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**Old DOOS > Heme 3 > Flashcards

Heme 3 Flashcards

1
Q

primary epistaxis is what?

A

platelets

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2
Q

what is secondary hemostasis

A

soluble, inactive protein-clotting factor change soluble fibrinogen to fibrin strands
clot containment
wound healing

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3
Q

what does nitric oxide cause

A

vasodilation

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4
Q

disurption of hemostasis leads to what

A

Bleeding

Thromboembolic events

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5
Q

causes of thrombocytopenia

A

Hemodilution
Decreased platelet production/bone marrow
Increased sequestration
Increased platelet destruction

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6
Q

labs to get with thrombocytopenia

A

CBC: platelet count, diff

% reticulated platelets

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7
Q

conditions w/ physiologic hemodiluation

A

pregnancy

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8
Q

causes of decreased platelet production

A

Cytotoxic chemo (usually reversible)
Aplastic anemia
Invasive malignancy (leukemia, multiple myeloma, myelofibrosis)
Stem cell defects
Metabolic issues/affect maturation (B12, folate, ETOH)

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9
Q

what causes increased sequestration theombocytopenia

A

splenomegaly
adavnced liver dz
myeloproliferative disorders (CML, myelofibrosis or splenic CA)

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10
Q

what causes increased platelet destruction

A 
Autoimmune TCP (primary/platelets or 2ndary (SLE)
Inc’d polyclonal antibodies against platelet membrane glycoprotein receptors (GPIIb/IIIa)
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11
Q

patient presents with petechial hemorrhage, mucosal bleeding, organomegaly, LAD (low grade fever possibly)

A

immune thrombocytopenia purpura (ITP)

signs and symptoms when platelets <20,000

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12
Q

what conditions are associated w/ thrombocytopenia in adults

A 
HIV
Hep C
SLE
IBD
autoimmune hemolytic anemia (evans syndrome)
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13
Q

tx for thrombocytopenia

A

Manage underlying conditions
Steroids (daily prednisone vs. high dose dexamethasone/pulsed q 1-2 weeks x 6-8 doses); IVIG
Pre-op: consider platelet transfusion; life threatening

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14
Q

if a person has HIT what else may they react to?

A

LMWH (but seen more w/ UFH)

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15
Q

for patients on heparin therapy how many develop antibodies to heaprin and platelet factor 4 complex?

A

25%

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16
Q

labs for heparin induced TCP (HIT)

A

heparin-PF4 antibody complex (sensitive , non-specific)

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17
Q

Tx for HIT

A

direct thrombin inhibitor - lepirudin (renal) or argatroban (hepatic)

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18
Q

Non-immune cause TCP

A

thrombotic thrombocytopenia purpura (TTP)

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19
Q

what is congenital TTP?

A

due to a higher circulating leves of high molecular wt VFR multimers= increased platelet adhesion

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20
Q

tx for TTP?

A

steroids
ASA
plasmapheresis

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21
Q

Non-immune platelet destruction

Causes: sepsis, malignancy, liver dz, PIH/eclampsia

A

DIC

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22
Q

tx for HELLP syndrome

A

delivery of fetus and placenta

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23
Q

Labs w/ DIC

A

CBC: schistocytes/smear, prolonged PT & PTT, low fibrinogen, increased fibrin-split products

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24
Q

Tx for DIC

A

platelets
cryopreceipitate
FFP
disrupt cascade effect

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25
Q

secondary causes of VW dz

A

2ndary myeloma, myeloproliferative dz, monoclonal gammopathies = abnormal clearance of the larger vWF proteins in pt w/out hx bleeding

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26
Q

what is the most common hemophilia

A

hemophilia A

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27
Q

S&S: childhood origin (crawl, walk) or spontaneous bleeding into joints, muscles, soft tissue, retroperitoneum, intracranial bleed, mucosa, urine
Mild trauma, any surgery

A

Hemophilia

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28
Q

what does the prothrombin 20210 mutations cause?

A

increased prothrombin levels

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29
Q

what does a protein S deficiency lead to

A

superficial thrombophlebitis, DVT, PE

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30
Q

Protein C deficiency leads to what?

A

superficial phelbitis, DVT

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31
Q

inc’d marrow RBC & platelet production, inc’d viscosity & risk thromboembolism
Labs: elevated Hct, RBC parameter

A

polycythemia vera

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32
Q

tx for P vera

A

reduce RBCs - phlebotomy, hydroxyurea & prevent platelet activation - ASA

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33
Q

hypercoag state d/t platelets > 900,000/mcL

A

thrombocytosis

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34
Q

tx for thrombocytosis

A

hydroxyurea & bone marrow biopsy

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35
Q

Excessive RBC sensitivity to complement = inc’d clotting (intra-abdominal, cerebral), hemolysis, bone marrow aplasia
Smoky color urine (excess Hb)

A

Paroxysmal nocturnal hemoglobinuria

36
Q

what test do you do for paroxysmal nocturnal hemoglobinuria

A

Ham’s test- RBC sensitivity to complement

37
Q

how does smoking cause a prothrombotic state?

A

Endothelial damage  platelet adhesion, reduced tPA production & TFPI = prothrombotic state

38
Q

what is the most frequent test for HIT

A

HIPA- herparin-induced platelet aggregation assay

39
Q

what is a platelet-activation test: patient’s serum is mixed w/donor platelets in presence of heparin; Positive test = aggregation of donor platelets = presence of antibodies to the heparin–PF4 complex

A

HIPA

40
Q

tx for HIT

A

d/c heparin

may need direct thrombin inhibitor

41
Q

tx for hyperhomocysteinemia

A

Rx: B12, B6 & folate supplementation

42
Q

Binds heparin on EC to inactivate thrombin/common cascad

A

antithrombin III

43
Q

(rare, genetic)

Arterial or venous clotting d/t excess circulating thrombin & reduced fibrinolytic activity

A

Dysfibrinogenemia

44
Q

Vascular endothelial dysfunction, reduced NO, inc’d viscosity, inc’d vWF, inc’d fibrinogen = prothrombotic state & platelet activation

A

CHF

45
Q

d/t infection, SLE/RA, CA, meds

Inc’d circulating TF & thrombin, dec’d fibrinolysis, reduced protein C activity

A

antiphospholipid syndrome

46
Q

labs for antiphospholipid syndrome

A

high titers anti-hpospholipid antibodies

47
Q

Endothelial dysfunction d/t renal failure, reduced NO production, inc’d circulating cytokines = hypercoag state

A

Uremia

48
Q

tx for uremia

A

NO precursor L-arginine may help

49
Q

how long should excessive clotting prophylaxis be given most surgery

A

Preventive therapy: 10 days post-op (up to 3 months/ortho)

50
Q

how does estrogen effect clotting

A

Inc’d clotting factor levels, reduced effect protein S & antithrombin III

51
Q

why are people w/ DM at a higher risk of clotting?

A

decreased insulin= NO production and increased platelet activation
increased insulin= blocked fibrinolytic pathway

52
Q

what mutation Blocks anticoag effects of activated protein C to inactivate V

A

Leiden factor V mutation

53
Q

why does cancer cause excessive clotting?

A

Tumor cells procoag effect = activation clotting cascade & inhibit fibrinolytic system

54
Q

why does obesity/ elevated lipis cause excessive clotting

A

Lipoproteins can activate platelets & clotting pathway
VLDL: up regulates expression plasminogen activator inhibitor 1 gene & plasminogen activator inhibitor 1 antigen leads to platelet aggregation/clot formation

55
Q

subclinical hyperthyroid causes increased what?

A

increased circulating clotting factor X

56
Q

how does hypothyroid affect clotting?

A

inc’d fibrinogen, factor VII & plasminogen activator inhibitor, dec’d antithrombin III

57
Q

how do thallassemia and sickel cell lead to excessive clotting

A

Inc’d platelet activation & thrombin

Dec’d NO & proteins C & S

58
Q

why does sepsis put someone at risk for excessive clotting.

A

Inc’d tissue factor & activation extrinsic pathway

59
Q

management of excessive clotting

A

reduce modifiable factors

alternative non-estrogen therapy

60
Q

what are 2 anti-platelet drugs?

A

ASA

61
Q

what are anti-thrombolytic drugs?

A

heparin and warfarin

62
Q

irreversible inhibition COX-1 pathway

A

ASA

63
Q

block platelet activation (blocks ADP receptor)

can combine w/ ASA

A

clopidogrel

64
Q

increases platelet cyclic AMP = blocks activation

Best in combo w/ASA

A

Dipyridamole (Persantine)

65
Q

inc antithrombin III & blocks intrinsic pathway; reverse w/protamine sulfate
Routine aPTT, heparin levels, platelet counts
if Low platelets – do HIT assay

A

Unfractionated heparin (UFH)

66
Q

for HIT what do you give?

A

fondaparinux

danaproid

67
Q

how can you reverse heparin

A

protamine sulfate

68
Q

oral agent inhibits vitamin K dependent factors/extrinsic pathway; reversed w/Vit K, FFP
Monitor PT, INR

A

warfarin

69
Q

contraindications w/ warfarin

A

frank bleeding, IUP, alcoholism, bleeding diathesis

70
Q

Assess platelet function & body’s ability to form a clot

A

bleeding time

71
Q

what is normal bleeding time?

A

1-9 minutes

72
Q

Uses: detect a bleeding disorder, diagnose liver problems, screen people having surgery for unrecognized bleeding problems, monitor anticoagulant therapy

A

PT (prothrombin time)

73
Q

Reflects activity most of the coagulation factors, including factor XII as well as “contact factors” (prekallikrein [PK] & high molecular weight kininogen [HMWK]) & factors XI, IX, and VIII in the intrinsic procoagulant pathway, as well as coagulation factors X, V, II & fibrinogen (factor I) in the common procoagulant pathway

A

aPTT (activated partial thromboplastin)

74
Q

what is aPTT useful for?

A

monitor heparin therapy
screen for certain coagulation factor deficiencies
detect coagulation inhibitos (such as lupus anticoag), sepcific factor inhibitors and nonspecific inhibitors

75
Q

what test evaluates the extrinsic and common pathways of the coagulation cascade

A

PT

76
Q

what test evaluates the intrinsic and common pathway

A

PTT

77
Q

Is PT is abnormal what should you consider

A

deficiencies II, V, VII, X

vitamin K dependent

78
Q

if PT is prolonged and PTT is normal waht should you look at?

A

Liver disease
decreased vitamin K
decreased or defective factor VII
chronic low-grade DIC anticoagulation drug (warfarin) therapy

79
Q

with normal PT and prolonged PTT what should you look at

A

decreased/ defective factor VIII, IX, or XI
VW disease
presence of lupus anticoag

80
Q

is someon ehas prolonged PT and PTT what should you look at

A

decreased or defective factor I, II, V< or X
severe liver dz
acute DIC

81
Q

basic labs for someone who is hypercoagable (CMP)

A

CMP: glucose, BUN, creatinine, lipid profile, TSH

82
Q

what is a hypercoagulation panel

A

Protein S, protein C, antithrombin III, Leiden factor V mutation, prothrombin 20210A mutation, homocysteine level, antiphospholipid antibodies, fibrinogen level, anticardiolipin/antinuclear/lupus anticoagulant

83
Q

what labs to look at if someone is on warfarin

A

Pt and INR

84
Q

what labs to look at if someone is on heparin therapy

A

aPTT

85
Q

what factor interact w/ Vit K synthesis

A

II, VII, IX & X & proteins C &S

**Old DOOS (11 decks)

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