7/5

Question 1

Invx difference between NSTEMI and unstable angina?

Answer 1

Troponin levels are raised in NSTEMI

Question 2

If >4hrs till scan/d-dimer what should be done in the interm?

What should be done if inital scan -ve but d-dimer +ve?

Answer 2

start on doac

stop the doac and repeat scan in 1 week

Question 3

Management of torsades de pointes?

Answer 3

IV magnesium sulphate

Question 4

What are the 6 Ps of limb ischaemia?

What are the two which are most relevant for ACUTE?

What kind of dermatological can you get? WHat does it mean?

Answer 4

Pallor
Pain
Parasthesia
Pulseless
Paralysis
Persingly cold

fixed mottled skin
= irreversibly ischaemia - cannot reperfuse as will release all the dead tissue (remove or pallitate)

Question 5

Invx of critical limb ischaemia

How do you determine who needs immediate surgery?

Answer 5

Bedside
- limb exam
-
Bloods
- FBC, U+Es
- Coagulation screen
- CK

Imaging
- Duplex - elective
- CT/MRI angiogram - emergency

based on sx

Question 6

locate the brachial artery

Answer 6

Medial to the brachial tendon

Question 7

If it is a thrombosis-in-situ that has caused acute limb ischaemia - how is it managed?

Answer 7

Bypass or stenting

Question 8

What is the most common cause of critical limb ischaemia?

Answer 8

AF

Question 9

Symptoms of anaemia?

Answer 9

Fatigue
Headaches
Dysponea
Faintness
Palpitations
Angina

Pallor
(rarely high output HF)

Question 10

What are examination findings of iron deficency anaemia?

Answer 10

Glossitis
Koilonychia
Angular stomatitis
Pallor

Question 11

How long must you have iron replacement with iron deficent anaemia?

Answer 11

3 months

Question 12

What is Romberg’s test?

What is +ve?

What does it allow us to test?

Answer 12

Standing still with ur eyes closed

If swaying with eyes shut but fine when open = +ve

= sensory neuropathy - (could indicate subacute combined degeneration of the cord)

if -ve (sway when eyes open and closed) likely to be cerebellar in nature

Question 13

Causes of megalobastic anaemia vs non-megaloblastic MACROCYTIC anaemia.

How can you tell the difference?

Answer 13

Blood film

Megalobastic
- Folate
-B12 deficeny
- methotrexate

Non-megaloblastic
- Alcohol - v important in OSCE setting
- Hypothyroidism

Question 14

How is polycythemia vera managed?

Answer 14

Vensection - remove excess Hb
Hydroxyurea - myelosuppresor (reduces bone marrow activity)
Aspirin - anti-platelet

Question 15

What is the relationship between platelets and the liver?

Answer 15

Liver produces thrombopoietin (TPO) which causes platelet formation

Cirrhosis of the liver causes reduced TPO and reduced platlets

Question 16

Link the INR to secondary haemostasis

Does a higher INR mean you are more or less anti-coagulated? If a patient is still clotting at INR 2-3 what do you do?

Answer 16

INR is a measure of PT (extrinsic pathway

Higher INR means more anti-coagulated (more bleeding)
If clotting at 2-3 up to 3-4

Question 17

Link PT time and PTT to the intrinsic and extrisinic pathways

Answer 17

Extrinsic = PT = Playing Tennis = outdoor sport

Intrinsic = PTT = Playing Table Tennis = indoor sport

Question 18

Why is the clotting cascade important?
Draw it out

What is factor II and I?

What factors does warfarin hit?

Answer 18

formation of fibrin clot

TF and VII - intrinisic

VIII and IX - extrinsic

Both link to common pathway - X and V which activates prothrombin -> thrombin

Thrombin causes fibrinogen -> fibrin

II = prothrombin
I = fibrinogen

Warfarin is a vit K anatgonist (vit K activates II, VII, IX and X)

Question 19

How can you differentiate between intravascular and extravascular haemolysis

Answer 19

Extravascular
- riased bilirubin (lots of blood cells broken down)

Intravascular
- Raised LDH
- urinary haemosiderin (Hb in urine)

Question 20

How do you counter major bleeding in someone taking warfarin?

Answer 20

STOP warfarin
Prothrombin concentrate or FFP (contains all coagulation apart from platletes)
Give 5mg of vit K

Question 21

What kind of anaemia is haemolytic anaemia?

What are hereditary causes of haemolytic anaemia?

What can cause AIHA (autoimmune haemolytic anaemia)? How can you test? How is it managed?

Answer 21

Normocytic

Hereditary spherocytosis
G6PD deficiency
Sickle cell Hb

Infections e.g. mycoplasma
Lymphoma
SLE
+ve coombe’s test

Management of AIHA with AIHA
Anti-inflam - steroids
Incision - splenocetomy
Haemoglobin replacement - transfusion
Antibody - monoclonal rituximab

Question 22

What causes DIC?

What is the invx and symptoms?

What is the most important management after treating underlying?

Answer 22

DIC
Delivery - obesteric emergencies
Infections/immunological - sepsis
Cancer

Thromboyctonenia
Raised PTT and PT
Low fibrinogen
Raised D-dimer

Brusing and haematuria

FFP (clotting factors)

Question 23

Explain von willebrand’s disease - autosomal dominant or recessive?
What are the findings?

Answer 23

abnormality in VWF - can’t aggregrate platletes - but have normal platletes
Dominant
Reduced VIII activity - raised PTT (extrinsic pathway)

Prolonged bleeding time
Raised PTT

Dominant

Question 24

How is B12 injections given?

Answer 24

3xwk for 2 weeks then every 3mth

Question 25

If giving blood transfusion and patient get sa bit febrile but otherwise well (febrile non-heamolytic transfusion reaction) - no problems do what?

How can you tell if they are having acute haemolytic transfusion reaction? What do you do?

What is TACO? How is it managed?

Answer 25

Slow down transfusion and give paracetomol

High fever, “feeling of impending doom”, systemic features e.g. hypotension - STOP tranfusion, give saline and if develops to DIC treat it

TACO = transfusion-assoc. circulatory overload - slow transfusion and give furosemide - presents with fluid overload