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Pathology > 4.9 Bleeding disorders > Flashcards

4.9 Bleeding disorders Flashcards

1
Q

coagulation tests

A

bleeding time,
prothrombin time (PT),
Partial thromboplastin time (PTT)

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2
Q

PT longer than normal tells you

A

dec platelet function

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3
Q

PT looks at

A

external path

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4
Q

Partial thrombo-plastin time (PTT) looks at

A

intrinsic path

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5
Q

genetics of hemophilia A and B

A

x -linkend

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6
Q

Hemophilia A

A

def in 8 (most common)

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7
Q

Hemophilia B

A

def in 9

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8
Q

severe activity

A

<1% - see internal bleeding and hemoarthrosis

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9
Q

moderate activity

A

1-5% - has variable course

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10
Q

mild activity

A

5-40% - may not even be diagnosed

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11
Q

in hemophilia PTT is

A

abnormal

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12
Q

what is the most common coagulation disorder

A

von Willebrand Disease

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13
Q

Von Willebrand Disease

A

dec amount of function of vWB factor - rirmber vWBF also carries and stabilizes factor 8 in the ciruculation

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14
Q

von Willebrand Disease subtypes

A

1 2 and 3 each with subtypes

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15
Q

Most common von Willebrand Disease subtype

A

Type 1 (60-80%)

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16
Q

Type I vWB diisease

A

heterozygous quantitative reduction in the amount of vWB factor (10-45% or normal),
frequently asymptomatic and not diagnosed under normal condition

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17
Q

Type 2 vWB disease

A

20-30%, qualitative defect in fn but normal levels of protein, subtypes A B M N

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18
Q

Type 2 vWB disease -A

A

inability to form HMW multimers

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19
Q

Type 2 vWB disease - B

A

gain of fn causing binding of platelets to HMW multimers and abnormal clearance

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20
Q

Type 2 vWB disease - M

A

qualitative deficit in native protein not in the ability to form multimers

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21
Q

Type 2 vWB disease - N

A

decrease ability to bind factor 8 but platelet fn is normal

22
Q

Type 2 vWB disease - N is commonly misdiagnosed as

A

hemophilia A bc of the dec activity of factor 8

23
Q

Type 3 vWB disease

A

homozygous defect so extremely low levels of vWBF, most serious bleeding with reduced 8 can have hemarthrosis as observed in hemophilia

24
Q

Platelet disorders

A

bernard-soulier syndrome,

glandzman thrombasthenia

25
Q

Bernard soulier syndrom

A

def in Gp1b the receptor for vWBF

26
Q

Glandzman Thrombasthenia

A

def in Gp2b/3a the receptor for fibrinogen and required for platelet aggregation

27
Q

DIC

A

disseminated intravascular coagultion

28
Q

DIC is

A

consumptive coagulopathy,
widespread fibrin thrombi in the microcirculation using up platelets and coagultion factors,
activates fibrinolytic system,
fibrin split products appear in blood,
not a primary disease but occurs in very sick people

29
Q

DIC becomes apparent by

A

bleeding - due to all the coagulation you eat up all your platelets

30
Q

in DIC you see fibrin split products bc

A

plasmin can eat up the small thrombi that are wide spread froming the fibrin split products

31
Q

so if you see someone that is Sick with GI bleed and fibrin split products think

A

DIC

32
Q

Infarction

A

ischemic necrosis caused by occlusion of the arterial supply or the venous drainage, 99% caused by thrombotic or embolic events

33
Q

occlusion of the arterial supply

A

wedge shape (but must be con correct plane)

34
Q

red infarcts

A

venous - red indicates that the part before the occlusion is getting too much blod –hemorragic dead tissue results

35
Q

and MI might look red due to

A

reperfusion - even though the artery was pinched off it got catherized and reprofused

36
Q

if you see many areas with occlusions think

A

left heart problems/vegetation

37
Q

factors affecting infarction

A

anatomy of vasculature,
rate of occlusion,
organ dependence on aerobic metabolism,
oxygen content of blood

38
Q

sudden occlusion is prone to

A

infarctin

39
Q

slow occlusion

A

might have nagina but since tissue gets mildly ischemic this tells the body to brow more collateral vessesl

40
Q

Shock

A

cardiovascular collapse due to reduction in cardiac output or reduction in blood volume.
Results in systemic hypotension,
hypoperfusion, and
hypoxia

41
Q

Three forms of schock

A

cardiogenic,
hypvolumic,
septic

42
Q

cardiogenic shock

A 
pump failure, 
muscle damage bye infarction, 
cardiomyopathies, 
extrinsic compression, 
arrythmias, 
outflow obstruction
43
Q

hypovolumic shock

A

blood loss from hemorrhage,
fluid loss from burns,
vomiting,
diarrhea

44
Q

Septic shock

A

25-75% mortality rate, usual cause is endotoxin from gram negative bacteria, but other bacteria and fungal products are also inducers and organisms don’t have to be alive

45
Q

LPS and Serum will induce macrophages to produce

A

TNF IL1 and IL6

46
Q

TNF and IL1

A 
leukocyte/endothelium activation, 
complement activation, 
fever/acute phase reactants, 
systemic vasodialation, 
lowered cardiac output, 
vessel damage and thrombosis, 
ARDS and DIC
47
Q

Stages of Schock

A

nonprogressive,
progressive,
irreversible

48
Q

nonprogressive shock

A

compensatory mechanisms maintain perfusion

49
Q

pregressive shock

A

tissue hypoporfusion and beginning of dwonward spiral

50
Q

irreversible shock

A

ischemic damage to tissues such that correction in hemodynamics cannot rescue

51
Q

nightmare of shock

A

overcompensation leading to vasoconstriction, tachycardia,
reanl fluid retention__hypoxia leads to anaerobic metabolism and lactic acid production inducing vasodialtion_..
cardiac output decreases, hypoxia worsens, hypoxic heart lower output, angiotensin activated, worsened systemic hypoxia

Pathology (26 decks)

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