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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
What is the clinical manifestation of Heparin induced thrombocytopenia
Unexplained platelet loss or sudden bleeding
26
What is the treatment of Heparin induced thrombocytopenia
Withdraw agents, get assay for previous hx
27
Who is affected by Hemolytic Uremic Syndrome
Infants and young children
28
What is the clinical manifestation of Hemolytic Uremic Syndrome
Similar to ITP or TTP without neuro and more *severe renal disease often progressing to ARF.
29
What is HUS be associated
1] E coli toxins, 2] Chemotherapeutic agents, 3] Diarrhea and URI are MC inciting factors
30
What is the treatment of Hemolytic Uremic Syndrome
plasmapheresis
31
What should be avoided in HUS and why
antimotility agents in Diarrhea may increase risk of HUS. Immune complexes implicated, Trapping of pathogens and toxins in the body
32
What are the causes of coagulation factor Deficiency?
1] Production, 2] Inhibition, 3] Consumption, 4] Liver disease
33
What is Factor VIII deficiency also known as
also known as Hemophilia A (Classic),
34
What synthesis Factor VIII
liver
35
What is the function of Factor VIII
Factor 8 required for activation of factor X by intrinsic pathway, Bound to subendothelium by vWF
36
What is the etiology of Factor VIII deficiency
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
Who is more commonly affected by hemophilia A?
Males
38
What is the presentation of Hemophilia 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
What is the lab findings of Hemophilia 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
Why is BT, platelets, and PT normal in Hemophilia A?
Loss of factor VIII results in inhibition of intrinsic pathway, does not involve loss of platelet
41
What is the treatment of Hemophilia A
1] Factor replacement, 2] Desmopressin Acetate (vasoconstrictor) for smaller bleeds, DVVAP
42
What is the Christmas factor
1] Spontaneous bleeding, 2] Prolonged Bleeding Time-cut pt watch, 3] Normal PT/INR-prothrombin, warfarin 4] Normal PTT heparin 5] Low count
43
How is hemophilia A and B differentiated
factor assay
44
What is the presentation of Von Willebrand Disease
Presentation with spontaneous bleeding from mucous membrane, oozing after procedure, menorrhagia
45
What are the different forms of Von Willebrand disease
AD and AR forms
46
What is the pathophysiology of Von Willebrand disease
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
List the laboratory work up consistent with Von Willebrand disease
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
What is Ristocetin aggregation test
Antibiotic facilitating binding of VIII:vWF complexes to GPIb receptor on the platelet. Absence of aggregation predicts low VIII, vWF or receptor deficiency.
49
What is Disseminated intravascular coagulation (DIC)
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
What disorders are associated with DIC
1] Abruptio placenta 2] Infection (meningococcemia, GN sepsis), 3] Metastatic CA, 4] Burn pts, 5] Hemolytic transfusion reactions
51
What is the pathophysiology of DIC
Activation of coagulation and fibrinolytic systems
52
What is the activation of coagulation in DIC
Release of tissue factor (thromboplastin) activates extrinsic pathway (placenta, leukemic cells, endotoxins). Widespread endothelial injury activates intrinsic pathway
53
What is the activation of bleeding in DIC
Factor XII activates kinins - vasodilation (shock) - also activates fibrinolysis (D Dimers formed)
54
What is the diagnostic test of choice for DIC
D-dimer test
55
What two factors regulate hemostasis
Balance between activation of coagulation and fibrinogen
56
What is the issue with excess clotting?
1] Ischemia, 2] Impaired organ perfusion, 3] End-Organ Damage
57
What is the issue with excess bleeding
1] Shock, 2] Hypotension, 3] Increased vascular permeability
58
What is the presentation of DIC
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
What are the lab tests consistent with DIC
1] Platelets low - bc they are tied into all these clots, 2] PT/aPTT prolonged, **3] D-Dimer elevation is diagnostic
60
What is Hemolytic transfusion reaction
Autoimmune pt reacts to donor antigens usually due to Usually ABO incompatibility
61
What is the result of a Hemolytic transfusion reaction
Hemoglobinemia, hemoglobinuria, DIC, anaphylaxis
62
What increases the risk of Hemolytic transfusion reaction
Massive transfusions dangerous (entire volume < 24 hr, 10u in 12 hr
63
What medications decrease clotting?
Heparin, LMWH, warfarin, antiplatelets, thrombolytics
64
What medications increase clotting?
Vit K, FFP (fresh frozen plasma, has all the clotting factors in it), factor replacement, antifibrinolytics, desmopressin
65
List the possible treatments for transfusion?
Blood (PRBC-packed red blood cells), FFP, platelets, cell saver (salvage), pre-op banking, clotting factors
66
What is the pharmacokinetics of heparin
Short t1/2, preg C
67
What factors are affected by heparin
Factors 2, 9, 10, 11, antithrombin 3
68
What test is used to monitor heparin therapy
aPTT used to monitor
69
What is the benefit of LMWH
reliable dose-dependent effects, 6-12 hr t1/2, injectable
70
What is the benefit of heparin
50% reduction in DVT rates with post-op use
71
What reverses heparin
Protamine sulfate reverses heparin
72
What is the MOA of Warfarin (coumadin)
Vit k analog inhibits metabolism of vit K dependent factors
73
What is the reversal of Warfarin (coumadin)
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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