Exam 2 Flashcards
1
Q
Eosinophil Function
A
Killing of antibody coated parasite
2
Q
Basophil Function
A
Promotion of allergic response and augmentation of anti-parasitic immunity (asthma/allergy)
3
Q
Mast Cell Function
A
Role in Allergy: Release histamine and proteases (increases permeability to WBC - inflammation occurs)
4
Q
Monocyte/Macrophage
A
Monocytes become macrophages
Phagocytosis and activation of bactericidal mechanisms and antigen presentation
5
Q
WBC Normal
A
4500-11000
6
Q
Order (Most abundant to least abundant) WBC (never leave me every baby)
A
Neutrophil
Lymphocyte
Monocyte
Eosinophil
Basophil
7
Q
Antigen Function
A
molecule that triggers an immune response and becomes target of response
8
Q
What is central tolerance?
A
Negative selection - Eliminating any developing T/B lymphocytes that reactive to itself
9
Q
Mechanical Barrier of immunity
A
Epithelial cells, mucus by cilia, tears, nasal cilia
10
Q
Chemical Barrier of immunity
A
Skin, Gut pH, Gut enzymes, Pulmonary Surfactant, Enzymes in tears/saliva
11
Q
Phagocytosis Steps
A
- Neutrophil forms barrier around and engulfs
- Lysosomes help degrade
- Combine with phagocytes
- Lysis of bacteria
Further macrophage/apoptosis
12
Q
Phagolysosome
A
Fusion of phagosome with lysosome (process)
13
Q
Cytokines that lead to fever
A
IL-1B, TNF-a, IL-6
14
Q
Acute Phase Respoonse
A
Promote phagocytosis and fibrinogens
15
Q
IL-6 functioon
A
Stimulate liver to secrete various APP
16
Q
Fever steps
A
Tissue becomes infected, WBC (leukocytes) respond and release IL-1, IL-1 stimulates production of prostaglandins, crosses blood-brain barrier and signals hypothalamus, POA/AH raises body temp
17
Q
NK Cell Function
A
Recognize ligands on virally infected cells, kill cells, recognize ligands on uninfected cells (MHC C1)
18
Q
Complement System Function
A
Activation of C3 (cascade)
- Opsonins (phagocytosis)
- Anaphylatoxin (recruitment on WBC)
19
Q
Clotting System Function
A
Fibrinogen
- Trapping pathogens
- Increase permeability
20
Q
Kinin System
A
Bradykinin (increases permeability and onsets pain)
21
Q
Clonal Diversity
A
Production of T/B cell in lymphoid organs
22
Q
Fab Region
A
Site that binds with antigen (variable region)
23
Q
Fc Region
A
Responsible for biological functions of antibodies
24
Q
IgA Antibody
A
Dimer
SECRETION
Mucousal Surfaces
Breast Milk
25
IgD Antibody
Early B cells
26
IgM Antibody
Pentamer
First antibody to repond
27
IgG Antibody
Monomer
Fights off most infections
Passed in utero
28
IgE
Monomer
Mediator of common allergic responses
Defense against parasitic infections
29
MHC 1
Interacts with CD8 (cytotoxic cells) and presents ENDOgenous antigens
30
Cytotoxic T Cell
CD8, MHC 1
Cell-Mediated destruction of cells (adheres via MHC 1)
Recognizes antigens on surface of type of cell
30
MHC 2
Interacts on CD4 (helper T) and B cells
EXOgenous antigens
31
Helper T Cell
CD4 - Help other. cells make important proteins (cytokines)
Th1 Cytokine: Provide help in developing cytotoxic T cells
Th2 Cytokine: B-Cell Clonal Selection
Th17: Lymphokine-secretion
Treg: Suppresses response and maintains tolerance against self-antigens (prevents autoimmunity)
32
Memory T Cell
Remain inactive until exposure occurs
33
When are combinations of Abx appropriate?
Tx of several infections, more than one organism, Tuberculosis Tx
34
Indications for Abx prophylaxis
Dental surgeries, Neutropenia, UTI, endocarditis
35
Bacterial Cell Wall Abx
Penicillin
Cephalosporin
36
Bacterial Protein Synthesis Abx
Tetracyclines (static)
Macrolides (static)
Aminoglycosides (cidal)
37
DNA/RNA Abx
Fluroquinoles
38
Enzymes Abx (Folic acid)
Sulfonamides/Trimethoprim (static)
39
SNS reponse to stress
1. Neuropeptide: Vasoconstriction, growth, angiogenic
2. Norepinephrine: Increased BP, Sweat, Pupil Dil., Piloerection, Smooth muscle conc.
3. Epinephrine: Bronchodilation, lipolysis (free fatty acids), increased cardiac contraction, C/O, glucogenesis, glycogenesis
40
Alarm Stage
Emergency reaction - triggers HPA axis
41
Adaption Stage
Takes hormones into account - continues coping - ready to fight back
42
Exhaustion Stage
Body Systems no longer coping to stressors - chronic
43
HPA axis
Hypothalamus - Secretes corticotopin-releasing hormone
Pituitary - Releases adrenocorticotropic hormone
Adrenal Gland - releases cortisol and adrenaline
44
Cortisol
Stimulates gluconeogensis (glucose production)
45
Adrenaline/Epinephrine
Increase HR, RR, Blood Sugar
46
Catecholamines
Epinephrine and Norepinephrine
- Hormones released and responsible for "fight-or-flight"
47
Alpha 1 Response
Increased vasoconstriction, increased contractility
48
Alpha 2 Response
Inhibition of Nerves
49
Beta 1 Response
Increased HR, conduction, contractility, increased glucagon/renin
50
Beta 2 Response
Bronchodilation, less motility, gluconeogensis, glycogenolysis
51
Primary Immune Deficiencies
Congenital (Genetic) - Inherited
52
Secondary Immune Deficiencies
Caused by another Illness - Acquired
53
HIV Pathophysiology
Virus infects and destroys T Helper Cells which are necessary for the development of cytotoxic T cells and B cells
54
Reverse Transcriptase - HIV
Enzyme used to convert RNA to DNA
55
Protease - HIV
Processing proteins needed from virus itself
56
Integrase - HIV
Inserts new DNA to infected cells genetic material (becomes virion)
57
Acute Phase - HIV
2-4 weeks after infection
"HIV Syndrome"
Flu-like symptoms
58
Lab Tests for AIDs
Western blot analysis, presence of antibodies against HIV, atypical/opportunistic infections
59
Chronic HIV Infection
Continues to multiply in body - not yet symptomatic - decades?
60
AIDS Diagnosis
<200 cells/mm3 CD4 count
61
Antiretroviral Therapy Function
Blocks enzymes in virus where certain actions would happen
62
ART Examples
1. Reverse transcriptase inhibitors
2. Protease Inhibitors
3. Integrase Inhibitors
4. Fusion Inhibitors
5. CCR5 antagonist
63
Highly Active Antiretroviral Therapy
1. HAART - COMBINATION
- 30-45 pills
- costly
64
Primary Intention Wound Healing
Wound that heals under conditions of minimal tissue loss
65
Secondary Intention Wound Healing
Wounds that require more tissue replacement
e.g. open wound (cardiac cells after myocardial infarction)
66
Ischemia - Wound Healing
Tissue is deprived of O2 (collagen synthesis is impaired)
67
Excessive Bleeding - Wound Healing
Affects O2 diffusion, pooled/stagnant blood is not good for oxygenation
68
Common issues for wound healing
Diabetes, Obesity, drugs, tobacco
69
Dysfunctional Collagen Synthesis
Keloid - raised scars that extends beyond normal boundary
Scar/Hypertrophic Scar - Raised but remain within boundary
70
Wound Disruption
Dehiscence - when a wound opens back up **infection risk**
71
Impaired Contraction
Contracture
72
Organ Rejection - Hypersensitivity
1. Hyperacute Reaction - Type II (preexisting antibodies to HLA)
2. Acute Reject - Type IV (cell-mediated response that occurs within a few days)
3. Chronic Reaction - Type IV reaction(results from chronic inflammation and weak cell-mediated immune response)
73
GVHD (graft vs. host disease)
Type IV
T cells in graft are mature against recipients HLA
74
Hemolytic Anemia
Type II
Red Blood cells are destroyed faster than they are. made
75
Type I Hypersensitivity
Common allergies
IgE
Anaphylaxis is the worst type of reaction
MOA:
1. Allergen
2. Processed by APC
3. B Cell transformed to Plasma
4. Plasma releases IgE
5. IgE attach to mast cell
6. Mast cell is sensitized
7. Degranulating
8. Release of histamines
9. Quick reaction
76
Type II Hypersensitivity
Tissue/Cell-Specific Antigen
Localized to tissue (NOT SOLUBLE)
IgG
e.g. Autoimmune hemolytic anemia, Goodpasture, graves disease, drug allergy, myasthenia gravis
77
Type III Hypersensitivity
Immune complex Mediated - NOT organ specific
- Antigen-Antibody complex formed in circulation and are deposited in EXTRA tissues (SOLUBLE)
e.g Systemic Lupus Erythematosus, Serum Sickness (Raynaud phenomenon)
Delayed response = not acute
IgG
78
Type IV Hypersentitivity
Cell-Mediated Hypersensitivity
- NO antibodies
Key player: Cytotoxic T cell
e.g. Graft Rejection, TB Skin test, poison ivy, etc.
79
Allergic Reaction
Runny nose, conjunctivitis, Hypotension
80
Anaphylactic Reaction
Pruritis, Erythema, Vomiting, Ab cramps, Diarrhea, SHOCK/DEATH
81
Principle Cells in allergy/anaphylactic
MAST Cells/B Cells
82
Bullous Pemphigoid
Massive, fluid-filled blisters
83
Goodpastures
Body attacks basement cell membranes - AGGRESSIVE bleeding
84
Vitiligo
Melanin response
85
Polymyositis
Systemic - Inflammation of group of muscles (organs can be impacted by muscle inflammation)
86
Myasthenia Gravis
Hummoral Immune Dysfunction - Progressive weakness and loss of muscle control (B-Cell disease)
*autoantibodies against nicotinic acetylcholine receptors*
87
Multiple Sclerosis
Cell-Mediated
Self-reactive T cells attack myelin sheath of CNS
88
Sjorgrens
Secretioons in mouth/tear glands
89
Graves
Hypre metabolism due to thyroid related issues
90
Organ Specific Autoimmune Diseases
Type 1 Diabetes, Hashimotos, Autoimmune hemolytic anemia, additons disease, myasthenia gravis
91
Systemic Autoimmune Disease
RA, Scleroderma, SLE,
92
Type A blood
A antigen - Anti-B antibodies
93
Type B blood
B antigen, Anti-A antibodies
94
Type AB blood
A and B antigen - no antibodies
95
Type O
No antigen, Anti-A/Anti-B antiobdies (presence of D antigen = positive)
96
Herpes Drugs
Acyclovir
Ganciclovir
97
Hep C Drugs
Pegylated INF-A combined with Ribavirin (drug maintains)
98
Hep C Drug Effects
Flu-like symptoms, depression, fatigue, thyroid dysfunction
99
Hep B Drugs
INF-a 2B
Lamivudine
100
Reverse Transcriptase Inhibitors
- inhibit conversion of RNA to DNA
101
Nucleoside Reverse Transcriptase Inhibitors
Zidovudine (Retrovir) - suppress synth of viral DNA
ADE: Hematologic toxicity, lactic acidosis, CNS reactions
102
Non Nucleoside Reverse Transcriptase Inhibitors
Efavirenz (Sustiva)
103
Integrase Strand Transfer Inhibitors
Inhibits integration of viral DNA
1. Raltegravir (Isentress)
104
Protease Inhibitors
Inhibits release of virus host from cell
105
Fusion Inhibitors
Prevents membranes from fusion/entrance intro cell
106
CCR5 antagonists
Takes up the receptor which blocks entry into the cell
107
Influenza Nueraminidase Inhibitors
Tamiflu/Relenza
MOA: Neurominidase in an enzyme which releases the virus from cells (prevent spreading)
108
Histamine
Mast Cells/Basophils
Release: an allergic reaction
109
H1 Antagonists
Block actions of histamine at H1 receptor
Vasodilation, Increase CP, Bronchoconstriction, CNS
110
1st generation
Bendaryl Dramamine
111
2nd Generation
Zyrtec, Allegra, Claritin (no sedating effects)
112
H1 Antagonists
Mild allergy/Sever allergy
Motion sickness
Common Cold
113
Overdose of Antihistamines
Paradoxical Excitation:
CNS Stim, Insomnia, Tremors, etc
114
Anticholinergic Syndrome
Weak atropine-line (dryness, confusion, blurred vision, photophobia, confusion, memory loss)
115
Glucocorticoid Therapy Function
Used to suppress immune response, suppress allograft rejection, asthma/RA, SLE, MS
116
Glucocorticoid Concerns
Increased ROI, Thinning of skin, Bone dissolution, Impaired growth
117
Glucocorticoid MOA
Corticosteroids* (identical to adrenal cortex steroids)
Modulate glucose metabolism in adrenocortical insufficiency (low dose)
Suppress inflammation (large dose)
118
Glucocorticoid Electrolyte Impact
Promote retention of NA/H2O and increase excretion of Potassium
119
ADE Glucocorticoids
Infection (PCP), glucose intolerance, adrenal insufficiency, osteoporosis, myopathy, cushings syndrome
120
Drug Interactions Glucocorticoids
Potassium loss - diuretics
NSAID
Insulin
Vaccines
121
Contraindications Glucocorticoid
Systemic Fungal Infection
Live vaccines
Pediatric/pregnancy
122
MOA - Anti-inflammatory
Inhibit COX (enzyme that converts arachidonic acid into prostanoids)
123
Drugs with antinflammatory properties
NSAIDS (ibuprofen, asprin)
124
Drugs without anti-inflammatory properties
Acetaminophen
125
Inhibition of COX-1 Effects
Gastric ulceration, bleeding, renal impair (prevents myocardial infarction/stroke)
126
Inhibition of COX-2 Effects
Suppress inflammation, alleviation of pain, reduce fever, protect against colorectal cancer
127
First Generation NSAIDS
Inhibits COX 1/2
Treats inflammatory disorders (RA/Osteo)
128
Aspirin
Nonselective inhibitor of COX (non. reversible)
Pain relief, suppress platalet aggregation, dysmennorrhea, alzeim (protects against MI/Stroke)
129
Non-Aspirin First Gen
Fewer Gi/renal effects
Inhibition of COX is reversible
130
2nd Gen NSAIDS
Target COX-2 ONLY
Lower GI risk
Cause HTN/Edema
131
Acetaminophen
Analgesic, Antipyretic
No anti-inflammatory actions
Inhibits prostaglandin synth in CNS
*Hepatotoxicity*
*Hepatic Necrosis with eTOH*
132
Treatment for Acetaminophen OD
Acetylcysteine (Mucomyst)
133
Aspirin Drug Interactions
Warfarin/Heparin
Glucocorticoids
Alc
Ibu
ACE inhibitors
134
Hyponatremia
Cell swelling, ability to polarize, LOC
135
Hypernatremia
Thirst, weight gain, big pulse, increased BP
136
Hypokalemia
Dysrhythmias and muscles weakness
137
Hyperkalemia
Dysrythmia, neuromuscular irritability
138
Metabolic Acidosis Causes
Loss of bicarb (diarrhea), ketoacidosis, lactic acids, renal failure
(lungs breath more and renal eliminates H+)
139
Metabolic Alkalosis Causes
Vomiting, Renal Loss, H+ moving into cells
H+moves out of cells, less breathing, eliminate Bicarb)
140
Nephrotic Syndrome
Presence of PROTEIN (glomerulonephritis)
141
Nephritic Syndrome
BLOOD in urine (infection)
142
Loop Diuretics
Loop
Block NaCl Reabsorption
Most effective
143
Thiazide Diuretics
Early Distal CT
Blocks absorption of NA,Cl
144
K+ Sparing
Late CT/Collecting Duct
Blocks aldosterone in DT
Excretion of sodium/retention of K+
145
Osmotic Diuretics
PCT, ICP!
146
virulence
causes disease
147
infectivity
ability to invade and multiply in host
148
