chapter 4

Question 1

hyperemia

Answer 1

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

Question 2

congestion

Answer 2

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

Question 3

acute pulmonary congestion

Answer 3

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

Question 4

chronic pulmonary congestion

Answer 4

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

Question 5

acute hepatic congestion

Answer 5

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

Question 6

chronic passive hepatic congestion

Answer 6

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

Question 7

hemorrhagic distheses

Answer 7

collective term for clinical disorder which increase tendancy for hemorrhage

Question 8

petechia

Answer 8

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

Question 9

purpura

Answer 9

greater then 3mm

occur in thrombocytopenia or uremia

Question 10

ecchymosis

Answer 10

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

Question 11

primary homeostasis

Answer 11

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

Question 12

secondary hemostasis

Answer 12

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

Question 13

t-PA

Answer 13

limits hemostatic plug to site of injury

Question 14

antiplatelet molecules of endothelium

Answer 14

NO and PGI2

adenosine diphosphotase breaks down ADP blocks aggregation

Question 15

heparin like molecules

Answer 15

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

Question 16

protein C

Answer 16

inhibits Va VIIIa

Question 17

protein s

Answer 17

cofactor for protein C and TRFI

Question 18

tissue factor

Answer 18

activates extrinsic clotting coagulation cascade

Question 19

alpha platelet granules

Answer 19

adhesion molecule P-selectin on surface

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

Question 20

delta platelet granules

Answer 20

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

Question 21

Adhesion

Answer 21

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

Question 22

Secretion

Answer 22

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

Question 23

aggregation

Answer 23

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

Question 24

bernard-soulier syndrome

Answer 24

deficiency in GpIB

Question 25

glazmannthrobothenia

Answer 25

GpIIb/IIa complex

Question 26

Vit K dependent

Answer 26

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

Question 27

PT

Answer 27

prothrombin time extrinsic VII, X, II, fibrinogen

Question 28

PTT

Answer 28

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

Question 29

pro-inflammatory effects of thrombin

Answer 29

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

Question 30

vichows triad

Answer 30

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

Question 31

tubulence

Answer 31

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

Question 32

stasis

Answer 32

major contributor to venous thrombi

Question 33

leiden mutation

Answer 33

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

Question 34

prothrombin gene mutation

Answer 34

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

Question 35

increased homocysteine

Answer 35

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

Question 36

decrease homocysteine

Answer 36

folic acid, pyridoxine, vit B12 | but does not decrease risk of thrombosis

Question 37

rare causes of hypercoagulability

Answer 37

deficiencies in antithrombin III, protein C, protein S

Question 38

heparin-induced thrombocytopenia syndrome

Answer 38

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

Question 39

antiphospholipid Ab syndrome

Answer 39

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

Question 40

lines of Zahn

Answer 40

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

Question 41

mural thrombi

Answer 41

in heart chambers or in aortic lumen

Question 42

arterial thrombi

Answer 42

occlusive | frequency: coronary > cerebral > femoral

Question 43

venous thrombus/phlebothrombosis

Answer 43

occlusive red/stasis thrombi vv of LL most common

Question 44

postmortem clots

Answer 44

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

Question 45

vegetation

Answer 45

thrombi of heart valves | blood borne bacteria and fungi -> infective endocarditis

Question 46

libman-sacks endocaditis

Answer 46

due to SLE

Question 47

DIC

Answer 47

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

Question 48

systemic thromboembolism

Answer 48

80% arise from intracardial mural thrombi | 75% occur in LL

Question 49

fat and marrow embolism

Answer 49

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

Question 50

red infarctions

Answer 50

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

Question 51

white

Answer 51

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

Question 52

metabolic abnormalities of septic shock

Answer 52

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

Question 53

clinical presentation of hypovolemic and cardogenic shock

Answer 53

hypotensive, cool, clammy, cyantotic

Question 54

clinical presentation of septic shock

Answer 54

initially warm and flushed