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cardiovascular system > haemostasis > Flashcards

haemostasis Flashcards

1
Q

what is the condition where you lack coagulation factors 8 and 9

A

haemophilia

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2
Q

wwhat are the characteristics of a normal bleed

A

spontaneous - eg bruise with no bump, nose bleeds
out of proportion to the trauma/injury - bleeding into joints
unduly prolonged (not faster it just doesn’t stop)
restarts after appearing to stop

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3
Q

problem with the ‘characteristics’ of abnormal bleeding

A

approx. 12% population had easy bleeding

ddoesnt mean that they have a bleeding disorder

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4
Q

name for nosebleed

A

epistaxis

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5
Q

signs of a bleeding disorder

A

epistaxis not stopped after 10mins or need medical attention
cutaneous haemorrhage or bleeding without trauma
bleeding for >15mins from trivial wounds or in the oral cavity
spontaneous bleeding 7days after wound
spontaneous bleeding of GI tract
menorrhagia - requiring treatment or leading to anaemia - not because of structural lesions of the uterus
heavy or prolongued bleeding after surgery or dental extractions

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6
Q

what can be defected in primary haemostasis

A

collagen vessel wall
vWF
platelets - more complicated

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7
Q

cause of collagen defect

A

steroids - break down supporting tissue, make bv more fragile
age - less able to support bv = senile purapura
scurvy - need bit c to cross link fibrinogen
platelets - complicated, so more things can go wrong with them neurafen, volterol?) - inhibit platelet like activity
hereditary - molecules on surface of platelets missing (Gp1B or tP38?)
or people don’t have enough platelets

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8
Q

what causes the defect in vWF

A

not assembled in the right way - genetic deficiency - vW disease

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9
Q

what causes the defects with platelets

A

aspirin and other drugs
thrombocytopenia - inhibit platelet activity
people don’t have enough platelets

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10
Q

describe vWD

A

no vWF so the platelet cant stick
cant bind to collagen because it is going too fast
cant form the plug
nothing for coagulation factor to hold together

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11
Q

what is a pattern of bleeding specifically caused by thrombocytopenia

A

petechiae

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12
Q

when does bleeding start if there is a primary failure (and where)

A

immediately
gum bleeding
and the previous examples of bleeding

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13
Q

describe petechiae

A

distal
back of pallet in mouth
confused with vasculitis and vascular disorder
all the time there are small breaks in the bv - with thrombocytopenia you can’t plug the small holes

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14
Q

describe the thrombin generaction in haemophiliacs

A

feeble - not surprising that they bleed

genetics is the most common cause

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15
Q

why does haemophilia cause bleeding

A

cant make fibrin to stabilise the platelet plug

the primary haemostatic plug is formed but not stabalised so it falls apart - start bleeding again

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16
Q

what are the defects of secondary haemostasis

A

deficiency or defect of coagulation factors - poor thrombin burst = pore thrombin mesh eg
genetic - haemophilia - factor 8 or 9 deficiency
acquired - liver disease, most coagulation factors are made in the liver (cirrhosis) don’t make enough factors, including coagulation ones
- drugs: warfarin inhibit synthesis of factors, others block function
- dilution: volume replacement but coagulation factors are not returned
- consumption: disseminated intravascular coagulation

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17
Q

what is disseminated intravascular coagulation

A

widespread inflammation - sepsis, incompatable blood transfusion, major tissue damage
inf reaction put tissue factor in bv on monocytes and endothelium
generalised activation of coagulation - tissue factor inside the microvasculature
associated with sepsis, major tissue damage and inflammation
consumes and depletes coagulation factor and platelets
activation of fibrinolysis - depletes fibrinogen because all made into fibrin which is deposited into bv - not good - organ dysfunction, chopped as well
platelets used up
antiplatelets degrade the coagulation factors - run out of those too
bleed spontaneously

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18
Q

consequences of DIC

A

widespread bleeding from iv lines, bruising, internal

deposition of fibrin in vessels causes organ failure

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19
Q

pattern of bleeding when there are secondary defects

A

delayed - after primary haemostasis - apparently fine then plug falls apart and you start bleeding
prolonged
deeper - joints and muscles
do the bleeding time test - no bleeding from small cuts
nosebleeds are rare
bleeding after trauma/surgery
after I/m injections

20
Q

what is easy bruising called

A

ecchymosis

21
Q

what is haemarthrosis

A

spontaneous bleeding into the elbow
sign of inflammamation - joint swollen
cause severe joint damage
hallmark of haemophilia

22
Q

what 2 things cause excess fibrinolysis

A 
excess fibrinolytic factors - plasmin or tPA 
deficient antifibrinolytic (antiplasmin)
23
Q

examples of excess fibrinolytic factors

A

therapeutic admisistration - give tPA to people with strokes to break down clots
some tumours

24
Q

example of deficient antifibrinolytic

A

genetic - antiplasmin deficiency

25
Q

why would there be an anticoagulant excess

A

eg excess antithrombin
due to therapeutic administration eh heparin, thrombin and Xa inhibitors
activate antithrombin
these drugs are given with good reason but they encourage bleeding

26
Q

describe thrombosis

A 
intravascular coagulation 
inappropriate coagulation 
coagulation inside a bv 
coagulation not preceded by bleeding 
can be venous or arterial 
caused because too much factor 8 or 11, or too little anticoagulant
27
Q

what are the effects of the thrombus obstructing the flow of blood

A

in artery - MI, stroke, limb ischemia (more serious back flow to tissue, unique blood supply, tissue dies)
in vein - causes pain and swelling, there are a few ways for the blood to return

28
Q

effects of a thrombus embolising

A

venous emboli - in legs, to hear, to pulmonary circulation which is low pressure so not built to take it
arterial emboli - usually from the heart, form in left side in atrial fibrillation enter arterial circulation lodge in brain cause cardioembolic stroke, can cause limb ischemia - peripheral, pain in foot

29
Q

describe DVT

A

venous return of blood is obstructed - painful, swollen leg

cause pulmonary embolism

30
Q

symptoms of pulmonary embolism

A

shortness of breath
chest pain
sudden death
lung infarction

31
Q

prevalence of venous thromboembolism

A

1 in 1000-10000 cases a year (10000 younger, 1000 older)
incidence doubles with each decade
PE cause of 10% of hospital deaths
25k preventable deaths a year

32
Q

relationship between PE and age and DVT and age

A

both increase with age

PE more steeply

33
Q

consequences of thromboembolism

A

case mortality 5%
20% recurrence in 1st 2 years, 4% per anum after that
thrombophlebitic syndrome - swelling and discomfort doesn’t get better, ulcer in leg from disturbance in flow to the heart - sever in 23% people at 2 years, 11% with stockings
pulmonary hypertension because the remodelling isn’t good for the heart - high mortality rate

34
Q

risk factors for thrombosis

A

genetic constitution
effect of age, previous events, illnesses and medications
acute stimulus

35
Q

explain the thrombosis risk

A

multi causal
caused by interacting genetic and acquired risk factors
genetic risk - from higher or lower level of thrombin or factor 8
then risk increases with age
and you can have acquired risk which could push you over the thrombotic threshold
some acquired risks can be removed - eg a broken leg will get better, stop the pill

36
Q

what are the factors in virchows triad

A

factors in blood - dominant in venous thrombosis
factors in the vessel wall - dominant in arterial thrombosis
flow 0 complex, contributes to both

these can be inherited or acquired

37
Q

describe how factors in the blood cause venous thrombosis

A

increase in coagulation factors and platelets (factor 8, 2, factor 5 leiden, thrombocytosis - increased platelets)
decrease in fibrinolytic factors and anticoagulant proteins (AT, protein C and S)

38
Q

describe factor 5 leiden

A

5% of people have it - tip in favour of thrombosis
polymorphic
hereditary
of factor 5
factor 5 is resistant to protein C - balance in favour of thrombosis
present with thrombosis
in white Caucasians, a little in Africa and asia

39
Q

what causes an increase risk of thrombus on the vessel wall

A

anticoagulant molecules on the surface
thrombomodulin, tissue factor, tissue factor inhibitor are all on endothelial cells
expression is altered in inflammation - malignancy, infection, immune disorders - down regulate thrombomodulin, increase thrombosis

40
Q

what causes an increase risk of thrombus with flow

A

stasis

eg in surgery, fracture, long haul flight, bed rest

41
Q

describe the clinical aspects of thrombophilia

A 
increased tendancy to form a thrombus 
thrombosis at a young age 
idiopathic thrombosis 
multiple thrombosis 
thrombosis whilst anticoagulated
42
Q

describe the labatory aspects of thrombophilia

A

identifiable cause of increased risk
AT deficiency
factor 5 leiden
global measures of coagulation deficiency

43
Q

what conditions causes combined risks for thrombosis

A

pregnancy - coagulation factor increases
malignancy - physical obstruction, and inflammation of bv cause increased fibrinogen, factor 8 and vWF
surgery
inflammatory response
reduce mobility and flow

44
Q

describe the risk for post operative VTE

A

surgery is a major risk

even day surgery is 15-16% higher - lack of mobility, inflammation, underlying disorder

45
Q

therapy and venous thrombosis

A

treatment: lyse clot - eg tPA high risk of bleeding
treatment: limit recurrence, extension or emboli - increased anticoagulant activity, eg heparin, immediate acting, parenteral, restore the haemostatic balance
- lower procoagulant factors eg warfarin, oral, slow acting for long term therapy
- inhibit procoagulant factors, direct inhibitors Rivaroxaban, Apixaban, Dibigatran (inhibits throimbin)
all of these prevent clot and propagation

46
Q

prevention of thrombosis

A

assess individual and circumstantial risk - acquired, genetic, and circumstantial
all patients who enter hospital should have a VTE risk assessment
give prophylactic antithrombotic therapy eg heparin and TED stockings - use balance, don’t give to haemophiliacs

47
Q

hwo do you restore the balance

A

just do the things that would tip it the lother way
decrease procoagulant factors with warfarin, or give antiplatelet agents (aspirin)
or increase anticoag - heparin
or drugs that inhibit anticoag activity

cardiovascular system (22 decks)

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