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Y3 Medicine > Nephrology > Flashcards

Nephrology Flashcards

1
Q

How can Addisonian crisis present?

A
  • can present vaguely with fever, abdo pain and collapse
  • can cause hyperkalaemic hyperchloraemic (normal anion gap) metabolic acidosis due to loss of aldosterone
  • even when managed with steroids, think of triggers e.g. recent infection
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2
Q

What are the main extra renal manifestation of ADPCKD?

A

liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly

berry aneurysms (8%): rupture can cause subarachnoid haemorrhage

cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection

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3
Q

How does acute interstitial nephritis present? What will be seen on investigation?

A

Usually drug induced kidney injury
Triad of rash, fever and eosinophilia
Common to see arthralgia

Sterile pyuria and white cell casts on investigation

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4
Q

What blood result would make you think of dehydration as the cause of AKI?

A

rise in urea proportionally bigger than rise in creatinine

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5
Q

Drugs to stop in AKI?

A

(DAMN AKI)

Diuretics
Aminoglycosides and ACE inhibitors
Metformin
NSAIDs (bar aspirin at cardioprotective dose and paracetamol)

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6
Q

What are the indications for haemodialysis in a patient with acute kidney injury?

A

haemodialysis always pulls up

Hyperkalaemia (severe)
Acidosis
Pulmonary oedema
Uraemia- (encephalopathy or pericarditis)

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7
Q

What serum urea:creatinine ratio indicates a likely pre-renal cause of AKI?

A

do urea/creatinine/1000 to calculate - above 100 is likely a prerenal injury

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8
Q

What is Alport’s syndrome? Describe the key features and how it is diagnosed

A

Alport syndrome : inherited defect in IV collagen (X linked dominant) that usually presents in childhood

  • GBM abnormality (splitting of lamina densa on microscopy)
  • progressive renal failure (microscopic haematuria)
  • sensorineural hearing loss
  • ocular issues, smooth muscle tumours (leiomyomas) and rarely aortic dissection

Diagnosed with genetic testing and renal biopsy

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9
Q

Give 3 causes of acidosis with a raised anion gap

A

Sepsis, DKA and methanol poisoning all cause metabolic acidosis with a raised anion gap

-they all result in the formation of a new anion that is not included in the calculation- lactic acid, ketones and formic acid

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10
Q

How long does an AV fistula take to develop?

A

6-8 weeks

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11
Q

CKD commonly causes anaemia, due to reduced EPO , toxic effects of uraemia on bone marrow and reduced iron absorption. What features might this present with, and how should treatment be optimised?

A

Features:
Classical signs of anaemia e.g. fatigue and pallor
Aortic flow murmur (soft ejection systolic murmur)

Tx optimisation:
Iron deficiency should be corrected (eg with ferrous sulphate) before starting erythropoiesis-stimulating agents
Patients on haemodialysis often require IV iron

target haemoglobin of 10 - 12 g/dl

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12
Q

What is the most common cause of death in CKD patients on haemodialysis?

A

Ischaemic heart disease

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13
Q

When should a GP consider referring to a nephrologist (eGFR)?

A

if eGFR falls below 30 or progressively by > 15 in a year

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14
Q

What variables are considered to affect eGFR in the Modification of Diet in Renal Disease (MDRD) equation?

A

eGFR variables
- CAGE - Creatinine, Age, Gender, Ethnicity

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15
Q

Outline the management of bone mineral disease in CKD

A
  • reduced dietary intake of phosphate is the first-line management
  • phosphate binders
  • vitamin D: alfacalcidol, calcitriol
  • parathyroidectomy may be needed in some cases
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16
Q

What should you give in CKD when concerned about fracture risk? (e.g. when post menopausal/ has fam hx to exacerbate bone mineral disease)

A

alendronic acid - a bisphosphonate that reduces the rate of bone turnover and strengthens the bone.

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17
Q

What should be done in all patients with a clinically raised ACR (albumin:creatinine ratio >3mg/mmol) and co-existent diabetes mellitus?

A

ACE-i should be commenced to reduce risk of diabetic nephropathy

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18
Q

What type of diabetes insipidus is commonly caused by lithium (mood stabiliser)?

A

Nephrogenic DI- lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts

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19
Q

What is diabetes insipidus? How do you test for it?

A

Diabetes insipidus is a condition characterised by either a decreased secretion of ADH from the pituitary (cranial DI) or an insensitivity to ADH (nephrogenic DI).

Causes polyuria and polydipsia.

Investigation:
- high plasma osmolality, low urine osmolality
- a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
- can do a water deprivation test

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20
Q

What is involved in annual screening for diabetic nephropathy? Why is it done?

A

urinary albumin:creatinine ratio (ACR)
- should be an early morning specimen
- ACR > 2.5 = microalbuminuria

ACR may be measured on a spot sample if a first-pass sample is not provided (but should be repeated on a first-pass specimen if abnormal)

Microalbuminuria is the earliest, clinically detectable manifestation of classic diabetic kidney disease

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21
Q

What investigation should be carried out for older patients with iron deficiency anaemia?

A

refer for endoscopy/colonoscopy to rule out GI cancer

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22
Q

What diagnoses should be considered when AKI develops after initiating ACEi?

A

In young women - think fibromuscular dysplasia (causing renal artery stenosis)
In older pts - think atherosclerosis of renal arteries

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23
Q

What are the requirements for maintenance fluids?

A

25-30 ml/kg/day of water
approximately 1 mmol/kg/day of potassium, sodium and chloride
approximately 50-100 g/day of glucose to limit starvation ketosis

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24
Q

What is the risk when using 0.9% Sodium Chloride for fluid therapy in patients requiring large volumes?

A

hyperchloraemic metabolic acidosis

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25
Q

Which cancer is most commonly associated with varicocele?

A

RCC

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26
Q

When should a 2 week wait referral happen for haematuria?

A

Aged > 45 years AND:
-unexplained visible haematuria without urinary tract infection, or
- visible haematuria that persists or recurs after successful treatment of urinary tract infection

Aged > 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised WCC

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27
Q

What is HUS? What are the common causes? Tx?

A

Haemolytic uraemic syndrome is generally seen in young children and produces a triad of:
- AKI
- microangiopathic haemolytic anaemia
- thrombocytopenia

Often follows diarrhoeal infection

Common cause - E.coli (shiga tox) , pneumococcus, HIV

Give supportive tx only unless underlying infection to correct

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28
Q

What is Henoch-Schonlein purpura (HSP)? How should it be managed?

A

an IgA mediated small vessel vasculitis, commonly seem in children (following infection)

classically presents with abdominal pain, arthritis, haematuria and a purpuric rash over the buttocks and extensor surfaces of arms and legs

blood pressure and urinalysis should be monitored to detect progressive renal involvement

Tx is usually supportive as it is self-limiting

29
Q

Outline the key steps in management of hyperkalaemia

A

Always do an ECG first in new hyperkalaemia

If K+ > 6.5 mmol/l or if there are ECG changes:

Administer calcium gluconate 10% 10-20ml by slow IV injection titrated to ECG response
Give 10 U Actrapid in 50 ml of 50% glucose over 10-15 minutes
Consider use of nebulised salbutamol (temporarily lower K+)
Consider correcting acidosis with sodium bicarbonate infusion

30
Q

What can happen when hyperkalaemia goes untreated?

A

Untreated hyperkalaemia can cause ventricular tachycardia- reduced CO, hypotension, and dyspnoea from pulmonary congestion

31
Q

How does IgA nephropathy (Berger’s disease) typically present?

A

Frank haematuria following upper respiratory tract infection in young people

It is the commonest cause of glomerulonephritis worldwide!

32
Q

What malignancy is associated with membranous glomerulonephritis?

A

prostate, lung, lymphoma, leukaemia

33
Q

How does aspirin overdose present? Tx?

A

initially presents with nausea, vomiting, tinnitus and headache

In more severe overdoses, hyperventilation and a secondary respiratory alkalosis develops

Over ~24 hours, this progresses to a metabolic acidosis and hypokalaemia. Confusion, coma, seizures, hypoglycaemia and fever may also develop.

Tx: IV sodium bicarb

34
Q

What is the most common cause of peritonitis secondary to peritoneal dialysis? Tx?

A

Coagulase-negative Staphylococcus e.g. staph epidermidis

vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth

35
Q

What hormonal change may be seen in nephrotic syndrome?

A

Low total thyroxine

36
Q

Describe hyperacute rejection and acute graft failure following renal transplant

A

Hyperacute rejection (minutes to hours)

  • pre-existing antibodies against ABO or HLA antigen (type II hypersensitivity reaction)
  • leads to widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
  • no treatment is possible and the graft must be removed

Acute graft failure (< 6 months)

  • usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
  • usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
  • may be reversible with steroids and immunosuppressants
37
Q

Most common viral infection in solid organ transplant patients? Tx?

A

Cytomegalovirus- Ganciclovir is the treatment of choice

38
Q

Patients on long-term immunosuppression for renal transplantation require regular monitoring for complications such as:

A

Cardiovascular disease - tacrolimus and ciclosporin can cause hypertension and hyperglycaemia so patients should be monitored for accelerated CVD

Renal failure - due to nephrotoxic effects of tacrolimus and ciclosporin/graft rejection/recurrence of original disease

Malignancy - patients should be educated about minimising sun exposure to reduce the risk of squamous cell carcinomas and basal cell carcinomas

39
Q

Name the diagnosis from each urine microscopy finding:

  1. Hyaline casts
  2. Brown ‘muddy’ granular casts
  3. Red cell casts
  4. ‘Bland’ urinary sediment
A

1.seen in normal urine, after exercise, during fever or with loop diuretics
2. Acute tubular necrosis
3. nephritic syndrome
4. pre-renal uraemia (azotemia)

40
Q

When should patients with CKD be started on an ACEi?

A

if they have an ACR > 30 mg/mmol

41
Q

What is the potential complication for patients with CKD who take calcium based phosphate binders?

A

hypercalcaemia and vascular calcification

42
Q

Why is Nephrotic syndrome associated with a hypercoagulable state?

A

Loss of antithrombin 3 by the kidneys

43
Q

Most likely diagnosis in an older patient with painless visible haematuria?

A

TCC of the bladder

44
Q

What vitamin D supplement is used in end-stage renal disease?

A

Alfacalcidol is used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys

45
Q

Spot diagnosis- haemoptysis + sudden onset AKI/proteinuria/haematuria ?

A

Goodpasture’s: anti-glomerular basement membrane (GBM) disease

small-vessel vasculitis associated with pulmonary haemorrhage and rapidly progressive glomerulonephritis

The disease is more common in men and can be exacerbated by a respiratory tract infection

46
Q

Causes of a normal anion gap metabolic acidosis?

A

ABCD

Addison’s
Bicarb loss- e.g. diarrhoea
Chloride (ammonium chloride injection)
Drugs- e.g. acetazolamide

47
Q

First line tx for ascites?

A

spironolactone

48
Q

What can spironolactone be replaced with in cases of troublesome gynaecomastia?

A

Eplerenone

49
Q

How do you differentiate between IgA nephropathy and Post-streptococcal glomerulonephritis when they both present with nephritic syndrome following an infection? (just based on clinical picture)

A

Post-streptococcal glomerulonephritis is more delayed (occurs 7-14 days after infection) and the infection is always streptococcal e.g. tonsilitis

50
Q

What is the first line investigation for rhabdomyolysis? What is the treatment?

A

Serum creatine kinase

rapid IV fluid rehydration- normal saline

51
Q

What drug should all CKD patients be started on?

A

a statin

52
Q

What are the main complications of haemodialysis?

A

CHASED

Cardiac arrhythmia
Hypotension
Air embolus
Stenosis/infection at the site
Endocarditis
Disequilibration syndrome

53
Q

What are the main complications of peritoneal dialysis?

A

Peritonitis
Catheter blockage/infection
Fluid retention
Constipation
Hyperglycaemia
Hernias

54
Q

What are the main complications of renal transplantation?

A

Graft rejection
Disease recurrence
Opportunistic infection
Malignancy (esp lymphoma and skin cancer)
DVT/PE
Urinary tract obstruction

55
Q

The symptoms of renal failure that is not being adequately managed with RRT are:

A

breathlessness
fatigue/insomnia
pruritus
poor appetite
swelling
weakness
weight gain/loss
abdominal cramps and nausea
muscle cramps
headaches
cognitive impairment
anxiety and depression
sexual dysfunction

56
Q

One of the best ways to differentiate between AKI and CKD is renal ultrasound - most patients with CKD have bilaterally small kidneys.

Exceptions to this rule include:

A

autosomal dominant polycystic kidney disease
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy

57
Q

What feature on blood tests can help you to differentiate between acute and chronic kidney injury?

A

Calcium levels

Hypocalcaemia = CKD

In chronic kidney disease, the kidneys cannot activate vitamin D effectively, meaning less calcium is absorbed from the gut, causing its levels to fall.

58
Q

How can you prevent contrast induced nephropathy?

A

Volume expansion with 0.9% saline pre and post procedure

59
Q

What is required in all patients with AKI of unknown cause?

A

renal USS

60
Q

AKI with raised urinary sodium makes you think of…

A

acute tubular necrosis (ATN) (the most common renal cause of an AKI)

The kidneys lose their ability to retain sodium

61
Q

What is seen on histology in membranous glomerulonephritis?

A

basement membrane thickening on light microscopy
subepithelial spikes on silver stain
positive immunohistochemistry for PLA2

62
Q

How should membranous glomerulonephritis be managed?

A

all patients should receive an ACE inhibitor or an angiotensin II receptor blocker (ARB)

immunosuppression (only patients with severe or progressive disease) :
A combination of corticosteroid + another agent such as cyclophosphamide is often used

consider anticoagulation for high-risk patients- increased risk of VTE

63
Q

Prognosis of membranous glomerulonephritis?

A

rule of thirds:
one-third: spontaneous remission
one-third: remain proteinuric
one-third: develop ESRF

64
Q

What patient factors may affect eGFR result?

A

pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being taken

65
Q

What should be prescribed to reduce the rate of CKD progression in ADPKD?

A

Tolvaptan - selective vasopressin antagonist

reduces cell proliferation, cyst formation and fluid excretion

66
Q

What can be used to treat hyperphosphataemia in patients with CKD mineral bone disease?

A

Sevelamer - a non-calcium based phosphate binder

67
Q

How do you manage nephrogenic diabetes insipidus?

A

thiazides, low salt/protein diet

68
Q

What is the SALT LOSS mnemonic for sxs of hyponatraemia?

A

stupor
anorexia
lethargy
tendon reflexes decreased

limp muscles
orthostatic hypotension
stomach ache
seizures

Y3 Medicine (9 decks)

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