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clinical lab > hemostasis > Flashcards

hemostasis Flashcards

1
Q

what is the algorithm of homeostasis ?

A

vascular spasm occurs when a vessel wall is severed or punctured - the endothelin released by endothelial cells and pain receptors causes contraction of smooth muscle cells

platelet plug formation starts -
platelets are activated by chemicals released from the injury site and by contact with subendothelilal collagen
von Hillebrand factor helps stabilise the platelet plug
the platelets themselves now release chemicals to attract other platelets

then there is coagulation - fibrinogen is converted to fibrin
a mesh forms that traps more platelets and erythrocytes

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2
Q

what is the morphological characteristics of a blood clot ?

A

gelatinus but robust clot made up of a mesh of fibrin

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3
Q

what are the pathways for homeostasis ?

A

the extrinsic pathway - triggered by damage occurring to surrounding tissues

the intrinsic pathway - begins in blood stream and triggered by internal damage of the vessel wall

both of these merge into a third pathway - called the common pathway

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4
Q

all the three pathways in homeostasis are dependant on what ?

A

calcium and vitamin K

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5
Q

clotting factors are derived from where

A

liver and platelets

liver needs vit K to produce many of them

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6
Q

the intrinsic or the extrinsic pathway is more quicker responding ?

A

the extrinsic pathway - tissue factor pathway

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7
Q

what is the cascade of the extrinsic pathway?

A

damaged extravascular cells come in contact with the blood plasma

they release factor 3 (thromboplastin/ tissue factor)

then factor 7 is activated by factor 3 to factor 7a

then a tissue factor and 7 a enzyme complex is made

leading to activation of factor 10 with calcium to 10a

leading to the common pathway

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8
Q

what is the process of activation in intrinsic pathway ?

A

when factor 12 come in contact with foriegn materials , negatively charged molecules
it becomes activated
or there can be surface activation

factor 12a —-> factor 11a —–> factor 9a ——> factor 10a

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9
Q

what is the common pathway

A

factor 10a —-pro thrombin —-> thrombin

thrombin—– fibrinogen —- soluble fibrin —–> polymerised fibrin clot

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10
Q

what is fibrinolysis ?

A

protien plasminogen converted to active plasmin breaking down the fibrin of the clot

bradykinin is a vasodilator
reversing effects of serotonin and prostaglandin’s from platelets - smooth muscles in the walls relax

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11
Q

what are the anticoagulants?

A

protein C

tissue factor pathway inhibitor - inhibits factor 7 activation

antithrombin inactivates factor 10
opposes conversion of prothrombin

basophls releasing heparin - also opposing porthrombin

heparin found on the surfaces of cells lining the blood vessels

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12
Q

what are the types of homeostasis ?

A

primary hemostasis

secondary hemostasis

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13
Q

what are the characteristics of primary hemostasis?

A

refers to platelet reactivity at the site of vessel injury

the onset is spontaneous immediately after trauma

sites - skin and mucus membranes

form - petechiae , ecchymosis, purpura

other sites - rare

clinical examples - thrombocytopnea , platelet defect - in number and function , von willebrand disease , scurvy

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14
Q

what is the characteristics of secondary homeostasis ?

A

coagulation of plasma due to coagulation factors - intrinsic system , extrinsic system and common pathway

delayed after trauma

sites - deep tissues

forms - hematomas

other sites - joint , muscle , CNS , retropeitoneal space

clinical examples - factor deficiency , liver disease , acquired inhibitors

factor deficiency
hemophilia A - factor 8 deficiency

hemophilia B - factor 9 deficiency

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15
Q

what is APTT induced by ?

activated partial thromboplastin time

A

asses the intrinsic system and common pathway

surface contact activation
factor 12 in the presence of artificial negatively charged particles (phospholipid) is activated
and calcium

addded to sodium citrate- rversable chelator of calcium

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16
Q

what is PT induced by ?

A

asses the extrinsic pathway and common pathway

excess of tissue factor / thromboplastin (reconbiant human or isolated animal tissue factor) , with exogenous phospholipid

and calcium
allowing factor 7 to overcome the inhibitory effects of TFPI and favouring activation

17
Q

what is thrombin time?

A

time for fibrinogen to go to fibrin

direct measure of fibrinogen function

adding purified exogenous thrombin

18
Q

in APTT examination what should be the ratio of anticoagulant to blood plasma ?

A

1 :9

anticoagulant / sodium citrate : blood plasma

19
Q

which assay serves as the basis for internationally normalised ratio (INR)?

A

PT - prothrombin time

for oral anticoagulant monitoring such as warfarin measurement

20
Q

what is INR ?

A

ratio of patient prothrombin time / mean of normal prothrombin time in local lab - on normal individuals

rasied to the power of international sensitivity index

21
Q

in patients with non warfarin treatment what is used to measure the homeostasis ?

A

pt vales in seconds

22
Q

antigen assays establish what ?

A

presence of coagulation factors

23
Q

combining antigen assays and coagulation based assays which measure the function does what ?

A

characterize any protein with reduced function but with normal antigen levels - dysfunctional proteins or inhibitors

A dysfunctional protein has reduced protein function with normal levels of antigen.

The most useful means to determine whether fibrinogen is abnormal (i.e., dysfibrinogenemia) is to measure clottable fibrinogen and fibrinogen antigen
If fibrinogen clottability is less than 90% of the amount of fibrinogen antigen present, this finding would suggest that the protein produced is abnormal in some way

24
Q

what are chromogenic assays used for ?

A

used to measure certain enzymes (plasmin, activated protein C) and various plasma protease inhibitors (antithrombin, C1 inhibitor, α2-antiplasmin, PAI, tPA).

measure the therapeutic levels of unfractionated heparin, low molecular weight heparin, or fondaparinux

25
Q

what are the findings and diagnosis associated with it ?

A

if aPTT is long and PT and TT normal

intrinsic factor defects 
factor 8 deficiency haemophilia A 
factor 9 deff - hemophilia B 
ONLY IN MALES
factor 12 deficny

contact deficiency - no bleeding
factor 11, prekalikrien, high molecular weight kininogen
lupus anticoagulant

PT long , and aPTT and TT normal ?
extrisic factor defect
factor 7 deficiency

(deficiency of fibrinogen , factor 2 , factor 5 , factor 10)

TT long , aPTT and PT normal?
fibrinogen defect - fibrinogen deficiency - by 30-40 percent detectable
low conc of fibrinogen inhibitors

aPTT and PT long , TCT normal
common pathway - thrombin- factor 2 , factor 5 , factor 10 defect or deficiency

combined deficiency
vit K dependant - thrombin (factor 2)
factor 7 , factor 9 , factor 10

diffrential diagnosis : anticoagulation therapy ,
DIC - sepsis , maligancy , obstetrics , abrution of placenta , surgery of uterus / prostate gland

liver disease ,
vit k deficiency
massive transfusions

all tests long
sever deficiency in fibrinogen
high conc inhibitors of fibrinogen

combined deficiency of fibrinogen , intrinsic and extrinsic pathways

26
Q

hemophilia A and B has hat type of hereditary pattern ?

A

X linked recessive disorder
females can be carrier
males are affected

or de novo mutation one third of haemophilia A

27
Q

which type of haemophilia can affect women and how?

A

Hemophilia a can affect women through lyonisation of the normal x chromosome

turner syndrome xo

daughter of affected male and carrier female

28
Q

severe hemophilia has what clinical presentation ?

A

spontaneous bleeding two or four times a month

needs replacement of factor therapy

29
Q

mild hemophilia has what clinical presentation ?

A

prolonged bleeding after trauma or major surgery - rarely need iv factor replacement

30
Q

mild to moderate deficiency of Factor 8 for whom a diagnosis of hemophilia A may be less apparent needs more diagnostic why ?

A

for a female patient with factor 8 defficiency that is autosomal inheritance

von Hillebrand disease - secondary deficiency of factor 8 may occur - because factor 8 is normally bound to von willebrand factor

31
Q

what is haemophilia b leyden ?

A

factor 9 levels at childhood 75 percent of adulthood

increases during post puberty - result of steroid hormone action

hemophila B leyden - present with haemophilia b in childhood ranging from 1-33 percent , plasma levels rise to 70 percent after puberty and the bleeding complication resolves

32
Q

what is the standard treatment for haemophilia a and b ?

A

recombiant factor products

inhibitor antibodies to favtor 9 and 9 - complicated therapy

33
Q

Afibrinogenmia is what type of inheritance ?

and what are its clinical manifestations

A

autosomal recessive - represent tota absence of fibrinogen

umbilical stump , mucosal bleeding , musculoskeletal and cns bleeding
poor wound healing

associated with recurrent miscarriage , and antepartum and postpartum haemorrhage

34
Q

what is hypofibrinogenima clinical manifestations

A

milder form of bleeding

associated with reoccurring misscarriage and antepartum and postpartum haemorrhage

35
Q

what is the cause of dysfibrinogenemia?

A

associated with liver diseases - post transitional modifications

common in hepatitis b and C

36
Q

what is the clinical manifestation of dysfibrinogenemia ?

A

usually asymptomatic , have mild bleeding
some cases thrombosis
with or without bleeding history

37
Q

what is the diagnosis of DIC ?

A

prolonged APTT and PT
reduced fibrinogen and platelet count - thrombocytopnea

in prothrombtic state -normal PT and APTT
mildly reduced platlet count and normal or elevated fibrinogen

made through - test showing simultaneous presence of thrombin and plasmin formation
D - dimer essay confimatroy test
positive - both thrombin and plasmin form

clinical lab (9 decks)

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