Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MSRA > Renal > Flashcards

Renal Flashcards

1
Q

What are some causes of AKI? Categorise them

A

Prerenal:
- volume depletion
- reduced cardiac output
- systemic vasodilation => renal hypoperfusion
- drugs e.g. NSAIDs, ACE-i

Renal:
- acute tubular necrosis
- acute interstitial nephritis
- vascular
- glomerular

Postrenal:
- obstruction - stones, tumours, strictures, prostatic hypertrophy

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

What urine analysis findings can help investigate AKI?

A

🔹urine dipstick
- urinary tract infection: leucocytes +/- nitrites
- glomerulonephritis: haematuria + leucocytes
- acute interstitial nephritis: leucocytes by themselves

🔹microscopy, culture and sensitivity if any evidence of UTI on the urine dipstick

🔹protein:creatinine ratio if glomerulonephritis is suspected

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

What is the NICE criteria for diagnosis of AKI?

A

Any of the following:
🔹rise in serum Cr of >=26umol/L / 48hrs

🔹>50% inc in serum Cr over past 7 days

🔹UO < 0.5ml/kg/hr for >6 hrs

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

What is the RIFLE criteria? What is AKIN criteria?

A

RIFLE - Risk, Injury, Failure, Loss, End-stage renal disease
Uses serum Cr and UO to classify kidney injury
:::::
AKIN - uses stages 1-3 to classify AKI

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

What is the KDIGO classification?

A

Staging of AKI

1 = Cr x 1.5-1.9 or >26umol/L / 48 hrs
:: = UO < 0.5 ml/kg/hr > 6hrs

2 = Cr x 2.0-2.9
:: = UO < 0.5 ml/kg/hr >12hrs

3 = Cr x >3.0 baseline or >353.6 umol/L
:: = UO < 0.3 ml/kg/hr >24hr or anuria > 12hrs

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

What is the management of AKI?

A

Replace fluids
Hold nephrotoxics and review meds (NSAIDs, aminoglycosides, ACE-i, ARB, diuretics)
Treat underlying cause

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

What are some early and late clinical manifestations of CKD?

A

Early:
- fatigue (toxins, anaemia from reduced EPO)
- polyuria/nocturia
- HTN
- puffiness/swelling - fluid retention

Late:
- reduced UO
- fluid overload
- uraemia - N+V, anorexia, metallic taste, pruritis
- Neuro - poor concentration, fatigue, seizures, coma
- CVD
- anaemia
- bone and mineral disease - bone pain, fractures, renal osteodystrophy
- metabolic acidosis - Kussmaul breathing, confusion, lethargy

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

What causes anaemia in CKD?

A
  • reduced EPO levels
  • reduced erythropoiesis due to toxic effect of uraemia on bone marrow
  • reduced iron absorption
  • anorexia/nausea due to uraemia
  • reduced red cell survival
  • blood loss due to capillary fragility and poor platelet function
  • stress ulceration => blood loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the management of mineral bone disease in CKD?

A

aim to reduce phosphate and PTH levels
- reduce dietary intake
- phosphate binders
- vitamin D
- parathyroidectomy in some cases

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

How do ACE inhibitors have a renoprotective effect, particularly in diabetic nephropathy?

A

They cause dilation of the efferent glomerular arterioles, reducing glomerular capillary pressure and protecting the filtration barriers.

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

What is the role of the glomerulus in the kidney?

A

It filters fluid from the capillaries into the renal tubule, the first step in urine formation.

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

What is nephritic syndrome? What are the key signs of nephritic syndrome?

A

A group of features associated with nephritis, including:
- haematuria
- oliguria
- proteinuria (<3g/day)
- fluid retention.

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

What is nephrotic syndrome? What are the key features of nephrotic syndrome?

A

A condition where the glomerular basement membrane becomes highly permeable, leading to significant proteinuria and associated features.

  • Massive Proteinuria (>3g/day)
  • Hypoalbuminaemia (<25g/L)
  • Peripheral oedema
  • Hypercholesterolaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease, which is usually idiopathic and responds well to steroids.

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

Name the top causes of nephrotic syndrome in adults.

A
  • Membranous nephropathy
  • Focal segmental glomerulosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is IgA nephropathy, and who is typically affected?

A

Also known as Berger’s disease, it is the most common primary glomerulonephritis, usually affecting people in their 20s with haematuria.

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

What is membranous nephropathy, and what does histology show?

A

A cause of nephrotic syndrome in adults, involving immune deposits in the basement membrane. Histology shows IgG and complement deposits.

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

What is post-streptococcal glomerulonephritis?

A

A condition affecting people under 30, presenting 1-3 weeks after a streptococcal infection, with most patients making a full recovery.

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

What is Goodpasture syndrome, and what are its features?

A

Also known as anti-GBM disease, it involves anti-GBM antibodies attacking the glomerular and pulmonary basement membranes, causing acute kidney failure and haemoptysis.

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

Name systemic diseases that can cause glomerulonephritis.

A
  • Henoch-Schönlein purpura (HSP)
  • Vasculitis (e.g., microscopic polyangiitis, granulomatosis with polyangiitis)
  • Lupus nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How can antibodies help differentiate conditions with acute kidney injury and haemoptysis?

A
  • Anti-GBM antibodies: Goodpasture syndrome
  • p-ANCA/MPO antibodies: Microscopic polyangiitis
  • c-ANCA/PR3 antibodies: Granulomatosis with polyangiitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the main management approaches for glomerulonephritis?

A
  • Supportive care (e.g., blood pressure control, dialysis)
  • Immunosuppression (e.g., corticosteroids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is renal tubular acidosis (RTA)?

A

Metabolic acidosis due to pathology in the renal tubules, which disrupt the balance of hydrogen (H⁺) and bicarbonate (HCO₃⁻) ions between blood and urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the pathology, urinary pH and serum K in Type 1 renal tubular acidosis?

A

aka Distal RTA

Pathology: Distal tubule cannot excrete hydrogen ions

Urinary pH: High

Serum K: Low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the pathology, urinary pH and serum K in Type 2 renal tubular acidosis?

A

aka proximal RTA

Pathology: Proximal tubule cannot reabsorb bicarbonate

Urinary pH: High

Serum K: Low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the pathology, urinary pH and serum K in Type 4 renal tubular acidosis?

A

aka hyperkalaemic RTA

Pathology: Low aldosterone or impaired aldosterone function

Urinary pH: Low

Serum K: High

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What causes type 1 RTA?

A
  • Genetic (autosomal dominant or recessive)
  • SLE
  • Sjögren’s syndrome
  • Primary biliary cholangitis
  • Hyperthyroidism
  • Sickle cell anaemia
  • Marfan’s syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the biochemical presentation of Type 1 renal tubular acidosis?

A
  • High urinary pH (above 6) due to the absence of hydrogen ions
  • Metabolic acidosis, due to retained hydrogen ions in the blood
  • Hypokalaemia, due to failure of the hydrogen and potassium exchange (H+/K+ ATPase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the clinical features of type 1 RTA?

A
  • Failure to thrive in children
  • Recurrent UTIs (due to alkaline urine)
  • Bone disease (rickets or osteomalacia)
  • Muscle weakness
  • Arrhythmias (due to hypokalaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is type 1 RTA treated?

A

Oral bicarbonate to correct acidosis and electrolyte imbalances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What causes type 2 RTA?

A
  • Genetic (autosomal dominant or recessive)
  • Multiple myeloma
  • Fanconi’s syndrome
32
Q

What is the biochemical presentation of Type 2 renal tubular acidosis?

A
  • High urinary pH (above 6) due to the excess bicarbonate in the urine
  • Metabolic acidosis, due to inadequate bicarbonate in the blood
  • Hypokalaemia, due to urinary loss of potassium along with bicarbonate
33
Q

How is type 2 RTA treated?

A

Oral bicarbonate.

34
Q

What is type 3 RTA?

A

A rare combination of type 1 and 2 RTA involving pathology in both the proximal and distal tubules.

35
Q

What causes type 4 RTA?

A
  • Adrenal insufficiency
  • Diabetic nephropathy
  • Medications (e.g., ACE inhibitors, spironolactone, or eplerenone)
36
Q

What are the clinical features of type 4 RTA?

A
  • Metabolic acidosis (retained hydrogen ions in blood)
  • Hyperkalaemia (retained potassium in blood)
  • Low urinary pH (reduced ammonia production in response to hyperkalaemia)
37
Q

How is type 4 RTA managed?

A
  • Treat the underlying cause
  • Fludrocortisone for aldosterone deficiency
  • Oral bicarbonate
  • Treatment of hyperkalaemia
38
Q

What is haemolytic uraemic syndrome (HUS)?

A

A condition involving thrombosis in small blood vessels throughout the body, usually triggered by Shiga toxins from E. coli O157 or Shigella.

39
Q

Which patient population is most affected by HUS?

A

Children, typically following an episode of gastroenteritis.

40
Q

What increases the risk of HUS in gastroenteritis caused by E. coli O157 or Shigella?

A
  • Antibiotics
  • Anti-motility medications (e.g., loperamide)
41
Q

What is the classic triad of features in HUS?

A
  1. Microangiopathic haemolytic anaemia (MAHA)
  2. Acute kidney injury (AKI)
  3. Thrombocytopenia (low platelets)
42
Q

How does HUS cause thrombocytopenia?

A

The formation of blood clots consumes platelets, reducing their availability in the bloodstream.

43
Q

What causes acute kidney injury in HUS?

A

Thrombi and damaged red blood cells obstruct blood flow through the kidneys.

44
Q

What is microangiopathic haemolytic anaemia (MAHA)?

A

Destruction of red blood cells due to pathology in small vessels where thrombi damage the red blood cells, causing haemolysis.

45
Q

What is the typical progression of symptoms in HUS following gastroenteritis?

A
  1. Diarrhoea (initial symptom, becomes bloody within 3 days)
  2. Around 1 week later, features of HUS develop, including:
    - Fever
    - Abdominal pain
    - Lethargy
    - Pallor
    - Reduced urine output (oliguria)
    - Haematuria
    - Hypertension
    - Bruising
    - Jaundice (due to haemolysis)
    - Confusion
46
Q

How is the causative organism in HUS identified?

A

Stool culture.

47
Q

What is the management approach for HUS?

A

Hospital admission (HUS is a medical emergency)
Supportive care for:
- Hypovolaemia (IV fluids)
- Hypertension
- Severe anaemia (blood transfusions)
- Severe renal failure (haemodialysis)

Self-limiting disease

48
Q

What are the key substances released from muscle cells during rhabdomyolysis?

A
  • Myoglobin
  • Potassium (most immediately dangerous)
  • Phosphate
  • Creatine kinase
49
Q

What is the primary renal complication of rhabdomyolysis?

A

AKI esp bc myoglobin

50
Q

What are potential complications of rhabdomyolysis?

A
  • Cardiac arrhythmia bc hyperkalaemia
  • AKI bc myoglobin
  • compartment syndrome
  • DIC
51
Q

List some common causes of rhabdomyolysis.

A
  • Prolonged immobility (e.g., frail patients after a fall)
  • Extremely rigorous exercise beyond fitness level (e.g., endurance events, CrossFit)
  • Crush injuries
  • Seizures
  • Statins
52
Q

What are the main symptoms of rhabdomyolysis?

A
  • Muscle pain, weakness, and swelling
  • Reduced urine output (oliguria)
  • Red-brown urine (myoglobinuria)
  • Fatigue
  • Nausea and vomiting
  • Confusion (particularly in frail patients)
53
Q

What blood test is crucial for diagnosing rhabdomyolysis?

A

Creatine kinase (CK): Normally <150 U/L; in rhabdomyolysis, it can range from 1,000-100,000 U/L.

54
Q

What is myoglobinuria, and how is it detected?

A

The presence of myoglobin in urine, giving it a red-brown color. It is detected with a urine dipstick that tests positive for blood.

55
Q

Which investigations are necessary in rhabdomyolysis?

A
  1. Creatine kinase (CK) to confirm the diagnosis.
  2. Urea and electrolytes (U&E) to assess for acute kidney injury and hyperkalaemia.
  3. ECG to monitor the effects of hyperkalaemia on the heart.
56
Q

What is the primary treatment for rhabdomyolysis?

A

Intravenous fluids to correct hypovolaemia and promote filtration of breakdown products.

57
Q

What additional treatments for rhabdomyolysis are debated and why?

A
  • Intravenous sodium bicarbonate: To increase urinary pH and reduce the toxicity of myoglobin.
  • Intravenous mannitol: To increase urine output and reduce oedema.
    Both have associated risks and are not always recommended.
58
Q

How is hyperkalaemia classified by serum potassium levels?

A
  • Mild: 5.4 - 6
  • Moderate: 6 - 6.5
  • Severe - >6.5
59
Q

List common causes of hyperkalaemia.

A
  • Acute kidney injury
  • Chronic kidney disease (stage 4 or 5)
  • Rhabdomyolysis
  • Adrenal insufficiency
  • Tumour lysis syndrome
60
Q

Which medications can cause hyperkalaemia? (4)

A
  • Aldosterone antagonists (e.g., spironolactone, eplerenone)
  • ACE inhibitors (e.g., ramipril)
  • Angiotensin II receptor blockers (e.g., candesartan)
  • NSAIDs (e.g., naproxen)
61
Q

What are the key ECG changes seen in hyperkalaemia?

A
  • Tall peaked T waves
  • Flattening or absence of P waves
  • Prolonged PR interval
  • Broad QRS complexes
62
Q

When does hyperkalaemia require urgent treatment?

A
  • Serum potassium >6.5 mmol/L
  • Presence of ECG changes
63
Q

What are the primary treatments for urgent hyperkalaemia?

A
  • Insulin and dextrose infusion: Drives potassium into cells.
  • IV calcium gluconate: Stabilises cardiac muscle and prevents arrhythmias.
64
Q

What additional treatments are available for hyperkalaemia?

A
  • Nebulised salbutamol: Temporarily shifts potassium into cells.
  • Oral calcium resonium: Reduces GI potassium absorption (slow action, causes constipation).
  • Sodium bicarbonate: Used in acidosis (renal advice needed).
  • Haemodialysis: For severe or persistent hyperkalaemia.
65
Q

What should be done for mild hyperkalaemia without ECG changes?

A

Address the underlying cause, such as:
- Treating acute kidney injury.
- Stopping causative medications (e.g., spironolactone, ACE inhibitors).

66
Q

What is polycystic kidney disease (PKD)?

A

A genetic disorder where healthy kidney tissue is replaced with fluid-filled cysts, leading to renal failure. Enlarged kidneys may be palpable on abdominal examination.

67
Q

Which genes are affected in Autosomal Dominant Polycystic Kidney Disease (ADPKD)?

A
  • PKD1 on chromosome 16 (85% of cases)
  • PKD2 on chromosome 4 (15% of cases)
68
Q

What are the extra-renal manifestations of AutDomPKD?

A
  • Cerebral aneurysms
  • Hepatic, splenic, pancreatic, ovarian, and prostatic cysts
  • Mitral regurgitation
  • Colonic diverticula
69
Q

What are the complications of ADPKD?

A
  • Chronic loin/flank pain
  • Hypertension
  • Gross haematuria (from cyst rupture)
  • Recurrent urinary tract infections
  • Renal stones
  • End-stage renal failure (mean age ~50 years)
70
Q

Which gene is affected in Autosomal Recessive Polycystic Kidney Disease (ARPKD)?

A

PKHD1 on chromosome 6.

71
Q

How does ARPKD typically present?

A

Antenatal signs: Oligohydramnios (reduced amniotic fluid).

Neonatal features:
- Pulmonary hypoplasia (underdeveloped lungs) leading to respiratory failure.
- Dysmorphic features: underdeveloped ear cartilage, low-set ears, flat nasal bridge.
- End-stage renal failure often before adulthood.

72
Q

How is PKD diagnosed?

A
  • Ultrasound: Identifies kidney cysts.
  • Genetic testing: Confirms mutations in PKD1, PKD2, or PKHD1.
73
Q

What is the role of tolvaptan in ADPKD?

A

A vasopressin receptor antagonist that slows the progression of cyst development and renal failure. Requires specific criteria and specialist monitoring.

74
Q

What are the management strategies for PKD?

A
  • Hypertension: ACE inhibitors (e.g., ramipril).
  • Pain management: Analgesia.
  • Infections: Antibiotics for UTIs or cyst infections.
  • Symptomatic cysts: Aspiration or surgical drainage.
  • Renal failure: Dialysis and/or renal transplant.
75
Q

What are additional precautions in PKD management?

A
  • Genetic counselling.
  • Avoiding contact sports (risk of cyst rupture).
  • Avoiding NSAIDs and anticoagulants.
  • MR angiography (MRA): Screen for cerebral aneurysms.

MSRA (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions