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FOP/TAS > Renal > Flashcards

Renal Flashcards

1
Q

ECG changes in hypokalaemia

A

ST depression
flat T wave
u wave

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2
Q

ECG changes in hyperkalaemia

A

peaked T waves

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3
Q

where is K regulated in the kidney

A

collecting duct - aldosterone causes K to be exchanged for Na

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4
Q

causes of hyperkalaemia

A

medications - ACE-I, ARBs, beta blockers, trimethoprim
rhabdomyolysis
tumour lysis syndrome
renal failure
acidosis
adrenal insufficiency - CAH, addisons

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5
Q

management of hyperkalaemia

A
  1. insulin glucose infusion - drives K intracellulalry
  2. salbutamol nebuliser
  3. calcium resonium - eliminates K from the body
  4. IV calcium gluconate - stabilises myocardium
  5. bicarbonate - correct acidosis
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6
Q

causes of hypokalaemia

A

diarrhoea
alkalsosis
volume depletion
hyperaldosteronism e.g. conns syndrome
renal artery stensosis
renal tubular acidosis

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7
Q

describe the renin-angiotensin system

A
  1. liver produces angiotensinogen
  2. angiotensinogen -> angiotensin 1 via renin
  3. angiotensin 1 -> angiotensin 2 via ACE (produced in lungs + kidney)
  4. angiotensin 2 causes:
    - increase sympathetic activity
    - produce aldosterone from adrenal cortex to cause reabsorption of Na and Cl and k execretion and water retention
    - arteriole vasoconstriction to increase bP
    - stimulate ADH secretion from pituitary to cause water reabsorption in collecting duct
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8
Q

mechanism of action of loop diuretics

A

e.g. furosemide
block Na K 2Cl co transporter in ascending loop of henle so there is increased excretion of Na, K and Cl and wate.

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9
Q

side effect of loop diuretics

A

metabolic alkalosis - secretion of H
hypokalaemia
hyponatraemia
hypochloraemia
hypomagnesasemia

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10
Q

mechanism of action of thiazide diuretics

A

act in DCT by inhibiting sodium chloride reabsorption
weak diuretics

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11
Q

mechanism of action of aldosterone antagonists e.g. spironolactone

A

block action of aldosterone in the DCt and collecting ducts so sodium and water excretion is increased

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12
Q

side effects of aldosterone antagonists

A

metabolic acidosis
hyperkalaemia

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13
Q

mechanism of action of osmotic diuretics e.g. mannitol

A

freely filtered in the bowmans capsule and increase osmolality of the filtrate within the tubule so reduces water reabsorption.

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14
Q

management of indirect inguinal hernias

A
  1. incarcerated (obstruction) -> manual reduction then surgery in 2-3 days
  2. strangulated (obstruction and toxic) -> emergency surgery
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15
Q

describe nephronophthisis

A

polydipsia
polyuria
end stage renal disease
retinal degeneration
ocular motor aprexia
b/l small kidneys
liver abnormalities

= medullary small cystic kidney disease, AR

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16
Q

pathophysiology of HUS

A

damage to renal endothelial cells

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17
Q

pathophysiology of lupus nephritis

A

diffuse proliferative glomerulonepritis with deposits of IgM, IgG, and C3
type IV reaction

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18
Q

blood results of post strep glomerulonephritis

A

low C3, normal C4
low CH50
raised ASOT

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19
Q

risk factors for UTI

A

girls > 6 months / boys < 6 months old
constipation
spinal lesions
VUR
renal calculi

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20
Q

common causes of UTI

A

e.coli ***
klebsiella
enterococcus
proteus

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21
Q

presentation of UTI

A

dysuria
increased frequency/ urgency / nocturia / enureusis
fever
vomiting
abdo pain / flank pain
signs of sepsis

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22
Q

gold standard test for uTI

A

clean and catch mid stream urine dip and microscopy

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23
Q

atypical UTI features

A

non E.coli organism
poor urine output
septicaemia / ill child
creatine raised
failure to respond to abx within 48 hours

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24
Q

scans required in < 6 month old with UTI

A

uncomplicated: USS within 6 weeks

complicated: USS during acute infection + DMSA + MCUG

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25
Q

Scans required in 6 month - 3 y/o with UTI

A

atypical -> USS during acute infection + DMSA in 4-6 months

recurrent -> USS within 6 weeks + dmsa IN 4-6 Months

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26
Q

scans required > 3 y/o with UTI

A

Atypical -> USS during acute infection

recurrent -> USS within 6 weeks and DMSA in 4-6 months

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27
Q

abx treatment for UTI

A

<3 months = IV abx
> 3 months + well = oral nitrofurantoin or trimethoprim / PO cefalexin if pyelonephritis
>3 months and unwell -> IV co-amox

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28
Q

describe vesico-ureteric reflux

A

retrograde flow of urine from bladder into urinary tract
1% newborns

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29
Q

severity grades of VUR

A

1 - tracks into non dilated ureter
2 - tracks into renal pelvis without any dilatation
3 - mild to moderate dilatation of ureter
4 - ureteral tuberosity with pelvicalcyeal dilatation
5 - gross dilatation of ureteral torturosity with blunted fornices

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30
Q

causes of VUR

A
  1. primary ** - congenital, AD, short ureter
  2. secondary - caused by high voiding pressures in bladder e.g. posterior urethral valves, neurogenic bladder, duplex ureter, uterocele
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31
Q

complications of vUR

A

recurrent urine infections
neuropathic bladder
AKI
urinary retention
hypertension
renal failure

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32
Q

how is VUR picked up antenatally

A

bilateral hydronephrosis with oligohydramnios

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33
Q

which scans are required post natally for VUR

A

MCUG ** - contrast dye to look at passing of urine via x ray

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34
Q

management of VUR

A
  1. bladder training e.g. double voiding
  2. prophylactic abx if recurrent UTIs
  3. oxybutynin
  4. surgery at age 2-3 if severe and recurrent UTI (otherwise normally resolves by age 5)
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35
Q

describe posterior urethral valves

A

most common cause of urinary tract obstruction in boys

congenital malformation of posterior urethra where mucosa folds -> dilatation of renal tract proximal to obstruction -> hypertrophied bladder

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36
Q

presentation of posterior urethral valves

A

often diagnosed pre natally - oligohydramnios
poor urine stream and dribbling
urinary retention
frequent UTIs
renal damage and post renal failure

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37
Q

investigations for posterior urethral valves

A

MCUG ***
USS - shows hydrophrosis (dilated renal pelvis > 20mm)
U&E and egFR

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38
Q

management of posterior urethral valves

A
  1. suprapubic catheterisation - relieves obstruction
  2. surgical management with resection of valves- ablation via cystoscopy
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39
Q

describe the primary and secondary causes of glomerulonephritis

A

PRIMARY (RENAL CAUSES)
- IgA nephropathy ** - days after URTI
- post strep glomerulonephritis **
- focal segmental glomerulosclerosis
- Goodpastures disease
- membranoproloiferative glomerulonephritis - circulating antigen complexes with low complement

SECONDARY (SYSTEMIC ILLNESS CAUSES)
- lupus nephritis
- HUS
- alport syndrome
- HSP
- ANCA +VE - wegeners granulomatosis

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40
Q

presentation of glomerulonephrits

A
  1. macroscopic haematuria
  2. proteinuria
  3. nephrotic syndrome
  4. nephritic syndrome
  5. hypertension
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41
Q

what are the features of nephritic syndrome

A
  1. haematuria ‘coca coloured urine’
  2. reduced renal function
  3. oliguria
  4. hypertension
42
Q

tests for glomerulonephritis

A

FBC, U&E, LFT, bone, ANCA, dsDNA
urinanalysis , PCR
complement levels
renal biopsy

43
Q

renal biopsy of IgA nephropathy

A

deposits of igA in glomerular mesangium

44
Q

most common cause and presentation of glomerulonephritis

A

POST GROUP A STREP INFECTION
1-2 weeks prior to throat infection / 3-6 weeks prior to skin infection

45
Q

renal biopsy findings in post strep glomerulonephritis

A
  1. type 3 hypersensitivity reaction
  2. granular deposits of IgG and C3 in capillary loop
  3. sub endothelial humps
46
Q

investigations of post strep glomerulonephritis

A
  1. U&E
  2. ASOT - high
  3. C3 low, C4 normal
  4. reduced CH50
  5. urine - haematuria and proteinuria and tubular casts
47
Q

when is a renal biopsy indicated in glomerulonephritis

A
  1. creatinine abnromal in 6 weeks
  2. C3 persists low beyond 3 months
  3. proteinuria persists low beyond 6 months
48
Q

management of post strep glomerulonephritis

A
  1. penicillin
  2. furosemide - can help salt and water retention
  3. anti hypertensives

1% develop CKD

49
Q

pathophysiology of good pastures disease

A

anti GBM antibodies target basement membrane in kidenys and lungs (against alpha 3 chain of type IV collagen in alveolar and glomerulus)

50
Q

how does goodpastures disease present

A
  1. RENAL
    rapidly progressive glomerulonephritis
  2. RESP
    haemoptysis, cough, fatigue, SOB
51
Q

diagnosis of goodpastures disease

A

anti GBM antibdoies **
30% have ANCA
renal biopsy
CT chets - b/l diffuse infiltrates in lower zones (pulmonary haemorrhage)

52
Q

describe Bartter syndrome

A

defective reabsorption of Na, K and Cl at thick ascending loop of henle

Type 1 -4 = autosomal recessive
Type 5 = X linked recessive
type 6 - AD

53
Q

blood results for Bartter syndrome

A

hypochloraemia
hypokalaemia
hypercalcuria
metabolic alkalosis
increased renin and aldosterone levels
normal Mg

54
Q

describe Gitelman syndrome

A

tubular loss of Na and Cl and excess loss of K in the DCT

55
Q

presentation of bartter syndrome

A

dysmorphic features - triangular face, protruding ears, large eyes
severe salt wasting
faltering growth
muscle cramps
nephrocalcinosis

56
Q

describe pathology of HSP

A

igA mediated vasculitis causing small vessel inflammation

57
Q

presentation of HSP

A

70% have renal involvement - microscopic haematuria and proteinuria

skin - purpura raised rash and oedema

arthritis

GI involvement - intussception risk

58
Q

causes of nephrotic syndrome

A
  1. minimal change disease (90%)*** - fusion of podocyte foot processes
  2. focal segmental glomerulosclerosis (10%)- steroid resistant, strcutural damage to glomerulus
58
Q

when is a biopsy indicated in HSP

A

proteinuria > 4 weeks
nephrotic syndrome
nephritic syndrome
HTN
macroscopic haematuria

58
Q

complications and risks with nephrotic syndrome

A
  1. thrombotic risk - loss of anti-thrombin 3, protein C and S -> hypercoagulable state
    risk of renal artery stenosis (macroscopic haematuria) + sinus thrombosis
  2. infection risk
    risk of pneumococcal, cellulitis and peritonitis
  3. cholesterol - hyperlipidaemia
  4. hypertension
59
Q

triad of nephrotic syndrome

A
  1. proteinuria >1g
  2. hypoalbuminaemia <25 g/L
  3. oedema
60
Q

atypical features of nephrotic syndrome

A

age < 1 y/o or > 12 y/o
macroscopic haematuria
HTN
high creatinine
low C3
family hx
unresponsive to steroids

61
Q

management of nephrotic syndrome

A

prednisolone 60mg/m2/day for 16 weeks and then 40 mg for another 4 weeks
+ penicillin
+ PPI
+ fluid monitoring

90% respond to steroids within 4 weeks

62
Q

if steroid resistant after 4-6 weeks in nephrotic syndrome…

A

BIOPSY

to try ACE-I + tacrolimus (calcineurin inhibitor) and mycophenolate (purine synthesis modulator)

63
Q

cause of haemolytic uraemic syndrome

A

shiga toxin producing E.coli (0157:h7 variant) ** - contaminated food/ farmyard animals , 10% risk of HUS
streptococcus
HIV
EBV

64
Q

presentation of HUS

A
  1. bloody diarrhoea
  2. vomiting + dehydration + fever
  3. develop 1 week later, reduced urine output + malaise + pallor
65
Q

pathology of HUS

A

microangiopathic haemolytic anaemia with thrombocytopenia + AKI

damage to renal endothelial cells, formation of intravascular microthrombi to cause vessel occlusion

66
Q

investigations for HUS

A
  1. stool sample
  2. bloods - reduced platelets, anaemia, increase urea/creat (haemolytic anaemia)
  3. blood film - fragmented RCC
67
Q

management of hUS

A
  1. IV fluids and hydration
  2. blood transfusions
  3. eculizumab (monoclonal antibody to C5)
  4. may require dialysis
68
Q

definition of AKI

A
  1. urine volume < 0.5ml/kg/hr for 6 hours
  2. increase serum creatinine to 1.5 x baseline or increase by 26.5 umol/l within 48 hours
69
Q

pre renal causes of AKI

A
  1. volume depletion e.g. haemorrhage, diarrhoea, DKA, burns
  2. 3rd space losses e.g. sepsis
  3. heart failure e.g. CHD, myocarditis, coarction
70
Q

renal causes of AKI

A
  1. medications E.G. NSAIDs, furosemide, gentamicin, contrast dye
  2. acute tubular necrosis + glomerulonephritis
  3. congenital renal disease
  4. vascular - b/l renal vein thrombosis, HUS *
71
Q

post renal causes of AKI

A
  1. obstruction e.g. PUV, stones, mass
  2. neuropathic bladder e.g. trauma, spinal tumour , transverse myelitis
72
Q

causes of proteinuria

A

NON PATHOLOGICAL
UTI
exercise
fever
transient
postural

PATHOLOGICAL
nephrotic syndrome
glomerulonephritis
CKD
tubular interstitial disease

73
Q

causes of haematuria

A

UTI
glomerulonephritis
stones
trauma
renal tract tumour
PKD
renal vein thrombosis
exercise induced

74
Q

inheritance of PKD

A

most commonly autosomal dominant
chromosome 16 , PKD 1 gene

75
Q

presentation of PKD

A

multiple renal cysts -> end stage renal disease
proteinuria
HTN
berry aneuryms in circle of willis -> SAH

76
Q

features of alport syndrome

A

microscopic haemturia
sensorineural deafness
b/l lenticlonus

77
Q

features of Potter syndrome

A

associated with oligohydramnios
small kidneys b/l
resp distress secondary to hypoplastic lungs
low set ears
micrognathia
beaked nose

78
Q

describe type 1 renal tubular acidosis

A

most common type in children
inherited - mutation in ATP6VIB autosomal recessive

mutations in distal tubular transporters (H+ ATPase) causing defects in H ion secretion and causing acidosis
results in RENAL STONES
ph > 5.5 in urine

79
Q

describe type 2 renal tubular acidosis

A

usually secondary to metabolic disease e.g. cystinosis, wilsons, galactosaemia

defect in bicarb reabsorption causing acidic urine
can lead to fanconi syndrome

80
Q

describe fanconi syndrome

A

generalised proximal tubular disorder causing
- growth flatering
- polyuria
- rickets

usually congenital e.g. familial, cystinosis, galactosaemia

81
Q

blood results of fanconi syndrome

A

metabolic acidosis wit normal anion gap
low phosphate
low potassium

82
Q

management of renal transplant

A
  1. cross match and tissue typing
  2. recent serology checked for CMV, toxoplasmosis, herpes, varicella, EBV, HIV, hep, syphilis
  3. immunosuppressants
  4. infection prophylaxis - co trimoxazole
  5. BCG and live vaccines contraindicated
83
Q

which immunosuppressants used in renal transplant

A
  1. calcineurin inhibitors e.g. tacrolimus
  2. anti proliferative agents e.g. azathioprine
  3. corticosteroids
84
Q

complications with renal transplants

A
  1. Hyper acute rejection (mins-hour) - T cell mediated, circulating antibodies with MHC class antigens
  2. hypertension
  3. infection
  4. vascular thrombosis
  5. maligancny
  6. chronic allograft nephropathy
85
Q

indications for dialysis

A
  1. severe volume overload and no response to diuretics
  2. severe hyperkalaemia and unresponsive to treatment
  3. severe symptomatic uraemia - urea >40 mmol/l, seizure
  4. hyponatraemia or hypernatraemia
  5. severe metabolic acidosis
  6. removal of toxins
86
Q

define noctural enuresis

A

involuntary wetting during sleep at least twice a week in children over 5 years old

87
Q

risk factors for nocturnal enuresis

A

family history
male sex
developmental delay
constipation
sleep apnoea
obesity
psychological stress

88
Q

management of nocturnal enuresis

A
  1. good fluid intake, avoid caffeine
  2. toileting patterns , motivational therapy and rewards
  3. enuresis alarm = 1st line

for short term relief e.g. sleepovers -> desmopressin 200 micrograms for 6 months +/- anticholinergic

for detrusor instability, can try oxybutynin

89
Q

describe descent of testes in utero

A
  1. testicular development starts along mesodermal ridge or posterior abdominal wall
  2. by 28 weeks, testes reach inguinal canal
  3. from 28-40 weeks, descend from inguinal canal into scrotum
  4. descent controlled by INSULIN LIKE 3 PEPTIDE and mullerian inhibiting factor
90
Q

cause of undescended testes

A
  1. retractile = exaggerated cremasteric reflex and testes can be manipulated into scrotum (usually resolves spontaneously)
  2. ascending testes = shortened spermatic cord pulls testes up
  3. anorchia = congenital absence
  4. idiopathic **
  5. syndromes e.g. prader willi, kallmann, prune belly, laurence moon
91
Q

tests if b/l undescended testes

A

USS abdomen and pelvis and endocrine if one not felt at 3-6 months
laparoscopy >6 months if unable to palpate both
(no surgery >18 months old)

92
Q

presentation of testicular torsion

A

acute testicular pain (pain can improve with necrosis)
nausea and vomiting
secondary hydrocele
erythematous hemi scrotum
swollen, tender, retracted, horizontal lie

93
Q

signs in testicular torsion

A

absent cremasteric reflex
Prehns sign = negative (lifting testes does not releive the pain - +ve in epididmytis)

94
Q

management of testicular torsion

A
  1. pain relief
  2. urgent surgical scrotal expliration within 6 hours
    if testes not viable -> resect and orchidopexy on opposite side
95
Q

describe torsion of appendix of epididymis

A

wolffian duct remnant present in 22% testest
gradual pain in upper part of scrotum
‘blue dot’ sign
management in supportive

96
Q

differentials for testicular pain

A
  1. torsion
  2. torsion of appendix of epidymis
  3. torsion of appendix of testes (hydatid of morgani)
  4. acute epididymo-orchitis
  5. trauma
  6. testicular tumour (gradual)
  7. hydrocele (normally painless, transilluminates)
97
Q

3 features of hypospadias

A
  1. abnormal urethral opening - urethral meatus at ventral aspect of penis
  2. foreskin incomplete
  3. chordee- penile curvature so abnormal stream of urine

DO NOT CIRCUMCISE

98
Q

describe autosomal recessive polycystic kidney disease

A

cysts in the collection system leading to dilatation of the ducts
cysts also in liver

99
Q

blood results in gitelman syndrome

A

hypomagnesiumaemia **
hypokalaemia
hypocalciuria
metabolic alkalosis

100
Q

types of kidney stones

A
  1. struvite (large, staghorn, radioopaque, impaired renal function)
    - uTI
  2. urate
    - tumour lysis syndrome
    - lesch nyhan syndrome (developmental delay)
  3. oxalate
    - excessive absorption of oxalate in the gut e.g. short gut syndrome or crohns
    - pnacreatitis
    - cystic fibrosis

FOP/TAS (12 decks)

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