Dec Exam Flashcards
What is the primary location of ALT (Alanine Aminotransferase)?
Found primarily in the liver.
What condition is indicated by elevated ALT levels?
Hepatocellular damage (e.g., hepatitis, fatty liver).
What are the primary locations of AST (Aspartate Aminotransferase)?
Found in the liver, heart, and muscles.
What other conditions can cause elevated AST levels besides liver diseases?
Myocardial infarction and muscle injury.
What ALT:AST ratio indicates alcoholic liver disease?
ALT:AST ratio >2.
What is the pathophysiology of macrocytic anaemia?
Impaired DNA synthesis leads to delayed nuclear maturation, resulting in large, immature RBCs.
What vitamin deficiencies are commonly associated with macrocytic anaemia?
- Vitamin B12 deficiency
- Folate deficiency
What laboratory finding is characteristic of macrocytic anaemia?
Elevated MCV (>100 fL).
What is a key lab finding in macrocytic anaemia on a blood film?
Hypersegmented neutrophils.
What does the faecal elastase-1 test measure?
Elastase enzyme in stool.
What do low levels of faecal elastase-1 indicate?
Pancreatic insufficiency (e.g., chronic pancreatitis, cystic fibrosis).
Why is faecal elastase-1 considered more reliable than serum amylase and lipase?
More stable and non-invasive marker.
What is the rationale for irradiating blood products?
Prevent transfusion-associated graft-versus-host disease (TA-GVHD).
Who are the primary recipients for irradiated blood products?
- Immunocompromised patients
- Bone marrow transplant recipients
- Patients receiving transfusions from relatives
What is the principle of the urea breath test in diagnosing H. pylori infection?
H. pylori produces urease, which breaks down urea into ammonia and CO2.
What does isotopically labeled urea detect in the urea breath test?
CO2 levels in exhaled breath.
What is the clinical utility of the urea breath test?
Non-invasive; detects active infection and confirms eradication after treatment.
What is serum creatinine a byproduct of?
Muscle metabolism.
What factors can affect serum creatinine levels?
- Muscle mass
- Age
- Diet
What is cystatin C and its relevance in kidney function?
Produced by all nucleated cells; independent of muscle mass.
Why is cystatin C considered more sensitive in early kidney dysfunction?
It is less affected by muscle mass compared to creatinine.
What is the role of troponins (T and I) in diagnosing acute myocardial infarction?
Highly specific for myocardial injury.
When do troponin levels typically elevate after myocardial injury?
Within 4–6 hours.
How long do troponin levels remain elevated after myocardial injury?
10–14 days.
What is the pathophysiology of microcytic anaemia?
Impaired haemoglobin synthesis leads to smaller RBCs (low MCV).
What are common causes of microcytic anaemia?
- Iron deficiency (dietary, blood loss)
- Thalassaemia (genetic globin chain deficiency)
- Chronic disease anaemia (cytokine-mediated iron sequestration)
What are key lab findings in microcytic anaemia?
Low Hb, low MCV, microcytic hypochromic RBCs on film.
What is the role of intrinsic factor in vitamin B12 absorption?
Binds B12, enabling absorption in the ileum.
What condition results from intrinsic factor deficiency?
Pernicious anaemia.
What are the consequences of intrinsic factor deficiency?
Megaloblastic anaemia and neurological symptoms.
What biochemical markers indicate cholestasis?
- Elevated ALP
- Elevated GGT
- Elevated conjugated bilirubin
What are the clinical features of cholestasis?
- Jaundice
- Dark urine
- Pale stools
- Pruritus due to bile salt accumulation
What is obstructive jaundice?
A condition caused by bile duct obstruction leading to bile accumulation in the liver and elevated conjugated bilirubin in the bloodstream.
Common causes include gallstones and malignancy.
What are the main diagnostic tests for obstructive jaundice?
Blood tests and imaging studies
Blood tests show elevated conjugated bilirubin, ALP, and GGT. Imaging can include ultrasound and MRCP.
What is the clinical management for obstructive jaundice?
Address the underlying cause and provide symptom relief
This may include ERCP for gallstones and cholestyramine for pruritus.
What is the likely cause of iron deficiency anaemia in a patient with low Hb and low MCV?
Chronic blood loss or dietary insufficiency.
Common sources of chronic blood loss include gastrointestinal bleeding.
What is the pathophysiology of iron deficiency anaemia?
Impaired haemoglobin synthesis due to lack of iron, resulting in smaller, hypochromic RBCs.
This condition is characterized by microcytic hypochromic red blood cells.
What is the treatment for iron deficiency anaemia?
Oral or IV iron supplementation and addressing underlying causes.
For example, a colonoscopy may be performed to investigate GI bleeding.
What diagnosis is indicated by elevated troponin levels with normal ECG findings?
Non-ST-Elevation Myocardial Infarction (NSTEMI).
This condition is characterized by myocardial injury without ST-segment elevation.
What is the pathophysiology of NSTEMI?
Partial occlusion of a coronary artery leading to myocardial injury.
This occurs without ST-segment elevation on the ECG.
What is the management for NSTEMI?
Antiplatelets, anticoagulants, beta-blockers, ACE inhibitors, and lifestyle changes.
Aspirin and clopidogrel are common antiplatelet medications.
What is Antiphospholipid Syndrome (APS)?
A condition characterized by autoantibodies targeting phospholipid-binding proteins, leading to thrombosis and miscarriage.
APS is associated with arterial and venous thrombosis.
What are the clinical features of APS?
Arterial and venous thrombosis, recurrent pregnancy loss.
Women with APS may experience multiple miscarriages.
What is the management for APS?
Anticoagulation, including low molecular weight heparin during pregnancy and lifelong warfarin for thrombosis.
Management is critical to reduce the risk of thrombosis.
What roles do serum amylase and lipase play in acute pancreatitis?
Serum amylase rises quickly but is non-specific; serum lipase is more specific and remains elevated longer.
Lipase is preferred for assessing recovery from pancreatitis.
What causes febrile non-haemolytic transfusion reactions?
Cytokines released by donor leukocytes in stored blood.
This reaction is common and typically mild.
What is the pathophysiology of febrile non-haemolytic transfusion reactions?
Accumulated cytokines trigger a febrile response in the recipient.
Symptoms include fever and chills during or after transfusion.
What is the management for febrile non-haemolytic transfusion reactions?
Stop the transfusion and use leukocyte-reduced blood products for future transfusions.
This approach helps to prevent recurrence.
What does an AST:ALT ratio of 3:1 indicate in a patient with alcoholic liver disease?
Strongly suggests alcoholic liver disease.
AST is located in mitochondria, which are damaged by alcohol.
What is the pathophysiology of anaemia in chronic kidney disease (CKD)?
Reduced erythropoietin production by damaged kidneys and chronic inflammation reducing iron availability.
This leads to normocytic anaemia.
What is the treatment for anaemia in CKD?
EPO-stimulating agents and iron supplementation if ferritin is low.
Darbepoetin is an example of an EPO-stimulating agent.
What is the pathophysiology of haemolytic disease of the newborn (HDN)?
Maternal anti-D antibodies attack fetal Rh-positive RBCs, leading to haemolysis.
This condition can cause significant neonatal complications.
What are the clinical features of HDN?
Neonatal jaundice, anaemia, hydrops fetalis.
Hydrops fetalis is a severe condition characterized by fluid accumulation.
How can HDN be prevented?
Administer anti-D immunoglobulin (RhoGAM) to Rh-negative mothers.
This prevents the formation of maternal anti-D antibodies.
What is the cause of myocardial injury with ST-elevation?
Coronary artery thrombosis leading to myocardial infarction (STEMI).
This is a critical condition requiring immediate intervention.
What are the diagnostic features of STEMI?
Symptoms include chest pain and diaphoresis; ECG shows ST-segment elevation; troponin is elevated within 4–6 hours.
Immediate recognition is crucial for management.
What is the management for STEMI?
Immediate PCI or thrombolysis, followed by antiplatelets, beta-blockers, and lifestyle changes.
These interventions aim to restore blood flow and prevent further damage.
