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D2 - FALL - PAR 1 > Pathology > Flashcards

Pathology Flashcards

(75 cards)

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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
fever = role of which mediators?
IL-1, TNF, PGs
26
pain = role of which mediators?
PGs, bradykinin
27
tissue dmg= role of which mediators?
neutrophil & mac lysosomal enzymes, O2 metabolites, NO
28
tissues are divided into 3 types in wound healing based on regenerative capacity... what are they?
labile, stable, permanent
29
activated mac's synthesize and secrete what enzyme to remodel the ECM?
matrix zinc metalloproteinases
30
what is angiogenesis?
formation of new capillaries from existing blood vessels
31
proud flesh?
exuberant amounts of granulation tissue
32
pyogenic granuloma?
tumor-like mass of excessive granulation tissue
33
elastin?
core protein glycine & proline random coils
34
fibrillin?
peripheral microfibrils w/ unknown function
35
fibronectin?
binds to ECM, cell surface integrins, bacteria, and DNA; type of glycoprotein
36
what is the order of remodeling of ECM?
fibrin/fibronectin > PGs & GAGs > collagen III > collagen I
37
Tensile strength of a wound will return. T/F?
Tensile strength will NEVER return to original! only 80% of original tensile strength returns in 3 months.
38
mechanisms of edema formation?
1. inc hydrostatic pressure 2. lymphatic obstruction 3. decreased plasma oncotic pressure 4. increased vascular permeability 5. sodium & water retention
39
ascites?
fluid accumulation in the anterior peritoneal cavity
40
anasarca?
generalized subcutaneous edema
41
shock is systemic hyperperfusion of the tissue. t/f?
FALSE, shock is systemic HYPOperfusion of the tissue.
42
types of shock?
1. cardiogenic - heart failure 2. hypovolemic - loss of fluid vol 3. neurogenic - spinal injury; anesthesia 4. septic - infection 5. anaphylactic - allergy
43
where is renin made? angiotensin? ACE? aldosterone?
kidney, liver, lungs, adrenal gland
44
if initial changes in nonprogressive shock continues, what happens?
go into progressive shock where tissue becomes hypoxic, anaerobic metabolism inc, inc in lactic acid, metabolic acidosis
45
what type of shock involves disseminated intravascular coagulation (DIC)?
irreversible shock
46
what do hyperemia and congestion suggest?
local inc in blood volume in particular tissue
47
diff betw hyperemia and congestion?
hyperemia: active; fresh blood; red/flushed tissue congestion: passive; older blood; blue-red tissue color
48
ex of hyperemia?
erythema - inc flow; due to exercise or inflamm
49
ex of congestion?
cyanosis/hypoxia; dec outflow; due to local obstruction, congestive heart failure
50
telangiectasia?
widened venules that cause red lines or patterns on the skin--not a hemorrhage (unlike petechiae); blanches w/ pressure
51
purpura (peliosis)?
bluish or purplish discolration of skin or mucous memb due to extravasation of blood.
52
ecchymosis?
larger subcutaneous hemorrhages
53
types of hermorrhage?
petechiae, purpura, ecchymosis
54
diff sources of hemorrhaging?
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
heparin acts by?
accelerating antithrombin III rxn.
56
antithrombin does what?
neutralizes clotting factors | neutralizes thrombin (IIa) and factor Xa
57
which clotting cascade pathway is sensitive to heparin?
intrinsic (dmg to platelets)
58
extrinsic pathway is characterized by trauma to...?
a tissue other than blood, hence extrinsic (to blood)
59
factor 2 aka?
prothrombin; activated = thrombin
60
factor 1 aka?
fibrinogen; activated = fibrin
61
heparin cofactor II?
neutralizes thrombin (IIa)
62
c-1-esterase inhibitor?
neutralizes XIIa and kallikrein
63
protein C system?
inactivates active factor V and VIII in presece of cofactor Protein S
64
tissue factor pathway inhibitor?
binds to factor Xa & VIIa, thereby inhibiting enzymatic activity of factor VIIa
65
deficiency of tissue plasminogen results in accumulation of excessive amounts of fibrin aka..?
ligneous conjunctivitis
66
DIC is...?
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
to diagnose for DIC what should we look for in blood?
d-dimers!
68
diff betw white thrombi and red thrombi?
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
lines of zahn?
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
recanalization of a thrombus?
holes will form in the clot for blood to flow
71
what does factor VLeiden do?
it is a mutated factor V that cannot be inactivated by protein C, so inc in clot formation
72
most common type of emboli?
thromboemboli; mostly arise in deep vv of legs
73
coagulation necrosis?
replacement of necrotic tissue by a scar
74
liquefaction necrosis?
necrotic area liquefies and forms a cystic area (i.e. brain)
75
septic infact?
abscess formation; presence of bacteria

D2 - FALL - PAR 1 (5 decks)

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