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Physio II > Bleeding disorders > Flashcards

Bleeding disorders Flashcards

1
Q

difference between the coagulation effect from a medicine like ASA vs a medicine like coumadin

A
  1. ASA - platelet toxin (resists clotting)

2. Coumadin - inhibits clotting

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2
Q

examples of dzs that effect primary hemostasis

A 
ITP
TTP
HUS
DIC
VwFD
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3
Q

briefly describe primary hemostasis

A

platelets form a plug
aggregate send
ADP and thromboxane A2 which attract other platelets

PT and PTT unaffected because these are clotting factors

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4
Q

dzs of primary hemostasis typically involve sxs like

A

petechiae and mucotaneous bleeding

oral
GI
menorrhagia

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5
Q

dzs that affect secondary hemostasis

A

hemophilia
DIC
vWD

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6
Q

sxs associated with dzsz of secondary hemostasis

A

deep delayed bleeding

hemarhtrosis seen with bleeding into the joints and delayed bleeding after surgery

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7
Q

PTT measures what factors

A

12
11
9
8

major intrinsic
alos

5
2
1

heparin DIC vWD heophilia

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8
Q

PT measures

A

7 and 10

also
1
2 5

warfarin
vitamin K deficiency
DIC

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9
Q

Hereditary Hemorrhagic Telangiectasia shows what type of inheritance pattern

A

AD

Osler, Weber, Rendu

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10
Q

what is the pathophys behind heridditary hemorrhagic talangictasia

A

defects of TGF beta-1 effect formation of connective tissue necessary for BV formation

results in knots of blood vessels b/c lack of normal basement membrane

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11
Q

when do you usually see hereditary hemorrhagic talangictasia

A

during adolescents Mucosla and during adulthood they are cutaneous on the muscosal membranes (nasal and orolabial), face, and distal extremities.

seen with reoccurent epistaxis and GIB

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12
Q

vascular disorder that effects all collagen sturctures

A

ehler danlos syndrome

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13
Q

sxs of ehler danlos

A

” Easy bruising, hyperelasticity of skin, hypermobility of joints, weakness of tissues

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14
Q

fibrilin 1 binds TGF beta creating inflammatory effects that damage the aorta and heart

A

marfans

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15
Q

this vascular disorder is associated with AVM in the brain lungs and liver

A

HHT

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16
Q

thrombocytopenia can result from

A

decreased bone marrow production

sequestration from the spleen

increased platelet destruction

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17
Q

features of a platelet d/o

A

normal PT and PTT
prlonged bleeding time
spontaneous bleeding
decrease platelets

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18
Q

causes of thrombocytopenia

A
  1. aplastic-bad bone marrow
  2. leukemia-bone marrow infultration
  3. ineffective thrombopoiesis (B12/Folate def)
  4. increased destruction
  5. infection –> will lower
  6. consumption (DIC)
19
Q

ITP is characterized by this imnune reaction

A

IgG Vs GPIIb/IIIA

MCC thombocytopenia in children

20
Q

pentad of TTP

A 
"	Thrombocytopenia
"	Microangiopathic anemia
"	Neurologic changes
"	Renal failure
"	Fever

Adams 13
FAR to TAN
splendid
plasma TV

21
Q

pathophys of TTP

A

” Extensive microscopic clotting in small blood vessels by failure to cleave vWF polymers (enzyme ADAMTS13). Shear stress on RBC –> hemolysis

22
Q

sxs associated with TTP

A

” Darkening of urine from hemolytic anemia
“ Small clots lead to widespread areas of ischemia (multi organ damage)
“ N/V from gut ischemia

23
Q

this platelet disorder can occur with recent use of heparin

A

ii. IgG mediated complexes destroy platelets
iii. Unexplained platelet loss or sudden bleeding
iv. Withdraw agents, get assay for previous hx; get platelet counts

24
Q

MCC of AKI in children

A

HUS

25
Q

what is hemolytic uremic syndrome

A

similar to TTP but associated with E. Coli toxins and chemotherapeutic agents

these exotoxins cause platelet activation and lead to damage in the vascular endothelieum that eventually leads to paltelet deletion thrombocytopenia and damage to to

26
Q

difference between HUS and TTP

A

HUS= AKI and RF no fever

TTP= mental sxs

27
Q

MC initiating facotrs of HUS

A

Diarrhea and URI are MC inciting factors

28
Q

suspect HUS in children with

A

AKI and diarrhea prodrome

29
Q

dx with HUS

A

increase in BUN and Creatinin

and of course thrombocytopenia

30
Q

what dxs would we expect to see associated with the microangiopathic anemia in HUS and TTP

A 
we would expect to see 
reticulocytes increase in the peripheral smear 
scistocytes (bile/fragmented cells) 
increase in LDH
increase in indirect bili 
decrease in haptoglobin

coombs negative
and spleenomegaly

31
Q

broad categories of coagulation disorders

A

production
inhibition
consumptaion
and liver dz

32
Q

Factor VIII Deficiency

A

hemophilia A

MCC of hemophilia

33
Q

pathophys of hemophilia A

A

required for activation of factor X by intrinsic pathway

liver synthesis
bound to subendothelium by vWF

34
Q

inheritance characteristics of hemophilia

A

sxs usually occur before 18 and it is x linked recessive

30% random mutation so Fhx Can’t rule out

10% have normal facotr levels but are inhibited by AB

35
Q

presentation of hem A

A

late rebleeding
hemarthroses
bruise easily
massive hemorrhage

36
Q

how would you dx hem A

A

PTT
low levels VIII

ALSO SEEN WITH bt

37
Q

TX for hem A

A

o Factor VIII replacement

o Desmopressin Acetate for smaller bleeds (it is vasoconstricting)

38
Q

christmas disease

A

hem B caused by factor IX deficiency

39
Q

sxs of xmas dz

A 
indistinguishable form hem A
late rebleeding 
hemarthroses 
bruise easily
massive hemorrhage

need factor assay

40
Q

what reverses heparin

A
  1. Protamine sulfate reverses
41
Q

what reverses warfarin

A

Reversed by administration of Vit K!

42
Q

iv. ASA (De Rosa’s favorite) í Acetylsalicylic acid

works by

A
  1. COX 1 and 2 inhibitor
  2. Inhibits prostaglandin and thromboxane production
  3. Blocking thromboxane A2 production prevents platelet aggregation
43
Q

what increases clotting

A

i. Vit K, FFP (fresh frozen plasma), factor replacement, antifibrinolytics, desmopressin

Physio II (18 decks)

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