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Pathology -- Cardiology > Fluid and Hemodynamic Alterations II > Flashcards

Fluid and Hemodynamic Alterations II Flashcards

1
Q

What is a thrombus?

A

Ante-mortem blood clot formation on vascular wall within the CV system

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2
Q

What are thrombi made of?

A

Platelets, Fibrin, and Entrapped Cellular elements

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3
Q

What circumstances do you see clots in?

A

Extravascular (hematoma) and intravascular (postmortem space)

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4
Q

What are the components of a postmortem clot?

A

Coagulation factors and erythrocytes only

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5
Q

Gross appearance of a postmortem clot?

A

Currant-jelly clot

Chicken Fat Clot

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6
Q

Describe a currant jelly clot

A

Dark to red-black, smooth and shiney, rubbery, uniform, molded to the shape of the vessel, not attached, increased RBC levels

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7
Q

Describe a chicken fat clot

A

Like currant jelly, but yellow

Result of settling and separation of RBC and plasma

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8
Q

Gross appearance of thrombus

A

Heterogenous
More organized than clots, attached to wall
Laminated

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9
Q

Appearance of an arterial thrombi?

A

Pale. grey-tan, dry, friable, concentric layers, attached to vessel wall

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10
Q

Appearance of venous thrombi?

A

Red, friable, attached to vessel wall, confused with clot, often occlusive

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11
Q

Contents of a thrombus?

A

Fibrin, Platelets, WBCs, RBCs, +/- bacteria

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12
Q

What are the laminated lines of Zahn?

A

arterial thrombi, alternating layers of platelets/fibrin (pale) and RBCs (dark)

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13
Q

Thrombus vs. PM Clot. Formation?

A

T – Ante-mortem

C – Post-mortem

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14
Q

Thrombus vs. PM Clot. Cause

A

T – Endothelial Injury

C – Stagnant blood of dead animal

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15
Q

Thrombus vs. PM Clot. Attachment

A

T – Vessel Wall

C – None

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16
Q

Thrombus vs. PM Clot. Consistency.

A

T – Dry

C – Moist

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17
Q

Thrombus vs. PM Clot. Surface

A

T – Granular, Rough

C – Smooth, Glistening

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18
Q

Thrombus vs. PM Clot. Vascular endothelium?

A

T – Damaged, Rough

C – Smooth, Intact

19
Q

Thrombus vs. PM Clot. Organization.

A

T – Partial

C – None

20
Q

Thrombus vs. PM Clot. Structure.

A

T – Laminated.

C – Homogenous

21
Q

Three primary causes of thrombosis.

A

Endothelial Injury (Most Common)
Alterations in Blood Flow
Hypercoagulability

22
Q

Causes of endothelial injury leading to thrombosis?

A

Endocardium: Infar./myocarditis, Immune Rxn, valve prbs
Arteries: Atherosclerosis, Vasculitis
Radiation, Bacterial agents, catheter

23
Q

Two types of blood flow alterations that can lead to thrombosis?

A

Turbulence (Arterial/Cardiac)

Stasis (Venous Thrombi)

24
Q

Mechanism of blood flow alterations leading to thrombosis?

A

Stasis/Turbulence fuck up laminar flow. Platelets hit the endothelium. Coagulation factors aren’t diluted by fresh blood. Retard inflow of coag. inhibitor. Promote endothelial cell activiation

25
Q

Four examples of alterations in normal blood flow

A

Aneurysms – Abnormal dilation of vessels
MI – Necrotic myofibers do not contract
Ulcerated atherosclerotic plaques – local turbulence
Hyperviscosity syndromes (polycythemia) – slow BF

26
Q

Causes of primary hypercoagulability?

A 
Factor V Leiden
Prothrombin mutation
Elevated homocysteine levels
antithrombin III deficiency
protein C deficiency, protein S deficiency
Defects in fibrinolysis
27
Q

Causes of secondary hypercoagulability?

A 
Oral contraceptives -- increased synth of coag. factors
Cancer -- tumor products
Tissue damage  -- stasis of injury site
Aging -- increased platelet aggregation
Heparin-induced thrombocytopenia
antiphospholipid antibody (lupus)
28
Q

What happens after a thrombus has formed

A

Propagation (grows larger – tail)
Detachment (embolization)
Stays attached

29
Q

What do you do with a thrombus that stays attached?

A

Lysis
Retraction (incorporate into vessel walls)
Organization (endothelial growth over surface, hyalinization, Calcification)
Recanalization

30
Q

Where do you typically see artherial thrombi?

A

Coronary, Cerebral, and Femoral Arteries

31
Q

Significance of thrombi?

A

Obstruction – Infarction, Congestion

Embolization

32
Q

What is an embolism?

A

Detached IV solid, liquid, or gasseous masses carrid by the blood stream to distant sites

33
Q

Almost all emboli are…

A

Fibrinous thromboembolus

34
Q

Sequale of Pulmonary emboli (not including silent ones)

A

Sudden Death – R Heart failure, CV collapse (big ones)
Pulmonary Hemorrhage (obs. of medium vessels)
Infarction - Obs. of small vessels
Pulmonary HTN – from multiple. leads to R sides HF

35
Q

Almost all systemic emboli come from….

Others from…

A

Intracardiac mural thrombi (LV wall infarct, dilated atria, fib)
Aneurysms, Atherosclerotic plaques, Septal Defect

36
Q

Whats it called when an emboli hits systemic circulation by goign through a septal defect?

A

Paradoxical emboli

37
Q

List some causes of infarction

A 
Thrombus/Thromboemboli
Local vasospasm
Tumor
Torsion
Edema causing vascular compromise
38
Q

What is a white (anemic) infarcts

A

Arterial occlusion in solid tissue

39
Q

What is a red (hemorrhagic) infarct

A

Venous occlusion
Tissues with dual blood supplies
Previously congested tissues, sluggish venous outflow

40
Q

Microscopic features of infarcts

A

Coagulative necrosis (except brain), sharply demarcated
+/- occluded vessels, +/- congestion
Congestion and leukocyte influx in tissues
Fibrosis

41
Q

Which type of thrombus is most prone to be occlusive

A

Venous

42
Q

Name for the triad of endothelial injury, abnormal blood flow, and hypercoagulability

A

Virchow’s Triad

43
Q

Common symptom of L sided embolism

A

Gangrene

44
Q

Fat emboli are typically surrounded by cells from

A

Marrow

Pathology -- Cardiology (13 decks)

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