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General Medicine > Renal > Flashcards

Renal Flashcards

1
Q

What is the definition of oliguria

A

<0.5ml/kg/hr

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2
Q

How do you collect an MSU?

A

The aim is to collect urine from the bladder
Hold open labia/ retract foreskin
Pee into toilet then divert stream into sterile bottle
Do NOT touch the sample or bottle neck
Hand in ASAP

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3
Q

Action and SE or furesomide

A

Inhibit the K/ Na/ 2Cl transporter in the ascending loop of Henle resulting in massive NaCl excretion
Hypokalaemia is main side effect

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4
Q

Mechanism and SE of thiazides

A

Inhibit Na/Cl transporter in distal tubule
They also increase reabsorption of Ca
Low Na and K
Increased lipid and uric acid levels - CI in gout

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5
Q

Thiazides are CI in gout

A

Thiazides are CI in gout

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6
Q

Mechanism and SE of spironolactone

A

Aldosterone antagonist in collecting duct

Hyperkalaemia and gynaecomastia

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7
Q

What do urinary RBC casts prove?

A

Haematuria is glomerular in origin e.g. vasculitis, glomerulonephritis

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8
Q

What is the significance of tubular cast cells?

A

They occur only in acute tubular necrosis

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9
Q

Bacterial diagnosis of UTI

A

Growth of >10^5 organisms/ ml of fresh MSU

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10
Q

Presentation of prostatitis

A

Fever, back pain, possibly urinary symptoms + swollen or tender prostate on PR

Treat with analgesia and ciprofloxacin for 28 days

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11
Q

Uncomplicated UTI treatment

A 
Female = nitrifurantoin for 3 days
Males = 5 days
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12
Q

UTI in pregnancy

A

Nitrofurantoin for 7 days if trimester 1or 2

Trimethoprim for 7 days if trimester 3

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13
Q

Presentation of nephritic syndrome

A

Haematuria + proteinuria + RBC casts + high BP and progressive renal failure

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14
Q

Target BP for patients with glomerulonephritis

A

130/80

125/ 75 if proteinuria >1g/day

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15
Q

What is the commonest glomerulonephritis in the UK

A

IgA nephropathy
Typically a young male who presents with micro/macroscopic haematuria after a URTI.
IgA is elevated and deposited in mesangial cells causing inflammation
Role for immunosuppression with steroids/ cyclophosphamide

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16
Q

Anti-glomerular basement membrane

A

Goodpastures disease
Kidney biopsy will show crescenteric GN
Lungs are also involved resulting in pulmonary haemorrhage
Treatment = plasma exchange + steroids

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17
Q

Renal disease + lung symptoms

A

Goodpastures

Cresenteric GN caused by anti-glomerular basement membrane antibodies

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18
Q

Post strep throat is the commonest cause of a proliferative GN

A

It typically causes nephritic syndrome

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19
Q

What is the treatment for a patient with IgA nephropathy and rapidly deteriorating renal function?

A

Cyclophosphamide

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20
Q

HSP =

A

Purpuric rash + IgA nephropathy + polyarthritis

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21
Q

How does rapidly progressing GN presenting

A

Acute renal failure

Treat with high dose steroids, cyclophoshamide and plasma exchange (to remove existing antibodies)

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22
Q

Triad of nephrotic syndrome

A

Proteinuria (>3g/ 24 hours)
Hypoalbuminaemia (<25g/L)
Oedema

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23
Q

Periorbital oedema is relatively specific for renal disease e.g. nephrotic

A

Periorbital oedema is relatively specific for renal disease e.g. nephritic

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24
Q

What is the key diagnostic test for a patient with GN?

A

Kidney biopsy

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25
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change GN
Associated with Hodgkins
‘Fusion of podocytes’
Steroid are effective but relapse likely >need cyclophosphamide

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26
Q

Investigation shows fusion of podocytes?

A

Minimal change GN

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27
Q

What is the commonest cause of nephrotic syndrome in ADULTS?

A

Membranous nephropathy - associated with malignancy and drugs e.g. gold
Thickened GBM with IgG and C3 deposits
Risk of renal vein thrombosis

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28
Q

‘Tramline’ appearance of double basement membrane

A

Mesangiocapillary GN

RARE, presents with nephrotic syndrome

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29
Q

Focal segmental glomerulosclerosis can be primary or secondary to IgA nephropathy, sickle cell or HIV

A

Focal sclerosis on biopsy

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30
Q

General management points of GN

A 
Reduce Na intake
Moderate fluid intake
Diuretics
ACEI - very important 
Manage HT
Be aware that nephrotic syndrome (especially membranous nephropathy) is a hypercoagulable state > renal vein thrombosis is a problem
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31
Q

What is the effect of PTH?

A
  • Released in response to low Ca
  • increases osteoclasts activity to release calcium and phosphate
  • increased calcium and decreased phosphate reabsorption from kidneys
  • increases active vit D production
  • high calcium, low phosphate results
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32
Q

What are the symptoms of hyperparathyroidism?

A
  • due to increased calcium e.g. stones, bones, polyuria, polydipsia etc
  • due to bone damage e.g. fracture
  • HT = always check BP

Patients who are young, or symptomatic need a excision of the adenoma

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33
Q

Treatment option for patient with primary hyperparathyroidismn in which excision is unsuitable?

Also for patients with secondary hyperparathyroidism e.g. in renal failure

A

Cinacelet

It increases the sensitivity of parathyroid cells to Ca

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34
Q

Blood result for patient with secondary hyperparathyroidism?

A

High PTH
Low Ca
Caused by chronic renal failure or poor vit D intake
Treat with cinacelet

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35
Q

Tertiary hyperparathyroidism follows chronic secondary hyperparathyroidism

A

It results in high Ca with inappropriately high PTH

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36
Q

Features of MEN 1

A

Pituitary tumour
Pancreatic tumours
Parathyroid tumours

Associated with MEN 1 gene

Remember the 3P’s

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37
Q

Features of MEN 2a

A

The TAP features

Thyroid medullary carcinoma
Adrenal phaeochromocytoma
Parathyroid hyperplasia

Ret proto-oncogene is involved

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38
Q

Features of MEN 2b

A

The TAM one

Thyroid medullary carcinoma
Adrenal phaeochromocytoma
Marfinoid appearance

Related to ret oncogene

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39
Q

Which hormone stimulates the release of ACTH from the anterior pituitary?

A

Corticotrophin releasing hormone from the hypothalamus

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40
Q

Name the 3 classes of steroids release by the adrenal cortex

A

1) Glucocorticoids - e.g. cortisol involved CHO and lipid metabolism
2) Mineralocorticoids e.g aldosterone involved in Na and Water balance
3) Androgens e.g. tesotosterone

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41
Q

Cushing’s syndrome can be caused in ACTH dependant causes e.g.

  • Cushing’s disease = adrenal hyperplasia from a ACTH secreting pituitary tumour
  • Ectopic ACTH production e.g. small cell lung cancer
A

Can also be from ACTH independent causes e.g.

Iatrogenic - high dose steroids
Adrenal adenoma/ cancer

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42
Q

2 steps in diagnosing Cushing’s disease

1 - identify raised cortisol level
2 - find the cause (1st line is overnight dexamethasonen suppression test)

In a normal person, cortisol should reduce to <50nmol/L

A

In Cushing’s disease a high dose dexamethasone may be enough to suppress cortisol - this is not the case in ectopic ACTH production

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43
Q

Investigation for lady with suspected Addison’s disease?

Low Na, high K and low glucose due to low mineralocorticoid and cortisol level

Remember this is adrenal insufficiency with the potential for life threatening hypovolaemia to occur

A

Short synacthen test

  • Primary Addison’s e.g. autoimmune destruction
  • TB
  • adrenal mets
  • sepsis
  • adrenal haemorrhage

All are potentials

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44
Q

High ACTH can lead to pigmentation. This helps distinguish primary (hyperpigmentation) and secondary (no -pigmentation) adrenal insufficiency

A

Long term steroid therapy is commonest secondary cause

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45
Q

Management of hyperaldosteronism?

A

Conn’s = surgically remove the singular adenoma and use spironolactone for BP and K control for 4 weeks pre-op

Bilateral adrenal enlargement = spironolactone or eplerenone (no gynaecomastia)

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46
Q

What is the classic triad of phaeochromocytoma?

A

Episodic headache
Sweating
Tachycardia

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47
Q

Management of phaeochromocytoma?

A

Diagnosed with 3 x 24hr urinary catecholamines

Surgical removal of the catecholamine producing tumour

Use ALPHA blocker first (phenoxybenzamine BEFORE beta blocker!

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48
Q

Refractory HT and low K

A

Exclude:

1) Renal artery stenosis
2) Conn’s disease

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49
Q

Differtial diagnosis of hirsutism?

A

Excess androgen secretion has several causes:

1) Ovarian secretion e.g. PCOS or ovarian cancer
2) Adrenal secretion e.g. Cushing’s or carcinoma
3) Drugs e.g. steroids

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50
Q

Definition of acute renal failure

A

Significant reduction in renal function resulting in an increase in serum creatinine and urea

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51
Q

What are the 3 main complications of acute renal failure e.g. that people die of?

A

1) Volume overload
2) Hyperkalaemia
3) metabolic acidosis

Urine output is so important - measure continuously

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52
Q

What is acute tubular necrosis?

A

Damage to renal tubular cells due to ischaemia or nephrotixins
E.g. drugs, radiology contrast, rhabdomyolysis or myeloma

53
Q

In pre-renal failure, the urine is concentrate and sodium is reabsorbed by working tubular cells:
Urine Na will be low and urine osmolarity high

A

In ascute tubular necrosis this does not happen so urine sodium is high and urine osmolality is low

54
Q

Management of acute renal failure

A

1) History, Examination and investigations - especially U&E and urinalysis
2) Identify and stop any nephrotixic drugs
3) Treat any reversible causes e.g. fluids for hypovolaemia
4) Insert catheter - daily fluid balance
5) Correct any underlying cause e.g. antibiotics

55
Q

What are the indications for dialysis in patients with acute renal failure?

A

1) Hyperkalaemia (>7)
2) Severe Metabolic acidosis (pH <7.2)
3) Refractory pulmonary oedema
4) Uraemic encephalopathy

56
Q

What are the classifications for different degrees of chronic renal failure?

A 
1 = GFR>90
2 = 60 -89 
3a = 45-59
3b = 30-44
4 =15-29
5 = <15
57
Q

Define end stage renal failure

A

GFR< 15 or need for dialysis

58
Q

Causes of chronic renal failure?

A 
DM
HT
GN
Polycystic kidney disease 
Myeloma
59
Q

Symptoms of uraemia/ renal failure

A

Pallor, yellow skin, pigmentation, easy bruising etc

60
Q

What is the main cause of death in patients with chronic renal disease?

A

Cardiovascular disease

61
Q

List some nephrotoxic drugs!

A 
ACEI
Digoxin
Trimethoprim
Gentamicin
Ethambutol (TB drug)
Lithium
Tetracycline
62
Q

Target BP in patients with CKD

A

140/85

130/80 diabetic - all people with DM and kidney disease should be on an ACEI, regardless of BP

63
Q

Indications for renal biopsy

A

Unexplained acute renal failure
Nephritic syndrome
Systemic disease e.g. SLE

(Remember that biopsy is useless in chronic disease as kidneys are often small, shrunken and will bleed - A LOT)

64
Q

What are the complications of heamodialysis?

A

1) Disequilibrium syndrome e.g. nausea, vomiting, headache and confusion/ seizure due to rapid changes in plasma osmolality
2) Fistula problems e.g. thrombosis, infection, stenosis etc
3) Time consuming and expensive

65
Q

What are the complications of peritoneal dialysis?

A

1) Peritonitis
2) Loss of membrane effectiveness
3) Tenchkoff catheter problem e.g. infection

66
Q

What are the complications of renal replacement therapy?

A

Cardiovascular disease
Platelet dysfunction —> bleeding tendency
Anaemia
Renal bone disease

67
Q

Complications of kidney transplant?

A

1) Acute graft rejection - rising urea, fever and flank pain
2) Chronic graft rejection
3) Infection - immunocompromised due to drugs
4) Malignancy - immunocompromised due to drugs
5) Hypertension - unknown

68
Q

Balkan nephropathy

A

Common cause of progressive renal impairment along the river Danube
Causes anaemia, glycosuria, skin pigmentation of hands and soles

69
Q

Urate nephropathy

A
  • acute crystal nephropathy
  • most common in lymphoma and other chemo patients
  • renal tubules fail due to precipitation of urate crystals
  • plasma urate very high and bright renal parenchyma on US
  • bifringent crystals on microscopy
  • prevent with fluids, allopurinol before chemo and sodium bicarbonate to alkalize urine
70
Q

How to prevent radiocontrast nephropathy?

A

1) Identify high risk patients e.g. DM, poor renal function
2) Stop nephrotoxic drugs pre procedure e.g. metformin
3) Prehydrate with saline
4) Consider IV acetylcysteine/ sodium bicarbonate to alkalize and protect kidneys

71
Q

How does rhabdomyolysis cause renal failure?

A

1) Release of muscle breakdown components e.g. myoglobin, K, phosphate, urea and creatinine
2) myoglobin is filtered by the glomeruli and precipitates —> blocked renal tubules
3) beware brown pee!

72
Q

What is the ‘gold standard’ investigation for a suspected renovascular disease?

Remember renovascular disease is essentially renal artery stenosis due to atherosclerosis, post-renal transplant or a giant cell arteritis

A

Renal angiography

(Done after US (uneven kidney size) and CT/ MRI

73
Q

HUS leads to intravascular haemolysis and red cell fragmentation —> thrombocytopenia and ARF .
90% are due to 0157. What will the blood film show?

A

Fragmented RBC (shistocytes)

74
Q

What are the 6 features of thrombotic thrombocytopenia purpura? TTP

A

1) Fever
2) Fluctuating CNS signs e.g. seizures
3) Haemolytic anaemia (microangipathic)
4) Haematuria/ proteinuria
5) Low platelets
6) Renal failure

This is a medical emergency precipitated by some drugs e.g. clopidogrel
Consider in anyone with unexplained anaemia and thrombocytopenia
Treat with plasma exchange +/- steroids, immunoglobulin or splenectomy

75
Q

What is renal tubular acidosis (RTA)?

A

Metabolic acidosis due to impaired renal function
Type 1 = distal —> impaired excretion of H+ ions from the distal tubule e.g. Treatment is with sodium bicarbonate but complications are renal calculus
Type 2 = proximal —> impaired reabsorption of bicarbonate ions from the proximal tubule —> excess bicarbonate in urine (Faconi syndrome is a common cause)

76
Q

Associations of AD polycystic kidney disease

A

1) Liver cysts
2) Intracranial anuerysms —> SAH
3) Mitral valve prolapse

Features of the disease itself = loin pain, haematuria, HT and renal failure

77
Q

Medullary cystic disease

A

Rare inherited kidney disorder

1) Tubular loss —> polyuria, polydipsia, salty wasting
2) Medullary cysts —> shrunken kidney, ESRF
3) Extra-renal —> retinal changes, skeletal changes etc

78
Q

Alport’s syndrome

A

1) type 4 collagen disease
2) haematuria, proteinuria and progressive renal failure
3) sensorineural deafness
4) lens defects

79
Q

Indication for fluid resuscitation

A

Signs of being systemically unwell e.g. NEWS 5 or more

Tachycardia
Hypotension
Cold peripheries
Cap refill> 2seconds 
Rapid resp rate etc
80
Q

Regime for patient needing fluid resuscitation

A 
500ml NaCl bolus over <15minutes
Reassess using ABCDE approach
Give repeated 500ml bolus as required
Keep reassessing
In HF patient, consider 250ml bolus after initial 500ml bolus
81
Q

What are daily fluid requirements for maintenance?

A

30ml/kg water
1mmol/L Na, K and Cl
50-100g/day glucose

82
Q

What is the maximum rate of delivery of K?

A

10mmol/L

E.g. if you add 40mmol to a bag then you can only give that bag over 4 hours

83
Q

What test should be done at every diabetic review to assess for signs of nephropathy?

A

Early morning albumin: ratio

>3 = bad

84
Q

Causes of a metabolic acidosis with a normal and increased anion gap

A

Anion gap = (Na + K) - (Cl + HCO3)
Gap is increased in the presence of the molecules such as ketones, phosphate etc
Normal anion gap = ABCD (Addisons, bicarbonate loss, chloride retention and rugs such as acetazolamide)
High anion gap = DKA, renal failure, dehydration, salicylic acid etc

85
Q

What is dabigatran?

A

A direct thrombin inhibitor

86
Q

Mechanism of action of rivaroxiban and apixiban?

A

Direct factor Xa inhibitors

87
Q

What is the cause of secondary hyperparathyroidism?

A

Usually due to Vit D deficiency (e.g. renal failure) which prevents calcium being absorbed –> increase in PTH

88
Q

What is the commonest inherited thrombophilia in the UK?

A

Factor V leiden deficiency

Factor 5 is a clotting factor, in this disease the clotting factor is inactivated 10 times faster –> bleeding

89
Q

Investigations in a young patient with unprovoked DVT?

A 
FBC
CXR
UE, LFT
CT pelvis if initial tests ok --> need to look for underlying malignancy 
Anti-phospholipid screen
90
Q

List 4 ‘common’ causes of polyuria

A

1) heart failure
2) Caffeine/ alcohol
3) lithium
4) dm

91
Q

US finding of a patient with diabetic nephropathy

A

Bilaterally enlarged kidneys (unusual - other types of chronic renal disease e.g. HT etc cause shrunken kidneys)

92
Q

What is the classification of different grades of AKI?

A 
1 = creatinine 1.5-1.9 x baseline + <0.5ml/kg/hr for 6 hours
2 = creatinine 2-2.9 x baseline + <0.5ml/kg/hr for 12 hours
3 = creatinine >3 x baseline or >354 + <0.3ml/kg/hr for 24  hours or anuric
93
Q

What is the commonest cause of infection in patient with peritoneal dialysis?

A

Staph epidermidis

94
Q

What is the 60, 40 , 20 rule?

A

60% of body weight is water
40% is intracellular
20% is extra cellular

95
Q

Cation = +

A

Anion = -ve

96
Q

Which drug causes blue/green pee?

A

Amitryptilline

Propofol

97
Q

Give a cause of hyaline casts?

A

Diuretics

98
Q

Cause of red cell casts?

A

Glomerulonephritis/ vasculitis

99
Q

Epithelial cells in urine microscopy?

A

Acute tubular necrosis/ Glomerulonephritis

100
Q

Nephrotic syndrome?

A

1) Proteinuria >3.5g/day
2) hypoalbuminaemia
3) oedema
4) Hyperlipidaemia and lipiduria

101
Q

Minimal change = commonest GN in children

A

Damage to podocytes foot process
Usuallly idiopathic
Associated with Hodgkin’s Lymphoma

102
Q

How does the membrane in membranous GN look?

A

Thickened
Immune complexes
SPike and dome pattern

103
Q

List some causes of focal segmental glomerulosclerosis?

A

Sickle cell
HIV
Heroin abuse

Segmental sclerosis and hyalinosis on histology

104
Q

List some causes of rapidly progressive glomerulonephritis?

A

Type 1 = ANti-GBM antibodies e.g. goodpasture (linear)
Type 2 = Immune complex e.g. IgA or SLE (granular)
Type 3 = ANCA e.g. Churg Strauss (negative)

All cause formation of crescent shape in glomerulus due to inflammation

105
Q

What are the features of nephritic syndrome?

A 
Haematuria
Proteinuria (mild)
Raised BP
Rapid decline in eGFR
Casts

(Post-streptococcal, SLE, Goodpastures, ANCA)

106
Q

Remember people with nephrotic syndrome are hypercoagulable so are at increased risk of thrombosis

A

The high cholesterol may be an important cause of this

107
Q

What are the key features of HUS?

A

1) Microangiopathic haemolytic anaemia (inappropriate clots act as boulder which break up the RBC)
2) Low platelets (the platelets are used up forming inappropriate clots)
3) Uraemia (due to clots in the kidneys causing renal damage —> proteinuria, haematuria)

Remember TTP is HUS + fever + neuro signs e.g. confusion and seizure - it is caused by lack of an enzyme (ADAMTT) which breaks up clots)

108
Q

Remember that autosomal PKD causes renal failure in utero leading to oligohydramnios

A

Other complications occur in liver, bile ducts and lungs

109
Q

List some risk factors for renal artery stenosis?

A

1) Coronary/ carotid artery disease
2) PVD
3) Smoking/ obesity
4) DM

110
Q

Why does renal artery stenosis cause hypertension?

A

The kidney senses low blood flow and acts as though pressure is low (not as if there is a block) —> activate RAAS to raise BP

111
Q

The macula densa cells detect Na in reabsorbed fluid. If BP is low then less Na will be absorbed —> low BP detected —> release of prostaglandins to encourage juxtaglomerular apparatus to release renin

A

The macula densa cells detect Na in reabsorbed fluid. If BP is low then less Na will be absorbed —> low BP detected —> release of prostaglandins to encourage juxtaglomerular apparatus to release renin

112
Q

MR angiogram shows a string of beads…

A

Fibromuscular dysplasia

An important cause of renal artery stenosis —> hypertension

113
Q

The indications for dialysis in renal failure can be remembered as 4PE

A

4P:

  • pH <7.2
  • Potassium >6.5
  • Pulmonary oedema
  • pericarditis
  • Encephalopathy
114
Q

In HT renal disease the afferent artery becomes thickened which reduces blood supply to the kidney —> Ischaemic

A

In DM kidney disease, glucose sticks to the efferent arteriole which causes it to stiffen and causes pressure to back up into the kidney
—> hyperfiltration

Rates causes of chronic kidney disease:

  • SLE
  • RA
  • PKD
115
Q

In CKD less K and urea are excreted —> build up

A

The kidney normally helps activate vit D which increases absorption of calcium —> in CKD Ca is low —> bone resorption occurs

EPO levels falls —> low production of blood cells —> normochromic anaemia

116
Q

What is the investigation of choice for reflux nephropathy?

A

Micturating cystography

117
Q

Eosinophilic casts are suggestive of chronic pyelonephritis

A

Waxy casts indicate low urine flow e.g. in renal failure

118
Q

As well as causing an acute myositis, steroids can also cause rhabdomyloysis

A

All NSAIDs should be stopped in an AKI expect for low-dose aspirin which will do not harm

119
Q

Classic ABG in a septic patient?

A

Metabolic acidosis with raised anion gap (due to production of lactate)

Raised gap = increased production or reduced excretion e.g. renal failure or DKA

120
Q

Lab results of osteoporosis?

A

DEXA z -2.5

121
Q

Lab results of osteomalacia?

A

Low Ca
Low phospahte
High Alk Phos

(Remember that osteomalacia in children = rickets)

122
Q

Lab results of Paget’s?

A

Isolated high alk phos

ca and phosphate are normal

123
Q

Lab results in myeloma?

A

Ca high
Phospahte high/ normal
Alk phos normal

Hence jones proteins

124
Q

Lab results in bony mets?

A

Ca and alk phos high

Phospahte high/ normal

125
Q

Hyaline casts

A

Can be normal OR due to diuretic use

126
Q

Anti-streptolysin antibodies?

A

In a nephritic syndrome, suggests post- strep glomerulonephritis

127
Q

What is the renal cause of flash pulmonary oedema?

A

Renal artery stenosis

128
Q

Generally, what is the indication to start dialysis in CKD?

A

GFR <10ml/min or <15ml/min in diabetics

General Medicine (6 decks)

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