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MOD I Exam I > Chapter 4 > Flashcards

Chapter 4 Flashcards

1
Q

Differentiate hyperemia from congestion

A

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

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2
Q

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

A

Congestion

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3
Q

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

A

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

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4
Q

First event in hemostasis

A

Arteriolar vasoconstriction/vasospasm via neurogenic reflex, augmented by endothelin

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5
Q

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

A

vWF; GpIb

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6
Q

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

A

Factor VII

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7
Q

Differentiate Bernard Soulier syndrome from Glanzmann thrombasthenia

A

Bernard-Soulier = GpIb deficiency (defective platelet adhesion)

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

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8
Q

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
A

A. Factor II deficiency

This is a prothrombin deficiency

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9
Q

Differentiate PT and PTT

A

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)

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10
Q

Process of fibrinolysis

A

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

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11
Q

Main clinical marker for fibrinolysis

A

D-dimer

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12
Q

Clinical presentation of defects of primary hemostasis

A

Mucosal bleeding

Thrombocytopenia

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13
Q

Clinical features of defects in secondary hemostasis

A

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

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14
Q

Virchow triad of thrombosis

A

Endothelial injury
Abnormal blood flow
Hypercoagulability

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15
Q

Clinical settings associated with thrombosis due to turbulent blood flow

A 
Ulcerated atherosclerotic plaques
Aortic and arterial aneurysm
Acute MI
Rheumatic mitral valve stenosis + Afib
Polycythemia vera (HYPERVISCOSITY)
Sickle cell anemia
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16
Q

Describe factor V leiden mutation

A

Arg—>glu substitution at aa 506

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

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17
Q

Other primary+secondary causes of hypercoagulability besides factor V leiden

A 
Protein C and S deficiency
Heparin-induced thrombocytopenia
Antiphospholipid Ab syndrome (false+syphilis, present with SLE)
Cigarette smoking
Obesity
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18
Q

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

A

DIC

19
Q

Red vs. white infarct

A 
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
20
Q

Types of shock

A

Cardiogenic = low CO d/t myocardial pump failure

Hypovolemic = low CO d/t low blood volume

Systemic/inflammatory

21
Q

Stages of shock

A

Nonprogressive = tachycardia, peripheral vasoconstriction, renal conservation of fluid

Progressive = widespread tissue hypoxia, lactic acidosis

Irreversible = anuria, survival not possible

22
Q

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

A

Adrenal = cortical cell lipid depletion

Kidneys = acute tubular necrosis

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

Skin = petechial hemorrhage

23
Q

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

A

Renal

24
Q

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

A

Congestion

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

25
Q

Differentiate general purpose of primary vs secondary hemostasis

A

Primary = formation of platelet plug

Secondary = deposition of fibrin/stabilization of the clot

26
Q

Which of the following limits clot propagation?

A. TGF-B
B. TNF
C. PGI2
D. IL-2
E. vWF
A

C. PGI2

27
Q

Contents of platelet granules

A

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

Delta granules:
ADP, ionized Ca, 5HT

28
Q

Thrombin activates platelets through a GPCR called _____

A

PAR = protease-activated receptor

[recruitment occurs via positive feedback]

29
Q

Which of the following does indomethacin inhibit?

A. PAR
B. PGI
C. TxA
D. GpIIb
E. B and C
A

E. B and C

30
Q

What lab would you check in conjunction with heparin therapy?

A

PTT

31
Q

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

A

Factor XI

32
Q

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

A

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

33
Q

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

A

XI, V, and VIII

34
Q

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

A

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

35
Q

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

A

Anti-thrombin III

36
Q

Describe heparin-induced thrombocytopenia syndrome (HIT)

A

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

37
Q

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

A

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

38
Q

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

A

Antiphospholipid Ab syndrome

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

39
Q

_____ thrombi usually begin at sites of turbulence or endothelial injury

___ thrombi usually begin at sites of stasis

A

Arterial/cardiac

Venous

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

40
Q

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

A

Mycotic aneurysm

41
Q

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
A

C. Left ventricular wall infarct

42
Q

What causes thrombocytopenia in cases of fat embolism?

A

Platelets adhere to fat globules and aggregate in spleen

Often associated with diffuse petechial rash if rapid onset; consumption

43
Q

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

A

Amniotic fluid aneurysm

44
Q

Pulmonary edema is always seen in what bleeding condition?

A

DIC

MOD I Exam I (5 decks)

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