"<span style=""font-style: italic; font-weight: 700; text-decoration-line: underline;"">8.3 Innate Cells<br></span>What do Macrophages and Monocytes do? <br> <br> <br> <br> ""<div class=""back""> <b><div>Macrophages:<span style=""font-weight: 400;""> Patrols tissues and are activated by phagocytosis, initiates bactericidal mechanisms and mechanism antigen presentation</span><br></div><div><br></div><div>Monocyte: <span style=""font-weight: 400;"">Makes up 10% of white blood cells and upon activation does phagocytosis, production of pro-inflammatory mediators, and recruited to tissues (which can differentiate into macrophages).</span><br></div><div><span style=""font-weight: 400;""><br></span></div><div><span style=""font-weight: 400;""><br></span></div></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">8.3 Innate Cells</span></div></b>What do Eosinophils, Basophils and Natural Killer Cells do? <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">8.3 Innate Cells</span><br></div><div><br></div><div>Eosinophil:<span style=""font-weight: 400;"">&nbsp;Found in low numbers in the blood, its granules contain enzymes that can attach to the cell wall of parasites but will also damage the host tissue. Facilitates the killing of anti-body coated parasites and has a role in allergic disease.</span><br></div><div><br></div>Basophil: <span style=""font-weight: 400;"">Found in low numbers in blood, its granules contain potent inflammatory mediators that aid in defense against parasites as it promotes allergic response and augmentation of anti-parasitic immunity.<br></span></b><b><br>Natural Killer: <span style=""font-weight: 400;"">Can kill host cells and produces chemical mediators known as cytokines.</span></b><br> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">8.3 Innate Cells<br></span></b>Describe the process of phagocytosis as well as the species used. <br> <br> <br> <br> ""<div class=""back""> <b>Phagocytosis: </b>Engulfment by the formation of a vesicle, initiated by recognition of microbes and phagocyte receptors then its engulfment is followed by the fusion of lysosomal enzymes with the microbe with the help of Arginine and Inducible nitric oxide synthase to form nitric oxide and then O2 with phagocyte oxidase to form a reactive oxygen species.<br><br>Device: AINOS + OOPO&nbsp;<br> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">8.3 Innate Cells<br></span></b>What is oponization and how is its components made? <br> <br> <br> <br> ""<div class=""back""> Opsonization: In the case when microbes are difficult to phagocytose, coating of microbe with proteins such as antibodies or complement facilitates phagocytosis. Acute phase proteins produced by the liver will bind to phosphocholine on bacteria and act as an opsonin. These proteins are recognized by specific receptors of the phagocyte.<br><br><b>Words Of Interest: Acute Phase Proteins, Phosphocholine, Opsonin</b><br> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">8.3 Innate Cells<br></span></b>What are the three different types of NK Cell Activation? <br> <br> <br> <br> ""<div class=""back""> <ul><li><div><b>NK Cell Activation:&nbsp;</b></div></li><ul><li><div><b>CD16:</b> Which is on NK cells binds to antibodies and activates it to kill antibody-coated cells, this is called antibody-dependant cell cytotoxicity (ADCC)</div></li><li><div><b>NKG2D:</b> Binds to NKG2D ligands that are upregulated to cellular and metabolic stress e.g infection and cancer and leads to death of the cell</div></li><li><div><b>MHC Class 1:</b> Present on all nucleated cells and engages inhibitory receptors on NK cells so it can be downregulated in viral infection and in cancer, this process is known as “missing self”.</div></li></ul></ul> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">8.4 Innate Immunology</span></div><div>Define PAMP's and descibe its two different types of forms in regards to the immune response.</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>PAMPs:<span style=""font-weight: 400;""> Pattern recognition receptors (PRRs) are receptors on innate cells, capable of recognizing Pathogen Associated Molecular Patterns (PAMPS), PRRs may be located on the cell surface, endosomal membranes, in the cytosol and may be in the form of Toll-Like Receptors (TLRs)</span></div></li><ul><li><div><span style=""font-weight: 400;"">Detection of PAMPs by PRRs can initiate an innate immune response; if it is a soluble PRR then it is a direct attack of microorganisms, it may enhance phagocytosis and cause a proteolytic cascade resulting in lysis. If it's a cell-associated PRR then phagocytosis takes place and the release of inflammatory mediators amplifies the response.</span></div></li></ul></ul></b> "
"<span style=""font-style: italic; font-weight: 700; text-decoration-line: underline;"">8.4 Innate Immunology<br></span>Define DAMP's and outline its effects on the immune system <br> <br> <br> <br> ""<div class=""back""> <b><br>DAMPs: <span style=""font-weight: 400;"">Danger Associated Molecular Patterns (DAMPS) are host proteins that are released during cell injury, in the case of a mild injury DAMP remains in the cell and regulated death (apoptosis) takes place so DAMP remains hidden and phagocytosis continues so immune cell remains quiet. But in severe injury where necrosis occurs, DAMP is released from cells so PRR recognizes it and an immune response happens.</span></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">8.5 Complement: Soluble Mediators</span></div></b>Define a complement and descrive its 3 different types of pathways in initiating a cellular response. <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Complement:<span style=""font-weight: 400;""> Collection of soluble proteins that upon activation can aid in the immune system by; promoting phagocytosis through opsonization, inducing an inflammatory response, and directly killing pathogens.&nbsp;</span></div></li><li><div>Cellular Response:</div></li><ul><li><div>Activation: <span style=""font-weight: 400;"">Can be done in 3 different types of pathways</span></div></li><ul><li><div>Classical: <span style=""font-weight: 400;"">Triggered by the presence of antibody-antigen complex.</span></div></li><li><div>Alternative: <span style=""font-weight: 400;"">Triggered by microbial surface structures.</span></div></li><li><div><b>Lectin: <span style=""font-weight: 400;"">Triggered by mannose residues on pathogen glycoproteins binding to host lectins.</span></b></div></li></ul></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">8.5 Complement: Soluble Mediators<br></span></b>List and explain the 3 ways that complements aid in the immune system via activation.<br>(Inflammation, Opsonisation and MAC's) <br> <br> <br> <br> ""<div class=""back""> <ul><li><div><b>Inflammation: </b>C3 proteins break down into C3a and C3b, both of these are powerful anaphylatoxins that cause mass cell degranulation and promote vasodilation and increase vascular permeability. The C5a is a chemotactic factor that causes the directed movement of leukocytes up a gradient concentration.<br></div></li><li><div><b>Opsonization:</b> <span style=""font-weight: 400;"">C3b becomes attached outside of the microbe and is recognized by complement receptor 1 on phagocytes and promotes phagocytosis and destruction of the pathogen.</span></div></li><li><div><b>Membrane Attack Complex (MAC’s): <span style=""font-weight: 400;"">C5 breaks down into C5a and C5b and the C5a portion increases inflammation while C5b triggers the formation of a membrane attack complex which contains multiple copies of C9 that results in the lysis of bacterial, virus-infected or tumor cells.</span></b></div></li></ul><div><b>Anecdote:</b><br></div><div><b>Protein Vs Death -&gt; Permeability, Vasodilation, Degranulation</b></div><div><b>A's causes metabolic stress while B's attatch</b></div><div></div> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">8.7 Cell Recruitment</span></div><div style=""""><b><span style=""font-weight: 400;"">Describe and explain the 3 stages of neutrophil recruitment</span></b><br></div> <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Neutrophil Recruitment:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul style=""font-weight: bold;""><li><div>Rolling: <span style=""font-weight: 400;"">Activation by inflammatory cytokines induces expression of E-selectin on the endothelium, and the weak interactions with carbohydrate ligands on the neutrophils, slow the movement, causing rolling.</span></div></li><li><div>Adhesion: <span style=""font-weight: 400;"">Chemokines induce conformation changes in integrins allowing leukocytes to adhere tightly to endothelial cells via interactions with their ligands causing adhesion and eventually tight binding.</span></div></li><li><div><b>Transmigration: <span style=""font-weight: 400;"">Cells can cross the blood vessel walls through extravasation with the chemokine CXCL8 (aka IL-8) directing the migration of neutrophils along its concentration gradient.</span></b></div></li></ul></ul><div><b>Words Of Interest:&nbsp;</b>E-selectin, CXCL8/IL-8</div><div><b>Menemonic</b><br></div><div><b>R</b><br></div><div><b>A</b></div><div><b>T</b></div> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">8.7 Antigens</span></div></b>Describe the the difference of recognition of B cells and T cells by their receptors and, the two types of pathways as well as what differntiates these pathways. <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Recognition:<span style=""font-weight: 400;""> B cells and T cells require their appropriate receptor to allow them to recognize foreign antibodies. BCR can directly recognize an antigen but TCR cannot directly recognize an antigen and must be processed into peptides in MHC before T cell recognition.</span></div></li><li><div><b>Presentation: <span style=""font-weight: 400;"">T cells cannot recognize foreign proteins directly and recognize the proteins they must be processed into peptides and bound to Human Leukocyte Antigen (HLA). For intracellular pathogens where the foreign body is made by a host cell, it's an MHC Class 1 pathway, From extracellular pathogens - MHC Class 2 pathway.</span></b></div></li></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">8.7 Antigens<br></span></b>Describe the MHC Class 1 pathway in terms of where antigen presentation occus, what is it recognized by, its conseuqnces, whats it marker, what are they expressed on and name them. <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>MHC Class 1: <span style=""font-weight: 400;"">For when foreign protein is made in presenting cell, these are recognized by cytotoxic T cells and they have the marker CD8 and act as a co-receptor for MHC class 1, the consequence is the death of presenting cell.</span></div></li><ul style=""font-weight: bold;""><li><div>Structure:<span style=""font-weight: 400;""> Expressed on all nucleated cells, encoded on chromosome 6. Three types; HLA-A, HLB and HLA-C. Most polymorphic genes and differ in peptide-binding characteristics.</span></div></li></ul></ul><div><b>MNEMONIC:</b><br></div><div><b>Help</b></div><div><b>Lord</b></div><div><b>Antibody</b></div><div><b><br></b></div><div><b>Dont</b></div><div><b>Praise</b></div><div><b>All</b></div> "
"<div class=""centeredbox""><div class=""leftalign""></div></div><div class=""centeredbox""><div class=""leftalign""></div></div><div><b><span style=""font-style: italic; text-decoration-line: underline;"">7.1 Genetic Material</span></b></div><div>Describe and explain the 3 laws of inheritance</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Laws Of Inheritance:</div></li><ul><li><div>Independent Segregation:<span style=""font-weight: 400;""> An individual gamete will contain only one of the two alleles present in other cells that are randomly selected.</span></div></li><li><div>Independent Assortment: <span style=""font-weight: 400;"">Chance determines which factor for a particular trait is inherited and that is not influenced by other genes.</span></div></li><li><div>Dominance: <span style=""font-weight: 400;"">One allele will be dominant over the other and the dominant allele is the one observed in the phenotype.</span></div></li></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">7.1 Genetic Material<br></span></b>Name a dominant and recessive genetic condition due to alleles <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Genetic conditions due to alleles:</div></li><ul><li><div>Dominant:<span style=""font-weight: 400;""> Colorectal cancer is a very common cancer and 3% is attributable to Lynch syndrome, these involve an autosomal mutation in one of the MMR genes (MLH1, MSH2/6, and PMS2).</span></div></li><li><div><b>Recessive: <span style=""font-weight: 400;"">Haemoglobin synthesis is controlled by two multigene clusters chromosomes 16 encoding ⍺-globins and 15 encoding β encoding-globins in β-Thalassaemia (where Cyprus has a carrier rate of about 15% anemia, headaches, and fatigues are common ailments.</span></b></div></li></ul></ul></b> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">7.2 DNA Replication</span></b></div><div>Describe the process of okazaki fragments (use the 3 types of polymerase to explain your answer)</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Strands: <span style=""font-weight: 400;"">DNA helicase initially unwinds duplex DNA to separate DNA and form a replication fork and separated into 2 different strands:</span></div></li><ul><li><div>Leading: <span style=""font-weight: 400;"">Replication factor C (RFC) attaches to proliferating cell nuclear antigen (PCNA) and polymerase ε</span></div></li><li><div>Lagging: <span style=""font-weight: 400;"">Initially primed by DNA polymerase α complex, which synthesizes short RNA/DNA initiator primer. RFC displaces Pol α from the lagging strand to initiative move from priming to elongation mode. The initiator primer is extended by PCNA/DNA polymerase δ to form Okazaki fragments. Pol δ displaces the RNA/DNA initiator primer into a 5’ flap structure and the flap endonuclease 1 recognizes the 5’flap and cleaves it. DNA ligase I seal the nick to create a fully functional continuous double-stranded DNA.</span></div></li></ul></ul>WOI: Replication Factor C, Proliferating Cell Nuclear Antigen</b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.3 Transcription</span></div><div><b><span style=""font-weight: 400;"">Describe some features of transcription such as; location of landmarks, features of strands, introns and their landmarks as well as the process.</span></b></div></b> <br> <br> Where is the CAAT and TATA box located?<br>What is added at the beginning and end of the strands?<br>What series of coding helps identify introns? <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.3 Transcription</span></div><ul><li><div>Control and Location:<span style=""font-weight: 400;""> Certain</span> <span style=""font-weight: 400;"">elements can influence whether transcription starts and what level of transcription which can be bound by transcription factors. At 25 bases upstream is the start of the TATA box with 75 being the CAAT box.</span></div></li><li><div>Eukaryote: <span style=""font-weight: 400;"">Three different RNA polymerases with polymerase 2 having 12 protein subunits that require 5 general transcription factor proteins. Termination signals ensure no need for extra hairpin structures however poly-A-tail that s 250 adenine residues long present with cleavage about 10 to 35 pairs from it, 5’ end cap present makes it more stable.</span></div></li><li><div>Splicing:<span style=""font-weight: 400;""> Introns present in genes that are mediated by spliceosomes by its removal, generally begin with GU and end with AG preceded by a pyrimidine-rich tract (UC)</span></div></li><li><div>Process:</div></li><ul><li><div>Initiation:<span style=""font-weight: 400;""> RNA polymerase binds to the DNA at the promoter, ATP is used then DNA polymerase splits DNA into 2 strands along its length.</span></div></li><li><div>Elongation: <span style=""font-weight: 400;"">RNA polymerase then moves along the transcription unit, synthesizing the RNA&nbsp; template and as it moves along it constantly unzips forward DNA and rezips the DNA strands.</span></div></li><li><div><b>Termination: <span style=""font-weight: 400;"">When the termination region is reached, RNA polymerase dissociates from the DNA and a newly formed strand of RNA is released.</span></b></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">7.4 Proteins</span></div><div>Name and describe abrnormal protein functions of both primary and secondary as well as its associated disease</div> <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Abnormal protein functions:&nbsp;</div></li><ul style=""font-weight: bold;""><li><div>Primary:</div></li><ul><li><div>Sickle Cell: <span style=""font-weight: 400;"">Mutations leading to misfolding.</span></div></li><li><div>Cystic Fibrosis: <span style=""font-weight: 400;"">Mutations leading to trapping of protein in the ER.</span></div></li><li><div>Duchene Muscular Dystrophy: <span style=""font-weight: 400;"">Mutations leading to premature stop codons so hence unfinished proteins.</span></div></li></ul><li><div>Secondary:</div></li><li><div><b>Amyloidosis Prions:<span style=""font-weight: 400;""> Accumulation of amyloid (proteins that have folded abnormally, aggregated together, and not easily broken down). And are when alpha-helix are turned into beta-pleated sheets to form extracellular deposits (associated with Alzheimer's), they can cause a chain reaction so that nearby normal prion proteins become abnormal. Prions are typically used in cell adhesion and ion channel activity.</span></b></div></li></ul></ul><b>ANECDOTE<br>PRIMARY:&nbsp;SM, CT, DMS. S&amp;M Rihanna, Exa'CT'ly what ive been yearning for, Give it 'D'o 'M'e S'trong</b><br><br> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">7.4 Proteins</span></b><div>In regards to amino-acids; Name the amino acids fore methionine and the stop codon, Features of methionine and cysteine as well as describe the wobble hypothesis.</div><div style=""""><br></div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Codons:&nbsp;</div></li><ul><li><div>Methionine: <span style=""font-weight: 400;"">Always the first amino acid and is AUG</span></div></li><li><div>Stop: <span style=""font-weight: 400;"">Causes termination of transcription and is UAA, UAG, and UGA.</span></div></li></ul><li><div>Methionine and Cysteine:<span style=""font-weight: 400;""> Both contain sulphur, methionine is always the first amino acid in a polypeptide chain. The free suphydryl group of cysteine is highly reactive and is often used in enzyme activity to attach various chemical groups to proteins, cysteine can form disulfide bonds.</span></div></li><li><div>Wobble Hypothesis: <span style=""font-weight: 400;"">Third base of a codon is the most degenerate, the corresponding anti-codon may base-pair with more than one codon due to wobble such as if Guanosine is sometimes modified to Inosine.</span></div></li></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">7.4 Proteins<br></span></b>Describe the process of protein translation <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Process:</div></li><ul><li><div>Initiation:<span style=""font-weight: 400;""> Begins with the small ribosomal sub-unit recognizing and binding to the start codon on the mRNA and tRNA carrying the anticodon for methionine binds to mRNA at the P-site of the complex, then the large ribosomal subunit attaches to the small one.&nbsp;</span></div></li><li><div>Elongation: <span style=""font-weight: 400;"">A second tRNA and its attached amino acid into the A-site and then the 1st amino acid is enzymatically transferred onto the 2nd one through a peptide bond. This process is repeated increasing the chain.</span></div></li><li><div><b>Termination: <span style=""font-weight: 400;"">Translation is terminated when it encounters one stop codon and the release factor recognizes it and settles into the A-site and an enzyme releases the polypeptide chain via hydrolysis causing dissociation from the chain.</span></b></div></li></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">7.5 Cell Structure And Function</span></b><br>Explain what do microtubules do and name and describe its 3 different functions. <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Microtubules: <span style=""font-weight: 400;"">Originate from Microtubule Organising Centre and consists of ⍺ and β tubulin, during mitosis they form the mitotic spindle centered around the MTOC to move chromosomes and deploy cytoplasmic organelles and shuttle vesicles. Can have different functions depending on the cilia:</span></div></li><ul><li><div>Primary: <span style=""font-weight: 400;"">Mainly cell signaling function.</span></div></li><li><div>Motile: <span style=""font-weight: 400;"">Coordinated movement.</span></div></li><li><div><b>Nodal: <span style=""font-weight: 400;"">Left-right development.</span></b></div></li></ul></ul>MNEMONIC:<br>Microtubes<br>Penis<br>Must<br>Nut</b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">7.5 Cell Structure And Function<br></span></b>Explain the functions of microfilaments and describe its 4 different types<br><b><span style=""font-style: italic; text-decoration-line: underline;""><br><br></span></b> <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Microfilaments: <span style=""font-weight: 400;"">Thin (5-7nm) and very flexible and filamentous polymers of actin proteins monomers. Functionally they aid in exocytosis and endocytosis and cell movement and maintaining cell shape.&nbsp; Can come in four different types depending on the region of the cell it is located in:</span></div></li><ul style=""font-weight: bold;""><li><div>Stress Fibers: <span style=""font-weight: 400;"">Contracile bundle</span></div></li><li><div>Cell Cortex: <span style=""font-weight: 400;"">Gel-like network</span></div></li><li><div>Lamellipodium: <span style=""font-weight: 400;"">Dendritic network</span></div></li><li><div><b>Filopodium: <span style=""font-weight: 400;"">Tight parallel bundle</span></b></div></li></ul></ul><b>ANECDOTE:<br>Fill -&gt; 5 guys - 1 = 4<br><br>MNEMONIC:<br>My&nbsp;<br>Single<br>Cell<br>Loves<br>Fries</b><br><br><br> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">7.5 Cell Structure And Function<br></span></b>Explain the functions of the intermediate filaments and describe its 5 different types<b><span style=""font-style: italic; text-decoration-line: underline;""><br></span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Intermediate: <span style=""font-weight: 400;"">Elongated protein molecules with a central helical domain forming a rope-like structure, easy to bend but difficult to break so helpful in anchoring adhesion complexes and stabilizing cell structure. Comes in 5 different types:</span></div></li><ul><li><div>1 and 2 (Epithelial):<span style=""font-weight: 400;""> Keratin</span></div></li><li><div>3: <span style=""font-weight: 400;"">Vimentin, Desmin, and glial bibrillary acidic protein</span></div></li><li><div>4 (Axonal): <span style=""font-weight: 400;"">Neurofilaments</span></div></li><li><div><b>5 (Nucleus): <span style=""font-weight: 400;"">Lamins (stabilizing the nuclear membranes).&nbsp;</span></b></div></li></ul></ul></b> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">7.6 Membrane Trafficking</span></b></div><div>Describe the steps of the membrane trafficking flow</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li>From ER to the Golgi:<br></li><ul><li><div>In the RER: <span style=""font-weight: 400;"">New proteins are translocated into the ER cisternae, oligosaccharides are added and chaperones help to fold proteins.</span></div></li><li><div>In the Cis Golgi Network: <span style=""font-weight: 400;"">Mannose-6-phosphate is added to future lysosomal enzymes, and oligosaccharides can be modified at this stage.</span></div></li><li><div>In the medial Golgi cistern: <span style=""font-weight: 400;"">Glycolysation of lipids occurs here and modification of oligosaccharides is possible, glycoproteins and glycolipids are sorted into specific vesicles at this stage.</span></div></li><li><div><b>In the Trans-Golgi network: <span style=""font-weight: 400;"">The final modification of sugars happens here and specific vesicles with different destinations are separated and sorted.</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.13 2,3-BPG</span></div></b>Describe the effects of 2,3-BPG on RBC's <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>2,3-BPG<span style=""font-weight: 400;"">: Once O2 is unloaded in the tissues 2,3 biphosphoglycerate (BPG) binds to beta chains. This binding induces conformational changes on all chains that prevent further O2 binding. When 2,3 BPG is low (such as in the lungs) it dissociates from the Hb so O2 binding is possible</span></div></li></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">7.15 Reception and Receptors<br></span></b>List and explain the features of the 3 types of receptors <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Ion Channel Coupled Receptors:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Can be ligand-gated, voltage-gated, mechanically-gated</span></div></li><li><div><span style=""font-weight: 400;"">Rapid synaptic signaling&nbsp;</span></div></li><li><div><span style=""font-weight: 400;"">Mediates most forms of electrical signaling in the nervous system</span></div></li><li><div><span style=""font-weight: 400;"">Most anesthetic work via these receptors</span></div></li><li><div><span style=""font-weight: 400;"">Done in milliseconds, the Nicotinic/ACh receptor</span></div></li></ul><li><div>G-Protein Receptors:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Seven-transmembrane domain receptor and Trimer GTP-binding protein (G-protein)</span></div></li><li><div><span style=""font-weight: 400;"">Target protein can be an enzyme or also ion channel</span></div></li><li><div><span style=""font-weight: 400;"">Done in seconds, Muscarcinic/ ACh receptor</span></div></li></ul><li><div>Enzyme Coupled Receptors:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Functions as or associated with enzymes (often kinases)</span></div></li><li><div><span style=""font-weight: 400;"">Heterogenous, mostly single transmembrane protein</span></div></li><li><div><span style=""font-weight: 400;"">Done in hours, Growth factor receptors, Cytokine receptors</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">7.16 Intracellular Signalling Molecules</span></div><div>List the 3 types of proteins associated with intraceullular signalling and explain what a molecular switch is<br></div> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint1c61a0c2749d8101').style.display='block'; return false;""> Hint</a> <div id=""hint1c61a0c2749d8101"" class=hint style=""display: none"">There is no signal inside the SPA!</div> ""<div class=""back""> <div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">7.16 Intracellular Signalling Molecules</span></div><ul style=""""><li style=""font-weight: bold;""><div>Types:</div></li><ul style=""""><li style=""font-weight: bold;""><div>Scaffold proteins:<span style=""font-weight: 400;""> Intracellular proteins activates one by one until the final protein is activated causing a signal</span></div></li><li style=""font-weight: bold;""><div>Phosphoinositide:&nbsp;<span style=""font-weight: 400;"">Due to different signalling proteins being phosphorylated and working together</span></div></li><li style=""font-weight: bold;""><div>Activated receptor:<span style=""font-weight: 400;"">&nbsp;Activated all at the same time on the same receptor and they all work together to cause downstream signals</span></div></li><li style=""font-weight: bold;""><div><b>Molecular switches: <span style=""font-weight: 400;"">Molecules that can be reversibly shifted between two stable states. Can be switched on and off through phosphorylation and/or GTP binding.</span></b></div></li></ul></ul><b>Anecdote: No Signal At the SPA<br></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">7.17 Apoptosis</span></div><div>Explain Apoptosis, list some of its features then describe capsase activation as well as list its 2 pathways and what triggers them.</div> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hintb6722310445b81ca').style.display='block'; return false;""> Hint</a> <div id=""hintb6722310445b81ca"" class=hint style=""display: none"">Dont forgot defining capsase activation!</div> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.17 Apoptosis</span></div><ul><li><div>Apoptosis: <span style=""font-weight: 400;"">Programmed cell death as a result of an intracellular ‘suicide’ program. Is a normal and essential event that is a fast process that resembles mitotic cells. Does not lead to the lysis of cells and does not damage neighboring tissue.</span></div></li><li><div>Apoptotic cell characteristics:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">Membrane Blebbing</span></div></li><li><div><span style=""font-weight: 400;"">Cell Shrinkage, Dense Cytoplasm</span></div></li><li><div><span style=""font-weight: 400;"">Nuclear fragmentation</span></div></li><li><div><span style=""font-weight: 400;"">Chromatin condensation</span></div></li><li><div><span style=""font-weight: 400;"">Chromosomal DNA fragmentation</span></div></li><li><div><span style=""font-weight: 400;"">mRNA degradation</span></div></li><li><div><span style=""font-weight: 400;"">Separation of cell fragments into apoptotic bodies</span></div></li><li><div><span style=""font-weight: 400;"">Organelle integrity and membranes still intact</span></div></li></ul><li><div>Apoptotic Signalling:</div></li><ul><li><div>Caspase Activation: <span style=""font-weight: 400;"">Proteolytic cascade is mediated by caspases (protease with cysteine, that cleave their target at specific aspartic acid) that can be executioner and initiator. This process is irreversible.</span></div></li><li><div>Two main pathways<span style=""font-weight: 400;"">:</span></div></li><ul><li><div>Intrinsic pathway:<span style=""font-weight: 400;""> Triggered by chemical radiations, loss of attachment to extracellular matrix or growth factor withdrawal, depending on mitochondria.</span></div></li><li><div>Extrinsic pathway:<span style=""font-weight: 400;""> Triggered by cell surface death receptors.</span></div></li></ul></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.1 Muscle<br></span></b>List and explain the 3 types of muscles and name some features such as structure and voluntary/involuntary <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint784c3a842456ba39').style.display='block'; return false;""> Hint</a> <div id=""hint784c3a842456ba39"" class=hint style=""display: none"">Remeber the picture!</div> ""<div class=""back""> <b><ul><li><div>Skeletal:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">Attached to the bone, supports and moves the skeleton</span></div></li><li><div><span style=""font-weight: 400;"">Fibres are striated, tubular, and multinucleated as well as parallel and long.</span></div></li><li><div><span style=""font-weight: 400;"">Actions are voluntary</span></div></li></ul><li><div>Cardiac:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">The muscle of the heart propels blood through the circulatory system</span></div></li><li><div><span style=""font-weight: 400;"">Fibers are striated, branched, and uni-nucleated.</span></div></li><li><div><span style=""font-weight: 400;"">Actions are involuntary</span></div></li></ul><li><div>Smooth:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Surrounds hollow organs of the body, controls the movement of contents through the organ and is capable of slow and sustained contractions</span></div></li><li><div><span style=""font-weight: 400;"">Fibers are non-striated, spindle-shaped, and uni-nucleated.</span></div></li><li><div><span style=""font-weight: 400;"">Actions are involuntary</span></div></li></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.1 Muscle<br></span></b><br>""Muscles consist of many histological layers and coverings that make up the entirety of the whole muscle""<br>Q: List all of these layers <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Structure:&nbsp;</div></li><ul><li><div>Muscle/Epimsyium: <span style=""font-weight: 400;"">Outermost connective tissue sheath, surrounding the entire muscle.</span></div></li><li><div>Fascicle/Perimysium: <span style=""font-weight: 400;"">Connective tissue sheath covering fasciculus.&nbsp;</span></div></li><li><div>Endomysium: <span style=""font-weight: 400;"">Innermost sheath at individual muscle fibers.</span></div></li><li><div>External Lamina</div></li><li><div>Muscle Fiber/Sarcolemma&nbsp;</div></li><li><div>Myofibril/ Sarcomere&nbsp;</div></li><li><div>Myofilaments/Actin and Myosin&nbsp;</div></li></ul></ul><div>MNEMONICS:</div><div>Episodes</div><div>Permitting</div><div>Endings</div><div>Lamenting</div><div>Lemons&nbsp;</div><div>Acting</div></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.2 Contractions</span></div><div style=""""><div style=""""><br></div><div style="""">""Muscles provide movement for the body through the act of contractions that come in many different types""<br></div><div style="""">Identify the 3 main types of muscle movement contractions as well as compare and contrast their differences</div></div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Reflexive Contractions: <span style=""font-weight: 400;"">Involuntary muscles.</span></div></li><li><div>Tonic Contractions: <span style=""font-weight: 400;"">When relaxed it’s still contracted.</span></div></li><li><div>Phasic Contractions: <span style=""font-weight: 400;"">Active muscle contractions</span></div></li><ul><li><div>Isotonic: <span style=""font-weight: 400;"">Muscles change in relation to movement.</span></div></li><ul><li><div>Concentric Contractions: <span style=""font-weight: 400;"">Muscle tension rise to meet the resistance and remains stable as the muscle shortens.</span></div></li><li><div>Eccentric Contractions: <span style=""font-weight: 400;"">Muscle lengthens as resistance becomes greater than the force the muscle is producing.</span></div></li></ul><li><div>Isometric Contractions: <span style=""font-weight: 400;"">Muscle length remains the same, no movement occurs but the force is increased to tonic levels.</span></div></li></ul><li><div>Roles:</div></li><ul><li><div>Prime mover:<span style=""font-weight: 400;""> Responsible for producing specific movement</span></div></li><li><div>Fixator: <span style=""font-weight: 400;"">Steadies the limb during isometric contractions</span></div></li><li><div>Synergist: <span style=""font-weight: 400;"">Complements the action of the prime mover</span></div></li><li><div>Antagonist: <span style=""font-weight: 400;"">Opposes the action of another muscle</span></div></li><li><div><b>Shunts: <span style=""font-weight: 400;"">Maintaining contact between articular + joints</span></b></div></li></ul></ul></b> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">1.3 Skeletal Systems</span></b></div><div>Explain the features of catrilages and name and identify its three types</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Cartilages:</div></li><ul><li><div><span style=""font-weight: 400;"">Semirigid, is an avascular form of connective tissue located in areas where flexibility is required. Their functions are supporting soft tissues, providing a smooth gliding surface for bone articulations at joints as well as enabling the development and growth of long bones.</span></div></li><li><div><span style=""font-weight: 400;"">There are three types:</span></div></li><ul><li><div>Hyaline: <span style=""font-weight: 400;"">Most common and found in ribs and trachea.</span></div></li><li><div>Elastic: <span style=""font-weight: 400;"">Found in intervertebral discs and joint capsules.</span></div></li><li><div><b>Fibrocartilage: <span style=""font-weight: 400;"">Located in the external ear and epiglottis.</span></b></div></li></ul></ul></ul></b> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">1.4 Joints</span></b></div><div>Descibe and list the two types of ways of the classification of bones</div> <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Joints: <span style=""font-weight: 400;"">Can be classified into two ways:</span></div></li><ul style=""""><li style=""font-weight: bold;""><div>Functionally:</div></li><ul style=""font-weight: bold;""><li><div>Synarthroses - <span style=""font-weight: 400;"">Immovable</span></div></li><li><div>Amphiarthrosis - <span style=""font-weight: 400;"">Partially movable</span></div></li><li><div>Diarthroses - <span style=""font-weight: 400;"">Freely Movable</span></div></li></ul><li style=""font-weight: bold;""><div>Type Of Material:</div></li><ul style=""font-weight: bold;""><li><div>Synovial - <span style=""font-weight: 400;"">Joint</span></div></li><li><div>Fibrous - <span style=""font-weight: 400;"">Fibrous</span></div></li><li><div><b>Cartilaginous - <span style=""font-weight: 400;"">Fibrocartilidge/Hyaline (Synchandroses present between ribs and sternum, Symphyses present in the vertebral disk.</span></b></div></li></ul></ul></ul><div><b>Anecdote:</b><br></div><div><b>Syn'Chan'droses -&gt; ""Can"" -&gt; Can a matchbox? No but a tin can! -&gt; Boxing dont hit ribs</b></div><div><b>Sym'phy'ses -&gt; Phyrexia -&gt; Weird vertebral disk (Surgical Extraction)</b></div> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.5 Nervous System<br></span></b>Name the structures of the meninges and describe the matter composition. <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: bold;""><li><div>Meninges: <span style=""font-weight: 400;"">Skull &gt; Dura Mater &gt; Arachnoid mater &gt; Subarachnoid mater &gt; Pia Mater &gt; Brain. CNS is protected by Meninges and cerebrospinal fluid.</span></div></li><li><div>Matter Composition: <span style=""font-weight: 400;"">In the brain, Grey matter surrounds the outside and inside while the White matter is between the two, but in the spinal cord white matter is on the outside and grey matter is on the inside.</span></div></li></ul><div style=""""><b>MNEMONIC:&nbsp;</b><br></div><div style=""""><b>Stop</b></div><div style=""""><b>Dying</b></div><div style=""""><b>At&nbsp;</b></div><div style=""""><b>Shitty&nbsp;</b></div><div style=""""><b>Places&nbsp;</b></div><div style=""""><b>Brian</b></div> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.5 Nervous System<br></span></b>List and number the types of spinal nerves and descibe the ganlionic fivers in Sympatheic and Parasympathetic nervous system <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: bold;""><li><div>Spinal Nerves:&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</div></li><ul><li><div>8 Cervical&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</div></li><li><div>12 Thoracic</div></li><li><div>5 Lumbar</div></li><li><div>5 Sacral</div></li><li><div>1 Coccygeal</div></li></ul><li><b>Ganglionic Fibers: <span style=""font-weight: 400;"">Automatic NS has relay nerves and no ganglia in the somatic pathway. Sympathetic NS has short preganglionic and long postganglionic fibers. Parasympathetic NS has long preganglionic and short preganglionic fibers.</span></b><br></li></ul><div style=""""><b>MNEMONIC:</b><br></div><div style=""""><b>8 Chickens</b></div><div style=""""><b>12 Turkeys Tacos</b></div><div style=""""><b>5 Leeks</b></div><div style=""""><b>5 Sambal</b></div><div style=""""><b>1 Cock</b></div> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">1.7 Muscle Stretch Reflex Circuit</span></b></div><div>Describe the muscle stretch reflex cicruit</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Circuit: <span style=""font-weight: 400;"">Made of a sensory neuron and a motor neuron and only has one synapse, this will only result in a passively stretched skeletal muscle that will contract. Damage to this system can cause the reflex to be absent (areflexia) or diminished (hyporeflexia).</span></div></li><ul><li><div><span style=""font-weight: 400;"">The system requires spinal nerves containing primary sensory neuron cell bodies and a spinal cord that has lower motor neuron cell bodies. In stretch receptors a skeletal muscle that's stretched by the opening of ion channels is recognized by the nervous system, this is measured by muscle spindles that monitor muscle length 24/7.</span></div></li><li><div><span style=""font-weight: 400;"">Extension at the elbow joint requires contraction of the triceps by the lower motor neurons and inhibition of the biceps by the muscle motor neuron by the inhibitory interneuron in the spinal cord. Glutamate released by the sensory neuron goes to a lower motor neuron which causes it to release ACh on the stretched muscle making it contract, the glutamate also goes to the inhibitory neuron causing reciprocal inhibition.</span></div></li></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.9 Circulation from the heart<br></span></b>Describe some features of coronary circulation <br> <br> Where does it drain into? <br> <br> ""<div class=""back""> <b>Coronary Circulation: <span style=""font-weight: 400;"">Refers to the oxygenated blood sent to the heart for functional purposes. The left and right coronary arteries form the coronary sulcus that branches around the interventricular sulci converging to the apex of the heart. These drain through the cardiac veins emptying into the right atrium.</span></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.9 Circulation from the heart<br></span></b>List the steps of conduction of the heart <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Conduction: <span style=""font-weight: 400;"">The SA Node sends impulses to;</span></div></li><ul style=""font-weight: bold;""><li><div>Internodal Tracts:<span style=""font-weight: 400;""> Stimulate contraction of the right atrium</span></div></li><li><div>Bachmann’s Bundle: <span style=""font-weight: 400;"">Stimulate contraction of the left atrium</span></div></li><li><div>AV Node: <span style=""font-weight: 400;"">Passing signals to the ventricles</span></div></li><li><div><b>Bundle of His: <span style=""font-weight: 400;"">Splits into right and left branches that continue to Purkinje fibers.</span></b></div></li></ul></ul><div><b>MNEMONICS:</b><br></div><div><b>Saying</b></div><div><b>Interesting</b></div><div><b>Back&nbsp;</b></div><div><b>Avoids</b></div><div><b>Bundles Of&nbsp;</b></div><div><b>Purple</b></div> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">1.10 Lymphatic System</span></b></div><div><div>Describe the lymphatic system</div></div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Lymphatic System:<span style=""font-weight: 400;""> A series of organs, vessels, and nodes that collect and filter excess tissue fluid (lymph) before returning it to the venous circulation</span></div></li><li><div>Function:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">Drains excess interstitial fluid from tissues into the venous system</span></div></li><li><div><span style=""font-weight: 400;"">To produce and transport immune cells (lymphocytes) that will mount an immune response against pathogens.</span></div></li><li><div><span style=""font-weight: 400;"">To transport dietary lipids from the GI tract into the blood.</span></div></li></ul><li><div>Drainage: <span style=""font-weight: 400;"">Lymph drains back into venous circulation near the heart. However, the duct via which it drains depends on where in the body the lymph is.</span></div></li><ul><li><div>Thoracic Duct:<span style=""font-weight: 400;""> Collects lymph from the left head, neck, thorax, upper limb, and lower half of the body (40 cm long)</span></div></li><li><div>Right Lymphatic Duct: <span style=""font-weight: 400;"">Collects lymph from the right head, neck, thorax, and upper limb (1cm long)</span></div></li></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.13 Digestive System</span></b><br>Describe and list the components of the lower GI tract such as the small and large intestine <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Lower GI tract:</div></li><ul style=""font-weight: bold;""><li><div>Small Intestine: <span style=""font-weight: 400;"">Extends from the pylorus to the ileocecal valve,&nbsp; composed of the duodenum, jejunum, and ileum. The primary function is the absorption of vitamins and nutrients including electrolytes, iron, carbohydrates, proteins, and fats.</span></div></li><li><div><b>Large Intestine: <span style=""font-weight: 400;"">Terminal Ileum &gt; Ascending colon &gt; Traverse colon &gt; Descending colon &gt; Sigmoid colon &gt; Rectum. The main function is water absorption and the production and absorption of vitamins.</span></b></div></li></ul></ul><div><b>MNEMONIC:</b><br></div><div><b>Small:</b></div><div><b>Python&nbsp;</b></div><div><b>Duos!</b></div><div><b>Jack</b></div><div><b>I'll Umm...</b></div><div><b>Ill!</b></div><div><b><br></b></div><div><b>Large Intestine:</b></div><div><b>Temperature&nbsp;</b></div><div><b>Ascending</b></div><div><b>Traps</b></div><div><b>Sigmoid&nbsp;</b></div><div><b>Rex</b></div><div><b><br></b></div> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.14 General Microanatomy of GI tract</span></div><div><span style=""font-weight: 400;"">Describe and list the general microanatomy of the GI tract</span><br></div></b> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint8e38eae80999533b').style.display='block'; return false;""> Hint</a> <div id=""hint8e38eae80999533b"" class=hint style=""display: none""><b><div>MNEMONIC:</div><div>Episodes</div><div>Lasting Production</div><div>Must</div><div>Submit&nbsp; Plainy</div><div>Must&nbsp;</div><div>Advertise</div></b></div> ""<div class=""back""> <b><ul><li><div>Mucosa:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Epithelium: <span style=""font-weight: 400;"">Covers the inner surface of the digestive tract, starts as stratified squamous epithelial in esophagus and changes to simple columnar epithelium in the stomach. In the intestine it remains columnar but acquires microvillia to increase the surface area for absorption. Lies on the basement membrane.</span></div></li><li><div>Lamina Propria: <span style=""font-weight: 400;"">Thin layer of loose connective tissue.</span></div></li><li><div>Muscularis Mucosae: <span style=""font-weight: 400;"">Relatively thin layer of smooth muscle.</span></div></li></ul><li><div>Submucosa:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Submucosal plexus: <span style=""font-weight: 400;"">A set of large blood vessels, lymhatics and neuronrs.</span></div></li><li><div>Submucosal glands: <span style=""font-weight: 400;"">Layer of dense connective tissue.</span></div></li></ul><li><div>Muscularis:&nbsp;</div></li><ul><li><div>Myentric Plexus: <span style=""font-weight: 400;"">A layer of smooth muscles.</span></div></li><li><div>Plexus Of Auerbach: <span style=""font-weight: 400;"">Lies between circular and longitudinal layers of smooth muscle and contract to produce persitalsis.</span></div></li></ul><li><div>Serosa/Adventita</div></li></ul><div>Summed Up:</div><div>Outside -&gt; Connective (Lam), Smooth (Mus), Connective (Sub), Smooth (Mus)</div><div><br></div><div>Anecdote</div><div>SEE A SEC! -&gt; Stratified Squamous, Simple Columnar</div><div><br></div><div>MNEMONIC:</div><div>Episodes</div><div>Lasting Production</div><div>Must</div><div>Submit&nbsp; Plainy</div><div>Must&nbsp;</div><div>Advertise</div></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.16 Kidneys</span></div></b>Describe the structures of kidneys and describe the uretheras sphincter <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> Nephrons act as functional units of the kidney and are the place where filtration and urine production occurs. They mostly lie within the renal cortex.</span></div></li><li><div>Structure: <span style=""font-weight: 400;"">Renal cortex surrounds the kidney and extends inwards at points to form renal columns within the renal medulla that divides it into triangular-shaped tissues known as renal pyramids.</span></div></li><li><div>Renal Medullas:<span style=""font-weight: 400;""> Collect urine and transfers them into the minor calyces and then the major calyces. These drain into the widened areas of the kidney known as the renal pelvis, the renal pelvis leaves the kidney at the hilum and thins to continue as the ureter.</span></div></li><li><div>Urethra: <span style=""font-weight: 400;"">In males usually surrounded by the prostate before passing through the pelvic floor whilst in females it passes directly through the pelvic floor.Has two associated muscles:</span></div></li><ul><li><div>Internal Sphincter: <span style=""font-weight: 400;"">Keeps bladder neck and urethra free of urine until pressure builds in the bladder, Involuntary smooth muscle</span></div></li><li><div><b>External Sphincter: <span style=""font-weight: 400;"">Controls release of urine from the urethra. Voluntary skeletal muscle.</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.17 Reproductive System - Male</span></div></b>Explain what is the Ductus Deferens, Seminal Vesicle and Ejaculatory Vessel <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Ductus Deferens (External/Internal): <span style=""font-weight: 400;"">Transports sperm towards the ejaculatory duct during ejaculation.</span></div></li><li><div>Seminal Vesicles (Internal): <span style=""font-weight: 400;"">Accessory glands that contribute fluid to ejaculate.</span></div></li><li><div>Ejaculatory Vesicles (Internal): <span style=""font-weight: 400;"">Fusion of a ductus deferens and seminal vesicles to transmit ejaculate to the urethra.</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.18 Reproductive System - Female</span></div><div style="""">Explain the features of the ovary, uterine tube and uterus</div> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.18 Reproductive System - Female</span></div><ul><li><div>Ovary (Internal):<span style=""font-weight: 400;""> Site of egg production, Ovulates mature eggs towards the uterine tubes</span></div></li><li><div>Uterine tube (Internal):<span style=""font-weight: 400;""> ‘Catch’ ovulated eggs. Transports eggs/zygotes to the uterus which causes fertilization.</span></div></li><li><div>Uterus (Internal): <span style=""font-weight: 400;"">Muscular organ that can expand during pregnancy and where implantation of the zygote should occur and fetus growth takes place.</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.1 Heart Location and Mediastinum</span></div><div><span style=""font-style: italic; text-decoration-line: underline;"">1.2 Orientation of the heart</span></div><div><span style=""font-weight: 400;"">Describe the location of the heart as well as its orientation in terms of location and base and where does it move if cardiomegaly</span><br></div></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Location:<span style=""font-weight: 400;""> Located between the 2nd rib and 5th intercostal space, it is between vertebral levels T4-T9 and when supine T4/T5-T8 and if they are standing T6-T9 extends from the right medial border of the sternum to having its apex at the midclavicular line on the left. This can be changed due to cardiomegaly or it can be displaced where it usually moves inferiorly and laterally towards the axilla.</span></div></li><li><div>Base:<span style=""font-weight: 400;""> It is the posterior surface of the heart. Mainly in contact with the posterior mediastinum, the esophagus is immediately posterior and fixed to the pericardial wall at T5-T8 vertebral levels (moves one up when standing).</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.3 Pericardium</span></div><div><span style=""font-weight: 400;"">Describe the pericardium in terms of its layers and what it is supplied by</span><br></div></b> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hintb71e013ec4506582').style.display='block'; return false;""> Hint</a> <div id=""hintb71e013ec4506582"" class=hint style=""display: none"">VAN! And what is the most common one? A to Z and V to G</div> ""<div class=""back""> <b><ul><li><div>Pericardium:<span style=""font-weight: 400;""> The hearts and the roots of the great vessels are contained within the middle mediastinum in a specialized fibrous sac called the pericardium. Can be divided into:</span></div></li><ul><li><div><span style=""font-weight: 400;"">Fibrous Pericardium</span></div></li><li><div><span style=""font-weight: 400;"">Serous Pericardium</span></div></li><ul><li><div><span style=""font-weight: 400;"">Parietal Layer</span></div></li><li><div><span style=""font-weight: 400;"">Pericardial Layer</span></div></li><li><div><span style=""font-weight: 400;"">Visceral Layer</span></div></li></ul></ul><li><div>Pericardium Generally Supplied by:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Venous: <span style=""font-weight: 400;"">Azygos system, internal thoracic and superior phrenic veins</span></div></li><li><div><span style=""font-weight: 400;""><span style=""font-weight: 700;"">Arterial:&nbsp;</span>Branches from internal thoracic, pericardiophrenic, musculophrenic, and superior phrenic arteries, and the descending thoracic aorta.<br></span></div></li><li><div>Nervous: <span style=""font-weight: 400;"">Vagus nerve, sympathetic trunk, and phrenic nerves.</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.4 Pericardium: Clinical</span></div><div style="""">Describe the ailments associated with the epicardium</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Excess Fluid:<span style=""font-weight: 400;""> Fluid including blood can build up in the pericardial sac from aortic aneurysms, heart attacks, or penetrating injuries that may lead to pericardial effusion. This can put pressure on the heart as it cannot function well in a filled pericardium.</span></div></li><li><div>Cardiac Tamponade:<span style=""font-weight: 400;""> Fluid has accumulated too fast, and the heart is pressurized and can cause lots of distress to a patient, in order to treat this fluid must be withdrawn using a needle and syringe (pericardial tap/ pericardiocentesis)</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.5 Heart Chambers: Right Atrium</span></div><div><span style=""font-weight: 400;"">Describe the structures of the right atrium of the heart</span><br></div></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> Right atrium collects deoxygenated blood from 3 sources and transports them to the right ventricle to the right atrioventricular valve knowns as the tricuspid valve. (there is also small openings for the smallest cardiac veins along the surface of the atrium):</span></div></li><ul><li><div><span style=""font-weight: 400;"">Superior Vena Cava</span></div></li><li><div><span style=""font-weight: 400;"">Inferior Vena Cava</span></div></li><li><div><span style=""font-weight: 400;"">Coronary Sinus</span></div></li></ul><li><div>Internal Structures:<span style=""font-weight: 400;""> Internally it has two surfaces, divided by the crista terminalis:</span></div></li><ul><li><div><span style=""font-weight: 400;"">Smooth surface posteriorly called the sinus of venae cavae (both venae cavae drain here)</span></div></li><li><div><span style=""font-weight: 400;"">Smooth muscular ridged surface anteriorly called the atrium proper</span></div></li><ul><li><div><span style=""font-weight: 400;"">Also covered in ridges called pectinate muscles.</span></div></li><li><div><span style=""font-weight: 400;"">A structure called the right auricle helps the atrium hold more blood</span></div></li></ul></ul><li><div>Separation: <span style=""font-weight: 400;"">Separated from the left atrium via the interatrial septum, this has a depression known as fossa ovalis which is a remnant of foramen ovale that is present before birth. Failure of this to close after birth can lead to patent foramen ovale where some blood can pass straight to the left atrium.</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.6 Heart Chambers: Right Ventricle</span></div><div style="""">Describe the structure of the right ventricle of the heart</div> <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: bold;""><li><div>Overview:<span style=""font-weight: 400;""> Collects deoxygenated blood from the right atrium. From the right ventricle, blood passes to the pulmonary trunk taking deoxygenated blood to the lungs, through the right semi-lunar valve known as the pulmonary valve.</span></div></li><li><div>Outer Structures:</div></li><ul><li><div>Trabeculae Carnae: <span style=""font-weight: 400;"">The majority of the surface of the right ventricle is covered in muscular structures called ‘trabeculae carnae’, these are irregularly arranged around the walls, sometimes forming ridges or connecting with each other. They serve as attachments for structures called chordae tendinae that are fibrous tendon like chords that attach on to the cusps of the tricuspid valve</span></div></li></ul><li><div>Spetomarginal Trabecula: <span style=""font-weight: 400;"">Exists from the lower portion of the interventricular septum to the papillary, Also known as the moderator band, and is important in cardiac conduction.</span></div></li><li><div>Exit:<span style=""font-weight: 400;""> Towards the exit of the right ventricle there is the conus arteriosus that has smooth walls</span></div></li></ul><b>MNEMONIC:<br>TraCa ChTen (Cotten) SpeTra</b><br><br> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.7 Heart Chambers: Left Atrium</span></div><div style="""">Describe the structure of the left atrium of the heart</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> Left atrium collects oxygenated blood from the 4 pulmonary veins ( 2 left and 2 right) There is also a left auricle. Similar to the left atrium it has 2 distinct surfaces;</span></div></li><ul><li><div><span style=""font-weight: 400;"">The posterior surface is smooth-walled and is where the inflow from the pulmonary veins is.</span></div></li><li><div><span style=""font-weight: 400;"">The interior surface is covered in pectinate muscles.</span></div></li><li><div><span style=""font-weight: 400;"">Unlike the right atrium, no distance structure divides these two surfaces</span></div></li></ul><li><div>Septum:<span style=""font-weight: 400;""> The interatrial septum also has the other side of the fossa ovalis, however on this side, it is known as the valve of the foramen ovale.</span></div></li><li><div>Travel: <span style=""font-weight: 400;"">From the left atrium, blood passes to the left ventricle through the left atrioventricular valve known as the bicuspid or Mitral valve.</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.8 Heart Chambers: Left Ventricle</span></div></b>Describe the structure of the left ventricle of the heart <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: bold;""><li><div>Overview:<span style=""font-weight: 400;""> The left ventricle collects oxygenated blood from the left atrium. The left ventricle is longer, larger, and has a thicker layer of myocardium than the right ventricle because blood needs to get pumped to the rest of the body.</span></div></li><li><div>Structures:<span style=""font-weight: 400;""> Like the right ventricle it has similar structures:</span></div></li><ul><li><div>Trabeculae Carnae: <span style=""font-weight: 400;"">More delicate and fine than those of the right ventricle which appear more tortuous</span></div></li><li><div>Papillary Muscles:<span style=""font-weight: 400;""> Larger than in the right ventricle</span></div></li><li><div>Chordae Tendinae</div></li></ul><li><div>Septum:<span style=""font-weight: 400;""> Divided from the right ventricle by the interventricular septum which can be divided into two parts:</span></div></li><ul><li><div>Muscular Part:<span style=""font-weight: 400;""> Thickest and largest part&nbsp;</span></div></li><li><div>Membranous Part:<span style=""font-weight: 400;""> Thin and forms the upper part (short downward extension of the fibro collagenous tissue of the aortic valve ring from the cardiac skeleton.</span></div></li></ul><li><b>Exit/Travel: <span style=""font-weight: 400;"">Towards the exit of the left ventricle there is the aortic vestibule which has smooth walls. From the left ventricle, blood passes to the ascending aorta taking oxygenated blood to the body, through the left semi-lunar valve known as the aortic valve.</span></b><br></li></ul><b>MNEMONIC<br></b>TraCar, Papi, Cotton<br><br> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.9 Cardiac Skeleton</span></div><div><span style=""font-weight: 400;"">Describe the cardiac skeleton as well as its abnormalities</span><span style=""font-style: italic; text-decoration-line: underline;""><br></span></div></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Cardiac Skeleton:<span style=""font-weight: 400;""> In between the atria and the onward vessels of the heart there is a structure known as the cardiac skeleton which contains fibrous connective tissue that acts as the strut for the attachment of the cusps of the valves (this ensures structures always remain open).</span></div></li><li><div>Abnormalities</div></li><ul><li><div>Stenosis:<span style=""font-weight: 400;""> Narrowing of the valves meaning they don't open properly</span></div></li><li><div><b>Regurgitation: <span style=""font-weight: 400;"">Valve is compromised and cannot close properly</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.10 Heart Wall: Layers</span></div><div><span style=""font-weight: 400;"">Describe the histology/layers of skin of the heart in terms of epicardium</span><br></div></b> <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Epicardium:</div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Serous pericardium composed of compact fibrocollagenous and elastic tissue, with an internal lining of flat mesothelial cells that is that internal surface of the pericardial sac.</span></div></li><li><div><span style=""font-weight: 400;"">In conditions such as pericarditis, the smooth lining can be lost and cause pericardial friction rub as the two layers scratch together due to abnormal roughening</span></div></li><li><div><span style=""font-weight: 400;"">Fibrocollagenous layer also contains coronary vessels running on the surface of the heart, as well as epicardial fat. This superficial location is significant as it allows coronary bypass grafts to be performed.</span></div></li></ul></ul>Meso-Heart<br><br> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.11 Heart Conduction</span></div></b>Describe the process of heart conduction <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Conduction System:</div></li><ul><li><div>SA node:<span style=""font-weight: 400;""> Pacemaker of the heart</span></div></li><li><div>Internodal: <span style=""font-weight: 400;"">Stimulates contraction of right atrium</span></div></li><li><div>Baachmanns Bundle: <span style=""font-weight: 400;"">Contracts at the same time as right atrium contraction</span></div></li><li><div>AV Node: <span style=""font-weight: 400;"">Sends impulses to stimulate contraction of ventricles</span></div></li><li><div>Bundle of His:<span style=""font-weight: 400;""> Collection of nerve fibers extending into the interventricular septum.</span></div></li><li><div><b>Purkinje Fibers: <span style=""font-weight: 400;"">A series of smaller terminal branches that stimulate muscle cells to contract.</span></b></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.12 Sympathetic Innervation</span></div><div>Describe what constitutes reffered pain</div> <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Referred Pain:<span style=""font-weight: 400;""> Visceral sensory neurons from the myocardium enters the spinal cord at the same segmental levels at T1-T4 nerves which provide sensation to the skin. Occur because the brain cannot distinguish between sensory input from visceral sensory neurons within the ANS and spinal nerves from the somatic nervous system.</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Cardiac Plexus (Sympathetic innervation to the heart)</span></div></li><li><div><span style=""font-weight: 400;"">Cervical And Splanchnic nerves</span></div></li><li><div><span style=""font-weight: 400;"">(Post-sympathetic neurons)</span></div></li><li><div><span style=""font-weight: 400;"">Cervical and Thoracic ganglia</span></div></li><li><div><span style=""font-weight: 400;"">(Pre-sympathetic neurons)</span></div></li><li><div><span style=""font-weight: 400;"">CNS Spinal cord (T1-T4)</span></div></li></ul><li style="""">Sensory Visceral + Sensory Input /=/&nbsp; Somatic Nervous And Spinal</li></ul><b>MNEMONIC<br>VISS</b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.11 Coronary Circulation</span></div></b>Describe coronary circulation in terms of right and left coronary artery <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hintec965d07911994e1').style.display='block'; return false;""> Hint</a> <div id=""hintec965d07911994e1"" class=hint style=""display: none"">Rabies, Rams And Licking!</div> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Right Coronary Artery: <span style=""font-weight: 400;"">Descends vertically in the coronary sulcus between the right atrium and ventricle</span>. <span style=""font-weight: 400;"">It curves posteriorly and gives off a small branch to the AV node before branches as the posterior interventricular branch in the posterior interventricular sulcus (Posterior descending Artery), where it connects with its anterior half.</span></div></li><li style=""font-weight: bold;""><div>&nbsp;<span style=""font-weight: 400;"">It gives off multiple branches like:</span></div></li><ul style=""font-weight: bold;""><li><div>Atrial Branch: <span style=""font-weight: 400;"">Onto Sinu-atrial branch which supplies the SA node.</span></div></li><li><div>Right Marginal Artery: <span style=""font-weight: 400;"">Continues to the apex of the heart</span></div></li></ul><li style=""font-weight: bold;""><div>Left Coronary Artery:<span style=""font-weight: 400;""> Enters the coronary sulcus and divides into two branches:</span></div></li><ul style=""font-weight: bold;""><li><div>Anterior interventricular branch: <span style=""font-weight: 400;"">Continues towards the apex of the heart in the anterior interventricular sulcus and this branch is sometimes called the left anterior descending artery/</span></div></li><li><div>Circumflex Branch: <span style=""font-weight: 400;"">Curves round left in the coronary sulcus and ends just before the posterior interventricular sulcus where it gives off the left marginal artery which continues across the rounded obtuse edge of the heart.</span></div></li></ul></ul><b>MNEMONIC<br>RAM<br>LIC</b><br><br> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.14 Clinical Setting</span></div><div>Describe clinical diseases associated with the heart and its treatment (as well as how treat them and what does it require)</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Coronary Artery Bypass:<span style=""font-weight: 400;""> For when coronary arteries have become obstructed and revascularisation must occur by grafting an artery from elsewhere in the body to bypass the obstructed artery. Such as;</span></div></li><ul><li><div><span style=""font-weight: 400;"">Great Saphenous Vein: Leg</span></div></li><li><div><span style=""font-weight: 400;"">Internal Thoracic Artery: Thorax</span></div></li><li><div><span style=""font-weight: 400;"">Radial Artery: Arm</span></div></li></ul><li><div>Angiogenesis:</div></li><ul><li><div><span style=""font-weight: 400;"">Budding of new blood vessels to aid with revascularization</span></div></li><li><div><span style=""font-weight: 400;"">Vital for establishing blood flow to damaged areas</span></div></li><li><div><span style=""font-weight: 400;"">Can create more capillary networks or even connect two blood vessels</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.13 Circulatory System: Fetus To Adult</span></div><div><b><span style=""font-weight: 400;"">Describe the strucure of the circulatory system in the fetus</span></b></div></b> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint4338fe17b01a3b77').style.display='block'; return false;""> Hint</a> <div id=""hint4338fe17b01a3b77"" class=hint style=""display: none"">Ovale, Arteries and Veins (30)</div> ""<div class=""back""> <b><ul><li><div>Fetal:<span style=""font-weight: 400;""> Three vascular shunts (When blood comes elsewhere) exist in fetal circulation to allow blood to bypass the liver and non-functioning lungs.</span></div></li><ul><li><div>Foramen ovale:<span style=""font-weight: 400;""> Between the atria, Blood bypasses the pulmonary circulation</span></div></li><li><div>Ductus arteriousis: <span style=""font-weight: 400;"">Links the distal arch of the aorta with the pulmonary trunk, and blood bypasses the pulmonary circulation.</span></div></li><li><div>Ductus venosus: <span style=""font-weight: 400;"">Shunts 30% of umbilical blood from the primitive liver to the inferior vena cava to ensure enough oxygen reaches the developing brain</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.17 Structure of vascular structures</span></div><div>Describe the structure of the vascular structures (Tunica...)</div> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Structure of vascular structures</span></div><ul><li><div>Tunica Intima:<span style=""font-weight: 400;""> Innermost layer that is lined by the endothelium comprised of simple squamous epithelial cells. The basement membrane and connective tissue support overlying cells.</span></div></li><li><div>Tunica Media:<span style=""font-weight: 400;""> Intermediate and is a smooth muscular layer that contains alpha and beta receptors allowing for sympathetic regulation of blood pressure,</span></div></li><li><div>Tunica Externa: <span style=""font-weight: 400;"">Outermost layer that anchors vessels to organs. It is comprised of type 1 collagen and elastic connective tissue (in arteries)</span></div></li></ul><br></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.23 Lymphatic System: Return Process</span></div><div>Describe features of the lymphatic system</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Return Process:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">Fluid leaves the blood capillaries (due to hydrostatic pressure) and enters the interstitial space.</span></div></li><li><div><span style=""font-weight: 400;"">Fluid enters the lymphatic system through the lymphatic capillaries within the interstitial space, which unit to form lymphatic vessels.</span></div></li><li><div><span style=""font-weight: 400;"">Lymph flow is slow, in one direction, and passes through a series of lymph nodes before draining into lymphatic trunks (collecting vessels)</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.24 Great Vessels: Aorta</span></div><div>Describe the great vessels associated with the Aorta (in terms of arteries!)</div> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hintb3cd446d2e422bc6').style.display='block'; return false;""> Hint</a> <div id=""hintb3cd446d2e422bc6"" class=hint style=""display: none"">Bitches BCC</div> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Overview: <span style=""font-weight: 400;"">After leaving the left ventricle via the aortic valve the ascending aorta gives off the right and left coronary arteries. It then forms the aortic arch which branches off to multiple important arteries:</span></div></li><ul style=""font-weight: bold;""><li><div>Brachiocephalic artery:</div></li><ul><li><div>Right subclavian artery: <span style=""font-weight: 400;"">Supplies the right upper limb and some head and neck</span></div></li><li><div>Right common carotid artery: <span style=""font-weight: 400;"">Supplies the right head and neck including the brain</span></div></li></ul><li><div>Left common carotid artery: <span style=""font-weight: 400;"">Supplies the left head and neck (including the brain)</span></div></li><li><div>Left subclavian artery: <span style=""font-weight: 400;"">Supplies the left upper limb and some head and neck.</span></div></li></ul><li><div><b>Carotid Sinus:</b>&nbsp;Proximal internal carotid artery (near the bifurcation of common carotid artery) its baroreceptors are sensitive to blood pressure</div></li><li><div><b>Carotid Body:<span style=""font-weight: 400;"">&nbsp;At birufication of the common carotid artery and its chemoreceptors are sensitive to O2 levels</span></b></div></li></ul><br> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.25 Great Vessels: Venae Cavae</span></div><div><span style=""font-weight: 400;"">Describe the great vessels regarding the Venae Cavae (in terms of veins)</span><br></div></b> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hintff0a3cdccbc453cb').style.display='block'; return false;""> Hint</a> <div id=""hintff0a3cdccbc453cb"" class=hint style=""display: none"">Jugs and Subs from start to end</div> ""<div class=""back""> <b><ul><li><div>Right Branchiocephallic Vein:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Right Internal Jugular Vein: <span style=""font-weight: 400;"">Drains right head and neck</span></div></li><li><div>Right Subclavian: <span style=""font-weight: 400;"">Drains right upper limb that receives a contribution from the right external jugular</span></div></li></ul><li><div>Left Brachiocephalic Vein:</div></li><ul><li><div>Left Internal Jugular Vein: <span style=""font-weight: 400;"">Drains the left head and neck</span></div></li><li><div>Left Subclavian Vein: <span style=""font-weight: 400;"">Drains from the left upper limb</span></div></li></ul><li><div><b>Azygos Vein: <span style=""font-weight: 400;"">Enters the superior vena cava just before it drains into the right atrium.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.26 The Thoracic Cage</span></div><div>Describe the structures and features of the sternum and in temrs of facets</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Sternum:<span style=""font-weight: 400;""> Consisting of 3 parts being the Manubrium, Body, and Xiphoid process. The sternal angle AKA the angle of Louis where the Manubrium joins the body of the sternum at the T4 vertebrae, its superior aspect is concave and produces a depression called the jugular notch which is visible underneath the skin. Costal cartilages attach to the ribs anteriorly.</span></div></li><ul><li><div><span style=""font-weight: 400;"">On either side of the jugular notch are large fossa and these articulate with the medial ends of the clavicles forming the sternoclavicular joints.</span></div></li><li><div><span style=""font-weight: 400;"">On the lateral edges of the manubrium, there is a facet (attachment point) for articulation with the costal cartilage of the 1st rib, and a demifacet for articulation with part of the costal cartilage of the 2nd rib.</span></div></li><li><div><span style=""font-weight: 400;"">The lateral edges of the body of the sternum are marked by articular facets which articulate with the costal cartilages of ribs 3-6. There are 2 smaller demi-facets for ribs 2 and 7.</span></div></li><li><div><span style=""font-weight: 400;"">The xiphoid process is the smallest part of the sternum and is located in the T10 vertebrae, largely cartilaginous and completely turns to bone in adulthood, each side of its upper lateral margin is a demi-facet for articulation with the inferior end of the 7th costal cartilage.</span></div></li></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.26 The Thoracic Cage<br></span></b>Describe the structures of ribs as well as what is its classifications in terms of position and shape <br> <br> Name the typical and atypical <br> <br> ""<div class=""back""> <b><ul><li><div>Ribs: <span style=""font-weight: 400;"">A set of 12 pairs of bones that protect the thorax and have a role in breathing during chest expansion the ribcage moves to permit lung inflation.&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">That is classified into 3 different types by its position:</span></div></li><ul><li><div>True ribs: <span style=""font-weight: 400;"">Ribs 1-7 that articulate directly with the sternum.</span></div></li><li><div>False ribs: <span style=""font-weight: 400;"">Ribs 8-10 that attach to coastal cartilages superior to them (joint).</span></div></li><li><div>Floating ribs: <span style=""font-weight: 400;"">Have no anterior connection with other ribs or the sternum.</span></div></li></ul><li><div><span style=""font-weight: 400;"">They can also be classified by their shape:</span></div></li><ul><li><div>Typical (Ribs 3-9 classified as this):</div></li><ul><li><div>Head:<span style=""font-weight: 400;""> Have 2 articular facets separated by the wedge of bone with a higher and lower facet articulating with the corresponding vertebrae.</span></div></li><li><div>Neck: <span style=""font-weight: 400;"">Tubercle present which is a facet for articulation with the traverse process of the corresponding vertebrae.</span></div></li><li><div>Shaft:<span style=""font-weight: 400;""> Flat and curved with the internal surface having a coastal groove that protects blood vessels and nerves.</span></div></li></ul><li><div>A-typical ribs:</div></li><ul><li><div>Rib 1:<span style=""font-weight: 400;""> Shorter and wider than the other ribs, has only 1 facet for articulation and a superior surface marked by two grooves that make way for the subclavian vessels.</span></div></li><li><div>Rib 2: <span style=""font-weight: 400;"">Thinner and longer than rib 1 and has articular facets but contains a roughened area on its upper surface where the serratus anterior muscle attaches.</span></div></li><li><div>Rib 10:<span style=""font-weight: 400;""> Only has one facet for articulation.</span></div></li><li><div><b>Rib 11 and 12: <span style=""font-weight: 400;"">Articulates only with their own body and has no tubercle or necks, both ribs are short and curve very little.</span></b></div></li></ul></ul></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.26 The Thoracic Cage<br></span></b>Describe the costovertebral joints as well as what are the 2 types <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Costovertebral joints: <span style=""font-weight: 400;"">Twelve thoracic vertebrae are medium-sized and increase in size from superior to inferior, specialised function is to articulate with ribs. Each one has two demi-facets placed above each other on either side of its vertebral body. Each rib has two joints:</span></div></li><ul><li><div>Costovertebral joint: <span style=""font-weight: 400;"">Between the head of the rib, the superior costal facet of the corresponding vertebrae, and the inferior costal facet of the vertebrae above.</span></div></li><li><div><b>Costranverse joint: <span style=""font-weight: 400;"">Between the tubercle of the rib and the transverse process of the corresponding vertebrae.</span></b></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.27 The Respiratory Tract</span></div><div>Describe the upper anatomy of the respiratory tract in terms of conchae, oral cavity and pharynx</div> <br> <br> What is the use of the Conchae?<br>What is the different types of Pharynx?<br> <br> <br> ""<div class=""back""> <b><ul><li><div>Conchae:<span style=""font-weight: 400;""> Air enters the nose via the nasal cavity on the lateral wall of each nostril lies 3 bones covered in layers of mucosa. Its function is to increase surface area and spin the air so that inhaled air can be warmed and moistened ready to travel to the lungs to allow effective gaseous exchange.</span></div></li><li><div>Oral Cavity:<span style=""font-weight: 400;""> Acts as an air inlet in addition to the nasal cavity and lies inferior to the nasal cavity. The oral cavity is bordered superiorly by a hard palate and a soft palate posteriorly. The soft palate ends at a region known as the uvula.</span></div></li><li><div>Pharynx:</div></li><ul><li><div>Nasopharynx: <span style=""font-weight: 400;"">Posterior to nasal cavities and above soft palette.</span></div></li><li><div>Oropahrynx: <span style=""font-weight: 400;"">Posterior to the oral cavity, inferior to the level of the soft palate, and superior to the upper margin of the epiglottis.</span></div></li><li><div>Laryngopharynx: <span style=""font-weight: 400;"">Extends from the superior margin of the epiglottis to the top of the esophagus.</span></div></li></ul></ul></b> "
"<span style=""font-style: italic; font-weight: 700; text-decoration-line: underline;"">1.27 The Respiratory Tract<br></span>Describe the structure of the lower respiratory tract (bronchi and alveoli) <br> <br> Where is food most likely to get lodged in?<br>How many sectors are there?<br>What is the histology?<br>What is present in the alveoli? <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Bronchi:<span style=""font-weight: 400;""> Have characteristic hyaline cartilage supporting them like the trachea. The right is wider, shorter, and lies at a steep vertical angle whereas the left is narrower and more horizontal. So we can assume inhaled foreign objects most likely get lodged in the right side bronchus.</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Left and right primary bronchi decide further into secondary bronchi; 2 on the left and 3 on the right. These divide into further tertiary bronchi which are about 10 for each lung.</span></div></li><li><div><span style=""font-weight: 400;"">Each tertiary bronchi gives rise to many terminal bronchioles and no longer has hyaline cartilage in their walls and respiratory bronchioles branch from these and ends in an acinus of clustered alveoli.</span></div></li></ul><li><b>Alveoli:<span style=""font-weight: 400;""> Contains no cilia or smooth muscle and are instead lined by thin squamous epithelial cells called pneumocytes. Most are type 1 which helps in gas exchange but some are type 2 which releases a surfactant that decreases surface tension and helps keep them open which prevents them from collapsing and sticking to each other.</span></b><br></li></ul> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.27 The Respiratory Tract<br></span></b>Describe surfuctants and describe the disease associated with it and premature babies <br> <br> <br> <br> ""<div class=""back""> <ul><li><b>Surfactant and premature babies:<span style=""font-weight: 400;""> Surfactant is a mixture of fats and proteins and acts as a lubricant. Its production begins in the developing fetus at around 24-28 weeks gestation and they tend to produce enough surfactant at around 34 weeks. If born prematurely then most likely not enough surfactant is produced which can cause Respiratory Distress Syndrome (RDS) shortly after birth.</span></b></li></ul> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.27 The Respiratory Tract<br></span></b>Describe the structure of the lungs in terms of vasculature (where they get blood from), lymphatics and bronchoscopy <br> <br> Where does the trachea and bronchial tree recieve blood from?<br>What is the difference from the draining of the left and right bronchial drains?<br>What happens to a infected carina? <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint9010e948a4b4e68f').style.display='block'; return false;""> Hint</a> <div id=""hint9010e948a4b4e68f"" class=hint style=""display: none"">Thoracic, Bronchial, Accesory Hemiazygos, Azygos</div> ""<div class=""back""> <b><ul><li>Vasculature: <span style=""font-weight: 400;"">The trachea and bronchial tree receive their blood directly from the thoracic aorta, bronchial arteries branch from this or also branch from the posterior intercostal arteries.</span><br></li><ul><li><span style=""font-weight: 400;"">On the left, bronchial veins drain into the accessory hemiazygos vein which drains into azygos on the right into the superior vena cava.</span><br></li><li><span style=""font-weight: 400;"">On the right, bronchial veins drain into the azygos vein.</span><br></li></ul><li>Lymphatics: <span style=""font-weight: 400;"">The inferior tracheobronchial lymph nodes can blunt the carina when enlarged.</span></li><li>Bronchoscopy: <span style=""font-weight: 400;"">A bronchoscope travels down the trachea to enter the main bronchus and must navigate around to reach the carina if cancer cells have metastasized at the inferior tracheobronchial enlarged and the carina becomes distorted and immobile.</span></li></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.26 The Thoracic Cage<br></span></b>Describe the features of the diaphram in terms of sites of attatchment and crus <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Diaphragm: <span style=""font-weight: 400;"">Separates thoracic and abdominal cavity and is comprised of 2 domes. Peripherally muscular and muscle fibers unite as a central tendon of the diaphragm. It is innervated by the phrenic nerve which keeps it alive (C3-C5)</span></div></li><ul style=""""><li style=""font-weight: bold;""><div>Sites of attachment:</div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Coastal cartilages and inner surfaces of ribs 7-12</span></div></li><li><div><span style=""font-weight: 400;"">Lumbar vertebrae of associated discs</span></div></li><li><div><span style=""font-weight: 400;"">Xiphoid process of sternum</span></div></li></ul><li><div><span style=""font-weight: 700;"">Crus: </span>Parts of the diagram that arise from the vertebrae</div></li><ul><li><div>Right crus from L1 to L3</div></li><li><div>LEft crus from L1 to L2</div></li></ul></ul></ul><br> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.27 The Respiratory Tract</span></b><div>Describe the activity of muscles during respiration</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Accessory Muscles:</div></li><ul><li><div>Inhalation: <span style=""font-weight: 400;"">Sternocleidomastoid mass, Pectoralis minor mass and Scalene muscle mass.</span></div></li><li><div>Exhalation: <span style=""font-weight: 400;"">External oblique mass, internal oblique mass, transversus mass and rectus abdominis mass.</span></div></li></ul><li><div>Respiration (Relaxed vs Active):</div></li><ul><li><div>Relaxed:</div></li><ul><li><div>Inhalation: <span style=""font-weight: 400;"">Diaphragm contracts and external intercostals elevate the thoracic cavity.</span></div></li><li><div>Exhalation: <span style=""font-weight: 400;"">Muscles above relax, this allows the lungs to recoil and push air out.</span></div></li></ul><li><div>Active:&nbsp;</div></li><ul><li><div>Inhalation: <span style=""font-weight: 400;"">Diaphragm contracts and external intercostals elevate the thoracic cavity plus the accessory muscles elevate the ribs and sternum.</span></div></li><li><div>Exhalation:<span style=""font-weight: 400;""> Muscles above relax, allowing the lungs to recoil and push air out, internal and innermost intercoastal contract reducing transverse dimensions of the thoracic cavity. Plus the accessory muscles depress the ribs and squeeze the abdominal cavity.</span></div></li></ul></ul></ul></b> "
"<span style=""font-style: italic; font-weight: 700; text-decoration-line: underline;"">1.28 Clinical Diseases<br></span>Describe the clinical disease pneumothorax and pleaural effusion <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Pneumothorax:<span style=""font-weight: 400;"">&nbsp;When a lung is compressed by air that has accumulated within the pleural space. This can lead to a partial or complete collapse of the lung in certain cases, the mediastinum can shift to a particular side which can provide a negative or positive effect, and its severity can range very heavily.</span></div></li><ul><li><div>Symptoms:<span style=""font-weight: 400;"">&nbsp;Sharp, Stabbing chest pain and shortness of breath (most common in young and tall males)</span></div></li></ul><li>Pleural Effusion:<span style=""font-weight: 400;"">&nbsp;When more than the normal amount of fluid accumulates within the pleural space, usually due to inflammation or the fluid gathers in the plural spaces for a wide variety of reasons, though it only affects one lung. Overtime, as fluid gathers the pleural membranes separate and lose their cohesion during inspiration. This prevents the lungs from expanding as much and eventually leads to partial or complete collapse.</span><br></li><ul><li><b>Symptoms:<span style=""font-weight: 400;"">&nbsp;Chest pain, shortness of breath and difficulty breathing unless sitting up or standing up.</span></b></li></ul></ul></b> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">5.? Cell Reproduction</span></b></div><div>Describe the process of cell reproduction<br></div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Process:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">Cell Growth (G1 Phase):</span></div></li><ul><li><div><span style=""font-weight: 400;"">Rapid cell growth</span></div></li><li><div><span style=""font-weight: 400;"">Metabolically active</span></div></li><li><div><span style=""font-weight: 400;"">Duplication of cell organelle</span></div></li><li><div><span style=""font-weight: 400;"">Start of centriole replication</span></div></li></ul><li><div><span style=""font-weight: 400;"">DNA Replication (S Phase)</span></div></li><ul><li><div><span style=""font-weight: 400;"">DNA replication and further growth</span></div></li></ul><li><div><span style=""font-weight: 400;"">Preparation for division (G2 Phase)</span></div></li><ul><li><div><span style=""font-weight: 400;"">Cell growth continues</span></div></li><li><div><span style=""font-weight: 400;"">Preparation for cell division</span></div></li><li><div><span style=""font-weight: 400;"">Enzymes and other proteins are synthesized</span></div></li><li><div><span style=""font-weight: 400;"">Replication of centrioles completed</span></div></li></ul><li><div><span style=""font-weight: 400;"">Cell Divides and forms 2 cells (M Phase)</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.? Nomenclature</span></div><div style="""">Describe the nomenclature associated with cell reproduction and mitosis</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Chromatin:<span style=""font-weight: 400;""> Complex of DNA and histones that make up the basic material of eukaryotic chromosomes.</span></div></li><li><div>Nucleosome: <span style=""font-weight: 400;"">Structure in chromatin composed of short DNA wrapped around an octameric core of histone proteins</span></div></li><li><div>Chromosome: <span style=""font-weight: 400;"">Structure composed of condensed DNA and associated proteins, which carry the genetic information.</span></div></li><li><div>Chromatid: <span style=""font-weight: 400;"">One of the copies of a chromosome present after DNA replication.</span></div></li><li><div>Centromere: <span style=""font-weight: 400;"">Holds together 2 sister chromatids.</span></div></li><li><div>Centrosome: <span style=""font-weight: 400;"">Organelle which organizes the microtubule cytoskeleton</span></div></li><li><div>Spindle: <span style=""font-weight: 400;"">Structures formed by the microtubules, stretching between opposite poles of the cell and which guide the movement of the chromosomes.</span></div></li><li><div>Kinetochore: <span style=""font-weight: 400;"">The protein complex that binds to a region at the centromere of a chromosome to which spindle microtubules attach.</span></div></li><li><div>Histones: <span style=""font-weight: 400;"">They are quite small but abundant proteins that are rich in arginine and lysine, they can be subject to protein modifications and are important for structure and regulation</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.? Mitosis</span></div><div><b><span style=""font-style: italic; text-decoration-line: underline;"">5.? Mitotic Spindle</span></b><span style=""font-style: italic; text-decoration-line: underline;""><br></span></div></b>Describe the process of mitosis and describe the mitotic spindle microtubules <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Prophase:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">Spindle fibers appear</span></div></li><li><div><span style=""font-weight: 400;"">Chromosomes condense</span></div></li></ul><li><div>Prometaphase:</div></li><ul><li><div><span style=""font-weight: 400;"">Spindle fibers attach to the chromosome</span></div></li><li><div><span style=""font-weight: 400;"">Chromosome condense</span></div></li></ul><li><div>Metaphase:</div></li><ul><li><div><span style=""font-weight: 400;"">Chromosomes align</span></div></li></ul><li><div>Anaphase:</div></li><ul><li><div><span style=""font-weight: 400;"">Sister chromatids move to opposite poles</span></div></li></ul><li><div>Telophase:</div></li><ul><li><div><span style=""font-weight: 400;"">Nuclear membrane reforms&nbsp;</span></div></li><li><div><span style=""font-weight: 400;"">Chromosomes decondense</span></div></li><li><div><span style=""font-weight: 400;"">Spindle fibers disappear</span></div></li></ul><li><div>Cytokinesis:</div></li><ul><li><div><span style=""font-weight: 400;"">Cytoplasm divides</span></div></li><li><div><span style=""font-weight: 400;"">The parent cell becomes 2 daughter cells with identical genetic information</span></div></li></ul></ul><ul><li><div>Astral Microtubules:<span style=""font-weight: 400;""> Works with the spindle pole and centrosome</span></div></li><li><div>Kinetochore Microtibulules: <span style=""font-weight: 400;"">Works with the kinetochore</span></div></li><li><div><b>Interpolar Microtubules: <span style=""font-weight: 400;"">Works with the replicated chromosome</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.? Checkpoints</span></div><div style=""""><div style="""">Describe and name the checpoints of mitosis</div></div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview: <span style=""font-weight: 400;"">Response to information received back from the cells, triggers events and ensures there is appropriate timing and coordination. The switches are binary and biochemical and launch events in a complete and irreversible fashion.</span></div></li><li><div>G1/S Checkpoint:<span style=""font-weight: 400;""> Checks if the environment is favorable, if it is then enter the cell cycle and proceed to the S phase</span></div></li><ul><li><div><span style=""font-weight: 400;"">Mitogens push cells through the checkpoint and at this checkpoint pRb and E2F become phosphorylated by the kinase complexes of cyclins D and E. The phosphorylated pRb falls off the transcription factor and the genes can be transcribed</span></div></li></ul><li><div>G2/M Checkpoint: <span style=""font-weight: 400;"">Checks if all DNA is replicated and if the environment is favorable, if it is then enter Mitosis</span></div></li><ul><li><div><span style=""font-weight: 400;"">Responses to DNA damage are coordinated by phosphoprotein p53 which is a transcription factor that drives the expression of genes for growth arrest, DNA repair, senescence, and apoptosis. It is present in low concentrations at all times, damage activated protein kinases activate it.</span></div></li></ul><li><div>M Checkpoint: <span style=""font-weight: 400;"">Checks if all chromosomes are attached to the spindle, if it is then triggers anaphase to go to cytokinesis.</span></div></li><ul><li><div><span style=""font-weight: 400;"">Occurs prior to the entry of the anaphase, it senses the completion of the microtubules binding to kinetochores at metaphase. By default, it is on but silenced when every chromosome is properly attached to the spindle and so an unattached kinetochore sends an inhibitory signal. APC (anaphase-promoting complex/cyclosome) is bound to substrate recognition factor Cdc20 and so for the cell to move from metaphase to anaphase it must be degraded. Kinetochores without microtubules assemble the mitotic checkpoint complex (MCC) which is the inhibitor that activates APC/C</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.? Measuring Biomolecules</span></div></b>Describe the principal of the measuring of biomolecules and use an example <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Measurement:<span style=""font-weight: 400;""> Relies on the theory that each molecule absorbs light energy differently amd a certain wavelength of light energy is absorbed at the highest level specifically for that particular molecule.</span></div></li><ul><li><div><span style=""font-weight: 400;"">If a light source of a particular wavelength passes through a solution containing the biomolecules to be measured, the amount of light absorbed will be in direct proportion to the number of molecules within that solution.</span></div></li></ul><li><b>Blood Glucose: <span style=""font-weight: 400;"">Glucose is converted by Glucose oxidase to yield D-Gluconic Acid and simultaneously oxygen is also converted to hydrogen peroxide by the oxidase enzyme. Hydrogen peroxide will oxidize Horse Radish Peroxidase to form a color complex (with a specific wavelength absorption of 540-570nm). The absorption of light energy is directly proportional to the glucose molecules present in the sample.</span></b><br></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.? Biochemical Profiling</span></div><div>Describe the process and types of biochemical profiling</div> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.? Biochemical Profiling</span></div><ul><li><div>Screening:<span style=""font-weight: 400;""> Provides preliminary physiological data to reflect the general conditions of an individual. Less complicated tests are involved and normally can be performed within a short period of time.</span></div></li><li><div>Specific Function Test:<span style=""font-weight: 400;""> This will provide more details to indicate whether a particular body system is performing its normal function or if there's any damage to particular organs.</span></div></li><li><div>Screening:&nbsp;</div></li><ul><li><div>Blood Sugar:</div></li><ul><li><div><span style=""font-weight: 400;"">Effectiveness of the control of glucose metabolism by metabolism by insulin.</span></div></li><li><div><span style=""font-weight: 400;"">Performed on either randomly timed samples or samples taken after overnight/ 8 hours of fasting.</span></div></li><li><div><span style=""font-weight: 400;"">Patients with endocrine defects affecting their insulin production will show abnormal blood sugar levels.</span></div></li></ul><li><div>Urea and Electrolytes:</div></li><ul><li><div><span style=""font-weight: 400;"">Serum levels indicate the effectiveness of the renal function.</span></div></li><li><div><span style=""font-weight: 400;"">Electrolytes (sodium, potassium, and chloride) also indicate renal function but also other general or specific pathological conditions in which electrolyte balance is disrupted.</span></div></li></ul><li><div>Blood Sample Types:</div></li><ul><li><div><span style=""font-weight: 400;"">Serum which reflects plasma concentration or biomolecules in circulation. The whole blood was collected in non-anticoagulated containers and will be left to allow for clot formation then the clot with all blood cells is removed by centrifugation since fibrin and cellular components will interfere with assay results.</span></div></li><li><div><span style=""font-weight: 400;"">Plasma which may be for more specific tests, may require preservations of analytes by the addition of enzyme inhibitors or preservatives. For example blood glucose level, samples are to be preserved by fluoride oxalate to prevent metabolism (the degradation of glucose in the sample.</span></div></li></ul></ul></ul><br></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.? Blood Sampling Sites</span></div><div><span style=""font-weight: 400;"">Describe the sites of blood sampling sites</span><br></div></b> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.? Blood Sampling Sites</span></div><ul><li><div>Blood Sampling Sites:</div></li><ul><li><div>Venous:</div></li><ul><li><div><span style=""font-weight: 400;"">Glycosylated hemoglobin causes raised levels in diabetes such as leukemia (leukocytosis).</span></div></li><li><div><span style=""font-weight: 400;"">White blood cell count, which can detect elevated levels in diseases such as leukemia (leukocytosis).</span></div></li><li><div><span style=""font-weight: 400;"">Decreased levels in cases such as vitamin deficiency (leukopenia).</span></div></li></ul><li><div>Arterial:</div></li><ul><li><div><span style=""font-weight: 400;"">Blood gas analysis for arterial partial pressure of oxygen partial pressure of carbon dioxide and pH.</span></div></li><li><div><span style=""font-weight: 400;"">Blood gas analysis is of particular use to indicate hypoxemia and acid-base balance in circulation.</span></div></li><li><div><span style=""font-weight: 400;"">Some life-threatening metabolic conditions such as ketoacidosis included by diabetic coma will show extreme arterial pH values.</span></div></li></ul><li><div>Capillary:</div></li><ul><li><div><span style=""font-weight: 400;"">Combination of venous and arterial blood.</span></div></li><li><div><span style=""font-weight: 400;"">Used for infants and young children, patients with fragile veins such as the elderly, and patients with severe burns.</span></div></li></ul></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.? Urea and Electrolytes</span></div><div>Describe the measurement of Urea in the body and how changes in serum levels occur</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Measurement: <span style=""font-weight: 400;"">To measure blood urea you take a sample of clotted venous blood from your patient and extract the serum after centrifugation. Urease converts urea to ammonium, coupling of OG in the test solution, Glutamate dehydrogenase (GLDH) converter NH4 and OG to glutamate, NADH converted to NAD and NADH measured at 340 nm.</span></div></li><ul><li><div><span style=""font-weight: 400;"">Spectrophotometry is used for this as well, NADH declines in concentration in the forward reaction. The first substrate is urea and it drives the reaction forward. Therefore, the higher the urea concentration (as it is the substrate in the first reaction), the more NH4, and the more NADH is converted to NAD. The lower the absorbance of NADH the higher the concentration in the sample.</span></div></li></ul><li><div>Serum Urea:&nbsp;</div></li><ul><li><div>High Urea: <span style=""font-weight: 400;"">This may be an indication of kidney function alteration or dehydration (diarrhea, vomiting).</span></div></li><li><div>Low Urea: <span style=""font-weight: 400;"">Low urea may be due to chronic liver diseases or starvation but can also be pregnancy-related.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.? Cardiac Troponin</span></div><div><span style=""font-weight: 400;"">Briefly explain the mechanics of cardiac troponin occurs</span><br></div></b> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.? Cardiac Troponin</span></div><ul><li><div>Cardiac Troponin: <span style=""font-weight: 400;"">Heart damage is largely analyzed via cardiac troponin, abnormal levels indicate cardiac damage. Itss complex consinsts of the TnC, TnI and TnT. TnC is also released by other muscles and therefore lacks specificity and detection of TnI and TnT specific for cardiac muscle damage. Comparison between time points normally three hours pose onset of symptoms made to indicate a relative increase in Tn levels. If more than a 20% increase - indicative of cardiac muscle damage.</span></div></li><li><div>Mechanics:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">Anti-cTnI antibodies against cTnI are conjugated to make magnetic beads against one epitope.</span></div></li><li><div><span style=""font-weight: 400;"">Anti-cTnI antibodies against cTnI are conjugated to alkaline phosphate (ALP) for a second epitope.</span></div></li><li><div><span style=""font-weight: 400;"">This allows for the antigen in the patient serum (if present) to be sandwiched between two antibodies, and then a chemical is added (Lumi-Phos*350) which reacts with ALP to produce light which is then measured on a luminometer.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.17 Reproductive System - Male</span></div></b>Explain what is the Epipdidymis, Prostate, Urethera and Bulbo-Uretheral Glands<br> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Epipdidymis (External): <span style=""font-weight: 400;"">Stores mature spermatozoa</span></div></li><li><div>Prostate (Internal): <span style=""font-weight: 400;"">Accessory glands that contribute fluid to ejaculate.</span></div></li><li><div>Urethra (Internal): <span style=""font-weight: 400;"">Collects formed ejaculate and transmits it along the penis to the orifice as well as urine from the bladder.</span></div></li><li><div>Bulbo-Urethral Glands (Internal):<span style=""font-weight: 400;""> Accessory glands that lubricate the urethra before ejaculation.</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.18 Reproductive System - Female</span></div><div>Explain the features of the cervix, vulva and greater vestibular glands</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Cervix (Internal): <span style=""font-weight: 400;"">Inferior aspect of the uterus and boundary between uterus and vagina</span></div></li><li><div>Vulva (External): <span style=""font-weight: 400;"">External genitalia composed of the clitoris, labia minora and labia majora</span></div></li><li><div><b>Greater vestibular glands (Internal): <span style=""font-weight: 400;"">Accessory glands located at the inferior pole of bulbs of the vestibule that provide lubrication to the vestibule of the vagina during sexual stimulation.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">8.3 Innate Cells</span></div></b>What do Neutrophils and Mast Cells do?<br> <br> <br> <br> <br> ""<div class=""back""> <b>Neutrophil:&nbsp; <span style=""font-weight: 400;"">Multilobed and most abundant white blood cell, not found in tissues but can be recruited and usually has a short lifespan. Causes phagocytosis, activation of bactericidal and mechanism antigen presentation</span></b><span style=""font-weight: bold;""><br><br>Mast:&nbsp;</span>Not located in blood but in tissues containing potent inflammatory mediators such as histamine that aid in defense against parasites. "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">6.2 Absorption</span></b></div><div>In terms of Absorbtion in pharmacology describe the routes taken, gastric emptying, liver and first pass metabolism as well as bio availability<br></div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Routes:<span style=""font-weight: 400;""> Can be taken in the form of</span></div></li><ul><li><div><span style=""font-weight: 400;"">Sublingual/Buccal (Under the tongue) - Tablets, Sprays</span></div></li><li><div><span style=""font-weight: 400;"">Oral - Tablets, Capsules</span></div></li><li><div><span style=""font-weight: 400;"">Rectal - Suppositories, Rectal Foams</span></div></li></ul><li><div>Gastric Emptying<span style=""font-weight: 400;"">: Acid labile drugs require the protection of an enteric coat to prevent inactivation by gastric juices in the stomach while gastric emptying may be slowed by other drugs. Transit of the drugs may also be delayed by food.</span></div></li><li><div>Liver and First Pass Metabolism: <span style=""font-weight: 400;"">Drugs are absorbed from the small intestine and delivered to the liver via the hepatic portal vein before they enter systemic circulation. 1st pass metabolism refers to the amount of drug metabolized on its first pass through the liver. Drugs may be inactive and then metabolized into the liver into an active compound (called prodrugs) these are used in the treatment of heart failure.</span></div></li><li><div><b>Bioavailability: <span style=""font-weight: 400;"">Refers to the fraction of a dose reaching the systemic circulation after oral dosing involving the two factors which are absorption via the GI tract and 1st pass metabolism.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.3 Drug Distribution</span></div><div style="""">In terms of drug distribution in Pharmacology describe protein binding and blood flow</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Protein binding:<span style=""font-weight: 400;""> In systemic circulation, drugs are normally bound to plasma protein that reduces clearance for the body so it enhances the duration of action. It is only the unbound component that leaves circulation to perfuse the tissues (is a dynamic effect since as soon the free drug leaves circulation more become unbound from protein). Acidic drugs bind mainly to albumin and Basic drugs bind mainly to alpha glycoprotein.</span></div></li><li><div>Blood Flow<span style=""font-weight: 400;"">: Two major factors determine tissue delivery which are tissue blood supply and tissue permeability which is mainly a function of lipid solubility.</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.4 Drug Metabolism</span></div><div style="""">In terms of Drug metabolism describe lipid solubility and drug metabolism (both phases)<br><b>Drugs: (Penicilin, Lidocaine, Paracetemol)</b></div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Lipid Solubility:<span style=""font-weight: 400;""> Lipid-soluble drugs require metabolic conversion into more water-soluble products that can be excreted from the body normally through urine, water-soluble drugs in contrast may be directly excreted through the kidney terminating pharmacological effects. Penicillin is a good example of a water-soluble drug reaching high enough concentrations in urine to treat UTIs</span></div></li><li><div>Drug Metabolism<span style=""font-weight: 400;"">: Metabolism of drugs by the liver is divided into 2 phases:</span></div></li><ul><li><div><span style=""font-weight: 400;"">Phase 1: Deactivates the drug to produce a primary inactive metabolite which if water-soluble can be excreted through the kidney. Lidocaine is enzymatically degraded at 3 molecular sites by hydrolysis terminating its analgesic effect.</span></div></li><li><div><span style=""font-weight: 400;"">Phase 2: Adds onto or conjugates the drug with for example a sugar which produces a water-soluble product that can be excreted by the kidney. Paracetamol is conjugated in 3 separate pathways by the addition of sulphate or sugar or a protein producing a water-soluble product.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">6.5 Drug Excretion</span></div></b>In terms of Drug excretion in pharmacology describe glomerular filtration <br> <br> How does size of protein affect the duration of action?<br>What does Monoclonal antibodies have to do with this? <br> <br> ""<div class=""back""> <ul style=""font-weight: bold;""><li><div>Glomerular Filtration:<span style=""font-weight: 400;""> Most drugs have low molecular weight and filtration is not affected by the drug's lipid solubility, however, drugs bound to plasma proteins are too large to be filtered so only the free-form version of the drug is allowed. Some modern monoclonal antibodies with large weight have a longer duration of actions so administered at weekly intervals. Filtration may be reduced with age.</span></div></li></ul><div style=""""><br></div> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.7 G-protein coupled receptors</span></div><div>Descibe the different types of G-Protein coupled receptors&nbsp;</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> Largest receptor family by having known 865, and are ligand-activated by having a singly polypeptide with 7TM domains, linked to intracellular effect. They may induce an enzymatic signaling cascade - metabotropic however this can be slow.</span></div></li><li><div>Gs Protein<span style=""font-weight: 400;"">: Stimulate adenylate cyclase (increases cAMP/PKA)</span></div></li><li><div>Gi Protein: <span style=""font-weight: 400;"">Inhibit adenylate cyclase (decreases cAMP/PKA)</span></div></li><li><div>Gq Protein: <span style=""font-weight: 400;"">Activate phospholipase C (PKC/[Ca2+] ) so DAG and IP3 produced</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.9 Enzyme-linked and Nuclear Receptors</span></div><div>Describe enzyme-linked and nuclear receptors</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> Often activated by signaling molecules like cytokines and hormones and are usually involved in the regulation of cell processes and gene expression, normally have slow induction but very long-lasting effects.</span></div></li><li><div>Receptors<span style=""font-weight: 400;"">:</span></div></li><ul><li><div>Kinase:<span style=""font-weight: 400;""> Done by the signal monomer binding with the receptor causing kinase activity to be stimulated that leads to tyrosine phosphorylation, this causes proteins to bind to the docking sites on the kinase.</span></div></li><li><div>Nuclear: <span style=""font-weight: 400;"">Done by hormones and steroids targeting nuclear receptors. In the nucleus or cytoplasm, this results in usually and regulation of gene transcription. The process can recognize foreign molecules and initiate metabolic processes</span></div></li></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">6.10 Pharmodynamics Factors<br></span></b>Describe the types of pharmodynamic factors (Tolerance, Withdrawl and Desnsitization) <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Tolerance<span style=""font-weight: 400;"">: The drug may become less effective, which can be caused by:</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Increase in “opposite” activity such as increased excitatory signaling with CNS depressants</span></div></li><li><div><span style=""font-weight: 400;"">Pharmacokinetics using altered ADME for example induction of liver enzymes</span></div></li><li><div><span style=""font-weight: 400;"">Drug resistance such as the development of internal mechanisms of drug inactivation such as antibiotics</span></div></li></ul><li style=""font-weight: bold;""><div>Withdrawal: <span style=""font-weight: 400;"">Removal of the drug may cause a reverse rebound as the body has adjusted to a new baseline with the drug</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">The systemic presence of corticosteroids activates adrenal hypothalamic-pituitary system feedback to suppress endogenous cortisol production. Removal of corticosteroids may lead to cortisol deficit.</span></div></li></ul><li style=""font-weight: bold;""><div>Desensitization: <span style=""font-weight: 400;"">Reduction of the activity of a drug in response to a drug, the desensitization may be acute, rapid, and transient (tachyphylaxis)that is linked with numerous physiological causes.&nbsp;</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Rapid desensitization is due to feedback mechanisms like phosphorylation and other protein modifications or inhibitory products such as enzymes.</span></div></li><li><div><span style=""font-weight: 400;"">Desensitisation can be caused by drug-induced changes in protein level and thus decreased expression of the target, tolerance due to expression of proteins mediating opposite activity can also occur.</span></div></li></ul></ul><div><b>MNEMONIC</b></div><div><b>Tolerance: O R A</b></div> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.11 Binding Sites</span></div><div style="""">Define binding sites and explain what affinity, efficacy and potency<br></div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Binding sites:<span style=""font-weight: 400;""> Receptors have an active (orthosteric) binding site for their endogenous, activating ligand (agonist). These sites have high specificity to select the appropriate legend formed by protein amino acid residues. The binding induces conformational changes to activate the receptor. (May also contain secondary (allosteric) binding sites for other ligands</span></div></li><li><div>Affinity: <span style=""font-weight: 400;"">The ability of a ligand to bind to a target</span></div></li><li><div>Efficacy: <span style=""font-weight: 400;"">The ability of a ligand to generate an effect.</span></div></li><li><div><b>Potency: <span style=""font-weight: 400;"">Together, affinity and efficacy determine potency which is the ability of a ligand to generate a response.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">6.13 Agonist</span></div></b>Explain the full, partial and inverse agonists <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Full:<span style=""font-weight: 400;""> Induces a maximal response (100% of the endogenous agonist), more efficient than a partial agonist.</span></div></li><li><div>Partial:<span style=""font-weight: 400;""> Induces a submaximal response (&lt;100% of the endogenous agonist), unable to generate maximal response even at saturating concentrations.</span></div></li><li><div>Inverse: <span style=""font-weight: 400;"">Receptors have constitutive activity (they have acitivity even without agonist bound), inverse agonists block this.</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">6.14 Antogonists</span></div></b>Describe and explain all the types of antagonists (Compeitive, Non Compeitive, Irrversible and Allosteric Modulation) <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div><b>Competitive:<span style=""font-weight: 400;""> Competes with the agonist for the agonist binding site to prevent receptor activation.</span></b><br></div></li><li><div>Non-competitive Antagonist: <span style=""font-weight: 400;"">Does not bind to the active site and agonist can bind as normal. But when the agonist binds, the agonist-receptor complex does not generate a response.</span></div></li><li><div>Irreversible Antagonist: <span style=""font-weight: 400;"">Reduces maximal response irrespective of whether competitive or non–competitive. Inhibition increases with increased concentration and duration of exposure. Recovery only occurs with the expression of new receptors</span></div></li><li><div><b>Allosteric Modulation:<span style=""font-weight: 400;""> Bind to sites on the receptors other than the active site, these cause conformation changes to the structure of the receptor. Can produce positive or negative effects however, positive allosteric modulators do not generate a response in the absence of an agonist.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Side Effects</span></div><div>In terms of pharmacology define what are side effects and explain what they due to change the drug-receptor relationship</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Emergence:<span style=""font-weight: 400;""> This can come from excessive activity by the drug at the desired target or from activity by the drug at other targets.</span></div></li><li><div>Therapeutic Index: <span style=""font-weight: 400;"">The dose range between where a drug has minimal therapeutic benefit and where it is excessively harmful</span></div></li><ul><li><div>ED50:<span style=""font-weight: 400;""> Median therapeutic dose (benefits 50% of subjects)</span></div></li><li><div>LD50: <span style=""font-weight: 400;"">Median lethal dose (kills 50% of subjects)</span></div></li></ul><li><div>DRR: <span style=""font-weight: 400;"">Drug-Receptor Relationship&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">Steep DRRs mean small changes in dose will have large therapeutic effects</span></div></li><li><div><span style=""font-weight: 400;"">Flat DRRs mean small changes in dose have little clinical effect so it is usually safer.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.1 Prokaryotes and Eukaryotes</span></div><span style=""font-weight: 400;"">Compare and contrast the difference between prokaryotes and eukaryotes in terms of size, ribosomes (as well as number of proteins) and DNA Type<br><br></span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Prokaryotes:</div></li><ul><li><div>Cell Size: <span style=""font-weight: 400;"">0.5-10 micrometers</span></div></li><li><div>Ribosome: <span style=""font-weight: 400;"">50S + 30S subunits, 82 proteins</span></div></li><li><div>DNA: <span style=""font-weight: 400;"">Free floating and only one chromosome present.</span><span style=""font-weight: 400;"">.</span></div></li></ul><li><div>Eukaryotes:</div></li><ul><li><div>Cell Size: <span style=""font-weight: 400;"">10-100 micrometers</span></div></li><li><div>Ribosome: <span style=""font-weight: 400;"">60S + 40S subunits, 51 proteins</span></div></li><li><div>DNA: <span style=""font-weight: 400;"">Chromosome enclosed by nuclear membrane, many.</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.2 Microbiological Properties</span></div><div>Describe the types of gene expressions of microbiologiccal organisms</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Gene Expressions:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Monocistronic (Eukaryotes): <span style=""font-weight: 400;"">Produces only a singular protein due to a single cistron.</span></div></li><li><div>Polycistronic (Prokaryotes): <span style=""font-weight: 400;"">Can consist of two or more citrons so genes assemble in groups in such a way all proteins can be transcribed if needed.</span></div></li><li><div>Intronic (Eukaryotes): <span style=""font-weight: 400;"">Scans in such a way that only necessary genes are processed and appropriate proteins are made even if not present at the start of the strand.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.4 Viruses</span></div></b>Explain the structure of a virus&nbsp; <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Nucleocapsid<span style=""font-weight: 400;""> (protein capsid + tegument + dsDNA genome)</span></div></li><ul><li><div>Protein Capsid: <span style=""font-weight: 400;"">Shell that surrounds and protects the viral genome.</span></div></li><li><div>Tegument: <span style=""font-weight: 400;"">Cluster of proteins between the envelope and nucleocapsid that helps in transportation and entry etc.</span></div></li><li><div>dsDNA genome: <span style=""font-weight: 400;"">Two strands of DNA containing genetic information.&nbsp;</span></div></li></ul><li><div>Viral Envelope: <span style=""font-weight: 400;"">Protects the genetic material when traveling between host cells.</span></div></li><li><div>Glycoprotein Complex (I, II, III): <span style=""font-weight: 400;"">Helps them enter bodily cells through recognition and binding but can also have therapeutic or preventive targets.</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.6 Protista</span></div></b>Describe the growth cycle of the protista <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Growth cycle:&nbsp;</div></li><ul><li><div>Cyst: <span style=""font-weight: 400;"">Resistance stage, with the thickened cell wall.</span></div></li><li><div>Trophozoites:<span style=""font-weight: 400;""> Stage that protozoa actively feed and multiply.</span></div></li><li><div><b>Flagellated: <span style=""font-weight: 400;"">Temporary non-feeding stage.</span></b></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.7 Helminths</span></div><div>Define helminths</div> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint0b8af91c7e35af0c').style.display='block'; return false;""> Hint</a> <div id=""hint0b8af91c7e35af0c"" class=hint style=""display: none"">Nemo, Platapus, Little Mix, Fluke</div> ""<div class=""back""> <b><ul><li><div>Classification Principals:</div></li><ul><li><div>Nemathlimethes (Roundworms): <span style=""font-weight: 400;"">Worm-like, separated sex, unsegmented roundworms.</span></div></li><li><div>Platyhelminthes (Flatworms): <span style=""font-weight: 400;"">Flat (dorsoventral), no true body cavity.</span></div></li><ul><li><div>Cestoda (Tapeworms): <span style=""font-weight: 400;"">Band-like, segmented, no digestive system.</span></div></li><li><div><b>Trematoda (Flukes):<span style=""font-weight: 400;""> Mostly leaf-shaped and hermaphroditic, however some (schistosomes) are narrow and elongated and have their separate sex.</span></b></div></li></ul></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.8 Prions</span></div><span style=""font-weight: 400;"">In terms of Microbiology define prions</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Amyloidosis Prions:<span style=""font-weight: 400;""> Abnormal, pathogenic agents that are transmissible that can induce abnormal folding of specific normal cellular proteins mostly found in the brain.</span></div></li><li><div><b>Diseases: <span style=""font-weight: 400;"">CJD (Creutzfeldt-Jakob disease) that typically affects brain functions like memory loss, changes in personality, and loss of balance and coordination. Normally diagnosed via a brain biopsy or autopsy and its examination, no cure is present but symptoms can be treated such as antidepressants and painkillers.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.9 Gram Positive and Gram Negative</span></div><div>Differentiate and compare the difference between gram positive and gram negative bacteria</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Gram Positive Vs. Gram Negative:<span style=""font-weight: 400;""> Gram-positive have cell walls made of a thick layer of peptidoglycan but gram-negative have a thin layer yet they also contain an outer membrane.</span></div></li><ul><li><div><span style=""font-weight: 400;"">If the bacteria is gram-positive, the rich peptidoglycan layer in the cell walls will retain dye and will stain violet but if it is gram-negative then the dye will leak out of the thin peptidoglycan layer and will stain red.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.10 Bacterial Requirements and Conditions</span></div></b>Describe and explain the requirments, conditions and types of growth media for bacteria growth <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Requirements:<span style=""font-weight: 400;""> Water, Sugar, Protein, Salt, Liquid growth medium.</span></div></li><li><div>Conditions:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Lag:<span style=""font-weight: 400;""> Adaptation to the new environment</span></div></li><li><div>Log (Exponential)<span style=""font-weight: 400;"">: Optimal conditions for growth</span></div></li><li><div>Stationary:<span style=""font-weight: 400;""> Compromised resources and toxic products accumulate</span></div></li><li><div>Death (Decline): <span style=""font-weight: 400;"">Depleted resources and toxic products lead to cellular death.</span></div></li></ul><li><div>Growth Media:&nbsp;</div></li><ul><li><div>General (non-selective) growth medium:<span style=""font-weight: 400;""> Contains the nutrients necessary for general growth for a large variety of bacteria. It can be ‘rich’ or ‘minimal’.</span></div></li><li><div>Selective medium: <span style=""font-weight: 400;"">A rich or minimal medium that contains the nutrients and supplements necessary for the growth of selected organisms.</span></div></li><li><div><b>Differential medium: <span style=""font-weight: 400;"">A rich or minimal medium that contains the nutrients and supplements that enable the growth and differentiation of various organisms.</span></b></div></li></ul></ul>MNEMONIC:<br>P<br>G<br>S<br>D</b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.12 Staphylococcus Aureus</span></div></b>Partially explain the disease Staphylococcus Aureus <br> <br> <br> <br> ""<div class=""back""> <b><div><b>Overview:<span style=""font-weight: 400;""> ⅓ carry this disease, most present in moist skin areas and higher pH levels, in addition to fatty areas with limited oxygen such as hair follicles, sebaceous glands, and sweat-support anaerobic organisms. Results in a wide variety of skin disorders and internal issues like pneumonia and meningitis.</span></b><br></div></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.13 Pityriasis/Tinea Versicolor</span></div></b>Describe the disease Pityriasis/Tinea Versicolor <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint58995bd80623da5e').style.display='block'; return false;""> Hint</a> <div id=""hint58995bd80623da5e"" class=hint style=""display: none"">Mama Furfur</div> ""<div class=""back""> <b><ul><li><div>Cause:<span style=""font-weight: 400;""> Mlalasezia furfur (Basidiomycota - Fungus, Septate hyphae, conidia)</span></div></li><li><div>Commonality: <span style=""font-weight: 400;"">Typical skin microbiota.</span></div></li><li><div><b>Symptoms:<span style=""font-weight: 400;""> Scaly and discolored skin patches, Occasionally can be itchy (pruritic) and located in the chest, abdomen, back, and neck.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.14 Co-presence and Exclusion</span></div><div style="""">Briefly explain the signature bacteria in the oral cavity and gut as well as describe co-presence and exclusion</div> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint305fe5eea71c2cf3').style.display='block'; return false;""> Hint</a> <div id=""hint305fe5eea71c2cf3"" class=hint style=""display: none""><b>MNEMONIC<br>Vagina: VaLaPre (Valarie) (Lactating Italian Pre)<br>Skin: SkStPro (Statpronol) (Coccos and Ponis)<br>Mouth: MoStrTan (Stranny) (Tans And Cocks)</b></div> ""<div class=""back""> <ul style=""font-weight: bold;""><li><div>Overview: <span style=""font-weight: 400;"">Closely related microorganisms co-occur in the same niche, and most exclusive relationships occur between more distantly related organisms.</span></div></li><li><div>Streptococcus: <span style=""font-weight: 400;"">Signature bacterium in the oral cavity.</span></div></li><li><div>Bacteroidetes: <span style=""font-weight: 400;"">Signature bacterium in the gut.</span></div></li><li><div>Vagina Exclusion: <span style=""font-weight: 400;"">Either Prevotella or Lactobacillus.</span></div></li><li><div>Skin Exclusion: <span style=""font-weight: 400;"">Either Propionibacterium or Staphyloccous.</span></div></li><li><div>Mouth Exclusion: <span style=""font-weight: 400;"">Either Streptococcus or Tannerella</span></div></li><li><div><b>Mouth Co-presence:<span style=""font-weight: 400;""> Prevotella and Treponema can co-exist in the mouth at the same time.</span></b></div></li></ul><b>MNEMONIC<br>Vagina: VaLaPre (Valarie) (Lactating Italian Pre)<br>Skin: SkStPro (Statpronol) (Coccos and Ponis)<br>Mouth: MoStrTan (Stranny) (Tans And Cocks)</b><br><br> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.15 Dysbiosis</span></div><div style="""">Describe and explain dysbiosis<br></div> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hintaf9c0192e5b32b54').style.display='block'; return false;""> Hint</a> <div id=""hintaf9c0192e5b32b54"" class=hint style=""display: none"">Dont forget get Ciliac Acid!</div> ""<div class=""back""> <b><ul><li><div>Dysbiosis: <span style=""font-weight: 400;"">Imbalance in the gut microbial community that is associated with disease. Can be caused by the organism “Clostridium Difficile” than infects the person through the path of; Mild diarrhea, Psuedomembranous colitis, Sepsis-like picture and then eventually death.</span></div></li><li><div>Path:</div></li><ul><li><div><span style=""font-weight: 400;"">Commendal microbiotica changes intestinal environment and alters the internal biome.</span></div></li><li><div><span style=""font-weight: 400;"">Environment becomes vulnerable to pathogens who are after the newly available niche.</span></div></li><li><div><span style=""font-weight: 400;"">This leads to inflammation and mucosal tissue damage.</span></div></li></ul><li><div>Infection Establishment:<span style=""font-weight: 400;""> Mucus exposing sialic acid released due to sufficient bacteria/anti-biotic treatment forming its free form. There is a Siliac acid compeition which causes infllmation and disease from pathogenic C. difficile overgroth (prevented by anti-biotics)</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.16 Superorganismic Communication</span></div><div>Briefly explain superorganismic communication<br></div> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint1b1a47bd2cf65ae0').style.display='block'; return false;""> Hint</a> <div id=""hint1b1a47bd2cf65ae0"" class=hint style=""display: none"">HPAG, Courts and Perm</div> ""<div class=""back""> <ul><li style=""font-weight: bold;""><div>Axis:</div></li><ul><li style=""font-weight: bold;""><div><span style=""font-weight: 400;"">Environmental stress and cytokines activate Hypothalamic-Pituitary-Adrenal gland which initates cortisol production and brain function modulation.</span></div></li><li style=""font-weight: bold;""><div><span style=""font-weight: 400;"">Cortisol alters gut permeability and barrier function which affects microbiota composition.</span></div></li><li style=""font-weight: bold;""><div><span style=""font-weight: 400;"">Microbiota short acid fatty chains are able to:</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Improve in glucose metabolism</span></div></li><li><div><span style=""font-weight: 400;"">Cause insulin sensitivity</span></div></li><li><div><span style=""font-weight: 400;"">Become substrates for coloncytes</span></div></li><li><div><span style=""font-weight: 400;"">Decrease pro-inflammatory cytokines secretion</span></div></li></ul></ul></ul> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.3 Drug Distribution</span></div><div>In terms of drug distribution in Pharmacology describe body compartments and cell membrane<br>(<b>Drugs; Heroin, Morphine, Thipentome, Suxamethonium)<br></b></div> <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: 700;""><li><div>Body compartments:&nbsp;<span style=""font-weight: 400;"">The body contains major barriers to drug distribution including:</span></div></li><ul><li><div><span style=""font-weight: 400;"">Blood-Brain Barrier: Drugs such as heroin can easily penetrate through the brain due to its lipid solubility but morphine which is a weak base has difficulty due to ion trapping. Morphine in its lipid-soluble form can cross the blood-brain barrier where it dissociates at a more acidic pH to its more water-soluble form which is then trapped being impermeable to the blood-brain barrier.</span></div></li><li><div><span style=""font-weight: 400;"">Placenta: Thiopentone which is an un-ionized lipid-soluble barbiturate can reach fetal circulation easily but suxamethonium which is an ionized water-soluble muscle reluctant shows very little fetal circulation.</span></div></li></ul><li><b>Cell Membrane:&nbsp;<span style=""font-weight: 400;"">Drugs that target receptors present in the cell membrane don't need to penetrate cell membranes to exert their effects while steroids and some drugs have an intracellular target site.</span></b></li></ul> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.4 Drug Metabolism</span></div><div>In terms of Drug metabolism describe&nbsp; liver enzymes and drug interactions, genetic ploymorphism as well as pro-drugs</div> <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: 700;""><li><div>Liver Enzymes and drug interaction:&nbsp;<span style=""font-weight: 400;"">the enzymes located in the liver leading to drug metabolism are a group dubbed the liver cytochromes p450’s. 9 have been identified. Some antibiotics can deactivate these enzymes so the patient has higher drug concentration levels than without them, conversely, some drugs can induce these drug interactions.</span></div></li><li><div>Genetic Polymorphism:&nbsp;<span style=""font-weight: 400;"">The enzyme CYP2D6 is lacking in about 8% of caucasian people so the opiate drug codeine doesn't have an analgesic effect.</span></div></li><li><div>Pro-Drugs:&nbsp;<span style=""font-weight: 400;"">Drug metabolism in the liver usually produces metabolites with reduced pharmacological activity thus terminating therapeutic effects. But some drugs known as Prodrugs are designed to be inactive to aid absorption because they are converted to active drugs due to liver metabolism.</span></div></li></ul> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">8.7 Antigens<br></span></b>Describe the MHC Class 2 pathway in terms of where antigen presentation occus, what is it recognized by, its conseuqnces, whats it marker, what are they expressed on and name them. <br> <br> <br> <br> ""<div class=""back""> <ul><li style=""font-weight: bold;""><div>MHC Class 2:&nbsp;<span style=""font-weight: 400;"">For when foreign proteins are taken up by presenting cell, these are recognized by helper T cells that have the CD4 marker that acts as a co-receptor for MHC class 2 and the consequence is the activation of helper T cells.</span></div></li><ul style=""font-weight: bold;""><li><div>Structure:&nbsp;<span style=""font-weight: 400;"">Expressed by antigen presenting cells and includes dendritic cells, macrophages and B cells. Six main types; HLA-DPA1, HLA-DPB1, HLA-DQA1, HLA-DQB1. HLA-DRA1 and HLA-DRB1.</span></div></li></ul></ul><div><b>MNEMONIC:</b><br></div><div><b>Help</b></div><div><b>Lord</b></div><div><b>Antibody</b></div><div><b><br></b></div><div><b>Dont</b></div><div><b>Praise</b></div><div><b>All</b></div> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.1 The Cardiac Cycle</span></div></b>Describe the cardiac cycle in terms of the systole and diastole phases <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Cardiac Cycle:<span style=""font-weight: 400;""> A coordinated sequence of electrical and mechanical events occurring from the start of one heartbeat to the start of the next. A single cardiac cycle includes a complete relaxation and contraction of both atria and ventricles. Relaxation is Diastole and Contraction is Systole</span></div></li><li><div>Changes in pressure and volume: <span style=""font-weight: 400;"">A series of pressure changes take place within the heart during the cardiac cycle resulting in the movement of blood. Valves within the heart's direct movement of blood and pressure changes are brought about by conductive electrochemical changes within the myocardium that result in the contraction of cardiac muscle.</span></div></li><li><div>Phases:</div></li><ul><li><div>Atrial Systole:<span style=""font-weight: 400;""> Atrial contraction forces blood into the ventricles. Sets up the P-wave which covers the atria depolarization</span></div></li><li><div>Ventricular Systole: <span style=""font-weight: 400;"">Ventricular contraction pushes AV valves closed (first phase) and sets up the QRS complex which covers ventricle depolarization. Semilunar valves open and blood is ejected (second phase) and sets up the T-Wave which initiates ventricular repolarization.</span></div></li><li><div><b>Ventricular Diastole: <span style=""font-weight: 400;"">Semilunar valves close and blood flows into the atria (early), and then chambers relax and blood fills ventricles passively.</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.1 The Cardiac Cycle</span></div></b>Describe the cardiac cycle in terms of the ECG (P, QRS and T wave)<br> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>ECG:</div></li><ul><li><div>P: <span style=""font-weight: 400;"">Atrial Depolarization. Does not represent a contraction of the muscle or the firing of the SA node, we assume the SA node fires at its start and atrial contraction begins at its peak, atrial repolarization however is too minor of an amplitude to be recorded by surface electrodes</span></div></li><li><div>QRS: <span style=""font-weight: 400;"">Ventricular Depolarization. Q represents initial downward deflection, R represents initial upward deflection and S represents downward deflection and return to baseline - isoelectric point. Contraction commences at peak of the R portion of the complex. Can be confirmed clinically by palpitating pulse.</span></div></li><li><div>T: <span style=""font-weight: 400;"">Ventricular Repolarization.</span></div></li></ul></ul><br></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">2.2 Electrophysiology</span></div><div>Describe electrophysiology in terms of cardiac pacemakers and pacemaker potentials</div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Cardiac Pacemakers:<span style=""font-weight: 400;""> The cells of the SAN depolarise over time, with the movement of ions causing the resting membrane potential to gradually decrease (pacemaker potential), once the membrane potential exceeds a threshold, an action potential is triggered&nbsp; (this happens automatically about every 0.8 seconds at rest). The cells of the AVN do the same, but more slowly; the result of this is that an action potential is triggered in the AVN before they depolarise enough to trigger their own.</span></div></li><li><div>Pacemaker Potentials:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">At a membrane potential of about -60mv sodium channels open in the SAN cell membrane</span></div></li><li><div><span style=""font-weight: 400;"">Sodium enters the cell through the sodium channels taking a positive charge into the cell</span></div></li><li><div><span style=""font-weight: 400;"">The inside of the cell becomes less negative in relation to the outside</span></div></li><li><div><span style=""font-weight: 400;"">A voltage-gated calcium channel opens and calcium enters the cell slowly</span></div></li><li><div><span style=""font-weight: 400;"">The cell continues to depolarise gradually (pacemaker potential)</span></div></li><li><div><span style=""font-weight: 400;"">When the threshold is reached, another type of voltage-gated calcium channel opens and calcium enters the cell rapidly.</span></div></li><li><div><span style=""font-weight: 400;"">This results in rapid depolarisation which is the cardiac action potential.</span></div></li><li><div><span style=""font-weight: 400;"">Potassium outflow when some of its channels open and repolarization occurs when more potassium voltage-gated channels open.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.4 Respiration and Structures</span></div></b>Describe respiration and some main associated structures <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Respiration:<span style=""font-weight: 400;""> Exchange of gases between the atmosphere, blood, and cells. The combination of 3 processes required for respiration to occur is; Ventilation (breathing), External (pulmonary) respiration, and Internal (tissue) respiration.</span></div></li><li><div>Organization:<span style=""font-weight: 400;""> Two ways to organize the system:</span></div></li><ul><li><div>Structurally:<span style=""font-weight: 400;""> Upper respiratory system (nose, pharynx, and associated structures), Lower respiratory system (larynx, bronchi, and lungs)</span></div></li><li><div>Functionally:<span style=""font-weight: 400;"">&nbsp; Conducting zone and respiratory zone.</span></div></li></ul><li><div>Conducting Zone: <span style=""font-weight: 400;"">Trachea, Bronchi, Bronchioles, and Terminal Bronchioles. It Transports air to the lungs, and can be used to warm, humidify, filter, and clean the air as well as produced mucus and traps small particles and cilia away from the lungs. Also used in voice production.’</span></div></li><li><div><b>Terminal and Respiratory zones: <span style=""font-weight: 400;"">Respiratory bronchioles, Alveolar ducts and Alevolar sacs.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.4 Respiration and Structures</span></div></b>Describe respiration in regards to process of inhalation and ventilation<br> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Inhalation/Ventilation:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">During inhalation, the diaphragm contracts, and the external intercostals contract. The chest cavity expands as well as the volume of the lungs. The alveolar pressure drops below the atmospheric pressure and air flows into the lungs in response to the pressure gradient during deep inhalation, the scalene and sternocleidomastoid muscles expand the chest further, thereby creating a greater drop in alveolar pressure.</span></div></li><li><div><span style=""font-weight: 400;"">At rest when the diaphragm is relaxed the alveolar pressure is equal to atmospheric pressure so there is no airflow, but when exhalation occurs then the diaphragm relaxes and the external intercostals relax. The chest and lungs as such also recoil and the chest cavity contracts with the alveolar pressure increasing above atmospheric pressure so air flows out.</span></div></li><li><div><span style=""font-weight: 400;"">The alveolar surface is lined by type 1 and type 2 cells. The thin cytoplasm of the type 1 cell is ideal for gas diffusion whereas the type 2 cell is important for the production of surfactant which decreases the surface tension of the alveolus.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.8 Enteric Nervous System (ENS)</span></div></b>Briefly describe the Enteric Nervous System in terms of the myenteric plexus, submucosal and enteroendocrine cells <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: bold;""><li><div>Myenteric Plexus:<span style=""font-weight: 400;""> Between longitudinal and circular layers of muscle involved in the control of digestive tract motility.</span></div></li><li><div>Submucosal:<span style=""font-weight: 400;""> Located between the circular muscle and the luminal mucosa, can sense the environment of the lumen and regulates gastrointestinal blood flow and epithelial cell function.</span></div></li><li><div><b>Enteroendocrine cells:<span style=""font-weight: 400;""> Related to hormonal control by the production of about 22 hormones and paracrine and is present within the mucosa. However, they are single cells scattered about in the GI tract, densely packed secretory vesicles. They can sense luminal contents such as chemical, osmotic, and pH and thus can release hormones and paracrine to help fix any issues.</span></b></div></li></ul><div style=""""><b>MNEMONIC<br>Myenteric: DGM (Dungeon Master)</b></div><div style=""""><b>Submucosal:</b><br></div><div style=""""><b>B<br>E<br>L</b></div> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.9 Motility</span></div></b>In terms of intestinal physiology describe the types of contractions <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Phasic Contractions:<span style=""font-weight: 400;""> Short-lasting contractions that control the movement of material in the small intestine.</span></div></li><ul><li><div>Peristalsis<span style=""font-weight: 400;"">: Waves of contraction of about 20 cms. Food is moved distally along the tract in adjacent segments</span></div></li><li><div>Segmented: <span style=""font-weight: 400;"">Waves of contraction of about 10 cms. Food is moved forward and then backward in nonadjacent segments.</span></div></li></ul><li><b>Tonic Contractions:<span style=""font-weight: 400;""> Long-lasting contractions that result in the closing of the sphincter, it is a controlled movement of material through the tract in an ordered sequence of events that through ‘compartmentalization’ ensures processes are complete before passing to the next area.</span></b><br></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.11 Male reproductive organs and function</span></div></b>What do the sertoli and leydig cells produce and list the semen composition <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Scrotum:<span style=""font-weight: 400;""> Outside of the pelvis and 1’C&nbsp; less body temperature</span></div></li><li style=""font-weight: bold;""><div>Testis:<span style=""font-weight: 400;""> Seminiferous tubules (location of meiosis)</span></div></li><ul style=""font-weight: bold;""><li><div>Sertoli cells: <span style=""font-weight: 400;"">Sperms (spermatogenesis)</span></div></li><li><div>Leydig cells: <span style=""font-weight: 400;"">Testosterone</span></div></li></ul><li style=""font-weight: bold;""><div>Epididymis: <span style=""font-weight: 400;"">Functional maturation of sperm</span></div></li><li style=""font-weight: bold;""><div>Vas/ Ductus: <span style=""font-weight: 400;"">Transportation of sperm using smooth muscle and peristalsis</span></div></li><li style=""font-weight: bold;""><div>Semen Composition:</div></li><ul style=""font-weight: bold;""><li><div>Bulbourethral (10%):<span style=""font-weight: 400;""> Produces a clear lubricating fluid</span></div></li><li><div>Prostate (30%): <span style=""font-weight: 400;"">Silky white acidic milky white fluid, Prostatic fibrinolysin that is a decoagulant.</span></div></li><li><div><b>Seminal Vesicle (60%): <span style=""font-weight: 400;"">Alkaline solution, Fructose, Prosaglandis that stimulates uterine contraction and decreases cervical viscosity, Coagulate that turns semen into a bolus and readily propelled into the vagina.</span></b></div></li></ul></ul><div><br></div><div><b>MNEMONIC:</b></div><div><b>Boys</b></div><div><b>Penis</b></div><div><b>Sucks</b></div> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.12 Hypothalamic Pituitary Gondal Axis</span></div></b>Describe the Hypothalamic Pituitary Gondal Axis <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Hormones:<span style=""font-weight: 400;""> From the hypothalamus, the hormone GnRH every 2 hours is released into the blood, will arrive at the anterior pituitary and in response to this release there will be 2 hormones traveling via blood and will arrive at the testes</span></div></li><ul><li><div>Follicle Stimulating Hormone: <span style=""font-weight: 400;"">Act on the Sertoli cells and will produce sperm in the process of spermatogenesis</span></div></li><li><div><b>Luteinizing Hormone: <span style=""font-weight: 400;"">Act on the Leydig cells producing testosterone&nbsp;</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.13 Female reproductive organs and functions</span></div></b>Describe the female reproductive organs and functions in terms of the fallopian tube, uterus and cervix <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint727da984bc0a0ee3').style.display='block'; return false;""> Hint</a> <div id=""hint727da984bc0a0ee3"" class=hint style=""display: none"">FT: Cilia<br>Ut: Endo, Myo, Oxy<br>CV: CE</div> ""<div class=""back""> <b><ul><li><div>Fallopian tube:<span style=""font-weight: 400;""> Contains the infundibulum, ampulla, and fimbriae. Is the site of fertilization where the cilia can be used to help transport the zygote to the uterus</span></div></li><li><div>Uterus:<span style=""font-weight: 400;""> Has the Endometrium which sheds off monthly and where implantation of zygote takes place. There is also the Myometrium where smooth muscle is present and contacts during that are influenced by the hormone oxytocin.</span></div></li><li><div><b>Cervix: <span style=""font-weight: 400;"">The base of the uterus closed by a narrow passageway, has an alkaline pH as well as columnar epithelial with branched glands. It may be subject to hormonal changes such as during ovulation it is wet, slippery, and stretchable due to spinnbarkeit which is a stretchable mucus. During pre-or-post ovulation there it is in a dry state with thick mucus.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">2.14 Ovarian Cycle</span></div><div>Describe the ovarian cycle in terms of the mature ovum production and uterine cycle</div> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hintc5a7224499a7d144').style.display='block'; return false;""> Hint</a> <div id=""hintc5a7224499a7d144"" class=hint style=""display: none"">FOL and MPS!</div> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Mature Ovum Production:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Follicular Phase Days 1-13</span></div></li><li><div><span style=""font-weight: 400;"">Ovulation Day 14</span></div></li><li><div><span style=""font-weight: 400;"">Luteal Phase Days 15-28</span></div></li></ul><li style=""font-weight: bold;""><div>Uterine Cycle:</div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Menstrual Phase Days 1-6</span></div></li><li><div><span style=""font-weight: 400;"">Proliferate Phase Days 7-13</span></div></li><li><div><span style=""font-weight: 400;"">Secretory Phase Days 15-28</span></div></li></ul></ul><br> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">4.1 Cellular Behaviours</span></div></b>In terms of development describe cellular behaviours in terms of growth, positional information and cell signalling <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Growth:<span style=""font-weight: 400;""> Changes in cell shape and size can affect the shape of an embryo. It can be done in two ways either Hypertrophy (increase in cell size) or Hyperplasia (increase in cell number). Cellular growth creates thickened tissues as the cells grow in size and cell division greats growth by increasing cell number (mitosis), often both processes will be happening simultaneously.</span></div></li><li><div>Positional Information:<span style=""font-weight: 400;""> Involves in the creation of a body plan and establishing body axes, the blastomere cells know how to become the outer trophoblast cells or inner cell mass using cellular communication of both long and short range.</span></div></li><li><div>Cell Signalling: <span style=""font-weight: 400;"">Directional, and in the case of long-range often create gradients where they will behave differently depending on where they are on the gradient (this is called a morphogen)</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">4.2 Glossary</span></div><div style="""">Define and explain what a gamete, embryo and fetus is<br></div> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Gamete:<span style=""font-weight: 400;""> A specialized reproductive cell containing only one set of dissimilar chromosomes or half the genetic material necessary to form a complete organism, a sperm, and an egg.</span></div></li><li><div>Embryo:<span style=""font-weight: 400;""> Egg that has been fertilized by a sperm and undergone one or more divisions. Used to describe the structure of early human development following fertilization during the first 8 weeks.</span></div></li><li><div>Fetus:<span style=""font-weight: 400;""> A term used to describe human development following the embryonic period and is used to describe the first 9 to 37 weeks dubbed the fetal stage.</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">4.2 Glossary</span></div></b>In terms of Development define and explain what a teratogen and mutagen is <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Teratogen:<span style=""font-weight: 400;""> Any agent that can produce a birth defect or increase the incidence of a defect in a population. Teratogen affects only during the time of pregnancy</span></div></li><li><div><b>Mutagen: <span style=""font-weight: 400;"">A substance or an agent that can cause a change in DNA sequence. Mutagen effects can occur at any point during an individual's lifetime.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">4.3 Pre-Natal Development Timeline</span></div><div>Describe the pre-natal developmnet timeline</div> <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Period of cell division:<span style=""font-weight: 400;""> Week 1-2 after fertilization that includes blastogenesis and implantation.</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Cell division</span></div></li><li><div><span style=""font-weight: 400;"">Blastocyst formation</span></div></li><li><div><span style=""font-weight: 400;"">Implantation</span></div></li><li><div><span style=""font-weight: 400;"">Formation of 2 layers</span></div></li></ul><li style=""font-weight: bold;""><div>Embryonic period:<span style=""font-weight: 400;""> Week 3-8 that constitutes organogenesis. Both the cell division period and the embryonic period make up the first semester.</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Gastrulation</span></div></li><li><div><span style=""font-weight: 400;"">Basic body plan</span></div></li><li><div><span style=""font-weight: 400;"">Start of organogenesis</span></div></li></ul><li style=""font-weight: bold;""><div>Fetal Period: <span style=""font-weight: 400;"">Weeks 9-38 that constitutes a long period making up the second and third trimesters.</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Growth</span></div></li><li><div><span style=""font-weight: 400;"">Refinement</span></div></li><li><div><span style=""font-weight: 400;"">Cell Function</span></div></li></ul></ul><b>MNEMONIC:<br>C<br>E<br>F</b><br><br> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">4.4 Pre-Fertilization</span></div></b>What are some features of pre-fertilzation in regards to gametes, oocyte and sperm transport <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Gametes:<span style=""font-weight: 400;""> Fertilization occurs when the haploid gametes unite to form the diploid zygote. In preparation for this Primordial Germ Cells need to undergo gametogenesis to form gametes.</span></div></li><li><div>Oocyte Transport:<span style=""font-weight: 400;""> Egg is released by ovulation as a response to the hormones Prostaglandins and Luteinizing hormones. The egg is picked up by the infundibulum of the uterine tube/oviduct. Cilia wafting and muscular contraction of the uterine tube aid the movement of the egg.</span></div></li><li><div><b>Sperm Transport: <span style=""font-weight: 400;"">1-2% of sperm cells reach the isthmus of the oviduct because traveling from the cervical canal to the uterus is difficult for sperms because the cervix is convoluted and rough. However, during ovulation oestrogen and progesterone makes cervical mucus more watery to allow for motile swimming action of sperm. Little movement is done by sperm via propulsion and instead muscular contraction is done that is stimulated by oestrogen and progesterone.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">4.5 Fertilization</span></div><div>Describe some features during the process of fertilization (Corona Radiata, Zona Pellucia and Zona/Cortical)</div> <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Penetration of cumulus cell layer (Corona Radiata):<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">Capacitated sperm allows the key acrosomal enzymes to be released</span></div></li><li><div><span style=""font-weight: 400;"">Hyaluronidase enzyme digest and loosen the intracellular matrix of hyaluronic acid holding the layer of cumulus cells so sperm can penetrate.</span></div></li></ul><li style=""font-weight: bold;""><div>Penetration of zona pellucida and sperm binding:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">ZP is a tough non-cellular glycoprotein coat surrounding the oocyte</span></div></li><li><div><span style=""font-weight: 400;"">The sperm membrane binds with receptor protein in the ZP which causes the rest of the acrosome to dissolve and release enzymes that open a pathway for sperm head to the inside of the ovum.</span></div></li></ul><li style=""font-weight: bold;""><div>Plasma membrane of the oocyte and sperm fuses:&nbsp;</div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">The plasma membrane of the oocyte and sperm fuses and sperm releases its genetic material into the oocyte.&nbsp;</span></div></li><li><div><span style=""font-weight: 400;"">Initiation of zona/cortical reaction changes eggs structure and composition which blocks other sperms from entering (this prevents polyspermy)</span></div></li></ul></ul><br><b>WOI: Hhyaluronidase Enzyme</b><br><br> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">4.6 Products and Site of fertilization</span></div></b>What is the main product and site of fertilization <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Main Product:<span style=""font-weight: 400;""> Fertilisation ends with the intermingling of maternal and paternal chromosomes of the zygote.</span></div></li><ul><li><div><span style=""font-weight: 400;"">This restores the zygote's normal diploid to 46 chromosomes.</span></div></li><li><div><span style=""font-weight: 400;"">Triggers secondary oocyte to complete the second meiotic division producing a mature oocyte and a second polar body (this polar body is where damaged copies of chromosomes are sent to get apoptised)</span></div></li><li><div><span style=""font-weight: 400;"">The zygote is genetically unique with half chromosomes originating from the mother and half from the father. This results in variation</span></div></li></ul><li><b>Site:<span style=""font-weight: 400;""> Usual site of fertilization is the ampullary region of the fallopian tube or the first ⅓ of the tube, this part is the widest part of the tube but can also occur outside of the fallopian tube resulting in ectopic pregnancy mostly in the ampullary region.</span></b><br></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">4.7 Cell Division and Implantation</span></div></b>Describe and explain cell division and implantation <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Cell Division: <span style=""font-weight: 400;"">Cell cleavage occurs as the first divisions of the zygote when the zygote starts as a single cell and due to rapid mitotic divisions number of cells increases (blastomeres)</span></div></li><li><div>Stages:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">From the first 8 stages, the cells form a loosely arranged clump and cells are round and indistinguishable</span></div></li><li><div><span style=""font-weight: 400;"">After this stage the blastomeres form tight junctions in a process called compaction, During the 16-cell stage, the blastomeres are called a morula (mulberry).</span></div></li></ul><li><div>Compaction: <span style=""font-weight: 400;"">This is important for the generation of cell diversity/differentiation in the early embryo. This process forms two cell populations a superficial outer cell mass with a deep inner cell mass. The morula is divided into 2 parts:</span></div></li><ul><li><div>Outer Cell Mass: <span style=""font-weight: 400;"">Gives rise to the trophoblast layer (origin of the embryonic part of the placenta).</span></div></li><li><div><b>Inner Cell Mass: <span style=""font-weight: 400;"">&nbsp;Will exclusively form the embryoblast which forms the entire embryo.</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">4.8 Early Blastocyst and Starting Weeks</span></div></b>Describe and explain the early blastocyst stage in termss of what does it transform too and what does this outer layer become <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint8a2c49a8ba44ca21').style.display='block'; return false;""> Hint</a> <div id=""hint8a2c49a8ba44ca21"" class=hint style=""display: none"">Blastocyst becomes 2 things and the ""upper layers"" (BET!) become 2 more things (CS)!<br>""Bet on counter srike!""</div> ""<div class=""back""> <b><ul><li><div>Blastocyst:<span style=""font-weight: 400;""> The structure enabling the human embryo to implant is called the blastocyst and it consists of:</span></div></li><ul><li><div>Trophoblast: <span style=""font-weight: 400;"">Become part of the placenta.</span></div></li><li><div>Embryoblast: <span style=""font-weight: 400;"">Become part of the embryo.</span></div></li></ul><li><div>Zonal Pellucida:<span style=""font-weight: 400;""> Will shed to allow blastocyst to increase rapidly in size and derive nourishment from secretions of the uterine gland,</span></div></li><li><div>Outer Trophoblast Differentiation:&nbsp;</div></li><ul><li><div>Cytotrophoblast:<span style=""font-weight: 400;""> Cellular layer</span></div></li><li><div><b>Syncytiotrophoblast: <span style=""font-weight: 400;"">Syncytical layer (highly invasive layer with finger-like projections that expands rapidly)</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">4.9 Extraembryonic Membranes&nbsp;</span></div></b>Describe and explain the extraembryonic membrane in terms of Amnion, Allantosis, Chorion and Placenta <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Amnion: <span style=""font-weight: 400;"">Protective layer that allows the embryo to float and prevents drying out (desiccation).</span></div></li><li><div>Allantosis: <span style=""font-weight: 400;"">Helps in waste disposal and collection.</span></div></li><li><div>Chorion: <span style=""font-weight: 400;"">Part of the placenta and forms villi with blood vessels for exchange with the external environment.</span></div></li><li><div><b>Placenta: <span style=""font-weight: 400;"">Organ with maternal and fetal blood vessels.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">4.10 Weeks 2 and 3</span></div><div style="""">Describe and explain weeks 2 and 3 of development in terms of the bilaminar germ disc (embroblast) turning to epiblast tor hypoblast as well as they cell type</div> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hinta7bbdbcbbb9ae94f').style.display='block'; return false;""> Hint</a> <div id=""hinta7bbdbcbbb9ae94f"" class=hint style=""display: none"">Think about the cell type as well and what they become! Epipens are talls and column shaped, Hypnosis requires a small cuboid.</div> ""<div class=""back""> <b><ul><li><div>Bilaminar Germ Disc: <span style=""font-weight: 400;"">Embryoblast differentiates into two layers:</span></div></li><ul><li><div>Epiblast (tall columnar cells): <span style=""font-weight: 400;"">Pluripotent cells on the outer layer. These cells give rise to the embryonic tissue which also leads to body structures and organs. They are also the floor of the amniotic cavity.</span></div></li><li><div>Hypoblast (small cuboidal cells): <span style=""font-weight: 400;"">Transforms the blastocyst cavity into the yolk sac and gives rise to extraembryonic tissues.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">6.13 Agonist</span></div></b>List and explain the compeitive, non-compeitive, reversible and irreversible agonists<br> <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: 700;""><li><div>Competitive:&nbsp;<span style=""font-weight: 400;"">Compete for the agonist binding site to prevent receptor activation</span></div></li><li><div>Non-competitive:&nbsp;<span style=""font-weight: 400;"">Bind to the allosteric site to prevent receptor activation</span></div></li><li><div>Reversible:<span style=""font-weight: 400;"">&nbsp;Bind weakly and can dissociate from the receptor, thereby freeing it up for action.</span></div></li><li><div><b>Irreversible:&nbsp;<span style=""font-weight: 400;"">Bind covalently and permanently to disable the receptor.</span></b></div></li></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">6.5 Drug Excretion</span></div></b>In terms of Drug excretion in pharmacology describe active tubular secretion and passive tubular diffusion<br> <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: bold;""><li><div>Active Tubular Secretion:<span style=""font-weight: 400;"">&nbsp;Blood that leaves the glomerulus capillary perfuses the rest of the neuron, allowing the active secretion of both free and bound drugs into the tubular lumen. There are two major secretory pathways one for weak bases and another one for weak acids</span></div></li><li><div><b>Passive Tubular Diffusion:&nbsp;<span style=""font-weight: 400;"">Lipid-soluble drugs that are freely filtered by the glomerulus but subjected to passive reabsorption by the renal tubule is taken back into the blood by to be further metabolized by the liver. Water soluble drugs are not subject to passive tubular reabsorption so urinary excretion terminates their effect but lipid soluble transferred back to blood.</span></b></div></li></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.1 The Cardiac Cycle</span></div></b>Describe the cardiac cycle in terms of the PR interval and PR segment<br> <br> <br> <br> <br> ""<div class=""back""> <ul style=""font-weight: 700;""><li><div>PR interval:&nbsp;<span style=""font-weight: 400;"">Measured from the beginning of the P wave to the beginning of the R portion of the QRS complex, Starts with atrial muscle depolarization and ends with ventricular depolarization and it is assumed that an impulse passes through the AV node during this interval. Determines if impulse conduction from the atria to the ventricles is normal.</span></div></li><li><div>PR segment:&nbsp;<span style=""font-weight: 400;"">Flatline between the end of the P wave and onset of QRS complex and reflects the slow impulse contraction through the AV node, serves as a baseline for the isoelectric line of the ECG trace.</span></div></li></ul> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">7.2 DNA Replication</span></b></div><div>List and explain the 3 types of polymerase</div> <br> <br> <br> <br> ""<div class=""back""> <ul><ul><li><div><span style=""font-weight: 700;"">DNA Polymerase: </span>A biological replication machine that travels along each replication fork of a DNA that has 5 known types:</div></li><ul><li><div><span style=""font-weight: 700;"">DNA Polymerase α, δ, and ε: </span>Nuclear DNA</div></li><li><div><span style=""font-weight: 700;"">DNA Polymerase γ: </span>Mitochondrial DNA</div></li><li><div><span style=""font-weight: 700;"">DNA Polymerase β: </span>DNA repair and gap-filling</div></li></ul></ul></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.13 RBC Synthesis</span></div></b>Describe the proccess of synthesis for Hamoglobin <br> <br> <br> <br> ""<div class=""back""> <ul><li><div>Synthesis:&nbsp;</div></li><ul><li><div>HB synthesis occurs in the mitochondria of the immature red blood cells</div></li><li><div>Ferrous irons are delivered into the RBC by transferrin that is further translocated into the mitochondria</div></li><li><div>Inside the mitochondria, aminolaevulinic acid (ALA) is synthesized which is then transferred back into the cytoplasm which causes it to change into protoporphyrin.</div></li><li><div>Protoporphyrin binds to Fe2+ to form Haem groups that in addition to proteins form the final Hb molecule</div></li></ul></ul> "
"<div><span style=""font-style: italic; text-decoration-line: underline;""><b>2.14 Ovarian Cycle</b></span></div>List the sex hormones as well as where are they produced from and list the contents of mensuration <br> <br> <br> <br> ""<div class=""back""> <div><ul><li><div>Sex Hormones:</div></li><ul><li><div>Ovary - Oestrogen</div></li><li><div>Corpus Luteum - Progesterone</div></li></ul></ul><ul><li><div>Menstruation Contains:</div></li><ul><li><div>Stratum functionalist tissues</div></li><li><div>Blood</div></li><li><div>Mucus</div></li><li><div>Secondary Oocyte</div></li><li><div>Endometrial repair starts</div></li></ul></ul></div> "
"<div><span style=""font-style: italic; text-decoration-line: underline;""><b>4.10 Weeks 2 and 3</b></span></div><div>Describe and explain the notochord, mesoderm and somites</div> <br> <br> <br> <br> ""<div class=""back""> <ul><li><div><b>Notochord:</b>&nbsp;A cellular rod of cells that acts as a structural support for the embryo and a primary inducer to transform surrounding unspecialized embryonic cells into tissues/organs. It is a transient structure that will degenerate as bodies of the vertebral column develop but will persist as the intervertebral discs of the vertebral column.</div></li><li><div><b>Mesoderm:</b>&nbsp;Highly organized cells that migrate towards edges before differentiating into the Paraxial, Intermediate, and Lateral mesoderm. This is in response to Bone Morphogenetic Proteins (BMP’s).</div></li><li><div><b>Somites:</b>&nbsp;Bilateral blocks of condensed paraxial mesoderms on the sides of the notochord and neural tubes, the former induces it into somites. It gives rise to most of the skeleton of the trunk like ribs and vertebrae columns, musculature and vasculature, and dermis.</div></li></ul> "
"<div><span style=""font-style: italic; text-decoration-line: underline;""><b>4.10 Weeks 2 and 3</b></span></div><div>Describe and explain weeks 2 and 3 of development in terms of gastrulation</div> <br> <br> <br> <br> ""<div class=""back""> <ul><li><div>Gastrulation:&nbsp;Process of the transformation of epiblast and hypoblast into ectoderm, mesoderm, and endoderm. The formation of the primitive streak is its first sign, this is when epiblast cells ingress by embryonic growth factors so the streak elongates caudally, the cranial end expands as the primitive node, and a depression called the primitive pit.</div></li><ul><li><div>Epiblast cells continue to migrate in a process of ‘epithelial to mesenchymal transition (EMT), which causes the differentiation into endoderm and mesoderm layers. Later in the 3rd week, intraembryonic mesoderm separates the ecto and endoderm except in 2 regions; Oropharyngeal (future oral cavity) and Cloacal (future urinary tract and genital tract).</div></li></ul></ul> "
"<div><span style=""font-style: italic; text-decoration-line: underline;""><b>5.2 Microbiological Properties</b></span></div><div>Describe ecological relations of microbiological organisms</div> <br> <br> <br> <br> ""<div class=""back""> <ul><li><div><b>Ecological Relations:&nbsp;</b></div></li><ul><li><div><b>Mutualistic:</b>&nbsp;Association in which each organism benefits.</div></li><li><div><b>Commensal:</b>&nbsp;Act on the host immune system to induce protective responses to prevent invasion by pathogens.</div></li><li><div><b>Parasite:</b>&nbsp;Lives in host organisms and gets its food at the expense of its host.</div></li><li><div><b>Opportunistic:</b>&nbsp;Potential for most bacteria to transform too and typically non-pathogenic and dormant until the host's immune system is suppressed and seizes attack chance.</div></li><li><div><b>Pathogen:&nbsp;<span style=""font-weight: 400;"">Capable of causing diseases inside a host.</span></b></div></li></ul></ul><b>MNEMONIC<br>My<br>Chicken<br>Pox<br>Ordered<br>Pizza</b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.1 Ganglia</span></div>Descrive the ganglia as well as some of its associates agonists and antagonists <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> ANS nerves pass through the nerve cell clusters called ganglia. The sympathetic is located in the ventral and dorsal to the spinal cord, Parasympathetic ganglia are near the target organ. All automatic efferents from the CNS use the neurotransmitter acetylcholine</span></div></li><li><div>Drugs:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Agonists:&nbsp;</div></li><ul><li><div>Nicotine</div></li><li><div>Varenicline</div></li><ul><li><div>Complex effects: <span style=""font-weight: 400;"">Tachycardia, Blood pressure, Variable GI activity, increased secretory activity</span></div></li></ul></ul><li><div>Antagonists (Therapeutically Obsolete):&nbsp;</div></li><ul><li><div>Tubocurarine&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</div></li><li><div>Hexamethonium&nbsp;&nbsp;&nbsp;</div></li><ul><li><div>Complex effects: <span style=""font-weight: 400;"">Hypotension, loss of CV reflexes, inhibition of secretions, GI paralysis, reduced urination</span></div></li></ul></ul></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.2 Nicotinic Acetylcholine Receptor (nAChR)</span></div><div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.3 The Sympathetic Nervous System</span></div>Describe the nAChR and the sympathetic nervous system <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>nAChR: <span style=""font-weight: 400;"">Prototypical ligand-gated ion channel consisting of 5 subunits. The first discovered exogenous agonist is nicotine, it is permeable to Na+ ( and Ca2+, K+) ions, and allows depolarisation, and excitation of the postganglionic nerve.</span></div></li><li><div>Postganglionic Agonists:<span style=""font-weight: 400;""> The main postganglionic neurotransmitter in the SNS is noradrenaline, which is a catecholamine transmitter that is released from the adrenal gland as a hormone.</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.4 Neurotransmitter vs Hormones</span></div>Compare and contrast neurotransmitters and hormones <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> Hormones are released by glands into the circulatory system and have bodywide effects. Neurotransmitters are released by neurons and have local effects on postsynaptic targets.</span></div></li><li><div><span style=""font-weight: 400;"">Adrenaline is a hormone released by the adrenal gland. Noradrenaline can be either a neurotransmitter (released from the synapse) or a hormone (from the adrenal gland).</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.5 Adrenergenic a1 receptors</span></div><span style=""font-weight: 400;"">Explain and describe the Adrenergic a1 receptors</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> They are Gq protein-coupled receptors, which means when the receptor is activated the alpha subunit is going to bind to Phospholipase C and going to cause the formation of Diacylglycerol and inositol triphosphate-3 and this causes the increase of intracellular calcium concentration</span></div></li><li><div>Location: <span style=""font-weight: 400;"">Blood vessels, GI sphincter, Eye, Salivary Gland</span></div></li><li><div><b>Agonism: <span style=""font-weight: 400;"">Constriction, Vasoconstriction, Reduced urine flow, Mydriasis and salivary secretion</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.6 Adregenic a2 receptor</span></div><span style=""font-weight: 400;"">Describe and explain the Adregenic a2 receptors</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.6 Adregenic a2 receptor</span></div><ul><li><div>Overview:<span style=""font-weight: 400;""> They are Gi receptors so they decrease the activity of adenyl cyclase so there is less cAMP produced so decreases the concentration of calcium inside cells</span></div></li><li><div>Location:<span style=""font-weight: 400;""> CNS, Pre-synaptic SNS terminals.</span></div></li><li><div><b>Agonism: <span style=""font-weight: 400;"">Decreased synaptic output, decreased sympathetic activity.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.7 Adregenic b1 receptors</span></div>Describe and explain the adregenic b1 receptors <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> They are Gs protein-coupled so they increase the activity of adenyl cyclase so more release of cAMP</span></div></li><li><div>Location:<span style=""font-weight: 400;""> Heart and Kidney</span></div></li><li><div>Agonist: <span style=""font-weight: 400;"">Increased heart contractility, Increased heart rate</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.8 Adregenic b2 receptors</span></div><span style=""font-weight: 400;"">Describe and explain the adrengenic b2 receptors</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> They are Gs protein-coupled so they increase the activity of adenyl cyclase so more release of cAMP</span></div></li><li><div>Location:<span style=""font-weight: 400;""> Lungs, blood vessels, smooth muscle</span></div></li><li><div>Agonism:<span style=""font-weight: 400;""> Bronchodilation, Vasoldilation, Smooth muscle relaxation, uterine dilation, and glycogenolysis.</span></div></li><li><div><b>Note: <span style=""font-weight: 400;"">Noradrenaline has a very low affinity for b2 receptors.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.9 Adregenic b3 receptors</span></div>Describe and explain the adregenic b3 receptors <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> They are Gs protein-coupled so they increase the activity of adenyl cyclase so more release of cAMP</span></div></li><li><div>Location:<span style=""font-weight: 400;""> Fatty tissue, skeletal muscle, the bladder muscle</span></div></li><li><div>Agonism: <span style=""font-weight: 400;"">Lipolysis, Thermogenesis, Bladder relaxation.</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.10 Parasympathetic Nervous System</span></div>Describe and explain the parasympathetic nervous system in terms of receptors <br> <br> What are the preganglionic and postganglionic receptors and channels? <br> <br> ""<div class=""back""> <b><ul><li><div>Endogenous Agonist:<span style=""font-weight: 400;""> The main postganglionic neurotransmitter in the PNS is acetylcholine.</span></div></li><li><div>Receptors:</div></li><ul><li><div>Preganglionic: <span style=""font-weight: 400;"">Nicotinic acetylcholine receptor (nAChR), Ligand-gated ion channels.</span></div></li><li><div>Postganglionic: <span style=""font-weight: 400;"">Muscarinic acetylcholine receptor (mAChR), G-protein coupled receptors.</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.11 M1 receptors</span></div>Describe and explain the M1 receptors <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> They are Gq protein-coupled receptors, that means when the receptor is activated the alpha subunit is going to bind to Phospholipase C and going to cause the formation of Diacylglycerol and inositol triphosphate-3 and this causes the increase of intracellular calcium concentration</span></div></li><li><div>Located:<span style=""font-weight: 400;""> CNS, GI tract, salivary and lachrymal glands.</span></div></li><li><div><b>Agonism: <span style=""font-weight: 400;"">CNS Excitation, Gastric Secretion.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.12 M2 receptors</span></div><span style=""font-weight: 400;"">Describe and explain the M2 receptors</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;"">&nbsp; They are Gi receptors so they decrease the activity of adenyl cyclase so there is less cAMP produced which decreases the concentration of calcium inside cells</span></div></li><li><div>Located:<span style=""font-weight: 400;""> CNS, Heart</span></div></li><li><div><b>Agonism: <span style=""font-weight: 400;"">Cardiac inhibition, CNS inhibition</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.13 M3 receptors</span></div>Describe and explain the M3 receptors <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> They are Gq protein-coupled receptors, that means when the receptor is activated the alpha subunit is going to bind to Phospholipase C and going to cause the formation of Diacylglycerol and inositol triphophate-3 and this causes the increase of intracellular calcium concentration</span></div></li><li><div>Located:<span style=""font-weight: 400;""> CNS, Heart</span></div></li><li><div><b>Agonism: <span style=""font-weight: 400;"">Cardiac inhibition, CNS inhibition</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.16 nAChR agonists</span></div><span style=""font-weight: 400;"">Describe and explain a nAChR agonist</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> Suxamethonium is an nAChR agonist, depolarising blocker.</span></div></li><li><div>Clinical Use:<span style=""font-weight: 400;""> Surgery as it prevents muscle movement</span></div></li><li><div><b>Side effects: <span style=""font-weight: 400;"">Better to give after anesthetic as it is painful. Causes initial Tachycardia and too many causes bradycardia</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.17 Acetylcholinesterase Inhibitors</span></div>Describe and explain the acteylcholinesterase inhibitors <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Clinical Use:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Neostigmine, Pyridostigmine - Mysthithea Gravis</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.18 Botox (Botulinum Toxin)</span></div><span style=""font-weight: 400;"">Describe and explain Botulinum Toxin (Botox)</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;""> Inhibits synaptic vesicle release, used especially at cholinergic synapses.</span></div></li><li><div>Clinical Use:<span style=""font-weight: 400;""> Muscle spasms, Muscle overactivity, Cosmetic surgery</span></div></li><li><div><b>Side Effects: <span style=""font-weight: 400;"">Muscle weakness, flu-like side symptoms, allergic reactions.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.26 Atropine</span></div>Describe and explain atropine <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><b><ul><li><div><span style=""font-weight: 400;"">A non-selective muscarinic antagonist. Some of its clinical use includes:</span></div></li><ul><li><div><span style=""font-weight: 400;"">Cardiopulmonary resuscitation</span></div></li><li><div><span style=""font-weight: 400;"">Bradycardia (including intraoperative, drug overdose)</span></div></li><li><div><span style=""font-weight: 400;"">Preoperative urinary retention</span></div></li></ul></ul></b></li></ul> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.29 Drug Treatment Of Asthma</span></div>Briefly explain the drug treatment of asthma<br><br> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Treatment:<span style=""font-weight: 400;""> Drug treatment of asthma is centered around improving peak expiratory flow of the lung by targeting the bronchioles, the two major areas of drug action to influence the symptoms of asthma include inducing bronchodilation of smooth muscle to increase bronchiole diameter and reducing the inflammation which thickens the bronchiolar wall.</span></div></li><li><div>Drug Treatment:</div></li><ul><li><div>Intermittent Reliever Therapy</div></li><ul><li><div><span style=""font-weight: 400;"">Short-acting β2-adrenoreceptor agonists (inhaled SABA)</span></div></li></ul><li><div>Regular Preventer Therapy</div></li><ul><li><div><span style=""font-weight: 400;"">Low dose corticosteroid (inhaled)</span></div></li></ul><li><div>Initial Add-In Therapy</div></li><ul><li><div><span style=""font-weight: 400;"">Leukotriene Receptor Antagonist (Oral)</span></div></li><li><div><span style=""font-weight: 400;"">Long-acting β2-adrenoreceptor agonist (inhaled LABA)</span></div></li></ul><li><div>Additional Controller Therapy</div></li><ul><li><div><span style=""font-weight: 400;"">Theophylline (Oral)</span></div></li><li><div><span style=""font-weight: 400;"">Long-acting muscarinic antagonist (inhaled LAMA)</span></div></li></ul><li><div>Continous Corticosteroid</div></li><ul><li><div><span style=""font-weight: 400;"">Prednisolone</span></div></li></ul></ul></ul><br></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.30 Intermittent Reliever Therapy</span></div>Explain intermittent reliever therapy (explain salbutamol) <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Type Of Drug: <span style=""font-weight: 400;"">Beta 2 agonists</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Gq membrane, passes through it 7 times and inactivates myosin phosphorylation</span></div></li><li><div>Effect:<span style=""font-weight: 400;""> Bronchodilator, inhibits mediator release and mucous clearance.</span></div></li><li><div><b>Adverse Effects: <span style=""font-weight: 400;"">Tolerance. C16 from arginine to glycine causes tolerance and nocturnal worsening, C27 Glutamine becomes glutamate tolerance decreases</span></b></div></li></ul></b><b>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><ul><li><div>SABA:<span style=""font-weight: 400;""> Used in all patients and for those with infrequent, short-lived wheezes it may be the only treatment required. Adrenaline is the derivative hormone and its selectivity relies on the amine portion (normally activates a1b1 and a2bs)</span></div></li><li><div>Isoprenaline: <span style=""font-weight: 400;"">The result of increasing the size of the amine substituent preventing alpha activation that dilates bronchiolar muscles and stimulates the heart which results in cardiac arrhythmias.</span></div></li><li><div>Salbutamol And Terbutaline: <span style=""font-weight: 400;"">Produced by increasing the size of the amine group prevents the beta-1 effect producing a beta-2-agonist. Not a catecholamine so longer duration of action.</span></div></li><li><div>Mechanism Of Action:<span style=""font-weight: 400;""> Salbutamol spans the cell membrane 7 times at the beta-2 adrenoreceptor which activates adenylyl cyclase through a G-protein mechanism elevating cAMP levels. Smooth muscle relaxation is induced by inactivating the myosin enzyme light chain kinase decreasing myosin phosphorylation.</span></div></li><li><div>Metered Dose Aerosol: <span style=""font-weight: 400;"">Inhalation improves drug selectivity and reduces the potential widespread adverse effects. SABA is delivered via inhalation using a metered dose aerosol releasing a fixed dose. With bronchodilation, they inhibit mediator release from mast cells and increase mucous clearance.</span></div></li><li><div><b>Adverse Effects:<span style=""font-weight: 400;""> Results from systemic absorption or delivery through the GI tract. Most important adverse effect is tolerance which is a reduction in therapeutic effect due to frequent use. Receptor agonists down-regulate and receptor antagonists up-regulate receptor number. Genetic polymorphism is a major factor; 74% of patients experienced nocturnal worsening with increased tolerance perhaps due to glycine replacing arginine at amino acid 16 while a decrease in tolerance in patients with receptor variant C27 where glutamine becomes glutamate.</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.31 Regular Preventer Therapy</span></div>Describe and explain regular preventer therapy (Beclometasone) <br> <br> <br> <br> ""<div class=""back""> <div style=""""><div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.? Fluticasone/ Beclometasone/Budesonide</span></div><ul style=""""><li style=""""><div style=""""><b>Type Of Drug: </b>Glucocorticoid/Steroid</div></li><li style=""font-weight: bold;""><div>MOA/Effect:<span style=""font-weight: 400;""> BMM (Bronchodilator, Mediator and Mucous)</span></div></li><li style=""font-weight: bold;""><div><b>Adverse Effects:<span style=""font-weight: 400;""> Oral candidiasis resulting, pnemumonia&nbsp;</span></b></div></li></ul><span style=""font-weight: bold; font-style: italic;"">--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><u>5.31 Regular Preventer Therapy</u></span></div><ul style=""""><li style=""font-weight: bold;""><div>Regular Preventer (Maintenance) Therapy<span style=""font-weight: 400;"">: When more than 1 inhaler (200 doses required each month)</span></div></li><li style=""font-weight: bold;""><div>Corticosteroids:<span style=""font-weight: 400;""> Delivered by meter dose aerosol. Contains one of three major agents; beclometasone, fluticasone and budesonide. They inhibit inflammation and suppress the immune system. No bronchodilator activity so will not provide relief in an acute asthma attack and only reduce the need for reliever therapy from salbutamol.</span></div></li><li style=""""><div style=""""><b style="""">I</b><b style=""font-weight: bold;"">nhaled Steroids:<span style=""font-weight: 400;""> Adverse effects include fungal oral candidiasis resulting from immunosuppression by local delivery into the mouth with a potential risk being pneumonia, estimated 70% delivered to the GI tract instead. To prevent adrenal suppression from systemic absorption fluticasone is designed to be metabolized on first pass through the liver.</span></b></div></li></ul> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">5.32 Initial Add-In Therapy</span></div>Describe and explain initial add-in therapy (Montelukast, Formeterol) <br> <br> <br> <br> ""<div class=""back""> <div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.? Montelukast</span></div><ul style=""font-weight: bold;""><li><div>Type Of Drug: <span style=""font-weight: 400;"">Leukotriene receptor Antagonist</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Inhibits cysteinyl leukotrine&nbsp;</span></div></li><li><div>Effect:<span style=""font-weight: 400;""> BMM (Bronchodilator, Mucous, MEdiator)</span></div></li><li><div><b>Adverse Effects: <span style=""font-weight: 400;"">Fever, headache, and infection (Hi! Fuck Off)</span></b></div></li></ul><b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Formoterol/Salmeterol</span></div><ul><li><div>Type Of Drug: <span style=""font-weight: 400;"">β2-adrenoreceptor agonist</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Gs receptor, increases Adenylyl Cyclase production increasing cAMP so a greater concentration of Ca2+</span></div></li><li><div>Effect:<span style=""font-weight: 400;""> B (Maintainence)</span></div></li><li><div>Adverse Effects: <span style=""font-weight: 400;"">Must be delivered with steroids or risk of death&nbsp;</span></div></li><li><div><b>Features:<span style=""font-weight: 400;""> Salmeterol has high lipid solubility and is a partial α-agonist</span></b></div></li></ul></b><b>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><ul><li><div>Initial Add-In Therapy: <span style=""font-weight: 400;"">For when continued uncontrolled SABA and corticosteroid inefficient.</span></div></li><li><div>Leukotriene: <span style=""font-weight: 400;"">Derived from arachidonic acid released from the cell membrane like prostaglandin. Conversion is via a lipoxygenase rather than a cyclo-oxygenase pathway. They are fatty acids combined with amino acids, called cysteinyl leukotrienes which in combination form a mixture termed SRS-A which is a slow-reacting substance of anaphylaxis.</span></div></li><li><div>Montelukast:<span style=""font-weight: 400;""> Delivered via oral dosage and not inhalation, is an antagonist for the receptor cysteinyl leukotrienes called Cys LT-1 that inhibits lung inflammation, bronchoconstriction,&nbsp; and mucous secretion. Oral dose form may have GI tract adverse effects inducing fever, headache, and infection.</span></div></li><li><div><b>Long-acting β2 adrenoreceptor agonists: <span style=""font-weight: 400;"">Consists of salmeterol and formoterol containing large amine substituent and used as maintenance therapy, not acute relief. Must be delivered with steroids since alone are linked with asthma deaths. High lipid solubility helps tissue retention at the beta-2 adrenoreceptor to which salmeterol may also anchor and is a partial agonist, it also has a more rapid onset of action and higher receptor affinity.</span></b></div></li></ul></b><br> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.33 Additional Controller Therapies</span></div><span style=""font-weight: 400;"">Describe and explain additional controller therapies (Theophylline/ Tiotropin)</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Theophylline</span></div><ul><li><div>Type Of Drug:<span style=""font-weight: 400;""> Phosphodiesterase inhibiter</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Inhibits the phosphodiesterase receptor/ MOA undiscovered.</span></div></li><li><div>Effect:<span style=""font-weight: 400;""> Bronchodilator that reduces the sensitivity of bronchioles.</span></div></li><li><div>Adverse Effects:<span style=""font-weight: 400;""> Arrhythmia and seizures come from the saturation of liver metabolism.</span></div></li></ul><br><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Tiotropin</span></div><ul><li><div>Type Of Drug: <span style=""font-weight: 400;"">Muscarinic cholinoreceptor antagonist (LABA)</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Mediates the release of acetylcholine acting at the muscarinic receptor</span></div></li><li><div>Effects:<span style=""font-weight: 400;""> Bronchodilator.</span></div></li></ul></b><b>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><ul><li><div>Additional Controller Therapy: <span style=""font-weight: 400;"">For when agents described are ineffective and therefore stopped.</span></div></li><li><div>Theophylline:<span style=""font-weight: 400;""> A bronchodilator that reduces the sensitivity of bronchioles to inflammatory stimuli, Mechanism of action is still unresolved. Its water-soluble analog aminophylline has a narrow therapeutic window and requires drug monitoring. Its adverse effect is from the saturation of liver metabolism&nbsp; causing elevated plasma concentrations causing arrhythmia and seizures.</span></div></li><li><div><b>Long-Acting Muscarinic Receptor Antagonist:<span style=""font-weight: 400;""> Bronchiolar smooth muscle is also under the control of the parasympathetic nervous system. Bronchoconstriction is mediated by the release of acetylcholine acting on its muscarinic receptor. The classical muscarinic choline receptor antagonist is atropine with Tiotropine being its long-acting muscarinic agent.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.34 Continuous Corticosteroid</span></div><span style=""font-weight: 400;"">Descrobe and explain continuous corticosteroid (prednisolone/ mepolizumab)</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Prednisolone</span></div><ul><li><div>Type Of Drug: <span style=""font-weight: 400;"">Glucocorticoid Agonist</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Lipocortin releasing arachidonic acid inhibiting phospholipase A2 and upregulate β2-2-adrenoreceptor</span></div></li><li><div>Effects:<span style=""font-weight: 400;""> Anti-inflammatory, Immunosupreesant and IL-transcription</span></div></li><li><div>Adverse Effects: <span style=""font-weight: 400;"">Moon Face, Osteoporosis, Thinning Skin, Abdominal Fat, Addisonian Crisis</span></div></li></ul><br><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Mepolizumab</span></div><ul><li><div>Type Of Drug: <span style=""font-weight: 400;"">Cytokine inhibitor for IL-5</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Binds and neutalizes IL-5 reducing eosinophil production.</span></div></li><li><div>Effects:&nbsp;</div></li><li><div>Adverse Effects:</div></li></ul></b><b><br>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><ul><li><div>Prednisolone:<span style=""font-weight: 400;""> Normally kept quiet by binding to a heat shock protein, it stimulates an anti-inflammatory effect increasing the synthesis of lipocortin which release arachidonic acid from the cell membrane by enzyme inhibition of phospholipase A2. Steroids reduce vascular permeability and can upregulate beta-2adrenoreceptor, they also are immunosuppressants in addition to anti-inflammatory effects reducing IL-Transcription and thereby the clonal expansion of lymphocytes.</span></div></li><li><div>Adrenal Suppression: <span style=""font-weight: 400;"">The chronic use of steroids such as prednisolone can inhibit the endogenous production of cortisol by a negative feedback mechanism on the pituitary and hypothalamus. As a result, if oral steroids are withdrawn rapidly a patient can be left without any endogenous cortisol production including an Addisonian crisis.&nbsp;</span></div></li><li><div>Eosinophil:<span style=""font-weight: 400;""> Degranulation of the mast cell is associated with the release of any other mediators apart from histamine, including products of arachidonic acid metabolism such as prostaglandin D2, which can then recruit other cells of the immune system such as the eosinophil. PGD2 exerts a two-fold effect on it with direct activation and indirect recruitment (chemotaxis) through the release of IL-5 from T-helper cells which can be inhibited using monoclonal antibodies.</span></div></li><li><div><b>IL-5 Mediators:<span style=""font-weight: 400;""> Two monoclonal antibodies, mepolizumab, and reslizumab are available which bind and neutralize IL-5 directly, which reduces the production and attraction of eosinophils to the airway. Mepolizumab is given by subcutaneous injection, reslizumab is administered by intravenous infusion. Both require monthly administration and are indicated as add-on therapy for severe refractory eosinophilic asthma. Benralizumab is an IL-5 receptor antagonist.&nbsp;</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.35 Drugs In The Lungs And Histamines</span></div><span style=""font-weight: 400;"">Describe and explain drugs in the lungs and histamines</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">5.35 Drugs In The Lungs And Histamines</span></div><ul><li><div>Drugs:<span style=""font-weight: 400;""> The lungs can be a useful route for the systemic delivery of drugs in a gaseous form such as anesthetics, analgesics (nitrous oxide), or oxygen. Drugs may be used to stimulate respiration while muscle relaxants, required for abdominal surgery are nicotinic cholinergic antagonists which block the neuromuscular junction, inhibiting the diaphragm and requiring artificial ventilation. Other drugs may include antitussives which tend to be opioids that can cause respiratory depression. Nasal decongestants constrict nasal blood vessels and tend to be sympathomimetic amines while mucolytics thin the mucus. In addition to the systemic use of antibiotics, the local delivery of antibiotics into the lungs by inhalation is useful in the treatment of cystic fibrosis. Sodium cromoglycate is a mast cell stabilizer used as early preventer therapy for asthma but also allergies such as hay fever.</span></div></li><li><div><b>H1 - Antihistamines: <span style=""font-weight: 400;"">Antihistamines are selective for the H1 histamine receptor, known to be inverse agonists. They are not bronchodilators but inhibit vascular permeability due to histamine release from mast cells or allergic responses. /a major adverse effect is sedation for 1st generation agents, such as chlorphenamine with a high lipid solubility and ability to cross the blood-brain barrier. The 2nd generation agents such as loratadine, were designed to be more water soluble to reduce this effect</span></b></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.3 Pericardium</span></div>Briefly explain the fibrous and serous pericardium&nbsp; <br> <br> <br> <br> ""<div class=""back""> <ul><li><div><span style=""font-weight: 700;"">Fibrous Pericardium: </span>The fibrous pericardium extends from its inferior apex attachment at the diaphragm, all around the heart, and then blends with the adventitia (blood vessel layer) of the great vessels superiorly. Attached anteriorly to the sternum and helps to keep the heart in position in the thoracic cavity, attached loosely posteriorly to structures within the posterior mediastinum. Fibrous pericardium somatic sensory innervation is from the phrenic nerves and passes through the fibrous pericardium on its way to the diaphragm.</div></li><li><div><span style=""font-weight: 700;"">Serous Pericardium:</span> Divided into two layers</div></li><ul><li><div><span style=""font-weight: 700;"">Parietal Pericardium:</span> Lines the inner surface of the fibrous pericardium</div></li><li><div><span style=""font-weight: 700;"">Visceral Layer: </span>Also known as the epicardium and adheres to the heart and forms it's outer covering</div></li></ul></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.10 Heart Wall: Layers</span></div><div><span style=""font-weight: 400;"">Describe the histology/layers of skin of the heart in terms of Endocardium and Heart Valves</span></div></b> <br> <br> <br> <br> ""<div class=""back""> <ul><li><div><b>Endocardium:</b></div></li><ul><li><div>Internal layer of the heart wall that is in direct contact with blood, thicker in atria than ventricles because elastic fibers are needed in atria for expansion. It is composed of 3 layers:</div></li><ul><li><div>Contact:&nbsp;Collagen fibers merge with those surrounding cardiac muscle fibers. It can also contain Purkjne fibers</div></li><li><div>Middle:&nbsp;Collagen fibers with a variable number of elastic fibers.</div></li><li><div>Innermost:&nbsp;Flat endothelial cells that are continuous with the cells lining vessels associated with the heart.</div></li></ul></ul><li><b>Heart Valves:<span style=""font-weight: 400;"">&nbsp;Fibrocollagenous which extends from the cardiac skeleton. Superior and inferior surfaces are covered by fibroelastic tissue and an outer layer of flat endothelial cells. In atrioventricular valves, the inferior surface is roughened for where the chordae tendinae attach and merge with central fibrosa.</span></b></li></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.11 Coronary Circulation</span></div></b>Describe coronary circulation in terms of venous return as well as SA and AV node supply <br> <br> Describe the types of cardiac veins?<br>Describe the typical SA/AVN blood supply? <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint1a359c686f944475').style.display='block'; return false;""> Hint</a> <div id=""hint1a359c686f944475"" class=hint style=""display: none"">Great -&gt; AIV<br>Middle -&gt; AP S<br>Small -&gt; RL S<br>Marginal -&gt; Sm<br><br>RC then LC</div> ""<div class=""back""> <ul><li><div><b>Venous Return:</b>&nbsp;Primary drainage for cardiac veins, receives drainage from great, middle, small, and posterior cardiac veins. The great cardiac vein begins as the anterior interventricular vein in its sulcus as it reaches the coronary sulcus it becomes the great cardiac vein and curves posteriorly and takes in the posterior cardiac vein.</div></li><ul><li><div>The middle cardiac vein ascends from the apex of the heart in the posterior interventricular sulcus towards the coronary sinus.</div></li><li><div>The small cardiac vein begins in the coronary sulcus between the right atrium and right ventricle, gaining contribution from the earlier right marginal vein.</div></li><li><div>If the right marginal vein doesn't join the small cardiac vein it drains into the right atrium directly.</div></li></ul><li><div><b>SA And AVN Node Supply:&nbsp;</b></div></li><ul><li><div><b>SA Node:</b>&nbsp;Usually supplied by the right coronary artery in 60% of people, in the other 40% supplied by the left circumflex coronary artery.</div></li><li><div><b>AV Node:<span style=""font-weight: 400;"">&nbsp;Supplied by usually the right coronary artery in 90% of people with the remaining being the left circumflex</span></b></div></li></ul></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.16 Circulatory System: Fetus To Adult</span></div><div><b><span style=""font-weight: 400;"">Describe the transition of fetus circulation upon first breath</span></b></div></b> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hintc4de3caff8be172d').style.display='block'; return false;""> Hint</a> <div id=""hintc4de3caff8be172d"" class=hint style=""display: none"">Pulmonary Vasculature, Pressure, Foramen Ovale, O2, Prostaglandin, Ductus</div> ""<div class=""back""> <ul><li><b>Transition:<span style=""font-weight: 400;"">&nbsp;A baby’s first breath causes a decrease in pulmonary vasculature resistance which increase relative pressure in LA to RA and causes the foramen ovale to close. Increased O2 concentration within the blood leads to decreased prostaglandins (bradykinin), causing the walls of the ductus arteriosus and venosus to close and contract.</span></b></li></ul> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.18 Structure of capillaries</span></div>Describe the structure of the capillaries <br> <br> Which one has beds or gap junctions?<br>Where are they located? <br> <br> ""<div class=""back""> <b><ul><li><div>Overview:<span style=""font-weight: 400;"">&nbsp;Smallest vascular structures in the body, their main purpose is delivering blood to tissues. Have no tunica media or external as they only have a single layer endothelium plus basement membrane, Grouped by their arrangement on the vessel walls:</span></div></li><ul><li><div>Fenestrated:<span style=""font-weight: 400;"">&nbsp;Capillary beds have holes in them and because of that they facilitate rapid molecular exchange between capillaries and tissues. They can be located in the Bowman's capsule.</span></div></li><li><div>Discontinuous:&nbsp;<span style=""font-weight: 400;"">Has multiple bends and looks uncompleted and is located spaced out in the endothelial cells. They lack gap junctions which allow for direct transportation from the capillary lumen to surrounding tissues. They are found in the bone marrow, liver, and spleen,</span></div></li><li><div>Continuous:&nbsp;<span style=""font-weight: 400;"">Most common type, these cells are within close proximity and are fitted with gap junctions. They isolate luminal content from interstitial space and can be seen in the skin, connective and nervous tissue as well as muscle.</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.19 Arteries&nbsp;</span></div>Describe the two types of arteries <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Two main types:&nbsp;</div></li><ul><li><div>Elastic:<span style=""font-weight: 400;"">&nbsp;Substantial elastic tissue in tunica media, accommodates high pulsatile forces.</span></div></li><li><div>Muscular:<span style=""font-weight: 400;"">&nbsp;Elastic fibers only at the intersection of the intima and media or adventitia and media. Allows for contraction or relaxation.</span></div></li></ul></ul></b> "
"<div><span style=""font-style: italic; text-decoration-line: underline;"">1.27 The Respiratory Tract</span></div><div>Describe the upper anatomy of the respiratory tract in terms of larynx and treachea</div> <br> <br> What type of cartilidge surrounds the trachea and what is it held by?<br>What can be used to identify cancer in the lymph nodes? <br> <br> ""<div class=""back""> <ul><li><div><b>Larynx:</b>&nbsp;Choking occur because of an anatomical flaw that we share with most other air-breathing vertebrates. Our breathing tube, the trachea isn't segregated from the one we use for swallowing. The study flap of cartilage called the epiglottis keeps food and drink from going down the windpipe and is designed to snap up automatically when we swallow.</div></li><li><div><b>Trachea:</b>&nbsp;Through the larynx, the air then travels through the trachea which is the tube through which air is transported to the lungs. It runs from the lower border of the cricoid cartilage to around T5-T6, it bifurcates into the left and right primary bronchi.</div></li><ul><li><div>Formed of C-shaped rings of hyaline cartilage held together by dense connective tissue. Posteriorly the junction where the trachea is in contact with the oesophagus, the trachea has a membrane void of cartilage and covered in the smooth trachealis muscle.</div></li><li><div>At the bifurcation of the trachea lies the carina which is a ridge that can be seen on a bronchoscopy, its widening/distortion can indicate cancer in the lymph nodes that lie just inferior to it.</div></li></ul></ul> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.27 The Thoracic Cage<br></span></b>Name and describe the features of the intercostal muscles <br> <br> What are the types of muscle mass?<br>What is the groove in the ribs for? <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint907676242142652d').style.display='block'; return false;""> Hint</a> <div id=""hint907676242142652d"" class=hint style=""display: none"">Hands in pocket! Hands In chest! Arrested!</div> ""<div class=""back""> <ul><li><div><b>Intercostal spaces:</b>&nbsp;Space between the ribs (numbered according to the rib above it). Each space contains muscles that help to move the ribs during breathing changing the volume within the thoracic cavity during respiration.</div></li><ul><li><div><b>External Intercostal Muscle Mass:</b>&nbsp;A most superficial layer of intercostal muscle. It runs from the inferior border of one rib to the superior border of the rib below. The contraction causes the ribs to elevate.&nbsp;</div></li><li><div><b>Internal Intercoastal Muscle Mass:</b>&nbsp;Middle layer of intercostal muscle that runs from the superior border of one rib to the inferior border of the rib above. Contractions draw adjacent ribs nearer together, the only function is forced exhalation.</div></li><li><div><b>Innermost Intercoastal Muscle Mass:</b>&nbsp;The deepest layer of intercostal muscle that is separated from the other 2 layers of muscle by the neurovascular bundle that has the same attachment points as the internal intercostal.</div></li><li><div><b>Neurovascular Supply:<span style=""font-weight: 400;"">&nbsp;Each intercostal space gas separates blood and nervous supply with each bundle running along the inferior aspect rib of the costal groove and running anteriorly from the spinal column to the sternum.</span></b></div></li></ul></ul> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">1.? The Thoracic Cage<br></span></b>In terms of the diapghram describe the features the thoracic respiratory movement and major openings <br> <br> What is the thoracic respiratory movement?<br>What is the major openings? <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint7b40ebeec0ce0b8f').style.display='block'; return false;""> Hint</a> <div id=""hint7b40ebeec0ce0b8f"" class=hint style=""display: none"">For the major openings, use the letters dumbass! : )</div> ""<div class=""back""> <ul><li><div><b>Thoracic respiratory movement:</b></div></li><ul><li><div><b>Anteropsterior:&nbsp;</b>Increase is illustrated with pump handle movement by the superior and anterior movement of the sternum.</div></li><li><div><b>Transverse:</b>&nbsp;Increase is illustrated using a bucket with two handles. Lifting handles is like raising the right and left ribs at the costovertebral and costovertebral joints.</div></li><li><div><b>Vertical:</b>&nbsp;Dimension is increased by the downward pull of the diaphragm.</div></li></ul><li><div><b>Major openings:</b></div></li><ul><li><div>Inferior Vena Cava passes at T8 level</div></li><li><div>Oesophagus passes at T10 level</div></li><li><div>Aorta passes at T12 level</div></li></ul></ul> "
"<span style=""text-decoration-line: underline; font-style: italic; font-weight: 700;"">5.? Clinical Diseases<br></span>Describe the clinical disease asthma and pneumonia <br> <br> <br> <br> ""<div class=""back""> <ul><li><div><b>Asthma:</b> Chronic condition where the walls of the airways of the lungs are permanently inflamed, with increased mucous production. This decreases airflow along the bronchial tree, being classified as a lower airway obstruction but despite this, with medication it can be reversed and controlled.</div></li><ul><li><div><b>Symptoms:</b>&nbsp;Young age, shortness of breath, chest tightness, and wheezing when exhaling.</div></li></ul><li><div><b>Pneumonia:</b> Characterised by pulmonary inflammation that is caused by an infectious agent such as viral, bacterial, or fungal, and such agents enter the lungs via inhalation or aspiration. A specific type known as aspiration pneumonia occurs when contents from or bound for the GI tract end up within the lungs.</div></li><ul><li><div><b>Symptoms:</b>&nbsp;Productive cough, difficulty breathing, chest pain, and high temperature</div></li></ul></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.1 Physiology Of Cardiac Muscle</span></div><span style=""font-weight: 400;"">Describe the physiology of the cardiac muscle</span></b> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint52b2fffa628152aa').style.display='block'; return false;""> Hint</a> <div id=""hint52b2fffa628152aa"" class=hint style=""display: none"">My Dig!</div> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Cardiac Muscle:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul style=""""><li style=""font-weight: bold;""><div><b>Myocardial Cells:<span style=""font-weight: 400;"">&nbsp;Spontaneous depolarization (automaticity)</span></b><br></div></li><li style=""font-weight: bold;""><div>Desmosomes:<span style=""font-weight: 400;""> Holds the muscle cells together tightly</span></div></li><li style=""font-weight: bold;""><div>Gap Junctions:<span style=""font-weight: 400;""> Allow passage of action potentials</span></div></li><li style=""""><div style=""""><b>Fibrous Tissue:</b>&nbsp;Isolates atria from ventricles providing a border</div></li></ul></ul><br> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">2.4 Calcium Induced Calcium Release</span></div>Describe the calcium induced calcium release <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint2aab87b3d139f730').style.display='block'; return false;""> Hint</a> <div id=""hint2aab87b3d139f730"" class=hint style=""display: none"">Ryan</div> ""<div class=""back""> <b><ul><li><div>CICR:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Influx of Ca2+ into mycoytes via the L-type channels from phase 2 of the action potential is insufficient to trigger contraction. Signal is amplified by CICR mechanism triggering greater release of Ca2+ from sarcoplasmic renticulum</span></div></li><li><div><span style=""font-weight: 400;"">The sarcolemna contains invaginations (T-tubules) that bring L-type Ca2+ channels into close contact with ryanodine receptors which are specialized Ca2+ release receptors in the sarcoplasmic reticulum</span></div></li><li><div><span style=""font-weight: 400;"">When Ca2+ enters the cells through L-type channels, ryanodine receptors change conformation and induce a larger release of Ca2+ from abundant sarcoplasmic reticulum scores. Large levels of intracellular Ca2+ act on tropomyosin complexes to induce myocyte contraction</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.5 Regulation Of Stroke Volume</span></div><span style=""font-weight: 400;"">Describe the regulation of stroke volume</span></b> <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint0d0529525d4045e6').style.display='block'; return false;""> Hint</a> <div id=""hint0d0529525d4045e6"" class=hint style=""display: none"">PAC VPC</div> ""<div class=""back""> <b><ul><li><div>Volumes Of Ventricles:</div></li><ul><li><div>End Diastolic:<span style=""font-weight: 400;""> 130</span></div></li><li><div>End Systolic: <span style=""font-weight: 400;"">60</span></div></li><li><div>Stroke Volume: <span style=""font-weight: 400;"">End Diastolic - End Systolic&nbsp;</span></div></li><li><div>Cardiac Output: <span style=""font-weight: 400;"">Stroke Volume x Heartrate</span></div></li></ul><li><div>Preload:<span style=""font-weight: 400;""> Extent of the stretch of heart muscle, so more the heart fills with blood, the more the muscle is stretched. Venous return is increased during physical activity due to the skeletal muscle pump.</span></div></li><li><div>Afterload:<span style=""font-weight: 400;""> Pressure against which the heart needs to pump to expel blood, higher the arterial pressure the lower the stroke volume.&nbsp; If the artery wall is stiff due to aging they stretch less when blood is pumped increasing pressure and afterload.</span></div></li><li><div>Contractility:<span style=""font-weight: 400;""> The more forceful the muscle contracts, the more blood is expelled, inotropic agents such as adrenaline and the influence of the sympathetic nervous system increase contractility.</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">2.6 Frank-Starling Mechanism:</span></div>Describe the frank-starling mechanism <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Ruling:<span style=""font-weight: 400;""> Force of contraction is proportional to the initial fiber length in diastole so if an increase in blood returning to the heart increases the final diastolic volume causes an increase in the next contraction meaning the heart will pump out whatever volume it receives.</span></div></li><li><div><b>Basis:<span style=""font-weight: 400;""> An increased stretch of ventricular muscle results in increased overlap of actin and myosin filaments a greater number of cross-bridges are formed. The length-tension relationship states that there is an optional sarcomere length for maximum contraction, for an increased stretch it increases the sensitivity of the contractile proteins to Ca2+. The intracellular calcium required to generate 50% max tension is lowered when a muscle fiber is stretched.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.7 Neural factors, Hormones And The Heart</span></div><span style=""font-weight: 400;"">Describe the neural factors for the hormones and the heart</span></b> <br> <br> What is the effect of NA+ and Ca2+ on sympatheetic and parasympatheic NS<br>What is the baroreceptor reflex? <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint41413da55ca50763').style.display='block'; return false;""> Hint</a> <div id=""hint41413da55ca50763"" class=hint style=""display: none"">Ren and Angie at Aldi's</div> ""<div class=""back""> <b><ul><li><div>Neural Factors:</div></li><ul><li><div>Sympathetic NS: <span style=""font-weight: 400;"">Increases both heart rate and contractility. It does this by increasing the rate of influx of Na+ and Ca2+ so the pacemaker potential develops quickly, so cardiac potentials happen more quickly.</span></div></li><li><div>Parasympathetic NS: <span style=""font-weight: 400;"">Decreases heart rate but has little effect on contractility. It does this by decreasing the influx of Na+ through sodium channels and slowing the Ca2+ influx. This means it takes longer for the pacemaker potential to reach the threshold for an action potential.</span></div></li></ul><li><div>Blood Pressure Automatic And Hormonal Mechanisms:</div></li><ul><li><div>Baroreceptor Reflex:<span style=""font-weight: 400;""> Regulates blood pressure and is a stretch-sensitive sensory nerve root ending located in the carotid tissues and aortic arch. As arterial pressure rises the rate of firing of these neurons increases, causing a decrease in heart rate and arterial pressure. This is the primary mechanism for blood pressure in an acute setting and acts as the buffer in changes in blood volume, the Renin-Angiotensin-Aldosterone maintains long-term blood pressure.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.9 Heart Ailments And Diseases</span></div><span style=""font-weight: 400;"">Describe the hypotension and atheroscleorosis</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Hypertension:&nbsp;</div></li><ul><li><div>No single hypothesis: <span style=""font-weight: 400;"">Some studies suggest early elevations in blood volume and cardiac output early in life might initiate increased resistance in the systemic vasculature.</span></div></li><li><div>Effects: <span style=""font-weight: 400;"">Cardiac output and blood volumes are often normal, the hypertension, therefore, is sustained by elevation of the systemic vascular resistance rather than by an increase in cardiac output. This increased output is caused by thickening in vascular walls and lumen.</span></div></li><li><div>Symptoms: <span style=""font-weight: 400;"">Stroke due to brain hemorrhage, damage to capillaries in the eye, left ventricular hypertrophy. Damage to kidney vessels (renal failure)</span></div></li></ul><li><div>Atherosclerosis:&nbsp;</div></li><ul><li><div>Hypothesis: <span style=""font-weight: 400;"">The response to injury hypothesis states that the initial event in the pathogenesis of atherosclerosis is an injury to the epithelium. A variety of injurious agents produce an inflammatory response in which leukocytes migrate to the area of injury.&nbsp;</span></div></li><li><div>Effects: <span style=""font-weight: 400;"">Retention and oxidation of lipoproteins in the tunica intima and the transformation of monocytes into macrophages that ingest these lipids becoming lipid-filled foam cells and making a fatty streak, narrowing the artery. Further cap formation is possible if plaque from smooth muscle cells is stable</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">2.12 Structures (Epithelium, Cilia, Goblet, Special</span></div><div><span style=""font-style: italic; text-decoration-line: underline;"">Features)</span></div><span style=""font-weight: 400;"">Describe the histology of the respiratory system</span></b> <br> <br> <br> <br> ""<div class=""back""> <ul><li><b>Pharynx + Trachea + Bronchi: </b>Ciliated Columnar</li><li><b>Bronchioles: </b>Simple columnar</li><li><b>Alveoli: </b>Simple Squamous</li></ul><b>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><ul><li><div>Nose:</div></li><ul><li><div>Vestibule: <span style=""font-weight: 400;"">Nonkeratinized stratified squamous, No, No, Contain numerous hairs.</span></div></li><li><div>Respiratory region:<span style=""font-weight: 400;""> Pseudostratified ciliated columnar, Yes, Yes, Contains conchae and meatuses.</span></div></li></ul><li><div>Pharynx:</div></li><ul><li><div>Nasopharynx: <span style=""font-weight: 400;"">Pseudostratified ciliated columnar, Yes, Yes,&nbsp; Passageway for air and contains internal nares as well as pharyngeal tonsil.</span></div></li><li><div>Oropharynx: <span style=""font-weight: 400;"">Non-keratinized stratifies squamous, No, No Passageway for both air and intake as well as contains opening from the mouth.</span></div></li><li><div>Laryngopharynx: <span style=""font-weight: 400;"">Nonkeratinzied stratified squamous, No, No, Passageway for both air and intake.</span></div></li></ul><li><div>Larynx:<span style=""font-weight: 400;""> Nonkeratinzied stratified squamous above the vocal folds and pseudostratified below the vocal folds, No two both above folds and yes below the folds, Passageway for air, contains vocal folds for voice production.</span></div></li><li><div>Trachea: <span style=""font-weight: 400;"">Pseudostratified ciliated columnar, Yes, Yes, Passageway for air and contains C-shaped rings of cartilage to keep trachea open.</span></div></li><li><div>Bronchi:&nbsp;</div></li><ul><li><div>Main Bronchi: <span style=""font-weight: 400;"">Pseudostratified ciliated columnar, Yes, Yes, Contains C-shaped rings of cartilage to keep things open.</span></div></li><li><div>Lobar/ Segmental Bronchi: <span style=""font-weight: 400;"">Pseudostratified ciliated columnar, Yes, Yes, Contains plates of cartilage to keep things open.</span></div></li><li><div>Larger Bronchioles: <span style=""font-weight: 400;"">Ciliated simple columnar, Yes, Yes, Contains more smooth muscle than in bronchi.</span></div></li><li><div>Smaller Bronchioles: <span style=""font-weight: 400;"">Ciliated simple columnar, Yes, No, Contains more smooth muscle than in larger bronchioles.</span></div></li><li><div>Terminal Bronchioles: <span style=""font-weight: 400;"">Nonciliated simple columnar, No, No Contains more smooth muscle than in smaller bronchioles.</span></div></li></ul><li><div>Lungs:</div></li><ul><li><div>Respiratory Bronchioles: <span style=""font-weight: 400;"">Simple cuboidal to simple squamous, No, No, helps in gas exchange.</span></div></li><li><div>Alveolar Ducts: <span style=""font-weight: 400;"">Simple squamous, No, No, produce surfactant.</span></div></li><li><div>Alveoli: <span style=""font-weight: 400;"">Simple squamous, No, No, produce surfactant to keep things open</span></div></li></ul><li><b>Surface Tension:<span style=""font-weight: 400;""> This is the attraction between molecules at a gas/liquid interface that tends to pull those molecules together, in a spherical structure such as an alveolus, this increases the pressure within the alveolus - the smaller the alveolus, the greater the pressure. This means that smaller alveoli have more tendency to collapse than larger ones. Surfactant reduces surface tension and is essential to enable the expansion of alveoli.</span></b><br></li></ul></b><br> "
"<i><u><b>2.13 Mechanics Of Breathing<br></b></u></i>Describe the factors affecting gas exchange as well as pulmonary ventilation <br> <br> What is distance and surface area for the alveoli <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint3cfed05abb1d1a4a').style.display='block'; return false;""> Hint</a> <div id=""hint3cfed05abb1d1a4a"" class=hint style=""display: none"">Ficks Law</div> ""<div class=""back""> <b><ul><li><div>Alveolus Gas Exchange:<span style=""font-weight: 400;""> Oxygen enters the alveoli sac, and a capillary surrounding it containing red blood cells carrying CO2 moves around the sac and releases CO2 into it whilst taking in O2. The carbon dioxide is then released from the sac.</span></div></li><ul><li><div>Factors Affecting Gas Exchange:&nbsp;</div></li><ul><li><div>Fick’s Law:<span style=""font-weight: 400;""> Rate of diffusion is proportional to both the surface area and concentration difference and is inversely proportional to the thickness of the membrane.&nbsp;</span></div></li></ul></ul><li><div>Distance And Surface Area: <span style=""font-weight: 400;"">Increased if there is fluid in the lungs (pneumonia) or mucus in the lungs (cystic fibrosis).&nbsp;</span><b><span style=""font-weight: 400;"">Normally very short in healthy lungs (0.2 - 0.4 um) and high surface area (50-100m2)</span></b></div></li><li><div>Factors Affecting Pulmonary Ventilation:</div></li><ul><li><div>Lung Compliance:</div></li><ul><li><div><span style=""font-weight: 400;"">The ease with which the lungs and thoracic wall can be expanded.</span></div></li><li><div><span style=""font-weight: 400;"">Defined as the change in lung volume per change in transpulmonary pressure.</span></div></li><li><div><span style=""font-weight: 400;"">Will be reduced in conditions that make lung tissue stiffer such as pulmonary fibrosis.</span></div></li></ul><li><div>Elasticity:</div></li><ul><li><div><span style=""font-weight: 400;"">The lungs contain elastic tissue that stretches on inhalation.</span></div></li><li><div><span style=""font-weight: 400;"">During exhalation the elastic tissues recoil, which aids the flow of air out of the lungs.</span></div></li><li><div><span style=""font-weight: 400;"">Disorders that cause loss of elasticity such as emphysema can affect ventilation.</span></div></li></ul></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">2.13 Mechanics Of Breathing<br></span></b><b><span style=""font-weight: 400;"">Describe the structure of the alveolus as well as pulmoanry circulation</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Structure Of The Normal Alveolus: <span style=""font-weight: 400;"">Structure of the normal alveolus. The type 1 cell with its long thin cytoplasmic processes lines most of the alveolar surface, whereas the cuboidal type 2 cell which is more numerous, occupies only about 7% of the alveolar surface. Transmission electron micrograph of a pulmonary capillary in cross-sectional. Alveoli are on either side of the red blood cell. The diffusion pathway goes from the alveolar-capillary barrier, plasma, and then the erythrocyte.&nbsp;</span></div></li><li><div>Pulmonary Circulation:<span style=""font-weight: 400;""> Lung has two separate circulations. Pulmonary circulation brings deoxygenated blood from the right ventricle to the gas-exchange units. Bronchial circulation arises from the aorta and nourishes the lung parenchyma and the circulation to the lung is unique in its dual circulation and in its ability to accommodate large volumes of blood at low pressure.</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">2.14 Ventilation</span></div>Describe the ventilation perfusion ratio <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Perfusion: <span style=""font-weight: 400;"">Blood flow reaching alveoli.</span></div></li><li><div>Ventilation:<span style=""font-weight: 400;""> Amount of gas reaching alveoli.</span></div></li><li><div>Ventilation-Perfusion Ratio: <span style=""font-weight: 400;"">Normal ratio for the whole lungs is 0.8</span></div></li><ul><li><div>Apices: <span style=""font-weight: 400;"">Receive more ventilation than perfusion (x&gt;0.8)</span></div></li><li><div>Bases: <span style=""font-weight: 400;"">Receive more perfusion than ventilation (x&lt;0.8)</span></div></li></ul><li><div>Factors Affecting Ratio: <span style=""font-weight: 400;"">Although there is blood passing the alveoli, gas exchange is limited due to refreshing alveolar air and blood-oxygen level will fall and blood carbon dioxide level will rise.</span></div></li><ul><li><div>Increase VQ</div></li><ul><li><div><span style=""font-weight: 400;"">Pulmonary embolism causes a blood clot in the lungs and may block lung blood vessels resulting in limited perfusion to an area being ventilated effectively and the overall V-Q ratio will increase.</span></div></li><li><div><span style=""font-weight: 400;"">In COPD patients will have a high ventilation rate but poor perfusion due to damage to the alveoli so the V-Q ratio will increase.</span></div></li></ul><li><div>Decrease VQ:</div></li><ul><li><div><span style=""font-weight: 400;"">Chronic Bronchitis causing bronchospasm, inflammation, and airway obstruction.</span></div></li><li><div><span style=""font-weight: 400;"">Asthma causes excess mucus.</span></div></li><li><div><span style=""font-weight: 400;"">Pulmonary oedema which produces fluid build-up in the lungs.</span></div></li><li><div><span style=""font-weight: 400;"">Pulmonary fibrosis which decreases compliance.</span></div></li></ul></ul></ul></b> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">2.14 Ventilation</span></b><b><br></b></div>Describe the receptors related to the lungs <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint2c87bb7b78e1d322').style.display='block'; return false;""> Hint</a> <div id=""hint2c87bb7b78e1d322"" class=hint style=""display: none"">LCP</div> ""<div class=""back""> <b><ul><li><div>Receptors:</div></li><ul><li><div>Lung Receptors:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Pulmonary stretch receptors which are slowly adapting, lie within the airway smooth muscle.</span></div></li><li><div><span style=""font-weight: 400;"">Discharge in response to distension in the lungs.</span></div></li><li><div><span style=""font-weight: 400;"">Activity sustained with lung inflation.</span></div></li><li><div><span style=""font-weight: 400;"">Impulses travel in the vagus nerve via large myelinated fibers.</span></div></li><li><div><span style=""font-weight: 400;"">Main reflex effect of stimulating these receptors is a slowing of respiratory frequency.</span></div></li></ul><li><div>Central Chemoreceptors:</div></li><ul><li><div><span style=""font-weight: 400;"">Located near the ventral surface of the medulla.</span></div></li><li><div><span style=""font-weight: 400;"">Sensitive to PCO2 but not PO2 of blood</span></div></li><li><div><span style=""font-weight: 400;"">Respond to change in pH of the ECF/CSF when CO2 diffuses out of the cerebral capillaries</span></div></li></ul><li><div>Peripheral Chemoreceptors:</div></li><ul><li><div><span style=""font-weight: 400;"">Located in the carotid and aortic bodies</span></div></li><li><div><span style=""font-weight: 400;"">Respond to decreased arterial PO2 and increased PCO2 and H+&nbsp;</span></div></li><li><div><span style=""font-weight: 400;"">Rapidly responding</span></div></li></ul></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.1 Hematopoiesis</span></div><span style=""font-weight: 400;"">Describe the age landmarks of Hematopoiesis</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Haemoatopoeisis: <span style=""font-weight: 400;"">Process of differentiation that leads to the formation of all blood vessels from stem cells.</span></div></li><ul><li><div>Fetus:<span style=""font-weight: 400;""> Yolk sac, then liver and spleen (4 months)</span></div></li><li><div>Infants/Children:<span style=""font-weight: 400;""> Occurs in all bone marrows</span></div></li><li><div>Adults: <span style=""font-weight: 400;"">Cranium, vertebra, ribs and pelvis</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">7.2 Growth</span></div>Describe Granulopoiesis <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Granulopoiesis:<span style=""font-weight: 400;"">&nbsp;For the formation of neutrophils, eosinophils and basophils. Progression includes: a decrease in cell size; condensation of nuclear chromatin; changes in nuclear shape (Flattening - Indentation - Lobulation); accumulation of cytoplasmic granules. A small number of band cells present in circulation may appear in large numbers when granulopoiesis is hyper-stimulated.</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.3 Changes in Blood Count</span></div><span style=""font-weight: 400;"">Describe the changes in blood count</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Thrombocytopenia (Low Platelet Count):&nbsp;</div></li><ul><li><div>Cause: <span style=""font-weight: 400;"">Decrease bone marrow production, enlarged spleen, increased platelet destruction.</span></div></li><li><div>Symptoms: <span style=""font-weight: 400;"">Abnormal bleeding, spontaneous skin purpura, and mucosal hemorrhage.</span></div></li></ul><li><div>Thrombocytosis (High Platelet Count):</div></li><ul><li><div>Cause:<span style=""font-weight: 400;""> Iron deficiency, Inflammation, Cancer, or Infection.</span></div></li><li><div>Symptoms: <span style=""font-weight: 400;"">Asymptomatic.</span></div></li></ul><li><div>Leucopenia/Leucocytosis:</div></li><ul><li><div>Cause:<span style=""font-weight: 400;""> Infection, Trauma, Malignancy, Autoimmunity, Chemotherapy, or allergy.</span></div></li><li><div><b>Symptoms: <span style=""font-weight: 400;"">Internal Bleeding, Strokes, and General Fever.</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.4 Haemostasis</span></div><span style=""font-weight: 400;"">Describe the process of haemostasis</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Response:&nbsp;</div></li><ul><li><div>Vasoconstriction: <span style=""font-weight: 400;"">After vascular injury, local factors from Endothelium induce transient vasoconstriction.</span></div></li><li><div>Primary Hemostasis:<span style=""font-weight: 400;""> Platelets bind to collagen via ‘Von Willebrand Factor (a glycoprotein that helps in platelet adhesion) on exposed extracellular matrix (ECM) and are activated, undergoing a shape change and granule release. Released ADP and thromboxane-A2 induce platelet aggregation through binding to fibrinogen to form the primary hemostatic plug</span></div></li><li><div>Secondary Haemostasis: <span style=""font-weight: 400;"">Activation of the coagulation cascade results in fibrin polymerization due to the action of thrombin, solidifying the platelets to form a secondary hemostatic plug.</span></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.5 Coagulation Cascade</span></div><span style=""font-weight: 400;"">Describe the coagulation cascade</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Zymogens:<span style=""font-weight: 400;""> Inactivated proteins that are activated by cleavage</span></div></li><li><div>In Vitro Pathway:</div></li><ul><li><div>Intrinsic pathway:<span style=""font-weight: 400;""> 12 &lt; 11 &lt; 9(/8) &lt; 10*</span></div></li><li><div>Extrinsic pathway: <span style=""font-weight: 400;"">Tissue Factor &lt; 7 &lt; 10*</span></div></li><li><div>Common pathway: <span style=""font-weight: 400;"">10(/5) &lt; Prothrombin (2) &lt; Thrombin &lt; Fibrinogen &lt; Fibrin Clot</span></div></li></ul><li><div>In Vivo Pathway:&nbsp;</div></li><ul><li><div>Common pathway:<span style=""font-weight: 400;""> Tissue Factor &lt; 7 &lt; 9(/11)&nbsp; &lt; 10 &lt; Prothrombin &lt; Thrombin(&lt;11)</span></div></li><li><div>13:<span style=""font-weight: 400;""> Stabilises the fibrin clot</span></div></li><li><div>Thrombin: <span style=""font-weight: 400;"">Amplifies the loop</span></div></li></ul><li><b>Fibrinolytic System: <span style=""font-weight: 400;"">Fibrin clots are broken down by this system, central to the process is the conversion of plasminogen to plasmin which degrades fibrin for fibrin degradation products eventually becoming d-dimers. Plasminogen is activated by tissue plasminogen activator and is produced by endothelial cells</span></b><br></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.6 Regulation</span></div><span style=""font-weight: 400;"">Describe the regulation of blood clotting</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Prevention of primary hemostatic plug:<span style=""font-weight: 400;""> Intact endothelium releases factors (prostacyclin, NO) that inhibit platelet aggregation.</span></div></li><li><div>Confine clotting to single site:<span style=""font-weight: 400;""> Control mechanism mediated by tissue plasminogen activator and the thrombomodulin.</span></div></li><li><div>Limit coagulation cascade:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Thrombomodulin: <span style=""font-weight: 400;"">Binds to thrombin and complex leads to degradation of 5 and 13 via activation of protein C.</span></div></li><li><div>Antithrombin: <span style=""font-weight: 400;"">Inhibits 10 and thrombin.</span></div></li><li><div>Tissue factor pathway inhibitor:<span style=""font-weight: 400;""> Inhibits 10.</span></div></li></ul><li><b>Fibrinolytic system regulation: <span style=""font-weight: 400;"">Plasminogen activator inhibitor binds to tPA and a-antiplasmin binds to and inhibits plasmin.</span></b><br></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.7 Assessing Hemostasis</span></div><span style=""font-weight: 400;"">Describe the coagulation test</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Coagulation Tests:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Prothrombin Time (PT): <span style=""font-weight: 400;"">Tissue factor and phospholipids, Extrinsic pathway, Defect is 7</span></div></li><li><div>Partial Thromboplastin time (PTT): <span style=""font-weight: 400;"">Calcium and contact surface activator, intrinsic pathway, Defect is; 12, 11, 9,8</span></div></li><li><div>Thrombin Clotting Time: <span style=""font-weight: 400;"">Calcium and thrombin, common pathways, Defect is Fibrinogen or thrombin inhibitor</span></div></li><li><div><b>PT + PTT: <span style=""font-weight: 400;"">Defect is 5, 10, or prothrombin.</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.8 Disorders Of Haemostasis</span></div><span style=""font-weight: 400;"">Describe the disorders of haemostasis</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Genetic:</div></li><ul><li><div>Haemophilia A: <span style=""font-weight: 400;"">8</span></div></li><li><div>Haemophilia C: 9</div></li><li><div>Von Willebrand Disease:</div></li></ul><li><div>Acquired:</div></li><ul><li><div>Liver Disease</div></li><ul><li><div><span style=""font-weight: 400;"">May increase prothrombin time due to deficiency in coagulation factors, if severe decreases in fibrinogen levels.</span></div></li><li><div><span style=""font-weight: 400;"">May cause thrombocytopenia and platelet abnormalities.</span></div></li></ul><li><div>Thrombocytopenia</div></li><ul><li><div><span style=""font-weight: 400;"">Impaired production of platelets</span></div></li><li><div><span style=""font-weight: 400;"">Immune-mediated destruction of platelets</span></div></li><li><div><span style=""font-weight: 400;"">Excessive coagulation in disseminated intravascular coagulation.</span></div></li></ul></ul><li><div>Thrombosis:<span style=""font-weight: 400;""> Formation of a blood clot inside a vessel, obstructing the flow of blood through the circulatory system. If the clot detaches from the vessel and lodges in the lungs or other organs it can become a life-threatening embolus.</span></div></li><ul><li><div>Virchow’s Triad: <span style=""font-weight: 400;"">Factors that lead to thrombosis.</span></div></li><ul><li><div><span style=""font-weight: 400;"">Stasis (Reduced blood flow)</span></div></li><li><div><span style=""font-weight: 400;"">Vessel wall injury.</span></div></li><li><div><span style=""font-weight: 400;"">Hypercoagulability.</span></div></li></ul><li><b>Disseminated Intravascular Coagulation:<span style=""font-weight: 400;""> A life threatening disorder that occurs when there is a systematic activation of coagulation, caused by bacterial sepsis, metabolic stress, and malignancy.</span></b><br></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Class I</span></div>Describe the effects of Class Ia drugs <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Disopyramide</span></div><ul><li><div>Type Of Drug: <span style=""font-weight: 400;"">Class Ia drug</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Volume-gated Na+ channel blockers</span></div></li><li><div>Use: <span style=""font-weight: 400;"">Atrial and Ventricular Tachycardia</span></div></li><li><div>Tropic Effect: <span style=""font-weight: 400;"">Negative Intotrope</span></div></li><li><div>Effect: <span style=""font-weight: 400;"">Lengthens rapid polarisation (medium)</span></div></li><li><div>Intake Note: <span style=""font-weight: 400;"">Negative inotropic effect due to Ca2+ entry so avoid patients with hypotension or low ventricular output</span></div></li><li><div>Adverse Effect:<span style=""font-weight: 400;""> Anticholinergeric side effects</span></div></li></ul></b><b>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><ul><li><div>MOA:</div></li><ul><li><div>Class 1a:<span style=""font-weight: 400;""> Intermediate dissociation (medium block), blocks VG K+ channels and prolongs repolarization.</span>&nbsp;</div></li></ul><li><div>Class 1a:</div></li><ul><li><div>Classic Drugs:</div></li><ul><li><div><span style=""font-weight: 400;"">Quinidine: Classic but obsolete</span></div></li><li><div><span style=""font-weight: 400;"">Procaiamide: Obsolete</span></div></li><li><div><span style=""font-weight: 400;"">Disopyramide: Key Drug</span></div></li></ul><li><div>Features:</div></li><ul><li><div><span style=""font-weight: 400;"">Can be used for atrial and ventricular tachycardias</span></div></li><li><div><span style=""font-weight: 400;"">Anticholinergic side effects (especially disopyramide)</span></div></li><li><div><span style=""font-weight: 400;"">Negative inotropic effect (so reduced contractilitiy) due to Ca2+ entry thus avoid with hypotension</span></div></li></ul></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Lidocaine</span></div><span style=""font-weight: 400;"">Describe the effects of lidocaine</span></b> <br> <br> <br> <br> ""<div class=""back""> <div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.? Lidocaine</span></div><ul style=""font-weight: bold;""><li><div>Type Of Drug: <span style=""font-weight: 400;"">Class Ib drug</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Volume gated Na+ channel blockers</span></div></li><li><div>Use: <span style=""font-weight: 400;"">Ventricular tachycardia and fibrillation with little effectiveness for most tachycardia, no effect at slow heart rates.</span></div></li><li><div>Tropic Effect: <span style=""font-weight: 400;"">Negative Inotrope</span></div></li><li><div><b>Effect: <span style=""font-weight: 400;"">Lengthens rapid polarisation (Weak)</span></b></div></li></ul>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<b><br><ul><li><div>MOA:&nbsp;</div></li><ul><li><div>Class 1b: <span style=""font-weight: 400;"">Fast dissociation (weak block), shortens repolarisation.</span></div></li></ul><li><div>Class 1b:</div></li><ul><li><div>Classical Drugs:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Lidocaine: Key Drug, Used as an anaesthetic in IV form</span></div></li><li><div><span style=""font-weight: 400;"">Mexiletine: Orally avaialable but rare in UK</span></div></li><li><div><span style=""font-weight: 400;"">Tocainide: Obsolete</span></div></li></ul><li><div>Features:</div></li><ul><li><div><span style=""font-weight: 400;"">Rapid dissociation means little effect except at fast heart rates</span></div></li><li><div><span style=""font-weight: 400;"">Used for ventricular tachycardia and fibrillation; low effectiveness for most atrial tachycardia</span></div></li></ul></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Class I</span></div><ul><li><div>MOA:</div></li><ul><li><div>Class 1a:<span style=""font-weight: 400;""> Intermediate dissociation (medium block), blocks VG K+ channels and prolongs repolarization.</span>&nbsp;</div></li><li><div>Class 1b: <span style=""font-weight: 400;"">Fast dissociation (weak block), shortens repolarisation.</span></div></li><li><div>Class 1c: <span style=""font-weight: 400;"">Slow dissociation (strong block). Strong negative inotropes.</span></div></li></ul><li><div>Conduction Velocity:<span style=""font-weight: 400;""> Myocytes form syncytium which are cells directly connected by gap junctions so depolarisation depolarises successive cells. Slowed depolarisation means longer to depolarise successive cells to reduced conduction velocity.</span></div></li><li><div>Class 1a:</div></li><ul><li><div>Classic Drugs:</div></li><ul><li><div><span style=""font-weight: 400;"">Quinidine: Classic but obsolete</span></div></li><li><div><span style=""font-weight: 400;"">Procaiamide: Obsolete</span></div></li><li><div><span style=""font-weight: 400;"">Disopyramide: Key Drug</span></div></li></ul><li><div>Features:</div></li><ul><li><div><span style=""font-weight: 400;"">Can be used for atrial and ventricular tachycardias</span></div></li><li><div><span style=""font-weight: 400;"">Anticholinergic side effects (especially disopyramide)</span></div></li><li><div><span style=""font-weight: 400;"">Negative inotropic effect (so reduced contractilitiy) due to Ca2+ entry thus avoid with hypotension</span></div></li></ul></ul><li><div>Class 1b:</div></li><ul><li><div>Classical Drugs:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Lidocaine: Key Drug, Used as an anaesthetic in IV form</span></div></li><li><div><span style=""font-weight: 400;"">Mexiletine: Orally avaialable but rare in UK</span></div></li><li><div><span style=""font-weight: 400;"">Tocainide: Obsolete</span></div></li></ul><li><div>Features:</div></li><ul><li><div><span style=""font-weight: 400;"">Rapid dissociation means little effect except at fast heart rates</span></div></li><li><div><span style=""font-weight: 400;"">Used for ventricular tachycardia and fibrillation; low effectiveness for most atrial tachycardia</span></div></li></ul></ul><li><div>Classical 1c:</div></li><ul><li><div>Classical Drugs (Both Key Drugs):</div></li><ul><li><div><span style=""font-weight: 400;"">Flecainide: Can cause sudden death after MI</span></div></li><li><div><span style=""font-weight: 400;"">Propafenone: Additional β-blocker effects</span></div></li></ul><li><div>Features:</div></li><ul><li><div><span style=""font-weight: 400;"">Used for atrial fibrillations and some ventricular tachycardias (AV nodal re-entrant tachycardia)</span></div></li><li><div><span style=""font-weight: 400;"">Potent negative inotrope so risk of heart failure if a weak heart</span></div></li></ul></ul></ul></b> <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Propafenone</span></div><ul><li><div>Type Of Drug: <span style=""font-weight: 400;"">Class Ic drug</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Volume-gated Na+ channel blockers</span></div></li><li><div>Use: <span style=""font-weight: 400;"">Atrial fibrillation and some ventricular tachycardia</span></div></li><li><div>Tropic Effect:<span style=""font-weight: 400;""> Negative Inotrope</span></div></li><li><div>Effect: <span style=""font-weight: 400;"">Lengthens rapid polarisation (strong)</span></div></li><li><div>Intake Note/Adverse Effect: <span style=""font-weight: 400;"">Risk of heart failure if weak heart</span></div></li></ul></b>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><ul style=""font-weight: bold;""><li><div>MOA:</div></li><ul><li><div>Class 1c: <span style=""font-weight: 400;"">Slow dissociation (strong block). Strong negative inotropes.</span></div></li></ul><li><div>Classical 1c:</div></li><ul><li><div>Classical Drugs (Both Key Drugs):</div></li><ul><li><div><span style=""font-weight: 400;"">Flecainide: Can cause sudden death after MI</span></div></li><li><div><span style=""font-weight: 400;"">Propafenone: Additional β-blocker effects</span></div></li></ul><li><div>Features:</div></li><ul><li><div><span style=""font-weight: 400;"">Used for atrial fibrillations and some ventricular tachycardias (AV nodal re-entrant tachycardia)</span></div></li><li><div><span style=""font-weight: 400;"">Potent negative inotrope so risk of heart failure if a weak heart</span></div></li></ul></ul></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Class II&nbsp;</span></div></b>Describe the effects of Class II Drugs <br> <br> <br> <br> ""<div class=""back""> <div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.? Sotalol</span></div><ul style=""font-weight: bold;""><li><div>Type Of Drug: <span style=""font-weight: 400;"">Class II drug</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Adregenic β receptor antagonism</span></div></li><li><div>Use: <span style=""font-weight: 400;"">Reduce death following MI, reduce arrhythmias from excessive sympathetic activity</span></div></li><li><div>Tropic Effect:<span style=""font-weight: 400;""> Negative Inotrope</span></div></li><li><div>Effect: <span style=""font-weight: 400;"">Lengthens slow repolarisation</span></div></li><li><div>Intake Note: <span style=""font-weight: 400;"">Sotalol should be avoided if useful as it may cause TdP</span></div></li><li><div>Adverse Effect:<span style=""font-weight: 400;""> Hypotension, Vasoconstriction and Asthma Symptoms</span></div></li></ul>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><b><div><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Class II&nbsp;</span></div><ul><li><div>MOA:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Adrenergic β receptor antagonism so lowered cAMP, PKA, and Ca2+ (so affects nodal AP), therefore longer refractory period especially AV node meaning negative inotropic effect.</span></div></li></ul><li><div>Beta-Blockers:</div></li><ul><li><div><span style=""font-weight: 400;"">Reduced mortality following MI reducing arrhythmias due to excessive sympathetic activity</span></div></li></ul><li><div>Classical Drugs:</div></li><ul><li><div><span style=""font-weight: 400;"">Atenolol, metoprolol, and propranolol</span></div></li><li><div><span style=""font-weight: 400;"">Sotalol: Key Drug, however only in specific circumstances since has class III activity</span></div></li></ul><li><div>Side Effects:</div></li><ul><li><div><span style=""font-weight: 400;"">Hypotension (dizziness), fatigue, vasoconstriction</span></div></li><li><div><span style=""font-weight: 400;"">Sotalol may be more potent due to Class III effects so avoided due to TdP&nbsp;</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Class III</span></div>Describe the effects of Class III drugs <br> <br> <br> <br> ""<div class=""back""> <b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Amiodarone</span></div><ul><li><div>Type Of Drug: <span style=""font-weight: 400;"">Class III drug</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Volume-gated K+ channel blockers</span></div></li><li><div>Use: <span style=""font-weight: 400;"">Atrial and Ventricular Tachycardia (when refractory to other drugs; Wolfe-Parkinson-White Syndrome</span></div></li><li><div>Tropic Effect:<span style=""font-weight: 400;""> Negative chronotrope, positive inotrope</span></div></li><li><div>Effect: <span style=""font-weight: 400;"">Delays repolarisation</span></div></li><li><div>Intake Note: <span style=""font-weight: 400;"">Use dependency so more effective the slower the heart</span></div></li><li><div><b>Adverse Effect:<span style=""font-weight: 400;""> Toxicity, thyroid dysfunction and TdP</span></b></div></li></ul></b><b>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><ul><li><div>MOA:</div></li><ul><li><div><span style=""font-weight: 400;"">Blocks K+ channels. Have reverse use dependency so more effective the slower the heart is going making it dangerous for bradycardia slowing the heart even more.</span></div></li></ul><li><div>Effect:</div></li><ul><li><div><span style=""font-weight: 400;"">Extends refractory period by delaying repolarisation</span></div></li><li><div><span style=""font-weight: 400;"">Negative chronotropic and positive inotropic</span></div></li></ul><li><div>Classical Drugs:</div></li><ul><li><div><span style=""font-weight: 400;"">Amiodarone: Has Class Ia, II, and IV activity</span></div></li><li><div><span style=""font-weight: 400;"">Dronedarone: Less effective but less lipophilic so hence safer</span></div></li><li><div><span style=""font-weight: 400;"">Sotalo: Less effective class III drug</span></div></li></ul><li><div>Side Effects:</div></li><ul><li><div><span style=""font-weight: 400;"">Toxicity, thyroid dysfunction TdP, Skin discoloration, and photosensitivity.</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><b><div><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Class IV</span></div></b></div>Describe the effects of Class IV drugs <br> <br> <br> <br> ""<div class=""back""> <div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.? Verampil</span></div><ul style=""font-weight: bold;""><li><div>Type Of Drug: <span style=""font-weight: 400;"">Class IV drug</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Volume-gated Ca2+ channel blockers</span></div></li><li><div>Use: <span style=""font-weight: 400;"">Atrial fibrillation (can be used to dilate blood vessels)</span></div></li><li><div>Tropic Effect: <span style=""font-weight: 400;"">Negative Inotrope (at nodes)</span></div></li><li><div>Effect: <span style=""font-weight: 400;"">Lengthens Nodal AP</span></div></li><li><div><b>Adverse Effect:<span style=""font-weight: 400;""> Hypotension, Oedema and constipation</span></b></div></li></ul>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<br><b><ul><li><div>MOA:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Ca 2+ channel block (L-type). Provides therapeutic effect on Nodal AP by decreasing amplitude and increasing length of nodal AP. Causes negative inotrope as well as decreases length of myocyte AP causing risk of ventricular tachycardias.</span></div></li></ul><li><div>Features:</div></li><ul><li><div><span style=""font-weight: 400;"">Used in atrial fibrillation and paroxysmal superventricular tachycardia. Ca2+ also dilates blood vessels</span></div></li><li><div><span style=""font-weight: 400;"">May be used as a hypertensive and antianginal medication</span></div></li></ul><li><div>Classical Drugs (Both Key Drugs):</div></li><ul><li><div><span style=""font-weight: 400;"">Verapamil: Also α-blocker and Na+ channel blocker</span></div></li><li><div><span style=""font-weight: 400;"">Diltiazem</span></div></li></ul><li><div>Side Effects:</div></li><ul><li><div><span style=""font-weight: 400;"">Hypotension, oedema and constipation</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Digoxin (Cardiac Glycosides)</span></div>Describe the effects of Digoxin<br> <br> <br> <br> <br> ""<div class=""back""> <div style=""""><b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.? Digoxin</span></div><ul><li><div>Type Of Drug: <span style=""font-weight: 400;"">Other Arrhymia Drug</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">NA+/K+ pump inhibitor, depolarises cells making it easier to fire action potentials at vagus nerve, increasing ACh so Gi receptor. More K+ therefore hyperpolarisation</span></div></li><li><div>Use:</div></li><li><div>Tropic Effect: <span style=""font-weight: 400;"">Negative Chronotrope (at nodes), positive inotrope at myocyte</span></div></li><li><div>Effect: <span style=""font-weight: 400;"">Lengthens slow depolarisation at nodal, reduces peak of hyperpolarisation at myocyte.</span></div></li><li><div><b>Adverse Effect:<span style=""font-weight: 400;""> Unsafe (from low TI) causing death</span></b></div></li></ul></b>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------</div><ul style=""font-weight: bold;""><li><div>MOA:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Na+/K+ pump inhibitor by degrading the concentration gradients (potassium one more) and therefore depolarising the cells such as the vagus nerve, causing increased ACh release so more activity at M2 receptors (Gi). Since more K+ efflux in nodal cells than hyperpolarisation.</span></div></li><li><div><span style=""font-weight: 400;"">Myocytes are also depolarised so increased intracellular Ca2+ levels increasing a positive inotrope and reduced Ca2+ entry so shorter action potential.</span></div></li></ul><li><div>Features:</div></li><ul><li><div><span style=""font-weight: 400;"">Very low therapeutic index so extremely unsafe</span></div></li></ul><li><div>Side Effects:</div></li><ul><li><div><span style=""font-weight: 400;"">Dizziness, Confusion and Vomiting</span></div></li></ul></ul> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Adenosine</span></div>Describe the effects of the drug adenosine <br> <br> <br> <br> ""<div class=""back""> <div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.? Adenosine</span></div><ul style=""font-weight: bold;""><li><div>Type Of Drug: <span style=""font-weight: 400;"">Other Arrhymia Drug</span></div></li><li><div>MOA: <span style=""font-weight: 400;"">Gi receptor agonist at AV node so K+ permeability</span></div></li><li><div>Use: <span style=""font-weight: 400;"">Atrial fibrillation (can be used to dilate blood vessels)</span></div></li><li><div>Tropic Effect: <span style=""font-weight: 400;"">Negative Inotrope (at nodes)</span></div></li><li><div>Effect: <span style=""font-weight: 400;"">Lengthens Nodal AP (possible vasodilator)</span></div></li><li><div><b>Adverse Effect: <span style=""font-weight: 400;"">Chest pain nausea and dizziness</span></b></div></li></ul>--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------<b><br><ul><li><div>MOA:&nbsp;</div></li><ul><li><div><span style=""font-weight: 400;"">Activates A1 receptors (Gi) in AV node so increased K+ permeability and therefore hyperpolarisation</span></div></li></ul><li><div>Features:</div></li><ul><li><div><span style=""font-weight: 400;"">Safe to apply since readily available in the body</span></div></li><li><div><span style=""font-weight: 400;"">Preferred to verapamil for acute paroxysmal superventricular tachycardia and very short lasting</span></div></li><li><div><span style=""font-weight: 400;"">Potent Vasodilator</span></div></li></ul><li><div>Side Effects:</div></li><ul><li><div><span style=""font-weight: 400;"">Chess pain, shortness of breath and Nausea</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">6.15 Clinical Use</span></div>Describe the clinical use of drugs for rate control and rhythm control <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Bradycardia: <span style=""font-weight: 400;"">Used for emergencies and short term, if chronic then a pacemaker is fitted instead</span>&nbsp;</div></li><li><div>Control: <span style=""font-weight: 400;"">Key to ensure orderly activation of ventricles is preventing atrial tachycardia getting passed to ventricles:</span></div></li><ul><li><div>Rate Control (Target AV Node Cells):<span style=""font-weight: 400;""> Negative chronotropic agents used to prevent atrial tachycardia being passed to ventricles.</span></div></li><ul><li><div>First Line:<span style=""font-weight: 400;""> Class II (β-blockers), Class IV (diltiazem/verapamil)</span></div></li><li><div>Digoxin:<span style=""font-weight: 400;""> Only for patients with immobile lifestyles</span></div></li><li><div>Last Line: <span style=""font-weight: 400;"">Two of digoxin, Class II diltiazem</span></div></li></ul><li><div>Rhythm Control (Prevent Atrial Tachycardias Occurring): <span style=""font-weight: 400;"">Cardioversion to restore sinus rhythm (defibrilator), drugs to maintain sinus rhythm.</span></div></li><ul><li><div>First Line: <span style=""font-weight: 400;"">Class II (β-blockers)</span></div></li><li><div><b>Next:<span style=""font-weight: 400;""> Class III or Class Ic</span></b></div></li></ul></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">2.15 Lung Function</span></div>Describe the restrictive and obstructive disorder <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Disorders:<span style=""font-weight: 400;"">&nbsp;</span></div></li><ul><li><div>Restrictive Disorder:<span style=""font-weight: 400;""> Limitation on the expansion of the lungs making it more difficult for air to get in, potentially caused by stiff lungs or even weakness of muscles or damaged nerves.</span></div></li><li><div>Obstructive Disorder:<span style=""font-weight: 400;""> Airways are narrowed so exhaled air is slower than normal, and residual volume may be higher than normal causing more difficulty in the air getting out of the lungs. Can be caused by COPD, emphysema, asthma, and cystic fibrosis.</span></div></li></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">2.15 Lung Function<br></span></b>Describe the different ways to test lung function <br> <br> What is FEV1, FVC and FEW<br>How to check if cause is really normal or restrictive? <br> <br> ""<div class=""back""> <b><ul><li><div>Testing:</div></li><ul><li><div>Static Lung Function (Volume and Capacity): <span style=""font-weight: 400;"">Static lung volumes measure the maximal effort generated only at the beginning and end of the maneuver. (Tests based on volume and not airflow).</span></div></li><li><div>Dynamic Lung Function (Volume and Velocity):<span style=""font-weight: 400;""> Assessed during forced inspiration or expiration, or during forced breathing when the maximal effort is applied through the respiratory maneuver. (Text based on time just not volume).</span></div></li><li><div>FEV1 (Forced Expiratory Volume): <span style=""font-weight: 400;"">Measures how much air you can blow out in 1 second (rate of air-flow). Can be used to gauge whether the airway is narrowed.</span></div></li><li><div>FVC (Forced Vital Capacity):<span style=""font-weight: 400;""> Measures the total volume of air you can blow out after a maximal inhalation, is used as an independent measure of pulmonary function.</span></div></li><li><div>FER (Forced Expiratory Ratio):<span style=""font-weight: 400;""> The ratio of FEV1 to FVC is a measure of the quality of the airway. If x = 0.8 then normal, x &lt; 0.8 then constricted airway, and x &gt; 0.8 restrictive airway.</span></div></li><li><div><b><span style=""font-weight: 400;"">In a restrictive disease both values expect to be low so possibly mistaken for normal. Checked by whether a normal low forced vital capacity</span> <span style=""font-weight: 400;"">volume.</span></b></div></li></ul></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">2.15 Lung Function<br></span></b>Describe the signs of obstructive and restrictive disorder <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Obstructive Disorder:</div></li><ul><li><div>Signs: <span style=""font-weight: 400;"">Low FEV1, FVC, and FER</span></div></li><li><div><span style=""font-weight: 400;"">Flow fall rapidly after the peak (concave loop).</span></div></li><li><div><span style=""font-weight: 400;"">Small airways may be obstructed so airflow is significantly reduced in exhalation.</span></div></li><li><div><span style=""font-weight: 400;"">FEF-25-75 reduced and the central part of the curve dips due to lowered airflow.</span></div></li></ul><li><div>Restrictive Disorder:</div></li><ul><li><div>Signs:<span style=""font-weight: 400;""> FER is normal, FVC and FEV1 is reduced.</span></div></li><li><div><span style=""font-weight: 400;"">Patient unable to inhale and exhale fully so total lung volume is lower than normal.</span></div></li><li><div><span style=""font-weight: 400;"">FEV1 is usually reduced however reduction in FVC may result in FER appearing normal.</span></div></li><li><div><span style=""font-weight: 400;"">Because there is no airway narrowing the shape of the flow-volume loop is normal, but the volume expired is reduced.</span></div></li></ul></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">2.16 Diseases</span></div>Describe the disease COPD and Chronic Bronchitis <br> <br> CERS <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint3bbdb2ac45c09bb0').style.display='block'; return false;""> Hint</a> <div id=""hint3bbdb2ac45c09bb0"" class=hint style=""display: none"">CERS</div> ""<div class=""back""> <b><ul><li><div>COPD:&nbsp;</div></li><ul><li><div>Emphysema:</div></li><ul><li><div>Cause: <span style=""font-weight: 400;"">Phagocytes attracted by inflammatory mediators which release enzymes including elastase.</span></div></li><li><div>Effect:<span style=""font-weight: 400;""> Elastase breaks down the elastin in alveolar walls.</span></div></li><li><div>Result: <span style=""font-weight: 400;"">Alevoli collapsed during expiration so trapping occurs causing reduced gas exchange, also reduced surface area.</span></div></li><li><div>Symptoms: <span style=""font-weight: 400;"">Breathlessness</span></div></li></ul><li><div>Chronic Bronchitis</div></li><ul><li><div>Cause:<span style=""font-weight: 400;""> Smoke and dust particles stick to the surface of airways, these release inflammatory mediators.</span></div></li><li><div>Effect: <span style=""font-weight: 400;"">Inflammation of airways due to mediators.</span></div></li><li><div>Result: <span style=""font-weight: 400;"">Excessive production of sticky mucus</span></div></li><li><div><b>Symptoms: <span style=""font-weight: 400;"">Breathlessness</span></b></div></li></ul></ul></ul></b> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">2.16 Diseases</span></b><b><br></b></div>Describe and explain the diseases antitrypsin and asthma <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Antitrypsin:</div></li><ul><li><div><span style=""font-weight: 400;"">The lungs are normally protected from elastase by a-1 antitrypsin, which is produced in the liver.</span></div></li><li><div><span style=""font-weight: 400;"">If the degree of inflammation results in more elastase that can be blocked by AAT, then damage to the lungs occurs.</span></div></li><li><div><span style=""font-weight: 400;"">Some people have a defective gene for AAT and are at much higher risk of COPD, even if they have never smoked or been exposed to high levels of pollution.</span></div></li><li><div><span style=""font-weight: 400;"">AAt is an inherited disorder, which required both parents to pass on the defective gene.</span></div></li></ul><li><div>Asthma:</div></li><ul><li><div><span style=""font-weight: 400;"">A chronic inflammatory condition of the airways that causes inflammation which results in airways hyperresponsiveness.</span></div></li><li><div><span style=""font-weight: 400;"">Increased sensitivity to stimuli causes airway narrowing.</span></div></li><li><div><span style=""font-weight: 400;"">It is possible for it to be reversible by bronchodilator drugs.</span></div></li><li><div><span style=""font-weight: 400;"">Causes reduced ventilation and decreased surface area which results in mucus production.</span></div></li></ul></ul></b> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">2.16 Diseases</span></b><b><br></b></div>Describe the diseases pulmonary embolism and pneumothorax <br> <br> <br> <br> <a class=hint href=""#"" onclick=""this.style.display='none'; document.getElementById('hint8e8f83af4825e2bc').style.display='block'; return false;""> Hint</a> <div id=""hint8e8f83af4825e2bc"" class=hint style=""display: none"">SIC</div> ""<div class=""back""> <ul><li><div><b>Pulmonary Embolism:</b>&nbsp;Occurs when thrombi forms in large veins and travel to the lungs and become lodged and affect pulmonary circulation.</div></li><ul><li><div><b>Effects:</b>&nbsp;Reduced ventilation leads to pain, and reduced blood flow to the area due to blockage. Restricted blood flow can damage the lung resulting in hemorrhage and atelectasis.</div></li><li><div><b>Pathogenesis:</b>&nbsp;Often arise from deep veins of lower extremities but can originate from upper extremities such as the right side of the heart and pelvic veins.</div></li><li><div><b>Diagnosis:&nbsp;</b>Can be diagnosed using a CT pulmonary angiogram or a ventilation-perfusion scan,&nbsp;</div></li><ul><li><div><b>Virchow’s Triad</b></div></li><ul><li><div>Stasis</div></li><li><div>Injury</div></li><li><div>Hyper-coagulation</div></li></ul></ul></ul><li><b>Pneumothorax:&nbsp;<span style=""font-weight: 400;"">When air enters the intrapleural space causing the pressure to rise and the lung collapses inward. Both the chest wall and the thoracic cage have elastic properties and under equilibrium, the chest wall is pulled inward and the lung is pulled outwards.</span></b></li></ul> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">2.18 Graphing Curves On Saturation Of&nbsp;</span><span style=""font-style: italic; text-decoration-line: underline;"">Haemoglobin And Partial Pressure</span></div>Describe the graphing curves and variations in the haemglobin and partial pressures <br> <br> <br> <br> ""<div class=""back""> <ul style=""""><li style=""font-weight: bold;""><div>Normal:<span style=""font-weight: 400;""> In the alveoli, the partial pressure of oxygen is about 104mmHg, which means that Hb is almost 100% saturated; and has a high affinity for oxygen.</span></div></li><ul style=""font-weight: bold;""><li><div><span style=""font-weight: 400;"">In systemic veins, the partial pressure of oxygen is about 40mmHg and Hb is around 77% saturated. This means that some of the oxygen has been released for use in aerobic respiration. In systemic veins, Hb has a lower affinity for oxygen.</span></div></li><li><div>pH:<span style=""font-weight: 400;""> When pH has reduced the affinity for Hb for oxygen reduces so this means that at any partial pressure of oxygen the percentage saturation of oxygen from hemoglobin is lower so more oxygen has been released. So the curve shifts to the right.</span></div></li><li><div>pCO2:<span style=""font-weight: 400;""> Blood also carries carbon dioxide so when blood pCO2 is high the affinity of Hb for oxygen falls and the curve shifts to the right so hence more oxygen is released.</span></div></li><li><div>Temperature:<span style=""font-weight: 400;""> Increasing temperature reduces affinity and shifts the curve to the right and decreasing temperature shifts the curve to the left.</span></div></li><li><div>2,3 DPG:<span style=""font-weight: 400;""> 2,3-Biphosphocylcerate acid is a three-carbon isomer of glycolytic intermediate that is present in human red blood cells at 5mmol/L whose purpose is that it binds with greater affinity to deoxygenated hemoglobin so it promotes the release of oxygen. So its increase shifts the curve to the left, 2,3-BPG increases x5 within 1-2 hours in patients with chronic anemia, this is decreased with dialysis and transfusion.</span></div></li></ul></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.1 Epithelial Cells</span></div><span style=""font-weight: 400;"">Describe the cells that protect the epithelium</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Epithelial Cells: <span style=""font-weight: 400;"">Form tight junctions to prevent early entry into the lamina propria and expresses PRRs like TLRs on the basolateral surfaces.&nbsp;</span></div></li><ul><li><div>Goblet Cells:<span style=""font-weight: 400;""> Produces highly glycosylated proteins called mucins which generate a mucus barrier that prevents pathogen access, they can be upregulated and modified by cytokines and infection.</span></div></li><li><div>Paneth:<span style=""font-weight: 400;""> Found at invaginates of the epithelium and produces anti-microbial peptides. In the small intestine, a-defensins are produced as inactive precursors cleaved by trypsin. They produce REGIII blocking and killing bacteria.</span></div></li><li><div><b>Microfold Cells:<span style=""font-weight: 400;""> Sampling of antigens from the lumen</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.2 Innate Cells</span></div><span style=""font-weight: 400;"">Describe what the innate cell the macrophage does</span></b> <br> <br> <br> <br> ""<div class=""back""> <ul><li><b>Macrophage: <span style=""font-weight: 400;"">Produced by</span> <span style=""font-weight: 400;"">local signals such as TGF-β which are highly phagocytic and kill microbes but don't produce cytokine. They secrete anti-inflammatory cytokines such as IL-10 and support T cells in the GI tract.</span></b></li></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.3 Adaptive Cells</span></div><span style=""font-weight: 400;"">Explain what does the adaptive cells: The lymphocytes and peyers patches do</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Lymphocytes: <span style=""font-weight: 400;"">Scattered within the GI tract and found in the lamina propria and as intraepithelial lymphocytes mainly CD8+ T cells.</span></div></li><li><div><b>Peyers Patches:<span style=""font-weight: 400;""> Organised lymphoid tissue, having lymphoid follicles which is isolated and can be sites of immune activation in addition to draining the mesenteric lymph nodes.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.4 Intestinal Dendritic Cells</span></div><span style=""font-weight: 400;"">Describe the intestinal dentritic cells as well as how do M cells accompany them</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Intestinal Dendritic Cells: <span style=""font-weight: 400;"">Antigen-presenting cells such as dendritic cells are present in the GI tract and sample antigens from extending between epithelial cells to the lumen for presentation to T cells in GALT and mesenteric lymph nodes.&nbsp;</span></div></li><li><div><b>M Cells:<span style=""font-weight: 400;""> Involved in continuous antigen sampling from the lumen via endocytosis to dendritic cells to present them to T cells and has irregular ruffled surfaces instead. They do not produce digestive enzymes or mucus and therefore are not protected from pathogens. Some microbes can take advantage of this pathway.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.5 Lymphoid Tissue</span></div><span style=""font-weight: 400;"">Describe the features of Lymphoid tissue</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Secondary Lymphoid Organs: <span style=""font-weight: 400;"">Region where lymphocytes like T and B cells interact with antigens and become activated.</span></div></li><li><div>Circulation Of Lymphocytes:<span style=""font-weight: 400;""> Distinctive feature of recirculation between the blood, lymphoid organs, and tissues. This allows for low-frequency antigen-specific lymphocytes to sample antigens captured within the body (cell migration is similar to neutrophil recruitment).&nbsp;</span></div></li><ul><li><div><span style=""font-weight: 400;"">DC-bearing antigens enter the lymph nodes through lymphatic vessels which causes naive lymphocytes to leave the blood and enter lymph nodes across high endothelial venules that if activated can enter via efferent lymphatics.</span></div></li></ul><li><b>Lymph Node:<span style=""font-weight: 400;""> T cells are found in the paracortex, and B cells are found within the cortex. Germinal centers develop in response to antigenic stimulation and are sites of B cell proliferation, somatic hypermutation and selection as well as class switch recombinant.</span></b><br></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.6 GI Lymphocytes</span></div>Describe the features of GI lymphocytes <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Activation:<span style=""font-weight: 400;""> Peyer patch region is under the epithelial layer and is rich in APC, T cells, B cells zone, and germinal centers.</span></div></li><li><div>Circulations:<span style=""font-weight: 400;""> Cells activated by antigen as well as exposed to retinoic acid produced by dendrites inducing the expression of CCR9 ad and the integrin α4β7, and these are sent back into the gut because the chemokine CCL25 is the ligand for CCR9 and the adhesion molecule MadCAM is the ligand for α4β7.</span></div></li></ul></b> "
"<div style=""font-weight: bold;""><span style=""font-style: italic; text-decoration-line: underline;"">1.7 IgA</span></div>Describe the features of IgA antibodies <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Adaptive Cell:<span style=""font-weight: 400;""> Is the dominant form of adaptive immunity in the gut and tissue cells such as TGF-β promotes B cell isotype switching to IgA</span></div></li><li><div>Transcytosis:<span style=""font-weight: 400;""> IgA in the lamina propria is held as a dimer by&nbsp; the J-chain, it binds to the poly Ig receptor and is transported across the epithelial cell where it is released via proteolytic cleavage of the receptor which forms the secretory component still attached to IgA</span></div></li><li><div>Function:<span style=""font-weight: 400;""> Does not activate the complement but is a powerful neutralizing antibody by mediating anti-viral activity and neutralization of toxins</span></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.8 T Helper Cell’s</span></div><span style=""font-weight: 400;"">Explain the T helper cell Th17 and regulator T cells</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Th17: <span style=""font-weight: 400;"">Found in the GI tract primarily in the small intestine and maintains mucosal epithelial barrier function due to production of IL-17 and Il-22&nbsp; that act on intestinal epithelial cells that induce expressions of proteins important for barrier function like mucins and β-defensins. They can induce acute inflammation to indirectly kill invading pathogens.</span></div></li><li><div><b>Regulatory T Cell: <span style=""font-weight: 400;"">Subset of CD4+ helper cells whose function is to suppress immune responses and maintain self-tolerance and can express the transcription factor FoxP3. They are either natural Tregs by self-antigen recognition in the thymus or inducible Treg by antigen recognition in the lymph nodes. Most Treg cells in the GI tract are inducible and their differentiation is induced by TGF-β and retinoic acid but Natural Treg can migrate to expand the response.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.9 Hypersensitivity</span></div><span style=""font-weight: 400;"">Describe the 4 types of hypersensitivity</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Hypersensitivity:</div></li><ul><li><div>Allergic: <span style=""font-weight: 400;"">Engagement of IgE antibodies bound to mass cells leads to degranulation causing an allergic response</span></div></li><li><div>Cytotoxic: <span style=""font-weight: 400;"">IgG antibodies and cell surface/extracellular matrix-associated antigens, promote cell destruction and function blocks. Arises from blood transfusion rejection.</span></div></li><li><div>Complex-Mediated:<span style=""font-weight: 400;""> Recognition of soluble antigen leads to deposition of Ab-Ag complexes in tissues or serum. Comes from Glomerulonephritis</span></div></li><li><div><b>Cell Mediated: <span style=""font-weight: 400;"">Damage mediated through inflammation or direct cytotoxicity and can come from contact dermatitis and type 1 diabetes</span></b></div></li></ul></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.10 Coeliac Disease</span></div><span style=""font-weight: 400;"">Describe the GI tract ailment Coeiliac Disease</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Coeliac Disease:<span style=""font-weight: 400;""> Autoimmune disorder leading to inflammation of the small intestine as well as causing atrophy and impairment from digestion and is triggered by dietary gluten, it has strong MHC Class II association specifically HLA-DQ2/DQ8. It is detected by serum antibodies reacting with gliadin, endomysium, or transglutaminase but a definite diagnosis is done by jejunal biopsy confirming villus atrophy.</span></div></li><li><div><b>Pathogenesis:<span style=""font-weight: 400;""> Gluten-derived peptides reach the sub-epithelial region and transglutaminase 2 deamidation of glutamines generates an inflammatory response done by HLA-DQ8 on APC to CD4 T cells creating. Another process leads to the production of anti-TG2 autoantibodies.</span></b></div></li></ul></b> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">1.11 Inflammatory Bowel Disease</span></div><span style=""font-weight: 400;"">Describe the GI ailment, Inflammatory Bowel Disease</span></b> <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Types:</div></li><ul><li><div>Ulcerative Colitis: <span style=""font-weight: 400;"">Confined to the colon, mucosal layer only. It can cause bloody diarrhea and abdominal pain with fever and weight loss. Caused by Th2 profile gut microflora.</span></div></li><li><div>Crohn’s Disease: <span style=""font-weight: 400;"">Any part of the GI tract causing transmural inflammation. Symptoms are fever, abdominal pain, and diarrhea. Caused by Th1 profile gut microflora.</span></div></li></ul><li><div>Th Cells:<span style=""font-weight: 400;""> Lots of TGF-β present in the GI tract that promotes differentiation of Th17 and Treg cells but they also inhibit Th1 and Th2 effector cells.&nbsp;</span></div></li><li><div><b>Risk Factor: <span style=""font-weight: 400;"">NODs a PRR, NFkB signaling pathway protein, and autophagy clearance of intracellular bacteria. HBA-B*27 (MHC class I) is a strong risk factor for UC.</span></b></div></li></ul></b> "
"<div><b><span style=""font-style: italic; text-decoration-line: underline;"">2.14 Ventilation</span></b><b><br></b></div>Describe the Herning-Breierur inflation reflex as well as the Pre-Botzinger Complex <br> <br> <br> <br> ""<div class=""back""> <ul><li><div>Herning-Breierur inflation reflex:&nbsp;</div></li><ul><li><div>Provides self-regulatory negative feedback mechanism.</div></li><li><div>Inflation inhibits further inspiratory muscle activity.</div></li><li><div>Deflation initiates inspiratory activity</div></li></ul><li><div>Pre-Botzinger Complex:&nbsp;</div></li><ul><li><div>Dorsal respiratory group neurons become excited and fire in bursts.</div></li><li><div>Firing leads to the contraction of inspiratory muscles.</div></li><li><div>When firing stops passive expiration occurs.</div></li></ul></ul> "
"<b><div><span style=""font-style: italic; text-decoration-line: underline;"">7.1 Hematopoiesis</span></div><span style=""font-weight: 400;"">Describe the&nbsp;</span></b>Pluripotent Haematopoietic Stem Cells <br> <br> <br> <br> ""<div class=""back""> <ul><li><div><b>Pluripotent Haematopoietic Stem Cells:&nbsp;</b>Can self-renew and differentiate into a variety of cell types with paths determined by growth factors present.</div></li><ul><li><div><b>Multi-CSF (IL-3):</b> Most cells of the immune system</div></li><li><div><b>GM-CSF:</b>&nbsp;Granulocyte and macrophage.</div></li><li><div><b>EPO (erythropoietin):</b>&nbsp;Production of RBCs</div></li><li><div><b>TPO (thrombopoietin):</b>&nbsp;Production of megakaryocytes</div></li></ul></ul> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">7.2 Growth<br></span></b>Describe the proccess thrombopoiesis as well as platlet homeostasis <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Thrombopoiesis: <span style=""font-weight: 400;"">Thrombocytes (platelets) are produced from very large cells termed megakaryocytes. These cells undergo nuclear replication and growth in the cytoplasm without cell division. After the granulation of the cytoplasm, platelets are formed from the fragmentation of the cytoplasm.</span></div></li><ul><li><div><span style=""font-weight: 400;"">TPO is secreted constitutively by the liver, kidney, endothelial cells, and bone marrow stromal cells. Its cs activity is regulated through a competition between platelets and megakaryocyte progenitors for Tpo. When platelet levels fall, less TPO is bound by platelets. The level of free Tpo available to stimulate megakaryocytic precursors in the marrow rises.</span></div></li></ul><li><b>Platelet Homeostasis: <span style=""font-weight: 400;"">Released platelets stored in the spleen, can also provide negative feedback by binding and destroying thrombopoietin. Older platelets are destroyed in the liver and spleen by the phagocyte system.</span></b><br></li></ul></b> "
"<b><span style=""font-style: italic; text-decoration-line: underline;"">7.2 Growth<br></span></b>Describe the process of Erythropoiesis <br> <br> <br> <br> ""<div class=""back""> <b><ul><li><div>Erythropoiesis: <span style=""font-weight: 400;"">EPO produced in the kidney in response to anoxia or high altitude, stimulates erythropoiesis at the committed blast stage and stimulates hemoglobin synthesis.</span></div></li><li><div><b>Life Cycle:<span style=""font-weight: 400;""> Usually leaves the bone marrow as reticulocytes and undergoes final maturation within 24 to 48 hours. Mature red blood cells last for 120 days and are retired by macrophages usually in the spleen. The iron and amino acids in the hemoglobin are recycled and the haem ring is converted into bilirubin.</span></b></div></li></ul></b> "