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SUMPHYS2 > PHY-Bleeding DO > Flashcards

PHY-Bleeding DO Flashcards

1
Q

What is possible etiology of acquired bleeding disorders

A

1] complications p circumcision, 2] ASA, Coumadin, 3] Bleeding surgery, hemarthrosis, GI/urinary bleeding, 4] UE DVT (this is not common)

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2
Q

What are tendency associated with bleeding disorders

A

Epistaxis, bruising, ecchymoses, bleeding p venipuncture, gums p brushing

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3
Q

What is the pathophysiology of Hereditary Hemorrhagic Telangiectasia aka Osler, Weber, Rendu

A

AD inheritance results in defects of TGF beta-1 effect formation of connective tissue necessary for blood vessel formation resulting in arteriovenous malformation

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4
Q

What is the manifestations of Hereditary Hemorrhagic Telangiectasia aka Osler, Weber, Rendu

A

1] Vascular malformations, 2] Skin/mucosal malformations on tongue, hands/fingers, nose, lips, conjunctiva, 3] Also brain and lungs

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5
Q

What is the pathophysiology of Ehler-Danlos Syndromes

A

All effect collagen structure (28 genes, 19 types)

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6
Q

What is the manifestations of Ehler-Danlos Syndromes

A

Easy bruising, hyperelasticity of skin, hypermobility of joints, weakness of tissues (including blood vessel walls)

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7
Q

What is vascular type IV - Ehler-Danlos Syndromes

A

joint or blood vessel ruptures 20-40 yo due to weak vessel walls

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8
Q

What is Marfan syndrome

A

Genetic d/o of connective tissue due to mutation in Fibrillin-1 (Chr 15); Fibrillin 1 binds TGF-beta causing local inflammatory effects damaging aorta, valves and structure of the vasculature

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9
Q

What is the features of platelet disorders

A

1] Spontaneous bleeding, 2] Prolonged Bleeding Time-cut pt watch, 3] Normal PT-prothrombin, heparin 4] Normal PTT-INR warfarin 5] Low count

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10
Q

Why do platelet disorders have prolonged bleeding time?

A

prolonged BT is about platelet plugging. normally we stop bleed bc of the platelet plug, not always from clot

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11
Q

Why do platelet disorders have normal PT/PTT

A

regards clotting factors made by the liver- NOT about platelet activity.

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12
Q

List the different disorders that cause Thrombocytopenia

A

1] aplastic anemia, 2] Marrow infiltration (leukemia), 3] Ineffective thrombopoiesis (B12/folate), 4] Increased destruction, 5] Infection (HIV), 6] Consumption (DIC)

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13
Q

What are the drugs that affect platelets

A

1] Quinidine, 2] Sulfa, 3] PCN, 4] Heparin - HIT, Heparin induced thrombocytopenia, 5] Thiazides

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14
Q

What is the most common cause of thrombocytopenia in children

A

Idiopathic thrombocytopenic purpura

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15
Q

Who else is affected by Idiopathic thrombocytopenic purpura

A

Female 20-40, possibly assoc with SLE

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16
Q

What is the pathophysiology of Idiopathic thrombocytopenic purpura

A

IgG vs GPIIb/IIIa surface receptors which leads to Removal of targeted platelet by spleen

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17
Q

What is the findings of ITP

A

No splenomegaly, Must examine marrow for increased megakaryocytes

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18
Q

What is the treatment of ITP

A

Steroids, splenectomy

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19
Q

Who is more affected by thrombocytopenic purpura TTP ?

A

Primarily Women

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20
Q

What is the pentad for TTP

A

1] Thrombocytopenia, 2] Microangiopathic anemia (low MCV), 3] Neurologic changes, 4] Renal failure, 5] Fever

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21
Q

What is the pathophysiology of TTP

A

Extensive microscopic clotting in small blood vessels (will clot A LOT in small vessels. ) by failure to cleave vWF polymers (enzyme ADAMTS13). Shear stress on RBC hemolysis.

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22
Q

What are the clinical findings of TTP

A

1] Darkening of urine from hemolytic anemia, 2] Small clots lead to widespread areas of ischemia, 3] N/V if gut ischemia, 4] Purple splotches on the skin

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23
Q

What is the treatment of TTP

A

plasmapheresis

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24
Q

What is Heparin induced thrombocytopenia

A

Several days of heparin or LMWH tx which leads to IgG mediated complexes destroy platelets, autoimmune in nature

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25
Q

What is the clinical manifestation of Heparin induced thrombocytopenia

A

Unexplained platelet loss or sudden bleeding

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26
Q

What is the treatment of Heparin induced thrombocytopenia

A

Withdraw agents, get assay for previous hx

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27
Q

Who is affected by Hemolytic Uremic Syndrome

A

Infants and young children

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28
Q

What is the clinical manifestation of Hemolytic Uremic Syndrome

A

Similar to ITP or TTP without neuro and more *severe renal disease often progressing to ARF.

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29
Q

What is HUS be associated

A

1] E coli toxins, 2] Chemotherapeutic agents, 3] Diarrhea and URI are MC inciting factors

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30
Q

What is the treatment of Hemolytic Uremic Syndrome

A

plasmapheresis

31
Q

What should be avoided in HUS and why

A

antimotility agents in Diarrhea may increase risk of HUS. Immune complexes implicated, Trapping of pathogens and toxins in the body

32
Q

What are the causes of coagulation factor Deficiency?

A

1] Production, 2] Inhibition, 3] Consumption, 4] Liver disease

33
Q

What is Factor VIII deficiency also known as

A

also known as Hemophilia A (Classic),

34
Q

What synthesis Factor VIII

A

liver

35
Q

What is the function of Factor VIII

A

Factor 8 required for activation of factor X by intrinsic pathway, Bound to subendothelium by vWF

36
Q

What is the etiology of Factor VIII deficiency

A

1] Genetic Defect, X-linked, 2] In up to 30% of pts, spontaneous mutation, 3] 10% have normal factor levels, but inhibited by autoantibodies

37
Q

Who is more commonly affected by hemophilia A?

A

Males

38
Q

What is the presentation of Hemophilia A

A

1] Late rebleeding - no problem forming a platelet plug, but unable to form a fibrin clot, 2] Hemarthrosis - bleeding into joints, 3] Bruising, 4] Massive hemorrhage

39
Q

What is the lab findings of Hemophilia A

A

1] BT normal, 2] Platelets normal, 3] PT normal (measures only 5, 10, 2 not 8), 4] Prolonged aPTT - corrected by mixing with normal plasma containing factor, 5] Factor VIII assay decreased

40
Q

Why is BT, platelets, and PT normal in Hemophilia A?

A

Loss of factor VIII results in inhibition of intrinsic pathway, does not involve loss of platelet

41
Q

What is the treatment of Hemophilia A

A

1] Factor replacement, 2] Desmopressin Acetate (vasoconstrictor) for smaller bleeds, DVVAP

42
Q

What is the Christmas factor

A

1] Spontaneous bleeding, 2] Prolonged Bleeding Time-cut pt watch, 3] Normal PT/INR-prothrombin, warfarin 4] Normal PTT heparin 5] Low count

43
Q

How is hemophilia A and B differentiated

A

factor assay

44
Q

What is the presentation of Von Willebrand Disease

A

Presentation with spontaneous bleeding from mucous membrane, oozing after procedure, menorrhagia

45
Q

What are the different forms of Von Willebrand disease

A

AD and AR forms

46
Q

What is the pathophysiology of Von Willebrand disease

A

platelets need to attach to the vessel membrane. Platelet binds to sub endothelium through vWF. responsible for platelet aggregation too. it’s an adhesion molecule

47
Q

List the laboratory work up consistent with Von Willebrand disease

A

1] Prolonged BT, 2] Prolonged aPTT, normal PT, 3] Low vWF levels, 4] Possible low level of factor VIII d/t loss of stabilizing influence of vWF

48
Q

What is Ristocetin aggregation test

A

Antibiotic facilitating binding of VIII:vWF complexes to GPIb receptor on the platelet. Absence of aggregation predicts low VIII, vWF or receptor deficiency.

49
Q

What is Disseminated intravascular coagulation (DIC)

A

Systemic, intravascular thrombohemorrhagic disorder where there is Formation of thrombi widespread results in Consumption of platelets and factors, secondary activation of fibrinolysis. Always a Secondary manifestation

50
Q

What disorders are associated with DIC

A

1] Abruptio placenta 2] Infection (meningococcemia, GN sepsis), 3] Metastatic CA, 4] Burn pts, 5] Hemolytic transfusion reactions

51
Q

What is the pathophysiology of DIC

A

Activation of coagulation and fibrinolytic systems

52
Q

What is the activation of coagulation in DIC

A

Release of tissue factor (thromboplastin) activates extrinsic pathway (placenta, leukemic cells, endotoxins). Widespread endothelial injury activates intrinsic pathway

53
Q

What is the activation of bleeding in DIC

A

Factor XII activates kinins - vasodilation (shock) - also activates fibrinolysis (D Dimers formed)

54
Q

What is the diagnostic test of choice for DIC

A

D-dimer test

55
Q

What two factors regulate hemostasis

A

Balance between activation of coagulation and fibrinogen

56
Q

What is the issue with excess clotting?

A

1] Ischemia, 2] Impaired organ perfusion, 3] End-Organ Damage

57
Q

What is the issue with excess bleeding

A

1] Shock, 2] Hypotension, 3] Increased vascular permeability

58
Q

What is the presentation of DIC

A

1] ill or OB patient, 2] Oozing of blood from wounds, 3] Subcutaneous bleeds, 4] Microthrombi in kidneys leading to RF, 4] Microinfarction of heart, 5] ARDS, 6] Intracerebral bleeds/CVA, 7] Microangiopathic hemolytic anemia, 8] Anterior pituitary involvement (Sheehan Syndrome) - postpartum pituitary necrosis

59
Q

What are the lab tests consistent with DIC

A

1] Platelets low - bc they are tied into all these clots, 2] PT/aPTT prolonged, **3] D-Dimer elevation is diagnostic

60
Q

What is Hemolytic transfusion reaction

A

Autoimmune pt reacts to donor antigens usually due to Usually ABO incompatibility

61
Q

What is the result of a Hemolytic transfusion reaction

A

Hemoglobinemia, hemoglobinuria, DIC, anaphylaxis

62
Q

What increases the risk of Hemolytic transfusion reaction

A

Massive transfusions dangerous (entire volume < 24 hr, 10u in 12 hr

63
Q

What medications decrease clotting?

A

Heparin, LMWH, warfarin, antiplatelets, thrombolytics

64
Q

What medications increase clotting?

A

Vit K, FFP (fresh frozen plasma, has all the clotting factors in it), factor replacement, antifibrinolytics, desmopressin

65
Q

List the possible treatments for transfusion?

A

Blood (PRBC-packed red blood cells), FFP, platelets, cell saver (salvage), pre-op banking, clotting factors

66
Q

What is the pharmacokinetics of heparin

A

Short t1/2, preg C

67
Q

What factors are affected by heparin

A

Factors 2, 9, 10, 11, antithrombin 3

68
Q

What test is used to monitor heparin therapy

A

aPTT used to monitor

69
Q

What is the benefit of LMWH

A

reliable dose-dependent effects, 6-12 hr t1/2, injectable

70
Q

What is the benefit of heparin

A

50% reduction in DVT rates with post-op use

71
Q

What reverses heparin

A

Protamine sulfate reverses heparin

72
Q

What is the MOA of Warfarin (coumadin)

A

Vit k analog inhibits metabolism of vit K dependent factors

73
Q

What is the reversal of Warfarin (coumadin)

A

Reversed by administration of Vit K, vit K is not immediate, it takes time to repair all the clotting factor inhibition

SUMPHYS2 (27 decks)

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