Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
70 Cards in this Set
- Front
- Back
what is Virchow's triad and when is it seen?
|
1. endothelial injury
2. hypercoagulable state 3. circulatory stasis *seen in clotting disorders |
|
name some diseases that contribute to a hyperthrombotic state (5)
|
1. DM
2. hypertension 3. hyperlipidemia 4. cancer 5. obesity |
|
name some medications that contribute to a hypercoaguable state (4)
|
1. OCs
2. HRT 3. Thalidomide 4. Cox-2 inhibitors |
|
what are some mechanical factors that contribute to a prothrombitic state? (3)
|
1. surgery
2. immobilization 3. trauma |
|
anticoagulant therapies can target either the arterial or the venous side. for each of the following therapies: state what side they affect.
1. Aspirin 2. tPA 3. heparin 4. warfarin 5. clopidogrel |
1. arterial
2. arterial or venous 3. venous 4. venous 5. arterial |
|
which clotting factor does LMWH inhibit?
|
factor IIa
(also factor Xa) |
|
what test is used to monitor heparin?
|
PTT
|
|
1. which type of clot is known as a red clot?
2. which type of clot is known as a white clot? |
1. venous clot (contains primarily fibrin)
2. arterial clot (contains primarily platelets) |
|
what is the major complication seen in antiphospholipid antibody syndrome?
|
increased arterial and venous thrombotic risk
|
|
what are the two therapies for antiphospholipid antibody syndrome?
|
1. aspirin
2. warfarin |
|
what are the clinical risks of an antithrombin III, protein C or S deficiency?
|
DVT/PE
pregenancy associated with a high risk |
|
what is administered as therapy for hyperhomocysteinemia?
|
folate
B6 B12 |
|
what test is elevated in a case of DVT or PE?
|
D-Dimer
|
|
therapies for DVT? (2)
|
tPA
Heparin |
|
which anticoagulant cannot be used during pregnancy?
|
Warfarin
(Heparin can be used b/c it doesn't cross the placenta) |
|
whay are first trimester miscarriages more common in hypercoagulable states?
|
blood clots form in the placenta
|
|
what are some classic clinical s/s seen in disorders of platelet and blood vessel wall interaction?
|
1. epistaxis
2. external bleeding everywhere! 3. iron deficiency |
|
with what deficiency would you see the "fingerprint sign"?
(spontaneous bruising) |
disorders of fibrin generation
|
|
describe the bleeding seen in disorders of fibrin formation.
|
- internal bleeding
- delayed bleeding (ie. in surgery) - hematuria - iron deficiency NOT a feature |
|
how does a resting platelet become activated?
|
by coming into contact with collagen
|
|
what happens when a platelet is activated?
|
1. pseudopods form
2. granules "shoot out" via cannalicular system (need Ca++ for this to occur) 3. activated platelets then spit out ADP to activate surrounding platelets |
|
what molecule binds platelets together?
|
fibrinogen
(via glc IIB/IIIa receptors) |
|
what molecule binds platelets to the vessel wall?
|
vWF
(glc Ib is recepor on plts) |
|
besides collagen and ADP, what other molecules can stimulate platelet aggregation? (4)
|
1. Thrombin
2. Thromboxane A2 3. platelet activating factor 4. epinephrine |
|
describe the primary and secondary waves of platelet aggragation...
|
1. primary wave - activated by collagen
2. secondary wave - activated by already activated platelets (they spit out ADP which activates surrounding plts) |
|
a damaged endothelial cell releases __________, which activates the extrinsic coagulation cascade.
|
tissue factor
|
|
fibrin generation is restricted to the sites of injury. why?
|
this prevents generalized thrombosis / DIC
|
|
1. A red topped blood collection tube contains ?
2. what happens to blood when it enters the tube? |
1. nothing
2. blood coagulates, forming a serum level and a clot level |
|
1. a "tiger topped" tube contains?
2. blood looks like? |
1. coagulation activating gel
2. blood also separates into serum and clot |
|
1. a green topped tube contains?
2. blood looks like? |
1. heparin
2. NO CLOT |
|
1. a purple tube contains?
2. blood looks like? |
1. EDTA (Ca++ binder)
2. NO CLOT (EDTA removes Ca++ from plasma; plts can't bind to clotting factors without Ca++ = no clot) |
|
1. A yellow top tube contains?
2. blood looks like? |
1. citrate
2. same as purple tube |
|
when blood is in a tube and it doesn't clot - what layers does it separate into?
|
plasma (fibrinogen and clotting factors)
RBCs |
|
1. PTT measures the clotting time of which pathway?
2. PT measures clotting time of which pathway? |
1. intrinsic
2. extrinsic |
|
the TT test is a direct measure of?
|
thrombin (IIa) activity
|
|
inheritance pattern of vWD?
|
autosomal dominant
|
|
hemophilia A is primarily a disorder of?
|
factor VIII
(fibrin generation) |
|
inheritance pattern of hemophilia A?
|
XL
|
|
hemophilia A displays changes in which lab test?
|
prolonged PTT
|
|
inheritance pattern of severe (type III) vWD?
|
autosomal recessive
|
|
type III vWD presents with what lab abnormality?
|
prolonged PTT
|
|
Hemophilia B is a deficiency of?
|
factor IX
(fibrin generation disorder) |
|
hypofibrinogenemia is a deficiency in?
|
factor I
|
|
inheritance pattern of hypofibrinogenemia?
|
autosomal dominant
|
|
lab test changes seen in hypofibrinogenemia?
|
prolonged PTT, PT
(hemorrhagic and thrombotic risk) |
|
inheritance pattern of factor two deficiency
|
autosomal recessive
|
|
lab test changes seen in factor II deficiency?
|
prolonged PT, PTT
|
|
lab test seen in factor VII deficiency?
|
prolonged PT
|
|
factor VII deficiency in neonates carries an increased risk of?
|
neonatal CNS bleed
|
|
inheritance pattern of protein C or S deficiency?
|
autosomal dominant
|
|
factor V Leiden deficiency is associated with?
|
increased risk of DVT, PE
(risk of arterial disease not increased) |
|
describe the levels of the following in early DIC
1. coagulation factors 2. D-Dimer 3. PTT 4. platelets |
1. increased
2. increased 3. decreased 4. normal |
|
describe the levels of the following in late DIC
1. coagulation factors 2. D-Dimer 3. PTT/PT 4. platelets |
1. decreased
2. increased 3. increased 4. decreased |
|
this protozoa causes...?
Naegleria |
amoebic meningioencephalitis
|
|
this protozoa causes...?
Trympanosoma brucei |
african sleeping sickness
|
|
this protozoa causes...?
Trympanosoma cruzi |
Chagas disease
|
|
this protozoa causes...?
Leischmania donovani |
leischmaniasis
|
|
this protozoa causes...?
Plasmodium |
malaria
|
|
this protozoa causes...?
Toxoplasma gondii |
toxoplasmosis
|
|
this flatworm causes?
Schistosoma |
schistosomiasis
|
|
this filarial roundworm causes?
Wucheraria bancrofti, Brugia malayi |
elephantiasis
|
|
this filarial roundworm causes?
Loa loa |
calabar swelling
|
|
this filarial roundworm causes?
Onchocera volvulus? |
river blindness
|
|
main symptoms and presentation of amoebic meningioencephalitis caused by Naegleria fowleri?
|
- enters body via nasal mucosa
- meningioencephalitis causing death within one week |
|
reservoir of Trypanosoma brucei (af. sleeping sickness)?
|
Tse-tse fly
|
|
reservoir for Trypanosoma cruzi?
|
Reduviid bug
|
|
two phases of chagas disease? difference between the two?
|
1. Acute phase - periorbital edema, fever
2. chronic phase - UNDETECTABLE PARASITEMIA, causes cardiomyopathy, autoimmune disease |
|
what type of cells does Leischmania prefers to infect and where do they "live?"
|
macrophages in the skin and viscera
|
|
insect vector for leischmania
|
sandfly
|
|
what is the sole mammalian reservoir of plasmodium species?
|
human
|