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Heme and Lymph > Week 3 (Clotting) > Flashcards

Week 3 (Clotting) Flashcards

1
Q

Heparin

A

Anticoagulant
binds antithrombin, which binds factor Xa, thus inhibits thrombin
IV only, rapid action
Can cause heparin induced thrombocytopenia (HIC)

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2
Q

LMWH

A

enoxaparin and dalteparin
anticoagulants
same but better than heparin

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3
Q

Direct thrombin inhibitors

A

lepirudin and bivalirudin
anticoagulants
IV only

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4
Q

Factor Xa inhibitor

A

Fondaparinux
anticoagulant
subcu
fewer side effects than heparins

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5
Q

Warfarin

A

anticoagulant
inhibits vitamin K (thus factors II, VII, IX, X)
metabolized by CYP2C9

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6
Q

New oral anticoagulants

A

Dabigatran (prodrug, direct thrombin inhibitor)

Rivaroxaban (direct Xa inhibitor)

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7
Q

Alteplase

A

thrombolytic

plasminogen activator

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8
Q

Anti-platelet drugs

A

Aspirin (COX inhibitor)
Clopidogrel, Ticlopidine, Prasugrel, Ticagrelor (inhibit ADP-P2Y binding)
Dipyrimadole (inhibits adenosine deaminase and PDE, increases cAMP)
Abciximab, Eptifibatide (antibodies that prevent fibrinogen cross linking)

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9
Q

Things that happen when platelets activate

A 
Integrin activation
granule secretion (2ndary messengers, coag proteins)
cytoskeletal rearrangements
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10
Q

Platelet adhesion

A

GPIb (braking) and GPIIb/IIIa (arrest) on the platelet adhere to collagen via vWF
this binding activates the platelet
platelets co-adhere via fibrinogen bridges -> primary platelet plug

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11
Q

Coagulation cascade

A

Extrinsic (PT): Tissue factor + VII -> common pathway
Intrinsic (PTT): XI -> IX -VIII/vWF-> common pathway
Common: X -V-> II (Thrombin)
Fibrinogen -II-> Fibrin -XIII-> cross-linked

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12
Q

PT and PTT

A

PT: extrinsic, VII and common (also vitK, warfarin, liver disease)
PTT: intrinsic, XI, IX, VIII, vWF, and common (also lupus anti-coag and heparin)
PTT also uses XII/contact factor, but is not physiologically important
1:1 mixture separates factor deficits from inhibitors
Both prolonged: X, V, II, fibrinogen, severe liver disease or vitK def, DIC, lupus

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13
Q

Fibrinolytic system

A

tissue plasminogen activator (tPA) frees up the plasminogen in the clot, which degrades fibrin
Also: antithrombin (heparin),, Thrombomodulin (Protein C)

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14
Q

Immune Thrombocytopenia Purpura (ITP)

A

auto-antibody against platelets
petechiae, bruising, epistaxis
Childhood: abrupt severe thrombocytopenia, often antecedant virus, most recover well
Adult (women 20-40yo): insidious, most do not recover well
RBC, WBC usually normal,, see large platelets on smear

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15
Q

Heparin Induced Thrombocytopenia

A 
Immune disease (transient)
moderate thrombocytopenia
assoc with thrombotic events (venous and arterial) (paradoxical bc on heparin)
labs: PF-4-Heparin elisa
Tx: stop heparin, begin anti-coag
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16
Q

Thrombotic Microangiopathy

A

schistocytes on smear

DDX: TTP, HUS, DIC, others

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17
Q

Thrombotic Thrombocytopenic Purpura (TTP)

A

labs: microangiopathic hemolytic anemia and thrombocytopenia
also: organ dysfunction (renal, mental status, fever)
schistocytes on smear
ADAMTS13 deficiency (regulates vWF/platelet interactions (cleaves vWF polymer), platelet string)
Tx: plasma exchange (also maybe steroids)

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18
Q

Platelet function defects

A

Congenital absence of:
GPIb: Bernard Soulier syndrome (abn adhesion)
GPIIb/IIIa: Glanzman’s thrombasthenia (abn clumping)

19
Q

Hemophilia

A

Deficient VIII (A) or IX (B)
X-linked
hemarthrosis, deep muscle bleeds
long PTT and normal PT (corrects on 1:1 mix)

20
Q

Vit K deficiency

A

Factors II, VII, IX, X, Protein C,S
can be caused by liver disease, newborns, malabsorbtion, drugs
elevated PT and (less so) PTT

21
Q

Hemolytic uremic syndrome (HUS)

A

Like TTP, except NO mental status change, more renal disease, more in kids
often triggered by E coli (stool culture)

22
Q

vWF Disease

A

autosomal dominant
mucocutaneous bleeding, menorrhagia
Type 1: reduced levels
2: mutated protein,, 3: absent protein

23
Q

HPC (stem cell) transplants

A

best case= identical twin, then HLA-matched sibling (in this case, all GVH is due to minor HLA mismatch,, any polymorphic factor that can generate an immune response)
Threatable things: leukemias, thalassemias, SKID, much more (NOT Hemophilia)
Nowadays try for non-myeloablative chemo bc less harmful to person, more lymphocyte specific, good for non-neoplastic things
Long term risks: short stature, hypothyroid, infxn, relapse, new cancers
Alternate sources for cells: cord blood (less GVH, less engraftment,,, Peripheral blood (more chronic GVH, better engraftment)

24
Q

Physiological coag control

A

blood flow washes factors away
anti-thrombin (heparin): inactivates enzymes IIa and Xa
Protein C (and S) (vitK dep) degrades cofactors: V and VIII

25
Q

AT, Protein C,S deficiencies

A

familial venous thrombosis
risks increase after puberty,, usually clots are “provoked”
Tests: functional AT, PC, PS
PT/PTT will be normal

26
Q

Factor V Leiden

A

mild increase risk of venous thrombosis
common in caucasions
Arg506Gln
PTT fails to prolong with added protein C
Factor V is less susceptible to degradation by PC

27
Q

Prothrombin gene mutation

A

venous thrombosis
G20210A
elevated thrombin levels
similar risks as FV-Leiden

28
Q

Antiphospholipid Antibody Syndrome

A

venous and arterial thrombosis
pregnancy complications / fetal wasting
Labs: evidence of antiphospholipid auto-antibody (“Lupus-like” anticoagulant, anti-cardiolipin)
PT fails to correct with 1:1 mix,, does correct with added phospholipid
may have thrombocytopenia

29
Q

Dissiminated Intravascular Coagulation (DIC)

A

widespread activation of thrombin and plasmin mechanisms
consumption of platelets, coag proteins, control proteins,, schistocytes on smear
Caused by: extrinsic clot promoting material, intravascular elaboration of procoagulants, vascular injury (sepsis)
Purpura Fulminans: meningococcal sepsis, severe Protein C deficiency in newborn
Elevated PT and PTT,, also elevated D-Dimer,, low fibrinogen and platelets
Tx: underlying condition

30
Q

Warfarin-dependent skin necrosis

A

When warfarin is first started, inhibition of vitK leads to drop in all vitK dependent proteins, including ProC and ProS,, which paradoxically increases thrombosis risk temporarally. This can cause microthrombi and skin necrosis

31
Q

Things screened for in donated blood

A

Syphilis, HCV, HIV, West Nile, Chagas, HBV

32
Q

Things added to preserve donated blood

A

Citrate (anticoag)
Phosphate (maintain DPG)
Dextrose (metabolism)
Adenine (ATP production)

33
Q

Direct Antiglobulin Test (DAT)

A 
detects antibody attached to red blood cells
\+ in: autoimmune hemolytic anemia
drug induced hemolytic anemia
hemolytic transfusion rxn
hemolytic disease of newborn
34
Q

Indirect Antiglobulin Test (IAT)

A

detects antibody in serum
red cell typing, compatibility testing
Also crossmatch

35
Q

Whole blood transfusion

A

used for massive blood loss
can be given super rapidly
Matched ABO only

36
Q

Packed red blood cell transfusion

A 
used for symptomatic anemia in normovolemic pt
O is donor, AB is recipient
most commonly used
Hb 6-8: transfuse if symptomatic
Hb less than 6: transfuse
37
Q

Fresh Frozen Plasma transfusion

A

contains clotting factors and coag inhibitors
opposite compatibility to RBCs (AB is donor, O is recipient)
Used for plasma protein replacement,, surgery prophylaxis
Plasma exchange in TTP

38
Q

Cyroprecipitate Transfusion

A

Mostly to replace Fibrinogen

DIC, liver ds, etc

39
Q

Platelet transfusion

A

ABO is less important
used in marrow failure if less than 10k
used prophylaxis for surgery if less than 50k or 100k

40
Q

Transfusion related fever DDX

A 
FNHTR
hemolytic transfusion rxn
bacterial contamination
TRALI
allergic rxn
related to underlying disease
41
Q

Febrile non-hemolytic transfusion rxn (FNHTR)

A

Antibodies in recipient to the donor WBCs

rapid onset, fever

42
Q

Hemolytic Transfusion reaction

A

Immunologic incmpatibility
Acute: ABO error,, intravascular hemolysis
Delayed: low level, undetected antibodies,, extravascular hemolysis
fever, chills, bad,, cytokine storm
Tx: stop transfusion, supportive fluids, etc

43
Q

Immune transfusion reactions

A

IgE mediated
usually urticaria (hives)
can be more serious sometimes

44
Q

Transfusion Induced Acute Lung Injury (TRALI)

A

Pulmonary edema, hypoxemia, hypotension
antibody mediated, HLA antibodies from the donor
neutrophil specific antibodies
now avoided by not taking plasma from women that have been pregnant,, screened negative for HLA antibodies

Heme and Lymph (3 decks)

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