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D2 - FALL - PAR 1 > Pathology > Flashcards

Pathology Flashcards

1
Q

What are the 2 types of edema and their differences?

A
  1. Transudate - NO endothelium dmg; clear, yellow fluid; prot poor
  2. Exudate - can have endothelium dmg; can be pink/red fluid; prot rich
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2
Q

recognition and attachment of phagocytes is enhanced by what?

A

opsonins

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3
Q

what are the 2 types of digestion?

A
  1. O2-dependent (oxidative burst method)

2. O2-independent (lysosome method)

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4
Q

what is the life span of PMNs?

A

24 hrs

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5
Q

What type of receptors do PMNs and mac’s have for phagocytosis?

A

c3b & Fc receptors - these mediate phagocytosis & aid in recognition of molecules to be digested

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6
Q

what do mac’s secrete?

A
  1. enzymes: collagenases, proteases, lipases, phosphatases
  2. plasma proteins: complement components, coagulation factors, fibronectin, a2-macroglobulin
  3. monokines: mediate inflamm and healing
  4. arachidonic acid metabolites
  5. ROS & NO
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7
Q

what are the cells of chronic inflamm?

A

mac’s, lymphocytes, eosinophils, mast cells/basophils, plasma cells

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8
Q

what cell secretes histamine?

A

mast cells

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9
Q

what cell(s) is associated with chronic granulomatous inflamm?

A

multinucleated giant cells, epitheloid histocytes

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10
Q

types of chronic granulomatous inflamm?

A

foreign body & immune granulomas

difference? foreign body = non-infectious etiology; immune = intracellular pathogen

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11
Q

cell associated w/ immune granulomas?

A

Langhans-type giant cell

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12
Q

what plasma derived mediators does hageman factor (factor XIIa) activate?

A

coagulation & fibrinolytic systems, complement, and kinin system

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13
Q

what are the 3 pathways for complement?

A

lectin binding pathway (bact), classical (Ab-ag complex), and alternate (bact, IgA, C3)

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14
Q

what does thrombin do?

A

converts fibrinogen to fibrin; also activates endothelial cells & platelets

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15
Q

source of arachidonic acid?

A

released from phospholipid cell memb via phospholipase A2

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16
Q

how is arachadonic acid activated?

A

by COS or 5-lipooxygenase

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17
Q

PG encourage platelet aggregation. T/F?

A

false, they inhibit it.

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18
Q

thromboxane induces platelet aggregation. T/F?

A

true

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19
Q

what does aspirin do for clotting?

A

it competes for thromboxane receptors, so it prevents platelet aggregation/clotting

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20
Q

what are the products of cyclooxygenase pathway?

A

PGs & thromboxanes

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21
Q

what are the products of lipooxygenase pathway?

A

leukotrienes & lipoxins

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22
Q

vasodilation = role of which mediators?

A

PGs, NO, histamine

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23
Q

increased vascular permeability = role of which mediators?

A

vasoactive amines, PAF, substance P, c3a & c5a, bradykinin, leukotrienes c4, d4, e4, c5a, leukotriene b4, chemokines

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24
Q

Chemotaxis, leukocyte recruitment & activation = role of what mediators?

A

c5a, leukotriene B4, chemokines, IL-1, TNF, bacterial products

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25
Q

fever = role of which mediators?

A

IL-1, TNF, PGs

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26
Q

pain = role of which mediators?

A

PGs, bradykinin

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27
Q

tissue dmg= role of which mediators?

A

neutrophil & mac lysosomal enzymes, O2 metabolites, NO

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28
Q

tissues are divided into 3 types in wound healing based on regenerative capacity… what are they?

A

labile, stable, permanent

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29
Q

activated mac’s synthesize and secrete what enzyme to remodel the ECM?

A

matrix zinc metalloproteinases

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30
Q

what is angiogenesis?

A

formation of new capillaries from existing blood vessels

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31
Q

proud flesh?

A

exuberant amounts of granulation tissue

32
Q

pyogenic granuloma?

A

tumor-like mass of excessive granulation tissue

33
Q

elastin?

A

core protein glycine & proline random coils

34
Q

fibrillin?

A

peripheral microfibrils w/ unknown function

35
Q

fibronectin?

A

binds to ECM, cell surface integrins, bacteria, and DNA; type of glycoprotein

36
Q

what is the order of remodeling of ECM?

A

fibrin/fibronectin > PGs & GAGs > collagen III > collagen I

37
Q

Tensile strength of a wound will return. T/F?

A

Tensile strength will NEVER return to original! only 80% of original tensile strength returns in 3 months.

38
Q

mechanisms of edema formation?

A
  1. inc hydrostatic pressure
  2. lymphatic obstruction
  3. decreased plasma oncotic pressure
  4. increased vascular permeability
  5. sodium & water retention
39
Q

ascites?

A

fluid accumulation in the anterior peritoneal cavity

40
Q

anasarca?

A

generalized subcutaneous edema

41
Q

shock is systemic hyperperfusion of the tissue. t/f?

A

FALSE, shock is systemic HYPOperfusion of the tissue.

42
Q

types of shock?

A
  1. cardiogenic - heart failure
  2. hypovolemic - loss of fluid vol
  3. neurogenic - spinal injury; anesthesia
  4. septic - infection
  5. anaphylactic - allergy
43
Q

where is renin made? angiotensin? ACE? aldosterone?

A

kidney, liver, lungs, adrenal gland

44
Q

if initial changes in nonprogressive shock continues, what happens?

A

go into progressive shock where tissue becomes hypoxic, anaerobic metabolism inc, inc in lactic acid, metabolic acidosis

45
Q

what type of shock involves disseminated intravascular coagulation (DIC)?

A

irreversible shock

46
Q

what do hyperemia and congestion suggest?

A

local inc in blood volume in particular tissue

47
Q

diff betw hyperemia and congestion?

A

hyperemia: active; fresh blood; red/flushed tissue
congestion: passive; older blood; blue-red tissue color

48
Q

ex of hyperemia?

A

erythema - inc flow; due to exercise or inflamm

49
Q

ex of congestion?

A

cyanosis/hypoxia; dec outflow; due to local obstruction, congestive heart failure

50
Q

telangiectasia?

A

widened venules that cause red lines or patterns on the skin–not a hemorrhage (unlike petechiae); blanches w/ pressure

51
Q

purpura (peliosis)?

A

bluish or purplish discolration of skin or mucous memb due to extravasation of blood.

52
Q

ecchymosis?

A

larger subcutaneous hemorrhages

53
Q

types of hermorrhage?

A

petechiae, purpura, ecchymosis

54
Q

diff sources of hemorrhaging?

A
  1. hematoma -localized blood pooling
  2. epistaxis - nosebleed
  3. hematemesis -vomit blood
  4. hemoptysis - blood from resp tract
  5. melena - older bloody poo
  6. hematochezia - fresh bloody poo
  7. hemorrhagic diathesis - deficiency of vit C, platelets, clotting ffacotrs
  8. body cavity hemorrhage
55
Q

heparin acts by?

A

accelerating antithrombin III rxn.

56
Q

antithrombin does what?

A

neutralizes clotting factors

neutralizes thrombin (IIa) and factor Xa

57
Q

which clotting cascade pathway is sensitive to heparin?

A

intrinsic (dmg to platelets)

58
Q

extrinsic pathway is characterized by trauma to…?

A

a tissue other than blood, hence extrinsic (to blood)

59
Q

factor 2 aka?

A

prothrombin; activated = thrombin

60
Q

factor 1 aka?

A

fibrinogen; activated = fibrin

61
Q

heparin cofactor II?

A

neutralizes thrombin (IIa)

62
Q

c-1-esterase inhibitor?

A

neutralizes XIIa and kallikrein

63
Q

protein C system?

A

inactivates active factor V and VIII in presece of cofactor Protein S

64
Q

tissue factor pathway inhibitor?

A

binds to factor Xa & VIIa, thereby inhibiting enzymatic activity of factor VIIa

65
Q

deficiency of tissue plasminogen results in accumulation of excessive amounts of fibrin aka..?

A

ligneous conjunctivitis

66
Q

DIC is…?

A

overactivation of coagulation in the whole body; exceeds regulatory mechanisms; uses up all platelets and clotting factors; followed by massive fibrinolysis resulting in a massive hemorrhage

67
Q

to diagnose for DIC what should we look for in blood?

A

d-dimers!

68
Q

diff betw white thrombi and red thrombi?

A

white: in arterial circ; mostly of platelets & fibrin
red: in venous circ; mostly of platelets, fibrin, and trapped RBCs; due to slower blood flow

69
Q

lines of zahn?

A

laminations in thrombus produced by alternating pale layers of platelets admixed w/ fibrin & darker layers containing more red cells; signify thrombosis at a site of pulsatile blood flow (contraction, relaxation, contraction, etc)

70
Q

recanalization of a thrombus?

A

holes will form in the clot for blood to flow

71
Q

what does factor VLeiden do?

A

it is a mutated factor V that cannot be inactivated by protein C, so inc in clot formation

72
Q

most common type of emboli?

A

thromboemboli; mostly arise in deep vv of legs

73
Q

coagulation necrosis?

A

replacement of necrotic tissue by a scar

74
Q

liquefaction necrosis?

A

necrotic area liquefies and forms a cystic area (i.e. brain)

75
Q

septic infact?

A

abscess formation; presence of bacteria

D2 - FALL - PAR 1 (5 decks)

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