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MHD block 4 > Abnormal Hemostasis I and II > Flashcards

Abnormal Hemostasis I and II Flashcards

1
Q

Quantitative Disorders of platelets

A

A number of diseases result in a decrease or increase in the number of platelets.

thrombocytopenia, thrombocytosis, thrombocythemia

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2
Q

thrombocytopenia

A

A decreased platelet count results in bleeding

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3
Q

thrombocytosis

A

a benign increase in platelet count

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4
Q

thrombocythemia

A

when it is a clonal proliferation (neoplastic)

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5
Q

what causes Thrombocytopenia
s

A

Alterations in bone marrow

Hereditary thrombocytopenia

Abnormal hematopoiesis (acquired, B12/Folate deficiency, pre-leukemia)

Drug Induced thrombocytopenia (Heparin, gold, quinine, quinidine, sulfonamides, GP IIb/IIIa Inhibitors)

Dilutional (hemodialysis, heart lung machine)

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6
Q

what is a possible outcome of heparin complexing with PF-4

A

Ab are formed to the complex - the Ab lead to activation and aggregation of platelets - can block blood vessels leading to gangrene, ampuation, stroke exc. (complication of Heparin therapy)

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7
Q

ITP

A

Immune thrombocytopenic purpura (IgG mediated)

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8
Q

TTP

A

Thrombotic thrombocytopenic purpura (abnormal vWF multimers), arterial thrombi (platelet-rich)

get many small bruises due to increased bleeding

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9
Q

HUS

A

Hemolytic Uremic Syndrome- thrombocytopenia

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10
Q

Splenectomy

A

thrombocytosis (increased platelet count), platelet function is normal

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11
Q

Reactive thrombocytosis

A

thrombocytosis (increase) due to cancer, infection, drugs.

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12
Q

Autonomous thrombocytosis (thrombocythemia)

A

Platelets ↑ (> 1,000,000/µl): clusters of platelets in circulation. Bleeding may occur.

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13
Q

Qualitative Disorders
 of platelets

A

Platelet numbers are usually normal, however, platelet function is impaired

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14
Q

3 causes of qualitative platelet disorders

A

Disease induced platelet defects (Liver disorders, paraproteinemia)

Drug induced platelet defects (Aspirin, NSAIDS (non-steroidal anti-inflammatory drugs))

Diet induced platelet defects (Omega 3 fatty acids (ocean fish), Eskimos)

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15
Q

Inherited Disorders of Platelets


A

Glanzmann’s thrombasthenia

Bernard-Soulier disease

Storage pool disease (decrease dense granule content, no aggregation )

Other disorders (Purpura of unknown origin - gray platelet syndrome, lack of alpha granules)

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16
Q

Glanzmann’s thrombasthenia

A

Autosomal recessive, GPIIb/IIIa defect, aggregation defect, bleeding time ↑

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17
Q

Bernard-Soulier disease

A

Autosomal recessive, GP Ib defect, adhesion defect, bleeding time ↑

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18
Q

polycythemia vera

A

is a neoplasm in which the bone marrow makes too many red blood cells. It may also result in the overproduction of white blood cells and platelets

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19
Q

non-thrombocytopenic purpuras

A

vascular disorders

common, but do not result in severe bleeding diathesis.

Platelet function and coagulation are normal.

Easy bruising, bleeding from mucosa, purpura, vasculitis.

20
Q

Subendothelial Disorders

A

Congenital- *Ehler Danlos Syndrome-Hypermobile joints. Hyperflexible skin, osteogenesis imperfecta, drugs, infections, amyloidosis

Acquired- Purpura simplex, amyloids, drugs, steroid purpura (prednisone), Cushing’s syndrome (steroid excess), Henoch-Schonlin purpura (usually drug induced).

21
Q

Endothelial Disorders

A

Congenital- Most common, hereditary hemorrhagic, telangiectasia (HHT), arteriovenous malformation; giant hemangioma (Kasaback-Merritt syndrome)

Acquired- Inflammation, vasculitis (drugs,viruses, Rickettsia)

22
Q

other types of diseases that cause bleeding disorders

A 
non-thrombocytopenic purpuras
subendothelial disorders
endothelial disorders
mechanical disorders
nutritional disorders
23
Q

Protein C is activated by

A

thrombin-thrombomodulin with protein S as a cofactor

24
Q

activated Protein C’s function

A

it is a serine kinase that regulated the coagulation cascade by digesting factors V and VIII

25
Q

protein C resistance

A

defect in Factor V that prevents it from being degraded by protein C (once activated it is continuously active) can be determined by PCR

26
Q

Hemophilia A defect

A

factor VIII defect, Classical

27
Q

Hemophilia B defect

A

factor IX defect, Christmas Disease

28
Q

vitamin K dependent factors

A

C, S, II, VII, IX, X

29
Q

prothrombin time

A

a labatory test for extrinsic pathway.

II, V, VII, X and fibrinogen

use blood plasma and add activators to it tos ee how long it takes to clot

30
Q

APTT

A

lab test for intrinsic pathway activation. VIII, IX, XI and XII (actually measures all factors but FVII, FXIII, protein C and S).

31
Q

hemophilia’s transmission

A

Both are transmitted as sex linked recessive

32
Q

blood tests in hemophilias

A

APTT is elevated, no effect on platelets

33
Q

Von Willebrand’s Disease

A

Hemostatic defect due to von Willebrand factor (ristocetin co-factor, factor VIII antigen) defect.
vW factor binds to platelet receptors (glycoprotein Ib, IIb-IIIa) and to collagen and subendothelium.

34
Q

types of von Willebrand’s disease

A
  1. Type-1 and Type-3 von Willebrand’s diseases are characterized by a decrease in the circulating level of the factor.
  2. Type-2 von Willebrand’s disease is characterized by a qualitative defect in the protein.
35
Q

differences in hemophilias vs. von Willebrand’s disease

A

Hemophilias
APTT prolongation
Platelet function-normal
Bleeding time - no effect

Von Willebrand’s Disease
APTT slightly elevated due to mild reduction in factor VIIIc
Hemostatic function impaired due to impaired adhesion of platelets to collagen in-vivo.
Bleeding time elevated.

36
Q

what occurs in Primary Fibrinolysis

A

In primary fibrinolysis, only fibrinogen is converted into fibrinogen degradation products.
This condition is seen in dead fetus syndrome (Abruptio Placenta).

Fibrinogen →→→ Fibrinogen degradation products

37
Q

outcomes from primary fibrinolysis

A

Excessive fibrinolysis can result in bleeding due to decreased fibrinogen levels.

Fibrinogen degradation products can also produce anticoagulant effects.

Overdosage of thrombolytic (t-PA) agents can result in a primary fibrinolytic state and cause bleeding.

38
Q

Secondary Fibrinolysis 
aka

A

Disseminated intravascular coagulation

39
Q

what occurs during secondary fibrinolysis

A

In secondary fibrinolysis both fibrin and fibrinogen are digested by plasmin. Secondary finbinolysis is also associated with digestion of clotting factors and consumption of platelets.

commonly occurs when both fibrinolysis and coagulation are activated

get both synthesis and degradation of fibrin simultaneously

40
Q

D-dimer test

A

can indicate either a DVT or DIC (higher levels with DIC)

41
Q

Deficiency of a2-Antiplasmin

A

Results in increased fibrinolysis (Bleeding) due to a lack of inhibition on Plasmin

42
Q

a2-Antiplasmin (a2-AP)

A

inhibits plasmin when it binds to it

43
Q

Drug Induced Bleeding Disorders

A 
Bleeding with thrombolytic drugs.
Bleeding with anticoagulants (Heparin)
Bleeding with drugs
      - Anti-platelet drugs
	  - Thrombolytic drugs
Drug induced thrombocytopenia
Heparin induced thrombocytopenia (HIT)
44
Q

which test is used to diagnose hemophilias

A

Activated partial thromboplastin time

45
Q

which test is used to monitor therapeutic heparinization in treatment of a DVT

A

Activated partial thromboplastin time

46
Q

which test is used to monitor anticoagulating status (ie warfarin use)

A

PT/INR

MHD block 4 (9 decks)

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