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82 Cards in this Set

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Objectives


Review: primary hemostasis, 2ndary hemostasis, and resolution


review: 3 steps of platelet plug formation

adhesion: platelets stick to injured endothelium

aggregation: platelets attract each other


activation: procoagulatn stimulation of clotting cascade



review : disorders in 1º vs. 2º hemostasis and how they present


1. pattern of bleeding


2. site


3. onset


4. example conditions



Screening for bleeding disorder? 2 components

1. take the history


2. simple lab tests: CBC/diff, PBS, INR, PTT

questions to ask in the bleeding history.. 8

+ PMHx (liver, renal disease, CT disease) 
+ Meds (ASA, anticoags, NSAIDS) 
+ FMHx bleeding problems 

+ PMHx (liver, renal disease, CT disease)


+ Meds (ASA, anticoags, NSAIDS)


+ FMHx bleeding problems

Lab tests to screen for bleeding risk



Note: when is no further testing required




when is further testing required



How is thrombocytopenia defined?

<140x10^9 cells at the U of A




NOT a diagnosis. IS a lab value that must be explained.

Thrombocytopenia: typical bleeding pattern



note: threshold for minor spontaenous bleeds?


threshold for life threatening bleed?




wrt platelet counts

sx may not be evident until count drops below 30 or even 20 

sx may not be evident until count drops below 30 or even 20

Can approach low platelets by pathologic category: dec. production, inc. destruction, sequestration



dec. production: 5 to consider



increased PLT destruction: immune mediated vs. consumptive



PLT sequestration: 3



The 3 letter platelet conditions of thrombocytopenia. there are 4. 3 are emergencies..



pathophys of ITP



ITP in Kids:


1. age group


2. natural history


3. potential platelet counts



Rx of ITP in kids












IVIG:
flood system with ab’s, and it’s not as easy from immune
system to attack platelets. 



Rituximab:
wipes out b lymphs. This resets immune system and
hopefully when it grows back, it is not autoimmune

IVIG:flood system with ab’s, and it’s not as easy from immunesystem to attack platelets. Rituximab:wipes out b lymphs. This resets immune system andhopefully when it grows back, it is not autoimmune

ITP IN ADULTS


1. M:F


2. bleeding risk


3. platelet counts


4. natural history



ITP in adults: Tx



ITP is a diagnosis of exclusion

rule out the bad stuff... 

rule out the bad stuff...

the 3 letter platelet emergencies.. 3



note: DIC is a syndrome 2ndary to severe systemic illness

 k

k

pathophys of DIC



Clinical Features of DIC

1. Low PLT count on CBC with occasional red cell fragments


2. bleeding!


3. thrombosis: digital infarcts, stroke/neuro/end organ damage


4. other labs: anemia, prolonged PT, PTT, depleted clotting factors


5. low fibrinogen

lab findings in DIC 5

1. anemic


2. prolonged PT, PTT


3. depleted clotting factors


4. low fibrinogen


5. low platelet count

Therapy of DIC?

1. treat underlying disease


2. replace clotting factors (plasma) and fibrinogen (cryoprecipitate) if bleeding


3. low dose heparin if thrombosis dominates

two types of MAHA (microangiopathic hemolytic anemia)

TTP: thrombotic thrombocytopenic purpura


HUS: hemolytic uremic syndrome

TTP and HUS: clinnical features? 2



what is required to diagnose MAHA? 2

1. low platelets with hemolytic anemia


2. red cell fragmentation on blood film




if you have these 2, the diagnosis is made

Classical pentad of TTP?

only need first 2 for dx


1. hemolytic anemia


2. red cell fragmentation


----


3. Fever


4. renal failure


5. neuro symptoms




THE ABSENCE OF FULL PENTAD DOES NOT MAKE TTP LESS LIKELY

How to diff't HUS from TTP on basis of


age


neuro manifestations


renal manifestations



pathophys of TTP/HUS

depletion of vWF cleaving metalloprotease (ADAMTS13) is responsible for the syndrome

diagram: pathophys TTP/HUS



mech of red cell shearing in MAHA



normal vs. TTP blood film 

normal vs. TTP blood film



HUS;


1. etiology


2. prodrome..


3. Rx



Causes of TTP 

Causes of TTP

d

TTP:


1. definitive care


2. supportive care to do while arranging transfer?


3. Other Treatments



HIT:


1. clinical syndrome?


2. manifestations


3. when to consider


4. how to monitor...



HIT pathophysiology



Who gets HIT/HIT antibodies? 4



4T score gives a pretest probability for HIT. DNM



Diagnosis of HIT?


what rules in HIT? what rules out?



functional assays in HIT ..



Rx HIT:

1. stop heparin 
2. anticoagulate with alternate drug

1. stop heparin


2. anticoagulate with alternate drug



Hx to take in thrombocytopenia



PE in thrombocytopenia



investigations in thrombocytopenia



LOW PLT: what do we do if HB is low?

MUST LOOK FOR HEMOLYSIS: (retic count, LDH, Bilirubin, Haptoglobin)




consider TTP...

Investigation of low PLT.. coag tests? HIT suspected? Serologic tests?



features that separate ITP, DIC, and TTP/HUS


1. PLT levels


2. PT/PTT


3. Fibrinogen


4. red cell fragments


5. patient Gen. appearance...



Objectives: VTE



why does the Superficial femoral vein have the stupidest name in the world

because it is actually a DEEP vein

review: virchow's triad

1. stasis


2. vessel wall injury


3. hypercoagulability

example causes of venous stasis 5



example causes of hypercoagulability 6



causes of vascular injury



VTE risk factors




explain importance of additive risk factors, and age



VTE: importance of provoked vs. unprovoked



where do blood clots form?




note: weird clot sites may require workup..



relationship between DVT and PE...



Dx of VTE: clinical findings are neither sensitive nor specific ..



Sx DVT/PE





Modified wells 7



review: D dimer is sensitive but not specific for VTE



Imaging studies in VTE



Extra imaging pointers



Clotting cascade review



How to treat DVT? (drug, dosages, etc)



LMWH:



Coumadin: dosing, monitoring, target INR, timing of onset



Note: INR reflects the dose of coumadin given ___ hr earlier

48 hours

example coumadin dosing schedule



how to manage bleeding on warfarin?



minimum duration of anticoagulation?



thrombophilia workup//



note: hypercoagulable workup should NOT be routinely ordered on all patients with clot

d

mechanisms of increased clot risk in cancer



VTE treatment in cancer...