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PBD1 > chapter 4 > Flashcards

chapter 4 Flashcards

1
Q

hyperemia

A

active process where arteriolar dilation and increased blood flow affected -> erythema

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2
Q

congestion

A

passive process resulting from decreased outflow from tissues, local, or systemic -> cyanosis

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3
Q

acute pulmonary congestion

A

engourged alveolar capillaries w/alveolar septal edema and focal intraalveolar hemorrhage

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4
Q

chronic pulmonary congestion

A

septa thick and fibrotic and alveoli often contain numerous hemosiderin laden macrophages called heart failure cells

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5
Q

acute hepatic congestion

A

central v and sinusoids distended, centrilobular hepatocytes ischemic white, periportal hepatocytes better oxygenated and may develop fatty changes

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6
Q

chronic passive hepatic congestion

A

centrolobular regions grossly red brown, and slightly depressed and accentuated against surrounding zones of congested tan liver (nutmeg liver)
microscopically there is centrilobular hemorrhage with hemosiderin laden macrophages and degeneration of hepatocytes

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7
Q

hemorrhagic distheses

A

collective term for clinical disorder which increase tendancy for hemorrhage

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8
Q

petechia

A

minute 1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces
occur in thrombocytopenia or uremia

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9
Q

purpura

A

greater then 3mm

occur in thrombocytopenia or uremia

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10
Q

ecchymosis

A 
aka bruises 
1-2 cm subcutaneous bleeding
red/blue- hemoglobin
blue/green- bilirubin
gold/brown- hemosiderin
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11
Q

primary homeostasis

A

endothelial injury exposes highly thrombogenic ECM -> platelet adherence and activation -> change in shape to increase surface area and increase in secretory granules -> secretions recruit additional platelets (aggregation) -> primary homeostatic plug

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12
Q

secondary hemostasis

A

tissue factor is a membrane bound pro-coagulant glycoprotein synthesized by endothelial cells
acts with factor VII to initiate coagulation cascade -> activates thrombin -> cleave circulating fibrinogen -> fibrin -> consolidation -> secondary hemostatic plug

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13
Q

t-PA

A

limits hemostatic plug to site of injury

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14
Q

antiplatelet molecules of endothelium

A

NO and PGI2

adenosine diphosphotase breaks down ADP blocks aggregation

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15
Q

heparin like molecules

A

thrombomodulin and tissue repair factor pathway inhibitor
inactivate thrombin (TRFI)
once bound to thombin activates protein C

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16
Q

protein C

A

inhibits Va VIIIa

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17
Q

protein s

A

cofactor for protein C and TRFI

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18
Q

tissue factor

A

activates extrinsic clotting coagulation cascade

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19
Q

alpha platelet granules

A

adhesion molecule P-selectin on surface

contains fibrinogen, fibronectin, V, VIII, platelet factor 4, PDGF, TGFbeta

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20
Q

delta platelet granules

A

contain ADP, ATP, ionized Ca, histamine, seretonin, epi

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21
Q

Adhesion

A

to ECM via vWF which is a bridge btwn collagen and platelet IGpIb

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22
Q

Secretion

A

both granule types
delta granules especially important b/c Ca required for coagulation cascade and ADP potent activator of platelet aggregation

23
Q

aggregation

A

ADP and TxA2 from platelets amplifies aggregation -> primary hemostatic plug
thrombin binds protease activated receptor (PAR) on platelet with ADP and TxA2 -> further aggregation
platelet contraction (depends on cytoskeleton) -> secondary hemostatic plug
thrombin converts fibrinogen to fibrin -> cement plug in place

24
Q

bernard-soulier syndrome

A

deficiency in GpIB

25
Q

glazmannthrobothenia

A

GpIIb/IIa complex

26
Q

Vit K dependent

A

II, XII, IX, X in order to bind Ca
protein C and S
antagonized by coumadin

27
Q

PT

A

prothrombin time
extrinsic
VII, X, II, fibrinogen

28
Q

PTT

A

partial thromboplastin time
intrinsic
XII, XI, IX, VIII, X, V, II, fibrinogen

29
Q

pro-inflammatory effects of thrombin

A

binds PARs (GPCR) expressed on endothelium, monocytes, dendritic cells, T cells

30
Q

vichows triad

A

3 abnormalities leading the thrombus formation
endothelial injury
alterations in normal blood flow
hypercoaguability

31
Q

tubulence

A

endothelial injury and/or dysfunction and forms local pockets of stasis

32
Q

stasis

A

major contributor to venous thrombi

33
Q

leiden mutation

A

1-15% of caucasians
single mutation in V
frequent reoccuring DVT
glutamine -> arginine making V resistant to cleavage by protein C
heterozygotes have a 5x increased risk of DVT
homozygotes 50x increase

34
Q

prothrombin gene mutation

A

single nucleotide change
1-2% of population
3x increased chance of DVT

35
Q

increased homocysteine

A

contributes to thrombosis and atherosclerosis
can be caused by: inherited deficiency of cystathione beta synthetase, variant of 15.10 methyltetrahydrofolatereductase
10-15% caucasians and east asia

36
Q

decrease homocysteine

A

folic acid, pyridoxine, vit B12

but does not decrease risk of thrombosis

37
Q

rare causes of hypercoagulability

A

deficiencies in antithrombin III, protein C, protein S

38
Q

heparin-induced thrombocytopenia syndrome

A

administration of unfractionated heparin -> Abs to heparin and platelet factor 4 -> complexes on platelets and endothelium -> prothrombic state

39
Q

antiphospholipid Ab syndrome

A

recurrent thromboses, repeat miscarriages, cardiac vavulevegetations, thrombocytopenia, pulmonary embolism, pulmonary HTN,
gives false positive test for syphilis

40
Q

lines of Zahn

A

pale platelet and fibrin deposits alternating w/darker red cell rich layers
not present in post-mortem clots

41
Q

mural thrombi

A

in heart chambers or in aortic lumen

42
Q

arterial thrombi

A

occlusive

frequency: coronary > cerebral > femoral

43
Q

venous thrombus/phlebothrombosis

A

occlusive
red/stasis thrombi
vv of LL most common

44
Q

postmortem clots

A

gelantinous w/dark red dependent portion w/cells settled and yellow ‘chicken fat on top’

45
Q

vegetation

A

thrombi of heart valves

blood borne bacteria and fungi -> infective endocarditis

46
Q

libman-sacks endocaditis

A

due to SLE

47
Q

DIC

A

disseminated intravascular coagulation
not a disease, but potential complication of any condition associated w/widespread activation of thrombosis
sudden onset of widespread fibrin thrombi in microcirculation -> diffuse circulatory insufficiency

48
Q

systemic thromboembolism

A

80% arise from intracardial mural thrombi

75% occur in LL

49
Q

fat and marrow embolism

A

usually occur after a long bone fracture, soft tissue damage, or burns
sudden onset 1-3 days post injury of tachycardia, tachypnea, dyspnea, irritability, restlessness, delirium, coma, diffuse petechial rash

50
Q

red infarctions

A 
venous occlusions (ovaries)
loose CT (lung)
dual circulation (lung, GI)
previously congested tissues
occurs when flow restored to site
51
Q

white

A

arterial occlusion in solid organs w/end aa (heart, spleen, kidney)

52
Q

metabolic abnormalities of septic shock

A

TNF, IL1, stress induced hormones, and catecholamines drive gluconeogenesis
pro-inflammatory cytokines block insulin release and increase insulin resistance
hyperglycemia decreases neutrophil fxn, bactericidal activity, and increases adhesion molecules
acute transient surge of glucocorticoids followed by deficient glucocorticoids

53
Q

clinical presentation of hypovolemic and cardogenic shock

A

hypotensive, cool, clammy, cyantotic

54
Q

clinical presentation of septic shock

A

initially warm and flushed

PBD1 (6 decks)

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