Bruising And Bleeding Flashcards

1
Q

Major causes of bleeding disorders

A

. Structural
. Platelet-related
. Clotting factor-related (platelet plug not stable)

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2
Q

Leukemia

A

. Group of neoplasticism disorders affecting leukopoietic tissues in body
. Characterized by leukocytosis, immature leukocytes in peripheral blood
. Proliferation of immature cells in marrow suppressing normal cell growth (like MK cells)

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3
Q

Idiopathic thrombocytopenic purpura

A

. Platelet destruction inc. from circulating antiplatelet antibodies in plasma
. Platelet survival is shortened

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4
Q

Hemophilia A/B

A

. Genetic defect x-linked recessive
. Inc. bleeding from clotting disturbance
. 70% people are inherited, others from spontaneous mutation
. A is deficiency in factor VIII, b from IX deficiency

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5
Q

Disseminated intramuscular coagulopathy

A

. Systemic activation of blood coag resulting in generation and deposition of fibrin
. Leads to microvascular thrombi in organs causing dysfunction
. Possible consumption and subsequence exhaustion of coag proteins and platelets may cause severe bleeding

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6
Q

Diascopy

A

. Test for blanchability by applying pressure w/ finger and observing color change

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7
Q

Normal platelet count

A

. 150,000-400,000
. Thrombocytopenic: less than 150,000
. Thrombocytosis: over 400,000

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8
Q

Partial thromboplastin time

A

.blood test evaluating integrity of intrinsic and common coag pathway and to monitor patients on Heparin
. Normal 25-37 s.

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9
Q

Prothrombin time

A

. Blood test that measures how quickly blood clots

. Normal 10-14 s.

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10
Q

International normalized ratio (INR)

A

. 1.1 or below is normal

. 2-3 is therapeutic range when taking blood thinners

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11
Q

Bleeding time (BT)

A

. Standard filter paper should be every 30 s. Until blood completely stops
. Normal: 2-9 minutes
. Risk of bleeding inc. w/ time over 10 min.

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12
Q

Unexplained nosebleeds suggest ___

A

. Platelet defects

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13
Q

5 causes of dec. platelet production

A
. Meds
. Bone marrow replacement by malignancy, fibrosis, or granulomas 
. Bone marrow aplasia
. Alcohol 
. B12 deficiency
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14
Q

5 causes of inc. platelet consumption

A
. Splenic sequestration 
. Autoimmune thrombocytopenia (idiopathic, HIV, lupus, lymphoproliferative issues, meds)  
. Disseminated intravascular coag. 
. Thrombotic thrombocytopenic pupura
. Sepsis
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15
Q

Evaluation of bleeding patient

A

. Clinical context (post-surgical, sepsis, exposure to anticoags)
. Personal history (onset in infancy = heritable condition, as adults = milder heritable condition or acquired cause)
. Family history
. Location (mucocutaneous bleeding = suggests qualitative/quantitative platelet defects, joint/soft tissue= disorders of coag factors

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16
Q

Platelets

A

. Critical role in hemostasis

. Functions: adhesion, activation, aggregation

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17
Q

Bernard-soulier syndrome

A

. Deficiency in GpIb platelet Factor

18
Q

Glanzmann thrombasthenia

A

. Deficiency in GpIIb-IIIa complex in platelet clotting

19
Q

Von willebrand Disease

A

. Most common inherited bleeding disorder, most cases autosomal dominant
. Due to issues w/ Von willebrand factor (glycoprotein that binds platelets to subendothelium and is a carrier of factor VIII)

20
Q

Type I Von willebrand disease

A

. Type i: 75-80% pts, mild to moderate bleeding, don’t bleed spontaneously, involves skin and mucous membranes
. Keep in mind for teen patients
. Normally diagnosed when excessive bleeding occurs after procedure, heavy or long menstrual bleeding (changing of pad once an hour)

21
Q

Type II Von willebrand disease

A

. 15-20% patients
. Moderate to severe bleeding
. Usually present in childhood or adolescence

22
Q

Type 3 Von willebrand disease

A

. Severe bleeding in infancy and childhood

. Autosomal recessive inheritance

23
Q

Bernard-Soulier syndrome

A

. Autosomal recessive inheritance
. Reduced or abnormal platelet membrane expression of GIb/IX
. Failure of adhesion
. Severity of symptoms vary
. Clinical features: petechia, ecchymosis, recurrent epistaxis

24
Q

Glanszmann’s thrombasthenia

A

. Autosomal recessive
. Platelets contain low or defective glycoprotein GpIIb/IIa (fibrinogen receptor)
. Platelets aggregation impaired os no thrombus formation
. Clinical features: petechia, ecchymosis, recurrent epistaxis

25
Q

Idiopathic thrombocytopenia

A

. Acquired disorder
. Immune mediated destruction of platelets (antibodies against. Platelet membrane antigens)
. Only bleeding presentation, spontaneous bruising doesn’t occur until platelet count is under 30,000
. Fatigue common
. Diagnosis of exclusion
. Secondary causes: leukemia, meds, lupus, cirrhosis, HIV, hep C

26
Q

ITP in children

A

. Acute
. Follow after viral vaccines
. Resolves w/in a few weeks w/o treatment

27
Q

ITP in adults

A
. Chronic 
. No prodrome
. Idiopathic 
. Affects more women 
. Requires treatment
28
Q

Disseminated intravascular coagulation

A

. Always has underlying etiology
. Cause must be identified to treat coagulopathy triggering factor damages vessels
. Uncontrolled activation of coag cascade where many clots develop throughout vasculature
. Inc. clotting depletes platelets and clotting factors creating excessive bleeding
. May cause tissue ischemia from occlusive thrombi AND bleeding from consumption of platelets and clotting factors
. Caused from sepsis, trauma, burns, obstetric complications, and cancer
. Bleeding in multiple sites, petechia/ecchymosis, gangrene

29
Q

Drug induced thrombocytopenia

A

. Severe mucocutaneous bleeding 7-14 days after exposure
. Discontinuation of meds leads to resolution in 7-10 days
. Recovery kinetics depends on rate of drug clearance

30
Q

Heparin-induced thrombocytopenia

A

. Immunologically mediated adverse reaction causing formation of IgG antibodies to heparin-platelet factor 4 complexes
. Causes inappropriate activation of platelets, thrombocytopenia, and pro thrombi state
. Thrombosis in both arterial and venous systems occur in up to 50% of cases
. Decline in baseline platelet count of 50% or more
. Onset occurs w/in 5 to 14 days or exposure to heparin

31
Q

Aspirin

A

. Irreversibly binds to platelets
. Inhibits COX and TBA2 production
. Produces inhibitory effect of platelet aggregation

32
Q

NSAIDS

A

. Inhibits platelet COX and TXA2

. Reversible bind to platelets for limited time

33
Q

Plavix

A

. Platelet receptor inhibitor

. Inhibits platelet adhesion and aggregation

34
Q

Alcohol effect on platelets

A

. Dec. TXA2 release

35
Q

Hemophilia

A

A: VIII issue
. B: IX issue
. Severity inversely proportional to factor levels
. Mild: spontaneous bleeding rare but can occur w/ significant surgery or trauma
. Severe: presents in infants w/ spontaneous bleeding into joints
. Female carries asymptomatic

36
Q

Hemophilia C

A

. Factor XI deficiency
. Autosomal recessive
. Jew problem
. Most mild form of bleeding

37
Q

Factor XIII deficiency

A

. Involved w/ process of cross linking fibrin
. Delayedbleeding occurs hours to days after hemostatic challenge
. Spontaneous intracranial hemorrhage and recurrent pregnancy loss are indicators

38
Q

Acquired antibodies to factor VIII

A

. Acquired hemophilia A
. Spontaneous antibodies to factor VII in adults w/o prior history
. High risk: lymph malignancy, CT disease, post party’s, or post surgery
. Clinical presentation: soft tissue ecchymosis, hematoma, mucosal bleeding
. Leads to severe life threatening bleeding

39
Q

Liver disease effect on bleeding

A

.dec. synthesis of clotting factors
. Splenomegaly
. Thrombopoietin controls circulating platelets by stimulating marrow to produce megakaryocytes and is impaired
. Complication from cirrhosis may be esophageal varices

40
Q

Vit, K deficiency

A

. Dec. synthesis of factors II, VII, IX,

. Occurs as result of dietary deficiency, malabsorption, dec. production by intestinal bacteria

41
Q

Warfarin (Coumadin)

A

. Vit. K antagonist

. Inhibits vit. K dependent carboxylase important for coag factors II, VII, IX, and X