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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?

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?

25
What is the starting step in the shared pathway for the coagulation cascade?
Activation of 10
26
What is the function of thrombin (factor I)?
thrombin converts fibrinogen to fibrin | [hydrolysis]
27
What occurs during fibrinolysis?
plasminogen is converted to plasmin | plasmin then break down the fibrin clot
28
What are the 2 pathways that lead to fibrin formation in the coagulation cascade?
- intrinsic pathway (components already in the blood) | - extrinsic pathway needs TISSUE FACTOR to be released by damaged endothelium
29
Which factors are inhibited by anti-thrombin III?
factors II, IX, X does also inhibit factor XI but to a lesser extent
30
What is anti-thrombin III?
= ATIII - non-vitamin K dependent protease - inhibits coagulation cascade
31
What Sx triad is indicative of Budd-Chiari syndrome?
- abdo pain - ascites - hepatomegaly
32
What can cause the hypercoagulable states in Budd-Chiari syndrome?
Protein C and S deficiency
33
What changes are likely to be seen in the arteries of a patient with angina?
- smooth muscle proliferation - migration from the tunic media into the intima - causing a FIBROUS CAPSULE to form
34
What changes can be seen in atherosclerosis?
- 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
What factors can cause initial endothelial dysfunction in atherosclerosis?
- hypertension - hyperglycaemia - smoking
36
What complications can occur once an atherosclerotic plaque has formed?
- plaque forms physical blockage to blood flow and perfusion [ANGINA] - plaque rupture which may occlude artery [MI]
37
Which immune cells are derived from myeloid lineage?
- mQ - DCs - neutrophils - eosinophils - basophils - mast cells
38
Which immune cells are derived from lymphoid lineage?
- T cells - B cells - NK cells - DCs
39
What score is used to predict/stratify if a PE is likely Dx or not? What score is considered low/high risk?
Wells score >4 PE likely <4 PE unlikely
40
If 2-level Wells score indicates a PE, what is the next Ix recommended?
If wells >4 then perform CTPA if there is a delay until scan, then give low MW heparin in interim
41
If 2-level Wells score indicates that a PE is unlikely, what is the next Ix recommended?
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
When may a V/Q scan be performed for PE Ix?
V/Q scanning is also the investigation of choice if there is renal impairment (doesn't require the use of contrast unlike CTPA)
43
What is the sensitivity of the D-dimer test?
95-98% SENSITIVITY but poor specificity
44
What are the classic ECG changes seen in PE?
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
What possible findings may there be on a CXR in PE?
wedge-shaped opacification
46
What is the clinical severity of a-thal where 1 or 2 genes are affected?
hypochromic and microcytic | Hb level would be typically normal
47
What is the clinical severity of a-thal where 3 genes are affected?
hypochromic microcytic anaemia splenomegaly known as Hb H disease
48
Under which conditions would individuals with sickle trait become symptomatic?
(HbAS) underly very hypoxic conditions pO2: 2-4 kPa
49
What is the clinical severity of a-thal where all 4 genes are affected?
e.g. --/-- (homs) death in utero (hydrops fetalis, Bart's hydrops)
50
What are the features of beta-thalassemia major?
presents in first year of life failure to thrive hepatosplenomegaly microcytic anaemia HbA2 & HbF raised HbA absent
51
What is the Rx for beta-thalassemia major?
repeated transfusion → iron overload | s/c infusion of desferrioxamine (Fe chelation)

Life Support (13 decks)

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