Pathology

Question 1

Indications for acute dialysis

Answer 1

A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia symptoms such as seizures or reduced consciousness

Question 2

Complications of Peritoneal Dialysis

Answer 2

1. Bacterial peritonitis
2. Peritoneal sclerosis
3. Ultrafiltration failure
4. Weight gain
5. Psychosocial effects

Question 3

Peritoneal sclerosis

Answer 3

Involves thickening and scarring of the peritoneal membrane.

Question 4

A-V fistula

Answer 4

An artificial connection between an artery to a vein.
It bypasses the capillary system and allows blood to flow under high pressure from the artery directly into the vein. Creating an A-V fistula requires a surgical operation and a 4 week to 4 month maturation period without use.

Question 5

Interstitial nephritis

Answer 5

Describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney.

This is different to glomerulonephritis, where there is inflammation around the glomerulus.

There are two types of interstitial nephritis: acute interstitial nephritis and chronic tubulointerstitial nephritis.

Question 6

What are the two types of interstitial nephritis?

Answer 6

acute interstitial nephritis and chronic tubulointerstitial nephritis

Question 7

Acute interstitial nephritis

Answer 7

Presents with acute kidney injury and hypertension. There is acute inflammation of the tubules and interstitium. This is usually caused by a hypersensitivity reaction to drugs (e.g. NSAIDS or antibiotics) and infections

Question 8

What drugs cause acute interstitial nephritis

Answer 8

e.g. NSAIDS or antibiotics

Question 9

Features of acute interstitial nephritis

Answer 9

Acute kidney injury and hypertension
Rash
Fever
Eosinophilia

Question 10

Acute tubular necrosis

Answer 10

Is damage and death (necrosis) of the epithelial cells of the renal tubules. It is the most common cause of acute kidney injury.

Damage to the kidney cells occurs due to ischaemia or toxins. The epithelial cells have the ability to regenerate making acute tubular necrosis reversible. It usually takes 7-21 days to recover.

Question 11

How long does it take to recover from acute tubular necrosis?

Answer 11

Damage to the kidney cells occurs due to ischaemia or toxins. The epithelial cells have the ability to regenerate making acute tubular necrosis reversible. It usually takes 7-21 days to recover.

Question 12

What are the features of urinalysis of acute tubular necrosis?

Answer 12

Muddy brown casts

Question 13

Management of Acute tubular necrosis

Answer 13

Supportive management
IV fluids
Stop nephrotoxic medications
Treat complications

Question 14

Renal tubular acidosis

Answer 14

Where there is a metabolic acidosis due to pathology in the tubules of the kidney. The tubules are responsible for balancing the hydrogen and bicarbonate ions between the blood and urine and maintaining a normal pH. There are four types each with different pathophysiology.

Question 15

Type 1 Renal tubular acidosis

Answer 15

Due to pathology in the distal tubule. The distal tubule is unable to excrete hydrogen ions.

Question 16

Presentation of renal tubular acidosis

Answer 16

Failure to thrive in children
Hyperventilation to compensate for the metabolic acidosis
Chronic kidney disease
Bone disease (osteomalacia)

Question 17

Treatment of Type 1 & 2 renal tubular acidosis

Answer 17

Treatment is with oral bicarbonate. This corrects the other electrolyte imbalances.

Question 18

Type 2 renal tubular acidosis

Answer 18

Due to pathology in the proximal tubule. The proximal tubule is unable to reabsorb bicarbonate from the urine into the blood. Excessive bicarbonate is excreted in the urine. Fanconi’s syndrome is the main cause.

Question 19

Type 4 renal tubular acidosis

Answer 19

Caused by reduced aldosterone.

This can be due to adrenal insufficiency, medications such as ACE inhibitors and spironolactone or systemic conditions that affect the kidneys such as systemic lupus erythematosus, diabetes or HIV.

Question 20

Treatment of Type 4 renal tubular acidosis

Answer 20

Management is with fludrocortisone. Sodium bicarbonate and treatment of the hyperkalaemia may also be required.

Question 21

Hemodialysis

Answer 21

A person with complete kidney failure is connected to a dialysis machine, which filters the blood and returns it to the body. Hemodialysis is typically done 3 days per week in people with ESRD.

Question 22

Peritoneal dialysis

Answer 22

Placing large amounts of a special fluid in the abdomen through a catheter allows the body to filter the blood using the natural membrane lining the abdomen. After a while, the fluid with the waste is drained and discarded.

Question 23

Dialysis

Answer 23

Artificial filtering of the blood to replace the work that damaged kidneys can’t do. Hemodialysis is the most common method of dialysis in the U.S.

Question 24

Glomerulus

Answer 24

The glomerulus is actually a web of arterioles and capillaries, with a special filter which filters the blood that runs through the capillaries, the glomerular membrane.

Question 25

Afferent arteriole and efferent arteriole

Answer 25

The vessel which brings blood into the glomerulus is the afferent arteriole, whereas the vessel that carries the rest of the blood out that hasn’t been filtered out of the glomerulus is called the efferent arteriole.

Question 26

Glomerular membrane permeability

Answer 26

Designed in a way in which it is not permeable for big and important molecules in blood, such as plasma proteins, but it is permeable to the smaller substances such as sodium, potassium, amino acids and many others.

It is also permeable for the products of the metabolism, such are creatinine and drug metabolites.

Question 27

Renal tubules

Answer 27

The tubules are designed in a way that they reabsorb the necessary substances, (sodium, potassium, and amino acids) and carries them back to the blood; secrete unnecessary substances such as creatinine and drug metabolites for excretion from the body.

Question 28

Haemolytic uraemic syndrome (HUS)

Answer 28

Occurs when there is thrombosis in small blood vessels throughout the body. This is usually triggered by a bacterial toxin called the shiga toxin by Ecoli 057

Question 29

Classic triad in Haemolytic uraemic syndrome (HUS)

Answer 29

Haemolytic anaemia
Acute kidney injury
Low platelet count (thrombocytopenia)

Question 30

What causes the AKI seen in Haemolytic uraemic syndrome (HUS)?

Answer 30

The formation of blood clots consumes platelets, leading to thrombocytopenia. The blood clots within the small vessels chop up the red blood cells as they pass by (haemolysis), causing anaemia. The blood flow through the kidney is affected by the clots and damaged red blood cells, leading to acute kidney injury.

Question 31

What are the causes of Haemolytic uraemic syndrome (HUS)?

Answer 31

The most common cause is a toxin produced by the bacteria e. coli 0157 called the shiga toxin. Shigella also produces this toxin and can cause HUS. The use of antibiotics and anti-motility medications such as loperamide to treat the gastroenteritis increase the risk of developing HUS.

Question 32

What drugs can cause HUS?

Answer 32

The use of antibiotics and anti-motility medications such as loperamide to treat the gastroenteritis increase the risk of developing HUS.

Question 33

Presentation of HUS

Answer 33

E. coli 0157 causes a brief gastroenteritis often with bloody diarrhoea.

Around 5 days after the diarrhoea the person will start displaying symptoms of HUS:

Reduced urine output
Haematuria or dark brown urine
Abdominal pain
Lethargy and irritability
Confusion
Hypertension
Bruising

Question 34

Management of HUS

Answer 34

Antihypertensives
Blood transfusions
Dialysis

70-80% of patients make a full recovery.

Question 35

Rhabdomyolysis

Answer 35

A condition where skeletal muscle tissue breaks down and releases breakdown products into the blood. This is usually triggered by an event that causes the muscle to break down, such as extreme underuse or overuse or a traumatic injury.

Causes release of Myoglobin, Potassium, Phosphate and Creatine kinase leading to AKI.

Question 36

What are the causes of Rhabdomyolysis

Answer 36

Prolonged immobility
Extremely rigorous exercise beyond the person’s fitness level
Crush injuries
Seizures

Question 37

Diagnosis of Rhabdomyolysis

Answer 37

Creatine Kinase (CK) blood test is a key investigation in establishing the diagnosis. It will be in the thousands to hundreds of thousands of Units/L. CK typically rises until 12 hours, then remains elevated for 1-3 days, then falls gradually. A higher CK increases the risk of kidney injury.

Myoglobinurea is myoglobin in the urine. It gives urine a red-brown colour. This will cause a urine dipstick to be positive for blood.

Urea and electrolytes (U&E) blood tests for acute kidney injury and hyperkalaemia.

ECG is important in assessing the heart’s response to hyperkalaemia.

Question 38

Management of Rhabdomyolysis

Answer 38

IV fluids are the mainstay of treatment.
Consider IV sodium bicarbonate.
Consider IV mannitol
Treat complications, particularly hyperkalaemia.

Question 39

What medications cause hyperkeleamia?

Answer 39

Aldosterone antagonists (spironolactone and eplerenone)
ACE inhibitors
Angiotensin II receptor blockers
NSAIDs
Potassium supplements

Question 40

ECG signs of hyperkalemia

Answer 40

An ECG is required in all patients with a potassium above 6 mmol/L

Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes

Question 41

What are the treatments for hyperkalemia

Answer 41

Insulin (e.g. actrapid 10 units) and dextrose (e.g. 50mls of 50%) drives carbohydrates into cells and takes potassium with it, reducing the blood potassium.

Calcium gluconate stabilises the cardiac muscle cells and reduces the risk of arrhythmias.