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FRACP > Renal > Flashcards

Renal Flashcards

1
Q

What are the general features of a RTA

Why are they short

What is the general mainstay of treatment

A

Metabolic acidosis
Normal anion gap
High serum chloride

Boney phosphate is being used as a buffer

Replace bicarb
Furosemide for type 4

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2
Q

Where is the defect in a type 1 RTA
what will you see in the serum and urine
What is the classical age of presentation and how?
What can cause it

A

Distal convoluted tubule-impaired h+ secretion

Metabolic acidosis, urine is alkalotic, hypokalaemia, high urine calcium, high serum chloride

Stones, polyuria, rickets and FTT. 1st year of life

Medullary sponge kidney

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3
Q

Where is the defect in type 2 RTA?

What is seen in the serum and urine?

What is the syndrome associated called?
What are the congenital and acquired causes?

What is Lowe syndrome otherwise known as?

How does cystinosis present

A

Proximal convoluted tubule

Metabolic acidosis, high serum chloride, acidic urine, no stones, glucose, protein and amino acids in urine. Low serum K

Fanconi syndrome
Metabolic disease, cystinosis, heavy metal poisoning, chemo agents, gent, ranitidine, amyloid, myeloma

Occulocerebral renal syndrome
X linked recessive
Cataracts, behaviour change, growth failure

Photophobia and retinal detachment, hypothyroid, rickets

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4
Q

Where is the defect in type 4 RTA?

What is seen in blood and urine

A

Blocks aldosterone

Metabolic acidosis with acidosis urine hyperkalaemia, High urine sodium

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5
Q

What are general rules of thumb for transporter defects?

A

Metabolic alkalosis

Hypokalaemia

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6
Q

What diuretics do barters and gitlemans act like

What is another name for Lidle syndrome

A

Barters- like loop
Gitlemans- like thiazides
Liddle- pseudohyperaldosteronism

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7
Q

Where is the defect in barraters syndrome? What gets activated making things worse

When and how does it normally present?

What is seen in blood and urine

What might you see on renal biopsy?

Which subtype has deafness?

Which diuretic does it mimic? How do you know it’s not diuretic abuse?
How is it treated

A

Ascending Limb of henle Na-k-cl transporter RAAS

Birth- polyhydramnios, poor growth, polyuria and ? Stones

Infantile- polyuria,ftt

Metabolic alkalosis, high urine calcium, chloride, sodium and potassium
hypokalaemia and low serum chloride

Hyperplasia of the JGA

Type 4

Loop- BP normal
Replace electrolytes and give k sparing diuretics. NSAIDs to reduce prostaglandin

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8
Q

How is baratters syndrome treated (2 things)

A

Give sodium and potassium supps

Give NSAIDS- switches off the prostaglandin effect

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9
Q

Where is the defect in Gitleman syndrome?

What is seen in blood and urine

When does it present?

What diuretic does it mimic?

What might it overlap with?

A

DCT

Metabolic alkalosis, low serum magnesium, low urine ca

Adolescence

Thiazides

Type 3 barrters

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10
Q

Liddle syndrome
Where is the defect
What is seen on bloods
What measure is important in diagnosis

A

Collecting duct
Hypokalaemia, metabolic alkalosis and low RAAS
HYPERTENSION

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11
Q

What is the normal daily requirement for sodium

A

3mM/kg/day

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12
Q

How do you calculate osmolality

What is normal-

A

2xna + urea + glucose

280-320

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13
Q

How fast should hypernatraemia be corrected

A

No faster than 0.5mmol/ hour

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14
Q

How do you distinguish between renal and non renal causes of hypernatraemia
What is the calculation
What is normal

A

Urinary fractional excretion of sodium
High- renal issue- DI or HONK
Low not renal issue- diarrhoea or fever

Urine sodium x serum creat/ urine create serum Na
1%

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15
Q

What are the features of DI on blood and urine?

What causes DI

A

Hyperna , high serum osmolality, low urine osmolality

Not enough ADH- water can’t be reabsorbed

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16
Q

In DI what should be seen on a water deprivation test

When should the test be stopped?

A

Low urine osmolality (<700)
High serum osmolality (>300)
>3% weight loss

Too much weight loss

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17
Q

What is DDAVP?

What should it show?

A

Synthetic adh
No effect if nephrogenic
If central should increase urine osmolality by 50% or more

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18
Q

What are central causes of DI

A

Brain tumours or post pit dysfunction

Structural- SOD

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19
Q

What is the most likely genetic cause of nephrogenic DI

How is it treated

A

X linked- mutated adh receptor

Drink Lots of water, low sodium diet, diuretics

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20
Q

Why is desmopressin given in nocturnal enuresis

A

Brain hasn’t learned to turn on ADH overnight causing nocturnal enuresis

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21
Q

How do you calculate an anion gap?
What is normal?
What does a normal gap indicate?
What does a high gap indicate?

A

Na+K - Cl+HCO3
10-12
Loss of bicarb
Addition of h

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21
Q

How is DI treated

A

Low sodium diet, thiazides diuretics, NSAIDs

Desmopressin if central cause

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22
Q

What are causes of a high anion gap

A 
Methanol
Uraemia
Dka
Paraldehyde 
Isoniazid 
Lactic acidosis 
Ethylene glycol 
Salicytes
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23
Q

What are causes of a normal anion gap

What are the two most common causes

A

Addisons
Bicarb loss
Chloride Xs
Diuretics

GI losses or RTA

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24
Q

Excess of which 2 diuretics will cause a metabolic alkalosis

Which 2 will cause a metabolic acidosis

A

Furosemide and thiazides

Acetazolamide and k sparing

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26
Q

What do you see in the blood with laxative abuse.

How is this different from normal diarrhoea

A

Hypokalaemia and metabolic alkalosis
Usually also increased Mg

Normally diarrhoea causes a normal anion gap metabolic acidosis

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26
Q

Define elevated blood pressure
What is stage one
What is stage 2

A

Blood pressure greater than the 90th centile
>95th centile
>95th plus 12

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28
Q

What is the best pharmaceutical treatment for htn in children
What is the best treatment for hypertensive urgency. What classes of drugs are they
“Urgency

A 
Ace inhibitor 
Oral isradipine (calcium channel blocker)
Iv hydralazine (vasodilator)
Iv labetalol (beta blocker) or sodium nitroprusside ( vasodilator)
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29
Q

What percentage of PUVs go on to ESRF
What percentage have VUR
How are they managed

A

30%
50%
Relief of obstruction and monitoring renal function. Laser ablation

30
Q

Where does UPJ obstruction normally occur

What normally causes it

A

L sided

Intrinsic compression from an artery

31
Q

Outline the RAAS system

What is the role of ANP

A

Renin secreted from JG cells when the macula densa at DCT senses low Na or the efferent arteriole senses low Bp
Stimulates AT1 release from the liver. ACE from lungs causes conversion to AT2- causes vasoconstriction

Stimulates- aldosterone- CD- increased Na in exchange for K.
ADH- increases aquoporins in CD to increase water reabsorb

ANP- released when fluid overloaded- reduces Na so less renin-more naturesis

32
Q

Which syndrome is a horseshoe kidney associated with

What tumour is it associated with

A

Turners

Wilms-4x increased risk

33
Q 
AR cystic kidney disease 
How does it present 
What is seen on ultrasound 
What other organ is affected 
When does end stage renal disease usually start
A

Bilateral flank masses. Feeding difficulties or breathing issues if severe
Lack of corticomedullary differentiation and bulky kidneys
Liver- fibrosis
12 years

34
Q

AD PKD

What other organ may have cysts

A

Brain- Berry aneurysms causing SAH

35
Q

What is nephronoptosis
What is the usual phenotype
What happens the kidney over time
What is the gene associated

A

Medullary kidney cysts
Red hair,FTT and fanconi syndrome
Gets smaller causing CKD
NPHP1

36
Q

What three kidney things are seen with TS

A

Simple cysts
Angiomyplipomas
Renal cell carcinoma

37
Q

Outline the 3 stages of AKI

A

1- creat 2x baseline
2-2-3x baseline, u.o less than half ml/kg over 6-12h
3-3x plus with anuria

38
Q

What are the features to look for in AIN

A

Sterile pyuria, global tubular dysfunction and uveitis

39
Q

What fluid should be replaced in aki

How is insensible loss calculated

A

Insensible loses with urine output and all other loses

400ml/m2/day

40
Q

What is the most likely bug in PD peritonitis

What is the first line abx regime

A

Strep pneumonia and E. coli

Cefazolin and ceftazidime

41
Q

What are the 2 main side effects of cyclosporine

A

Hirsuitism

Gingival hypertrophy

42
Q

What are the 2 main side effects of tacrolimus

A

Alopecia
Diabetes
Low Mg

43
Q

What are three main side effects of MMF

A

Lukopenia, anaemia, GI side effects

44
Q

What is characteristic about haematuria in alports disease
Genetically what occurs
What are other phenotypically features

A

Microscopic, becomes macroscopic with infections
X linked, type 4 collagen defect
SN hearing loss and anterior lenticonus

45
Q

What happens in thin basement membrane disease

Will it progress to ESRF

A

Persistent microscopic haematuria

No!

46
Q

What is the classical presentation of HSP
What is it
What is a sign of poor prognosis
How long should urine dip and BP be monitored for
What might be useful to treat it

A 
Swelling and haematuria 1-3 weeks after URTI 
IgA mediated small vessel vasculitis 
Nephrotic range protein at diagnosis 
12 months 
Steroids
47
Q

When after a strep infection is PSGN usually seen
What happens complement levels
What would be seen on biopsy

A

10d after throat infection, 3 weeks after cellulitis
Low
Neutrophil infiltration

48
Q

How is igA nephropathy differentiated from post infectious (2 ways)

A

Haematuria at the time of the infection

Normal complement levels

49
Q

What are three causes of low complement in GN

A

PSGN
Mesangiocapillary
SLE

50
Q

What is cresentic GN also known as

A

Rapidly progressive

51
Q

In good pastures what are antibodies formed against

A

Type 4 collagen in basement membrane

52
Q

What is the triad of HUS

What happens to haptoglobins

A

AKI low platelets and microangiopathic haemolytic anaemia

Low!

53
Q

What infection can cause atypical HUS

What neutrophil count shows poor prognosis

A

Pneumococcus

Neuts >20

54
Q

What complement pathway is involved in complement mediated HUS
WHich MAB is useful

A

Alternative pathway

Ecilizumab

55
Q

What is AIN
what are the characteristic features
What is TINU
What drugs can cause it

A

Immune mediated kidney infiltration with inflammatory cells. Causes tubular damage

General tubular dysfunction, sterile pyuria, tired with polyuria

With uveitis

NSAIDs, PPIs, antibiotics and diuretics

56
Q

Loop diuretics

Give an example
Where do they work
How do they work
What is seen in the blood with excess

What diuretic works in a similar way with similar side effects
Where do they work

A

Loop of henle and DCT
Block nakcl transporter- keep na and k in the lumen and water follows

Hypo k and na
Metabolic alkalosis
High urine mg and ca

Thiazides-DCT

57
Q

K sparing diuretics
How do they work
What 2 main things are seen in blood

A

Block aldosterone

Hyper jalapeños and metabolic acidosis

58
Q

Nephrotic syndrome
Why is there an associated immunodeficiency?
What infections are most common

A

Reduced production of immunoglobulins

Encapsulated

59
Q

Nephrotic syndrome

Why is there an associated hupercoagulability and high cholesterol

A

Reduced oncotic pressure therefore reduced liver perfusion
Raised VLDL
raised clotting factor production

60
Q

Nephrotic syndrome
What dose of steroids is given and for how long
What defines a relapse
What defines remission
What defines steroid dependence
What defines steroid resistance- what is the risk to developing CKD

A

60mg/m2 for 6 weeks
>3+ protein over 3 consecutive days
Zero or trace protein “
Relapse on steroids or less than 2 weeks off
No improvement after 4 weeks- around 40 %

61
Q

What stain is likely to pick up FSGS

A

Trichrome staining

62
Q

Which three renal diseases can recurr in transplant

Which can change to another

A

FSGS, membranoproliferative, and 1/3 of igA

Alports- becomes anti GBM disease

63
Q

Congenital nephrotic syndrome
What is the most common genetic cause
What is another cause

A

NPHS1

WT1

64
Q

Which type of stones are most common
What happens citrate and Oxalate in the urine
What can cause them- 4 things and 2 meds

A

Calcium stones- oxalate and phosphate
High oxalate, low citrate
Malabsorption and short gut, RTA, hyper PTH
TOPIRAMATE AND ACETAZOLAMIDE

65
Q

What causes cysteine stones
Which 4 amino acids leak Into the urine

What causes Uric acid stones
What causes struvite stones

What type of stone is likely to cause a staghorn calculus

A

Cysteinuria- cystine, ornithine, arginine and lysine
Lesch nyhan syndrome
UTIs

Struvite stones

66
Q

What is dent disease
What are three main features
Which 2 genes are affected

A

X linked form of fanconi syndrome
Haematuria, polyuria and stones
OCRL1 CLCN5

67
Q

What medication is useful for giggle incontinence

A

Oxybutinin

68
Q

What does the mesonephros form

“ metanephros

A 
Ureteric bud (pelvis and collecting ducts) 
Everything else
69
Q

What does DMSA show

What do mag 3 and DTPA show

A

Structure and scarring

Function (?obstruction)

70
Q

What type of drugs are cyclosporine and tacrolimus

A

Calcineurin inhibitors

FRACP (23 decks)

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