Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology RCOA > Anaemia & Drugs > Flashcards

Anaemia & Drugs Flashcards

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
Q

Where does Dabigatran work?

A

Factor IIa

26
Q

Where does Aspirin work?

A

Irreversible cyclooxygenase inhibitor
Works on that platelet for the rest of it’s life until new platelets produced

27
Q

Where does Clopidogrel work?

A
  • 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
Q

Where does Dipyridamole work?

A
  • Inhibits plt adhesion to vessel wall
  • VasoD effects, particularly in coronaries
  • Phosphodiesterase inhibitor (inhibits metabolism of Adenosine)
  • Potentiates action of prostacyclin & stimulates release
29
Q

What is Alteplase an example of?

A

Tissue plasminogen activator (TPA)

30
Q

What is the mechanism of action of Warfarin?

A
  • Inhibits vitamin K dependent coagulation factors by inhibiting vitamin K epoxide reductase which is responsible for reducing vitamin K to active form
31
Q

What is the production of clotting factors dependent on?

A

Carboxylation of precursor proteins
Vit K oxidised to vit K epoxide (inactive) during this reaction

32
Q

What are the pharmacokinetics of Warfarin?

A
  • 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
Q

What drugs potentiate the effects of Warfarin?

A
  • Inhibit metabolism: ETOH, Cimetidine, Allopurinol, Erythromycin, Cipro, Metro
  • Displacement of proteins: NSAIDs
34
Q

Which drugs inhibit the effects of Warfarin?

A
  • Induction: Barbs, Rifamp, Carbamazepine
  • Decrease fat soluble vit absorption: Cholestyramine
35
Q

How long do prothrombin levels take to decrease?

A

3 days to decrease by 50%

36
Q

What are the effects of Warfarin in pregnancy?

A

Teratogenic - mainly in 1st trimester, later on = CNS disorders
Spont abortion
Stillbirth
Neonatal death
Preterm birth

37
Q

How do DOACs work?

A

Factor 10a inhibition
Similar to oral Heparin

38
Q

How does Fondaparinux work?

A
  • Factor 10a inhibition
  • Synthetic pentasaccharide similar to Heparin
  • Half life: 21hours- renally excreted
39
Q

How long to guidelines suggest waiting before attempting Neuraxial block following LMWH?

A

Minimum 12hours

40
Q

How do GPIIb/IIIa antagonists work?

A
  • Block receptor
  • Prevents binding of receptor to fibrinogen & plt adherence/aggregation inhibited
  • Appear as monoclonal antibodies to the receptor
41
Q

What does an Aspirin overdose do to the body?

A
  • 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

Haematology RCOA (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions