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MRCP Part 2 and PACES > Nephrology > Flashcards

Flashcards in Nephrology Deck (19)
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1
Q

What is the treatment for SBP in PD patients

A

Intraperitoneal antibiotics preferred unless systemically septic
Gram +ve cover and anaerobs

  • VANCOMYCIN
  • CEFUROXIME+ GENT

Sepsis:
Tazocin
Ciprofloxacin - watch out for photosensitive rash as SE

2
Q

What is nephrogenic systemic fibrosis

A

Defintion:
Systemic fibrosis of skin
-cuteanous demopathy seen in ESRF
-aetiology unknown

Triggers:
Gadolinium based contrast agent
metformin

presentation:
worsening skin tightetning with joint contractures
inpulling of umbilicus
cutaeneous dermopathy  = WOOD LIKE SKIN
pulmonary fibrosis + pulm htn
cardiomyopathy due to fibrosis
3
Q

How does renal cell carcinoma present?

A
Unilateral Renal mass
hydrocoele may be present if ocmpression or invasion of testicular vein occurs
metastases
haematuria
renal flank mass
loin pain

Mx:
Nephrectomy
small kinase inhibitors - Anti VEGF
-once primary removed - secondaries do tend to regress

portion of renal cell is bilateral - cannot perform nephrectomy in this case

no place for chemo radiotherapy

4
Q

Familial mediterranean fever

A

Abdominal pain - recurrent without cause
fever periodically
arthritis
nephrotic syndrome

Nephrotic syndrome is caused by Renal Amyloidosis

25% pericarditis and pleuritis

mediterranean and jewish descent

Mx:
Colchicine delays renal CKD
Renal transplant

5
Q

How does RTA 1 present - What is the defect?

A

CLASSIC RTA
DCT

Defect:
Failure to excrete H+ and reabsorb K+ at DCT exchanger
retain H+ - no urine acidification so can cause stones
no K reabsoprtion from passive diffusion back into lumen from LoH

Alakline urine
hypokalaemia
metabolic acidosis

renal stones - predisposition to stone formation in alkaline environment

6
Q

How is RTA 2 managed -how does it present?

A

PCT
Often associated with FANCONI SYNDROME = PCT absorption dysfunction

Failure to reasorb HCO3
Hypokalaemic metabolic acidosis

urinary alkalinisation typically
H+ excretion defect as well therefore K+ preferentially excreted to acidify urine and correct acidosis

Typically multiple other PCT defects go along with it

7
Q

How is RTA 4 managed -how does it present?

A

Actually an effect of hypoaldosteronism and nothing to do with RTA 1/2

Effect of lowered excretion of ammonia

Hypoaldosteronism = hyperkalaemia and Hyponatraemia
and hypotension

normal anion gap still

8
Q

What is renal tubular acidosis

A

Failure of the renal tubules to maintain Acid base balance leading to a metabolic acidosis

type dependent on RTA type

RTA 1 = DCT K+/H+ exchanger
HYPOKALAEMIC MET ACIDOSIS
NORMAL ANION GAP

RTA 2 = PCT
usually in assoc with FANCONI
multiple reabsorption defects
hypokal met acidosis as RTA 1
add
hypomag / hypocal / hypophos

RTA 4
Adrenal issue - secondary to hporeninemic hypoaldosteronism
i.e. hyperkalaemia and hyponatraemia

9
Q

What is Bartters syndrome?

A

Congenital defect in Thick Ascending limb of LoH
Defect Na/K/2Cl channel - SALT WASTING

Hypotension
Metabolic alkalosis (H+ excretion to reabsorb K+)
Hypokalaemia

EARLY PRESENTATION

Hypotension - lose salt concentration gradient medulla - water losing therapy also association with Mag loss / Cal loss
No reabsorption Na
No net movement water
No net movement of charge - no mag absorption
K+ remains in lumen
Compensatory exchange to sequester lost K+

10
Q

What is Gitelman syndrome

A

Congenital defect in Thiazide NaCl cotransporter channel in DCT

As defect is fairly small compared to barters patients are often asymptomatic

Hypokalaemia hypomagnesic metabolic alkalosis

The Na/K basolateral antiporter continues to function
Net movement of K+ from blood into luminal cell

K+ exchanged for Calcium and is lost.
Attempt to reabsorb K+ via H+ antiporter = alkalosis

Lack of net movement of Positive charge limits Magneisum absorption

11
Q

What does liquorice intoxication cause?

A

liquorice increase enzymatic conversion of cortisol to cortisone which has crossover mineralicorticoid activity

This results in hyperaldosteronism without adlosterone

low renin
low aldosterone
HTN
low K+ - excreted in excess
hypernatraemia
12
Q

Whats is SAME syndrome?

A

Syndrome of apparent mineralicorticoid excess

Overactive conversion of cortisol to cortisone - genetic

11BHSD2 gene

low renin
low aldosterone
HTN
low K+ - excreted in excess
hypernatraemia
13
Q

What condition is associated with renal failure in Caribbean descent?

A

Renal artery fibromuscular dysplasia

  • Hypertension - treatment resistant due to hyperreninaemic hyperaldosteronism
  • CKD
14
Q

How is membranous nephropathy treated?

A

Treatment:
Marked proteinurea
HTN
deteriorating renal function

prednisolone
cyclophosphamide

88% remission at 10 years follow-up

Rituximab may be used for steroid resistant disease

15
Q

What is membranous glomerulopathy associated with

A

2nd most common cause of nephrotic syndrome
steroid responsive

Also most commonly associated with chronic NSAID use

16
Q

What is FSGS associated with

A

HIV associated nephropathy
reflux nephropathy
scarring vascuitidies
most common cause of nephrotic syndrome as well

17
Q

PCKD type1 is inherited in what fashion and due to a mutation where?

A

Chr 16 85%

Autosomal dominant

18
Q

PCKD type 2 is inherited in what fashion and due to a mutation where?

A

chr 4

autosomal dominant

19
Q

How is scleroderma renal crisis managed and which Abs are most associated?

A

RNA-pol III
- renal and ild

slc 70
mainly ild

treat ace i and agressive bp control