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**Old DOOS > Heme 3 > Flashcards

Heme 3 Flashcards

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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
secondary causes of VW dz
2ndary myeloma, myeloproliferative dz, monoclonal gammopathies = abnormal clearance of the larger vWF proteins in pt w/out hx bleeding
26
what is the most common hemophilia
hemophilia A
27
S&S: childhood origin (crawl, walk) or spontaneous bleeding into joints, muscles, soft tissue, retroperitoneum, intracranial bleed, mucosa, urine Mild trauma, any surgery
Hemophilia
28
what does the prothrombin 20210 mutations cause?
increased prothrombin levels
29
what does a protein S deficiency lead to
superficial thrombophlebitis, DVT, PE
30
Protein C deficiency leads to what?
superficial phelbitis, DVT
31
inc’d marrow RBC & platelet production, inc’d viscosity & risk thromboembolism Labs: elevated Hct, RBC parameter
polycythemia vera
32
tx for P vera
reduce RBCs - phlebotomy, hydroxyurea & prevent platelet activation - ASA
33
hypercoag state d/t platelets > 900,000/mcL
thrombocytosis
34
tx for thrombocytosis
hydroxyurea & bone marrow biopsy
35
Excessive RBC sensitivity to complement = inc’d clotting (intra-abdominal, cerebral), hemolysis, bone marrow aplasia Smoky color urine (excess Hb)
Paroxysmal nocturnal hemoglobinuria
36
what test do you do for paroxysmal nocturnal hemoglobinuria
Ham's test- RBC sensitivity to complement
37
how does smoking cause a prothrombotic state?
Endothelial damage  platelet adhesion, reduced tPA production & TFPI = prothrombotic state
38
what is the most frequent test for HIT
HIPA- herparin-induced platelet aggregation assay
39
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
HIPA
40
tx for HIT
d/c heparin | may need direct thrombin inhibitor
41
tx for hyperhomocysteinemia
Rx: B12, B6 & folate supplementation
42
Binds heparin on EC to inactivate thrombin/common cascad
antithrombin III
43
(rare, genetic) | Arterial or venous clotting d/t excess circulating thrombin & reduced fibrinolytic activity
Dysfibrinogenemia
44
Vascular endothelial dysfunction, reduced NO, inc’d viscosity, inc’d vWF, inc’d fibrinogen = prothrombotic state & platelet activation
CHF
45
d/t infection, SLE/RA, CA, meds | Inc’d circulating TF & thrombin, dec’d fibrinolysis, reduced protein C activity
antiphospholipid syndrome
46
labs for antiphospholipid syndrome
high titers anti-hpospholipid antibodies
47
Endothelial dysfunction d/t renal failure, reduced NO production, inc’d circulating cytokines = hypercoag state
Uremia
48
tx for uremia
NO precursor L-arginine may help
49
how long should excessive clotting prophylaxis be given most surgery
Preventive therapy: 10 days post-op (up to 3 months/ortho)
50
how does estrogen effect clotting
Inc’d clotting factor levels, reduced effect protein S & antithrombin III
51
why are people w/ DM at a higher risk of clotting?
decreased insulin= NO production and increased platelet activation increased insulin= blocked fibrinolytic pathway
52
what mutation Blocks anticoag effects of activated protein C to inactivate V
Leiden factor V mutation
53
why does cancer cause excessive clotting?
Tumor cells procoag effect = activation clotting cascade & inhibit fibrinolytic system
54
why does obesity/ elevated lipis cause excessive clotting
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
subclinical hyperthyroid causes increased what?
increased circulating clotting factor X
56
how does hypothyroid affect clotting?
inc’d fibrinogen, factor VII & plasminogen activator inhibitor, dec’d antithrombin III
57
how do thallassemia and sickel cell lead to excessive clotting
Inc’d platelet activation & thrombin | Dec’d NO & proteins C & S
58
why does sepsis put someone at risk for excessive clotting.
Inc’d tissue factor & activation extrinsic pathway
59
management of excessive clotting
reduce modifiable factors | alternative non-estrogen therapy
60
what are 2 anti-platelet drugs?
ASA
61
what are anti-thrombolytic drugs?
heparin and warfarin
62
irreversible inhibition COX-1 pathway
ASA
63
block platelet activation (blocks ADP receptor) | can combine w/ ASA
clopidogrel
64
increases platelet cyclic AMP = blocks activation | Best in combo w/ASA
Dipyridamole (Persantine)
65
inc antithrombin III & blocks intrinsic pathway; reverse w/protamine sulfate Routine aPTT, heparin levels, platelet counts if Low platelets – do HIT assay
Unfractionated heparin (UFH)
66
for HIT what do you give?
fondaparinux | danaproid
67
how can you reverse heparin
protamine sulfate
68
oral agent inhibits vitamin K dependent factors/extrinsic pathway; reversed w/Vit K, FFP Monitor PT, INR
warfarin
69
contraindications w/ warfarin
frank bleeding, IUP, alcoholism, bleeding diathesis
70
Assess platelet function & body’s ability to form a clot
bleeding time
71
what is normal bleeding time?
1-9 minutes
72
Uses: detect a bleeding disorder, diagnose liver problems, screen people having surgery for unrecognized bleeding problems, monitor anticoagulant therapy
PT (prothrombin time)
73
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
aPTT (activated partial thromboplastin)
74
what is aPTT useful for?
monitor heparin therapy screen for certain coagulation factor deficiencies detect coagulation inhibitos (such as lupus anticoag), sepcific factor inhibitors and nonspecific inhibitors
75
what test evaluates the extrinsic and common pathways of the coagulation cascade
PT
76
what test evaluates the intrinsic and common pathway
PTT
77
Is PT is abnormal what should you consider
deficiencies II, V, VII, X | vitamin K dependent
78
if PT is prolonged and PTT is normal waht should you look at?
Liver disease decreased vitamin K decreased or defective factor VII chronic low-grade DIC anticoagulation drug (warfarin) therapy
79
with normal PT and prolonged PTT what should you look at
decreased/ defective factor VIII, IX, or XI VW disease presence of lupus anticoag
80
is someon ehas prolonged PT and PTT what should you look at
decreased or defective factor I, II, V< or X severe liver dz acute DIC
81
basic labs for someone who is hypercoagable (CMP)
CMP: glucose, BUN, creatinine, lipid profile, TSH
82
what is a hypercoagulation panel
Protein S, protein C, antithrombin III, Leiden factor V mutation, prothrombin 20210A mutation, homocysteine level, antiphospholipid antibodies, fibrinogen level, anticardiolipin/antinuclear/lupus anticoagulant
83
what labs to look at if someone is on warfarin
Pt and INR
84
what labs to look at if someone is on heparin therapy
aPTT
85
what factor interact w/ Vit K synthesis
II, VII, IX & X & proteins C &S

**Old DOOS (11 decks)

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