7/5 Flashcards

1
Q

Invx difference between NSTEMI and unstable angina?

A

Troponin levels are raised in NSTEMI

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2
Q

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?

A

start on doac

stop the doac and repeat scan in 1 week

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3
Q

Management of torsades de pointes?

A

IV magnesium sulphate

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4
Q

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?

A

Pallor
Pain
Parasthesia
Pulseless
Paralysis
Persingly cold

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

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5
Q

Invx of critical limb ischaemia

How do you determine who needs immediate surgery?

A

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

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

based on sx

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6
Q

locate the brachial artery

A

Medial to the brachial tendon

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7
Q

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

A

Bypass or stenting

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8
Q

What is the most common cause of critical limb ischaemia?

A

AF

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9
Q

Symptoms of anaemia?

A

Fatigue
Headaches
Dysponea
Faintness
Palpitations
Angina

Pallor
(rarely high output HF)

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10
Q

What are examination findings of iron deficency anaemia?

A

Glossitis
Koilonychia
Angular stomatitis
Pallor

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11
Q

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

A

3 months

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12
Q

What is Romberg’s test?

What is +ve?

What does it allow us to test?

A

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

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13
Q

Causes of megalobastic anaemia vs non-megaloblastic MACROCYTIC anaemia.

How can you tell the difference?

A

Blood film

Megalobastic
- Folate
-B12 deficeny
- methotrexate

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

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14
Q

How is polycythemia vera managed?

A

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

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15
Q

What is the relationship between platelets and the liver?

A

Liver produces thrombopoietin (TPO) which causes platelet formation

Cirrhosis of the liver causes reduced TPO and reduced platlets

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16
Q

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?

A

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

17
Q

Link PT time and PTT to the intrinsic and extrisinic pathways

A

Extrinsic = PT = Playing Tennis = outdoor sport

Intrinsic = PTT = Playing Table Tennis = indoor sport

18
Q

Why is the clotting cascade important?
Draw it out

What is factor II and I?

What factors does warfarin hit?

A

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)

19
Q

How can you differentiate between intravascular and extravascular haemolysis

A

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

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

20
Q

How do you counter major bleeding in someone taking warfarin?

A

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

21
Q

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?

A

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

22
Q

What causes DIC?

What is the invx and symptoms?

What is the most important management after treating underlying?

A

DIC
Delivery - obesteric emergencies
Infections/immunological - sepsis
Cancer

Thromboyctonenia
Raised PTT and PT
Low fibrinogen
Raised D-dimer

Brusing and haematuria

FFP (clotting factors)

23
Q

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

A

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

24
Q

How is B12 injections given?

A

3xwk for 2 weeks then every 3mth

25
Q

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?

A

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