Zero to Finals Flashcards

1
Q

What is the classic triad of HUS?

A

Haemolytic anaemia

Acute kidney injury

Low platelet count (thrombocytopenia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the ECG changes for hyperkalamia?

(MUST KNOW)

A

An ECG is required in all patients with a potassium above 6 mmol/L. It is worth memorising the ECG changes in hyperkalaemia:

Tall peaked T waves

Flattening or absence of P waves

Broad QRS complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the indications for Dialysis?

A

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.

End stage renal failure (CKD stage 5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 options for long term dialysis?

A

Continuous Ambulatory Peritoneal Dialysis

Automated Peritoneal Dialysis

Haemodialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the complications of peritoneal dialysis?

A

Bacterial peritonitis. Infusions of glucose solution make the peritoneum a great place for bacterial growth. Bacterial infection is a common and potentially serious complication of peritoneal dialysis.

Peritoneal sclerosis involves thickening and scarring of the peritoneal membrane.

Ultrafiltration failure can develop. This occurs when the patient starts to absorb the dextrose in the filtration solution. This reduces the filtration gradient making ultrafiltration less effective. This becomes more prominent over time.

Weight gain can occur as they absorb the carbohydrates in the dextrose solution.

Psychosocial effects. There are huge social and psychological effects of having to change dialysis solution and sleep with a machine every night.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Summary of Haemodialysis:

A

With haemodialysis, patients have their blood filtered by a haemodialysis machine. Regimes can vary but a typical regime might be 4 hours a day for 3 days a week.

They need good access to an abundant blood supply. The options for this are:

Tunnelled cuffed catheter

Arterio-venous fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the main complications with using a catheter for haemodialysis?

A

The main complications are infection and blood clots within the catheter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the complications of AV fistulas?

A

Aneurysm

Infection

Thrombosis

Stenosis

STEAL syndrome

High output heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is STEAL syndrome?

A

STEAL syndrome is where there is inadequate blood flow to the limb distal to the AV fistula. The AV fistula “steals” blood from the distal limb. The blood is diverted away from where is was supposed to supply and flows straight into the venous system. This causes distal ischaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is meant by nephritic syndrome?

A

Nephritic syndrome or acute nephritic syndrome refers to a group of symptoms, not a diagnosis. When we say a patient has “nephritic syndrome” it simply means they fit a clinical picture of having inflammation of their kidney and it does not represent a specific diagnosis or give the underlying cause. Unlike nephrotic syndrome, there are no set criteria. However, there are the following features in nephritic syndrome:

Haematuria means blood in the urine. This can be microscopic (not visible) or macroscopic (visible).

Oliguria means there is a significantly reduced urine output.

Proteinuria is protein in the urine. In nephritic syndrome, there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome.

Fluid retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

To have nephrotic syndrome a patient must fulfil what criteria:

A

Peripheral oedema

Proteinuria more than 3g / 24 hours

Serum albumin less than 25g / L

Hypercholesterolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is meant by glomerulonephritis?

e.g…

A

Glomerulonephritis is an umbrella term applied to conditions that cause inflammation of or around the glomerulus and nephron.

e.g Interstitial nephritis &glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Interstitial nephritis

A

Interstitial nephritis is a term to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney. It is important not to confuse this with glomerulonephritis. Under the umbrella term of interstitial nephritis, there are two key specific diagnoses: acute interstitial nephritis and chronic tubulointerstitial nephritis. These are discussed in a later section.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Glomerulosclerosis is a term to describe the pathological process of scarring of the tissue in the glomerulus. It is not a diagnosis in itself and is more a term used to describe the damage and scarring done by other diagnoses. Glomerulosclerosis can be caused by any type of glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by a specific disease called focal segmental glomerulosclerosis.

A

Glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most types of glomerulonephritis are treated with what?

A

Immunosuppression (e.g. steroids)

Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin-II receptor blockers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Goodpasture syndrome:

A

Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes. This causes glomerulonephritis and pulmonary haemorrhage. In your exam, there may be a patient that presents with acute kidney failure and haemoptysis (coughing up blood).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

If you come across a patient in your exam with the combination of acute renal failure and haemoptysis, think of two conditions: Goodpasture syndrome and granulomatosis with polyangiitis (AKA Wegener’s granulomatosis). Goodpasture syndrome is associated with anti-GBM antibodies, whereas Wegener’s granulomatosis is a type of vasculitis associated with anti-neutrophil cytoplasmic antibodies (ANCA). Patients with Wegener’s granulomatosis may also have a wheeze, sinusitis and a saddle-shaped nose.

A

If you come across a patient in your exam with the combination of acute renal failure and haemoptysis, think of two conditions: Goodpasture syndrome and granulomatosis with polyangiitis (AKA Wegener’s granulomatosis). Goodpasture syndrome is associated with anti-GBM antibodies, whereas Wegener’s granulomatosis is a type of vasculitis associated with anti-neutrophil cytoplasmic antibodies (ANCA). Patients with Wegener’s granulomatosis may also have a wheeze, sinusitis and a saddle-shaped nose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is diabetic nephropathy and what does it lead to?

A

Diabetic nephropathy is the most common cause of glomerular pathology and chronic kidney disease in the UK. The chronic high level of glucose passing through the glomerulus causes scarring. This is called glomerulosclerosis.

Proteinuria is a key feature of diabetic nephropathy. This is due to damage to the glomerulus allowing protein to be filtered from blood to urine.

Patients with diabetes should have regular screening for diabetic nephropathy by testing the albumin:creatinine ratio and U&Es.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is diabetic nephropathy managed?

A

Treatment is by optimising blood sugar levels and blood pressure.

ACE inhibitors are the treatment of choice in diabetics for blood pressure control. They should be started in patients with diabetic nephropathy even if they have a normal blood pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is meant by interstitial nephritis?

A

Interstitial nephritis is term to 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is acute interstitial nephritis and what is it usually caused by?

A

Acute interstitial nephritis 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 / antibiotics

Infection

Note: You may also see rash / fever / eosinophillia in the paitent (associated with the hypersensitivity).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Management of acute interstitial nephritis:

A

Management involves treating the underlying cause. Steroids have a role in reducing inflammation and improving recovery.

23
Q

Summarise acute tubular necrosis:

A

Acute tubular necrosis 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.

24
Q

Causes of acute tubular necrosis:

A

Ischaemia can occur secondary to hypoperfusion in:

  • Shock
  • Sepsis
  • Dehydration

Direct damage from toxins can occur due to:

  • Radiology contrast dye
  • Gentamycin
  • NSAIDs
25
Q

What specific finding is found on urinalysis for ATN?

A

“Muddy brown casts” found on urinalysis is a pathognomonic finding specific to acute tubular necrosis. There can also be renal tubular epithelial cells in the urine.

26
Q

How is ATN managed?

A

Supportive management

IV fluids

Stop nephrotoxic medications

Treat complications

27
Q

Summarise Type 4 renal tubular acidosis:

A

Type 4 renal tubular acidosis is caused by reduced aldosterone. This is probably the most common cause of renal tubular acidosis and the most likely to turn up in your exams and clinical practice.

28
Q

What causes type 4 renal tubular acidosis?

A

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.

29
Q

How does renal tubular acidosis present?

A

Hyperkalaemia

High chloride

Metabolic acidosis

Low urinary pH

30
Q

How is renal tubular acidosis managed?

A

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

31
Q

What is haemolytic uraemic syndrome?

A

Haemolytic uraemic syndrome (HUS) occurs when there is thrombosis in small blood vessels throughout the body. This is usually triggered by a bacterial toxin called the shiga toxin. It leads to the classic triad of:

Haemolytic anaemia

Acute kidney injury

Low platelet count (thrombocytopenia)

32
Q

Pathophysiology of HUS:

A

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.

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.

33
Q

How does HUS present?

A

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

34
Q

How is HUS managed?

A

HUS is a medical emergency and has up to 10% mortality. The condition is self limiting and supportive management is the mainstay of treatment:

  • Antihypertensives
  • Blood transfusions
  • Dialysis
35
Q

What can cause extreme damage to muscle cells and lead to Rhabdomyolysis?

A

Prolonged immobility, particularly frail patients that fall and spend time on the floor before being found

Extremely rigorous exercise beyond the person’s fitness level (e.g. ultramaraton, triathalon, crossfit competition)

Crush injuries

Seizures

36
Q

Signs and symptoms of rhabdomyolysis:

A

Suspect rhabdomyolysis in patients with trauma, crush injury, prolonged immobilisation or excessive exercise.

  • Muscle aches and pain
  • Oedema
  • Fatigue
  • Confusion (particularly in elderly frail patients)
  • Red-brown urine
37
Q

Investigations carried out for rhabdomyolysis:

A

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.

Myoglobinuria 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.

38
Q

How is rhabdomyolysis managed?

A

IV fluids are the mainstay of treatment. The aim is to rehydrate the patient and encourage filtration of the breakdown products.

Consider IV sodium bicarbonate. This aims to make the urine more alkaline (pH ≥ 6.5), reducing the toxicity of the myoglobin on the kidneys. The evidence on this is not clear and there is some debate about whether to use it.

Consider IV mannitol. This aims to increase the glomerular filtration rate to help flush the breakdown products and to reduce oedema surrounding muscles and nerves. Hypovolaemia should be corrected before giving mannitol. The evidence on this is not clear and there is some debate about whether to use it.

Treat complications, particularly hyperkalaemia. Hyperkalaemia can be immediately life threatening as it can cause arrhythmias (particularly ventricular fibrillation).

39
Q

What are the main complications of hyperkalaemia?

A

The main complication is cardiac arrhythmias such as ventricular fibrillation. These can be fatal.

40
Q

Causes of hyperkalaemia?

A

Conditions

  • Acute kidney injury
  • Chronic kidney disease
  • Rhabdomyolysis
  • Adrenal insufficiency
  • Tumour lysis syndrome

Medications

  • Aldosterone antagonists (spironolactone and eplerenone)
  • ACE inhibitors
  • Angiotensin II receptor blockers
  • NSAIDs
  • Potassium supplements
41
Q

How is hyperkalaemia diagnosed?

A

Hyperkalaemia is diagnosed on a formal urea and electrolytes (U&E) blood test.

Pay attention to creatinine, urea and eGFR. Acute or chronic renal failure is important as they will need discussion with the renal team and consideration of haemodialysis.

Haemolysis (breakdown of red blood cells) during sampling can result in a falsely elevated potassium. The lab might indicate that they have noticed some haemolysis and require a repeat sample to confirm the correct potassium result.

42
Q

What are the ECG changes for hyperkalamia?

(MUST KNOW)

A

An ECG is required in all patients with a potassium above 6 mmol/L. It is worth memorising the ECG changes in hyperkalaemia:

Tall peaked T waves

Flattening or absence of P waves

Broad QRS complexes

43
Q

How is hyperkalaemia treated?

A

The mainstay of treatment is with an insulin and dextrose infusion and IV calcium gluconate:

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.

44
Q

Summarise polycystic kidney disease:

A

Polycystic kidney disease is a genetic condition where the kidneys develop multiple fluid-filled cysts. Kidney function is also significantly impaired. There are a number of associated findings outside the kidneys such as hepatic cysts and cerebral aneurysms. Palpable, enlarged kidneys may be felt on examination.

45
Q

Diagnosis of PCKD:

A

Diagnosis is by kidney ultrasound scan and genetic testing.

46
Q

Extra-renal manifestation of pckd:

A

Cerebral aneurysms

Hepatic, splenic, pancreatic, ovarian and prostatic cysts

Cardiac valve disease (mitral regurgitation)

Colonic diverticula

Aortic root dilatation

Hirsuitism

Acanthosis nigricans

Acne

47
Q

Complications of PCKD:

A

Chronic loin pain

Hypertension

Cardiovascular disease

Gross haematuria can occur with cyst rupture (this usually resolves within a few days

Renal stones are more common in patients with PKD

End-stage renal failure occurs at a mean age of 50 years

48
Q

Management of PCKD:

A

Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease. It is recommended by NICE in certain situations although it should be initiated and monitored by a specialist.

Management of polycystic kidney disease is mainly supportive of the complications:

  • Antihypertensives for hypertension.
  • Analgesia for renal colic related to stones or cysts.
  • Antibiotics for infection. Drainage of infected cysts may be required.
  • Dialysis for end-stage renal failure.
  • Renal transplant for end-stage renal failure.
49
Q

What drugs should be stopped in AKI?

A

I was once told DAMN drugs should be stopped in AKI (diuretics, ACEI, metformin, NSAIDs).

50
Q

Worsening anaemia in a patient with CKD give…?

A

EPO

51
Q

Key symptoms of nephrOtic vs nephrITic syndrome

A

(Oedema for nephrOtic) (heamITuria for nephrITic)

52
Q

Young females develop AKI after starting an ACEi think…?

A

Consider fibromuscular dysplasia in young female patients who develop AKI after the initiation of an ACE inhibitor.

53
Q

Fibromuscular dysplasia

A

Fibromuscular dysplasia describes the proliferation of cells in the walls of the arteries causing the vessels to bulge or narrow. This most commonly affects women. These patients are susceptible to AKI after the initiation of an ACE inhibitor. The classic description is ‘string of beads’ appearance.

54
Q

Why is thrombosis associated with nephrotic syndrome?

A

Nephrotic syndrome is associated with a hypercoagulable state due to loss of antithrombin III via the kidneys.