Pathology 1.2 Flashcards

1
Q

inflammation

A

acute- neutrophils, vessels, mast cells
chronic- begins 1 day later. lymphos, macros, plasma cells
granulomatous- variant of chronic,

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2
Q

5 signs of inflamation

A

Rubor, tumor, calor, dolor, loss of function

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3
Q

leaky small vessels

A

redness, swelling, loval warmth

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4
Q

pus

A

lots of inflammatory cells,

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5
Q

fever

A

37.2 - 37.7 degrees celcius.

PgE2 chanfes temp regulation in hypothalamus.

serious tissue damage at 104-106 fahrenheit

“SELL at 106”

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6
Q

vessel’s role in inflammation

A

small vessels develop endothelial retraction and pinocytosis

plasma leaks out

forms exudate- clotting factors.

DDx - transudate from hemodynamic problems.

recruit inflammatory cells to site.

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7
Q

leukocytosis with neutrophilia

A

acute inflammation, bacterial infection
depleted PMNs,
left shift

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8
Q

leukocytocis with lymphocytocis

A

chronic inflamation, viral infection

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9
Q

Eosinophilia

A

parasitic infection, autoimmune, asthma/allergic, tumors

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10
Q

thrombocytosis

A

thrombocytopenia

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11
Q

laboratory signs of infection

A

increased sedimentation rate.
due to increased fibrinogen.

non-specific.

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12
Q

fibrinogen

A

acute phase protein

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13
Q

CRP

A

c-reactive protein
becomes abnormal after fast sedimentation rate
can increase by 1000 fold
mild increases can indicate atherosclerotic changes

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14
Q

procalcitonin

A

largely specific for bac infection

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15
Q

SAA

A

serum amyloid A prtein

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16
Q

Ceruloplasminin

A

copper binding protein

17
Q

troponin

A

myocardial samage, as an infarct

18
Q

transaminases

A

AST, ALT- liver injury

19
Q

alkaline phsophatase

A

liver biliary obstructive injury.

20
Q

CPK

A

creatine phsophokinase, muscle injury

21
Q

amylase and lipase

A

pancreatitis

22
Q

vascular changes in inflamation

A
23
Q

cells in acute inflammation

A

mast (first responders), PMNs, endothelial cells.

24
Q

mast cells

A

activated by trauma

degranulate and secrete histamine, TNF-alpha, chemokines, protesases, heparin

25
Q

Neutrophils

A

recruited by endothelial interactions, chemotactic stimuli, complement, leukotriene, chemokines.

phagosomes merge with lysosomes to kill phagocytosed organisms and destroy toxins.

Resperatory burst