NURS
365 Test 2
Exams consist
of
Study
Guide
True/False
and
-
RUBRIC
TEST 2
Comprehensive
and Rubric
multiple-choice
Content
questions.
10
Class 1- Cell/Intro to Pharm
4
Class 2 – Fluid Electrolyte/Acid-Base
3
Class 3 -
3
Renal
Class 4
13
Introduction to Immune
System
2
Innate Immunity
5
Adaptive Immunity
6
Class 5
20
Infectious
Disease
5
Stress and
Disease
4
Countermeasures for Infectious
Disease, vaccines
8
Immunodeficiencies
Class 6
3
17
Hypersensitivities
4
Wound
2
Healing
Autoimmunity, Alloimmunity
4
Anti-virals
2
Drugs: Antihistamines, Glucocorticoids,
5
Anti-inflammatories
Total
60
1. CLASS 4
a. Introduction to the Immune System
i.
The two major lymphoid organs (immature lymphocytes)
a
Bone Marrow
i
b
Central lymphoid tissue for B lymphocytes
Thymus
i
Central lymphoid tissue for T lymphocytes
ii. Secondary Lymphoid organs (mature lymphocytes)
a
Lymph nodes
b
Spleen
iii. The cell types including cell surface markers, location, and function
a
Cells of the immune system
i
Have a very specific developmental pattern
ii
Have highly specific functions and characteristics
iii
Can be identified by a specific protein on its cell
surface. This is called a Cluster of Differention or
CD marker
iv B cells
1
Develop in the bone Marrow
2
Have specific antigen receptor called the B cell
receptor (BCR)
3
Primary function of the B cell is to make
antibody. A fully differentiated B cell is called a
Plasma Cell
4
v
Identified by the presence of CD19 or CD20
T cells
1
Develop in the Thymus
2
All T cells are CD3+
3
Have a specific receptor – The cell receptor
(TCR) – used to identify antigen
4
Subsets
a
Cytotoxic T cells (CTL) – Kill tumor cells
and virus infected cells. CD8+
b
Helper T cells (TH) – help other cells by
making important proteins (cytokines).
CD4+
i
CD4+ cells can be divided into
even more groups
ii
HIV targets CD4 cells, disrupting
cell-mediated and antibody
immune response
vi Natural Killer Cells
1
Specialized cells that kill tumor or virus
infected cells
2
Do not have memory, if they see infected cell,
they kill it
3
Cell surface receptor: Killer Inhibitory Receptor
(KIR)
4
CD56+
vii Dendritic Cells
1
“Professional antigen presenting cells” best at
“eating” antigen and presenting it to T cells
and/or B cells
2
Found in tissues such as epidermis, mucous
membranes CD11c+
viii Granulocytes (major role = phagocytosis)
1
These cells are CD66b+ but can be
differentiated from one another by staining
2
Types
a
Neutrophils (60-70% of granulocytes)
i
Most abundant cell type in
circulation
ii
Professional phagocyte –
important in killing of
microorganism
iii
Part of the Pus at an infected site
iv Short lived at infected site
v
First immune cells to be
recruited, which can be through
the cytokines produced by
macrophages
b
Eosinophils
i
Important in parasite clearance
but is also associated with
allergic disease
ii
Gets its name because of “eosin”
stain
iii
Kills antibody-coated parasites
c
Basophils
i
Found in blood – least abundant
cell type
ii
Get name from “basic” staining
iii
Promotion of allergic responses
and augmentation of antiparasitic immunity
ix Monocytes and Macrophages
1
Primary function is phagocytosis
2
Develop in the bone marrow and enter the
circulation as monocyte
3
When monocytes are appropriately activated
or enter into appropriate tissues they become
macrophages
4
x
CD14+
Mast Cells
1
Best known role: in allergy, involved in wound
healing and defense against pathogens
2
Found in tissue
3
Release preformed granules containing
proteases and histamines
4
Histamines help get WBC to the cite of
infection
iv. The breakdown of a WBC
a
Men and nonpregnant women: 4500-11,000/mcL3
b
Differential:
i
Neutrophils: 50-62%
ii
Band neutrophils: 3-6%
iii
Lymphocytes:25-40%
iv Monocytes:3-7%
v
Eosinophils: 0-3%
vi Basophils: 0-1%
v. Definitions
a
Immunity: Ability to resist infection
b
Antigen: any substance capable of causing an immune
response
c
Tolerance: Immune system normally responds to non-self
antigens, but maintains tolerance to self antigens
d
Breakdown in tolerance: immune responses are not always
beneficial and cause tissue damage or death
e
Lymphatic vessels (lymphatics): carry lymph and work in
complement to blood vessels
b. Innate and Adaptive Immunity
i.
Innate (Not antigen-specific, rapid)
a
Defense mechanisms existing before antigen exposure
(rapid onset)
i
Does not distinguish among antigens (Not antigen
specific)
ii
No enhanced response on second antigen exposure
(No memory)
iii
Promotes initiation of adaptive responses (Antigen
presenting cells APCs)
iv
Although the innate immune system is non-specific, it
is selective and can distinguish self from non self
b
Physical/Mechanical/Chemical Barriers
i
Physical
1
Oral Mucosa: secretions
2
Gastric Secretions
3
Intact skin
ii
Mechanical Barriers
1. Cilia in lungs
2. Epithelial cells joined by tight junctions
iii
BioChemical Barriers
1
ii.
Surfactants in lungs
Phagocytosis
a
Steps
i
Bacterium is phagocytosed by neutrophil
ii
Phagosome fuses with granules
iii
pH of phagosome rises, antimicrobial response
is activated via lysosomes and bacterium is killed
iv
pH of phagosome decreases, fusion with
lysomes allows acid hydrolases to degrade the
bacterium completely
v
Neutrophil dies by apoptosis and is
phagocytosed by macrophage
b
Outputs of pathogen recognition: These are released
once we recognize these pathogens
i
Cytokines
1
Inflammation
2
Key cytokines
a
IL-1 (interleukin 1)
i
Fevers
ii
Production of IL-6
iii
Activates vascular
endothelium
iv
Activates lymphocytes
v
Local tissue destruction
vi
Increases access of
effector cells
b
TNF-alpha
i
Fever
ii
Mobilization of metabolites
iii
Shock
iv
Helps with increasing
vascular permeability to allow for
increased entry of IgG,
complement, and cells to tissues
and increased fluid drainage to
lymph nodes
c
IL-6
i
Fever
ii
Induces acute phase
protein production
ii
Chemokines
1
Subset of cytokines that use chemotaxis
to attract leukocytes and WBCs to the area for
iii
Surface co-stimulatory molecules
1
Help with enhancing immune cell
attraction, can form immune complexes to
increase immune response
iii.
Inflammation
a
Characteristics
i
Pain, redness, swelling, heat and loss of
function
ii
Increased vascular permeability and blood flow
(TNF-alpha)
iii
Exudation of plasma fluid (pus)
iv
Leukocyte recruitment and extravasation
v
Inflammation is a protective response intended
to isolate infected tissues and prevent the spread of
disease
vi
iv.
Initial response to injury or infection
Acute Phase Response (helps with innate immunity)
a
Acute phase proteins are important components of
innate immunity:
i
Promote phagocytosis (CRP, MBL (MBP),
collectins)
ii
Promote blood clots (fibrinogen) in small
vessels
1
Block spread of infection
iii
Complement activators (Complement system)
iv
TLR signaling induces IL-6, which stimulates
Liver to produce Acute-phase proteins
1
Bacteria induce macrophages to
produce IL-6, which acts on hepatocytes to
induce synthesis of acute-phase proteins
v.
Fever (pyrexia)
a
Steps
i
Tissue becomes infected with bacteria, virus,
etc
ii
White blood cells (leukocytes) respond to
infection & release a protein
iii
Interleukin-1 (IL-1) is produced and stimulates
production of Prostaglandins
iv
Prostaglandins cross blood brain barrier
stimulate the hypothalamus which triggers the Preoptic Area
v
Pre-optic area, in response to the
hypothalamus, causes ANS to raise body temperature
b
Elevated temps impede both viral and bacterial
replication
vi.
NK Cells and Antiviral Immunity
a
Type 1 Interferons (Interferons-alpha, IFN-beta)
b
Natural Killer (NK) cells
i
Directly recognize ligands on virally infected
cells
1
Kill virally infected cells
2
Ligands / receptors are poorly
characterized
3
ii
Involved in anti-tumor immunity
Recognize ligands on uninfected cells
1
Uninfected cells are spared
2
Ligands = MHC Class I proteins
3
Receptors
a
Killer lectin-like receptors (KLR)
b
Killer cell immunoglobulin-like
receptors (KIR)
vii.
Plasma Protein Systems
a
Complement System = activation of C3
i
Cascade of enzymes
ii
C3 is activated, leading to activation of other
enzymes, resulting in increased protein production
1
Opsonin,
a
assists with phagocytosis
iii
Part of the innate immune response
iv
Functions to destroy invaders and signal other
immune cells
v
Consists of 30 proteins synthesized in the liver
vi
Always present in high concentrations in the
blood and tissue
vii
b
Many complement proteins are inactive
Clotting System = trapping infection, while also
increasing permeability
i
ii
c
Fibrinogen
1
Blood clots
2
Chemotactic factor
3
Increased permeability
Kinin- interacts with clotting system
Kinin System = increasing permeability, and involved
with pain
i
ii
Bradykinin
1
Histamine like effects
2
Stimulates nerve endings
Work with Prostaglandins to induce pain
viii. Adaptive (Antigen-Specific, slow)
a
2 step Process
i
Clonal Diversity (Production of T and B cells with all
possible receptors for antigen)
1
Lymphoid Stem cells from Bone marrow
migrate to Thymus (T cells) or Bone Marrow (B
cells) to mature into immunocompetent T
cells/B cells that then reside in secondary
lymphoid organs (Spleen/Lymph Nodes)
2
Lymphoid Stem cells are still naïve at this point
as they have not encountered an antigen
3
Generation of Clonal Diversity
a
All necessary receptor specificities are
produced
b
Takes place in the primary (central)
lymphoid organs (thymus, bone marrow)
c
Results in naïve but immunocompetent
T and B cells
d
4
Primarily occurs in the fetus
T cell Development
i
The thymus is the central
lymphoid organ of T cell
development
ii
Development of antigen-specific
T cell receptors (TCRs), surface
molecules CD4 and CD8
iii
Leave thymus, travel to and
reside in secondary lymphoid
tissue as mature
immunocompetent cells
5
B Cell development
i
Production, proliferation,
differentiation in bone marrow
ii
Travel to lymphoid tissue and
reside there as
immunocompetent cells
iii
Each cell responds to only one
specific antigen
iv
B-cell receptor, CDRs (variable
region)
v
Central tolerance
1
Process in which B cells
learn how to distinguish
between self and non-self.
2
Any B cells that attack our
own tissue are filtered out
during the process of
central tolerance
ii
Clonal Selection (Selection, proliferation, and
differentiation of individual T and B cells with
receptors for a specific antigen)
1
2 Steps:
a
Antigen processing and presentation
i
Initiated when T and B cells
interact with an antigen
ii
Must first be processed and then
presented by APCs (from innate
immunity)
iii
Results
1
Differentiation of T cells
into effector cells, such as
T cytotoxic cells
2
Differentiation of B cells
into active antibody-
producing cells (plasma
cells)
iv
Major Histocompatibility complex
1
Two Classes
a
Class I
i
Present
endogenous
antigens
b
Class II (usually
involved in B cell
Clonal Selection)
i
Present
exogenous
antigens
2
Present on the surface of
all human cells (except
RBCs)
b
Complex cellular interactions
i
Results in production of effector
cells
b
1
Plasma Cells
2
Th
3
Tc cells
4
Memory cells
Cell-Mediated Immunity
i
Conversion of Immunocompetent T cells into Effector
T cells (i.e. Cytotoxic T Cell)
ii
TCR is similar to an Fab
iii
Structure is similar to immunoglobulins
1
Also have variable region (gives ability to
interact with multiple antigens)
2
TCR
3
MHC class I (cell mediated) or II (humoral)
4
Co-receptors
iv
CD3s are present on all T cells
v
T cells = MHC class I = CD8
vi
Antigens must be processed in order for T cells to
recognize them
vii
Sensitization for Killing by NK cells (Antibody
Dependent Cellular Cytotoxicity) = anti-cancer
antibody treatments
1
Similar to opsonization, falls under adaptive
immunity because it involves antibodies
2
Antibody binds antigens on the surface of
target cells
3
Fc receptors on NK cells recognize bound
antibody
4
Crosslinking of Fc receptors signals the NK cell
to kill the target cell
5
c
Target cell dies by apoptosis
Humoral Immunity
i
Differentiation of Immunocompetent B cells upon
encounter with antigen into Plasma Cells (secrete
antibodies)
ii
B Cell Clonal Selection
1
Antigen binds to B cell Receptor
2
Processed inside Cell
3
Presented on the surface by MHC Class II
(always interacts with CD4)
4
Antigen interacts with CD4 on T helper cell
5
T helper cells
a
Have TCR
b
CD4 on cell surface interacts with
antigen presented by MHC Class II
c
6
Release cytokine signal (IL-4)
B cell then differentiates into plasma cell that
then secretes antibodies
ix.
Innate/Adaptive connection
a
Antigen-presenting cells
i
Dendritic Cells
ii
Macrophages
x.
Definition of an antigen
xi.
How do we recognize self/non-self
xii. Seven aspects of innate immunity
xiii. Types of adaptive immunity: humoral, cellular
xiv. Components of an antibody
xv. Types of antibodies/immunoglobulins, where they are primarily
found and their function
a
Immunoglobulin (Ig) (more generic antibody)
i
Defined as the antigen binding molecules on B cells
ii
Antibodies = more specific antigen
iii
Produced by B cells
iv
Fab region = interacts with antigen
v
Fc region = constant region = where function comes
from = attaches to B cell
vi
Light Chains and Heavy Chains
vii
CDRs = variable region = gives antibodies ability to
interact with different antigens
b
Types of Ig
i
IgM = big = pentamer joined by J chain = 5
1
Stable in pentamer form
2
J chain joins 5 monomeric IgM together to form
pentameric IgM
ii
IgA = largely in secretions and in gut = 2
1
Dimeric (secretory) especially IgA protects
mucosal surfaces
2
Must be transported across epithelia
(membrane) into mucosal lumen
iii
3
Joined by J chain to form dimeric IgA
4
Secretory in nature
a
In breast milk
b
In GI tract
IgG = most abundant = Passed down from Mom
during pregnancy
1
IgG transferred from Mom to baby, acts as
babies immune system
a
Baby will begin to create their new IgG
once they grow older
b
2
Will start making IgA around 1 year
Fights most of our infections
xvi. Role of major histocompatibility complex (MHC), what cell types
a
Involved in Antigen Processing and Presentation
b
Glycoproteins on the surface of all human cells (except
RBCs)
c
Also called Human Leukocyte Antigens (HLAs)
d
Class I (always interacts with CD8)
i
e
Present endogenous antigens
Class 2 (always interacts with CD4)
i
Present exogenous antigens
xvii. Types of T cells and their functions
xviii.
Opsonization
a
Overlap between Innate and Adaptive immunity
b
Antibodies form a layer around bacterium to help with
engulfment process by macrophage
2. CLASS 5
a. Infection/Inflammation - some overlap with Class 4
i.
First line of defense against infection
1.
Physical Barriers
i
Skin
ii
Mucosa
iii
ii.
How inflammation aids in protecting against infection
iii.
Shapes of bacteria
1.
2.
3.
Spheres | Cocci
i
Diplococci
ii
Streptocci
iii
Tetrad
iv
Staphylococci
v
Sarcina
Rods (Bacilli)
i
Chain of Bacilli
ii
Flagellate rods
iii
Spore-Former
Spirals
i
Vibrios
ii
Spirilla
iii
Spirochaetes
iv. Factors for Infection
1.
Communicability: ability to spread from one individual to
others and cause disease
2.
Infectivity: ability of pathogen to invade and multiply in the
host
3.
Virulence: capacity of a pathogen to cause severe disease
i
Measles: Low
ii
Rabies: High
4.
Pathogenicity: Ability of an agent to produce disease (what
kind of damage it can do)
i
True pathogens have devised means to circumvent
normal immune responses
5.
Port of entry: route by which a pathogenic microorganism
infects the host
6.
Toxigenicity: ability to produce soluble toxins or endotoxins
i
v.
Goes hand in hand with virulence
Causes of infection – know each type
1. Viruses
i
Most common affliction of humans
ii
Need permissive host cell
iii Steps in Viral Reproduction
1 Attachment
2 Penetration
3 Uncoating
4 Replication
5 Assembly
6 Release
2. Bacteria
i
Prokaryotes: lack discrete nucleus
ii
Classified by
1 O2 metabolism
a Aerobic
b Anaerobic
2 Motility
3 Shape
4 Staining
a Gram Positive
i
Very thick Peptidoglycan outer
layer
ii
Absence of outer membrane
layer
iii E. Coli
b Gram Negative
i
Thinner peptidoglycan layer
ii
Have outer membrane layer
iii Diagnosed by culture & Sensitivity
1 Antibiotic susceptibility: figure out what kind of
medication
iv Bacteremia (presence) or septicemia (growth)
1 A result of a failure of the body’s defense
mechanisms
2 Septicemia – Usually caused by gram-negative
bacteria, release endotoxins in the blood
3 Toxins released in the blood
a Release of vasoactive peptides and proinflammatory cytokines
b Produce widespread vasodilation,
increased capillary permeability
i
Can lead to hypertension, and
further -> shock
c
Activate clotting cascades
i
Can lead to Disseminated
Intravascular Coagulation (DIC)
1 Leads to sepsis
d Leading to septic (endotoxic) shock
3. Fungi
i
Characteristics
1 Large eukaryotic microorganisms
2 thick, rigid cell walls without peptidoglycan
a Walls made up of polysaccharides
b Need different medications than
bacteria
3 Single celled = yeasts
4 Multi-celled = mold (filaments or hyphae)
5 Both = dimorphic
6 Reproduce by simple division or budding
ii
Fungal Infection
1 Mycoses: diseases caused by fungi
a Superficial, deep, or opportunistic
2 Dermatophytes: fungi that invade the skin, hair
or nails
a Diseases they produce are called tineas
(ringworm)
i
Tinea capitis, tinea pedis, and
tinea cruris
3 Pathogenicity
a Adapt to host environment
b Suppress the immune defenses
c
Usually controlled by phagocytes, T
lymphocytes
4 Candida albicans
a Most common cause of fungal infections
b Opportunistic
c
Found in normal microbiome of skin, GI
tract, vagina of many individuals
d Localized infection if overgrowth occurs
e Disseminated infection if
immunocompromised
i
Common in cancer patients
4. Parasitic Infection
i
Characteristics
1 Symbiotic (parasitic)
2 Unicellular protozoa to large worms (helminths)
3 Protozoa include malaria, amoebae, flagellates
4 More common in developing countries
5 Spread human to human via vectors
6 Usually ingested
7 Tissue damage
vi. Steps in Phagocytosis
vii. How bacteria evade our immune system/develop antibiotic
resistance
1.
Evasion techniques
i
Coating to evade phagocytes
ii
Degrade complement and IgA
1
These are important for our immunity
2
Some proteases (enzymes that break down
proteins) degrade these immunoglobulins
iii
Toxins
1
Ability to nullify effects of chemotaxis from
chemokines
iv
Molecular mimicry
1
Proteases from pathogens can mimic
immunoglobulin parts
2
v
Can lead to hypersensitivity reactions
Antibiotic resistance
1
Multi-drug Resistant Staph Aureus (MRSA)
example of antibiotic resistance
2
vi
Gotta stay one step ahead of the pathogens
Biofilm
1
Microorganisms exist as a complex of biofilms,
gives survival advantage to bacteria
vii
Change antigens
1
Antigenic Drift
a
More gradual mutations of surface
antigens
2
Antigenic Shift
a
Major shifts in genetic recombination,
usually in species jumping
viii. Antimicrobial/Antibacterial Drugs
1. Principles of antibiotic use
i
Narrow-spectrum
1 More specific to category of bacteria (i.e. gramnegative cocci, bacillus)
2 Active against very few species of organisms
3 Typically want to use narrow-spectrum
ii
Broad-spectrum
1 May start at offset with broad spectrum, then
with more cultures/labs can fine-tune
antimicrobial therapy, move to narrow
specturm
iii Bactericidial = kill
iv Bacteriostatic = suppress
v
Host defenses are essential to the success of
antibiotic therapy
vi Patient Education:
1 Patients should complete entire course to get
rid of the infection
2 Failure – promotes resistance
3 Drug reactions/allergies
vii Combinations of Antibiotics are appropriate
1 Treatment of severe infections
2 Infection > 1 organism
3 Tuberculosis treatment
4 Combination of bactericidal effects
viii Indications for Antibiotics prophylaxis
1 Certain surgeries (dental)
2 Neutropenia (immunosuppressed)
3 Recurrent UTI
4 Risk of bacterial endocarditis
ix Antibiotics misuses
1 Treatment of viral infections
2 Treatment of Fever of Unknown Origin (FUO) if
not immunocompromised
3 Treatment w/o information on bacteria
4 Treatment in the absence of drains/removal of
debris
2. Desirable traits of an antibiotic
i
Selective Toxicity
1 Ability to injure the pathogen without harming
healthy cells
2 Our cells are different than the pathogens so
drugs are tailored to take advantage of these
differences:
a Bacterial cell wall (structure/protoplasm)
inhibition
i
Penicillin’s, cephalosporins,
bacitracin, vancomycin
b Bacterial protein synthesis (ribosomes)
inhibition
i
Chloramphenicol, erythromycin,
tetracyclines, streptomycin
c
Bacterial DNA/RNA (nucleic
acid/enzymes) inhibition
i
Quinolones, rifampin
d Bacterial enzymes (folic acid synthesis)
inhibition
i
Sulfanilamide, trimethoprim
3. Know how antibiotics work
4. Bactericidal versus bacteriostatic
5. Major adverse side effects of all antibiotics (penicillin,
fluoroquinolones, macrolides)
i
Pencillin
1 Allergic reactions
2 Hyperkalemia
ii
Fluoroquinolones
1 Tendon Rupture
2 Phototoxicity
iii Macrolides
1 GI effects
2 Prolonged QT duration – sudden cardiac death
6. Classes of antibiotics
i
Bacterial Cell Wall Inhibition
1 Penicillins (PCNs)
a Therapeutic Uses
i
Primarily Gram (+); broad and
narrow spectrum
b Contraindications
i
Caution with Renal dysfunction
1 Increased PCN blood
levels
ii
Severe PCN allergy
1 Wear Medic Alert
c
Adverse effects
i
Allergy
ii
Electrolyte imbalances (IV)
1 Hyperkalemia – cardiac
2 Due to mixture of
potassium penicillin,
potassium comes with it
2 Cephalosporins (Ceph)
a Therapeutic Uses
i
Primarily Gram (+), multiple
generations
b Contraindications
c
i
Severe PCN allergy
ii
Do not drink alcohol with
Adverse effects
i
Bleeding
1 Monitor; use caution with
pts on anticoagulants
2 Interferes with prothrombin
levels by interfering with
Vit K
ii
ii
Thrombophlebitis
Bacterial Protein Synthesis: Bacteriostatic
1 Tetracyclines
a Therapeutic Uses:
i
Acne
ii
Gum disease (periodontal
disease)
b Contraindications
c
i
Pregnant women
ii
Children under 8
Adverse effects
i
Hepatotoxicity
ii
Nephrotoxicity
iii Photosensitivity
iv Discolor teeth
v
GI irritation
vi Suprainfection
1 C. diff diarrhea
2 Macrolides
a Therapeutic Uses
i
Substitute in PCN allergy
b Contraindications
i
Avoid admin with CYP3A4
inhibitors (increase risk of QT)
1 CYP3A4 are important in
med clearance
c
Adverse effects
i
GI effects
ii
QT prolongation – sudden
cardiac death
iii Bacterial Protein Synthesis: Bactericidal
1 Aminoglycosides
a Therapeutic uses
i
Narrow spectrum; serious
infections; aerobic gram (-) bacilli
b Contraindications
i
Pencillin (inactivates), do not
administer together
c
Adverse effects
i
Nephrotoxicity
ii
Ototoxicity (transient hearing
loss)
iii Neuromuscular blockade =
respiratory depression
iv Bacterial Metabolites Inhibition (folic acid)
1 Sulfanomides & Trimethoprim –
Bacterostatic
a Therapeutic Uses
i
UTIs
ii
Combination TMP/SMZ more
powerful
b Contraindicaitons
i
Pregnant women, nursing
mothers, infants under 2 months
1 Bilirubin build up in brain
c
Adverse effects
i
Hypersensitivity (StevensJohnson syndrome)
ii
Photosensitivity
iii Hematologic-hemolytic anemias
iv Renal (crystalluria)
1 Drink plenty of water
v
Bacterial DNA/RNA inhibition
1 Fluroquinolones (Cipro)
a Therapeutic uses
i
Broad-spectrum’ wide variety
b Contraindications
i
IV avoided in children due to risk
of tendon rupture
c
Adverse effects
i
Risk for tendon rupture
ii
Phototoxicity
iii Absorption can be reduced by
cationic solutions
1 Milk, antacids, etc
7. Classes of anti-fungals
i
Polyene antibiotics
1 Amphotericin B
a Broad Spectrum antifungal agent
b Highly toxic
i
Infusion reaction and renal
damage occur in many patients
ii
c
Given IV, no oral administration
Uses:
i
Drug of choice for most systemic
mycoses
ii
Before amphotericin B, systemic
fungal infections were usually
fatal
d Adverse effects
i
Infusion reaction
1 Fever, chills, rigors,
nausea, and headache
2 Pro-inflammatory
cytokines
3 Symptoms begin 1-3 hrs
after start of infusion
ii
Nephrotoxicity
iii Hypokalemia
1 Affects pores of renal
tubule collecting duct
leading to leakage of
potassium and loss
iv Bone marrow suppression
ii
Azoles
1 Example: Fluconazole [Diflucan]
2 Characteristics
a Broad Spectrum antifungal drugs
b Alternative to amphotericin B for most
systemic mycoses
c
Lower toxicity
d Can be given orally
e Disadvantage
i
Inhibit P450 drug-metabolizing
enzymes and can increase levels
of many other drugs
iii Echinocandins
iv Pyrimidine analogs
8. Vaccines
i
Preparation Types
1 Attenuated
2 Killed
a Typhoid
b Uses killed bacteria for delivery
3 Toxoid
a Diphteria, tetanus
b Antigenicity is preserved, but no longer
toxic
4 Subunits
a Pertussis, HepB, Pneumococcoal
b Attach to carrier proteins
5 Nucleic Acid
ii
Features of effective vaccines
1 Safe
2 Protective
3 Gives sustained protection
4 Induces neutralizing antibody
5 Induces protective T cells
6 Practical Considerations
b. Stress and disease
i.
What triggers a stress response and signs and symptoms
1. Stress is triggered by a perceived or anticipated threat that
disrupts a person’s homeostasis
i
May stem from
1
Psychological/emotional (fear, social rejection)
2
Physical (dramatic temp changes, abuse)
3
Physiologic (infection, inflammation) stimuli
2. Stress affects the immune system
i
Stress directly related to proinflammatory cytokines
ii
Link between stress, immune function, and
disease/cancer
iii
Immune system affected by neuroendocrine factors
iv
Stress response decreases T-cell cytotoxicity and Bcell function
v
3. Signs and Symptoms of Stress, precipitating factor for some
diseases and may worsen conditions
ii.
i
Ulcers
ii
Asthma
iii
Anxiety
iv
Depression
v
Diabetes
How the Sympathetic Nervous System (SNS) responds to stress
1. General Adaptation Syndrome
i
Alarm Stage
1
Stressor triggers the hypothalamic-pituitaryadrenal (HPA) axis
a
Activates sympathetic nervous system
2
Arousal of Body defenses
3
Steps
4
a
b
Brain
i
ACTH
ii
Nerve Signal
Adrenal Gland Releases
i
Cortex
1
Glucocorticoids (cortisol)
a
Liver releases
glucose
ii
Medulla
1
Adrenaline (epinephrine)
a
Increased heart
rate, breathing rate,
blood sugar
2. Resistance/adaptation stage
i
Begins with the actions of adrenal hormones
ii
Mobilization contributes to fight or flight
3. Exhaustion stage (allostatic overload)
i
Occurs only if stress continues and adaptation is not
successful
ii
Leads to stress-related disorders
iii
Allostasis
1
“Stability through change”
2
Brain continuously monitors for future events
and anticipates what is required from
neuroendocrine and autonomic systems
3
Allostatic Overload
a
Overactivation of adaptive systems
b
Highly individualized
iii. Catecholamines (Neuroendocrine regulation)
1. Released from chromaffin cells of the adrenal medulla
i
Epinephrine released binds to adrenergic receptors
2. α-adrenergic receptors
i
α1 and α2
3. β-adrenergic receptors
i
β1 and β2
4. Mimic direct sympathetic stimulation
iv. What are the effects of epinephrine
1. Increased heart rate, breathing rate, blood sugar
2. Stimulates both alpha and beta adrenergic receptors
3. Greatest influence on cardiac action
i
Increased heart rate – B1
ii
Increased force cardiac contraction: B1
4. Epinephrine also has metabolic effects
i
Increased hepatic gluconeogenesis: B2
ii
Increased hepatic and muscle glycogenolysis: B2
iii
Increased Glucagon and renin: B1
5. Pulmonary effects of epinephrine
i
Smooth muscle relaxation of bronchial smooth
muscles – cause bronchodilation: B2
v. Adrenergic receptors
1. What they are (alpha 1 and 2, beta 1 and 2)
2. What are the primary responses of each
3. How that relates to the stress response and clinical
manifestations (ex. If beta 1 is stimulated/blocked…you will
see x clinical response)
4. Alpha-adrenergic receptors
i
Alpha 1
1 Blood Vessels: Increased Vasoconstriction
2 Heart: Increased Contractility
ii
Alpha 2
1 Neurons: Inhibition
5. Beta-adrenergic receptors
i
Beta 1
1 Heart: Increased HR, conduction, contractility
ii
Beta 2
1 Lung: Bronchodilation
2 GI: decreased motility
vi. Hypothalamic-Pituitary-Adrenal (HPA) axis
1. Hypothalamus secretes corticotropin-releasing hormone
(CRH)
2. Pituitary releases adrenocorticotropic hormone (ACTH)
3. Adrenals secrete cortisol and catecholamines
i
Cortisol
1 Secreted during stress
2 Reaches all tissues
3 Stimulates gluconeogenesis
4 Elevates the blood glucose level
5 Affects protein metabolism
6 Powerful anti-inflammatory and
immunosuppressive agent
7 Effects:
a Used therapeutically as power antiinflammatory/immunosuppressive
agents
b Influence virtually all immune cells
c
Elevated Levels may decrease innate
immunity and increase autoimmune
responses
4. Stress triggers the HPA axis
c. Immunodeficiencies
i.
Know the dangers for patients with immune deficiencies
1. Major Concepts
a. Main symptoms is recurring infections
b. Types of infections indicate immune defect
c. Family history is important for diagnosis
d. Failure to thrive
1
Lack of adequate nutrition
e. The type of infection that the patient has is often the
first clue that something is wrong with the immune
system
ii.
Types of Immune Deficiencies (examples of disease diagnoses
and clinical Manifestations)
iii. Primary vs Secondary
1. Primary (congenital)
a. Genetic anomaly
b. Disease in which ther is a failure of immunological
functions as a result of defects in genes for
components of the immune system
c. Inherited – not acquired
d. Primary Immune defects are can involve one
defective gene
1
XLA
a
2
SCID
a
3
Aire gene
IPEX
a
5
Rag, y common chain gene
APECED
a
4
BTK gene
FoxP3 gene
Bare Lymphocyte Syndrome
a
MHC gene
2. Secondary (acquired)
a. Caused by another illness
b. More common
c. Unlike primary, these are not diseases that we are
born with and cannot be genetically passed on to our
offspring
iv. HIV causes AID
1. Pathophysiology
a. The cells involved and their roles
1 Affects CD4+ cells
a HIV’s Gp120 binds to CD4 cells
b. Pathogenesis
1 Retrovirus
a Genetic info is in the form of RNA
b Contains reverse transcriptase to
convert RNA into double stranded DNA
c
HIV Integrase
i
Inserts new DNA into the affected
cell
d Protease
i
Necessary for processing and
assembling virions
c. The HIV enzymes required for viral replication and
how they work
d. “Acute phase” and what it means in HIV, symptoms
e. “Clinical latency” and what it means in HIV, symptoms
2. Clinical Manifestations
a. Serologically negative, serologically positive but
asymptomatic, early stages of HIV, or AIDS
b. Window Period
c. Th cells <200 cells/mm3 diagnostic for AIDS
d. Diagnosis of AIDS is made in association with various
clinical conditions
1 Atypical or opportunistic infections and cancer
2 Presence of antibodies against HIV
3 Western Blot analysis
3. The clinical presentation of HIV – differentiate the 3 phases
a. Viral loads and CD4 counts in each phase in general
(not specific numbers)
4. What CD4 count is indicative of HIV progression to AIDS
(the number in cells/ml)
<200 cells/mm3
5. Pharmacological HIV Treatment
a. Define/describe mechanism of action of antiretroviral
therapy (ART; HAART)
1 Antiretroviral Therapy (ART) combination of
the following
a Reverse transcriptase inhibitors
b Protease inhibitors
c
Integrase Inhibitors
d Fusion inhibitors
e CCR5 antagonist
2 HAART – Combination therapy
a Most patients take around 30-45 pills a
day
b Cost is astronomical
b. Antibiotics/antifungals given prophylactically
c. Define protease enzyme
1
6. Laboratory Monitoring for HIV Infection and Efficacy of Drug
Therapy
7. Whats the overall treatment goal, CD4 T-cell counts
3. CLASS 6
a. Wound Healing
i.
Types of healing (first intention, second intention, etc.)
a
Primary Intention
i
Wounds that heal under conditions of minimal tissue
loss
b
Secondary intention
i
Wounds that require a great deal more tissue
replacement
1
Examples
a
open wound
b
Myocardial infarction replaced with
fibrous tissue
c
Regeneration = replacement of damaged tissue with healthy
tissue
i
Resolution =
ii
Return to original structure and function
d
Repair
i
Replacement of destroyed tissue with scar
tissue
1
Composed primarily of collagen to
restore the strength of the tissue but not its
function
e
Healing Processes
i
Filing in the wound
ii
Sealing the wound (epithelialization)
iii
Shrinking the wound (contraction)
ii. Phases of Wound Healing (overlapping)
a
Phase I: Inflammation
i
ii
iii
Coagulation
1
Immediate
2
Short and quick
Infiltration of wound-healing cells
1
Platelets
2
Neutrophils
3
macrophages
Angiogenesis
1
Forming of capillaries to provide area with
needed blood flow
b
Phase 2: Proliferative and new tissue formation
i
Granulation
1
Healthy tissue that surrounds and grows into
the wound
ii
Epithelization (Keratinocyte Migration)
1
iii
Occurs under the scab
Requires fibroblast proliferation, collagen formation,
wound contraction (myofibroblasts: important for
closing up the wound)
1
Connective protein proliferations
c
Phase 3: Remodeling and maturation phase
i
Continuation of cellular differentiation
1
End of angiogenesis
ii
Scar Tissue formation
iii
Scar remodeling
iii. Dysfunctional Wound healing
a
May occur during any phase of wound healing
i
Ischemia
ii
Excessive bleeding
iii
Excessive fibrin deposition
iv Predisposing disorders
1
Diabetes
2
Obesity
a
Elevated levels of proinflammatory
cytokines affecting leukocytes
3
Wound infection
4
Inadequate nutrients
5
Numerous drugs
a
6
b
NSAIDs
Tobacco Smoke
Dysfunction during reconstructive phase
i
Dysfunctional collagen synthesis, resulting in
1
Keloid scar
a
Raised, but extend beyond boundary of
affected tissue
b
2
Do not regress
Hypertrophic scar
a
Contained within the site of injury and
may regress over time
ii
Wound disruption
1
Dehiscence (increases risk of infection)
a
Wound pulls apart at a suture line
b
Obesity major risk factor
c
Calls for immediate attention due to
high risk for infection
iii
Contracture
1
Usually at joint sites
2
Term for meaning a decrease in passive range
of motion at a joint
iv. Terms: Dehiscence, keloid, etc. ]
b. Hypersensitivities
i. Types of hypersensitivity reactions (I-IV)
1. Definition and generally how hypersensitivity reactions work
i
Diseases caused by an exaggerated immune
response
ii
Could be response against a pathogen, nonpathogen or self
iii 4 Types of Hypersensitivity Reactions
1 Type 1 (IgE) = seasonal allergies = mast cell
activation
a IgE-mediated allergic reactions
i
Systemic anaphylaxis
ii
Acute urticaria
iii Seasonal rhinoconjunctivitis
iv Asthma
v
Food Allergy
b Effector mechanism = Mast-Cell
activation
c
Ige attaches to Mast cells
i
Mast cell is now sensitized
ii
Once enough IgE attaches to
mast cell, degranulation occurs
1 Release of histamines
(allergic reactions)
2 Type 2 (IgG) = some drug allergies (penicillin)
a Cell- or matrix- associated antigen with
cell-surface receptor
b Effector mechanism = complement,
FcR+ cells (phagocytes, NK cells)
i
c
Antibody alters signaling
Mediated by IgG
d Specific cell or tissue (tissue-specific
antigens) is the target of an immune
response
e Occur when antibodies react to altered
components of self
f
NOT a soluble antigen
g Five mechanisms:
i
Cell is destroyed by antibodies
and complement
ii
Cell destruction through
phagocytosis
iii Soluble antigen may enter the
circulation and deposit on
tissues; tissues destroyed by
complement and neutrophil
granules
iv Antibody-depended cell-mediated
cytotoxicity (ADCC)
v
Target cell malfunction (e.g.,
Graves – targets thyroid)
3 Type 3 (IgG)
a Immune complex mediated
b Antigen-antibody complexes are
formed in the circulation first and are
later deposited in vessel walls or
extravascular tissues
i
Large release of lysosomal
enzymes
c
Not organ specific
d Serum sickness
i
Raynaud phenomena
e Arthus reaction
4 Type 4 (does not involve any antibodies, cellmediated, cytotoxic T cells)
a Cell mediated hypersensitivity reactions
b Does not involve antibody
c
Cytotoxic T lymphocytes or lymphokineproducing Th1 and Th17 cells
i
Direct killing by Tc or recruitment
of phagocytic cells by Th1 and
Th17 cells
d Examples:
i
Graft rejection
ii
Tuberculosis skin test
iii Allergic reactions from poison ivy
or metals
iv Celiac
2. Apply these principles to organ rejection, GVHD, hemolytic
anemias
ii. Know Allergy/Anaphylactic Reactions, principle cells, Ab, clinical
signs/symptoms and processes involved in allergic reactions
c. Autoimmunity
i.
Know examples discussed in class of autoimmune disorders
a
b
Organ Specific
i
Goodpasture’s syndrome
ii
Type 1 diabetes mellitus
iii
Multiple sclerosis
iv
Graves’ disease
v
Vitiligo
vi
Bullous pemphigoid
Systemic: (throughout the body)
i
Polymyositis: “Many muscle inflammation”
1
Inflammation of a group of muscles, or
muscles in general
ii.
Understand the pathophysiology of autoimmune disorders
a
Causes
i
Environment
1
Pathogens, drugs, toxins, and hormones are
just a few ways that the environment can
trigger autoimmunity
ii
Genes and Autoimmunity
1
The concept that a single gene mutation leads
to a single autoimmune disease is the
EXCEPTION not the rule
2
Because of this, autoimmune diseases are
generally classified as COMPLEX diseases as
there is not a single “pinpoint-able” gene
b
Immune Regulation
i
A defect in any arm of the immune system can trigger
autoimmunity
a
Innate immunity (Neutrophils
Complement)
2
Acquired Immunity
a
Cell-Mediated Immunity (T Cells)
i
Multiple Sclerosis (Brain and
Spinal Cord demyelination)
1
T cells (predominantly)
attack the myelin sheath
surrounding the axons of
our nerve cells
2
MS patients can have
autoantibodies and/or selfreactive T cells which are
responsible for the
demyelination
b
Humoral Immunity (B Cells)
i
Myasthenia Gravis
1
Disease marked by
progressive weakness and
loss muscle control
2
Classified as “B Cell”
disease
3
Autoantibodies against
nicotinic acetylcholine
receptors
c
Symptoms
i
Initial diagnosis may be missed in patients as
diseases present with general symptoms
1
Fever, muscle ache, fatigue, joint pain,
changes in weight
ii
However, disease specific symptoms are often the
first sign of autoimmune illness
d
1
Dry mouth, dry eyes – Sjogren’s
2
Changes in metabolism – Grave’s
Diagnosis
i
General tests
1
Low RBC count (anemia)
2
C reactive protein
3
Autoantibody titers (anti DNA, anti
phospholipids, etc)  very telling if
autoimmune
4
ii
e
Presence of Rheumatoid factor
Disease specific tests
1
Neurologic exam – MS
2
Fasting glucose – Diabetes
3
TSH levels – Graves
Treatment
i
The key to treating autoimmunity is
immunomodulation
iii. Alloimmunity (immune response to nonself antigens from a
member of the same species)
a
Transfusion reactions
i
ABO Blood group
1
A and B carbohydrate antigens
2
Can be simultaneously expressed
a
Blood types passed on which
erythrocytes expressed
b
i
A
ii
B
iii
O (neither expressed)
iv
AB (both expressed)
Example
i
Person with blood type A
receives type AB or B blood,
transfused erythrocytes
destroyed
1
Type A people will have A
antigens on their
erythrocytes and Anti-B
antibodies in their serum
2
Type O – universal donor
(no antigens on their
erythrocytes)
ii
Type AB – universal recipient (no
antibodies in their serum)
ii
Rh blood group (antigen D)
1
Antigens expressed only on RBCs
2
Rh-positive
a
If baby is rh-positive (d positive),
3
Rh-negative
4
Hemolytic disease of newborn
iv. Know blood types, universal donor/recipient
v. Be able to apply this knowledge to what occurs in blood
transfusions
d. Drugs
i.
Antiviral Therapy/Drugs – for HIV and other diseases
a
Characteristics
i
Our ability to treat viral infections remains limited
ii
Viruses use biochemical machinery of host cells to
reproduce
iii
Difficult to suppress viral replication without doing
significant harm to the host
iv
Antivirals suppress biochemical processes unique to
viral reproduction
b
Herpes
i
Acyclovir (Zovirax)
1
Active only against members of the
herpesvirus family
2
Agent of first choice for herpes simplex virus
(hsv) or varicella-zoster virus infection
3
ii
Herpesvirus develops resistance to acyclovir
Cytomegalovirus Infection
1
CMV: member of the herpesvirus group
2
Transmitted by direct contact with body fluids
3
50% to 80^ of Americans age 40 years or older
harbor the virus
4
Can remain dormant for life
5
Immunosuppressed patients at high risk for
reactivation of dormant virus
iii
Ganciclovir [Cytovene, Vitrasert, Zirgan]
1
Synthetic antiviral agent
2
Uses
a
Herpes simplex virus, including CMV
b
Prevnetion and treatment of CMV
infection in immunocompromised
patients, including transplant patients,
those with HIV infection, and those
receiving immunosuppressive drugs
3
c
Serious side effects
a
Granulocytopenia
b
Thrombocytopenia
Hepatitis
i
Viral hepatitis is the most common liver disorder
ii
Millions of Americans are infected
iii
Six different viruses can cause acute hepatitis
(A,B,C,D,E, and G)
iv
Only B, C, and D can cause chronic hepatitis (B, C
account for 90%)
v
Hep C Virus (HCV)
1
Differences in HCV: 6 genotypes
2
Transmission: primarily through exchange of
blood; sexual transmission (rare)
3
Even with no symptoms, can be transmitted
4
Slow progression can lead to liver failure,
cancer, and death
5
Leading reason for liver transplantation
6
Drugs
a
Pegylated interferon alfa combined with
ribavirin
b
vi
Pegylated helps maintain drug in body
Interferon Alfa (drug use to treat)
1
Interferon family
a
Alpha, beta, gamma
b
Alpha used to treat hepatitis
c
None can be administered orally
2
Conventional versus long-acting interferons
3
Adverse effects
a
Flu-like symptoms
b
Neuropsychiatric effects, especially
depression
c
Fatigue, thyroid dysfunction, heart
damage, and bone marrow suppression,
manifesting as neutropenia and
thrombocytopenia
vii Hep B
1
1.4 million people have chronic hep B
2
11,000 require hospitalization for deep fatigue,
muscle pain, and jaundice
3
Chronic infection develops in 3%-5% of
infected adults
4
Chronic infection can lead to cirrhosis, hepatic
failure, hepatocellular carcinoma, and death
5
Transmission via blood and semen
6
HBV vaccine and drugs:
a
d
Interferon alpha 2beta, Lamivudine
Influenza
i
Characteristics
1
Serious respiratory tract infection
2
Major cause of morbidity and mortality
worldwide
3
Caused by influenza viruses, which are highly
variable and undergo constant evolution
ii
a
Type A (more infectious)
b
Type B
Management
1
Influenza managed by vaccination (primary
strategy) and drugs
2
Drugs
a
Adamantanes and neuraminidase
inhibitors
3
Vaccines
a
Influenza vaccines change yearly based
on identification of strains by CDC, FDA,
WHO
iii
Drugs for Influenza
1
Neuraminidase inhibitors
a
Oseltamivir (Tamiflu)
b
Zanamivir [Relenza]
c
Block the function of the viral
neuraminidase protein
e
HIV
i
Characteristics
1
HIV is a retrovirus (HIV1 and 2)
2
HIV has RNA as genetic material
3
Uses reverse transcriptase to convert RNA into
DNA and integrase to insert its DNA into ours
4
Target cells: CD4 T cells (helper lymphocytes)
5
Transmission via blood and body fluids (virus is
present in all body fluids)
ii
Classification of Antiretroviral Drugs
1
5 Types of antiretroviral drugs
a
Inhibit enzymes required for HIV
i
Reverse transcriptase inhibitors
1
Blocks reverse
transcriptase
2
Nucleoside Reverse
Transcriptase Inhibitors
(NRTIs)
a
Zidovudine
[Retrovir]
i
Inhibits HIV
replication by
suppressing
synthesis of
viral DNA
b
Adverse effects
i
Hematologic
toxicity
ii
Lactic
acidosis with
hepatomegal
y
iii
Myopathy
iv
Gastrointesti
nal effects
v
Central
nervous
system
(CNS)
reactions
vi
Others
c
Drug Interactions
d
Non-Nucleoside
Reverse
Transcriptase
Inhibitors (NNRTIs)
i
Efavirenz
[Sustiva]
ii
Preferred
agent for
treating HIV
iii
Only NNRTI
recommende
d for first-line
therapy of
HIV infection
iv
Drug
interactions
v
Adverse
effects
vi
Transient
adverse CNS
effects in
50% of
patients
vii Rash
viii Teratogenicit
y
ii
Integrase strand transfer
inhibitors
1
Blocks integration into
DNA
iii
Protease inhibitors (similar to
neuraminidase inhibitors)
1
Proteases are important
for release of virus to other
cells
b
Block viral entry into cells
i
Fusion inhibitors
ii
CCR5 antagonists
1
Blocks attachment point
for virus
iii
ii.
Antihistamine Drugs
iii. Treatment of anaphylactic reactions
iv. Know which drugs are used based upon severity of reaction
v. Know the clinical presentation of overdose of antihistamines,
anticholinergic syndrome
vi. Glucocorticoid therapy
1. Mechanism of action and considerations for safe use vii.
Anti-inflammatory,
1. Know mechanisms of action of NSAIDs and ASA viii.
NSAIDs, ASA
1. Clinical effects of COX-1 and COX-2 inhibition
2. Clinical indications/uses and precautions related to NSAIDs
3. Adverse side effects
4. Effects on platelet aggregation
5. Drug-Food interactions
COMPREHENSIVE CONTENT
CLASS 1: CELL, GENETICS, & INTRO TO PHARMACOLOGY
1. Altered cell biology
a. Types of cell & tissue alterations and injuries (hyperplasia, metaplasia,
dysplasia, hypertrophy, atrophy, etc.)
2. Genetics
i. Heterozygous vs. homozygous
3. Intro. to Pharmacology
a. Basic definitions/principles of absorption, metabolism, distribution and
excretion and how aging affects these
i. How drug route affects these concepts
ii. Principles associated with:
1. lipid solubility, water solubility, polar,
b. Routes of administration – enteral versus parenteral and first pass effect
c. Principles of safe medication administration and education about
medication - nursing responsibilities
CLASS 2: FLUID & ELECTROLYTES – ACID-BASE IMBALANCES
•
Fluid and Electrolytes o Hyper/Hypotonic fluid imbalances,
causes, and associated ICF/ECF fluid shifts
o Edema – what leads to edema

Oncotic/osmotic/capillary hydrostatic pressures o Types of
electrolyte imbalances (Sodium, Potassium, Chloride)

•
Causes
Acid-base o Know pH range (know actual values)
o Metabolic Acidosis and Alkalosis and Respiratory Acidosis and Alkalosis

Causes

Associated ABC changes - Know trends (ex. If PCO2 is increased
and HCO3 is decreased this means…)
o Interpretation of Blood Gas results

Know normal values (pH, HCO3, PaCO2, PaO2)
CLASS 3: RENAL
1. Renal Alterations
a. Definitions related to urine and urine output (anuria, oliguria, dysuria, polyuria,
hematuria, pyuria, bacteruria, etc.)
b. Nephrotic vs. Nephritic syndrome
c. Common causes and symptoms of:
i. Cystitis, Acute Pyelonephritis
ii. Renal calculi (most common type)
d. Acute Kidney injury (AKI)
i. Mechanisms/causes of (Prerenal, Intrarenal, Postrenal)
e. Definitions and Clinical Manifestations of:
i. Nephrolithiasis
2. Diuretics
a. Indications for use
i. General mechanism/site of action for each class of diuretics: loop,
thiazide, K+ sparing, osmotics