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Gen Path Final > Vascular Disorders II > Flashcards

Vascular Disorders II Flashcards

(47 cards)

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1
Q

Prothrombin activation is inhibited by

A

APC

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2
Q

Plasminogen activation is inhibited by

A

TAFIa

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3
Q

Prostacyclin (PGI2) and Nitric Oxide (NO)

A
  • Anti-thrombotic
  • Vasodilation inhibits platelet aggregation
  • SECRETED by endothelium
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4
Q

ADPase

A
  • Anti-thrombotic
  • SECRETED by endothelium
  • Inhibits platelet aggregation
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5
Q

Tissue Plasminogen Activator (tPA)

A
  • Anti-thrombotic
  • Leads to fibrinolysis
  • SECRETED by endothelium
  • Most active when plasminogen is bound to fibrin
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6
Q

Thrombomodulin and Proteins C and S

A
  • Anti-thrombotic
  • MEMBRANE-ASSOCIATED in endothelium
  • Thrombomodulin binds thrombin and activates Protein C
  • Proteins C and S degrade 5 (V) and 8 (VIII)
  • Proteins C and S depend on Vit K
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7
Q

Heparin-like molecules

A
  • Anti-thrombotic
  • MEMBRANE-ASSOCIATED in endothelium
  • Bind ATIII
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8
Q

Tissue Factor Pathway Inhibitor (TFPI)

A
  • Anti-thrombotic
  • MEMBRANE-ASSOCIATED
  • Inhibits the 3-7 complex
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9
Q

Endothelin

A
  • Pro-thrombotic

- Assists primary hemostasis via vasoconstriction

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10
Q

von Willebrand factor

A

Enhances platelet binding to collagen

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11
Q

Which substances are released from platelet granules to recruit additional platelets?

A
  • ADP
    • Activation
  • Thromboxane A2 (TXA2)
    • Vasoconstriction

Both enhance platelet aggregation, along w/ Ca

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12
Q

Liver produces all clotting factors EXCEPT

A
  • III [endo and fibroblasts]
  • IV [that’s calcium]
  • VI [does not exist]
  • XIII

8 production is shared w/ endo; liver is not 8’s primary source

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13
Q

Prothrombin time (PT) measures

A

Extrinsic System

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14
Q

Partial Thromboplastin Time (PTT) measures

A

Intrinsic System

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15
Q

What are the 3 steps of coagulation?

A
  1. Initiation
  2. Amplification
  3. Propagation
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16
Q

What happens during Initiation of Coagulation?

A
  • VII binds III (TF) on damaged endothelial cell

- 9, 10, and (some) thrombin produced

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17
Q

What happens during Amplification of Coagulation?

A
  • Thrombin activates platelets
  • Thrombin cleaves vWF-8 complex
  • Generates 5, 8, 11
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18
Q

What happens during Propagation of Coagulation?

A
  • 10 produced
  • 10 and 5 make thrombin
  • 10 separated from platelet surface complex and inhibited
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19
Q

Two main functions of thrombin

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A
  • Activate fibrinogen (-> fibrin)

- Activate Factor 13

20
Q

Compare and contrast urokinase-type plasminogen activator (uPA) from tissue plasminogen activator (tPA)

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A

uPA is made by many cells whereas tPA is made only by endothelial cells

uPA is less susceptible to inhibition than tPA

21
Q

a-2-antiplasmin

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A

Inhibits fibrinolysis by binding plasmin

22
Q

Plasminogen Activator Inhibitor (PAI)

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A
  • Inhibits fibrinolysis by inhibiting tPA and uPA

- Made by endothelial cells and platelets

23
Q

Thrombus vs Thrombosis vs Embolus

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A

Thrombus = aggregate of platelets, fibrin, and blood cells (may or may not be pathogenic)

Thrombosis = pathogenic thrombus

Embolus = translocated thrombus

24
Q

Virchow’s triad

Study These Flashcards
A

Abnormal blood flow and endothelial injury cause each other and both cause hyperoagulability

Only 1 of 3 is needed for thrombosis

25
Antithrombin III
- Most potent inhibitor of coagulation - Neutralizes thrombin and Factor X [common pathway] - Made in liver
26
How does inflammation lead to hyperocagulability?
Increased TF and fibrinogen
27
How does glomerular disease lead to hyper coagulability?
Selective loss of antithrombin III
28
Protein losing enteropathy
Leads to hyper coagulability via loss of antithrombin III and inflammation
29
Which endocrine disorder is associated with hypercoagulability?
Hyperadrenocorticism
30
What are 3 consequences of ischemia?
First, hypoxia decreases ATP production 1. Na pump failure -> swelling 2. Increased anaerobic glycolysis -> decreased pH -> clumping of chromatin 3. Ribosome detachment -> decreased protein production -> lipid deposition
31
Why does restoring blood flow to ischemic tissue cause complications?
Hypoxanthine (ATP metabolism byproduct) reacts w/ O2 to make ROS - Uric acid - H2O2 - Superoxide free radical
32
Describe the appearance of CHRONIC infarcts
"lumpy" margin of organ (i.e. kidney); where red blood cells and scars were broken down
33
True or false: propagation of embolus is always towards the heart, even in arteries.
True
34
Describe an antemortem thrombus
- Firm - Adheres to vessel wall - Red-to-tan - Granular
35
Describe a postmortem clot/thrombus
- Gelatinous - deep red (sometimes yellow chicken fat) - smooth
36
Arterial thrombi
- Pale (b/c faster flow, less time for blood cells to deposit) - Lamellations (Lines of Zahn) - Visible grossly - "bullseye" of fibrin and cell debris histologically
37
Venous thrombi
- Redder than arterial | - Attached to vessel wall
38
Heartworm/Dirofiliaria
- Sit within pulmonary artery
39
Hypertropic cardiomyopathy
- Thickened left ventricle - Left ventricle fills poorly - Clot develops in left atrium due to "traffic jam" of blood - Embolism in distal abdominal aorta ("saddle thrombus") - Clinical signs include blue toes, failure to use hind legs
40
Normal buccal mucosal bleeding time
< 4 min
41
Aside from decreased production or increased consumption of platelets, what else might cause thrombocytopenia?
Sequestration of platelets in spleen
42
Hemophilia A
- Affects factor 8 (VIII) - Variable severity - Dogs and cats - X-linked recessive
43
Hemophilia B
- Affects factor 9 (IX) - Severe - Labs esp., other dogs, cats - X-linked recessive
44
Vitamin K antagonists
- Warfarin - Dicoumarol (sweet clover) - Work by inhibiting epoxide-reductase - K is active when REDUCED
45
Disseminated Intravascular Coagulopathy
- Starts as clotting/ischemia but results in HEMMORRHAGE - Lab results: - PT and PTT up - Thrombocytopenia - FDP increased - ALWAYS secondary to another process - Poor prognosis
46
What are the clinical signs of PRIMARY hemostatic disorders?
- Petechiae/ecchymoses - Gingival bleeding - Hematuria / Melena (GI bleeding) - Hyphema (intraocular bleeding) Buccal bleeding time > 4 minutes
47
What are the clinical signs of SECONDARY hemostatic disorders?
- Hematomas ("mass" hemorrhage) - Cavitary hemorrhage - Delayed bleeding from venipuncture sites

Gen Path Final (5 decks)

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