7/5 Flashcards
Invx difference between NSTEMI and unstable angina?
Troponin levels are raised in NSTEMI
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?
start on doac
stop the doac and repeat scan in 1 week
Management of torsades de pointes?
IV magnesium sulphate
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?
Pallor
Pain
Parasthesia
Pulseless
Paralysis
Persingly cold
fixed mottled skin
= irreversibly ischaemia - cannot reperfuse as will release all the dead tissue (remove or pallitate)
Invx of critical limb ischaemia
How do you determine who needs immediate surgery?
Bedside
- limb exam
-
Bloods
- FBC, U+Es
- Coagulation screen
- CK
Imaging
- Duplex - elective
- CT/MRI angiogram - emergency
based on sx
locate the brachial artery
Medial to the brachial tendon
If it is a thrombosis-in-situ that has caused acute limb ischaemia - how is it managed?
Bypass or stenting
What is the most common cause of critical limb ischaemia?
AF
Symptoms of anaemia?
Fatigue
Headaches
Dysponea
Faintness
Palpitations
Angina
Pallor
(rarely high output HF)
What are examination findings of iron deficency anaemia?
Glossitis
Koilonychia
Angular stomatitis
Pallor
How long must you have iron replacement with iron deficent anaemia?
3 months
What is Romberg’s test?
What is +ve?
What does it allow us to test?
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
Causes of megalobastic anaemia vs non-megaloblastic MACROCYTIC anaemia.
How can you tell the difference?
Blood film
Megalobastic
- Folate
-B12 deficeny
- methotrexate
Non-megaloblastic
- Alcohol - v important in OSCE setting
- Hypothyroidism
How is polycythemia vera managed?
Vensection - remove excess Hb
Hydroxyurea - myelosuppresor (reduces bone marrow activity)
Aspirin - anti-platelet
What is the relationship between platelets and the liver?
Liver produces thrombopoietin (TPO) which causes platelet formation
Cirrhosis of the liver causes reduced TPO and reduced platlets
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?
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
Link PT time and PTT to the intrinsic and extrisinic pathways
Extrinsic = PT = Playing Tennis = outdoor sport
Intrinsic = PTT = Playing Table Tennis = indoor sport
Why is the clotting cascade important?
Draw it out
What is factor II and I?
What factors does warfarin hit?
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)
How can you differentiate between intravascular and extravascular haemolysis
Extravascular
- riased bilirubin (lots of blood cells broken down)
Intravascular
- Raised LDH
- urinary haemosiderin (Hb in urine)
How do you counter major bleeding in someone taking warfarin?
STOP warfarin
Prothrombin concentrate (contains all coagulation apart from platletes)
Give 5mg of vit K
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?
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
What causes DIC?
What is the invx and symptoms?
What is the most important management after treating underlying?
DIC
Delivery - obesteric emergencies
Infections/immunological - sepsis
Cancer
Thromboyctonenia
Raised PTT and PT
Low fibrinogen
Raised D-dimer
Brusing and haematuria
FFP (clotting factors)
Explain von willebrand’s disease - autosomal dominant or recessive?
What are the findings?
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
How is B12 injections given?
3xwk for 2 weeks then every 3mth
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?
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
