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Renal medicine > Renal medicine > Flashcards

Renal medicine Flashcards

1
Q

What are the 2 most common causes of CKD?

A
  1. HTN

2. DM

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2
Q

How much urine is produced by the kidneys each day?

A

1-1.5L

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3
Q

What are the 4 main functions of the kidneys?

A
  1. excretion (drugs and waste products)
  2. Homeostasis (inc acid-base balance)
  3. endocrine (renin, erythropoietin and prostoglandins)
  4. metabolism (vit D)
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4
Q

Where in the abdomen are the kidneys positioned?

A

retroperitoneal

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5
Q

What are the 2 types of nephrons?

A

This depends on the size of the nephron:

  1. cortical nephrons (85%)
    - renal corpuscle in outer part of cortex
    - short loop of henle
  2. juxtamedullary nephrons (15%)
    - larger renal corpuscle in inner 3rd of cortex
    - long loop of henle extending into medulla
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6
Q

What % of CO do the kidneys receive?

A

20-25%

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7
Q

How much of total erthyropoietin is produced by the kidneys?

A

85%

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8
Q

What is the half life of EPO?

A

5hrs

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9
Q

What stimulates the production of EPO?

A
  1. hypoxia
  2. anaemia
  3. renal ischaemia
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10
Q

What is the active metabolite of vitamin D ?

A

1,25-dihydroxycholecalciferol

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11
Q

List some congenital abnormalities of the kidneys.

A
  1. agenesis of the kidney
  2. hypoplasia
  3. ectopic
    4 horseshoe
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12
Q

What is potter’s syndrome?

A
  1. bilateral renal agenesis
  2. oligohydramnios
  3. pulmonary hypoplasia

it is incompatible with life

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13
Q

what is a horseshoe kidney?

A

fusion of the 2 kidneys at the lower poles
more common in boys than girls
prone to reflux, obstruction, infection and stone formation

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14
Q

What are mesangial cells?

A

specialised smooth muscle cells that support the glomerulus and regulate blood flow and GFR

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15
Q

What causes renin release from the macula densa (DCT)?

A 
low BP (detected by baroreceptors)
low NaCl
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16
Q

What is the function of PCT?

A
  1. 70% total Na reabsorption
  2. reabsorption of aa, glucose, cations
  3. bicarbonate reabsorbed (using carbonic anhydrase)
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17
Q

What electrolyte channel is found in the thick ascending limb of the loop of Henle?

A

NKCC2 (Na/K/2Cl triple symporter)

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18
Q

What electrolyte channel is found in the DCT?

A

NCC (NaCl co-transporter)

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19
Q

What is the function of the thick ascending loop of henle?

A

creation of osmolality gradient

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20
Q

Where is calcium reabsorbed in the nephron?

A

DCT

calcium reabsorption is under the control of PTH

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21
Q

What electrolyte channels are found in the medullary collecting ducts?

A

ENaC (basolateral aldosterone-sensitive Na/K pump)

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22
Q

What is the function of the cortical collecting duct?

A

regulation of water reabsorption

controlled by AQP2 channels

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23
Q

List the 5 classes of diuretics.

A
  1. carbonic anhydrase inhibitors
  2. loop diuretics
  3. thiazide diuretics
  4. potassium-sparing diuretics
  5. osmotic diuretics
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24
Q

What is the MOA of loop diuretics?

A

inhibit NKCC2 symporter in thick ascending limb
causes massive NaCl, K and Ca excretion

SEs: hypokalaemia, ototoxic, metabolic alkalosis

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25
Q

What is the MOA of thiazide diuretics?

A

inhibit NCC co-transporter in DCT
moderate NaCl excretion, increased calcium reabs.

SEs: hypokalaemia, hyperglycaemia, inc. urate

CI in gout

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26
Q

What are the side effects of potassium sparing diuretics?

A
  1. hyperkalaemia

2. gynecomastia (anti-androgenic)

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27
Q

What drugs cause haematuria?

A
  1. NSAIDs
  2. ciprofloxacin
  3. furosemide
  4. cephalosporins
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28
Q

What are the renal causes of haematuria?

A
  1. infection (pyelonephritis)
  2. inflammation/trauma
  3. neoplasm
  4. immune (glomerulonephritis)
  5. congenital (PCK)
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29
Q

What is the triad of nephrotic syndrome?

A
  1. proteinuria (>3.5g/24hr)
  2. hypoalbuminaemia
  3. oedema

NB hyperlipidaemia is often present

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30
Q

What are the 4 histological patterns of nephrotic syndrome?

A
  1. minimal change
  2. membranous nephropathy
  3. mesangiocapillary glomerulonephritis
  4. focal segmental glomerulosclerosis (FSGS)
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31
Q

What is the commonest type of nephrotic syndrome in children?

A

minimal change

90% undergo remission with steroids
if frequently relapsing or steroid-dependent give ciclosporin/tacrolimus

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32
Q

How is urea produced?

A

from ammonia by the liver in ornithine cycle

increased in dehydration as decreased flow increases urea

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33
Q

What happens to urea and creatinine in renal failure?

A

increase

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34
Q

What factors are considered when calculating eGFR?

A

serum creatinine
sex
age
race

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35
Q

Name some nephrotoxic drugs.

A
  1. NSAIDs
  2. ACEi
  3. gentamicin
  4. amphotericin (anti-fungal)
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36
Q

What ECG changes would you be worried about in AKI?

A

hyperkalaemia:

  • tall tented T waves
  • flattened P waves
  • increased PR interval
  • widened QRS
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37
Q

What are the risk factors for AKI?

A 
>75y/o
CKD
HF
PVD
diabetes
sepsis 
history of urinary symptoms
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38
Q

What will you see on blood film with haemolytic uraemic syndrome?

A

red cell fragmentation

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39
Q

What is the triad for haemolytic uraemic syndrome?

A
  1. microangiopathic haemolytic anaemia (Coomb’s negative)
  2. AKI
  3. thrombocytopenia
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40
Q

What is the most common cause of AKI in children?

A

haemolytic uraemic syndrome

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41
Q

What are patients at risk of if taking metformin with a rising creatinine?

A

lactic acidosis

stop metformin if creatinine >150mM

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42
Q

What are the complications of uraemia?

A

encephalopathy
pericarditis

treat with dialysis

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43
Q

What is the management of hyperkalaemia?

A

K>6-7mmol/L requires urgent treatment

  1. 10ml of 10% calcium gluconate over 2 mins
    - repeat as necessary until ECG improves
    - cardioprotective
  2. insulin and glucose
    - 10units actrapid in 50ml 20% glucose
    - drives potassium into cells
    - aim to low serum K by 1-2mmol/L over 60mins
  3. salbutamol nebuliser (10-20mg)
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44
Q

What is the complication of hyperkalaemia?

A

ventricular fibrillation

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45
Q

What staging system is used for AKI?

A

KDIGO

kidney disease improving global outcomes

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46
Q

What is the criteria for diagnosing AKI?

A

KDIGO:

  1. > 26micromol/L rise in creatinine in 48hrs
  2. > 1.5x rise in creatinine from baseline
  3. urine output <0.5ml/kg/hr for >6 consecutive hrs
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47
Q

What are the life-threatening complications of AKI?

A

hyperkalaemia

pulmonary oedema

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48
Q

How do you treat pulmonary oedema?

A
  1. oxygen - consider CPAP
  2. IV GTN
  3. IV furosemide 80-250mg
  4. IV diamorphine 2.5mg (venous vasodilator) + 10mg metoclopramide
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49
Q

Define AKI.

A

A significant decline in renal function over hours to days manifesting as an abrupt and sustained increase in creatinine and urea

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50
Q

What are the indications for acute dialysis?

A
  1. refractory pulmonary oedema
  2. persistent hyperkalaemia (>7mmol/L [3.5-5])
  3. symptomatic uraemia
  4. severe metabolic acidosis (pH<7.2)
  5. poisoning (aspirin - salicylate level >700mg/L)
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51
Q

What is the most likely cause of nephrotic syndrome is adults?

A

membranous nephropathy

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52
Q

What is Goodpasture’s?

A

anti-GBM antibodies against type IV collagen found in glomerular and alveolar basement membranes

haematuria + haemoptysis

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53
Q

What are the Sx of acute nephritis syndrome?

A
  1. oliguria
  2. haematuria
  3. proteinuria
  4. uraemia
  5. fluid retention
  6. HTN
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54
Q

What is an early indicator of glomerulosclerosis in diabetic patients?

A

microalbuminuria

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55
Q

Where does the majority of bicarbonate reabsorption occur?

A

90% in PCT

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56
Q

How do the convoluted tubules regulate body pH?

A

the reabsorption of bicarbonate

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57
Q

How does PTH affect kidneys handling of phosphate?

A

decreases phosphate reabsorption in the PCT

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58
Q

What treatment of hyperkalaemia actually removes potassium from the body?

A

calcium resonium

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59
Q

List some drugs that cause tubulointerstital nephritis.

A
  1. NSAIDs
  2. penicillin
  3. gold
  4. rifampicin
60
Q

Which part of the nephron is impermeable to water?

A

thin and thick ascending limbs

61
Q

Where is body fluid osmolality detected?

A

hypothalamus

triggers release of ADH

62
Q

Why might a psych patient taking lithium develop an abnormality in their serum osmolality ?

A

nephrogenic diabetes insipidus

63
Q

What is Conn’s syndrome?

A

primary hyperaldosteronism

overproduction of aldosterone causes fluid retention and hypertension

64
Q

Which fluid compartment contains the greatest volume of water?

A

intracellular fluid

65
Q

What does aldosterone do to electrolyte levels

A

causes reabsorption of sodium (increases sodium therefore increases ECF volume) and increases the excretion of potassium (lowers serum potassium)

66
Q

What process takes place in the kidneys when the baroreceptors detect hypotensive state?

A

increased sympathetic tone triggers the release of renin from the macula densa

67
Q

List some causes of secondary HTN.

A
  1. Cushing’s
  2. Conn’s
  3. oestrogen
  4. phaeochromocytoma
68
Q

How would adrenal insufficiency affect BP?

A

hypotension

69
Q

Why do you get a dry cough with ACEi?

A

inhibition of the breakdown of bradykinin

70
Q

Which diuretics cause hypokalaemia?

A

thiazide diuretics

loop diuretics

71
Q

What is the most common type of renal stone?

A

calcium oxalate (alkaline urine)

72
Q

What is adult PCK disease associated with? And what does this put these patients at risk of?

A

associated with berry aneurysms

at risk of SAH (PC: thunderclap headache)

73
Q

What can patients develop after a long time on dialysis?

A

acquired cystic disease

74
Q

What symptom triad do you get with renal cell carcinoma?

A
  1. frank haematuria
  2. flank pain
  3. loin mass
75
Q

What is the most common malignant renal tumour in children?

A

Wilm’s tumour

Most commonly occurs aged 1-4

76
Q

Describe the synthesis and storage of ADH.

A
  • ADH is a peptide hormone
  • it is synthesised in the supraoptic nucleus of the hypothalamus as a large precursor molecule
  • it is transported to the posterior pituitary gland
77
Q

What drugs affect ADH release?

A

increase ADH release:

  • nicotine
  • ether
  • morphine
  • barbiturates

inhibit ADH release:
- alcohol

78
Q

What are the CKD stages and their respective eGFRs?

A 
stage 1 >90
stage 2 60-89
stage 3a 45-59
stage 3b 30-44
stage 4 15-29
stage 5 <15
79
Q

How does HTN affect the size of the kidney?

A

makes it smaller

80
Q

What conditions result in an enlarged kidney?

A

diabetes
PKD
RCC
renal mets

81
Q

What is a sign of renal artery stenosis?

A

renal bruit

82
Q

What is the management of nocturnal enuresis?

A

desmopressin nasal spray

–> can be caused by a reduction in circulating ADH at night time

83
Q

What is the normal plasma osmolality (Posm)?

A

285-295mOsmol/kg H2O

84
Q

What is the maximum urine osmolality?

A

1400mOsm/kg H20

85
Q

define hyponatraemia.

A

plasma sodium <130mmol/L

86
Q

What are the causes of SIADH?

A
  1. CNS: abscess, stroke, SLE
  2. malignancy: small cell carcinoma of lungs
  3. lung disease: TB, pneumonia, aspergillosis
  4. drugs: opiates, chlorpropamide, oxytocin
  5. metabolic disease: porphyria, hypothyroidism
  6. other: pain, GBS, trauma
87
Q

What is diabetes insipidus?

A

the inability to reabsorb water from the distal part of the nephron due to failure of secretion/action of ADH

88
Q

What are the symptoms of diabetes insipidus?

A
  1. polyuria
  2. polydipsia
  3. low urine osmolality (dilute urine)
89
Q

What are the 2 types of diabetes insipidus?

A
  1. neurogenic

2. nephrogenic

90
Q

What is the cause of thrombotic thrombocytopenia purpura (TTP)
?

A

genetic/acquired deficiency of ADAMTS13

91
Q

What is rhabdomyolysis and how does it affect the kidneys?

A
  • muscle breakdown leading to the release of myoglobin into the blood
  • myoglobin is freely filtered by the kidneys
  • if the filtrate is acidic the myoglobin precipitate forming casts which block the normal flow of urine through tubules
  • causes v high creatine kinase and hyperkalaemia
92
Q

What is acute tubular necrosis?

A

the result of acute tubular cell damage by ischaemia of toxins

hyperkalaemia can develop

93
Q

What is Fanconi syndrome?

A

disturbance of PCT function leading to generalised impaired absorption

94
Q

List some complications of acute pyelonephritis.

A
  1. renal papillary necrosis
  2. perinephric abscess
  3. pyonephrosis (obstruction of pelvicalyceal system)
  4. chronic pyelonephritis
  5. fibrosis and scarring
95
Q

What are the risk factors for acute pyelonephritis?

A
  1. urinary tract obstruction
  2. vesicoureteric reflux
  3. instrumentation of urinary tract
  4. sexual intercourse
  5. DM
  6. immunosuppression
96
Q

What is the most common cause of chronic pyelonephritis?

A

reflux nephropathy (associated with vesicoureteric reflux which is congenital)

97
Q

What is found on histological examination for chronic pyelonephritis?

A

interstitial fibrosis
dilated tubules containing eosinophilic casts

(NB USS kidney is shrunken, scarred and misshapen)

98
Q

List the 2 hereditary nephritis syndromes.

A
  1. Alport’s syndrome

2. Fabry’s syndrome

99
Q

What is Alport’s syndrome?

A
  • X-linked disorder affecting basement membrane collagen IV
  • they lack the Goodpasture’s antigen
  • KIDNEY: glomerulonephritis + haematuria
  • EYES: lens dislocation, cataract, cornical cornea
  • EARS: sensorineural deafness
  • also associated with platelet dysfunction and hyperproteinaemia
100
Q

What is Fabry’s syndrome?

A
  • rare X linked disorder
  • deficiency of galacto-sidase A
  • accumulation of ceramide trihexoside in kidneys, skin and vascular system
101
Q

What are the secondary causes of glomerulonephritis?

A
  1. post-strep glomerulonephritis
  2. non-strep glomerulonephritis
  3. SLE
  4. HSP
  5. bacterial endocarditis
  6. diabetic glomerulosclerosis
  7. amyloidosis
  8. goodpasture’s syndrome
102
Q

What are the causes of asymptomatic haematuria?

A
  1. IgA nephropathy
  2. think basement membrane
  3. Alport’s syndrome
103
Q

At what stage of CKD do symptoms occur?

A

stage 4

104
Q

At what stage of CKD is renal replacement therapy required?

A

stage 5

105
Q

What are the 2 main categories of glomerulonephritis?

A
  1. nephrotic syndrome

2. nephritic syndrome

106
Q

What immune cells are thought to be involved in damage of the glomerulus?

A
  1. macrophages

2. T lymphocytes

107
Q

What is the general management of nephrotic syndrome?

A
  1. reduce oedema
    - furosemide
    - check daily weights and U&Es
    - fluid and salt restrict
  2. reduce proteinuria
    - ACEi/ARB for all pts
    - they reduce proteinuria and preserve renal function
  3. decrease risk of complications
    - statin to reduce cholesterol
    - anticoagulant if hypercoagulable
    - blood pressure control
  4. treat underlying cause
108
Q

What are the 4 primary causes of nephrotic syndrome?

A
  1. minimal change
  2. membranous nephropathy
  3. focal segmental glomerulosclerosis (FSGS)
  4. mesangiocapillary GN
109
Q

What does a kidney biopsy of minimal change disease show?

A
  • normal under light microscopy

- electron microscopy shows effacement of podocyte foot processes

110
Q

How do you treat minimal change disease?

A
  1. steroids

if frequent relapsing give cyclophosphamide/ciclosporin

prognosis good only 1% go on to ESRD

111
Q

What are the biopsy findings in membranous nephropathy?

A
  1. diffusely thickened GBM

2. subepithelial deposits of immune complexes - IgG + C3

112
Q

How do you treat membranous nephropathy?

A

immunosuppress pt if renal function declines

113
Q

How do you treat FSGS?

A
  1. steroids

2. OR cyclophosphamide/ciclosporin

114
Q

What are the subtypes of mesangiocapillary glomerulonephritis?

A

Type 1 (more common)

  • immune complex mediated
  • immune complexes deposited in kidneys
  • activates classical pathway
  • causes inflammation and capillary thickening

Type 2 (less common)

  • activation of alternative complement pathway
  • thickened capillaries caused by C3 deposition
115
Q

What is the most common type of glomerular disease worldwide?

A

IgA nephropathy (Berger’s disease)

116
Q

What are the renal biopsy findings for IgA nephropathy?

A

immune complex deposition of IgA and C3 in the mesangium

117
Q

What would be a typical history preceeding diagnosis of IgA nephropathy?

A

young man presents with recurrent haematuria post URTI

118
Q

What are the 4 primary causes of glomerulonephritis presenting with nephritic syndrome?

A
  1. IgA nephropathy
  2. rapidly progressive GN
  3. focal proliferative GN
  4. mesangiocapillary GN
119
Q

What are the 3 subtypes of rapidly progressive GN?

A

type 1
- anti-GBM

type 2

  • immune complex deposition
  • SLE, post=strep

type 3

  • pauci immune
  • cANCA = GPA
  • pANCA = churg strauss
120
Q

What is HSP and what are the systems affected?

A

immune-mediated (IgA) small-vessel vasculitis presenting with:

  1. purpura (over buttocks and extensor surfaces)
  2. glomerulonephritis
  3. abdo pain +/- intussusception
  4. polyarthritis
121
Q

What factors increase the risk of having SLE?

A
  1. female
  2. Asian
  3. HLA B8-, DR2-, DR3- positivity
122
Q

How does SLE affect the kidneys?

A
  1. immune complex deposition in glomerulus
  2. basement membrane thickening
  3. endothelial proliferation
123
Q

What are the main deposit sites of renal calculi?

A
  1. pelviureteric junction
  2. pelvic brim
  3. vesicoureteric junction
124
Q

Which type of calculi are likely to form in acidic urine?

A
  1. cystine

2. uric acid crystals

125
Q

Which type of calculi are likely to form in alkaline urine?

A
  1. calcium oxalate
  2. calcium phosphate
  3. magnesium ammonium phosphate
126
Q

Why should you do early morning urine sample?

A

to avoid orthostatic proteinuria

127
Q

What causes a staghorn calculus ?

A

struvite

128
Q

What is pyonephrosis?

A

infected hydronephritis

129
Q

What is the general management of renal stones?

A
  1. analgesia - diclofenac
  2. antibiotics if infected - cefuroxime/gentamycin
  3. IV fluids
130
Q

What is medical expulsive treatment for renal calculi?

A
  1. CCB e.g. nifedipine
  2. OR alpha-blocker e.g. Tamsulosin

they promote expulsion of the stone (<10mm), decrease pain relief requirements and reduce ureteric spasms

131
Q

List the 2 hereditary hypokalaemic tubulopathies.

A
  1. Bartter syndrome
    - mutation in co-transporter targeted by loop diuretics
    - therefore similar pattern
  2. Gitelman syndrome
    - mutation in co-transporter targeted by thiazide diuretics
    - therefore similar pattern
132
Q

What is the causative organism of haemolytic uraemic syndrome?

A

E.coli O157:H7

133
Q

Define UTI.

A

presence of pure growth of >10 to the 5 organisms per ml of fresh MSU

134
Q

List an example of an upper UTI.

A

pyelonephritis

135
Q

List examples of lower UTIs.

A

urethritis
cystitis
prostatitis

136
Q

List some common organisms causing UTI.

A
  1. E.coli (75-95% community)
  2. proteus mirabilis
  3. klebsiella pneumonia
  4. staph saprophyticus
137
Q

What is the treatment for cystitis?

A

nitrofurantoin

138
Q

What is the treatment of pyelonephritis?

A

cefotaxime

if no response: augmentin/gent

139
Q

Why are thiazide diuretics CI in pts with gout?

A

there action reduced uric acid excretion

140
Q

Give examples of loop diuretics.

A
  1. furosemide

2. bumetanide

141
Q

Give examples of thiazide diuretics.

A
  1. bendroflumethiazide
  2. indapamide
  3. metolazone
142
Q

Give examples of potassium sparing diuretics.

A
  1. spironolactone

2. eplerenone

143
Q

Give an example of an osmotic diuretic.

A

mannitol

144
Q

What are the indications for using an osmotic diuretic?

A
  1. raised ICP
  2. rhabdomyolisis
  3. haemolysis
145
Q

Give an example of a carbonic anhydrase inhibitor.

A

acetazolamide

  • -> acts on the PCT to increase excretion of bicarbonate
  • -> causes alkalinisation of urine and a subsequent mild metabolic acidosis
146
Q

What are the causes of Fanconi syndrome?

A

CONGENITAL:

  • idiopathic
  • cysteinosis
  • Wilson’s disease

ACQUIRED:

  • heavy metal poisoning
  • drugs (gentamicin, cisplatin)
  • light chains (myeloma, amyloid)
147
Q

What are the indications for dialysis?

A

pneumonic: AEIOU

A - acidosis
E - electrolyte disturbance
I - intoxication
O - overload (fluid)
U - uraemia

Renal medicine (1 decks)

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