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Renal Flashcards

1
Q

3 endocrine roles of the kidney

A

Renin (vasoconstriction as part of RAAS)

EPO

vit D metabolism

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2
Q

What stimulates EPO?

A

hypoxia
anaemia
renal ischaemia

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3
Q

When is EPO increased?

A

PKD and RCC

causes polycythaemia

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4
Q

When is EPO decreased?

A

CKD

causes normocytic normochromic anaemia

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5
Q

Describe metabolism of vit D

A

natural vit D (cholecalciferol) –> goes to liver, becomes 25(OH)D3 —> in proximal tubule, under 1a hydroxylase becomes 1,25 (OH)2 D3

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6
Q

What is vit D needed for?

A

bone mineralisation

absorption of calcium and phosphate from gut

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7
Q

What regulates the formation of 1,25 (OH)2 D3?

A

PTH, phosphate and negative feedback

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8
Q

What causes agenesis of the kidney?

A 
collecting duct (from ureteric buds) fails to fuse with nephrons (from metanephric mesoderm)
can be unilateral (or bilateral - Potter's syndrome -> death)

remaining kidney hypertrophies, may have abnormalities (hydronephrosis, malrotation)
renal function may be normal

often associated with other congenital abnormalities

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9
Q

What are common problems with congenital kidney issues, eg hypoplasia, horse-shoe kidney?

A

Often issues with malrotation and prone to reflux, obstruction, infection and stones

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10
Q

What are the 3 general causes of glomerulonephritis?

A

Hereditary (Alport’s, Fabry’s)
Primary
Secondary (SLE, DM)

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11
Q

5 levels of severity of glomerular disease

A
  1. asymptomatic haematuria/ proteinuria
  2. nephrotic syndrome
  3. nephritic syndrome
  4. rapidly progressive glomerulonephritis
  5. CKD
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12
Q

Clinical features of nephrotic syndrome

A

Proteinuria, hypoalbuminaemia, oedema, hyperlipidaemia (hepatic lipoprotein secondary to protein losses)

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13
Q

Clinical features of nephritic syndrome

A

Oliguria/ anuria, HTN, fluid retention, haematuria, uraemia, some proteinuria

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14
Q

Clinical features of rapidly-progressive glomerulonephritis?

A

Haematuria, oliguria, hypertension –> renal failure

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15
Q

Examples of primary glomerulonephritis typically giving nephrotic syndrome

A

Minimal change disease

Membranous glomerulonephropathy

Focal segmental glomerulosclerosis

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16
Q

Who usually gets minimal change disease?

A

typically kids under 6
seen on electron microscopy
cause unknown, maybe circulating immune-complexes

good prognosis in kids, variable in adults

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17
Q

Most common cause of nephrotic syndrome in adults?

A

Membranous glomerulonephropathy

chronic - causes 40% nephrotic

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18
Q

What is membranous glomerulonephropathy?

A

widespread glomerular basement thickening caused by Ig deposition - causes hyalinisation and death of individual nephrons

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19
Q

Causes of membranous glomerulonephropathy

A

85% are idiopathic

secondary causes:
infections (hep B, malaria, syphilis)
tumours (melanoma, Ca bronchus, lymphoma)
drugs
systemic (SLE)

Prognosis depends on cause - 1/3 get CKD

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20
Q

Examples of primary glomerulonephritis typically giving nephritic syndrome

A

Berger’s disease (IgA nephropathy)
Rapidly progressive glomerulonephritis
Focal proliferative glomerulonephritis

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21
Q

Most common cause of primary glomerulonephritis?

A

Berger’s

no effective treatment - 20% > CKD

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22
Q

What causes Berger’s disease?

A

IgA nephropathy

usually affects young men after an URTI

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23
Q

What are the causes of secondary glomerulonephritis?

A 
Post-streptococcal GN
Non-strep GN
SLE
Henoch-Schonlein purpura
Bacterial endocarditis
Diabetic glomerulosclerosis
Amyloidosis
Goodpasture's syndrome
Microscopic polyarteritis nodosa
Wegener's granulomatosis
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24
Q

When does post-strep GN occur?

A

1-3 weeks after group A beta-haemolytic strep infection (tonsils, pharynx, skin)

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25
How is post-strep GN treated?
Conservative/ abx for remaining infection Kids recover well but 40% adults develop HTN/ renal impairment
26
What % SLE have kidney involvement?
75% - often most significant of lesions | caused by immune-complex deposition
27
What causes HSP?
can follow URTI - immune-mediated systemic vasculitis
28
Which organs does HSP affect?
Skin (purpuric rash over legs, arms, arse) Joints (pain) Intestine (abdo pain, vomiting, bleeding) Kidney (third develop lesions identical to IgA nephropathy)
29
How does bacterial endocarditis cause glomerulonephritis?
Emboli Immune-complex deposition Presents with haematuria and fluid retention
30
Why can Alport's not get Goodpasture's?
Lack the Goodpasture's antigen - abnormality of BM collagen IV
31
Clinical features of Alport's syndrome
ocular abnormalities - sensorineural deafness - renal failure X-linked (female carriers may have microscopic haematuria)
32
Clinical features of Fabry's syndrome
X-linked metabolic defects due to missing enzyme deposits accumulate in kidney, skin, vascular system (associated with angina + HF) most die in 50s
33
How does acute tubular necrosis present?
Cause of AKI - high mortality, full recovery with prompt fluid/ electrolytes and dialysis
34
Causes of acute tubular necrosis
Ischaemic ATN Toxic ATN Rhabdomyolysis
35
When does PKD present?
30-40 years
36
What causes acquired cystic disease?
Dialysis | Small cysts throughout cortex and medulla
37
Are simple renal cysts painful?
Only if haemorrhages
38
Clinical features of AKI
Reduced renal function in days/ weeks increased urea increased creatinine usually oliguria usually reversible
39
Dangerous consequences of AKI
``` Fluid overload/ pulm oedema metabolic acidosis high K+ high phosphate low calcium (less marked than CKD) low Na ```
40
Causes of AKI
``` PRE-RENAL reduced kidney perfusion dehydration shock renal artery stenosis or emboli NSAIDs and ACEi (impair renal autoreg) ``` ``` RENAL ATN acute interstitial nephritis glomerular disease vascular disease ``` ``` POST-RENAL bladder outflow obstruction (BPH, strictures) tumour (prostate, bladder, gynae) stones (bilateral) retroperitoneal fibrosis ```
41
Who does NICE suggest have screening for CKD?
DM - HTN - CVD - obstruction - SLE - family hx - nephrotoxic drugs
42
How is the increased risk of CVD managed in CKD?
lifestyle, statin, aspirin
43
Indications for RRT in AKI
hyperkalaemia pulmonary oedema acidosis uraemic pericarditis
44
Where is the fistula usually for haemodialysis?
radial artery and cephalic vein
45
Triad for presentation of renal cell carcinoma
loin pain loin mass haematuria (rarely all 3)
46
Example of osmotic diuretic. Where does it act?
Mannitol | Proximal tubule
47
Example of loop diuretic
Furosemide, bumetanide
48
How much stronger is bumetanide?
x40
49
Example of thiazides/ thiazide-like diuretics. Where does it act?
Bendroflumethiazide Thiazide-like: indapamide, chlortalidone Distal tubule
50
Example of potassium-sparing diuretics. Where does it act?
Amiloride: distal tubule Spiro: collecting duct - alodosterone antagonist
51
Indications for osmotic diuretic
Increase urine volume/ prevent anuria Decrease ICP Decrease intraocular pressures before opthalmic surgery
52
Indications for loop diuretics
Relief of symptoms of fluid overload: pulm oedema, CHF, renal/ liver disease
53
What side-effects can happen with high furosemide doses?
Tinnitus, hearing loss
54
Indications for thiazides?
HTN only
55
What should be avoided with thiazides?
Loop diuretics (hypokalaemia)
56
ADRs thiazides
Low sodium | Exchange for K+ can lead to low potassium
57
Indications for potassium-sparing diuretics?
Treatment of hypokalaemia from loop or thiazide therapy (weak as diuretic alone) Spiro also used in: - ascites and oedema due to liver cirrhosis - HF - primary HYPERaldosteronism
58
In whom should potassium-sparing diuretics not be given?
severe renal impairment | hyperkalaemia
59
ADRs of spiro?
hyperkalaemia gynaecomastia stevens-Johnson syndrome
60
Normal urea
2.5 to 6.6
61
Normal creatinine
60 to 120 | creatinine is reciprocal relationship to GFR
62
When is urea increased?
renal disease, dehydration, high protein intake
63
Normal albumin
35 - 50
64
When might you see hypoalbuminaemia and hyperalbuminaemia in renal disease?
Hypo: nephrotic syndrome Hyper: dehydration
65
When might Hb be affected in renal disease?
Decreased: chronic renal failure, blood loss Increased: polycythaemia in renal tumours, renal cysts
66
Normal eGFR
Above 90
67
What should always be done in suspected UTI?
Urine culture > 100, 000 CFU/mL is diagnostic (otherwise prob contamination of sample)
68
When might urine be brown?
Concentrated cholestatic jaundice
69
What can discolour urine making it appear to be haematuria?
Beetroot Myoglobinuria Porphyria Phenolphthalein
70
eGFR in end-stage renal failure
less than 15
71
How to calculate anion gap?
[Na] - [Cl] + [HCO3]
72
What is MUDPILES?
Causes of high anion gap metabolic acidosis ``` Methanol Uraemia DKA Paraldehyde Isoniazid Lactic acidosis Ethylene glycol Salicylates ```
73
Causes of bilat enlarged kidneys
APKD bilateral hydronephrosis amyloidosis
74
causes of unilateral enlarged kidney
hydronephrosis renal ca renal cyst
75
cannonball mets associated with
RCC most common
76
contraindications catheter insertion
Trauma patient with suspected urethral injury as evidenced by: Blood at the urethral meatus High-riding prostate on rectal examination Penile, scrotal, perineal hematoma Radiographic evidence of urethral/bladder trauma (in many centers a gentle attempt at urethral catherisation by an experienced doctor is accepted practice) Postoperative urological patients. Always consult the urologist first if the patient has had bladder neck or prostate surgery. Known stricture or ‘impossible insertion‘ last time
77
What is haemolytic uraemic syndrome? Cause? Ix? mx?
combination of haemolysis with red cell fragmentation, thrombocytopenia, acute renal failure caused post-infections, esp E.coli FBC, blood film, u&e mx supportively: fluids/ transfusion - may need dialysis
78
how is contrast-induced nephropathy managed?
fluid bolus
79
define aki
creatinine x1.5 | fall in urine to 0.5 mL/kg/h for 6h+ in adults
80
what should pregnant patients be offered for stones?
uteroscopy

Medicine (30 decks)

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