Antiinflammatory Drugs + Immune Rxn's

Question 1

3 stages of inflammation

Answer 1

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

Question 2

plasma transporter of iron

Answer 2

Transferrin

Question 3

clotting factor

Answer 3

Fibrinogen (can lead to clotting disorder)

Question 4

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

Answer 4

Fever

Question 5

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

Answer 5

chemokines, interferon, interleukins, TNF,–

attract and activate

Question 6

Steps of inflammation

Answer 6

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

Question 7

step 3 of inflammation

Answer 7

red, warm, edema, pain

Question 8

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

Answer 8

• instructed cell death–apoptosis
• phagocytosis & degranulation & creates net (*bacteria)
• phagocytosis

Question 9

• Inflammation can be (2) + cell mediators

Answer 9

acute (neutrophil mediated) vs.

chronic (monocyte, macro, lymphocyte mediated)

Question 10

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

Answer 10

fibroblasts,

adhesions

Question 11

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

Answer 11

severe and progressive

“SMOLDERING”

Question 12

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

Answer 12

mild and self-limited,

prominent

Question 13

inflammation is associated w/

Answer 13

almost every disease–get used to it

Question 14

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

Answer 14

Granulomatous inflammation (a type of chronic inflammation)

Question 15

Systemic S&S of inflammation (3) PROSTAGLANDINS

Answer 15

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

Question 16

the process of inflammation is fundamental to virtually…

Answer 16

all of clinical medicine!!!!!

Question 17

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

Answer 17

bacteria

Question 18

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

Answer 18

C-reactive protein, Serum amyloid A

Question 19

2 classes of antiinflammatory drugs

Answer 19

1. steroidal (corticosteroids)

2. nonsteroidal (NSAIDS)

Question 20

ESR tests:

Answer 20

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.

Question 21

really good gram+ antibiotic

Answer 21

gentimycin

Question 22

___-______ not good at treating intracellular organisms

Answer 22

beta-lactams

Question 23

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

Answer 23

arachadonic acid,

prostaglandins

Question 24

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

Answer 24

arachidonic acid

Question 25

most common cause of cushings (^ cortisol)

Answer 25

steroid treatment (prednisone)

Question 26

glucocorticoids: desired effects: Undesired effects:

Answer 26

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

Question 27

glucocorticoid MO

Answer 27

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

Question 28

*equivalent physiological dose of prednisone

Answer 28

5 mg

Question 29

prednisone inhibits _________

Answer 29

phospholipases --/--> arachidonic acid

Question 30

prednisone dosing and duration dictated by

Answer 30

seriousness of condition

Question 31

* Prednisone dosing: acute inflammation: chronic:

Answer 31

- 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)

Question 32

Prednisone distributes __________ quickly; metabolized into _________

Answer 32

everywhere; - | prednisolone (more active form)

Question 33

Most common prednisone ADRs: | ADRs to concern us:

Answer 33

- GI upset and mood changes (anger) | - disturbance of HPA axis (Cushings)

Question 34

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

Answer 34

NSAIDs--via cyclooxygenase inhibition selectively or non-selectively

Question 35

antiinflammatory drugs in addition to steroids and NSAIDS

Answer 35

tetracyclines and macrolides--inhibit production of inflammatory mediators

Question 36

``` Hypersensitivity Rxn mne: ACID mediator? A: C: I: D: ```

Answer 36

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

Question 37

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

Answer 37

mast cells, | histamine

Question 38

angioedema mediated by

Answer 38

Type I or II (bradikinins or histamine)

Question 39

hypersensitivity rxn often caused by ________ rather than direct allergen

Answer 39

metabolite

Question 40

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

Answer 40

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

Question 41

anaphylaxis vs. | anaphylactoid

Answer 41

- IgE mediated | - drug itself acts as sensitivity mediator

Question 42

Difference btwn type II and III (video)

Answer 42

type II: IgG attaches directly to cell surface antigen | type III: IgG attaches to antibody--> immune complexes

Question 43

penicillin allergy most likely

Answer 43

Type I

Question 44

serum sickness caused from type ____ hypersensitivity

Answer 44

III

Question 45

ARTHUS reaction looks just like

Answer 45

cellulitis

Question 46

Initiation of the T-helper cell

Answer 46

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

Question 47

positive TB test is

Answer 47

type IV rxn