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Anatomy Test Block II > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

What are the principle characteristics of acute inflammation?

A

minutes lasting hours to days; EXUDATION of fluid and plasma proteins and emigrantion of WBCs; when offender is over inflammation subsides;

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2
Q

How may repair to inflammation occur?

A

regeneration of tissue (as in hepatitis) or scarring (mass of collagen laid down)

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3
Q

characteristics of TRANSUDATE

A

clear/pale yellow and water-like; no tissue fragments; no odor; alkaline; 1.015 specific gravity’ low (>3%) protein content; low cell count (b/c not infectious); low enzyme content; no bacteria or inflammation

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4
Q

What conditions would you find transudate?

A

renal failure; CHF; acites

usually has to do w/ hydrostatic or osmotic issues

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5
Q

Characteristics of EXUDATE

A

cloudy/white/yellow/red; thick and creamy w/ tissue fragments; may have odor; acidic; higher specific gravity and protein content; high cell ct; high enzyme content; bacteria may be present; associated w/ inflammation

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6
Q

explain the vascular response in acute inflammation

A

first vasocontriction b/c prevents bleeding and piles up cells that are needed; then vasodilation to bring in all cellular components needed for repair (what produces heat); then permeability changes in which the endothelium of venule becomes leaky so things can move in and out - causes swelling

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7
Q

what process of acute inflammation causes pain?

A

chemotaxis: chemoattractant chemicals activate sensory nerves to cause pain

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8
Q

Rouleaux phenomenon

A

stacks of RBCs aggregate in presence of inflammation to slow blood flow

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9
Q

What are examples of stimuli for acute inflammation?

A

infections - most commonly bacteria. viruses and fungi
tissue damage
foreing bodies (splinters, dirt, sutures) immune reactions: aunto immune disease, alergies

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10
Q

segs

A

segmented neutrophils; 60% of WBCs are segs; has 3-5 lobed nucleus; 4-10k per cubic mm of blood, normally. contain enzymes that are chemoattractants.

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11
Q

B lymphocytes

A

produce antibodies; activated b cell = plasma cell that pumps out abs against something

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12
Q

t helper lymphocytes

A

CD4+; when activated, induces b cells to become plasma cells

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13
Q

what happens w/o T helper cells?

A

b cells don’t mount an effective antibody response (ex. HIV kills CD4+ cells so lowered immune response = oportunistic infections)

humoral mediated immunity

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14
Q

T nk cells

A

CD8+; when activated, produce perforin which inserts into membrane of cells causing them to be leaky

cell mediated immuntity

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15
Q

monocytes

A

immature cells in circulation that when called up emigrate and become macrophages to eat debris and bacteria

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16
Q

eosinophils and basophils

A

WBCs - only about 1% of them; high eosinophil count would be seen in roundworm infection and in allergies

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17
Q

mast cells

A

in subQ tissue where there is an openeing in the body; have granules that produce and immune response when released

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18
Q

what would be the use of a mast cell stabilizing drug?

A

preventing the mast cell from releasing the granules

asthma drugs

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19
Q

histamine is found in

A

mast cells, basophils, plts

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20
Q

heparin found in

A

mast cells, plts

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21
Q

serotonin found in

A

plts

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22
Q

release of IL1 and IL6 produces what?

A

fever

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23
Q

bradykinin and substance p

A

made by neuron and packaged into granules and when release, causes pain and swelling

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24
Q

what is a drug that degrades the enzyme for substance p and bradykinin?

A

ACE inhibitors

when they build up in tissues, cough

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25
Q

TNF

A

involved in fever and chemotaxis

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26
Q

what drugs are anti TNF agents?

A

biologics (inbrel and rimicade) - reduce inflammation

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27
Q

what chemical mediators are involved in vasodilation?

A

prostaglandins
NO
histamine

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28
Q

What chemical mediators are involved in increased vascular permeability?

A 
histamine and seratonin
C3a & C5a
bradykinin
leukotrienes
substance P
29
Q

What chemical mediators are involved in chemotaxis?

A

TNF, IL1
chemokines
C3a C5a
leukotriene

30
Q

What chemical mediators are involved in fever?

A

IL1 and TNF

prostaglandins

31
Q

What chemical mediators are involved in pain?

A

prostaglandins

bradykinins

32
Q

What chemical mediators are involved in tissue damage?

A

leukocyte enzymes
ROS
NO

33
Q

Viagra/cialis

A

blocks degradation of NO, therfore producing vasodilation and an errection

34
Q

singular

A

leukotriene inhibitor

35
Q

chomalin sodium

A

mast cell stabilizer: used in exercise induce asthma

36
Q

what are some systemic manifestions of acute inflammation?

A

fever, shaking, weakness, aches, decreased appetite, increased sleep

37
Q

leukomoid rxn

A

in some people, WBC count will be 50k when normally it’s never overe 20k; you would think leukemia first but have to consider leukomoid rxn which is always present in acute inflammatory process

38
Q

left shift

A

increase in bands; (bands = banded immature segs pushed out by marrow during inflammatino) (normal is 4% bands)

39
Q

acute phase reactants

A

proteins present in the blood that increase in acute inflammatory process (CRP, complement, fibrinogne)

40
Q

what is responsible for the releaux phenom?

A

fibrinogen

41
Q

what tests both show that there is an inflammatory response, just that it is non specific?

A

CRP (goes up in presence of inflammaion)

ESR (erthyrocyte sedimentation rate) - sed rate increases (normal is 15) due to rouleaux.

42
Q

wheal and flare

A

allergic response - superficial skin rxns to ags. ex. poison ivy and dermatographism

43
Q

serous inflammation

A

one producing a serous exudate; esentially a filtrate of blood; could be caused by a friction burn or sunburn or effusion of joints

44
Q

catarrhal inflammation

A

affects mainly a mucous surface, originating from a mucous membrane; runny nose to conjuctivits

45
Q

supperative inflammation

A

marked by the presenve of pus

46
Q

paronychia

A

supperative type of inflammation - usually staph which is penicillin resistant; seen in mani pedis

47
Q

hydradenitis suppurativa

A

form recurrent furuncles and carbuncles in areas w/ apocrine glands

48
Q

abcess

A

cystic collection of pus w/i a tissue - liquifaction necrosis

49
Q

empyema

A

collection of pus w/i a naturally occuring anatomical cavity

ex: staph in lungs; gallbladder empyema

50
Q

lymphadenitis

A

swollen lymph nodes

51
Q

lymphadema

A

blocked lymph channels

52
Q

bubos

A

seen in lymphogranuloma venerum, bubonic plague, chalmydia, syphilis, chancroid, TB

53
Q

what organism causes chancroid?

A

homophiles duchrey (seen in sex workers in 3rd world countries)

54
Q

fibrinous inflammation

A

marked by an exudate of coagulated fibrin - may form adhesions.

ex: pericarditis

55
Q

serosanguinous inflammation

A

thin bloody fluid

56
Q

ulcerative inflammation

A

that in which necrosis on or near the surface leads to loss of tissue and creation of local defect (ulcer). tissue that forms when trying to heal is granultion tissue (starts around rim and works in - its active tissue) so dominant cell type is fibroblast and endothelium.

57
Q

examples of ulverative inflammation

A

ulcerative colitis; ulcerative gingivitis; duodenitis (peptic ulcer disease); decubiti

58
Q

gangrenous inflammation

A

implies enzymatic and bacterial decomp (putrefaction)

ex: TSS; decrotizing fascitis

59
Q

when acute, if gangrene is due to ischemia like a blood clot entering circulation and traveling to instestines, that is a what?

A

mesenteric ischemia (gangrenous inflammatory ex)

pt. present w/ pain out of proportion to physcial findings

60
Q

membranous/

pseudomembranous inflammation

A

matted fibrin, mucus and inflammatory cells on focally necrotic epithelial surface

61
Q

examples of membranous or pseudomembranous inflammation

A 
diptheria (grey membrane)
pseudomembranous colitis (c diff overgrowth in colon)
62
Q

if acute inflammation fails to clear invaders, what is the cause?

A

chronic inflammation

63
Q

immune mediated diseases examples

A 
asthma
myasthenia gravis (ab against Ach receptor which is on skeletal muscles so weakness)
64
Q

chronic inflammation caused by prolonged exposure ex

A

silicosis (glass making)

asbestos

65
Q

granulomatous inflamation

A

basically a cellular attempt to contain an offending agent that is difficult to eradicate - walls it off

66
Q

what are the 2 types of granulomatous inflammation?

A

caseous - turning to cheese meaning necrosis present

non caseous

67
Q

examples of granulomatous inflammation

A 
Tb (caseating)
syphilis (gumma is CNS)
sarcoidosis (noncaseating)
leprosy (non)
crohns (occasional caseation)
68
Q

cat scratch disease

A

granulomatous inflammation caused by bartonela hensalia from scratch of cat - produces huge lymph node

Anatomy Test Block II (7 decks)

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