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Finals > Renal > Flashcards

Renal Flashcards

1
Q

What are the NICE guidelines for diagnosing an acute kidney injury?

A

Rise in creatinine of more than 25 micromol/L in 48 hours
Rise in creatinine of more than 50% in 7 days
Urine output of less than 0.5 ml/kg/hour over at least 6 hours

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2
Q

State 5 risk factors that would predispose someone to developing an AKI?

A

Older age
Sepsis
Chronic kidney disease
Heart failure
Diabetes
Liver disease
Cognitive impairment (leading to reduced fluid intake)
Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
Radiocontrast agents

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3
Q

State 3 pre-renal causes of AKI?

A

Dehydration
Shock (e.g., sepsis or acute blood loss)
Heart failure

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4
Q

State 3 renal causes of AKI

A

Acute tubular necrosis
Glomerulonephritis
Acute interstitial nephritis
Haemolytic uraemic syndrome
Rhabdomyolysis

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5
Q

State 3 post-renal causes of AKI

A

Kidney stones
Tumours (e.g., retroperitoneal, bladder or prostate)
Strictures of the ureters or urethra
Benign prostatic hyperplasia (benign enlarged prostate)
Neurogenic bladder

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6
Q

What is acute tubular necrosis?

A

damage and death (necrosis) of the epithelial cells of the renal tubules. It is the most common intrinsic cause of acute kidney injury. Damage to the kidney cells occurs due to:

Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)
Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)

Recovery usually takes 1-3 weeks

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7
Q

How is a acute tubular necrosis diagnosed?

A

Muddy brown casts on urinalysis
Renal tubular epithelial cells may also be seen

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8
Q

What is acute interstitial nephritis?

A

involves acute inflammation of the interstitium (the space between the tubules and vessels). It is caused by an immune reaction associated with:

Drugs (e.g. NSAIDs or antibiotics)
Infections (e.g., E. coli or HIV)
Autoimmune conditions (e.g., sarcoidosis or SLE)

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9
Q

What other features can accompany AKI in acute interstitial nephritis?

A

Rash
Fever
Flank pain
Eosinophilia

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10
Q

What is the management of acute interstitial nephritis?

A

treat underlying cause
steroids may reduce inflammation

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11
Q

what investigation can be used to assess for obstruction post-renal cause of AKI?

A

Ultrasound of urinary tract

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12
Q

What are 3 ways to prevent an AKI?

A

Avoiding nephrotoxic medications where appropriate
Ensuring adequate fluid intake (including IV fluids if oral intake is inadequate)
Additional fluids before and after radiocontrast agents

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13
Q

What supportive management options are there for an AKI?

A

IV fluids for dehydration and hypovolaemia
Withhold medications that may worsen the condition (e.g., NSAIDs and ACE inhibitors)
Withhold/adjust medications that may accumulate with reduced renal function (e.g., metformin and opiates)
Relieve the obstruction in a post-renal AKI (e.g., insert a catheter in a patient with prostatic hyperplasia)
Dialysis may be required in severe cases

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14
Q

State 4 complications of AKI

A

Fluid overload, heart failure and pulmonary oedema
Hyperkalaemia
Metabolic acidosis
Uraemia (high urea), which can lead to encephalopathy and pericarditis

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15
Q

What defines kidney disease as chronic?

A

chronic reduction in kidney function sustained over three months

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16
Q

State 3 factors that can speed up a decline in kidney function

A

Diabetes
Hypertension
Medications (e.g., NSAIDs or lithium)
Glomerulonephritis
Polycystic kidney disease

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17
Q

Most patient with CKD are asymptomatic. What non-specific signs/symptoms may they have?

A

Fatigue
Pallor (due to anaemia)
Foamy urine (proteinuria)
Nausea
Loss of appetite
Pruritus (itching)
Oedema
Hypertension
Peripheral neuropathy

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18
Q

What investigations are done in CKD?

A

eGFR
urine:creatinine ratio (proteinuria)
Urine dipstick/microscopy (haematuria)
renal ultrasound (obstructions)
RF: BP, HbA1c, Lipid profile

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19
Q

When can a diagnoses of CKD be made?

A

when there are consistent results over three months of either:

Estimated glomerular filtration rate (eGFR) is sustained below 60 mL/min/1.73 m2
Urine albumin:creatinine ratio (ACR) is sustained above 3 mg/mmol

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20
Q

What are the stages of CKD?

A

G1 = Over 90
G2 = 60-89
G3a = 45-59
G3b = 30-44
G4 = 15-29
G5 = Under 15

A1 = Under 3 mg/mmol
A2 = 3-30 mg/mmol
A3 = Above 30 mg/mmol

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21
Q

What is accelerated progression of CKD?

A

sustained decline in the eGFR within one year of either 25% or 15 mL/min/1.73 m2

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22
Q

State 4 complications of CKD

A

Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
End-stage kidney disease
Dialysis-related complications

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23
Q

what can be used to estimate the 5-year risk of kidney failure requiring dialysis?

A

Kidney Failure Risk Equation

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24
Q

When should you refer someone with CKD to a specialist?

A

eGFR less than 30 mL/min/1.73 m2
Urine ACR more than 70 mg/mmol
Accelerated progression (a decrease in eGFR of 25% or 15 mL/min/1.73 m2 within 12 months)
5-year risk of requiring dialysis over 5%
Uncontrolled hypertension despite four or more antihypertensives

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25
Q

what is the blood pressure target in patients under 80 with CKD and an ACR above 70 mg/mmol.

A

less than 130/80

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26
Q

State 2 medications that can slow disease progression of CKD

A

ACE inhibitors (or angiotensin II receptor blockers)
SGLT-2 inhibitors (specifically dapagliflozin)

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27
Q

State 2 factors that can reduce the risk of complications in someone with CKD

A

Exercise, maintain a healthy weight and avoid smoking
Atorvastatin 20mg for primary prevention of cardiovascular disease (in all patients with CKD)

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28
Q

What management options are their for treating the complications of CKD?

A

Oral sodium bicarbonate to treat metabolic acidosis
Iron and erythropoietin to treat anaemia
Vitamin D, low phosphate diet and phosphate binders to treat renal bone disease

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29
Q

What are the management options for end-stage renal disease?

A

Special dietary advice
Dialysis
Renal transplant

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30
Q

what needs monitoring in a patient with CKD on ACE inhibitors?

A

serum potassium as both can cause hyperkalaemia

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31
Q

ACE inhibitors should be offered to all patients with:

A

Diabetes plus a urine ACR above 3 mg/mmol
Hypertension plus a urine ACR above 30 mg/mmol
All patients with a urine ACR above 70 mg/mmol

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32
Q

When should Dapagliflozin be offered for CKD?

A

Diabetes plus a urine ACR above 30 mg/mmol

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33
Q

what type of anaemia does CKD cause and why?

A

normocytic normochromic
reduced production of erythropoietin

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34
Q

How should anaemia in CKD be managed?

A

Iron replacement first then erythropoiesis-stimulating agents

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35
Q

What is raised/low in renal bone disease?

A

High serum phosphate
Low vitamin D activity
Low serum calcium

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36
Q

why can you get secondary hyperparathyroidism in CKD?

A

Chronic kidney disease leads to less vitamin D activity and low serum calcium, parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone

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37
Q

what is the characteristic sign on x-ray of renal bone disease?

A

Rugger jersey spine

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38
Q

What are the management options for renal bone disease?

A

Low phosphate diet
Phosphate binders
Active forms of vitamin D (alfacalcidol and calcitriol)
Ensuring adequate calcium intake

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39
Q

What are the indications for short-term dialysis?

A

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

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40
Q

What is the main indication for long-term dialysis?

A

End-stage renal failure (CKD stage 5)

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41
Q

What are the 2 options for long-term dialysis?

A

Haemodialysis
Peritoneal dialysis

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42
Q

What are the 2 options for longer term access in patients who have dialysis?

A

Tunnelled cuffed catheter
Arteriovenous fistula

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43
Q

What AV fistula features a key to examine?

A

Skin integrity
Aneurysms
Palpable thrill (a fine vibration felt over the anastomosis)
A “machinery murmur” on auscultation over the fistula

44
Q

What are the 3 options for an AV fistula?

A

Radiocephalic fistula at the wrist (radial artery to cephalic vein)
Brachiocephalic fistula at the antecubital fossa (brachial artery to cephalic vein)
Brachiobasilic fistula at the upper arm (less common and a more complex operation)

45
Q

State 4 complications of an AV fistula

A

Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output heart failure

46
Q

What is STEAL syndrome?

A

inadequate blood flow to the limb distal to the fistula. The AV fistula “steals” blood from the rest of the limb. Blood is diverted away from the part of the limb it was supposed to supply, leading to ischaemia. Instead, it flows through the fistula and into the venous system.

47
Q

state 4 complications of peritoneal dialysis

A

Bacterial peritonitis (infections in the high-sugar environment are common and serious)
Peritoneal sclerosis (thickening and scarring of the peritoneal membrane)
Ultrafiltration failure (the dextrose is absorbed, reducing the filtration gradient, making ultrafiltration less effective)
Weight gain (due to absorption of the dextrose)
Psychosocial implications

48
Q

What are patient and donor kidneys matched based on?

A

human leukocyte antigen (HLA) type A, B and C on chromosome 6.

49
Q

What is the name of the scar after a kidney transplant?

A

hockey stick scar

50
Q

What is given after kidney transplant surgery to prevent acute rejection?

A

Basiliximab

51
Q

state 2 lifelong immunosuppression options to reduce the risk of transplant rejection

A

Tacrolimus
Mycophenolate
Ciclosporin
Azathioprine
Prednisolone

52
Q

What immunosuppressant causes gum hypertrophy?

A

Cyclosporine

53
Q

What is a key side effect of Tacrolimus?

A

tremor

54
Q

state 2 complications relating to kidney transplant

A

Transplant rejection (hyperacute, acute or chronic)
Transplant failure
Electrolyte imbalances

55
Q

state 3 complications related to immunosuppressants following a kidney transplant

A

Ischaemic heart disease
Type 2 diabetes (steroids)
Infections are more likely, more severe and may involve unusual pathogens
Non-Hodgkin lymphoma
Skin cancer (particularly squamous cell carcinoma)

56
Q

state 3 unusual infections that can occur secondary to immunosuppressant medication

A

Pneumocystis jiroveci pneumonia (PCP/PJP)
Cytomegalovirus (CMV)
Tuberculosis (TB)

57
Q

What are the features of Nephritic syndrome?

A

Haematuria
Oliguria (significantly reduced urine output)
Proteinuria (protein in the urine), but less than 3g per 24 hours (higher protein suggests nephrotic syndrome)
Fluid retention

58
Q

What are the features of Nephrotic syndrome

A

Proteinuria (more than 3g per 24 hours)
Low serum albumin (less than 25g per litre)
Peripheral oedema
Hypercholesterolaemia

59
Q

What does nephrotic syndrome predispose patients too?

A

thrombosis, hypertension and high cholesterol

60
Q

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

A

minimal change disease

61
Q

What are the 2 top causes of nephrotic syndrome in adults?

A

Membranous nephropathy
Focal segmental glomerulosclerosis

62
Q

What is the most common cause of primary glomerulonephritis?

A

IgA nephropathy (Berger’s disease)

63
Q

What will histology show in IgA nephropathy?

A

IgA deposits and mesangial proliferation

64
Q

What would histology show in membranous nephropathy?

A

IgG and complement deposits on the basement membrane

65
Q

What is membranoproliferative glomerulonephritis?

A

typically affects patients under 30. It involves immune complex deposits and mesangial proliferation

66
Q

What is post-streptococcal glomerulonephritis?

A

tends to affect patients under 30. It presents 1-3 weeks after a streptococcal infection (e.g., tonsillitis or impetigo). Patients usually make a full recovery

67
Q

What is rapidly progressive glomerulonephritis (or crescentic glomerulonephritis)?

A

presents with an acute severe illness but tends to respond well to treatment. Histology shows glomerular crescents

68
Q

What is Goodpasture syndrome/anti-glomerular basement membrane disease?

A

Anti-GBM (glomerular basement membrane) antibodies attack the glomerulus and pulmonary basement membranes. It causes glomerulonephritis and pulmonary haemorrhage. The typical presentation is a patient in their 20s or 60s with acute kidney failure and haemoptysis

69
Q

State 3 systemic diseases that can cause glomerulonephritis?

A

Henoch-Schönlein purpura (HSP)
Vasculitis (e.g., microscopic polyangiitis or granulomatosis with polyangiitis)
Lupus nephritis (associated with systemic lupus erythematosus)

70
Q

what is the diagnostic investigation for glomerulonephritis?

A

renal biopsy for histology

71
Q

what are the management options for glomerulonephritis?

A

Supportive care (e.g., hypertension management and dialysis in severe disease)
Immunosuppression (e.g., corticosteroids)

72
Q

What is the pathology, urinary pH and serum potassium of renal tubular acidosis type 1?

A

Pathology: distal tubule cannot excrete hydrogen ions
pH: high
K: low

73
Q

What is the pathology, urinary pH and serum potassium of renal tubular acidosis type 2?

A

Pathology: proximal tubule cannot reabsorb bicarbonate
pH: high
K: low

74
Q

What is the pathology, urinary pH and serum potassium of renal tubular acidosis type 4?

A

Pathology: low aldosterone or impaired aldosterone function
pH: low
K: high

75
Q

how can type 1 renal tubular acidosis present?

A

Failure to thrive in children
Recurrent UTIs (due to alkaline urine)
Bone disease (rickets or osteomalacia)
Muscle weakness
Arrhythmias (due to hypokalaemia)

76
Q

What is the treatment of type 1 + 2 renal tubular acidosis

A

bicarbonate

77
Q

What are the key causes of type 2 renal tubular acidosis?

A

inherited
multiple myeloma
Fanconi’s syndrome

78
Q

What are some causes of type 4 renal tubular acidosis?

A

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

79
Q

what is haemolytic uraemic syndrome and what is the usual trigger?

A

Thrombosis in small blood vessels throughout the body, usually triggered by Shiga toxins from either E. coli O157 or Shigella

80
Q

What can increase the risk of haemolytic uraemic syndrome?

A

Antibiotics and anti-motility medication (e.g., loperamide) used to treat gastroenteritis caused by E. coli O157 or Shigella

81
Q

what is the classic triad of haemolytic uraemic syndrome ?

A

Microangiopathic haemolytic anaemia
Acute kidney injury
Thrombocytopenia (low platelets)

82
Q

What are the symptoms of HUS?

A

diarrhoea which turns bloody within 3 days - after a week:
et of diarrhoea, the features of HUS develop:

Fever
Abdominal pain
Lethargy
Pallor
Reduced urine output (oliguria)
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion

83
Q

What is the management of HUS?

A

Stool culture is used to establish the causative organism.

HUS is a medical emergency and requires hospital admission and supportive management with treatment of:
Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)

84
Q

What do muscle cells release when they undergo apoptosis?

A

Myoglobin
Potassium
Phosphate
Creatine kinase

85
Q

state 3 complications of rhabdomyolysis

A

AKI
compartment syndrome
disseminated intravascular coagulation

86
Q

state 3 causes of rhabdomyolysis

A

Prolonged immobility, particularly frail patients who fall and spend time on the floor before being found
Extremely rigorous exercise beyond the person’s fitness level (e.g., endurance events or CrossFit)
Crush injuries
Seizures
Statins

87
Q

state 4 signs/symptoms of rhabdomyolysis

A

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

88
Q

What is the diagnostic investigation for rhabdomyolysis?

A

Creatine kinase (CK)
(typically rises in the first 12 hours, then remains elevated for 1-3 days)

89
Q

What is the management of rhabdomyolysis?

A

IV fluids
management of hyperkalaemia

90
Q

What is the main complication of hyperkalaemia?

A

cardiac arrhythmias, such as ventricular fibrillation, which can lead to cardiac arrest

91
Q

what is the normal range of serum potassium?

A

3.5 – 5.3

92
Q

What is classed as severe hyperkalaemia?

A

Over 6.5

93
Q

state 3 conditions that can cause hyperkalaemia

A

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

94
Q

state 3 medications that can cause hyperkalaemia

A

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

95
Q

What can create a falsely elevated potassium?

A

haemolysis

96
Q

What are the ECG changes seen in hyperkalaemia ?

A

Tall peaked T-waves
Flattening or absence of P waves
Prolonged PR interval
Broad QRS complexes

97
Q

When do patients require urgent treatment for hyperkalaemia?

A

ECG changes
Serum potassium above 6.5 mmol/L

98
Q

What is the management of severe hyperkalaemia?

A

Insulin and dextrose infusion
Calcium gluconate

99
Q

What are some other options apart from insulin for lowering serum potassium?

A

Nebulised salbutamol temporarily drives potassium into cells
Oral calcium resonium reduces potassium absorption in the GI tract (this is slow and causes constipation)
Sodium bicarbonate (in acidotic patients on renal advice) drives potassium into cells as it corrects the acidosis
Haemodialysis may be required in severe or persistent cases

100
Q

what type of polycystic kidney disease is more common?

A

autosomal dominant

101
Q

What are the affected genes in ADPKD ?

A

PKD1 gene on chromosome 16 (85% of cases)
PKD2 gene on chromosome 4 (15% of cases)

102
Q

What are some extra-renal manifestations of ADPKD ?

A

Cerebral aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Mitral regurgitation
Colonic diverticula

103
Q

What are some complications of ADPKD?

A

Chronic loin/flank pain
Hypertension
Gross haematuria can occur with cyst rupture (usually resolves within a few days)
Recurrent urinary tract infections
Renal stones
End-stage renal failure occurs at a mean age of 50 years

104
Q

Mutation in what gene causes ARPKD?

A

polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6

105
Q

How can ARPKD be picked up in antenatal scans?

A

oligohydramnios

106
Q

What are the diagnostic investigations for polycystic kidney disease?

A

ultrasound and genetic testing

107
Q

What are the management options for PKD

A

Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant

Antihypertensives for hypertension (e.g., ACE inhibitors)
Analgesia for acute pain
Antibiotics for infections (e.g., UTIs or cyst infections)
Drainage of symptomatic can be performed by aspiration or surgery
Dialysis for end-stage renal failure
Renal transplant for end-stage renal failure

Finals (21 decks)

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