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Mechanisms of Disease Exam #1 > Hemodynamic Disorders, Thromboembolic Disease and Shock > Flashcards

Hemodynamic Disorders, Thromboembolic Disease and Shock Flashcards

1
Q

Where does fluid accumulate in:
Edema
Effusion

A

Edema: interstitial space.
Effusion: potential space (body cavities), i.e. pleural space, peritoneal space (ascites), pericardium, joint space, etc.

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2
Q

What pressure wants to push fluid out of capillary?

What pressure wants to pull fluid into the capillary?

A

Hydrostatic pressure

Colloid osmotic pressure

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3
Q

4 mechanisms of edema

A
  1. Increased intravascular hydrostatic pressure (Na+ and water retention, congestion).
  2. Reduced plasma oncotic pressure.
  3. Increased vascular permeability.
  4. Lymphatic obstruction
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4
Q

Hyperemia

Congestion

A

Too much blood arriving (physiologic, arterial).

Not enough blood leaving (pathologic).

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5
Q

What sorts of edema does heart failure cause? (3)

A

Soft tissue, pulmonary edema, pulmonary effusion.

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6
Q

Mechanisms of heart failure leading to edema/effusion (2)

A

Retention of Na+ and water due to increased volume and decreased oncotic pressure.

Decreased pump activity –> back-up of pulmonary venous circulation (congestion).

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7
Q

2 ways renal disease can result in edema

A
  1. Retained Na+ and water –> increased intravascular hydrostatic pressure.
  2. Nephrotic syndrome (excess protein loss in urine) –> decreased plasma oncotic pressure.
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8
Q

Kwashiorkor is a deficiency in:

A

Deficiency in protein –> reduced plasma oncotic pressure

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9
Q

3 ways we can have low protein (low plasma oncotic pressure)

A
  1. Not enough ingested: malnutrition.
  2. Not enough made: liver failure.
  3. Too much lost: kidney disease w/ nephrotic syndrome.
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10
Q

What kind of edema does lymphedema typically cause:

What would be in the differential?

A

Localized edema.

Infection, inflammation, trauma, tumors, surgery, malformations, etc.

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11
Q

Types of fluid leaving the intravascular compartment are transudate or eudate. What causes them? What is their makeup?

A

Transudate: increased hydrostatic pressure (venous obstruction, CHF, etc). Low protein, few cells.

Exudate: increased interendothelial spaces (gaps in endothelium). High protein content and may contain RBCs and/or WBCs. Found in places with increased inflammation.

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12
Q

3 causes of chronic congestion

A

Edema
Hemosiderosis
Tissue damage

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13
Q

What are “heart-failure cells”?

A

Hemosiderin-laden macrophages in areas of chronic congestion.

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14
Q

Main cause of hepatic congestion?

What is the pathology?

A

Advanced HF.

Central vein obstruction or flow reduction.

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15
Q

What is “nutmeg liver”?

A

Liver is nutmeg color (alternating brown and white) indicative of chronic hepatic congestion.

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16
Q

1st step in hemostasis

Primary hemostasis (1st step)

Primary hemostasis (2nd step)

Primary hemostasis (3rd step)

A

Site of injury causes a reflex constriction by releasing Endothelin.

Platelets adhere to the sub-endothelial surface.

Platelet activation.

Platelet aggregation.

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17
Q

What proteins are involved in the adhesion of platelets to the sub-endothelial surface?

A

GpIb on platelet bins to von Willebrand factor (vWF) on the surface.

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18
Q

Fibrinogen binds to what on the platelet?

A

Binds to GpIIb-IIIa on platelets and allows aggregation.

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19
Q

Disease caused by deficiency in GpIIb-IIIa

A

Glanzmann thrombasthenia

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20
Q

Disease caused by deficiency in GpIb

A

Bernard-Soulier syndrome

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21
Q

Disease caused by deficiency in vWF

A

von Willebrand disease

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22
Q

Weibel Palade bodies

A

Storage granules in endothelial cells that contain vWF (also integrins).

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23
Q

What is the structure of Weibel Palade bodies?

A

Coiled, looks like a spring.

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24
Q

What us ADAMTS13?

A

Can limit thrombus formation by cleaving vWF.

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25
Q

What is clustered in pairs at platelet attachment sites?

A

Alpha-Beta integrins

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26
Q

What disease is known to have “giant platelets”?

Again, what is its pathology?

A

Bernard-Soulier syndrome

Lack of GpIb

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27
Q

What 3 things allow for platelet activation (post adhesion)?

A 
Conformational change (increase in SA).
Its negatively charged surface.
GpIIb-IIIa change - fibrinogen links.
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28
Q

What triggers secretion of molecules once the platelet is activated?

What does it cause the secretion of and what do they do? (2)

A

Thrombin initiates it.

ADP (more activation) and Thromboxane A2 (more aggregation).

FYI that thrombin also has antithrombotic effects.

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29
Q

What does aspirin inhibit?

A

Thromboxane A and COX

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30
Q

End result of primary hemostasis:

A

Formation of the platelet plug

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31
Q

Clinical sign of problems with primary hemostasis: (1)

Laboratory sign of problems with primary hemostasis: (3)

A

Mucocutaneous bleeding (gums, nosebleeds).

Bleeding time (not really used anymore), platelet function studies, PFA-100.

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32
Q

Modern techniques for determining platelet malfunction (2)

A

Flow cytometry

PFA-100 (adhesion, aggregation)

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33
Q

Thrombocytopenia

Mechanism:
Platelet count:
Platelet adhesion:
Platelet aggregation (Y/N):

A 
Mechanism: loss or impaired production of platelets.
Platelet count: very low.
Platelet adhesion (Y/N): yes
Platelet aggregation (Y/N): yes
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34
Q

von Willebrand disease

Mechanism:
Platelet count:
Platelet adhesion:
Platelet aggregation (Y/N):

A 
Mechanism: inherited lack of vWF.
Platelet count: normal.
Platelet adhesion (Y/N): no.
Platelet aggregation (Y/N): yes.
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35
Q

Bernard-Soulier disease

Mechanism:
Platelet count:
Platelet adhesion (Y/N):
Platelet aggregation (Y/N):
A 
Mechanism: abnormal GpIb.
Platelet count: low to normal.
Platelet adhesion (Y/N): no.
Platelet aggregation (Y/N): yes.
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36
Q

Glanzmann’s thrombasthenia

Mechanism:
Platelet count:
Platelet adhesion (Y/N):
Platelet aggregation (Y/N):
A 
Mechanism: abnormal GpIIb-IIa.
Platelet count: normal.
Platelet adhesion (Y/N): yes.
Platelet aggregation (Y/N): no.
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37
Q

Adhesion disorders (2)

A

B-S syndrome

vWF

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38
Q

Aggregation disorder (1)

A

Glanzmann thrombasthenia

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39
Q

What word should I associate with fibrinogen?

A

Stabilization during primary hemostasis

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40
Q

Secondary hemostasis is AKA:

A

The coagulation cascade

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41
Q

Diagram the intrinsic/extrinsic pathways (slide 65)

A

Draw it

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42
Q

Aliases for:
I
II
VIII

A

I - fibrinogen
II - prothrombin
VIII - antihemophilic A factor (AHF)

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43
Q

Vitamin K-dependent factors in coagulation cascade (6)

A

II, VII, IX, X, protein C, protein S. This means they use vit K to bind Ca++.

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44
Q

Functions of Thrombin (3)

A 
Stabilizes fibrin
Activates platelets (protease-activated receptor)
Activates receptors on inflammatory cells and endothelium.
45
Q

End result of secondary hemostasis:

A

Coagulation cascade has stabilized the clot.

46
Q

Dermatologic manifestations of defects in hemostasis and their size (3)

A

Petechiae: small (< 3mm)
Purpura: larger
Ecchymosis: palpable

47
Q

2 causes of visceral and intracranial bleeding

A 
Factor deficiencies (poor coagulation cascade)
Profound thrombocytopenia
48
Q

What is hemarthrosis?

A

Blood within a joint capsule. Occurs as a result of factor deficiencies.

49
Q

What can limit coagulation? (3)

A

Blood flow - washes away clotting factors.
No more platelet surface.
Plasmin - breaks apart fibrin.

50
Q

What is t-PA?

A

The clot-buster.

It is a potent activator of Plasmin.

51
Q

What are some platelet inhibitors? (3)

A

Adenosine diphosphatase
Prostacyclin
Nitric Oxide

52
Q

Thrombomodulin and protein C

A

Thrombomodulin activates protein C which helps in anticoagulation.

53
Q

What protein causes fibrinolysis?

A

t-PA

54
Q

Virchow’s triad includes which 3 general causes for Thrombosis?

A

Endothelial injury
Abnormal blood flow
Hypercoagulation

55
Q

What can cause endothelial injury?

How does it cause a thrombus?

A

Direct injury, infection, toxins, inflammation, hypercholesterolemia, smoking, turbulent flow.

The endothelial dysfunction leads to low NO which causes endothelial activation and increased adhesion molecules.

Promthrombotic: downregulation of thrombomodulin and activated protein C. Also, elaboration of plasminogen activator inhibitors.

56
Q

Which blood flow is good?

Which blood flow is bad?

A

Good - laminar flow

Bad - turbulent flow

57
Q

Where in circulation can alterations in blood flow occur? (5)

A 
Bifurcation of vessels.
Dilated vessels (aneurysm, hemorrhoids)
Internal obstruction
External compression
Poor heart function
58
Q

Primary (genetic) causes of hypercoagulability:

Deficiencies (3):

Increased amounts of (2):

A

Deficiencies:
Antithrombin (III) deficiency
Protein C deficiency
Protein S deficiency

Increased amounts of:
Factor Va (Factor V Leiden)
Prothrobin

59
Q

Risk factors for DVT

A 
Genetic disorders
Inactivity
Injury
Birth control
Smoking
Pregnancy
Cancers
Obesity
60
Q

What is a thrombus called when it is dislodged?

A

Embolus

61
Q

Symptoms of the following emboli:
Large saddle emboli
Small emboli
Very small emboli

A

Large saddle emboli - typically instantly fatal.
Small emboli - can travel more peripherally can cause SOB.
Very small emboli - can be asymptomatic.

62
Q

Factor V Leiden mutation

MOA

How to test for it?

A

Most common heritable hypercoagulopathy.

MOA: mutation in factor V that makes it resistant to cleavage by protein C.

Can test by direct genetic testing or activated protein C testing.

63
Q

How do you conduct an APCR test?

A

Measure clotting time before and after APC is added to a blood sample clotted w/ snake venom.

64
Q

How to suspect primary hypercoagulable states:

A

An initial event (DVT, PE) w/o family history, provoking factors, etc.

Tests: ATIII, protein C, S, factor V Leiden, Prothrombin mutation.

65
Q

Heparin-induced thrombocytopenia cause:

A

Abs to PF4-heparin.

  1. exposure to unfractionated heparin.
  2. formation of PF4-heparin complexes.
  3. IgG cross-linking of platelet Fc receptors and PF4-heparin complexes.
  4. platelet activation and aggregation.
66
Q

Antiphospholipid antibody syndrome (Lupus anticoagulant) cause:

What is present with thrombotic complications?

A

Abs against plasma proteins that bind to phospholipids.

Vascular: arterial or venous thrombosis.
Obstetric: unexplained miscarriage/stillbirth.

67
Q

Coumadin does what?

A

Blocks the action of vitamin K

68
Q

How can dissolution of thrombi occur? (2)

A

Spontaneous dissolution via endogenous fibrinolytic pathways.
Therapeutic fibrinolysis vis exogenous t-PA if within 6 hrs of onset.

69
Q

What is recanalization of a thrombus?

A

Basically the thrombus is eaten away.

70
Q

What are Lines of Zahn?

A

A way to tell if a thrombus/embolus occured during active blood flow (means there was antemortem clot).
There are alternating red and pale areas of RBCs and platelets/fibrin.

71
Q

Postmortem clots

A

Would not contribute to cause of death.

Simply pooled blood that has coagulated after demise.

72
Q

Types of emboli (5)

A 
Thromboemboli
Fat/marrow emboli
Air emboli
Septic emboli
Amniotic fluid emboli
73
Q

Fat emboli cause:

A

Fx or soft tissue trauma introduces fat or marrow into circulation.

Sx: respiratory distress, mental status changes.

74
Q

Air embolism cause:

A

Cardiac catheterization, changes in pressure.

“Decompression illness”

75
Q

Amniotic fluid embolism

A

Sudden dyspnea, cyanosis and shock.
Can cause subsequent pulmonary edema.
Introduces squamous cells, hair, fat, mucin into vessels.
Has an anaphylactic component as the embolus has foreign tissue (baby’s).
Possibly fatal.

76
Q

Septic emboli

What condition can cause it?

A

Bloodborne infective material.

Endocarditis - valve vegetations break off and manifest in other sites, like skin, retina and nail bed microemboli.

77
Q

White thrombus

A 
Arterial
Platelet-rich
Occurs in areas of high shear stress
Atherosclerosis*
Coronary, cerebral arteries.
78
Q

Red thrombus

A

Venous
Red cell rich
Stasis*
Lower extremities

79
Q

Rate of occlusion is associated with:

A

Collateral circulation. Less likely to lead to an infarct.

80
Q

3 causes of shock

A

Low cardiogenic output
Hypovolemia
Increased systemic inflammatory response syndrome

81
Q

What happens in neurogenic shock physiologically?

A

Vasodilation, decreased vascular resistance due to autonomic disruption.

82
Q

What happens in anaphylactic shock physiologically?

A

IgE-mediated decrease in vascular resistance.

83
Q

How do we get from pathogens to decreased tissue oxygenation?

A

PAMPs on pathgens bind TLRs on immune cells.
Release of cytokines (IL-1, IL-12, IL-18, IFNy, TNF).
Activation of complement, leading to leakage and vasodilation and procoagulation of endothelial cells.

84
Q

Final result of pathogens’ effect in shock:

A

Hypotension, hypovolemia and thrombosis leading to decreased tissue oxygenation.

85
Q

In what diseases are non-inflammatory edema and effusions common?

A

HF
Liver failure
Renal disease
Severe nutritional disorders

86
Q

What kinds of disorders can increase hydrostatic pressure?

A

Disorders caused by impaired venous return.

87
Q

What can cause lymphatic obstruction?

What microbes in particular can cause it?

A

Trauma, fibrosis, tumors, infections.

Wuchereria bancrofti, Brugia malayi, Brugia timori. Can lead to elephantitis.

88
Q

Subcutaneous edema is generally caused by what?

What diseases should be correlated with it?

What can it complicate?

A

High hydrostatic pressures.

Cardiac or renal disease.

Wound healing and clearance of infections.

89
Q

How can cardiac disease lead to subcutaneous edema?

A

The heart has lower pumping leading to congestion in the lungs (edema, effusions) and decreased blood arriving at the kidneys.
The decreased blood flow to the kidneys activates the RAAS system and increases blood volume, thus leading to edema.

90
Q

Pulmonary edema is a common clinical problem in patients with what diseases?

A

Left ventricular failure, renal failure, respiratory distress, pulmonary infection or inflammation.

91
Q

Pulmonary effusions are a symptom of:

A

HF

92
Q

How are peritoneal effusions caused?

A

Usually by portal HTN or can be due to liver failure.

Commonly becomes infected.

93
Q

What are hemosiderin-laden macrophages and how do they develop?

A

The are “heart failure cells”.

Chronic pulmonary congestion, from HF, causes thickening and fibrosis of the septa. This causes the alveoli to have many H-L Mo.

94
Q

How does nutmeg liver develop?

What is congested in particular?

What does chronic congestion lead to?

A

Chronic hepatic congestion.

The centrolobular regions are brown and depressed (cell death) and the surrounding zones are tan (non-congested).

Central v.

Hemosiderosis

95
Q

What is the histological identifier for endothelial cells?

A

Weibel-Palade bodies

96
Q

Explain thrombin and fibrinogen’s interactions:

A

Cleaves fibrinogen to fibrin which is insoluble.

Creates a fibrin meshwork -> aggregation.

97
Q

What are alpha-granules and dense cytoplasmic granules in endothelium?

A

alpha-granules: have P-selectin and contain fibrinogen, factor V, and vWF and factors involved in wound healing (fibronectin, PF4, PDGF, TGF-beta).

Dense granules: contain ADP, ATP, Ca++, serotinin and epinephrine.

98
Q

Intrinsic pathway pathology would show a long:

Extrinsic pathway pathology would show a long:

A

aPTT

PT

99
Q

What are 2 limiting factors in coagulation?

A

Blood flow

Loss of surface area of the endothlium.

100
Q

D-dimer is from what?

A

An elevated breakdown of fibrinogen.

101
Q

What is alpha2-antiplasmin?

A

Produced by plasmin that actually inhibits plasmin. Helps to buffer its effects.

102
Q

What does protein C/S inhibit?

A

Factors V and VIII

103
Q

What are the prothrombotic (procoagulant and antifibrinolytic) roles of the endothelium?.

A

Procoagulant: If activated by cytokines, it can downregulate thrombomodulin, protein C and tissue factor inhibitor.

Antifibrinolytic: PAIs are secreted by endothelium which limits fibrinolysis by downregulating t-PA.

104
Q

Primary vs. secondary hypercoagulability

A

Primary: genetic

Secondary: acquired

105
Q

Superficial venous thrombus

A

Typically occurs in saphenous vs. in setting of varicosities.

Generally do not embolize.

106
Q

What are the 4 fates of a thrombus?

A

Propagation
Embolization
Dissolution
Organization and recanalization

107
Q

What is disseminated intravascular coagulation (DIC)?

A

Not a disease, but a complication of a number of conditions associated w/ systemic activation of thrombin.

They are microvascular thrombi in microcirculation.

108
Q

Most systemic thromboembolism arise from what?

Where do they usually come to rest?

A

Intracardiac mural thrombi most from the LV.

In the LE usually, but can be in brain, kidneys, spleen, etc.

109
Q

What is the detailed pathogenesis of septic shock? (3 then 2)

A
  1. Inflammatory and counter-inflammatory respones
    - -complement cascade
    - -resulting immunosuppression
  2. Endothelial activation and injury
    - -vascular leakage
    - -hypotension
  3. Induction of a procoagulant states
    - -increased factor XII, tissue factor and decreased antithrombin and protein C.
    - -DIC

Mechanisms of Disease Exam #1 (5 decks)

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