Chapter 4

Question 1

Differentiate hyperemia from congestion

Answer 1

Hyperemia = active process in which arteriolar dilation leads to increased blood flow; affected tissues turn red

Congestion = passive process d/t reduced outflow of blood from tissue

Question 2

In chronic hepatic ________, centrilobular regions are grossly red-brown and slightly depressed, accentuated against surrounding zones of uncongested tan liver (nutmeg liver)

Answer 2

Congestion

Question 3

Describe effects of chronic pulmonary congestion (often d/t CHF)

Answer 3

Septa are thickened and fibrotic, alveoli contain numerous hemosiderin-laden macrophages (heart failure cells)

Question 4

First event in hemostasis

Answer 4

Arteriolar vasoconstriction/vasospasm via neurogenic reflex, augmented by endothelin

Question 5

During primary hemostasis, platelets bind _____ using _____ receptors, then release their granules containing ADP and TXA2

Answer 5

vWF; GpIb

Question 6

During secondary hemostasis, tissue factor is exposed at the site of injury, which binds and activates _______ leading to thrombin formation

Answer 6

Factor VII

Question 7

Differentiate Bernard Soulier syndrome from Glanzmann thrombasthenia

Answer 7

Bernard-Soulier = GpIb deficiency (defective platelet adhesion)

Glanzmann thrombasthenia = GpIIb-IIIa deficiency (defective platelet aggregation)

Question 8

Which of the following is incompatible with life?

A. Factor II deficiency
B. Factor XI deficiency
C. Factor XII deficiency
D. Factor V deficiency
E. Factor VII deficiency

Answer 8

A. Factor II deficiency

This is a prothrombin deficiency

Question 9

Differentiate PT and PTT

Answer 9

PT = prothrombin time
Assesses function of proteins of extrinsic pathway (VII, X, V, II, fibrinogen)

PTT = partial thromboplastin time
Assesses function of proteins of intrinsic pathway (XII, XI, IX, VIII, X, V, II, fibrinogen)

Question 10

Process of fibrinolysis

Answer 10

Plasmin (activated by t-Pa) breaks down fibrin and interferes with its polymerization

Question 11

Main clinical marker for fibrinolysis

Answer 11

D-dimer

Question 12

Clinical presentation of defects of primary hemostasis

Answer 12

Mucosal bleeding

Thrombocytopenia

Question 13

Clinical features of defects in secondary hemostasis

Answer 13

Bleeding in soft tissues or joints (often d/t hemophilias)

Question 14

Virchow triad of thrombosis

Answer 14

Endothelial injury
Abnormal blood flow
Hypercoagulability

Question 15

Clinical settings associated with thrombosis due to turbulent blood flow

Answer 15

Ulcerated atherosclerotic plaques
Aortic and arterial aneurysm
Acute MI
Rheumatic mitral valve stenosis + Afib
Polycythemia vera (HYPERVISCOSITY)
Sickle cell anemia

Question 16

Describe factor V leiden mutation

Answer 16

Arg—>glu substitution at aa 506

Makes factor V resistant to cleavage and inactivation by protein C. Makes pt prone to thrombosis

Question 17

Other primary+secondary causes of hypercoagulability besides factor V leiden

Answer 17

Protein C and S deficiency
Heparin-induced thrombocytopenia
Antiphospholipid Ab syndrome (false+syphilis, present with SLE)
Cigarette smoking
Obesity

Question 18

Condition characterized by widespread formation of thrombi in microcirculation causing diffuse circulatory insufficiency and organ dysfunction; particularly in lungs, brain, heart, kidneys

Answer 18

DIC

Question 19

Red vs. white infarct

Answer 19

Red infarct (typically venous)
Occurs in tissues with dual circulation

White infarct (typically arterial)
Occurs in solid organs with end-arterial circulation like heart, spleen, kidney

Question 20

Types of shock

Answer 20

Cardiogenic = low CO d/t myocardial pump failure

Hypovolemic = low CO d/t low blood volume

Systemic/inflammatory

Question 21

Stages of shock

Answer 21

Nonprogressive = tachycardia, peripheral vasoconstriction, renal conservation of fluid

Progressive = widespread tissue hypoxia, lactic acidosis

Irreversible = anuria, survival not possible

Question 22

Shock’s effect on adrenals, kidneys, lungs, and skin

Answer 22

Adrenal = cortical cell lipid depletion

Kidneys = acute tubular necrosis

Lungs = diffuse alveolar damage, deposition of fibrin-rich microthrombi

Skin = petechial hemorrhage

Question 23

Periorbital edema is a characteristic sign of dysfunction of what organ system?

Answer 23

Renal

Question 24

Cells that morphologically appear as “blue and bloated” indicate what pathologic process?

Answer 24

Congestion

Congestion tissues appear cyanotic d/t blood stasis and accumulation of deoxygenated Hgb

Question 25

Differentiate general purpose of primary vs secondary hemostasis

Answer 25

Primary = formation of platelet plug Secondary = deposition of fibrin/stabilization of the clot

Question 26

Which of the following limits clot propagation? ``` A. TGF-B B. TNF C. PGI2 D. IL-2 E. vWF ```

Answer 26

C. PGI2

Question 27

Contents of platelet granules

Answer 27

Alpha granules: Coagulative proteins = fibrinogen, factor V, vWF Proteins that heal = fibronectin, PF4 (binds heparin), TGF-B, PDGF Delta granules: ADP, ionized Ca, 5HT

Question 28

Thrombin activates platelets through a GPCR called _____

Answer 28

PAR = protease-activated receptor [recruitment occurs via positive feedback]

Question 29

Which of the following does indomethacin inhibit? ``` A. PAR B. PGI C. TxA D. GpIIb E. B and C ```

Answer 29

E. B and C

Question 30

What lab would you check in conjunction with heparin therapy?

Answer 30

PTT

Question 31

______ deficiency leads to mild bleeding d/t thrombin’s ability to activate factor V, VIII, and XI via positive feedback

Answer 31

Factor XI

Question 32

Why do patients with Factor XII (Hageman) deficiency not tend to bleed and actually have higher risk of thrombosis?

Answer 32

Factor XII is involved in fibrinolysis; pt will have high PTT but be asymptomatic Because factor XII is only involved in the in vitro assay and TF is major initiator of coagulation cascade in vivo

Question 33

Thrombin activates factor ___, ___ and ____ which amplifies the coagulation pathway

Answer 33

XI, V, and VIII

Question 34

T/F: t-Pa is released as a platelet inhibitor factor that stops platelets from activating and aggregating

Answer 34

False; t-Pa works on clots that have already formed

Question 35

Clinical utility of heparin and related drugs is based on their ability to stimulate _____ activity

Answer 35

Anti-thrombin III

Question 36

Describe heparin-induced thrombocytopenia syndrome (HIT)

Answer 36

Abs are developed against heparin and platelet factor 4 after administration of unfractionated heparin leading to hypercoagulable state Labs will show elevated PT and PTT

Question 37

What is trousseau’s syndrome, seen in some disseminated cancers/malignancies?

Answer 37

Increased risk of thrombosis d/t hypercoagulable state which was likely induced by unregulated gene expression in malignant cells

Question 38

What condition typically presents as thrombocytopenia, repeated miscarriages from ab-mdiated interference with growth of trophoblasts, and cardiac valve vegetations?

Answer 38

Antiphospholipid Ab syndrome [also likely mentioned with false positive syphilis test since Ag in syphilis assay is embedded in cardiolipin]

Question 39

_____ thrombi usually begin at sites of turbulence or endothelial injury ___ thrombi usually begin at sites of stasis

Answer 39

Arterial/cardiac Venous [both extend toward heart bc arterial grow retrograde and venous extend in direction of blood flow]

Question 40

Condition characterized by weakening of the vessel wall that can occur from trapped leukocytes releasing granules within the center of a thrombus that becomes infected

Answer 40

Mycotic aneurysm

Question 41

Which of the following is most likely to cause intracardiac mural thrombi? ``` A. Left atrial dilation and fibrillation B. Aortic aneurysm C. Left ventricular wall infarct D. Atherosclerosis E. Mitral valve vegetation ```

Answer 41

C. Left ventricular wall infarct

Question 42

What causes thrombocytopenia in cases of fat embolism?

Answer 42

Platelets adhere to fat globules and aggregate in spleen Often associated with diffuse petechial rash if rapid onset; consumption

Question 43

What type of embolus is characterized by sudden severe dyspnea, cyanosis, and shock followed by neurological problems like headaches, seizures, and coma?

Answer 43

Amniotic fluid aneurysm

Question 44

Pulmonary edema is always seen in what bleeding condition?

Answer 44

DIC