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1
Q

Type I hypersensitivities

A

Allergic/atopic reactions

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2
Q

Type II hypersensitivities

A

Antibody binding to cell surface proteins

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3
Q

Type III hypersensitivities

A

Soluble antigen (floating around; no membrane involved), IgG binds, forms immune complex; followed by complement activation and acute inflammation

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4
Q

Type IV hypersensitivities

A

No antibody; involves T cell-instigated/mediated tissue damage

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5
Q 
Myasthenia gravis
Pemphigus vulgaris
Goodpasture's syndrome
Graves disease
Hemolytic disease of the newborn
Loss of RBCs in hemolytic anemia
A

Type II hypersensitivities

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6
Q

Systemic lupus erythematous
Glomerulonephritis
Arthritis/arthralgia
Arteritis

A

Type III hypersensitivities

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7
Q

Lesion seen after positive TB test
Granuloma formation in latent TB
Poison ivy rash
Contact dermatitis

A

Type IV hypersensitivities

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8
Q

Type III rheumatoid arthritis

A

Rheumatoid factor plus IgG complexes, deposit in joint space (synovial fluid)

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9
Q

Type IV rheumatoid arthritis

A

Reaction occurs in synovial membrane-mononuclear cell infiltration leads to reorganization of joint tissue and resorption of bone

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10
Q

What causes granuloma formation in TB?

A

Tuberculosis and histoplasma replicate in alveolar macrophages

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11
Q

What are the three stages of Type I hypersensitivity?

A
  1. SENSITIZATION
    Antigen exposure –> production of IgE
  2. IMMEDIATE PHASE
    Occurs within minutes of mast cell degranulation
  3. LATE-PHASE
    Results from the cytokines released from the mast cells
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12
Q

What induces B cell switching to IgE?

A

IL-4 release

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13
Q

What activates eosinophils?

A

IL-5

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14
Q

What cell types are involved in Type IV hypersensitivities?

A

CD4 T-cells
Macrophages
CD8 T-cells

**no antibodies involved*

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15
Q

What type of tissue damage is involved in Type III hypersensitivities?

A

Neutrophil-mediated tissue damage

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16
Q

Which alleles are most important when matching for transplantation?

A

MHC Class I B and Class II DR

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17
Q

Which cells are involved in acute rejection and chronic rejection?

A

Acute: CD8 and CD4
Chronic: CD4 only

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18
Q

A antigen has ______

A

N-acetylgalactosamine

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19
Q

B antigen has ______

A

D-galactosyltransferase

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20
Q

What is the difference between forward and reverse typing?

A

Forward: determines antigens on patient’s or donor’s blood
Reverse: determines antibodies in patient’s or donor’s serum or plasma

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21
Q

What occurs during hyperacute rejection?

A

Preformed antibodies specific to MHC, therefore B-cell mediated

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22
Q

What poses the greatest risk for Graft vs. Host Disease?

A

Bone marrow

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23
Q

This legislation, passed in 1962, was largely in response to reports of severe malformations in
the offspring of women in Europe who took thalidomide for sedation during their pregnancy. It
required proof of efficacy and safety for new drugs.

A

Kefauver-Harris Amendments

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24
Q

What is the mechanism of an agonist?

A

Mimics the actions of an endogenous ligand

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25
Q

What is an indication of the presence of spare receptors?

A

EC50 less than Kd

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26
Q

Concentration at which 50% of receptors are occupied by drug

A

Kd

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27
Q

True/False: The relationship between [drug] at target site and [drug-receptor complex] is linear.

A

False

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28
Q

True/False: The relationship between dose and [drug] at target site is linear.

A

True

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29
Q

[Drug] which causes 1/2 maximum response

A

EC50

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30
Q

What is tachyphylaxis?

A

RAPID development of tolerance

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31
Q

Enhanced response to a drug due to an increase in the number of receptors

A

Supersensitivity

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32
Q

Enhancement of the effect of one drug by another which has no effect by itself

A

Potentiation

parallel shift of the log dose-response curve to the left

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33
Q

Production of a greater response than two drugs that act individually

A

Synergism

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34
Q

List the 3 classes of host pattern recognition receptors which respond to influenza virus

A

TLR-7: recognizes virus genomic DNA
NLRP3: recruited to the mitochondria to form the NLRP3 inflammasome
RIG-1: cytosolic sensor that directly interacts with the viral nucleocapsid; detects the uncapped RNA of the viral genome

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35
Q

What is the basic purpose of the NS1 protein study?

A

To analyze and identify the pathway that NS1 inhibits the secretion of IL-1B. This is done by inhibiting inflammasome formation.

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36
Q

What are the roles of EGFP, hCUP-2, and NS-1 plasmids?

A 
EGFP = control; green fluorescent for control; lacked subunits of the inflammasome
hCUP-2 = inhibitory action of IL-1B via mt. membrane dissipation. Uncoupling proteins that reduce flow out of membrane for flow cytometry
NS-1 = used to infect macrophages
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37
Q

In the influenza study, they demonstrate that the function of the influenza NS1 protein differs from that of the influenza PB1-F2 protein in that the PB1 protein has what effect on cells?

A

PB1 dissipates the mitochondrial membrane potential. They didn’t find that the mitochondrial membrane was affected by NS1.

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38
Q

What is the function of influenza virus NS1 protein in cell infections?

A

NS1 interacts with the inflammasome formation by reducing the speck formation and not by reducing mitochondrial membrane formation.

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39
Q

Fluoxetine

A

Transport inhibitor

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40
Q

Minoxidil

A

Ion channel opener (potassium)

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41
Q

Phenylephrine

A

Cell surface receptor agonist

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42
Q

Aspirin

A

Enzyme (cyclooxygenase) inhibitor

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43
Q

Vinca alkaloids

A

Disrupt structural proteins (tubulin)

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44
Q

Dimercaprol

A

Bind free molecules –> chelating agent for heavy metal poisoning

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45
Q

Fomivirsen

A

Antisense

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46
Q

Diltiazem

A

Calcium channel blocker

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47
Q

Tamoxifen

A

Estrogen receptor antagonist (nuclear)

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48
Q

Mannitol

A

Exerts actions due to physical properties (osmotic diuretic)

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49
Q

Cyclophosphamide

A

DNA alkylating agent

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50
Q

Pralidoxime

A

Enzyme activator

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51
Q

Propanalol

A

Cell surface receptor antagonist

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52
Q

Sildenafil

A

Inhibits signal transduction proteins

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53
Q

Loading dose equation

A

LD = Cp x Vd

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54
Q

Maintenace dose equation

A

MD / DI = [Cp x Cl] / B

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55
Q

Css equation

A

Css = R0 / CL = B x MD / DI x CL

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56
Q

This phase converts lipophilic molecules into more polar molecules by introducing/unmasking a polar functional group

57
Q

This phase converts the drug molecule to an even more polar molecule in order to be excreted in urine

58
Q

Which isozymes are responsible for metabolism of the largest number of drugs?

A
  1. CYP3A4

2. CYP2D6

59
Q

Where is CYP3A4 found?

A

GI tract

Liver

60
Q

What do these drugs inhibit?

Ketoconazole
Itraconazole
Fluconazole
Amiodarone
Ritonavir
Grapefruit juice
61
Q

What do these drugs induce?

St. John’s Wort
Barbiturates

62
Q

What isozyme catalyzes primary metabolism of codeine and Beta-blockers?

63
Q

What inhibits CYP2D6?

64
Q

What does CYP2C9 metabolize?

A

NSAIDs
Warfarin
Phenytoin

65
Q

What inhibits CYP2C9?

A

Fluconazole

66
Q

What drug reaction is CYP2D6-dependente?

A

Activation of codeine by methylation

67
Q

Which isozyme is induced by tobacco?

68
Q

Which isozyme is the primary catalyst of propanolol metabolism?

69
Q

What drugs should St. John’s Wort not be taken with?

A

Idinavir (induces CYP3A4)
Cyclosporin
Digoxin

70
Q

What is the best studied drug transporter?

A

P-glycoprotein

71
Q

Which drugs inhibit p-glycoprotein?

A

Diltiazem
Quinidine
Verapamil

72
Q

Fusion protein that blocks T cell activation by inhibiting co-stimulation
Blocks T-cell activation by BINDING B7/CD80/CD86 ON APCs

73
Q

Inhibits JAK kinases, thereby blocking cytokine signaling

A

Corticosteroids

74
Q

Inhibits calceneurin from activating NFAT thereby blocking transcription of genes for IL-2 and other cytokines

A

Cyclosporine

Tacrolimus

75
Q

Recombinant TNF receptor fused to Fc of human IgG

A

Etancercept

76
Q

Myasthenia gravis muscle weakness pathogenesis

A

Antibody to a receptor acts as an antagonist

77
Q

Desquamation in pemphigus vulgaris

A

Antibody to desmoglein inhibits function of desmosomes that binds cells tightly together

78
Q

Pathogenesis of hematuria in Goodpastures

A

Antibody to the non-collagenous domain of type 4 collagen leads to complement activation, neutrophil infiltration, and subsequent tissue damage

79
Q

Myasthenia gravis hyperthyroidism pathogenesis

A

Antibody to a receptor acts as agonist

80
Q

Due to generation of leukotriene B4 from activated mast cells

A

Shortness of breath in atopic asthma

81
Q

Example of a T cell response to a hapten

A

Erythematous, itchy rash of poison ivy

82
Q

Memory T cells elicit a Type IV hypersensitivity response with mononuclear cell infiltration into the site of antigen encounter

A

Granuloma formation in TB

83
Q

Results from release of mast cell mediators that lead to vasodilation and increased vascular permeability

A

Wheal and flair in atopic skin test reactions

84
Q

Activation of macrophages

A

Gamma-interferon

85
Q

Bronchoconstriction

86
Q

Causes B cells to switch to production of IgE

87
Q

Chemotactic for eosinophils

88
Q

Chemotactic for mononuclear cells

A

MIP, MCP, RANTES

89
Q

Chemotactic for neutrophils

A

IL-8

Complement C5a

90
Q

Enhanced mucuous production

91
Q

Increase vascular permeability

A

C3a
C5a
IL-4
TNF

92
Q

Necessary for differentiation of Th1 cells

93
Q

Necessary for differentiation of Th17 cells

94
Q

Necessary for proliferation of T cells

95
Q

Kinins induce ____ and ____

A

Pain / itch

96
Q

Vasodilation mediators

A

Leukotriene B4

Histamine

97
Q

Risk factors for ankylosing spondylitis

A

HLA-B27

Klebsiella infections

98
Q

What do corticosteroids block?

A

Phospholipase

Arachidonic acid metabolism

99
Q

Which drugs block calcineurin from activating NFAT?

A

Tacrolimus

Cyclosporine

100
Q

Anti-TNF drugs are used to treat…..

A

Rheumatoid arthritis
Psoriasis
Crohn’s disease

101
Q

What does methotrexate block?

A

Folate synthesis

102
Q

Key cytokines in rheumatoid arthritis and their treatment

A

TNF: Infliximab, Adalimumab, Entanercept
IL-1: Anakinra
IL-6: Tocilizumab

103
Q

Which mediators promote expression of selectin/integrin ligands?

104
Q

IL-6 function

A

Induces release of acute phase proteins from liver

105
Q

Endothelial effects

A 
Increase:
Leukocyte adherence
PGI synthesis
Procoagulant activity
IL-1, IL-8, IL-6, PDGF
106
Q

Where are MIP, MCP, and RANTES produced? What is their function?

A

Produced by Th1 cells, endothelial cells, and macrophages

Recruit of mononuclear cells and eosinophils

107
Q

True/False: DAMPs interact with DRRs and PRRs.

108
Q

SIRS criteria

A

Two of the following:

  1. Fever of more than 38C or less than 36C
  2. Pulse > 90
  3. RR > 20 breaths per minute
  4. Abnormal WBC count ( >12,000 ; <4,000 ; >10% bands)
109
Q

THE bronchodilator

A

Leukotriene

110
Q

What type of RA does Infliximab treat?

111
Q

What type of graph curve is used to determine the variation in sensitivity of subjects to the drug?

A

Quantal dose curve

112
Q

Which inflammatory mediators are primarily responsible for prolonged swelling?

113
Q

Drugs with zero order eliminatin

A

PEA

Phenytoin
Ethanol
Aspirin

114
Q

Treat amphetamine OD with ______

A

Ammonium chloride

115
Q

Treat methotrexate/aspirin/phenobarbital OD with ______

116
Q

DI equation

A

DI = 1.44 x t1/2 x ln(TW)

117
Q

Xerostomia
Xerophthalmia
Enlarged parotid
Antibodies SS-A and SS-B

A

Sjogren’s syndrome

Type III

118
Q

Hematuria
Hemoptysis
Autoantibodies against collagen IV in pulmonary and glomerular basement membranes

A

Goodpasture’s

Type II

119
Q

Risk factors for Reiter’s syndrome

A 
HLA-B27
Shigella
Yersinia
Salmonella
Chlamydia
120
Q

Risk factors for MS

A 
Living in higher latitudes
Females 2:1
Syphilis
Measles
Herpes
121
Q

Myasthenia gravis receptor site

A

Acetylcholine receptors

122
Q

Graves disease receptor site

A

TSH receptors

123
Q

What are NOD-Like Receptors?

A

Nucleotide-binding Oligomerization Domain-like receptors

Intracellular PAMP sensors

Regulate immune response

124
Q

What does YopM inhibit?

A

Activation of the Pyrin inflammasome that is initially induced by YopE

125
Q

What is the function of caspase?

A

Protease that matures and cleaves pro-IL1B

126
Q

What is the T3SSe strain of Y. pestis?

A

Lacks Yops but has basic machinery

127
Q

HAV vs. HBV

A

HAV: regeneration (no scar)
HBV: repair by scarring

128
Q

Sites of stem cells in the skin

A

Epidermis
Sebaceous gland
Hair follicle bulge

129
Q

Functions of the ECM in tissue repair

A

Sequester water and minerals from circulation
Store presynthesized growth factors
Give cells a scaffolding upon which to adhere to do their tasks

130
Q

Regeneration of labile tissues occurs under what condition?

A

ECM must be intact and containing healthy stem cells

131
Q

When an incision occurs, what is the first response?

A

Blood clot in seconds –> begins with PDGF

132
Q

Wounds that will heal by first intention

A

Small wounds that close easily:

Paper cuts
Closely approximated surgical incisions
Well vascularized, no dead tissue

133
Q

Extravascular fluid with low protein content and low specific gravity
Key cells: mononuclear
Example: ultrafiltrate of blood

A

Transudate

134
Q

Example of a serous transudate

A

Friction blister

Pitting edema in CHF

135
Q

Example of a serous exudate

A

Non pitting edema in cellulitis

Middle ear infection

136
Q

Example of a fibrinous exudate

A

Fluid on the heart

137
Q

Triple response of Lewis

A

Red line
Flare
Wheal

138
Q

Primary immune cell in foreign body suture granuloma

A

Giant cell

CMBM E5 CB (1 decks)

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