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Pathophysiology > Exam 2: Ch 16 > Flashcards

Exam 2: Ch 16 Flashcards

1
Q

4 types of hypersensitivity disorder

A

type 1: allergic reactions

type 2: antibody-mediated disorders

type 3: immune complex mediated disorders

type 4: cell mediated disorders

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2
Q

type 1: allergic reactions 2 subtypes

A

local (atopic) reactions

systemic (anaphylactic) reactions

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3
Q

when do type 1 allergic reactions begin

A

almost immediately after exposure to allergen

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4
Q

allergens are usually what type of molecule

A

proteins

pollen, food, animal dander, dust mites

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5
Q

immune system response to type 1: allergens

A

processed by macrophages

T helper cells (CD4) release cytokines which stimulate plasma cells to make and release IgE antibodies

IgE binds to mast cells (sensitized like memory cells)

hours later, esinophils recruited

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6
Q

mast cells that have been sensitized…

A

degranulate on subsequent exposure

release histamine, cytokines, etc

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7
Q

symptoms of type 1: allergic rxns

A

vasodilation

smooth muscle contraction

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8
Q

anaphylactic reaction (systemic)

A

can produce shock

must stabilize airway and give epi

prevent exposure, wear bracelet

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9
Q

local (atopic) allergic rxn examples

A

hives

dermatitis

hay fever

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10
Q

esinophils can also fight off _____

A

parasites

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11
Q

type 2: Ab mediated description

A

IgG or IgM mediated

directed against antigens on cell surfaces or in conn. tissue

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12
Q

3 types of type 2: Ab mediated

A

complement & Ab mediated cell destruction

complement & Ab mediated inflammation

Ab mediated cell dysfunction

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13
Q

complement & Ab mediated cell destruction

A

Ab coat abnormal cells

cells killed by complement system or phagocytosis

ex. blood transfusion rxn

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14
Q

complement & Ab mediated inflammation

A

Ab coat abnormal cells or react with extracellular proteins

complement activated –> chemotaxic factors

monocytes and neutrophils recruited

causes inflammation and tissue damage

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15
Q

examples of complement & Ab mediated inflammation

A

Goodpasture syndrome

glomerulonephritis and pulmonary hemorrhage from basement memb. inflammation

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16
Q

Ab mediated cell dysfunction

A

Ab inactivate/destroy or activate cells (receptors)

ex. Graves disease: Ab activate TSHr (hyperthyroidism)

Myasthenia Gravis: Ab inactivate AChr

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17
Q

type 3: immune complex mediated disorders

A

antigen-Ab complexes form in circulation and activate complement

inflammation and damage within blood vessels

ex. allergic rxns to drugs or food

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18
Q

type 4: cell mediated disorders

A

antigen presented to CD4 by APC

CD4 activates CD8 –> kill target cells w/ antigen

common response to intracellular parasites and part of autoimmune diseases

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19
Q

type 4 can also produce…

A

a delayed hypersensitivity rxn

CD4 secretes cytokines that recruit lymphocytes

inflammation results

ex. contact dermatitis, pneumonitis from inhaled antigens

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20
Q

HLA/MHC

A

human leukocyte antigen/major histocompatibility complex

antigens on surface of all body cells, individual specific

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21
Q

transplantation

A

taking tissue from 1 person and giving it to another

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22
Q

rejection

A

recipient’s (host) immune system sees donor HLAs as foreign and attacks the graft

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23
Q

autologous graft

A

donor & recipient are the same person

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24
Q

syngenic graft

A

donor and recipient are identical twins

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25
Q

allogenic graft

A

donor and recipient differ genetically

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26
Q

allograft rejection

A

host immune system recognizes graft antigens on organ surface or APCs

activates CD4 –> CD8 –> type 4 rxn

Ab may contribute

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27
Q

3 patterns of rejection

A

hyper acute

acute

chronic

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28
Q

hyper acute rejection

A

almost immediate type 3 rxn

results from preexisting Ab from previous blood transfusions

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29
Q

acute rejection

A

within months

involves T cells

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30
Q

chronic rejection

A

may involve fibrosis

cytokines

takes time

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31
Q

graft vs. host disease

A

most common following bone marrow transplant

graft attacks the host’s organs

host’s immune system compromised and can’t destroy graft

produces rash, GI sloughing, organ (liver) failure

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32
Q

what is an autoimmune disease

A

when the immune system attacks self

organ-specific or systemic

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33
Q

examples of organ-specific autoimmune diseases

A

thyrotoxicosis (Graves): TSH

pernicious anemia

Hashimoto thyroiditis

Addison’s disease

34
Q

examples of systemic autoimmune diseases

A

lupus

scleroderma

rheumatoid arthritis

ulcerative colitis

35
Q

immune tolerance

A

immune system “tolerates” self, only attacks foreign antigen

develops in fetal development

36
Q

central tolerance

A

T cells reacting against self are eliminated in thymus

37
Q

peripheral tolerance

A

immune cells including B cells that react against self are eliminated in the lymph organs

38
Q

genetic susceptibility to autoimmune disease

A

families with specific HLAs prone

not everyone with HLA type gets disease, mechanism unclear

39
Q

environmental factors of autoimmune disease (mechanisms)

A

T cells active against self when co-stimulators present

self-antigens that were held during development are released, prompting an immune response

molecular mimicry: microbe has antigen similar to self

super-antigens on microbes stim T cells w/o processing and binding to normal receptors

40
Q

diagnosis of autoimmune disease

A

assay for Ab in patients with symptoms (fever, rash, inflammation)

41
Q

treatment of autoimmune disease

A

steroids

immunosuppressants

42
Q

primary immunodeficiency disorders

A

inherited or congenital – most recessive and x-linked

some traced to cytokines/signaling pathways

warning signs: multiple infections

many types

43
Q

some signs of primary immunodeficiency disorders

A

8+ ear infections in a year

2+ sinus infections in a year

2+ pneumonia in a year

2+ deep-seated infections

2+ months on antibiotics that doesn’t help

44
Q

b-cell immunodeficiency

A

most common primary immunodeficiency

stem cells –> pre-B in marrow –> lymph tissue maturation

mature B cells make specific Ab –> plasma cells when stim

45
Q

transient hypogammaglobuinemia of infancy

A

delayed production of IgG –> multiple respiratory infections

usually resolves spontaneously

(infants protected by maternal IgG until 6mo of age)

46
Q

X-linked agammaglobulinemia

A

recessive, more common in males

bruton tyrosine kinase needed for pre-B maturation

symptoms at 6-9mo, respond poorly to antibiotics

Rx: IVIG (intravenous immunoglobulin)

47
Q

common variable immunodeficiency

A

differentiation of B cells to plasma cells blocked (affects 1+ types)

symptoms in teens to early adult

48
Q

immunoglobulin G deficiency

A

respiratory infections

IVIG

49
Q

T-cell immunodeficiency

A

more severe than B-cell deficiency

DiGeorge syndrome (thymic hypoplasia)

50
Q

DiGeorge syndrome (thymic hypoplasia)

A

T-cell deficiency

developmental defect of thymus and parathyroid

associated w/ facial and cardiac defects

extent of defect variable

51
Q

SCID severe combined immunodeficiency disorders

A

most x-linked and recessive, more common in males

survival rate w/o bone marrow transplantation

1 type: T, B, NK cells deficient

2nd type: T, NK, CD4 cells deficient, B cells elevated, Ab production abnomal,

52
Q

AIDS is caused by ___ infection

A

HIV

34m ppl living, 1.7m died, 2.5m get it

most new infections in underdeveloped countries

sub-sarahan africa, racial minorities in US

recognized in 1981, IDed in 1984

53
Q

transmission of HIV

A

sexual contact: body fluid contact w/ mucosa or open sore

blood to blood contact: shared needles

perinatal transmission: in utero or during delivery

occupational

54
Q

seroconversion

A

when HIV Ab develop and become detectable

1-6 mo after infection

55
Q

HIV virus structure

A

HIV 1 & 2 (1 most common in US & europe, 2 in africa)

retrovirus (RNA)–core surrounded by lipid envelope

2 copies of RNA in core, p24 protein (target of Ab screen) and p17 protein (surrounds core)

3 enzymes: Rev. transcriptase, integrase, protease

56
Q

enzyme order HIV

A

reverse transcriptase (transcribes RNA into dsDNA)

integrase (dsDNA integrated into CD4 genome)

(transcription, translation happens)

protease (breaks polyprotein into pieces)

new virus built from pieces and HIV released from cell

57
Q

HIV infects which type of cells

A

CD4–binds to receptors and other surface molecules (CCR5)

requires glycoproteins gp120, gp41

virus memb. fuses to CD4 so RNA and enzymes can enter cell

58
Q

HIV replication starts at…

A

site of infection

many CD4 cells infected by day 10

people with HIV generally asymptomatic until CD4 count falls

59
Q

classification of HIV phases

A

HIV+ said to have AIDS if:

CD4 count less than 200cells/microliter

or have an AIDS-defining illness

60
Q

HIV stage 1 and 2 and 3 (AIDS)

A

T cells greater than or equal to 500

2: T cells between 200-499
3: T cells less than 200

61
Q

primary HIV infection

A

mono-like symptoms (fever, fatigue, myalgia, sore throat)

viral replication rapid

CD4 count falls

treatment beneficial

62
Q

latent period of HIV infection

A

viral load is low, but CD4 count falls over time

lymphadenopathy develops

63
Q

overt AIDS

A

viral load climbs

CD4 count less than 200/ul or AIDS-defining illness

opportunistic infections and cancer develops

64
Q

what is the leading cause of death for AIDS

A

TB

65
Q

respiratory manifestations of AIDS

A

pneumocystis pneumonia (fungal spores)

common pneumonia like strep, pseudomonas, H flu

PCP–less common since HAART

mycobacterium TB: multiple drug resistant strains

66
Q

GI manifestations of AIDS

A

esophageal candidiasis

herpes simplex (esophageal)

gastroenteritis: protozoal or bacterial (stool culture)

67
Q

NS manifestations of AIDS

A

HIV-associated neurocognitive disorders (HAND)
cognitive and motor impairment

toxoplasmosis: parasitic brain infection
antibiotics

68
Q

Kaposi sarcoma

A

endothelial cell malignanacy in AIDS

opportunistic cancer linked to herpes

lesions on skin and in mouth, in internal organs (lungs)

HAART may be effective

69
Q

non-hodgkin lymphoma

A

AIDS cancer

may undergo remission with HAART

70
Q

cervical and anal carcinoma

A

AIDS cancer

from HPV

71
Q

wasting syndrome

A

AIDS

weight loss, diarrhea, chronic weakness, fever

Rx: appetite stimulants

72
Q

3 metabolic disorders associated with AIDS

A

insulin resistance

hypercholesterolemia/triglyceridemia

lipohypertrophy

might need to switch anti-retroviral drugs

73
Q

insulin resistance (AIDS)

A

higher among those with HIV

medications may contribute to development

74
Q

hypercholesterolemia/triglyceridemia

A

HIV and medications contribute to development

monitor lipids closely

use statins with caution

75
Q

lipohypertrophy

A

buffalo hump right below back of neck

76
Q

prevention of HIV infection

A

condoms

avoid recreational drug use, sharing needles

routine screening

education

77
Q

diagnosis of HIV

A

HIV Ab test: ELISA + western blot if initial is ( + )

western blot is more specific (less false pos)

oral swab for at home use (both ELISA and western blot)

PCR: detects HIV, not Ab (used earlier)

78
Q

HAART

A

combination of 2 or 3 anti-retroviral drugs

reverse transcriptase inhibitors

protease inhibitors

entry inhibitors

integrase inhibitors

79
Q

reverse transcriptase inhibitors

A

block RNA –> DNA conversion

block elongation of DNA by adding fake nucleotide or inhibit enzyme

80
Q

integrase inhibitors

A

prevent integration of viral cDNA into cell genome

81
Q

protease inhibitors

A

block cleavage of viral proteins by binding and inhibiting enzyme

82
Q

entry inhibitors

A

prevent HIV from binding to or entering CD4 cells

Pathophysiology (24 decks)

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