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Life Support > Coagulation > Flashcards

Coagulation Flashcards

1
Q

What are the main causes of drug-induced thrombocytopenia?

A
  • quinine
  • abciximab
  • NSAIDs
  • diuretics (furosemide)
  • Abx (penicillins, sulphonamides, rifampicin)
  • anticonvulsants (carbamazepine, sodium valproate)
  • heparin
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2
Q

Which clotting factors are affected by heparin?

A

prevents activation of factors 2, 9, 10, 11

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3
Q

Which clotting factors are affected by warfarin?

A

prevents synthesis of factor 10, 9, 7, 2

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4
Q

How does DIC affect clotting factors?

A

DIC = disseminated intravascular coagulopathy

factors 1, 2, 5, 8, 11

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5
Q

Which clotting factors does liver disease affect?

A

factors 1, 2 5, 7, 9, 10, 11

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6
Q

What are the 2 clotting cascades that lead to fibrin formation?

A
  • intrinsic (components already present in the blood)

- extrinsic (needs tissue factor released by damaged tissue)

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7
Q

What are the roles of the INTRINSIC pathway of the clotting cascade?

A

Minor role in clotting

Subendothelial damage e.g. collagen

Formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK) and Factor 12

Factor 12 activates Factor 11
Factor 11 activates Factor 9,

Factor 9 with its co-factor Factor 8a form a complex

This activates Factor 10

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8
Q

What are the roles of the EXTRINSIC pathway of the clotting cascade?

A

Tissue damage

Factor 7 binds to Tissue factor (III)

This complex activates Factor 9

Activated Factor 9 works with Factor 8 to activate Factor 10

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9
Q

What is the common pathway of the clotting cascade?

A

Activated Factor 10 causes the conversion of prothrombin to thrombin

Thrombin hydrolyses fibrinogen -> fibrin

Activation of factor 8 to form links between fibrin molecules

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10
Q

What is fibrinolysis?

A

Plasminogen is converted to plasmin to facilitate clot resorption

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11
Q

Which factors are involved in extrinsic/PT measures?

A 
PT = prothrombin time 
(standardised = INR), extrinsic

factors: 2, 7, 9, 10

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12
Q

Which factors are involved in intrinsic/APTT measures?

A

APTT = intrinsic clotting time

factors: 8, 9, 11, 12

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13
Q

How does jaundice affect clotting time?

A

will affect production of vitamin K dependent clotting factors (PT/extrinsic)

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14
Q

Why is APTT affected by vitamin K deficiency?

A

APTT: factors 8, 9, 11, 12

factor 9 is Vit K dependent

can be affected but to a lesser extent (than in PT). Is usually associated with severe liver disease

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15
Q

What does warfarin do to clotting?

A

affects synthesis of factors 10, 9, 7, 2

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16
Q

What does heparin do to clotting time?

A

Prevents activation of factors 2, 9, 10, 11

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17
Q

What does DIC affect in clotting?

A

DIC = disseminated intravascular coagulopathy

factors: 1, 2, 5, 8, 11

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18
Q

What does liver disease affect in clotting?

A

factos: 1, 2, 5, 7, 9, 10, 11

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19
Q

How will Haemophiia affect clotting times?

A

APTT: Increased
PT: normal
bleeding time: normal

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20
Q

How does von Willebrand’s disease affect clotting time?

A

APTT: increased
PT: normal
bleeding time: increased

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21
Q

How does vitamin K deficiency affect clotting times?

A

APTT: increased
PT: increased
bleeding time: normal

22
Q

Which clotting test represents the intrinsic pathway?

A

APTT

23
Q

Which clotting test represents the extrinsic pathway?

A

PT

If this is standardised then this becomes INR

24
Q

Which pathway of the coagulation cascade is most important?

A

Extrinsic

25
Q

What is the starting step in the shared pathway for the coagulation cascade?

A

Activation of 10

26
Q

What is the function of thrombin (factor I)?

A

thrombin converts fibrinogen to fibrin

[hydrolysis]

27
Q

What occurs during fibrinolysis?

A

plasminogen is converted to plasmin

plasmin then break down the fibrin clot

28
Q

What are the 2 pathways that lead to fibrin formation in the coagulation cascade?

A
  • intrinsic pathway (components already in the blood)

- extrinsic pathway
needs TISSUE FACTOR to be released by damaged endothelium

29
Q

Which factors are inhibited by anti-thrombin III?

A

factors II, IX, X

does also inhibit factor XI but to a lesser extent

30
Q

What is anti-thrombin III?

A

= ATIII

  • non-vitamin K dependent protease
  • inhibits coagulation cascade
31
Q

What Sx triad is indicative of Budd-Chiari syndrome?

A
  • abdo pain
  • ascites
  • hepatomegaly
32
Q

What can cause the hypercoagulable states in Budd-Chiari syndrome?

A

Protein C and S deficiency

33
Q

What changes are likely to be seen in the arteries of a patient with angina?

A
  • smooth muscle proliferation
  • migration from the tunic media into the intima
  • causing a FIBROUS CAPSULE to form
34
Q

What changes can be seen in atherosclerosis?

A
  • endothelia dysfunction
  • inflammation, oxidative and proliferative changes to endothelium
  • reduced NO availability
  • fatty infiltration of the sub endothelial space by LDLs
  • monocytes migrate from blood forming MQ
  • As MQ engulf LDLs and die, they become foam cells
  • fibrous plaque formation over fatty plaque
35
Q

What factors can cause initial endothelial dysfunction in atherosclerosis?

A
  • hypertension
  • hyperglycaemia
  • smoking
36
Q

What complications can occur once an atherosclerotic plaque has formed?

A
  • plaque forms physical blockage to blood flow and perfusion [ANGINA]
  • plaque rupture which may occlude artery [MI]
37
Q

Which immune cells are derived from myeloid lineage?

A
  • mQ
  • DCs
  • neutrophils
  • eosinophils
  • basophils
  • mast cells
38
Q

Which immune cells are derived from lymphoid lineage?

A
  • T cells
  • B cells
  • NK cells
  • DCs
39
Q

What score is used to predict/stratify if a PE is likely Dx or not? What score is considered low/high risk?

A

Wells score
>4 PE likely
<4 PE unlikely

40
Q

If 2-level Wells score indicates a PE, what is the next Ix recommended?

A

If wells >4
then perform CTPA
if there is a delay until scan, then give low MW heparin in interim

41
Q

If 2-level Wells score indicates that a PE is unlikely, what is the next Ix recommended?

A

D-dimer blood test
if this is positive, then perform a CTPA
if there is a delay until scan, then give low MW heparin in interim

42
Q

When may a V/Q scan be performed for PE Ix?

A

V/Q scanning is also the investigation of choice if there is renal impairment

(doesn’t require the use of contrast unlike CTPA)

43
Q

What is the sensitivity of the D-dimer test?

A

95-98% SENSITIVITY
but
poor specificity

44
Q

What are the classic ECG changes seen in PE?

A

S1Q3T3
large S wave in lead 1
large Q wave in lead 3
inverted T wave in lead 3

other changes:

  • RBBB and right axis deviation
  • sinus tachycardia
45
Q

What possible findings may there be on a CXR in PE?

A

wedge-shaped opacification

46
Q

What is the clinical severity of a-thal where 1 or 2 genes are affected?

A

hypochromic and microcytic

Hb level would be typically normal

47
Q

What is the clinical severity of a-thal where 3 genes are affected?

A

hypochromic microcytic anaemia
splenomegaly
known as Hb H disease

48
Q

Under which conditions would individuals with sickle trait become symptomatic?

A

(HbAS)
underly very hypoxic conditions
pO2: 2-4 kPa

49
Q

What is the clinical severity of a-thal where all 4 genes are affected?

A

e.g. –/– (homs)
death in utero
(hydrops fetalis, Bart’s hydrops)

50
Q

What are the features of beta-thalassemia major?

A

presents in first year of life
failure to thrive
hepatosplenomegaly
microcytic anaemia

HbA2 & HbF raised
HbA absent

51
Q

What is the Rx for beta-thalassemia major?

A

repeated transfusion → iron overload

s/c infusion of desferrioxamine (Fe chelation)

Life Support (13 decks)

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