Intro To Physiology

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Intro To Physiology

Nervous System

Master regulator for the body

Takes sensory input, integrates it, and elicits motor output

Two divisions o CNS

 Consists of the brain and the spinal cord

 Mostly responsible for integration o PNS

 Spinal nerves

 Afferent/Sensory

Towards the CNS

Sensory input from sensory receptors

Enters the dorsal side of the spinal cord

No synapses- cell bodies exist in a dorsal root ganglion

 Efferent/Motor

Away from the CNS to effectors

Effectors are muscles and glands

Two divisions o ANS (Autonomic NS)

 Involuntary

 Visceral motor control of glands and smooth muscle

 Two divisions

Sympathetic-fight or flight o Synapses right outside the spinal cord in sympathetic trunks o Uses ACH in the first path, Epi or Norepi in the second path

Parasympathetic-rest and digest o Synapses close to the effector organ o Uses ACH for both paths

Both divisions have their first path myelinated while the second path is unmyelinated o Somatic NS

 Voluntary motor control

 From the CNS to skeletal muscles

 Single neuron all myelinated

 Uses ACH as the neurotransmitter

Glial cells-non neuronal cells in the nervous system o Many more glial cells than neurons

o Insulation (myelin)

 Oligodendrocytes in the CNS

Can wrap more than 1 neuron

 Schwann Cells in the PNS

Can only wrap 1 o Protection

 Astrocytes

The majority of glial cells

Provide nourishment to the cells

Create the Blood Brain Barrier o Circulation

 Ependymal cells

Ciliated

Circulate (do not produce) CSF o CSF is produced by a choroid plexus o Immunity

 Microglia

Macrophages

Immune system isn’t allowed into nervous system

Neuron o Dendrites

 The receptive region of the neuron

 Contains Na and K ion channels to start depolarization

 Receives neurotransmitter via receptors

 Post synapse

The signal goes electrical, chemical, electrical o Membrane potential

 Resting cells are at -70 mv

 Action potential brings them to +30

 Opening of Na channels brings + charges into the cell

Causes the climb in charge

Depolarization

 Repolarization is caused by the delayed opening of the K gated ion channel

(activated at the same time but delayed) allowing K ions out of the cell

 Also slow to close, causing hyperpolarization

This has the added benefit of making sure the neuron cant fire too much too fast

 Na/K pump restores ion concentrations after

 The anions in the cell are mostly responsible for the negative charge

 Charges balance out

An electrical equilibrium is created based on the regular charge of the cell, or based on an outside charge (experimentally)

Charges flow to make the charges equal

Add + charge to cell, it wants to decrease the potential so it flows out

Add – charge to cell, it wants to increase the potential so ions flow in

 Threshold potential of the neuron is reached at -55 mv

Reached at the axon hillock

 -58 mv is the K ion potential equilibrium o Graded potentials

 Depolarizes one region of the cell

 Can be any level

-34

-24

-85 (so it can even be hyperpolarization)

Etc

 The cell region is depolarized yet does not reach threshold at -55 mv

 Graded potentials can lead to Action potentials

 Can be summed in time or in space

Temporal summation o One after another, they add up

Spatial summation o In the same space, add together o Action potential

 Reaches threshold

 Generated at the axon hillock

 Depolarization due to Na channels opening

 Reaches about +30

 Then K ion channels open up and there is repolarization

 Then hyperpolarization as they are slow to shut

 Then the gradient is reestablished by the Na/K pump

 Another one cannot be fired for 4-5 ms

 Needs to be strong to overcome hyperpolarization

Absolute refractory- nothing can be fired

Relative refractory-only a very strong graded potential will lead to an AP

 The number of AP’s determines the stimulus strength o Variables

 Size

Increase diameter, the speed increases

 Myelination

Myelination increases speed by a lot

Saltatory conduction

o In jumps only to the nodes of ranvier o Makes it so that only at the nodes of ranvier does the AP have to occur o Three types of neurons

 Multipolar

Most common

 Bipolar

Found only in special senses

 Unipolar

Sensory receptors o Three functions

 Sensory (afferent)

 Motor (efferent)

 Interneurons

CNS

Most common (99%)

Neurotransmitters o Diffuse from high to low gradient across the synaptic cleft o IPSP

 Inhibitory

 Hyperpolarizes

 EX: Cl- or GABA o EPSP

 Excitatory

 Depolarizes

 EX: glutamate o EPSP and IPSP can fight each other to try and create (or not create) an AP o The distance from the axon hillock makes a difference, as the depolarization decreases as the distance increases

Terminal bulbs o Ca ion channels (voltage gated) open when the AP reaches, and the influx of Ca pushes vesicles containing NTs to the wall of the terminal bulb o This causes their release into the synapse

Ionotropic receptors o Everything discussed here o Fast

Metabotropic receptors o Use second messengers o Usually G-protein linked o And takes longer due to the second messengers

Endocrine System

Method of communication in the body o Use the blood stream o Hormones are long distance

Hypothalamus- top of the pituitary gland- master control

Pituitary-second in command

Lipid soluble hormones can go directly through the bilayer and attach to a receptor inside the cell

Hormones are usually controlled by metabotropic receptors o Their effect takes longer than neurotransmitters

 Due to amplification

Target cell activation depends on 3 factors o Number of hormones in the blood o Number of receptors o Affinity for receptors (how tightly they bind)

 cAMP second messenger o G s

on a G-protein receptor o Response is amplified o Activates PKA o Hormones that use this cAMP

 Cattecholamines

 Acth

 FSH

 LH

 Glucagon

 PTH

 TSH

 Calcitonin

Pip second messenger o DAG and IP3 activated Calcium ion release and therefore PKC o Hormones

 Catecholamines

 TRH

 ADH

 GnRH

 Ocytocin o G q

subuinits

Hormone interactions o Antagonism o Permissiveness o Synergism

Endocrine gland stimulations o Humoral (nutrients in blood) o Hormones o Neuronal

 Faster than hormonal

Pituitary gland portal system o Regular portal system is arteriole-capillary-venule o Pituitary portal system is capillary-vein-capillary

 Goes quickly from hypothalamus to pituitary

 More concentrated hormones in a shorter distance

Speed and concentration

Pituitary o Posterior pituitary

 Oxytocin

Made in the paraventricular nuclei of the hypothalamus and sent to the posterior pituitary to be released

 ADH

Supraoptic nuclei in the hypothalamus make it o Anterior pituitary

 TSH, GH, ACTH, prolactin, LH, FSH

Aneurysm o Saccular-bulb at risk of rupturing o Fusiform-not as dangerous-> longer elongation o Ruptured-broken open

Kidneys o Adh production

 Mechanism?

Triggers kidneys to reabsorb water, therefore increasing blood volume and pressure

Based on osmolality

Thyroid hormone o Major metabolic hormone o T3 and T4 (needs IODINE) o Path

 Hypothalamus-TSH (ant pituitary)-thyroid-thyroid hormones

PTH vs Calcitonin o PTH increases the blood Ca level and breaks the bone down o Calcitonin decreases blood Ca level by building the bone up

Insulin vs Glucagon o Insulin decreases blood glucose level o Glucagon increases glucose level

Aldosterone o Directly brings in Na and water into the blood in the kidneys o Controlled

 Increased K+ level in blood

 Decreased blood volume or blood pressure

 Acth released by anterior pituitary

 Increased blood pressure or volume

Inhibitory o Targets kidney tubules o Antagonized by ANP release by the heart

Stress response o CRH released by hypothalamus (corticotropin releasing hormone) o Causes the adrenal medulla to release catecholamines (epi/norepi) o Catecholamines release ACTH to raise the blood pressure o Catecholamines short term stress response o Mineralo and glucocorticoids=long term stress response

Different behavior? o Due to different receptors

Muscles

Smooth, cardiac, and skeletal

Skeletal is under conscious control

Smooth and cardiac are unconscious

Four functional characteristics of muscle tissue o Contraction o Extension o Elastic o Excitability

Skeletal o Striated o Multinucleated o Cylindrical o ACH binds to it and is always excitatory

Cardiac o Striated o Multibranched o Pacemaker o Cells connected by calated discs

Smooth o No striations o Spindle shaped

o Shortens with calmodulin

Skeletal muscles o Contract small to large o Smaller motor units first

Each bundle separated by perimysium o Bundle=fascicle

Muscle fiber (cell) o Surrounded by the endomysium

Myofibrils o Contains two filaments (myofilaments)

 Actin and myosin

Each muscle fiber contains many myofibrils

Motor unit o The motor neuron and all of the muscle fibers it innervates o Vary in size

Myosin and actin o Work together to contract the muscle

T tubules o Allow the AP to go down into cell and release Ca from the sarcoplasmic reticulum

Sarcoplasmic reticulum o Calcium ion storage

Glycosomes o Storage of glycogen for quick energy

Sarcomere o The smallest unit of the muscle o Z disc to z disc o H zone is based on thick filaments only o I bands only thin o A band length of myosin

Calcium o The final trigger for the muscle contraction, what is the initial trigger for the muscle cell

Muscle contraction steps o Na enters and AP propagated along the cell and down the t tubule o AP triggers Ca channel in the SR to open o Ca binds to troponin

 Changes the shape of tropomyosin and actin active sites are exposed o Contraction

 Myosin heads bind to active sites on actin and use energy by ATP to push o Removal of calcium from the cytosol o Tropomyosin blockage restored

Thin filaments

o Actin o Two actin molecules helix shape o Actin associated with troponin and tropomyosin o Troponin binds to Ca ions o Tropomyosin covers active sites

Myosin o Thick filaments o 2 lobed heads

Cross bridge o Myosin head attaches and forms a cross bridge o ATP is released to push the cross bridge

 Power stroke o ATP attaches to dislodge crossbridge o The ATP to ADP charges it for its next powerstroke

Sliding filament theory o Myosin pulls actin closer o The H band gets smaller

Rigor mortis o Crossbridge remain engaged after death

 High tension o Muscles need ATP to relax

Motor unit recruitment and wave summation o Increasely strong muscle contractions o Motor unit recruitment recruits more motor units o Wave summation work for one motor unit increasing in force (not calling more)

Size principle for motor units o Small-meduim-large

Muscle contaction o Isometric

 Same length

 No shortening of the sarcomere

 Develop tension in the muscle o Isotonic

 Shortening

 Same tension

 Tension is at or above the load so the muscle shortens

Energy o Creatine phosphate

 Directly converts ADP to ATP for quick energy o Anaerobic mechanism

 Hlycolysis and lactic acid forms

o Aerobic mechanism

 Glucose and fatty acids from fat tissue

 Provides hours of energy

3 types of fibers o Slow oxidative

 Endurance activities

 First recruited o Fast oxidative

 Sprinting/walking o Fast glycolytic

 Short term intense movement

Oxygen debt o Spend more energy than can be provided o Lactic acid build up needs to be corrected

Blood Vessels

Deoxygenated blood comes from a capillary into the right atrium from the vena cava

Pulmonary circuit is lower pressure

Systemic circuit is high pressure

Arterioles go away from the heart

Veins go towards the heart

Pulmonary veins-left atrium-left ventricle-aorta-arterioles-capillary-venules-veins-vena cavaright atrium-right ventricle-pulmonary arteries

Cardiac output o HR X (EDV-ESV) o EDV- amount of blood left in ventricle when the heart is relaxed o ESV- amount of blood left in ventricle during contraction

The highest pressure of anywhere in the circulatory system is in the left ventricle (to get it into the aorta)

Average of 5.25L of blood per minute

Preload o Greater preload leads to a higher stroke volume o Unless they are too high, which decreases stroke volume

 Stretches the sarcomere too much

Contractility o The contractile force of the heart o Increased by the amount of Ca ions released

 More calcium, more crossbridges

Afterload o The amount left over o Greater left over, need more pressure to push the blood out

Sympathetic nervous system increases the heart rate

Parasymp decreases the heart rate

ADH and aldosterone can affect the volume of the blood

CHF caused by MI, high Bp, etc o Pulmonary CHF

 Left side fails first and the blood backs up in the lungs o Peripheral CHF

 Right side fails first and the blood pools in extremities

Norepi or epi o Released in adrenal medulla o Activate cAMP mechanisms o Allows more Ca into the cell and cause a stronger contraction

Vessels o Capillaries are responsible for a gas exchange o Types

 Fenestrated

Holes in the walls (window)

Intestines

Filtration or absorption is their function

SI is the site of most absorption

Endocrine glands also use fenestrated capillaries

 Continuous

No holes/spaces

Lungs-gasses are small enough you just need PM

Specialized continuous capillaries are in the brain

 Sinusoidal

Allows cells to go through

WBC’s move around

Arteries o Elastic-conducting o Muscular-distributing o More elastic tissue

 Withstand higher pressure o Thicker tunica media

Veins o Valves o Lower pressure

Capillary beds o Perfusion depends on the sphincter of arteriole o Can control which capillary beds are open or closed at a time

Mean arteriole pressure pushes blood through the heart

o Diastolic pressure + 1/3 (pulse pressure (difference between systole and diastole)) o

Pressure through blood vessels is steady-does not vary up and down

How do the veins return blood to the heart o Skeletal muscle contractions o Breathing o Valves in the veins preventing backflow

Contractility is defined by a sarcomere length o At a stable sarcomere length still get increased contraction due to higher calcium levels

Kidney compensation o Multiple ways the kidneys can affect BP o Renin Angiotensin aldosterone system

 Angiotensin II causes an increase in BP

 Constricts blood vessels by impairing NO synthesis o Increases aldosterone production

 Retains Na and water increasing blood volume and blood pressure

Intrinsic mechanisms o Local o Distribute blood flow to individual organs as needed o Metabolic controls and myogenic controls

Extrinsic mechanisms o Global o Nerves and hormones o Control levels all over the body, not just to specific places

Factors determine fluid in and out

o Hydrostatic pressure-force fluid out o Osmotic pressure-water moving in o Net filtration pressure

Respiratory System

4 processes of respiration o Inspiration o Expiration o External respiration o Internal respiration

Continuous capillaries

Breathing o Air passes to alveoli where gas exchange occurs o Inspiration

 O

2

into the body o Exhalation

 CO2 out

Conducting zone o Filter and warm (nasal cavity) o Moisten the air o Rigid tube with cartilage o Cilia/structures that help filter

Bronchi split until they reach the terminal bronchioles

Alveoli pop up in the respiratory bronchioles

Dividing line is between the terminal bronchioles and respiratory bronchioles

Respiratory zone o Less rigid o Some smooth muscle o Smooth muscle wrapped around the respiratory bronchioles

What controls the dilation of the airway o Smooth muscle controlled by

 Gas

 Sympathetic

Dilates!!!!!!!!!

 α receptors constrict (found in the vessels)

 β receptors dilate (found in the lungs)

 also found in coronary arteries and skeletal muscle arteries

 external respiration membrane o 3 or 4 structures o Alveoli o Continuous capillaries

o 2 types of cells that make up an alveolus

 Type 1-shared respiratory membrane

 Type 2-surfacant secreting

Detergent that breaks surface tension

 Basement membrane (fused) o Immune cells in our lungs

 Macrophages constantly hunt for bacteria and pathogens

 Macrophage is stuck in alveoli

Negative pressure breathing o Generate a negative pressure to pull air in o Inhalation is active

 Contract the muscles o Exhalation is passive

 Relax muscles and push air out o Breathing muscles

 Diaphragm and intercostal muscles

Lungs automatically want to collapse, chest pushing out

Creates an interplural pressure that is always negative relative to the atmospheric pressure

Visceral pleura lines lungs

Parietal pleura lines the inside of the chest wall

Relative to ATM o Interpulmonary pressure negative on inspiration, zero at break, and positive on expiration

Transpulmonary pressure at 0? o Pneumothorax

P p

=P

T

X C o Partial pressure= total pressure X concentration

Gasses diffuse from high to low o Tissues are in need of oxygen, oxygen diffuses into them

Dead air space o Mixes oxygen o 150 mL o Conducting structures

Dead air space causes expired O2 to be higher than alveolar O2 o The alveolar oxygen is low due to it perfusing into the capillaries

High altitude o Breathing rate increases o More Red Blood cell production

Respiratory groups o Ventral respiratory group

 Generate normal breathing

 GABA o Dorsal Respiratory Group

 Modulates the VRG

 Can sense changes in parameters, to then effect o Pontine respiratory center

 Can change rate

Respiratory stimulant o CO2 levels drive breathing o CO2 produced from tissues o Decreases the PH of the blood by being converted to carbonic acid which lowers the PH

Hyperventilation o Usually a V/Q match o Ventilation o Perfusion o Need to match

Oxygen carried in the blood by hemoglobin (Hb)

90% of Oxygen attached to Hb o Gives it more solubility o 4 bonds pere Heme

The affinity of hemoglobin for oxygen changes with the extent of oxygen saturation

More oxygen there is, the more affinity there is for O2

High levels of O2 sat o Usually unladed fast to the tissues, and difficult to load to the Hb

Decreased CO2 pressure leads it to be harder to unload

Increased CO2 pressure? Easier to unload

Lower body temperature triggers decreased co2 levels

High metabolic activity leads to increased CO2

CO2 o Typically carried in the blood o Bicarbonate ion o 70% is bicarbonate ion o 20% is dissolved directly in the plasma o 10% bound to Hb

Carbonic anhydrase o Converts CO2 to carbonic acid o In the Red Blood Cell

Cl- comes into the RBC as the HCO3- ion leaves to balance the charges

Haldane effect o Lower O2 levels?

 Higher PCO2 o Higher O2 levels?

 Lower PCO2

If oxygen is saturated, harder for CO2 to bind to Hb

BPG o Helps push O2 off of the Hb so high levels in systemic capillaries causes O2 unloading

HAPE o High altitude pulmonary edema o Fluid in the lungs o Causes a decrease in alveolar ventilation

Digestive system

Nutrient competition in the gut between good and bad bacteria

Leptin is made by bacteria and signals body to feed

Many organs have dual functions o Liver o Pancreas o Pharynx

Accessory organs o Support the digestive system (not a part of the alimentary canal) o The alimentary canal is the path from the mouth to the anus

 The “tube within the tube” o Pancreas o Gallbladder o Liver o Stomach cells

Mechanical digestion o Occurs via the teeth

Chemical digestion o Chemically breaks down food o First is salivary amylase

 Breaks down carbohydrates o HCl degrades food in the stomach

 Creates chime

 Acid also kills many bacteria o SI

 Major place of chemical digestion

 Proteins, fats, carbs are all degraded and absorbed

Gallbladder o Stores concentrated bile from the liver o Shunts it to the small intestine via the common bile duct (with the pancreas)

Large intestine o Major site of water reabsorption

o Also produces the feces

The goal of digestion is to get the components of food broken down into usable parts

Long reflexes o Go all the way to the CNS and get integrated o Prepare the body to receive food

Short reflexes o Local (enteric) nerve plexus

Reflexes are stimulated by food

Antacids work by blocking H+ ion production and making the stomach acid less acidic o Has the effect of not killing some of the bacteria o Acid is usually 2-3 pH

Stomach digestion o Breaks down food mechanically and chemically

 Mechanical is churning

 Chemical is acid and peptidases o Gastrin

 Stimulates the secretion of HCl and pepsinogen which works to chemically digest proteins (in its active pepsin form) o Pepsinogen

 Activated by HCl

 Into pepsin

 Pepsin then works to break down proteins o Parietal cells

 Make the HCl

 Secreted by goblet cells o Chief cells

 Make the pepsinogen o Enteroendocrine cells

 Hormone producing cells

How does the brain control gastric juice production o Brain senses food and secretes additional gastric juice

 Reflect of food…saliva o Symp-less o Parasymp-more o Ph based

 Low pH-less gastric juice

Vagus nerve of the parasymp NS stimulates the digestive system

Which 3 chemicals are necessary for maximum HCl production? o Gastrin o ACH

 From the parasymp (vagus)

o Histamine

Chyme gets sent to the duodenum o The duodenum produces many hormones

 Secretin

 CCK (Cholecystokinin)

 VIP (vasoactive intestinal peptide) o All of these hormones are known under the collective name enterogastrones

SI o Nutrient absorption

 Microvilli

 Folds (gyri)

 Increased surface area o Microvilli contain brush border enzyme

 Bring things to the monomer form

Nutrients absorbed go to the liver o Hepatic portal system o Liver creates bile o Bile salts

 Emulsifiers

Help break down fats o Lacteals take the fats to the liver

 Triglycerides pass into lacteals

 Called chylomicrons

Liver o Processes SI blood o Liver stores the glycogen o Detoxifies compounds o Arterioles and venules send blood the same way

 Arterioles supply oxygen

 Venules supply nutriets

 o Kupffer cells

 WBC (macrophages) o Liver can regenerate o Bile production

 CCK-singals the gallbladder to release

 Secretin

Tells the liver to make bile

H+ is neutralized in the SI by bicarbonate ion o Comes from the pancreatic juice

CCK induces the pancreas to produce pancreatic juice

Secretin binds and causes copious release of bicarbonate ions in pancreatic juice

Pancreas hormones (in juice) o Trypsinogen  trypsin o Chemotrypsinogen  chemotrypsin o Procarboxypeptidase  carboxypeptidase o Activated by brush boarder enzymes

Large intestine o Water reabsorption o Some absorption of ions occurs with the water o A lot of bacteria in the LI, some good others bad

Immune System

Adaptive vs innate immune system o Innate

 First line of defense

Skin barrier

Mucus membranes

Skin secretions

 Doesn’t require previous exposure

 Present at birth

 Enzymes that can directly kill bacteria

 Faster and more immediate

 Has internal nonspecific defenses

Phagocytes

Fever

Natural killer cells

Antimicrobial proteins

Inflammation

 NK cells recognize antigen (just that it has an antigen) and releases chemicals called granzymes to perforate the membrane

 Macrophages

Derived from monocytes

Stem cell is the hemocytoblast

General macrophages eat bacteria

Search for food and engulf them through a process known as phagocytosis

Arrive after neutrophils (part of innate defense)

 Phagocytosis

Success rate increased (opsonization)

Antibodies specific to the antigen are produces and coat the bacteria o Neutralization o Agglutination

 o Precipitation

Inflammatory response o Neutrophils enter blood from the bone marrow o Margination

 They stick to the sides of the blood vessel wall via CAM (cell adhesion molecules) o Diapediesis

 Walk to the site o Positive chemotaxis

 Call more WBC o Four cardinal signs

 Swelling

Edema

 Heat

Increased blood flow

 Pain

Leaked protein rich fluid

Histamine released

 Redness

Increased blood flow

Increased temperature short term helps fight the infection

Long term fever can be dangerous for the organism

Interferons and complement proteins enhance the innate defenses by attacking microbes directly o Interferons are local o Complement proteins are more whole body

Adative immune system o Specific o Made to attack very specific microbes o Vascular o Antibodies o Lymphocytes vs leukeocytes

 Lymphocyte is one of three specific types of WBC

 Leukeocytes are WBC overall (larger category) o Immunocompetance (need to get educated)

 Happens in the T gland for T cells

 Bone marrow for B cells

 Have not been exposed to antigen? Naïve o APC (antigen presenting cells)

 Big 3?

Dendritic cells

B cells

Macrophages o T cells

 Recognize our own MHC proteins

 If they recognize it? They are killed off to avoid an autoimmune reaction

 Surviving cells are self tolerant o Activated immune cells are “selected” and begin to divide o B cells

 Plasma B cells-antibody secreted

 Memory B cells-stay around for next reaction for less of a lag time o Humoral immunity-antibody mediated (B-cell)

 Active-make antibodies

Natural-antibodies/reaction

Artificial-vaccine

 Passive-pass antibodies

Natural-passed from mom

Artificial-serum (antibodies) o Cell mediated immunity

 T cell response

Helper T cells recognize and help mount an attack o CD4 o Respond to class II MHC’s via the APC’s

Cytotoxic T cells kill directly o Induce apoptosis with granzymes and perforin o CD8 o Respond directly to class I MHC proteins

 MHCII

Only present in APC

Taken in by APC cells (endocytosed) and combined with a MHCII receptor

Only an antigen fragment is displayed (antigenic determinant)

 MHCI

All cells carry it

Display any antigens that invade the cell

Urinary System

Kidney is at the center of the urinary system o Major functions

 Filter blood

 Excrete urine

 pH balance is important

o blood comes from the aorta and feeds the kidneys o pair of ureters collects the urine

 nephrons-functional unit of the kidney o also the urine forming units

Proximal convoluted tubule (PCT) o Cells have lots of mitochondria and microvilli

 Absorption function

Kidneys modulate the systemic BP o Catcholamines o Angiotensin o Renin o ADH

Glomerulus is where renin is released o Can sense the BP o Renin raises the BP (vasoconstrict)

Proteins cannot pass throught he glomerular filtration membrane because it is too selective

 three forces determine the filtrate formation o glomerular hydrostatic pressure

 out o osmotic pressure

 in o capsular hydrostatic pressure

 in o net outward pressure is 10mm hg

 three mechanisms help maintain glomerular filtration rate when systemic bp is altered o myogenic o tubuloglomerular o hormonal

 afferent arterioles enter the glomerular capsul

 efferent arterioles leave

 the macula densa cells in the ascending loop of henle sense alteration of the filtrate flow and the NaCl concentration

The water in kidneys follows solutes out passively

Proximal Convoluted Tubule o Contains the Na/K pump that establishes the gradient to maintain ion balance

Primary and secondary active transport for absorption

Transport maximum exists for everything but Na ion o Maximum number of carriers are operating

DCT o Primary control of tubular secretion/reabsorption

 Sends things back IN to the Tube if there is too much in the blood

o Aldosterone-sends Na in o Parathyroid hormone (PTH)-sends Ca in

Loop of henle o Descending limb-water reabsorption passive o Ascending limb-solute reabsorption (mostly active)

Collecting duct o Water reuptake

 Concentrates the urine o ADH affects it

 Higher levels, more aquaporins, more water reabsorption o Water is reabsorbed into the vasa recta as to not affect the ion concentrations

Reproduction

Meiosis evolved o Mechanism to correct for error without cell division o Ploidy cycle-sometimes benefit from being haploid

Genes required for mitosis were repurposed for meiosis

Sex started-evolution occurred rapidly

Meiosis o Two stages

 Meiosis I-hapliod but still replicated

 Meiosis II-haploid and only one copy o Genetic variability

 Random assortment in metaphase I

 Crossing over in prophase I

 Random fertilization o 4 gametes out of the male process o 1 viable gamete for females (3 polar bodies)

Male gametes made in the seminiferous tubules o Edge cells move towards the lumen and become sperm

Spermatogonia o The male stem cells o Type A and B daughter cells

Sustentacular cells (sertoli cells) o Surround and protect the spermatogonia o Keep the immune system out

 Tight junctions o Produce ABP (andreogen binding proteins)

 Respond to FSH and LH o APB and testosterone combine to form the complex needed to form mature sperm

FSH and LH

o Stimulated by GnRH

Females o Meiosis produces polar bodies

 These polar bodies are not viable gametes

 Nonfunctional o 1 function oocyte is produced o a woman has 2 million primary oocytes present at birth o only 10% make it to primary follicle stage o Always more than one oocyte going through stages

 Only one responds best to the hormones o Follicular phase and luteal phase

 Follicular phase

Initial follicle to the thick follicle

Primary to secondary oocyte

14 days average

 Lueteal phase

Almost always 14 days

Antrum, secondary oocyte, and its release o Thecal cells

 Release male hormones (androgens) o Granulosa cells

 Convert androgens to estrogens o Sometimes more than one oocyte is released

 Fertilized by 2 different sperm?

Fraternal twins o Fertilized

 Once it is fertilized, the blastocyst is implanted into the uterine wall to allow it to grow o Sperm cell is only good for 1-2 days because the mitochondria die out and use up all the energy o 3-4 days for an oocyte

 Has all of the cytoplasm and organelles needed to survive o Increasing LH/FSH surge

 Induces the follicle growth o LH

 Receptors on the thecal cells create androgens o FSH

 Receptors on the follicle cells o Estrogen release in the blood causes a burst of FSH/LH release (not production)

 Positive feedback mechanism o Follicle gets larger, produces more estrogen, this triggers a shut off

o FSH and LH surge occurs around 14 days

 Estrogen dependent o Surge causes ovulation o After ovulation, the follicle ruptures and this leads to declining estrogen levels in the blood o Estrogen levels decrease, progesterone increases o Follicular cells become the corpus luteum

 Under control of LH

 Degraded if no fertilization o Estrogen and progesterone

 Estrogen=ovulation

Also allows sperm into the uterus by making the mucus slimy

 Progesterone=changing in the uterus to prepare for ovulation

Blocks the uterus again o No fertilization?

 The uterine lining is shed o Regular bleeding and shedding (monthly)

 The purpose is to make sure the uterine wall is responding to the hormones

 Also helps disinfect the uterus o Uterine cycle

 Menstrual phase (shed lining)

 Proliferative phase (builds up)

 Secretory phase (postovulatory)

The endometrium prepares for the implantation of the embryo o Implantation occurs

 Now the uterus needs to keep the nutrients up o Inner cell mass develops into the blastocyte o The lungs of the baby develop last o Human chorionic gonadotropic (HCG)

 Spike helps initially develop the placenta

 Develops the corpus luteum

That secretes estrogen and progesterone o Hormones from the corpus luteum maintain the uterus structure o The HCG comes from the oocyte itself if fertilized o HCG drops off?

 This leads to estrogen and progesterone getting released from the placenta

This occurs after the embryo is implanted o Fetus is not rejected by the mother because the mother recognizes it

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