What questions are important to ask to rule out uveitis in a case of conjunctivitis?
Pain?
Is vision affected?
Conjunctivitis should only be itchy and not affect vision
Acne order of treatment
What do you have to check for before giving oral anti fungal?
Liver function test
What questions should you ask in the case of a UTI?
Back pain, fever? Rule out spread to pyelonephritis
Any chance of pregnancy? For antibiotic choice and asymptomatic treatment
Where is midazolam metabolised? What does this mean about cautions?
Metabolised in the kidney.
Caution must be given dose-wise in kidney injury as the half-life is extended massively
What blood test do you order with suspected ovarian cancer?
CA125
What blood test do you order with suspected prostate cancer?
Prostate specific antigen
What blood test do you order with suspected testicular cancer?
hCG
If a patient might have hypotension and you don’t have a way to measure to blood pressure or you are worried about a faulty cuff.
How can you use pulses to measure minimum diastolic blood pressure?
What are reticulocytes? What does they tell you about the cause of macrocytic anemia?
Reticulocytes are immature red blood cells (RBCs) released from the bone marrow, containing residual RNA that forms a mesh-like network, making them slightly larger than mature RBCs.
Macrocytosis + high reticulocytes = haemolysis or actute blood loss, prescence of aneamia causes bone marrow to release RBCs early to compensate.
Macrocytosis + low reticulocytes = megaloblastic anaemia, problem with dna synthesis
What is megaloblastic anaemia? What are the common causes?
This is a form of macrocytic anemia caused by an inability to synthesise DNA.
Main causes are B12/Folate deficiency (including pernicious anemia)
Does alcoholism cause macrocytic aneamia? is it megaloblastic?
It’s always macrocytic.
Whether or not it’s megaloblastic it depends.
Can lead to folate deficiency causing megaloblastic anemia.
But is also directly toxic to bone marrow causing non-megaloblastic aneamia.
What happens to MCV in blood loss anemia?
It depends.
In an acute bleed initially it’s normocytic as bone marrow hasn’t had time to respond, but then 3-5 days later it becomes macrocytic as Erythropoietin rises stimulating release of reticulocytes (mimiking hemolysis).
In chronic bleeding you end up with IDA as iron stores are depleted (different to hemolysis as in hemolysis iron is recovered). This results in microcytic aneamia.
Why is aneamia of chronic disease often normocytic?
Inflammation suppresses erythropoiesis, including EPO and bone marrow response to EPO.
So there is less RBCs getting made however they are normal.
Although it also causes functional iron deficiency due to hepcidin increase surpressing iron release from stores this doesn’t reduce it enough to affect hemoglobin quality as only a little is being made anyway. It can, however, sometimes lead to microcytic anaemia if inflammation is extreme and very chronic. The way to tell the difference will be ferritin/transferrin studies.
What is thalassemia?
Inherited anemia caused by gene mutations affected ability to make haemoglobin properly.
Causes of microcytic anaemia?
How to tell the difference?
IDA (includes chronic bleeds)
Thalassemia
AoCD (in extreme cases)
Can tell apart with ferritin/transferrin/free iron/RBC count
Causes of normocytic anaemia?
Aneamia of chronic disease
CKD/Low erythropoietin
Bone marrow failure (in this case all other white cells and platelets would also be low)
Causes of macrocytic aneamia?
B12/ Folate deficiency
Alcoholism
Heamolysis
Acute bleeds
In a coagulation screen what coagulation pathways do PT and APTT represent?
Prothrombin Time
extrinsic pathway – PeT
Activated Partial Thromboplastin Time
intrinsic pathway – APinTT
Solve this
Result 1: PT ↑, APTT normal, fibrinogen normal
PT measures: extrinsic pathway (Factor VII)
APTT normal → intrinsic pathway fine
✅ This pattern fits Warfarin therapy (affects vitamin K-dependent factors like VII → PT prolonged first).
Result 2: PT normal, APTT ↑, fibrinogen normal
APTT measures: intrinsic pathway (Factors VIII, IX, XI, XII)
PT normal → extrinsic pathway fine
✅ This fits Boy with factor VIII deficiency (Hemophilia A).
Result 3: PT ↑, APTT ↑, fibrinogen ↓
Both pathways prolonged + low fibrinogen
✅ Classic for advanced liver failure (all clotting factors produced in liver, plus fibrinogen can drop).
In an FBC, what happens to neutrophils, leukocytes and platelets during infection/inflammation?
All can be raised
(sometimes neutrophils are reduced in acute infection due ot all being used up)
In an FBC, what happens to neutrophils, leukocytes and platelets during bone marrow failure?
All can be lowered
What can happen to platelet count in IDA?
Raised
What can happen to platelet count in blood loss?
Lowered