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CLS > Dec Exam > Flashcards

Dec Exam Flashcards

1
Q

What is the primary location of ALT (Alanine Aminotransferase)?

A

Found primarily in the liver.

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2
Q

What condition is indicated by elevated ALT levels?

A

Hepatocellular damage (e.g., hepatitis, fatty liver).

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3
Q

What are the primary locations of AST (Aspartate Aminotransferase)?

A

Found in the liver, heart, and muscles.

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4
Q

What other conditions can cause elevated AST levels besides liver diseases?

A

Myocardial infarction and muscle injury.

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5
Q

What ALT:AST ratio indicates alcoholic liver disease?

A

ALT:AST ratio >2.

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6
Q

What is the pathophysiology of macrocytic anaemia?

A

Impaired DNA synthesis leads to delayed nuclear maturation, resulting in large, immature RBCs.

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7
Q

What vitamin deficiencies are commonly associated with macrocytic anaemia?

A
  • Vitamin B12 deficiency
  • Folate deficiency
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8
Q

What laboratory finding is characteristic of macrocytic anaemia?

A

Elevated MCV (>100 fL).

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9
Q

What is a key lab finding in macrocytic anaemia on a blood film?

A

Hypersegmented neutrophils.

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10
Q

What does the faecal elastase-1 test measure?

A

Elastase enzyme in stool.

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11
Q

What do low levels of faecal elastase-1 indicate?

A

Pancreatic insufficiency (e.g., chronic pancreatitis, cystic fibrosis).

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12
Q

Why is faecal elastase-1 considered more reliable than serum amylase and lipase?

A

More stable and non-invasive marker.

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13
Q

What is the rationale for irradiating blood products?

A

Prevent transfusion-associated graft-versus-host disease (TA-GVHD).

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14
Q

Who are the primary recipients for irradiated blood products?

A
  • Immunocompromised patients
  • Bone marrow transplant recipients
  • Patients receiving transfusions from relatives
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15
Q

What is the principle of the urea breath test in diagnosing H. pylori infection?

A

H. pylori produces urease, which breaks down urea into ammonia and CO2.

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16
Q

What does isotopically labeled urea detect in the urea breath test?

A

CO2 levels in exhaled breath.

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17
Q

What is the clinical utility of the urea breath test?

A

Non-invasive; detects active infection and confirms eradication after treatment.

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18
Q

What is serum creatinine a byproduct of?

A

Muscle metabolism.

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19
Q

What factors can affect serum creatinine levels?

A
  • Muscle mass
  • Age
  • Diet
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20
Q

What is cystatin C and its relevance in kidney function?

A

Produced by all nucleated cells; independent of muscle mass.

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21
Q

Why is cystatin C considered more sensitive in early kidney dysfunction?

A

It is less affected by muscle mass compared to creatinine.

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22
Q

What is the role of troponins (T and I) in diagnosing acute myocardial infarction?

A

Highly specific for myocardial injury.

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23
Q

When do troponin levels typically elevate after myocardial injury?

A

Within 4–6 hours.

24
Q

How long do troponin levels remain elevated after myocardial injury?

A

10–14 days.

25
Q

What is the pathophysiology of microcytic anaemia?

A

Impaired haemoglobin synthesis leads to smaller RBCs (low MCV).

26
Q

What are common causes of microcytic anaemia?

A
  • Iron deficiency (dietary, blood loss)
  • Thalassaemia (genetic globin chain deficiency)
  • Chronic disease anaemia (cytokine-mediated iron sequestration)
27
Q

What are key lab findings in microcytic anaemia?

A

Low Hb, low MCV, microcytic hypochromic RBCs on film.

28
Q

What is the role of intrinsic factor in vitamin B12 absorption?

A

Binds B12, enabling absorption in the ileum.

29
Q

What condition results from intrinsic factor deficiency?

A

Pernicious anaemia.

30
Q

What are the consequences of intrinsic factor deficiency?

A

Megaloblastic anaemia and neurological symptoms.

31
Q

What biochemical markers indicate cholestasis?

A
  • Elevated ALP
  • Elevated GGT
  • Elevated conjugated bilirubin
32
Q

What are the clinical features of cholestasis?

A
  • Jaundice
  • Dark urine
  • Pale stools
  • Pruritus due to bile salt accumulation
33
Q

What is obstructive jaundice?

A

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.

34
Q

What are the main diagnostic tests for obstructive jaundice?

A

Blood tests and imaging studies

Blood tests show elevated conjugated bilirubin, ALP, and GGT. Imaging can include ultrasound and MRCP.

35
Q

What is the clinical management for obstructive jaundice?

A

Address the underlying cause and provide symptom relief

This may include ERCP for gallstones and cholestyramine for pruritus.

36
Q

What is the likely cause of iron deficiency anaemia in a patient with low Hb and low MCV?

A

Chronic blood loss or dietary insufficiency.

Common sources of chronic blood loss include gastrointestinal bleeding.

37
Q

What is the pathophysiology of iron deficiency anaemia?

A

Impaired haemoglobin synthesis due to lack of iron, resulting in smaller, hypochromic RBCs.

This condition is characterized by microcytic hypochromic red blood cells.

38
Q

What is the treatment for iron deficiency anaemia?

A

Oral or IV iron supplementation and addressing underlying causes.

For example, a colonoscopy may be performed to investigate GI bleeding.

39
Q

What diagnosis is indicated by elevated troponin levels with normal ECG findings?

A

Non-ST-Elevation Myocardial Infarction (NSTEMI).

This condition is characterized by myocardial injury without ST-segment elevation.

40
Q

What is the pathophysiology of NSTEMI?

A

Partial occlusion of a coronary artery leading to myocardial injury.

This occurs without ST-segment elevation on the ECG.

41
Q

What is the management for NSTEMI?

A

Antiplatelets, anticoagulants, beta-blockers, ACE inhibitors, and lifestyle changes.

Aspirin and clopidogrel are common antiplatelet medications.

42
Q

What is Antiphospholipid Syndrome (APS)?

A

A condition characterized by autoantibodies targeting phospholipid-binding proteins, leading to thrombosis and miscarriage.

APS is associated with arterial and venous thrombosis.

43
Q

What are the clinical features of APS?

A

Arterial and venous thrombosis, recurrent pregnancy loss.

Women with APS may experience multiple miscarriages.

44
Q

What is the management for APS?

A

Anticoagulation, including low molecular weight heparin during pregnancy and lifelong warfarin for thrombosis.

Management is critical to reduce the risk of thrombosis.

45
Q

What roles do serum amylase and lipase play in acute pancreatitis?

A

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.

46
Q

What causes febrile non-haemolytic transfusion reactions?

A

Cytokines released by donor leukocytes in stored blood.

This reaction is common and typically mild.

47
Q

What is the pathophysiology of febrile non-haemolytic transfusion reactions?

A

Accumulated cytokines trigger a febrile response in the recipient.

Symptoms include fever and chills during or after transfusion.

48
Q

What is the management for febrile non-haemolytic transfusion reactions?

A

Stop the transfusion and use leukocyte-reduced blood products for future transfusions.

This approach helps to prevent recurrence.

49
Q

What does an AST:ALT ratio of 3:1 indicate in a patient with alcoholic liver disease?

A

Strongly suggests alcoholic liver disease.

AST is located in mitochondria, which are damaged by alcohol.

50
Q

What is the pathophysiology of anaemia in chronic kidney disease (CKD)?

A

Reduced erythropoietin production by damaged kidneys and chronic inflammation reducing iron availability.

This leads to normocytic anaemia.

51
Q

What is the treatment for anaemia in CKD?

A

EPO-stimulating agents and iron supplementation if ferritin is low.

Darbepoetin is an example of an EPO-stimulating agent.

52
Q

What is the pathophysiology of haemolytic disease of the newborn (HDN)?

A

Maternal anti-D antibodies attack fetal Rh-positive RBCs, leading to haemolysis.

This condition can cause significant neonatal complications.

53
Q

What are the clinical features of HDN?

A

Neonatal jaundice, anaemia, hydrops fetalis.

Hydrops fetalis is a severe condition characterized by fluid accumulation.

54
Q

How can HDN be prevented?

A

Administer anti-D immunoglobulin (RhoGAM) to Rh-negative mothers.

This prevents the formation of maternal anti-D antibodies.

55
Q

What is the cause of myocardial injury with ST-elevation?

A

Coronary artery thrombosis leading to myocardial infarction (STEMI).

This is a critical condition requiring immediate intervention.

56
Q

What are the diagnostic features of STEMI?

A

Symptoms include chest pain and diaphoresis; ECG shows ST-segment elevation; troponin is elevated within 4–6 hours.

Immediate recognition is crucial for management.

57
Q

What is the management for STEMI?

A

Immediate PCI or thrombolysis, followed by antiplatelets, beta-blockers, and lifestyle changes.

These interventions aim to restore blood flow and prevent further damage.

CLS (2 decks)

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