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Infection and Immunology > Antiinflammatory Drugs + Immune Rxn's > Flashcards

Antiinflammatory Drugs + Immune Rxn's Flashcards

1
Q

3 stages of inflammation

A
  1. acute 1-3 days hot, red, and painful
  2. subacute 3 days - 1 month–cleaning
  3. chronic–month-years
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2
Q

plasma transporter of iron

A

Transferrin

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3
Q

clotting factor

A

Fibrinogen (can lead to clotting disorder)

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4
Q

in the hypothalamus, prostaglandins stimulte the production of nt’s which function to reset the temp set point at a higher leverl

A

Fever

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5
Q

damage to cells releases cytokines i.e. (4) that ______ and ______ local immune cells to site

A

chemokines, interferon, interleukins, TNF,–

attract and activate

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6
Q

Steps of inflammation

A
  1. injury occurs–invasion of organism
  2. Activation of local macrophages
  3. biochemical messages released (part of step 2)
  4. Dendritic cells = ^ espionage (gain info) and responses
  5. Arrival of killer T cells (specialized for viruses)
  6. Return to homeostasis
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7
Q

step 3 of inflammation

A

red, warm, edema, pain

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8
Q

T-cells kill by
neutrophils (earliest) kill by
dendritic cells kill by

A
  • instructed cell death–apoptosis
  • phagocytosis & degranulation & creates net (*bacteria)
  • phagocytosis
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9
Q
  • Inflammation can be (2) + cell mediators
A

acute (neutrophil mediated) vs.

chronic (monocyte, macro, lymphocyte mediated)

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10
Q

in phase 6 of inflammation–the tissue engineers are_____, may lead to ______ as after ab surgery

A

fibroblasts,

adhesions

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11
Q

chronic inflammation is often ______ and ________–usually due to overactive fibroblasts

A

severe and progressive

“SMOLDERING”

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12
Q

Acute inflammation is usually ____ and ___-______–local S&Ss are often _____

A

mild and self-limited,

prominent

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13
Q

inflammation is associated w/

A

almost every disease–get used to it

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14
Q

a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages w/ scattered lymphocytes (walling off isolated foreign materials and debris) i.e TB, Syphilis

A

Granulomatous inflammation (a type of chronic inflammation)

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15
Q

Systemic S&S of inflammation (3) PROSTAGLANDINS

A
  1. Fever (hypothalamus–adjusted “set-point”)
  2. Production of acute-phase proteins (C-reactive)
  3. Leukocytosis (^ WBCs)
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16
Q

the process of inflammation is fundamental to virtually…

A

all of clinical medicine!!!!!

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17
Q

leukocytosis in common to inflammatory rxn’s–esp those induced by ________

A

bacteria

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18
Q
  • Plasma levels of _______ and _______ raise dramatically during inflammation–produced by LIVER–checked via “Sed rate” (sedimentation rate)/ ESR
A

C-reactive protein, Serum amyloid A

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19
Q

2 classes of antiinflammatory drugs

A
  1. steroidal (corticosteroids)

2. nonsteroidal (NSAIDS)

20
Q

ESR tests:

A

how quickly red blood cells (erythrocytes) settle in a test tube in one hour. The more red cells that fall to the bottom of the test tube in one hour, the higher the sed rate.

21
Q

really good gram+ antibiotic

A

gentimycin

22
Q

___-______ not good at treating intracellular organisms

A

beta-lactams

23
Q

cell membrane phospholipids can become -_______ ______ which can become _____________ —> inflammation

A

arachadonic acid,

prostaglandins

24
Q

Corticosteroids (prednisone) blocks synthesis of ______ _____–blocking much downstream

A

arachidonic acid

25
Q

most common cause of cushings (^ cortisol)

A

steroid treatment (prednisone)

26
Q

glucocorticoids:
desired effects:
Undesired effects:

A
  • antiinflammation, lower immune funciton

- lower immune function, ^gluconeogenesis, ^lipolysis, fat redistribution, ^insulin resistance, mood changes (ANGER)

27
Q

glucocorticoid MO

A

involved in concentration, distribution and function of peripheral leukocytes–> suppression on cytokine release

28
Q

*equivalent physiological dose of prednisone

A

5 mg

29
Q

prednisone inhibits _________

A

phospholipases –/–> arachidonic acid

30
Q

prednisone dosing and duration dictated by

A

seriousness of condition

31
Q
  • Prednisone dosing:
    acute inflammation:
    chronic:
A
  • high dose short duration

- low dose long term–taper if over 2 weeks (over 2 is when ADRs emerge) (stunted growth in kids–monitor growth)

32
Q

Prednisone distributes __________ quickly; metabolized into _________

A

everywhere; -

prednisolone (more active form)

33
Q

Most common prednisone ADRs:

ADRs to concern us:

A
  • GI upset and mood changes (anger)

- disturbance of HPA axis (Cushings)

34
Q

All agents w/in these classes are antiinflammatory, antipyretic, and analgesic via inhibition of prostaglandin synthesis

A

NSAIDs–via cyclooxygenase inhibition selectively or non-selectively

35
Q

antiinflammatory drugs in addition to steroids and NSAIDS

A

tetracyclines and macrolides–inhibit production of inflammatory mediators

36
Q 
Hypersensitivity Rxn mne: ACID 
mediator?
A:
C:
I:
D:
A

A: IgE–allergin binds to mast cells and basophils=> degran
C: IgG– Antigen=Antibody –>compliment mediated lysis
I: IgG – Compliment activation attracts POLYMORPHONUCLEAR cells–>release lysosomal enzymes
D: Cell– Help T cell –> lymphokines => inflammation + Macrophages

37
Q

Type I hypersensitivity induces ____ ______ or eosinophile to release ______ (rhinnorrhea, anaphylaxis, angioedema)

A

mast cells,

histamine

38
Q

angioedema mediated by

A

Type I or II (bradikinins or histamine)

39
Q

hypersensitivity rxn often caused by ________ rather than direct allergen

A

metabolite

40
Q

IgG binds to antigen on cell surface + compliment system => cytotoxic (cell is killed)

A

Type II hypersensitivity rxn (i.e. wrong blood type infusion–AUTOIMMUNE disorder)

41
Q

anaphylaxis vs.

anaphylactoid

A
  • IgE mediated

- drug itself acts as sensitivity mediator

42
Q

Difference btwn type II and III (video)

A

type II: IgG attaches directly to cell surface antigen

type III: IgG attaches to antibody–> immune complexes

43
Q

penicillin allergy most likely

A

Type I

44
Q

serum sickness caused from type ____ hypersensitivity

A

III

45
Q

ARTHUS reaction looks just like

A

cellulitis

46
Q

Initiation of the T-helper cell

A

Type IV hypersensitivity rxn–activation of B and Killer T cells (can lead to most dangerous autoimmune diseases i.e. diabetes)

47
Q

positive TB test is

A

type IV rxn

Infection and Immunology (17 decks)

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