Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 2019 First Aid Flashcards > Immuno FA part II p109 - 122 > Flashcards

Immuno FA part II p109 - 122 Flashcards

1
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What makes sputum a green color?

A

Myeloperoxidase contains a blue-green, heme-containing pigment that gives sputum its color.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Patients with CGD are at risk for infection of what organisms?

A

Catalase + organisms -

Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E coli, Staphylococci, Serratia, B cepacia, H pylori.

Cats Need PLACESS to Belch their Hairballs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Enzyme def in Chronic granulomatous disease? Inheritance pattern?

A

Defect of NADPH oxidase –> dec reactive oxygen species (eg, superoxide) and –> dec respiratory burst in neutrophils; X-linked form most common.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

_____ plays a role in both the creation and neutralization of ROS.

A

NADPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do catalase + organisms prevent respiratory burst in pts with CGD?

A

catalase ⊕ species (eg, S aureus, Aspergillus) capable of neutralizing their own H2O2, leaving phagocytes without ROS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

_____ of _____ generates ROS to kill competing pathogens

A

Pyocyanin of P aeruginosa generates ROS to kill competing pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Oxidative burst also leads to ____ influx, which releases __________.

A

Oxidative burst also leads to K+ influx, which releases lysosomal enzymes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

_______ is a protein found in secretory fluids and neutrophils that inhibits microbial growth via ____ _________

A

Lactoferrin is a protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How to interferons fight virus infections?

A

by downregulating protein synthesis to resist potential viral replication and by upregulating MHC expression to facilitate recognition of infected cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical use of Interferons

A

Chronic HBV and HCV, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma, multiple sclerosis, chronic granulomatous disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cell surface proteins on T cells

A

TCR (binds antigen-MHC complex)

CD3 (associated with TCR for signal transduction) CD28 (binds B7 on APC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cell surface proteins of Th cells?

A

CD4, CD40L, CXCR4/CCR5 (co-receptors for HIV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tc cell surface proteins?

A

CD8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treg cell surface proteins?

A

CD4, CD25

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

B cell - cell surface proteins?

A

Ig (binds antigen)

CD19, CD20, CD21 (receptor for Epstein-Barr virus), CD40

MHC II, B7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Macrophages - cell surface proteins?

A

CD14 (receptor for PAMPs, eg, LPS), CD40

CCR5

MHC II, B7 (CD80/86)

Fc and C3b receptors (enhanced phagocytosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

NK cells - cell surface proteins and fxn?

A

CD16 (binds Fc of IgG),

CD56 (suggestive marker for NK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Hematopoietic stem cells - cell surface proteins?

A

CD34

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is anergy?

A

State during which a cell cannot become activated by exposure to its antigen. T and B cells become anergic when exposed to their antigen without costimulatory signal (signal 2). Another mechanism of self-tolerance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Passive vs Active immunity - means of acquisition

A

passive - receiving preformed antibodies

active - exposure to foreign antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Onset of action and duration of Passive vs Active immunity?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Examples of Passive vs Active immunity

A

Passive - IgA in breast milk, maternal IgG crossing placenta, antitoxin, humanized monoclonal antibody

Active - natural infection, vaccines, toxoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Combined passive and active immunizations can be given for exposure to what?

A

hepatitis B or rabies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Live attenuated vaccines - (+) what immune response? Pros? and Cons?

A

Induces cellular and humoral responses.

Pros: induces strong, often lifelong immunity.

Cons: may revert to virulent form. Often contraindicated in pregnancy and immunodeficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

If HIV patients CD4 cell count >= 200cells/mm^3, what vaccines are given? what type?

A

MMR and varicella vaccines can be given to HIV ⊕ patients without evidence of immunity if CD4 cell count ≥ 200 cells/ mm3.
- live attenuated vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Ex of live attenuated vaccines?

A

Adenovirus (nonattenuated, given to military recruits), Typhoid (Ty21a, oral), Polio (Sabin), Varicella (chickenpox), Smallpox, BCG, Yellow fever, Influenza (intranasal), MMR, Rotavirus

“Attention Teachers! Please Vaccinate Small, Beautiful Young Infants with MMR Regularly!”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Killed or inactivated vaccine - induces what kind of immune response? Pros/Cons?

A

Pathogen is inactivated by heat or chemicals. Maintaining epitope structure on surface antigens is important for immune response. Mainly induces a humoral response.

Pros: safer than live vaccines.

Cons: weaker immune response; booster shots usually required.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Examples of killed vaccines?

A

Rabies, Influenza (injection), Polio (Salk), hepatitis A, typhoid (Vi polysaccharide, intramuscular)

SalK = Killed

RIP Always

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a subunit vaccine?

A

Includes only the antigens that best stimulate the immune system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Ex of subunit vaccine?

A

HBV (antigen = HBsAg),

HPV (types 6, 11, 16, and 18),

acellular pertussis (aP),

Neisseria meningitidis (various strains), Streptococcus pneumoniae,

Haemophilus influenzae type b.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is a toxoid vaccine? Pros/Cons?

A

Denatured bacterial toxin with an intact receptor binding site. Stimulates the immune system to make antibodies without potential for causing disease.
Pros: protects against the bacterial toxins. Cons: antitoxin levels decrease with time, may require a booster.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Ex of toxoid vaccine

A

Clostridium tetani,

Corynebacterium diphtheriae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

List types of hypersensitivity reactions - which are are antibody mediated?

A

Four types (ABCD): Anaphylactic and Atopic (type I), AntiBody-mediated (type II), Immune Complex (type III), Delayed (cell-mediated, type IV). Types I, II, and III are all antibody-mediated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Two phases of HS-I?

A

Anaphylactic and atopic—two phases:

ƒ Immediate (minutes): antigen crosslinks preformed IgE on presensitized mast cells –> immediate degranulation –> release of histamine (a vasoactive amine) and tryptase (a marker of mast cell activation).

ƒ Late (hours): chemokines (attract inflammatory cells, eg, eosinophils) and other mediators (eg, leukotrienes) from mast cells –> inflammation and tissue damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How to test for HS-I?

A

Test: skin test or blood test (ELISA) for allergenspecific IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What happens in type II HS?

A

Antibodies bind to cell-surface antigens –> cellular destruction, inflammation, and cellular dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

HS-II - cellular destruction happens how? Diseases where this happens?

A

Cellular destruction—cell is opsonized (coated) by antibodies, leading to either:

ƒ Phagocytosis and/or activation of complement system.

ƒ NK cell killing (antibody-dependent cellular cytotoxicity).

Ex/ƒ Autoimmune-hemolytic anemia ƒ Immune thrombocytopenia ƒ Transfusion reactions ƒ Hemolytic disease of the newborn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

HS-II - how inflammation occurs? Diseases where this happens?

A

Inflammation—binding of antibodies to cell surfaces –> activation of complement system and Fc receptor-mediated inflammation.

Ex/ƒ Goodpasture syndrome ƒ Rheumatic fever ƒ Hyperacute transplant rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

HS-II - how does cellular dysfunction happen? Diseases where this process happens?

A

Cellular dysfunction—antibodies bind to cell surface receptors –> abnormal blockade or activation of downstream process.

ex/ ƒ Myasthenia gravis ƒ Graves disease ƒ Pemphigus vulgaris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

HS-III - what happens?

A

Immune complex—antigen-antibody (mostly IgG) complexes activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes.

In type III reaction, imagine an immune complex as 3 things stuck together: antigenantibody-complement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Ex of diseases with HS-III?

A

ƒ SLE ƒ Polyarteritis nodosa ƒ Poststreptococcal glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What happens in serum sickness? sx?

A

Serum sickness—the prototypic immune complex disease. Antibodies to foreign proteins are produced and 1–2 weeks later, antibodyantigen complexes form and deposit in tissues –> complement activation –> inflammation and tissue damage.

Fever, urticaria, arthralgia, proteinuria, lymphadenopathy occur 1–2 weeks after antigen exposure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Serum sickness- like reactions are associated with which drugs/infections?

A

penicillin, hep B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What’s an arthus reaction?

A

Arthus reaction—a local subacute immune complex-mediated hypersensitivity reaction. Intradermal injection of antigen into a presensitized (has circulating IgG) individual leads to immune complex formation in the skin. Characterized by edema, necrosis, and activation of complement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Two mech of HS-IV?

A
  1. Direct cell cytotoxicity: CD8+ cytotoxic T cells kill targeted cells.
  2. Inflammatory reaction: effector CD4+ T cells recognize antigen and release inflammation-inducing cytokines (shown in illustration).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

T or F HS-IV response does not involve antibodies

A

True! (Type 1, 2,3 do)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Ex of HS-IV?

A

contact dermatitis (eg, poison ivy, nickel allergy) and graft-versus-host disease.

[MS, T1DB, Hashimoto]

Tests: PPD for TB infection; patch test for contact dermatitis; Candida skin test for T cell immune function.

4T’s: T cells, Transplant rejections, TB skin tests, Touching (contact dermatitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Explain the allergic/anaphylactic reaction to blood transfusion? sx? timing?

A

Type I hypersensitivity reaction against plasma proteins in transfused blood. IgA deficient individuals must receive blood products without IgA.

Sx/ Urticaria, pruritus, fever, wheezing, hypotension, respiratory arrest, shock.

Within minutes to 2-3 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Explain acute hemolytic transfusion reaction? What type of HS? Sx? timeline?

A
  • *Type II hypersensitivity reaction.**
  • *Intravascular hemolysis** (ABO blood group incompatibility) or extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs).

Sx/Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinuria (intravascular hemolysis), jaundice (extravascular).

Within 1 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Explain mech of febrile non hemolytic transfusion reaction?

A

febrile non hemolytic transfusion reaction:

Two known mechanisms: most likely induced by cytokines that are created and accumulate during the storage of blood products; or associated with type II hypersensitivity reaction with host antibodies directed against donor HLA and WBCs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Sx and timeline of febrile nonhemolytic transfusion rxn?

A

sx/ Fever, headaches, chills, flushing. Reaction prevented by leukoreduction of blood products.

Within 1-6 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Transfusion related acute lung injury - mech and sx? timeline?

A

Transfusion related acute lung injury :

Donor anti-leukocyte antibodies against recipient neutrophils and pulmonary endothelial cells.

sx/ respiratory distress and noncardiogenic pulmonary edema

within 6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

X-linked (Bruton) agammaglobulinemia

A

Defect in BTK, a tyrosine kinase gene Ž no B-cell maturation. X-linked recessive (Inc in Boys).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What disease leads to inc susceptibility to giardiasis?

A

Selective IgA def

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Presents after age 2, with risk of autoimmune disease, bronchiectasis, lymphoma and sinopulm infections

A

CVID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Dec immunoglobulins on blood work - of any type

A

X linked agammaglobulinemia - no B cell maturation

CVID - no B cell differ’n

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pt has no lymph nodes or tonsils - primary follicles and germinal centers absent

A

X linked agammaglobulinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Which immunodef can present with hypocalcemia? why? whats the sx?

A

Thymic aplasia - ex/DiGeorge syndrome bc of No PTH hormone –> leads to tetany

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Disease that has deficiency of cells that produce IL17, IL21, IL 22?

A

Hyper IgE - def of Th17 cells

61
Q

Disease with defects in self antigen expression in the thymus

A

Chronic mucocutaneous candidiasis - defect in Auto Immune Regulator (AIRE)

62
Q

What embryonic structure fails to develop in thymic aplasia?

A

3rd & 4th pharyngeal pouches

63
Q

Sx of DiGeorge and Velocardiofacial syndrome?

A

DiGeorge syndrome—thymic, parathyroid, cardiac defects.

Velocardiofacial syndrome— palate, facial, cardiac defects

CATCH-22: Cardiac defects (conotruncal abnormalities [eg, tetralogy of Fallot, truncus arteriosus]), Abnormal facies, Thymic hypoplasia Ž T-cell deficiency (recurrent viral/ fungal infections), Cleft palate, Hypocalcemia 2° to parathyroid aplasia –> tetany.

64
Q

Presentation of selective IgA def?

A

Majority Asymptomatic. Can see Airway and GI infections, Autoimmune disease, Atopy, Anaphylaxis to IgA-containing products.

65
Q

Why won’t you see immediate issues with X linked agammaglobulinemia?

A

They are protected by maternal IgG for the first 6 months

66
Q

What receptor def leads to dec Th1 response?

A

IL 12 R def

Remember, IL 12 causes Th–> Th1 cells

67
Q

Present with dec IFN-gamma/

A

IL 12 R def

Bc IL 12 (+) Th –> Th1 cells and Th1 cells prod IFN y (& IL 2)

68
Q

Child presents with facial deformities, eczema, bone fractures, and still has his baby teeth?

A

Autosomal dominant hyper-IgE syndrome (Job syndrome)

Cold (noninflamed) staphylococcal Abscesses, retained Baby teeth, Coarse facies, Dermatologic problems (eczema), Inc IgE, bone Fractures from minor trauma. Learn the ABCDEF’s to get a Job!

69
Q

Leads to noninvasive candida albicans infections of skin and mucuos membranes?

A

Chronic mucocutaneous candidiasis

70
Q

Chronic mucocutaneous candidiasis is a dysfunction of what part of the immune system?

A

T cells

71
Q

Due to STAT3 mutation?

A

Autosomal dominant hyper-IgE syndrome (Job syndrome)

72
Q

Cerebellar defects, spider angiomas, and IgA def?

A

Ataxia-telangiectasia

73
Q

Genetic Issue in Ataxia-telangiectasia? MoI?

A

Defects in ATM gene –> failure to detect DNA damage –> failure to halt progression of cell cycle –> mutations accumulate;
autosomal recessive

74
Q

Blood findings in ataxia telangiectasia?

A

Inc AFP. dec IgA, IgG, and IgE

75
Q

Ataxia telangiectasia - risk of developing which disease?

A

Inc risk of lymphoma and leukemia

76
Q

Due to defect in CD40L on Th cells?

A

Hyper-IgM syndrome

77
Q

Which immune def are X linked rec ?

A

Hyper IgM syndrome, Wiskott Aldrich syndrome, Chronic granulomatous disease, Bruton agammaglobulinemia, SCID (defective IL-2R gamma chain)

78
Q

Due to failure to detect DNA damage?

A

Ataxia telangiectasia

79
Q

Diseases seen with Hyper-IgM syndrome?

A

Severe pyogenic infections early in life; opportunistic infection with Pneumocystis, Cryptosporidium, CMV

80
Q

Findings in Hyper IgM syndrome?

A

Normal or Inc IgM. DEC IgG, IgA, IgE. Failure to make germinal centers

81
Q

Underlying issue in Wiskott Aldrich syndrome?

A

Mutation in WAS gene; leukocytes and platelets unable to reorganize actin cytoskeleton –> defective antigen presentation

82
Q

Sx of Wiskott Aldrich?

A

WATER: Wiskott-Aldrich: Thrombocytopenia, Eczema, Recurrent (pyogenic) infections.

83
Q

Lab findings of Wiskott Aldrich syndrome?

A

dec to normal IgG, IgM.

Inc IgE, IgA.

Fewer and smaller platelets

84
Q

Defect in CD18?

A

Leukocyte Adhesion def - Defect in LFA-1 integrin aka CD18

85
Q

1st sx of Leukocyte adhesion def?

A

umbilical stump takes a long time to fall off

86
Q

T or F - there is no pus in bacterial infections with LAD type 1

A

True!

87
Q

Defect in LFA-1 integrin protein? - what’s the consequence?

A

Leukocyte adhesion def - leads to impaired migration and chemotaxis

88
Q

Lab findings with Leukocyte adhesion def?

A

Inc neutrophils in blood. Absence of neutrophils at infection sites.

89
Q

Defect in lysosomal trafficking regulator gene? What does it lead to?

A

Chédiak-Higashi syndrome
Defect in lysosomal trafficking regulator gene (LYST). Microtubule dysfunction in phagosome-lysosome fusion;

90
Q

Sx of Chediak Higashi?

A

PLAIN: Progressive neurodegeneration, Lymphohistiocytosis, Albinism (partial), recurrent pyogenic Infections, peripheral Neuropathy.

Note that there’s no pus in LAD, and this has pus errrrryyywhere

91
Q

Giant granules in granulocytes and platelets + pancytopenia + coag issues

A

Chédiak-Higashi syndrome

92
Q

High neutrophils in the blood, but none at infection sites?

A

LAD 1

93
Q

Defect in NADPH oxidase?

A

Chronic granulomatous disease.

94
Q

Lab test for chronic granulomatous disease?

A

Abnormal dihydrorhodamine (flow cytometry) test (dec green fluorescence). Nitroblue tetrazolium dye reduction test (obsolete) fails to turn blue

95
Q

Which immune def has issues with class switching?

A

Hyper IgM syndrome

96
Q

Patients with Hyper IgM are more prone to which infections?

A

opportunistic infection with Pneumocystis, Cryptosporidium, CMV.

97
Q

If you have dec T cells, then what diseases are you more prone to?

A
98
Q

If you have dec B cells, you’re more prone to which infections?

A
99
Q

Dec granulocytes leads to which infections?

A

Some Bacteria Produce No Serious granules

100
Q

Dec complement leads one to be prone to which STI?

A

Neisseria

101
Q

What happens in hyperacute transplant rejection? Timeline?

A

Within min!!

Pre-existing recipient antibodies react to donor antigen (type II hypersensitivity reaction), activate complement.
Widespread thrombosis of graft vessels (arrows within glomerulus A) –> ischemia/necrosis. Graft must be removed.

102
Q

Cellular vs Humoral acute transplant rejection?

A

Cellular: CD8+ T cells and/ or CD4+ T cells activated against donor MHCs (type IV hypersensitivity reaction).

Humoral: similar to hyperacute, except antibodies develop after transplant.

103
Q

If a patient is non compliant with their immunosuppressant meds post transplant - what will one see within weeks/months of their body histologically?

A

Vasculitis of graft vessels with dense interstitial lymphocytic cellular infiltrate

104
Q

Chronic transplant rejection is due to which hypersensitivity reaction?

A

Both type II and IV hypersensitivity reactions

105
Q

Pathogenesis of Chronic transplant rejection?

A

CD4+ T cells respond to recipient APCs presenting donor peptides, including allogeneic MHC

106
Q

What is the major patho feature of Chronic transplant rejection? why? ex?

A

Arteriosclerosis

Recipient T cells react and secrete cytokines –> proliferation of vascular smooth muscle, parenchymal atrophy, interstitial fibrosis.

Organ-specific examples: ƒ Bronchiolitis obliterans (lung) ƒ Accelerated atherosclerosis (heart) ƒ Chronic graft nephropathy (kidney) ƒ Vanishing bile duct syndrome (liver)

107
Q

Why are GVH disease more likely in bone marrow or liver transplant pt?

A

bc liver and bone marrow ( from the donor) is rich in lymphocytes

108
Q

Type of HS rxn in G v H disease? explain pathogenesis

A

HS-IV -

Grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with “foreign” proteins –> severe organ dysfunction.

109
Q

Pt presents post liver transplant with maculopapular rash, jaundice, and diarrhea - How does his liver look like histologically?

A

NORMAL!

It is the immunocompent T cells from the graft that attacks the host - so the transplanted liver itself will not be affected.

110
Q

Pathogenesis of Graft v Host disease?

A

Grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with “foreign” proteins Ž severe organ dysfunction

111
Q

2 drugs that (-) IL2 transcription? How does that immunosuppress?

A

Cyclosporine, Tacrolimus - (-) IL2 transcription blocks T cell activation

112
Q

Uses of Cyclosporine/Tacrolimus?

A

RA and Psoriasis

113
Q

Toxicity of Cyclosporine vs tacrolimus?

A

Cyclosporin - Nephrotox, hypertension, hyperlipidemia, neurotoxicity, gingival hyperplasia, hirsutism.

Tacrolimus - similar, but no gingival hyperplasia/hirsutism

114
Q

Another drug that has gingival hyperplasia as SE?

A

Phenytoin, CCB

Can Cause Puffy gums

115
Q

How does mech of action of Tacrolimus compare to Sirolimus?

A

Both block T cell activation, but Tacrolimus blocks transcription of IL 2 and Sirolimus (-) IL 2 response, so also stops B cells differentiation

116
Q

SE/ of Sirolimus?

A

Pansirtopenia (pancytopenia), insulin resistance, hyperlipidemia; not nephrotoxic.

117
Q

MoA of Basiliximab?

A

blocks IL2 -R

118
Q

SE/ of Basiliximab?

A

edema, HTN, tremor

119
Q

AZT toxicity is increased with the addition of what drug?

A

6-MP degraded by xanthine oxidase; toxicity inc by allopurinol.

120
Q

MoA of AZT? SE/

A

Antimetabolite precursor of 6-mercaptopurine. Inhibits lymphocyte proliferation by blocking nucleotide synthesis.
SE/pancytopenia

121
Q

MoA of mycophenolate?

A

Reversibly inhibits IMP dehydrogenase, preventing purine synthesis of B and T cells.

122
Q

Another rx that (-) IMP DH?

A

Ribavirin

123
Q

SE of Mycophenolate?

A

GI upset, pancytopenia, hypertension, hyperglycemia. Less nephrotoxic and neurotoxic

124
Q

Mycophenolate is associated with infections with which virus?

A

CMV

125
Q

Glucocorticoids MoA?

A

Inhibit NF-κB. Suppress both B- and T-cell function by dec transcription of many cytokines. Induce T cell apoptosis

126
Q

Major side effect if you stop glucocorticoids abruptly after chronic use?

A

adrenal insufficiency

127
Q

SE/ of glucocorticoids?

A

Cushing syndrome, osteoporosis, hyperglycemia, diabetes, amenorrhea, adrenocortical atrophy, peptic ulcers, psychosis, cataracts, avascular necrosis (femoral head).

128
Q
A
129
Q

When do we use EPO analogs? name?

A

Epoetin alfa - Anemias with renal failure

130
Q

Rx used in Leukopenia

A

Filgrastim (G-CSF), Sargramostim (GM-CSF)

131
Q

Recombinant thrombopoietin?

A

Romiplostim (TPO analog), eltrombopag (TPO receptor agonist)

132
Q

Aldesleukin is recombinant what? used when?

A

IL-2, used in Renal cell carcinoma, metastatic melanoma

133
Q

IFN alpha used in?

A

Chronic hepatitis C (not preferred) and B, renal cell carcinoma

134
Q

IFN beta is used for?

A

Multiple sclerosis

135
Q

IFN gamma used when?

A

Chronic granulomatous disease

136
Q

Target of Alemtuzumab? used when?

A

CD52; CLL, MS

“Alymtuzumab”—chronic lymphocytic leukemia

137
Q

Target and use of Bevacizumab?

A

VEGF

Colorectal cancer, renal cell carcinoma, non-small cell lung cancer
Also used for neovascular agerelated macular degeneration, proliferative diabetic retinopathy, and macular edema

138
Q

Target and use of Rituximab?

A

CD20 B-cell non-Hodgkin lymphoma, CLL, rheumatoid arthritis, ITP, MS
Risk of PML in patients with JC virus

Ri2Ximab

139
Q

Target and use of Trastuzumab?

A

HER2;

Breast cancer, gastric cancer HER2—“tras2zumab”

That’s theirs - I prefer Titstuzumab

140
Q

Diff between adalimumab and etanercept?

A

Etanercept is a decoy TNF alpha R, not a mAb

141
Q

Clinical use of adalimumab and infliximab?

A

RA, IBD, Ankylosing spondylitis, psoriasis

Adali (Ideally), you should be more flexible (Inflixi) with inflammatory diseases.

142
Q

Eculizumab - target and use?

A

C5, PNH

Excuse me (Eculi), I pee red at night

Eculi - EC –> 5th letter, and C = C5

143
Q

Natalizumab - target and disease?

A

α4-integrin, MS & Crohn disease

Natali has A+ integrity

144
Q

Ustekinumab - target/use?

A

IL-12, IL-23

Psoriasis, Psoriatic arthritis

145
Q

Abciximab - target/use?

A

Platelet glycoproteins IIb/IIIa

Antiplatelet agent for prevention of ischemic complications in patients undergoing percutaneous coronary intervention

ABC is as easy as 123

146
Q

Denosumab - target/use?

A

RANKL

Osteoporosis; inhibits osteoclast maturation (mimics osteoprotegerin)

Denosumab helps make dense bones

147
Q

Omalizumab

A

IgE

Refractory allergic asthma; prevents IgE binding to FcεRI

OMygod - my allergies are bad!

148
Q

Palivizumab - target/use?

A

RSV F protein

RSV prophylaxis for high-risk infants
PaliVIzumab—VIrus

149
Q
A

Step 1 2019 First Aid Flashcards (63 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions