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Med Year 3 > clotting disorders > Flashcards

clotting disorders Flashcards

1
Q

what is the clotting cascade

A

check ipad for full thing but:

intrinsic (damaged tissue): 12-12a, 11-11a, 9-9a, 10-10a

extrinsic (trauma): 7-7a, then with TF to 10-10a

10a activates prothrombin-thrombin, fibrinogen - fibrin

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2
Q

what factors does thrombin activate

A

5,7,8,11,13

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3
Q

what do protein c and protein s do

A

prevent constant clotting; protein c and thrombomudulin in presence of protein s stop 10-10a and 13-13a

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4
Q

how does warfarin work

A

acts on vit-k dependent factors like factors 2, 7, 9,10 and proteins C and S to prevent clotting

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5
Q

what does plasmin do

A

thrombin converts plasminogen to plasmin, which dissolves the fibrin clot

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6
Q

what is the diagnostic triad for bleeding disorders

A

personal history of bleeding
family history of bleeding
supportive lab tests

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7
Q

what do you ask about history of bleeding

A

bruising, surgical and dental history, epistaxis >30 minutes, GI tract bleeding, menses: clots, flooding, duration
urine: haematuria

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8
Q

what do you ask about FH of bleeding

A

known bleeding disorders; when, where and who tested

surgical history and if abnormal bleeding

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9
Q

what are the main lab tests done for clotting disorders

A
  • FBC
  • Hb, haematocrit and WBC
  • platelets
  • PT = normal 10-12 seconds
  • APTT normal is 20-30s

microscopy: large, small platelets or neutrophil or platelet inclusions all indicate certain syndromes

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10
Q

how do you test whether there is a factor deficiency or a coagulation factor inhibitor present?

A
  • do a 50/50 mixture study of patients plasma and normal plasma if times are prolonged
  • if inhibitor is present: APTT and PT will still be prolonged
  • if deficiency is present: adding in 50% normal WILL correct it; hence could be factor 8 or 9 deficiency
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11
Q

what do you do if nothing is found in the investigations but good bleeding history?

A

tests for vWD: factor 8, vWF antigen and vWF activity

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12
Q

what are APTT and PT

A

prothrombin time - measures intrinsic pathway

activated partial thromboplastin time - meausres extrinsic pathway

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13
Q

what does a prolonged PT mean

A

they are:

  • on warfarin
  • have a factor 7 deficiency - common
  • have a factor 2,5,10 deficiency
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14
Q

what does a prolonged APTT mean

A

heparin
8,9,11 deficiencies
12 deficiency but no bleeding
vWD (however in types 1 and 2 may be a normal APTT)

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15
Q

what do prolonged both pT and APTT mean

A

vitamin k deficiency and low fibrinogen = liver disease so malabsorption

disseminated intravascular coagulation (small blood clots form throughout body causing CP, SOB, leg pain etc)

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16
Q

how do you test clot stability and what is it for

A

euglobin clot lysis (make clot on orange stick, place in fridge, is it still there after 24 hours)

checks for factor 13

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17
Q

what is the physiology of vWF

A

plasma protein that carries factor 8

endothelilal cells attached to the subendothelial collagen by vWF (they produce it)

stored in welbei-palade bodies

platelets store it as well; helps to clump them together

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18
Q

what is vWD

A

loss of ability to clot the blood due to defect in vWF or decrease in plasma levels

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19
Q

what are the types of vWD

A

type 1 - mildest, reduced amount of vwd
type 2 - abnormal vw protein
type 3 - little or no vw protein

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20
Q

how do you test for vwd?

A

factor 8
vw antigen
vw activity
all normal ranges 50-250

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21
Q

how do you differentiate between type 1 and type 2

A

ratio of vwF activity: antigen

ratio >0.6 = type 1
ratio <0.6 = type 2

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22
Q

symptoms of type 1 vwd

A

bruising, menorrhagia, mucosal bleeding

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23
Q

treatment of type 1 vwd

A

DDAVP (desmopressin) and transexamic acid
increase level of vw protein, for last 24 hours

watch for diminishing returns in major surgery bc may need to give vwF

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24
Q

how does DDAVP work

A

increases vWF secretion from endothelial cells

25
Q

what is the issue with type 2 vwd

A

clinically indistinguishable from type 1

26
Q

what is type 2b

A

overactive protein (abnormal) which results in thrombocytopaenia

avoid desmopressin bc increases vwF from endothelial cells and don’t need an increase

to diagnose from type 2: give DDAVP when well and meausre BP and iron ?

27
Q

how do you treat type 2b

A

vwF concentrates or replacement therapy

28
Q

how do you treat type 2

A

DDAVP

29
Q

what is type 3 vwd

A

severe, life threatening

serious mucosal bleeding and operative treatment will cause severe bleeding

30
Q

what is haemophilia

A

is a genetic disorder that is inherited and impairs clotting, there are 3 types but 2 main ones (A and B)

31
Q

what is haemophilia A

A

reduction in factor 8

32
Q

what is haemophilia B

A

reduction in factor 9

33
Q

what is haemophilia C

A

known as plasma thromboplastin antecedent (PTA) deficiency = mild form of haemophilia affecting both sexes due to factor 11 deficiency

34
Q

how do you grade haemophilia in terms of severity?

A

factor level, <1, 1-5, >5 (severe, moderate, mild)

bleeding: spontaneous, slight injury, trauma
frequency: 1-2x a week, 1x per month, rare

35
Q

how is haemophilia A treated?

A 
home therapy (explained in another FC)
DDAVP useful for mild haemophiliacs, it raises levels by 2 or 3; given SC, IV or intranasally

also transamexic acid

36
Q

haemophilia B differences

A

factor 9 - recombinant small molecule; bigger distribution than above

amount needed = rise x weight

37
Q

how does transamexic acid work

A

anti-fibrinolytic agent, given orally, which slows down the plasminogen system allowing any clot that’s formed to stay longer

38
Q

what is the home therapy for haemophilia?

A

primary - start when patient is 18 months - 3 years old
secondary - start after 3 joint bleeds

injections:
factor 8 - alternate days but still often 3x a week
factor 9 - 2x a week

39
Q

what is a VTE

A

DVT and PE

40
Q

physiology of blood in legs

A

contraction of calf muscles normally squeeze blood up the deep veins of the leg and internal venous valves prevent it flooding back

in diseased states: varicose veins bc systems don’t work well so back wash of blood, veins bulge and blood pools in the deep veins

41
Q

what is virchow’s triad

A

stasis of blood flow (immobile)

endothelial injury - esp leg operation

hypercoagulability - acute phase reactant proteins including fibrinogen, factor 8 and vWF

42
Q

what are the risk factors for VTE

A

-hip or knee replacement surgery patients
-anasthesia
-post-op period bed rest
> 60 years
-prev DVT or family history of DVT

43
Q

how do you prevent DVT

A

mechanically: pneumatic compression stockings
pharmacologically: low does LMWH or low dose unfractionated heparin

direct anti-Xa and DOAC’s

44
Q

how do you manage a suspected VTE

A

do not investigate first unless this can be done within 1 hour for PE or 4 hours for DVT

  • use LMWH or UFH heparin, or clexane
  • at the same time, begin oral warfarin for 48-72 hours until INR is 2 then discontinued
45
Q

how is warfarin reversed

A

vitamin K1, and immediately via prothrombin complex concentrate and FFP

46
Q

what is the pathophysiology of the thrombus

A

-dissolution
-propagation
-recanalization - growth of SMC, fibroblasts and endothelium to form a fibrin rich thrombus –> capillaries may form into the thrombus, providing further nutrient supply to the clot
embolisation

47
Q

what is an embolus

A

-material which is transported in blood stream and lodges in a blood vessel at a different site

when it impedes or blocks blood flow in artery = embolism

48
Q

what causes a DVT

A

clot, muscle haematoma, baker’s cyst or cellulitis

49
Q

what are the 4 most common signs of a DVT

A

warm, swollen, tender on palpation and in calf, redness

also: homan’s sign: pain in calf upon dorsiflexion of ankle

50
Q

pathophys of a PE

A

thrombus breaks off, travels in venous system into right atrium, to pulmonary arteries and blocks it

51
Q

what is a massive PE

A

large clot which lodges in right side of heart or in both pulmonary arteries

classically presents with syncope and other symptoms of PE

clinically defined as a massive PE by presence

52
Q

physical signs of a PE

A

-increased respiratory rate
-tachyarrhythmias
-possible signs of DVT
-pleural rub can be heard
-sudden onset of pleuritic chest pain and worse on breathing in
(sharp pain)

  • shortness of breath
  • haemoptysis
53
Q

how do you compare leg swelling and checking for DVT

A

-measure 10 cm down from tibial tuberosity

54
Q

what are the investigations for a PE

A

ECG; right heart strain like RBBB
CHEST x ray
ABG: hypoxia, type 1 resp

55
Q

how do you diagnose a PE

A

look at diagram in notes - wells score

56
Q

what are the investigations for a DVT

A

0 on wells score = lower risk
no need for doppler but d-dimer anyway
if d-dimer is positive, then do a doppler and a CTPA

if higher clinical probability = go straight for doppler on CTPA

57
Q

how do you manage a PE

A

LMWH followed by doac’s; however if religious reasons give fondaparinux bc porcine in heparin

58
Q

what are the guidelines for doac’s

A

apixaban or rivaroxaban
to TREAT DVT or PE:
- 15mg rivaroxaban should be taken twice a day for 21 days and then 20mg oD for 3 months

if these are not suitable; LMWH for at least 5 days followed by dabigatran or edoxaban or LMWH concurrently with a VKA (warfarin) till therapeutic anticoagulation

59
Q

what is the well’s score

A

for DVT >2

for PE>4

Med Year 3 (25 decks)

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