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MMI133 > MMI133_Lecture11 > Flashcards

MMI133_Lecture11 Flashcards

1
Q

Hypersensitivity

A

immune system goes haywire/doesn;t work properly

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2
Q

4 types of hypersensitivity

A

Type 1: Allergy
- localized or general anaphylaxix/shock
IgE mediated
Type 2: Cytotoxic
- blood attacks
Type 3: Immune complex mediated
Type 4: Delayed cell-mediated

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3
Q

all hypersensitivity reactions that cause tissue damage require

A

previous exposure to antigen/allergen

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4
Q

Type 1 Reactions

A

localized - hives/ urticaria
hay fever, allergic rhinitis

systemic or general
shock, need epi-pen, peanut allergies

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5
Q

Type 1 reactions phases

A
  1. sensitization - result of classical antigen presntation with T helper cell involvement + B cell activation
  2. activation - cross linking of at least 2 IgE molecules bound to Fc receptors on mast cell - triggers mast cell/basophil degranulation
  3. effector
    - phase 1 primary mediators released - histamine, eosinophil, chemotactic factor, neutrophilchemotactic factor, proteases
    - phase 2 secondary mediators released leukotrienes + prostaglandins
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6
Q

the only type of hypersensitivity with no antibodies involved is

A

type 4 - delayed cell-mediated

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7
Q

type 1 systemic reactions

A

immediate reaction (minutes)
life threatening impaired breathing to swelling of airways
uterine cramps, involuntary urination/defecation = due to smooth muscle contraction
edema from fluid leaking into tissue spaces
blood pressure drops leading to life-threatening anaphylactic shock bec BV’s widen and blood leaks out

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8
Q

mediators from primarily mast cells + basophils

A

histamine + other lipid moelcs + cytokines

collectively act to:
- inc permeability + dilate BV’s - lead to edema + erythema/redness
- inc mucus secretion + contract smooth muscle

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9
Q

treatment of anaphylaxis

A

antihistamines to block action of histamine

epinephrine (epi-pen) - to contrict BV’s + raise BP
dilates air passages in lunges, effects smooth muscles

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10
Q

Type 2 cytotoxic reactiosn

A

due to diff blood types having diff antigens on their surfaces, getting anoth kind of blood that has diff antigens and teh immune system sees the blood as non-self and attacks + kills RBC - leads to hemolysis of RBC’s

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11
Q

blood type A has

A

anti B antigens

compatable blood types are A + O

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12
Q

blood type B has

A

anti A antigens

compatable blood types are B + O

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13
Q

AB blood type has

A

no antibodies in plasma

compatable blood types: A, B, AB, O

universal recipient - can get anything

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14
Q

O blood type has

A

anti A + anti B antibodies and no antigens

compatable blood types are O

it is the universal donor, but can only accept O blood types

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15
Q

key components of type 2

A

complement system
cell-bound antigens
antibodies IgG + IgM

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16
Q

HDN = hemolytic disease of newborn = blue baby

A

mother Rh- baby Rh+
with first baby, mother is exposed to Rh+ blood which has D+ antigen, so mother becomes sensitized to that antigen + immune system produces D+ antibodies

next baby, more baby blood leaks into mum, mum’s antibodies are small enough to get into placenta + attack baby blood + cause hemolysis of baby’s blood, results in baby with less blood + annemia + at risk of respiratory issues + bad for baby maybe death
ne

17
Q

baby blue

A

not enough o2 due to hemolysis

18
Q

prevention of Rh sensitization as treatment to prevent hymolytic disease of newborn

A

rhogam administration to Rh- mothers before + after delivery
to rapidly eliminate fetal Rh+ RBC’s from maternal circulation + hide them from mothers immune system
prevents maternal B cell activation against Rh antigens

19
Q

Type 3 Immune complex mediated

A

immune complex binds to endothelium then activates complement which generates chemoattractants for neutrophils which arrive then release their granules + enzymes to damage tissue

poststreptococcal glomerulonephritis or SLE
immune complex deposition is typically in skin, joints, + kidney (glomerular basement membrane)

immune complex AB+AG circulate in blood circulation which is called soluble

20
Q

Type 4 delayed cell mediated reaction

A

no antibodies involved
takes several days to develop
T cells involved
poison oak + ivy
Tb tests
Th1 cells + macrophages
requires previous exposure + presence of T memory cells

principal effector cell is activated macrophages which release lytic enzymes that cause local tissue destruction

mechanisms of tissue destruction: cytotoxic T lymphocytes induced by Th1 cells to assist in tissue damage

21
Q

allergic response of type 4 delayed cell mediated

A

contact dermatitis
triggered by poison oak + ivy
oils from plant act as haptens binding to skin proteins
complexes are presented by skin dendritic cells to Th1 cells initiating immune response

treatment with corticosteroids for contact dermatitis immunosuppressive drugs including cortisone for transplant rejection

22
Q

other type 4 reactions

A

tuberculin test: assesses immune response to Tb
transplant rejection: immune reaction against foreign tissues

23
Q

how does Tuberculin skin test work?

A

determines prev exposure to TB by Iding memory cells reactive to TB antigens
widesly used in NA bec not many people immunized against TB

cell mediated reaction type 4
involves infiltration of lymphocytes + macrophages due to mobilization by pre-existing memory cells

24
Q

limitations of tuberculin tests

A

inapplicaability to certain pops
anergic individs are unresponsive to immune stimuli like AIDS
immunosuppressed patients won’t react redictably to test which can make it unreliable

lack of specificity
those vacc with BCG vax give false positives

25
Q

quantiFERON-TB Gold test

A

tests for memory cells + activated T lymphocytes thru interferon production

helps confirm + rule out latent TB + active tb + prev BCG effects,
pateints don’t need to go back to have it read
requires blood sample to be processed within 12 hrs
deals with BCG effects

26
Q

caparison of hypersensitivty reactions

A

type 1: IgE, exogenous antigen, 15-30 min response, wheal + flare, mast cells, allergic asthma, hay fever

type 2: IgG, IgM, cell bound antigen, min-hrs response, lysis + necrosis, no cells, arythroblastosis foetalis HDN

type 3: IgG, IgM, soluble antigen, 3-8 hrs response, erythema, edema, necrosis, no cells, SLE, farmer’s lung

type 4: no antibodies, tissues + organs antigens, 48-72 hrs, erythema, induration, T-cells + macrophages, Tb test, poison ivy, granuloma

27
Q

jenner observed that milkmaids who contracted cowpox were immune to more severe

A

smallpox disease

28
Q

types of vaccines

A

attenuated whole-agent

inactivated whole-agent/subunit

toxoids

conjugated

nucleic acid (DNA or RNA)

29
Q

Attenuated whole agent vaccines

A

live attenuated vaccines with weakned microbes that mimic real infections

95% effective often providing life-long immunity
stimulates both humoral antibody + cell-mediated immunity + creates memory cells

Sabin (polio)
MMRV (measles, mumps, rubella, varicella)

risk of mutation back to virulent form
can’t use for immunocompromised or pregnant women

30
Q

inactivated + subunit vaccines

A

use killed whole microbes or parts of organisms like glycoproteins

rabies, salk (polio), influenza, gardasil, hepatitis B

safe for immunocompromised + preg women
no risk of reverting back to wild-type

limited cell-mediated immunity no CD8+ response, shorter lasting immunity
stimulates B cell memory, needs boosters

31
Q

toxoids

A

toxin isolated + chemically treated to preserve autigenicity but make toxin non-functional
toxoid used as vax to produce antibodies to toxin not microbe - only humoral immunity
requires boosters for full immunity

diphtheria tetanus

32
Q

conjugated vaccines

A

for organisms with polysaccharide capsules, poor antigens
doesn’t work for children <2yrs

polysaccharides from capsules are combined with a protein which is highly immunogenic which fools immune system into reacting to protein + get immunity to carbohydrates

Haemophilus influenzae type b
Neisseria meningitidis
Streptococcus pneumoniae

33
Q

Nucleic acid vaccines

A

DNA vaccines: gene from organisms into human host cell to get transcribed
covid Astra-Zeneca + johnson/johnson vax

RNA: changed mRNA + produce protein that stimulates our usual adaptive immune system. leaves cells within 3 wks
works 95% effectivity, needs boosters
Pfizer + Moderna

34
Q

what is vax controversy all about

A

MMR causes autism
too many vax for infant immune systems to handle
toxic chemicals used to preserve vax
use of fetal cells for growing (TRUE) virus used in vax
too many vax for baby to tolerate
natural infection produces better immunity + makes immune system stronger

35
Q

naturally acquired active immunity

A

indiv exposed to antigens in course of daily life where clinical or subclinical infectiosn can confer immunity
child gets chickenpox

36
Q

naturally acquired passive immunity

A

natural transfer of antibodies
maternal transfer of IgG antibodies over placenta
IgA antibodies in mothers’s breast milk

37
Q

artificially acquired active immunity

A

result of vax, where specialized prepared antigens (vaccines) are introduced into body
susbstances are altered so that they can no longer cause disease, but can stimulate an immune response
immunity after mump vaccine

38
Q

artificially acquired passive immunity

A

involves introduction of antibodies form an animal or person who is already immune tot eh disease
varicella immunoglobulin given after exposure of unimmunized person to varicell (antibodies pooled from blood donor sera)

39
Q

the tuberculin test is

A

not a vax, but a diagnostic test using the type 4 hypersensitivity reaction to gauge patient exposure

MMI133 (16 decks)

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