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Medicine > Renal And GUS > Flashcards

Renal And GUS Flashcards

1
Q

criteria for nephrotic syndrome

A 
proteinuria >3.5g in 24h
hypoalbuminemia <3g/DL
generalised oedema
hyperlipidemia and lipiduria 
(hypercoagubility)
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2
Q

criteria of nephritic syndrome

A

haematuria
hypertension
proteinuria (less than nephrotic)
oliguria and azotemia

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3
Q

size of largest molecules to be filtered in health

A

4nm (max diameter of gaps in podocytes) also +> - charge due to negative collagen

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4
Q

mechanism of linear v granular immune deposits in glomeruli

A

linear: anti-GBM (TIV collagen alpha3 chain)
granular: circulating Ag (endogenous or exogenous) deposited OR Ab v GBM (to PLA2-R in membranous nephropathy only)

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5
Q

exogenous antigens that can deposit in glomeruli

A

hep C At, HBsAg l, strep protein, treponema, plasmodium.

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6
Q

where are subendothelial deposits in the glomeruli

A

side near blood

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7
Q

where are subepithelial deposits in glomeruli

A

on the side near bowman’s capsule.

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8
Q

Risk factors for Renal cell carcinoma?

A

Smoking, HTN, obesity
Acquired polycystic kidney disease (dialysis) RRx30
Occupational: cadmium, asbestos, pertrol
Chronic analgesia use (paracetamol, aspirin)
Family history

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9
Q

Age and sex for Renal cell carcinoma?

A

M>F. 60-80y

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10
Q

Classical triad of RCC?

A

Haematuria
Abdominal pain
Flank mass
(Only present in 10%)

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11
Q

Typical blood findings for RCC?

A

Anaemia (normocytic) + Raised ALP

Or Hypercalcaemia or polycythaemia

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12
Q

Ways of RCC presentation?

A

Incidental finding
Classical triad: haematuria, abdo pain, flank mass
Local invasion: IVCO, Buddchiari, scrotal varicocoele, limb oedema
Paraneoplastic: anaemia, B symptoms, cahexia, lytic bone lesions, polycythaemia (EPO), feminisation, masculinisation, HTN, PMR, amyloidosis
Metastatic: (30% at present) lung, lymph, liver, bone, brain,

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13
Q

How would you investigate ?RCC

A 
Urine dip: haematuria (not great)
FBC: paraneoplastic syndrome
LDH: marker of advanced disease
LFTs + coag: metastases, Stauffer's syndrome
Corr Ca: raised (advanced disease)
U+Es
Imaging: US abdo/pelvis OR CT
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14
Q

What is stauffer’s syndrome?

A

Non-metastatic (paraneoplastic) nephrogenic hepatic dysfunction. Cholestasis (elevated bilirubin, alk phos, GGT) + elevated PT, thrombocytosis and hepatosplenomegaly

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15
Q

DDX for renal mass:

A

Benign: simple renal cysts (NB. USS to confirm not complex/malignant); or
Angiomyolipoma; or Oncocytoma.
Malignant: renal cell carcinoma, metastases.

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16
Q

How to distinguish oncocytoma from RCC?

A

With difficulty! But management is similar anyway!
Mx: nephrectomy (to prevent complications/spont haemorrhage)
Biopsy: central stellate scar. Granular cytoplasm (looks like clear cell)

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17
Q

Subtypes of RCC?

A

Clear cell (65%)
Papillary renal cell (10-15%)
Chromophobe renal carcinomas (5%)

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18
Q

Biochemistry of excess aldosterone?

A

Hypokalaemic, alkalosis, high to normal sodium.

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19
Q

How to differentiate primary and secondary hyperaldosteronism?

A

Primary: normal-high Na, HTN, pH high. [renin] plasma LOW
Secondary: low Na (<138), ±HTN, pH maybe normal. (Look for causes: CCF, ascites, nephrotic syndrome) [renin] plasma HIGH
BOTH: K excretion >30mmol pd.

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20
Q

What is Conn’s syndrome?

A

Primary adrenal disease with excess aldosterone.

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21
Q

signs and symptoms of Conn’s syndrome?

A

Hypertension, muscle weakness, latent tenant, paraesthesia, polydipsia, polyuria, nocturia

22
Q

Cause of HTN + low K

A

Thiazide diuretics

?conn’s syndrome

23
Q

How to investigate ?raised aldosterone?

A

[aldosterone]/[renin]
Renin activity + renin mass
If both are low (<800, <80) excludes diagnosis
If both are high (>2000, >200) likely diagnosis

24
Q

How to confirm diagnosis of Conn’s syndrome?

A
  1. Saline suppression test: 2l IVI 0.9% over 4h. Should decrease aldosterone. Diagnostic if aldosterone >140pmol/. (But risk of inducing cardiac failure esp in elderly)
  2. Sodium loading + fludrocortisone over 4d
    But needs admission to hospital and risks of serious hypokalaemia
25
Q

Causes of conn’s syndrome?

A

Adrenal adenoma
Bilateral adrenal hyperplasia
GC remediable hyperaldosteronism (genetic)

26
Q

How to calculate plasma osmolality?

A

2x[Na] + [urea] + [glucose] (mmol/l)

27
Q

Diagnostic criteria of SIAD

A

Hyponatraemia (<135)
Hypo-osmolar plasma <270
Inappropriate concentrated urine >100mmol/kg
No adrenal, renal ro thyroid dysfunction
(Do NOT measure ADH, it’s raised in most people with hyponatraemia anyway)

28
Q

Causes of hyponatraemia?

A

(Sick cell, pseudo)
Na losses (hypovolaemic)
Inability to excrete free water (hypervolaemic)
SIAD (normovolaemic)

29
Q

Management of dilutional hyponatraemia?

A

(Correct at rate of onset, monitor carefully)
Water restrict
Demclocycline (v ADH-R antag @ collecting duct)

30
Q

Risk of rapid correction of hyponatraemia?

A

Central pontine myelinolysis

31
Q

Urgent correction of dilutional hyponatraemia?

A

Hypertonic saline (1.8/2.7/3%) to increase [Na] by 1mmol/l/h
(Correct 0.5mmol/l/h if >48h onset)
NOT if fluid overloaded.

32
Q

Max increase of [Na]plasma per day?

A

Do NOT correct more than 10mmol/l over 24h.

33
Q

When to stop treating urgent hyponatraemia?

A

When Na 120mmol/l or pt asymptomatic

34
Q

How to correct dilutional hyponatraemia in fluid overloaded pt?

A

Loop diuretic + hypertonic saline?

35
Q

Min Na, K, Cl intake pd?

A

1mmol/kg per day

36
Q

Min water intake pd?

A

25-30ml/kg/day

37
Q

Min glucose needed pd?

A

50-100g per day

38
Q

Max K replacement?

A

<240mmol in 24h

39
Q

What is Addison’s disease?

A

Primary adrenal insufficiency. reduced aldosterone and cortisol.

40
Q

How to distinguish hypervolaemic hyponatraemia due to CKD or CCF?

A

Urine osmolality: if >20mmol/l suggests renal cause.

Urine osmolality <20mmol/l suggests non-renal cause

41
Q

Disorders associated with hypokalaemic alkalosis

A

Liddle’s syndrome
Gitelman’s syndrome
Bartter’s syndrome

42
Q

Baby presents with polyuria and low BP. Urinary Ca high. Na 138; K 2.8; Urea 3.4; Cr 62; pH 7.51; HCO3 33. Likely diagnosis?

A

Hypokalaemic Metabolic alkalosis.

Bartter’s syndrome: salt wasting (hypercalciuria, Mg). Impaired Na resorption in LoH (NKCC2 defect)

43
Q

What is Bartter’s syndrome?

A

Defect in thick asc LoH. Direct/indirect impairment of NKCC2. Hypokalaemia, alkalosis, hypotension.
Onset 24-30w. High renin and Aldosterone.
Salt wasting: lose Ca, Mg, Cl, K in urine.
PC: polyhydramnios, polyuria, polydipsia
Autosomal recessive

44
Q

What is Liddle’s syndrome?

A

Activating mutation in ENaC (DCT Na channel): always active.
Pseudohyperaldosteronism. Retain Na and H2O
PC: infant-early adult. Autosomal dominant.
HTN, hypernatraemia, hypokalaemia (high HCO3, low renin and aldosterone)

45
Q

4 ways NSAIDs kill the kidneys

A

Dysregulation of blood flow
Toxic Tubulointerstitial insult
Membranous GN
Minimal change GN

46
Q

Cause of patchy tubular necrosis?

A

Renal hypoperfusion/prerenal AKI.

47
Q

Causes of confluous tubular necrosis?

A

Exogenous: solvents, gentamycin, heavy metals, radiocontrast
Endogenous: HbC, myoglobin, light chain (myeloma)

48
Q

Stages of AKI?

A

1: 1.5xincrease in [Cr] (>0.3mg/dl) OR <0.5ml/kg/h for 6h
2. 2-3xincrease in [Cr] OR <0.5ml/kg/h for >12h
3. >3xincrease in [Cr] OR <0.5ml/kg/h for >24h OR anuria for 12h OR renal replacement therapy needed

49
Q

Indications for dialysis?

A 
AEIOU
Acidosis
Electrolytes (K)
Ingested toxins
Overload
Uraemic
50
Q

Stages of CKD?

A

(GFR in ml/min)

1: >90 + something else e.g. ACR>3
2. 60-90
3. 30-59
4. 15-49
5. <15 AKA ESRF

Medicine (16 decks)

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