Anaemia & Drugs Flashcards

(41 cards)

1
Q

What are the types of normocytic anaemia?

A

Chronic disease
BM failure
Renal failure
Haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of anaemia is thalassaemia?

A

Microcytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What would be seen in a blood film of someone with IDA?

A

Poikilocytosis
Anisocytosis
Hypochromic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is seen on a microcytic anaemia blood film?

A

Hypersegmented neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is intrinsic factor produced?

A

Fundus of stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is haemolytic anaemia?

A

Premature breakdown of RBCs before their normal lifespan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the features of haemolytic anaemia?

A

Jaundice
Hepatosplenomegaly
Gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens in the direct Coombs test?

A

Detects antibodies already bound to RBCs
Used in haemolytic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens in the indirect Coombs test?

A

Detects antibodies against RBCs in the serum
Used in pregnancy & before transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the causes of haemolytic anaemia?

A

Acquired: Immune-mediated, Drugs (Pen, quinine), autoimmune, prosthetic heart valves
Hereditary: G6PD def, hereditary spherocytosis, Sickle cell, thalassaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is G6PD passed on?

A

X-linked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What’s the commonest RBC enzyme deficiency?

A

G6PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can precipitate a crisis in G6PD deficiency?

A

Illness
Fava/broad beans
Drugs (Aspirin, sulphonamides, antimalarials)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where in Hb is the abnormal protein found in SCA?

A

Beta chain creating HbS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are people with SCA prone to?

A

Painful crises
Bone pain
Aplastic crisis
Splenic infarction
Osteomyelitis
Dactylitis
Stroke
Avascular necrosis
Priapism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can trigger a sickle cell crisis?

A

Cold
Dehydration
Infection
Hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What virus can cause an aplastic crisis in SCA?

A

Parvovirus B19

18
Q

What is normal Hb made up of?

A

Normal = HbA
2 alpha chains
2 beta chains

19
Q

What would be seen on the FBC of someone with beta Thalassaemia minor?

A

Mild anaemia (>90)
Very low MCV (<75)
Raised HbA2
Often confused with iron def anaemia

20
Q

What are the features of beta thalassaemia major?

A

Severe anaemia in childhood
Splenomegaly
Iron overload

21
Q

What Heparin and how does it work?

A
  • Glycosaminoglycan (mucopolysaccharide) occurring naturally in liver & mast cells
  • Reversibly binds & potentiates antithrombin 3 (protease inhibitor)
  • This inhibits factors 2, 7, 9, 10, 11, plasmin
  • Antiplatelets effects mediated through effects on fibrin
22
Q

What are the pharmacokinetics of Heparin?

A
  • Highly bound to plasma proteins
  • Low lipid solubility
  • Doesn’t cross BBB or placenta
  • 1/2 life: 30-60mins
  • Metabolised by hepatic heparinase & excreted in urine
  • Monitored: PTT
23
Q

What has an INR target of 2.5 & 3.5?

A

2.5: DVT/PE, AF, Biological heart valves
3.5: Mechanical valves

24
Q

How do LMWHs work?

A
  • Produced by depolymerisation or fractionation of heparin
  • Anti - Xa action
25
Where does Dabigatran work?
Factor IIa
26
Where does Aspirin work?
Irreversible cyclooxygenase inhibitor Works on that platelet for the rest of it's life until new platelets produced
27
Where does Clopidogrel work?
- Prodrug activated by oxidation of the thiophene ring by cP450 - Blocks ADP induced plt activation pathway - Prevents plt activation after acute vessel injury - Has irreversible plt effects
28
Where does Dipyridamole work?
- Inhibits plt adhesion to vessel wall - VasoD effects, particularly in coronaries - Phosphodiesterase inhibitor (inhibits metabolism of Adenosine) - Potentiates action of prostacyclin & stimulates release
29
What is Alteplase an example of?
Tissue plasminogen activator (TPA)
30
What is the mechanism of action of Warfarin?
- Inhibits vitamin K dependent coagulation factors by inhibiting vitamin K epoxide reductase which is responsible for reducing vitamin K to active form
31
What is the production of clotting factors dependent on?
Carboxylation of precursor proteins Vit K oxidised to vit K epoxide (inactive) during this reaction
32
What are the pharmacokinetics of Warfarin?
- 99% plasma protein bound - Metabolised by liver & excreted in urine & faeces - 1/2 life: 35-45hours - Significant drug interactions by displaced plasma proteins & liver induction/inhibition
33
What drugs potentiate the effects of Warfarin?
- Inhibit metabolism: ETOH, Cimetidine, Allopurinol, Erythromycin, Cipro, Metro - Displacement of proteins: NSAIDs
34
Which drugs inhibit the effects of Warfarin?
- Induction: Barbs, Rifamp, Carbamazepine - Decrease fat soluble vit absorption: Cholestyramine
35
How long do prothrombin levels take to decrease?
3 days to decrease by 50%
36
What are the effects of Warfarin in pregnancy?
Teratogenic - mainly in 1st trimester, later on = CNS disorders Spont abortion Stillbirth Neonatal death Preterm birth
37
How do DOACs work?
Factor 10a inhibition Similar to oral Heparin
38
How does Fondaparinux work?
- Factor 10a inhibition - Synthetic pentasaccharide similar to Heparin - Half life: 21hours- renally excreted
39
How long to guidelines suggest waiting before attempting Neuraxial block following LMWH?
Minimum 12hours
40
How do GPIIb/IIIa antagonists work?
- Block receptor - Prevents binding of receptor to fibrinogen & plt adherence/aggregation inhibited - Appear as monoclonal antibodies to the receptor
41
What does an Aspirin overdose do to the body?
- Uncouples oxidative phosphorylation which increases O2 consumption & CO2 production - Minute ventilation increases to keep PaCO2 static - Resp increases further due to stimulation of the resp centres = resp alkalosis - Impaired aerobic metabolism = metabolic acidosis