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Patho/Pharm > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Eosinophil Function

A

Killing of antibody coated parasite

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2
Q

Basophil Function

A

Promotion of allergic response and augmentation of anti-parasitic immunity (asthma/allergy)

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3
Q

Mast Cell Function

A

Role in Allergy: Release histamine and proteases (increases permeability to WBC - inflammation occurs)

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4
Q

Monocyte/Macrophage

A

Monocytes become macrophages
Phagocytosis and activation of bactericidal mechanisms and antigen presentation

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5
Q

WBC Normal

A

4500-11000

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6
Q

Order (Most abundant to least abundant) WBC (never leave me every baby)

A

Neutrophil
Lymphocyte
Monocyte
Eosinophil
Basophil

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7
Q

Antigen Function

A

molecule that triggers an immune response and becomes target of response

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8
Q

What is central tolerance?

A

Negative selection - Eliminating any developing T/B lymphocytes that reactive to itself

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9
Q

Mechanical Barrier of immunity

A

Epithelial cells, mucus by cilia, tears, nasal cilia

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10
Q

Chemical Barrier of immunity

A

Skin, Gut pH, Gut enzymes, Pulmonary Surfactant, Enzymes in tears/saliva

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11
Q

Phagocytosis Steps

A
  1. Neutrophil forms barrier around and engulfs
  2. Lysosomes help degrade
  3. Combine with phagocytes
  4. Lysis of bacteria
    Further macrophage/apoptosis
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12
Q

Phagolysosome

A

Fusion of phagosome with lysosome (process)

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13
Q

Cytokines that lead to fever

A

IL-1B, TNF-a, IL-6

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14
Q

Acute Phase Respoonse

A

Promote phagocytosis and fibrinogens

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15
Q

IL-6 functioon

A

Stimulate liver to secrete various APP

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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

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17
Q

NK Cell Function

A

Recognize ligands on virally infected cells, kill cells, recognize ligands on uninfected cells (MHC C1)

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18
Q

Complement System Function

A

Activation of C3 (cascade)
- Opsonins (phagocytosis)
- Anaphylatoxin (recruitment on WBC)

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19
Q

Clotting System Function

A

Fibrinogen
- Trapping pathogens
- Increase permeability

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20
Q

Kinin System

A

Bradykinin (increases permeability and onsets pain)

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21
Q

Clonal Diversity

A

Production of T/B cell in lymphoid organs

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22
Q

Fab Region

A

Site that binds with antigen (variable region)

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23
Q

Fc Region

A

Responsible for biological functions of antibodies

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24
Q

IgA Antibody

A

Dimer
SECRETION
Mucousal Surfaces
Breast Milk

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25
Q

IgD Antibody

A

Early B cells

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26
Q

IgM Antibody

A

Pentamer
First antibody to repond

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27
Q

IgG Antibody

A

Monomer
Fights off most infections
Passed in utero

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28
Q

IgE

A

Monomer
Mediator of common allergic responses
Defense against parasitic infections

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29
Q

MHC 1

A

Interacts with CD8 (cytotoxic cells) and presents ENDOgenous antigens

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30
Q

Cytotoxic T Cell

A

CD8, MHC 1
Cell-Mediated destruction of cells (adheres via MHC 1)
Recognizes antigens on surface of type of cell

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30
Q

MHC 2

A

Interacts on CD4 (helper T) and B cells
EXOgenous antigens

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31
Q

Helper T Cell

A

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)

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32
Q

Memory T Cell

A

Remain inactive until exposure occurs

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33
Q

When are combinations of Abx appropriate?

A

Tx of several infections, more than one organism, Tuberculosis Tx

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34
Q

Indications for Abx prophylaxis

A

Dental surgeries, Neutropenia, UTI, endocarditis

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35
Q

Bacterial Cell Wall Abx

A

Penicillin
Cephalosporin

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36
Q

Bacterial Protein Synthesis Abx

A

Tetracyclines (static)
Macrolides (static)
Aminoglycosides (cidal)

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37
Q

DNA/RNA Abx

A

Fluroquinoles

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38
Q

Enzymes Abx (Folic acid)

A

Sulfonamides/Trimethoprim (static)

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39
Q

SNS reponse to stress

A
  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
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40
Q

Alarm Stage

A

Emergency reaction - triggers HPA axis

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41
Q

Adaption Stage

A

Takes hormones into account - continues coping - ready to fight back

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42
Q

Exhaustion Stage

A

Body Systems no longer coping to stressors - chronic

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43
Q

HPA axis

A

Hypothalamus - Secretes corticotopin-releasing hormone
Pituitary - Releases adrenocorticotropic hormone
Adrenal Gland - releases cortisol and adrenaline

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44
Q

Cortisol

A

Stimulates gluconeogensis (glucose production)

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45
Q

Adrenaline/Epinephrine

A

Increase HR, RR, Blood Sugar

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46
Q

Catecholamines

A

Epinephrine and Norepinephrine
- Hormones released and responsible for “fight-or-flight”

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47
Q

Alpha 1 Response

A

Increased vasoconstriction, increased contractility

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48
Q

Alpha 2 Response

A

Inhibition of Nerves

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49
Q

Beta 1 Response

A

Increased HR, conduction, contractility, increased glucagon/renin

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50
Q

Beta 2 Response

A

Bronchodilation, less motility, gluconeogensis, glycogenolysis

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51
Q

Primary Immune Deficiencies

A

Congenital (Genetic) - Inherited

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52
Q

Secondary Immune Deficiencies

A

Caused by another Illness - Acquired

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53
Q

HIV Pathophysiology

A

Virus infects and destroys T Helper Cells which are necessary for the development of cytotoxic T cells and B cells

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54
Q

Reverse Transcriptase - HIV

A

Enzyme used to convert RNA to DNA

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55
Q

Protease - HIV

A

Processing proteins needed from virus itself

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56
Q

Integrase - HIV

A

Inserts new DNA to infected cells genetic material (becomes virion)

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57
Q

Acute Phase - HIV

A

2-4 weeks after infection
“HIV Syndrome”
Flu-like symptoms

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58
Q

Lab Tests for AIDs

A

Western blot analysis, presence of antibodies against HIV, atypical/opportunistic infections

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59
Q

Chronic HIV Infection

A

Continues to multiply in body - not yet symptomatic - decades?

60
Q

AIDS Diagnosis

A

<200 cells/mm3 CD4 count

61
Q

Antiretroviral Therapy Function

A

Blocks enzymes in virus where certain actions would happen

62
Q

ART Examples

A
  1. Reverse transcriptase inhibitors
  2. Protease Inhibitors
  3. Integrase Inhibitors
  4. Fusion Inhibitors
  5. CCR5 antagonist
63
Q

Highly Active Antiretroviral Therapy

A
  1. HAART - COMBINATION
    - 30-45 pills
    - costly
64
Q

Primary Intention Wound Healing

A

Wound that heals under conditions of minimal tissue loss

65
Q

Secondary Intention Wound Healing

A

Wounds that require more tissue replacement
e.g. open wound (cardiac cells after myocardial infarction)

66
Q

Ischemia - Wound Healing

A

Tissue is deprived of O2 (collagen synthesis is impaired)

67
Q

Excessive Bleeding - Wound Healing

A

Affects O2 diffusion, pooled/stagnant blood is not good for oxygenation

68
Q

Common issues for wound healing

A

Diabetes, Obesity, drugs, tobacco

69
Q

Dysfunctional Collagen Synthesis

A

Keloid - raised scars that extends beyond normal boundary
Scar/Hypertrophic Scar - Raised but remain within boundary

70
Q

Wound Disruption

A

Dehiscence - when a wound opens back up infection risk

71
Q

Impaired Contraction

A

Contracture

72
Q

Organ Rejection - Hypersensitivity

A
  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
Q

GVHD (graft vs. host disease)

A

Type IV
T cells in graft are mature against recipients HLA

74
Q

Hemolytic Anemia

A

Type II
Red Blood cells are destroyed faster than they are. made

75
Q

Type I Hypersensitivity

A

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
Q

Type II Hypersensitivity

A

Tissue/Cell-Specific Antigen
Localized to tissue (NOT SOLUBLE)
IgG
e.g. Autoimmune hemolytic anemia, Goodpasture, graves disease, drug allergy, myasthenia gravis

77
Q

Type III Hypersensitivity

A

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
Q

Type IV Hypersentitivity

A

Cell-Mediated Hypersensitivity
- NO antibodies
Key player: Cytotoxic T cell
e.g. Graft Rejection, TB Skin test, poison ivy, etc.

79
Q

Allergic Reaction

A

Runny nose, conjunctivitis, Hypotension

80
Q

Anaphylactic Reaction

A

Pruritis, Erythema, Vomiting, Ab cramps, Diarrhea, SHOCK/DEATH

81
Q

Principle Cells in allergy/anaphylactic

A

MAST Cells/B Cells

82
Q

Bullous Pemphigoid

A

Massive, fluid-filled blisters

83
Q

Goodpastures

A

Body attacks basement cell membranes - AGGRESSIVE bleeding

84
Q

Vitiligo

A

Melanin response

85
Q

Polymyositis

A

Systemic - Inflammation of group of muscles (organs can be impacted by muscle inflammation)

86
Q

Myasthenia Gravis

A

Hummoral Immune Dysfunction - Progressive weakness and loss of muscle control (B-Cell disease)
autoantibodies against nicotinic acetylcholine receptors

87
Q

Multiple Sclerosis

A

Cell-Mediated
Self-reactive T cells attack myelin sheath of CNS

88
Q

Sjorgrens

A

Secretioons in mouth/tear glands

89
Q

Graves

A

Hypre metabolism due to thyroid related issues

90
Q

Organ Specific Autoimmune Diseases

A

Type 1 Diabetes, Hashimotos, Autoimmune hemolytic anemia, additons disease, myasthenia gravis

91
Q

Systemic Autoimmune Disease

A

RA, Scleroderma, SLE,

92
Q

Type A blood

A

A antigen - Anti-B antibodies

93
Q

Type B blood

A

B antigen, Anti-A antibodies

94
Q

Type AB blood

A

A and B antigen - no antibodies

95
Q

Type O

A

No antigen, Anti-A/Anti-B antiobdies (presence of D antigen = positive)

96
Q

Herpes Drugs

A

Acyclovir
Ganciclovir

97
Q

Hep C Drugs

A

Pegylated INF-A combined with Ribavirin (drug maintains)

98
Q

Hep C Drug Effects

A

Flu-like symptoms, depression, fatigue, thyroid dysfunction

99
Q

Hep B Drugs

A

INF-a 2B
Lamivudine

100
Q

Reverse Transcriptase Inhibitors

A
  • inhibit conversion of RNA to DNA
101
Q

Nucleoside Reverse Transcriptase Inhibitors

A

Zidovudine (Retrovir) - suppress synth of viral DNA
ADE: Hematologic toxicity, lactic acidosis, CNS reactions

102
Q

Non Nucleoside Reverse Transcriptase Inhibitors

A

Efavirenz (Sustiva)

103
Q

Integrase Strand Transfer Inhibitors

A

Inhibits integration of viral DNA
1. Raltegravir (Isentress)

104
Q

Protease Inhibitors

A

Inhibits release of virus host from cell

105
Q

Fusion Inhibitors

A

Prevents membranes from fusion/entrance intro cell

106
Q

CCR5 antagonists

A

Takes up the receptor which blocks entry into the cell

107
Q

Influenza Nueraminidase Inhibitors

A

Tamiflu/Relenza
MOA: Neurominidase in an enzyme which releases the virus from cells (prevent spreading)

108
Q

Histamine

A

Mast Cells/Basophils
Release: an allergic reaction

109
Q

H1 Antagonists

A

Block actions of histamine at H1 receptor
Vasodilation, Increase CP, Bronchoconstriction, CNS

110
Q

1st generation

A

Bendaryl Dramamine

111
Q

2nd Generation

A

Zyrtec, Allegra, Claritin (no sedating effects)

112
Q

H1 Antagonists

A

Mild allergy/Sever allergy
Motion sickness
Common Cold

113
Q

Overdose of Antihistamines

A

Paradoxical Excitation:
CNS Stim, Insomnia, Tremors, etc

114
Q

Anticholinergic Syndrome

A

Weak atropine-line (dryness, confusion, blurred vision, photophobia, confusion, memory loss)

115
Q

Glucocorticoid Therapy Function

A

Used to suppress immune response, suppress allograft rejection, asthma/RA, SLE, MS

116
Q

Glucocorticoid Concerns

A

Increased ROI, Thinning of skin, Bone dissolution, Impaired growth

117
Q

Glucocorticoid MOA

A

Corticosteroids* (identical to adrenal cortex steroids)
Modulate glucose metabolism in adrenocortical insufficiency (low dose)
Suppress inflammation (large dose)

118
Q

Glucocorticoid Electrolyte Impact

A

Promote retention of NA/H2O and increase excretion of Potassium

119
Q

ADE Glucocorticoids

A

Infection (PCP), glucose intolerance, adrenal insufficiency, osteoporosis, myopathy, cushings syndrome

120
Q

Drug Interactions Glucocorticoids

A

Potassium loss - diuretics
NSAID
Insulin
Vaccines

121
Q

Contraindications Glucocorticoid

A

Systemic Fungal Infection
Live vaccines
Pediatric/pregnancy

122
Q

MOA - Anti-inflammatory

A

Inhibit COX (enzyme that converts arachidonic acid into prostanoids)

123
Q

Drugs with antinflammatory properties

A

NSAIDS (ibuprofen, asprin)

124
Q

Drugs without anti-inflammatory properties

A

Acetaminophen

125
Q

Inhibition of COX-1 Effects

A

Gastric ulceration, bleeding, renal impair (prevents myocardial infarction/stroke)

126
Q

Inhibition of COX-2 Effects

A

Suppress inflammation, alleviation of pain, reduce fever, protect against colorectal cancer

127
Q

First Generation NSAIDS

A

Inhibits COX 1/2
Treats inflammatory disorders (RA/Osteo)

128
Q

Aspirin

A

Nonselective inhibitor of COX (non. reversible)
Pain relief, suppress platalet aggregation, dysmennorrhea, alzeim (protects against MI/Stroke)

129
Q

Non-Aspirin First Gen

A

Fewer Gi/renal effects
Inhibition of COX is reversible

130
Q

2nd Gen NSAIDS

A

Target COX-2 ONLY
Lower GI risk
Cause HTN/Edema

131
Q

Acetaminophen

A

Analgesic, Antipyretic
No anti-inflammatory actions
Inhibits prostaglandin synth in CNS
Hepatotoxicity
Hepatic Necrosis with eTOH

132
Q

Treatment for Acetaminophen OD

A

Acetylcysteine (Mucomyst)

133
Q

Aspirin Drug Interactions

A

Warfarin/Heparin
Glucocorticoids
Alc
Ibu
ACE inhibitors

134
Q

Hyponatremia

A

Cell swelling, ability to polarize, LOC

135
Q

Hypernatremia

A

Thirst, weight gain, big pulse, increased BP

136
Q

Hypokalemia

A

Dysrhythmias and muscles weakness

137
Q

Hyperkalemia

A

Dysrythmia, neuromuscular irritability

138
Q

Metabolic Acidosis Causes

A

Loss of bicarb (diarrhea), ketoacidosis, lactic acids, renal failure
(lungs breath more and renal eliminates H+)

139
Q

Metabolic Alkalosis Causes

A

Vomiting, Renal Loss, H+ moving into cells
H+moves out of cells, less breathing, eliminate Bicarb)

140
Q

Nephrotic Syndrome

A

Presence of PROTEIN (glomerulonephritis)

141
Q

Nephritic Syndrome

A

BLOOD in urine (infection)

142
Q

Loop Diuretics

A

Loop
Block NaCl Reabsorption
Most effective

143
Q

Thiazide Diuretics

A

Early Distal CT
Blocks absorption of NA,Cl

144
Q

K+ Sparing

A

Late CT/Collecting Duct
Blocks aldosterone in DT
Excretion of sodium/retention of K+

145
Q

Osmotic Diuretics

A

PCT, ICP!

146
Q

virulence

A

causes disease

147
Q

infectivity

A

ability to invade and multiply in host

148
Q
A

Patho/Pharm (2 decks)

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