MICROBIOLOGGY AND LAB ANALYSIS
Histology and Embryology
Pharmacology and Physiology
Anat Path
Chem, Anat Path and Biochemistry
100

A 25-year-old non-pregnant woman with a history of vesicoureteric reflux and recurrent urinary tract infections presents with a 3-day history of dysuria, urinary frequency, urgency and suprapubic pain. An MSU specimen is collected before antibiotics are started.

Urine dipstick

  • Leukocyte esterase: Positive
  • Nitrites: Positive

Urine culture

  • Pure bacterial growth (>10⁴ CFU/mL)
  • Leucocytes 3+
  • No epithelial cells

Question 1.1: What is the most likely diagnosis?

Question 1.2: Which two dipstick findings support a urinary tract infection?

Question 1.3: Is this UTI likely to be complicated or uncomplicated?

Answers:

  • Acute pyelonephritis
  • Nitrites and leucocytes
  • Complicated UTI
100

Question: Which cells in the kidney produce renin?

Juxtaglomerular cells

100

Question: What three processes are involved in drug elimination by the kidneys?

  • Glomerular filtration
  • Passive tubular reabsorption
  • Active tubular secretion
100

Question: Why do immune-mediated glomerular diseases occur? Name the three main causes.

Answer:
Immune-mediated glomerular diseases occur when the immune system mistakenly causes damage to the glomeruli, the filtering units of the kidney. In most cases, the injury is caused by immune complexes, complement activation, and type III hypersensitivity reactions which occur as a result of the first two.

100

Question: A patient with liver failure develops confusion due to high ammonia levels. Why?


Answer:
Ammonia depletes α-ketoglutarate. α-ketoglutarate is a key intermediate in the Krebs cycle so depletion in it will lead to Krebs cycle impairment, reducing ATP produced, affecting the brain and causing confusion.

200

A 25-year-old non-pregnant woman with a history of vesicoureteric reflux and recurrent urinary tract infections presents with a 3-day history of dysuria, urinary frequency, urgency and suprapubic pain. An MSU specimen is collected before antibiotics are started.

Urine dipstick

  • Leukocyte esterase: Positive
  • Nitrites: Positive

Urine culture

  • Pure bacterial growth (>10⁴ CFU/mL)
  • Leucocytes 3+
  • No epithelial cells

Question: Give two reasons why a urine dipstick test might produce a false negative nitrite test.

Answer:

  • Not allowing enough time for reaction of nitrate to nitrite conversion to take place.
  • Infection is caused by gram-positive bacteria.
200

Question: How can you distinguish the distal convoluted tubule from the proximal convoluted tubule under the microscope?

Answer (Any of each):

  • Epithelium (both cuboidal) – PCT has brush borders and DCT does not.
  • Lumen – PCT lumen ain't clear but DCT is.
  • Cell appearance – DCT has distinct cell borders.
  • Cell size – PCT larger than DCT. 
200

Question: What class of drugs often require a higher dose in patients with renal failure?

Answer:
Loop diuretics

200

Question: What are the characteristic findings on Electron Microscopy and Immunofluorescence for Acute Post-Infectious Glomerulonephritis (APGN)?

Answer:
EM: Large, subepithelial electron-dense "humps". IF: Granular "starry sky" deposits of IgG and C3 along capillary walls and mesangium.

200

Question 1.1: Where do the major nitrogenous waste products come from?

Question 1.2: Which nitrogenous waste product is the biggest indicator of GFR: Urea or Creatinine? Why? List factors of each marker

 

Answer 1.1:

  • Proteins/amino acids
  • Creatine phosphate, muscle
  • Purines, DNA/RNA 

Answer 1.2:
Creatinine

  • Produced at constant rate
  • 100% filtered
  • None of it is reabsorbed, only a small amount is excreted therefore making it an ideal marker for measuring GFR

Urea

  • Dependent on hydration
  • Protein intake therefore it is not an ideal clearance marker
300

Question: Why are ASOT and anti-DNase B titres useful in diagnosing acute post-streptococcal glomerulonephritis even though they do not diagnose active infection?

Answer:
These antibody tests provide evidence of a recent streptococcal infection, which is necessary because APSGN develops after the infection has resolved. They support the diagnosis but do not indicate that bacteria are still present.

300

Question: Starting at the renal artery, describe the complete pathway of blood until it leaves the kidney via the renal vein.

Renal artery → Segmental arteries → Interlobar arteries → Arcuate arteries → Interlobular arteries → Afferent arteriole → Glomerulus → Efferent arteriole → Peritubular capillaries (or vasa recta) → Interlobular veins → Arcuate veins → Interlobar veins → Renal vein.

300

Question: What is aciclovir nephrotoxicity caused by?

Answer:
By crystals

Aciclovir nephrotoxicity is caused by precipitation of aciclovir crystals in the renal tubules, resulting in crystal-induced obstructive nephropathy (acute kidney injury).

300

Question: Which specific cell types proliferate to form the crescents in Rapidly Progressive Glomerulonephritis (RPGN)?

Answer:
Parietal epithelial cells of Bowman's capsule and infiltrating monocytes/macrophages.

300

Question: Why can a patient with severe heart failure develop acute kidney injury even though the kidneys are receiving more total body fluid than normal?

  • Poor pumping power: The weak heart cannot pump blood forward effectively.
  • Low effective volume: Even though total body fluid is high, the fluid inside the actual arteries (which feed organs) is dangerously low.
  • Congestion/Backlog: Blood backs up into the veins, creating high pressure in the renal veins.
  • Pressure trap: High backward pressure in the veins stops fresh, oxygen-rich blood from entering the kidneys.
  • Starvation: The kidneys starve of oxygen and nutrients, leading to rapid tissue injury.
400

Question 1.1: Why is acute post-streptococcal glomerulonephritis considered an immune-mediated disease rather than a direct bacterial infection of the kidney?

Question 1.2: Explain why serum C3 is decreased in acute post-streptococcal glomerulonephritis and describe its clinical significance.  

Answer 1.1:
The kidneys are damaged by immune complex deposition and complement activation rather than by direct invasion of the kidney by streptococci. By the time nephritis develops, the original infection has usually resolved.

Answer 1.2:
C3 is decreased because it is consumed during activation of the alternative complement pathway by immune complexes. A low C3 level supports the diagnosis of APSGN and usually returns to normal within 6–8 weeks.  

400

Question 1.1: What two structures form the permanent kidney?


Question 1.2: Why does a horseshoe kidney remain lower than normal?


 

Answer 1.1:
The ureteric bud and metanephric mesenchyme.

Answer 1.2:
Its fused lower poles become trapped beneath the inferior mesenteric artery.  

400

Describe how the kidneys maintain fluid and electrolyte homeostasis. In your answer, explain the role of glomerular filtration, tubular reabsorption, tubular secretion, and hormonal regulation (ADH and aldosterone).

The kidneys maintain fluid and electrolyte homeostasis by regulating the volume and composition of the extracellular fluid.

The nephron performs four basic processes:

  1. Glomerular filtration – Water and small solutes (Na⁺, K⁺, Cl⁻, glucose, urea) are filtered from the glomerular capillaries into Bowman's capsule, while blood cells and plasma proteins remain in the circulation.
  2. Tubular reabsorption – Approximately 99% of filtered water and most useful solutes are reabsorbed back into the bloodstream. About 65% of sodium and water are reabsorbed in the proximal convoluted tubule, with further regulation occurring in the loop of Henle, distal convoluted tubule, and collecting duct.
  3. Tubular secretion – Substances such as H⁺, K⁺, NH₄⁺, creatinine, and many drugs are actively secreted into the tubular fluid for excretion. This process helps regulate electrolyte balance and acid-base homeostasis.
  4. Urinary excretion – The final urine contains excess water, electrolytes, metabolic waste, and toxins.

Hormones regulate the final composition of urine:

  • ADH (antidiuretic hormone) increases water reabsorption in the collecting ducts by inserting aquaporin-2 water channels, reducing urine volume and increasing urine concentration.
  • Aldosterone increases sodium reabsorption and potassium secretion in the distal nephron, helping maintain blood volume, blood pressure, and potassium balance.

Through these mechanisms, the kidneys regulate extracellular fluid volume, osmolarity, electrolyte concentrations, and blood pressure.

400

Question: How do the macroscopic renal scars of Chronic Pyelonephritis differ from typical vascular scars?

Answer:
Chronic pyelonephritis scars are coarse, irregular, asymmetric scars that directly overlie blunted or deformed calyces (vascular scars are typically V-shaped, superficial, and do not deform the underlying calyces).

400

During sepsis, patients often develop acute kidney injury even when there is no obstruction or direct damage to the kidneys. Explain the mechanisms responsible.

  • Micro-clots: Severe inflammation triggers tiny blood clots that block the microscopic blood vessels inside the kidneys.
  • Blood vessel leakage: Inflammation makes the tiny kidney blood vessels leaky, causing fluid to pool outside the vessels and crush the internal structures.
500

Question: The urine culture reports pure bacterial growth (<10⁴ CFU/mL). Is this result clinically significant? Explain your answer and state the next appropriate step.

Answer:
This is likely clinically significant. Although bacteriuria of <10⁴ is typically considered insignificant in a properly collected MSU, urine culture results should always be interpreted in conjunction with the patient's clinical presentation and other lab findings. In this case, the presence of 3+ leucocytes on dipstick and the absence of squamous epithelial cells on urine microscopy support a true urinary tract infection rather than contamination.

500

A 28-week premature infant is born with bilateral renal agenesis. Explain, with precise reference to developmental timing, tissue interactions, and sequential kidney systems, why this condition is incompatible with extrauterine life

Bilateral renal agenesis results from failure of reciprocal induction between the ureteric bud and metanephric mesenchyme during the 5th week of embryonic development, preventing formation of the permanent kidneys. Although the pronephros and mesonephros develop earlier, they are either non-functional or only transiently functional and cannot support postnatal life. Absence of metanephric kidneys prevents fetal urine production from approximately 9–10 weeks, causing severe oligohydramnios, which leads to pulmonary hypoplasia (Potter sequence). Consequently, the infant is born without functional kidneys and with severely underdeveloped lungs, making extrauterine life incompatible with survival.

500

A patient with chronic kidney disease presents with fluid overload, hyperkalaemia, metabolic acidosis, and hypertension. Using your knowledge of renal physiology, explain how impaired kidney function leads to each of these abnormalities.

Chronic kidney disease causes a progressive loss of functioning nephrons, reducing the kidneys' ability to regulate fluid, electrolytes, and acid-base balance.

1. Fluid overload

Reduced GFR decreases filtration of sodium and water. Excess sodium and water are retained, expanding extracellular fluid volume and causing peripheral oedema and pulmonary oedema.

2. Hyperkalaemia

Normally, potassium is secreted by principal cells in the distal tubule and collecting duct. In CKD, reduced nephron number and decreased tubular secretion result in potassium retention, leading to hyperkalaemia, which increases the risk of life-threatening cardiac arrhythmias.

3. Metabolic acidosis

The kidneys are unable to:

  • Excrete sufficient hydrogen ions.
  • Generate enough new bicarbonate.
  • Reabsorb all filtered bicarbonate.

As a result, acid accumulates and plasma bicarbonate falls, producing metabolic acidosis.

4. Hypertension

Reduced sodium and water excretion causes expansion of blood volume. In addition, impaired renal perfusion activates the renin–angiotensin–aldosterone system (RAAS), producing vasoconstriction and further sodium retention, increasing blood pressure.

Overall physiological consequence

Loss of nephron function impairs the kidneys' ability to:

  • Maintain fluid balance.
  • Regulate electrolytes.
  • Maintain acid-base homeostasis.
  • Excrete metabolic waste.
  • Regulate blood pressure.

This explains why patients with CKD commonly present with fluid overload, hyperkalaemia, metabolic acidosis, hypertension, and eventually uraemia.

500

A 58-year-old man develops acute kidney injury (AKI) following severe dehydration from gastroenteritis. Two days later, he has reduced urine output, ankle oedema, and a blood pressure of 165/95 mmHg.

His blood tests show:

  • ↑ Potassium
  • ↑ Phosphate
  • ↓ Calcium
  • ↓ Bicarbonate

Using your knowledge of renal physiology, explain the mechanisms responsible for each of the patient's clinical signs and biochemical abnormalities. In your answer, relate your explanation to the effects of reduced glomerular filtration rate (GFR) and impaired kidney function.

Acute kidney injury causes a reduced glomerular filtration rate (GFR) and impaired tubular function, resulting in:

  • Oedema: Reduced sodium and water excretion causes fluid retention, increasing extracellular fluid volume.
  • Hypertension: Sodium and water retention expand blood volume, increasing blood pressure.
  • Hyperkalaemia: Reduced potassium excretion leads to potassium accumulation in the blood.
  • Hyperphosphataemia: Impaired phosphate excretion causes phosphate retention.
  • Hypocalcaemia: Elevated phosphate binds calcium, reducing free calcium levels, while reduced vitamin D activation decreases intestinal calcium absorption.
  • Metabolic acidosis (↓ bicarbonate): Impaired hydrogen ion excretion and reduced bicarbonate reabsorption/regeneration lead to acid retention and decreased blood pH.

Overall: Reduced GFR and impaired tubular function prevent the kidneys from maintaining normal fluid, electrolyte, and acid–base homeostasi

500

Question: A patient with nephrotic syndrome has massive proteinuria, oedema, and hyperlipidaemia. Explain how damage to podocytes eventually leads to each of these findings.

Massive Proteinuria (Protein in Urine)

  • Broken filter: Healthy podocytes keep large molecules like albumin in the blood.
  • Leaking mesh: Damaged podocytes lose their structure and negative charge, allowing massive amounts of protein to slip through into the urine.

Oedema (Severe Swelling)

  • Lost sponge effect: Protein in the blood acts like a sponge to hold water inside blood vessels.
  • Fluid escape: When blood protein drops dangerously low, water leaks out of blood vessels into surrounding tissues.
  • Salt retention: The body tries to save fluid by hoarding salt and water, which worsens the swelling.

Hyperlipidaemia (High Blood Cholesterol/Lipids)

  • Liver overdrive: The liver notices that blood protein levels are dangerously low.
  • Accidental factory output: In a desperate rush to manufacture new proteins, the liver accidentally overproduces cholesterol and fats at the same time.
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