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MRCP > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Within ADPKD, what are the two different types, which chromosomes cause the mutations and when do they usually reach ESRF?

A

PKD1 (85%) - Chr16, ESRF by 50s
PKD2 (15%) - Chr4, ESRF by 70s

T1 = most common (1st), Chr (1)6, reaches ESRF 1st

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2
Q

In patients with a positive FH, what is the USS criteria for diagnosing PKD?

A

two cysts, unilateral or bilateral, if aged < 30 years
two cysts in both kidneys if aged 30-59 years
four cysts in both kidneys if aged > 60 years

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3
Q

What are the main symptoms of PKD and what complications may occur in the kidney?

A

Abdo pain +/- haematuria

Cyst infection
Renal calculi
Increased BP
Progressive kidney failure

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4
Q

What are the extra-renal manifestations of PKD?

A

Liver cysts -> hepatomegaly
Intra-cranial aneurysm -> SAH
Cysts: pancreas, ovaries, testes, liver
Mitral valve prolapse (systolic apical murmur) and diverticular disease

  • essentially all cystic/out-pouching structures
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5
Q

Management of PKD?

A

HIGH BP SHOULD BE TREATED AGGRESSIVELY (aim <130/80mmHg)

Strict criteria, but some patients may be offered tolvaptan (vasopressin receptor 2 antagonist) to slow cyst development
No other regular treatment
Treat infections + monitor U&Es
To help pain -> cyst removal/nephrectomy
Increased water intake, decreased sodium intake and avoid caffeine may also help

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6
Q

If a patient develops a SAH with a history of PKD, what might you offer their family members?

A

Magnetic resonance angiography screening may be done in 1st degree relatives of those with SAH + ADPKD

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7
Q

Which Ab is idiopathic membranous glomerulonephritis related to?

A

Anti-phospholipase A2 antibodies

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8
Q

What are the three defining features of nephrotic syndrome? + extra finding

A

Proteinuria (>3g/24hrs)
Hypoalbuminaemia (<30g/L)
Oedema
- also severe hyperlipidaemia

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9
Q

What are the three primary causes of nephrotic syndrome?

A

Minimal change disease
Membranous nephropathy
Focal segmental glomerulosclerosis

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10
Q

What can cause secondary nephrotic syndrome?

A

infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

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11
Q

What is minimal change disease, causes, how is it Ix and Tx?

A

fusion of foot processes, more common in children
Can see loss of foot processes on electron microscopy (light microscopy normal)
80% idiopathic, but can be caused by:
drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
infectious mononucleosis

Tx = steroids 
Prognosis = 1/3 one episode, 1/3 infreq relapses 1/3 freq relapses (stop before adulthood)
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12
Q

What is membranous nephropathy, how is it Ix and Tx?

A

thickened glomerular BM, more common in adults, usually idiopathic – may be assoc with AI disease e.g. SLE
Tx = ACEi, immunosuppression (steroids + another agent) if severe/progressive
Prognosis = , 1/3 remission, 1/3 remain proteinuric, 1/3 renal failure

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13
Q

What is the pathophysiology of nephrotic syndrome?

A

Injury to the podocytes appears to be the main cause – usually they wrap around the glomerular capillaries and maintain the filtration barrier, preventing large protein molecules from getting through. Damage can cause a large protein loss.

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14
Q

What are good prognostic indicated of membranous nephropathy?

A

Female
Young age
Asymptomatic proteinuria at the time of presentation

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15
Q

What is focal segmental glomerulosclerosis, how is it Tx?

A

Segments of glomeruli develop sclerosis, 50% will get better, 50% develop ESRF, Tx = steroids

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16
Q

What is the presentation of nephritic syndrome?

A

Haematuria (micro/macro), HTN, drop in GFR
Also - fluid retention + oedema, and proteinuria

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17
Q

Causes of nephritic syndrome?

A

Post-strep infection
IgA nephropathy
Rapidly progressive GN
Membranoproliferative GN
Goodpastures disease

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18
Q

What is post infectious (post-strep) GN?

A

Post-infection with Group A B-haemolytic streptococcus (pyogenes)
• Causes inflammation in the glomeruli + defective filtration, causing blood to leak through
• Typically occurs in children
ASSOCIATED WITH LOW COMPLEMENT

  • Occurs 1-2 weeks after throat/skin infection
  • Tx = supportive, potentially Tx oedema with furosemide, >95% recover renal function
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19
Q

What is IgA nephropathy?

A
  • Commonest GN in HICs in adults - typical: young man with haematuria that recovers rapidly after attacks
  • Usually present with macroscopic haematuria, may present 1-2 days after a viral infection
  • Renal biopsy – IgA deposits seen in the matrix
  • Tx – BP control with ACEi, immunosuppression may slow the decline of renal function
  • 20% of adults develop ESRF over 20 years
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20
Q

What is rapidly progressive GN?

A
  • The most aggressive GN
  • Different causes – all have crescents (fibrin thickening) in the glomeruli seen on biopsy
  • Examples: Goodpasture’s, granulomatosis with polyangiitis, microscopic polyangiitis
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21
Q

What is Goodpasture’s disease?

A

• Also known as anti-glomerular BM disease
• Caused by auto-Abs to T4 collagen (an essential component of the GBM)
o Features
–> pulmonary haemorrhage
–> rapidly progressive glomerulonephritis (rapid AKI)
• Tx – plasma exchange, steroids +/- cyclophosphamide, if started early full recovery is possible

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22
Q

What are some common causes of polyuria?

A

diuretics, caffeine & alcohol
diabetes mellitus
lithium
heart failure

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23
Q

What is the mechanism by which alcohol intake causes polyuria?

A

Alcohol acts to inhibit ADH. This causes reduce aquaporin insertion in the collecting tubules

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24
Q

What is diabetes insipidus?

A

Either a deficiency of ADH (cranial) or an insensitivity to ADH (nephrogenic)

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25
Q

Causes of cranial diabetes insipidus?

A
  • Idiopathic
  • Trauma – post-head injury
  • Pituitary surgery
  • Craniopharyngiomas

• Histiocytosis X

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26
Q

Causes of nephrogenic diabetes insipidus?

A
  • Genetics (AVPR2)
  • Electrolytes (high Ca, low K)
  • Drugs (demeclocycline (abx), lithium)
  • Tubulo-interstitial disease – obstruction, sickle-cell, pyelonephritis
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27
Q

What is Wolfram’s syndrome?

A

DIDMOAD - the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness

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28
Q

Presentation of DI?

A

Polyuria + polydipsia

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29
Q

Investigations of DI?

A

High plasma osmolality, low urine osmolality (urine osmolality >700 excludes DI)

Water deprivation test: give desmopression after period of no water
If nephrogenic - no change
If crania - osmolality will fall
MRI head if cranial suspected

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30
Q

Management of DI?

A

Nephrogenic - thiazides, low Na/protein diet
Cranial - desmopressin

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31
Q

How to calculate the anion gap? Normal range?

A

(Na + K) - (Cl + HCO3)
normal range = 8-14 mmol/L

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32
Q

What are the causes of a raised anion gap?

A

CO, CN
Alcoholic ketoacidosis and starvation ketoacidosis
Toluene
Metformin, Methanol
Uremia
DKA
Phenformin, paraladehyde
Iron, Isoniazid
Lactic acidosis
Ethylene glycol (antifreeze)
Salicylates

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33
Q

What is Alport’s syndrome?

A

a genetic condition that causes abnormalities in T4 collagen -> characterized by kidney disease, hearing loss, and eye abnormalities

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34
Q

What is the inheritance pattern of Alport’s?

A

X-linked dominant

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35
Q

In which gender is Alport’s worse?

A

Males

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36
Q

What is the genetic abnormality on Alport’s syndrome?

A

D/t defect in gene coding for T4 collagen = abnormal glomerular BM

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37
Q

THINK Alport, in?

A
  1. Renal failure
  2. Bilateral sensorineural hearing loss
  3. Ocular abnormalities
  • microscopic haematuria almost universal
  • lenticonus: protrusion of the lens surface into the anterior chamber
  • retinitis pigmentosa
    Usually presents in childhood
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38
Q

Investigations in Alport’s syndrome?

A

Molecular genetic testing
Renal biopsy, electron microscopy - longitudinal splitting of the lamina densa of the glomerular BM -> ‘basket-weave’ appearance

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39
Q

In DI, what are the two genetic causes that result in a nephrogenic picture?

A

the more common form affects the vasopression (ADH) receptor
Less common form results from a mutation in the gene that encodes the aquaporin 2 channel

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40
Q

How much Na, K, water and glucose do you need/day?

A

Sodium - 1mmol/kg
Potassium - 1mmol/kg
Water - 30ml/Kg
Glucose - 50-100g

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41
Q

Which immunoglobulins are responsible for hyperacute graft rejection?

A

IgG (d/t pre-existing Abs against HLA/ABO)
Example of a T2 hypersensitivity reaction

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42
Q

when HLA matching for a renal transplant, what is the relative importance of the HLA antigens?

A

DR > B > A

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43
Q

Name of few post-op problems after kidney transplant?

A

ATN of graft
vascular thrombosis
urine leakage
UTI

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44
Q

What occurs in/causes acute graft rejection (<6 months)?

A

usually due to mismatched HLA. Cell-mediated (cytotoxic T cells)
usually asymptomatic and is picked up by a rising creatinine, pyuria and proteinuria
other causes include CMV infection (Tx ganciclovir)
may be reversible with steroids and immunosuppressants

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45
Q

What occurs in/causes chronic graft rejection (>6 months)?

A

both antibody and cell-mediated mechanisms cause fibrosis to the transplanted kidney (chronic allograft nephropathy)
Or recurrence of original renal disease (MCGN > IgA > FSGS)

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46
Q

What are the 3 most common sites for stones to obstruct in the urinary system?

A

Pelvi-uteric junction
Pelvic brim
Vesico-ureteric junction

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47
Q

What is the firstline scan in suspected renal calculi for all patients?

A

CT KUB

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48
Q

Below which size of renal stones is an expectant approach usually adopted?

A

<5mm

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49
Q

How would you manage a pregnant women with a renal stone >5mm?

A

Ureteroscopy (uses laser to break up the stone) - in most cases a stent is left in situ for 4/52 after the procedure

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50
Q

How would you manage a healthy patient with a renal stone >5mm?

A

Shockwave lithotripsy

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51
Q

In who would you perform percutaneous nephrolithotomy?

A

Patients with complex renal calculi and staghorn calculi

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52
Q

How to treat calcium stones?

A 
High fluid intake
**Low protein**, low salt
thiazides diuretics (increase distal tubular calcium excretion)
Interestingly, changing Ca dietary intake is not effective
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53
Q

How to treat oxalate stones?

A

cholestyramine/pyridoxine (vit B6)
-> both reduce urinary oxalate secretion

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54
Q

How to treat uric acid stones?

A

Allopurinol/oral bicarbonate

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55
Q

Lifestyle management of BPH?

A

Avoid caffeine/alcohol/relax when voiding/void twice in a row to aid emptying/train bladder by holding on to increase the time between voiding

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56
Q

Medication to manage of BPH?

A

Alpha-blockers are 1st line (decrease SM tone)
5alpha-reductase inhibitors (finasteride) can be added

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57
Q

Surgical management of BPH?

A
  • TURP – risk to sexual function, 20% need redoing within 10 years
    o Comp: TURP syndrome
  • Transurethral incision of the prostate (TUIP) – less destruction than TURP, relieves pressure on the urethra
  • Retropubic prostatectomy – open operation if prostate very large
  • Transurethral laser-induced prostatectomy (TULIP) – may be as good as TURP
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58
Q

What is TURP syndrome?

A

It occurs as a consequence of the absorption of the fluids used to irrigate the bladder during the operation into the prostatic venous sinuses.

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59
Q

What is TURP syndrome?

A

It occurs as a consequence of the absorption of the fluids used to irrigate the bladder during the operation into the prostatic venous sinuses.

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60
Q

Most common ethnicities effected by BPH?

A

black > white > Asian

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61
Q

What is the mechanism of action of alpha-1 antagonists?

A

decrease smooth muscle tone (prostate and bladder)

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62
Q

What are the side effects of alpha-1 antagonist?

A

dizziness, postural hypotension, dry mouth, depression

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63
Q

What is the mechanism of action of 5 alpha-reductase inhibitors?

A

block the conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH - causes a reduction in prostate volume and hence may slow disease progression

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64
Q

What are the side effects of 5 alpha-reductase inhibitors?

A

erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia

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65
Q

What is contrast induced nephrotoxicity?

A

25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media

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66
Q

RFs for contrast induced nephrotoxicity?

A

known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs

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67
Q

How to prevent contrast induced nephrotoxicity?

A

IV 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure

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68
Q

Which medication should be held prior to giving contrast and why?

A

metformin - withhold for a minimum of 48 hours/until the renal function has been shown to be normal. This is due to the risk of lactic acidosis.

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69
Q

Pre-renal causes of AKI?

A

Pre-renal (40-70%) – due to renal hypoperfusion (FIRST)

  • Failure – heart/liver
  • Infection/sepsis or Iatrogenic (drugs)
  • Red cell haemorrhage
  • Stenosis (RAS) or Sick (GI losses)
  • Thrombosis
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70
Q

In AKI, what does the presence of protein indicate?

A

Presence of protein in urine effectively rules out a pre- or post-renal cause

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71
Q

What are the renal causes of AKI?

A
  • Tubular (acute tubular necrosis, radiological contract, myoglobinuria in rhabdomyolysis)
  • Glomerular (autoimmune such as SLE, HSP, drugs, infection)
  • Interstitial (acute interstitial nephritis caused by drugs – NSAIDs/abx, infiltration with tumour/infection)
  • Vascular (vasculitis, malignant BP)
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72
Q

What are the post-renal causes of AKI?

A

Luminal (clots, stones, sloughed papillae)
Mural (tumour, strictures)
Extrinsic compression (tumour, retroperitoneal fibrosis)

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73
Q

What will you see on microscopy in acute tubular necrosis?

A

Muddy brown urine casts

74
Q

What is cystinuria?

A

Cystinuria is an AR disorder characterised by the formation of recurrent renal stones.
Due to a defect in the membrane transport of cystine, ornithine, lysine, arginine (COLA)

75
Q

What tests can identify cystinuria?

A

cyanide-nitroprusside test - turns reddish if presence of excess amino acids

76
Q

Management of cystinuria?

A

hydration
D-penicillamine
urinary alkalinisation

77
Q

Management of cystinuria?

A

hydration
D-penicillamine
urinary alkalinisation

78
Q

What is cystinosis?

A

an AR condition causing defective cystine storage and therefore cystine builds up in the cell -> fanconi syndrome -> ESRD

79
Q

Causes of renal papillary necrosis?

A

POSTCARDS: pyelonephritis, obstruction of the urogenital tract, sickle cell disease, tuberculosis, cirrhosis of the liver, analgesia/alcohol abuse, renal vein thrombosis, diabetes mellitus, and systemic vasculitis

80
Q

What are the symptoms of renal papillary necrosis?

A

fever, loin pain, haematuria
IVU - papillary necrosis with renal scarring - ‘cup & spill’

81
Q

What is the preferred method of access for haemodialysis?

A

AV fistula

82
Q

How long does it take for an AV fistula to develop?

A

6-8 weeks

83
Q

What are stag-horn calculi made of?

A

Struvite

84
Q

What are the features of prostatitis?

A

UTIs, retention, pain, haematospermia, swollen prostate on DRE

85
Q

What is the management of acute prostatitis?

A

Analgesia
Levofloxacin for 28 days

86
Q

Management of chronic prostatitis?

A

Non-bacterial has no response to abx, Anti-inflammatories, alpha-blockers and prostatic massage have a place

87
Q

What is the most common cell type in prostate cancer?

A

Adenocarcinoma

88
Q

Treatment options for prostate cancer?

A

Radical prostatectomy
Radical radiotherapy
Hormone (androgen) therapy
Active surveillance

89
Q

What are the types of hormone therapy for prostate cancer?

A 
GnRH agonists (Goserelin) or antagonists – first stimulate, then inhibit pituitary gonadotrophs
-\> Risk: tumour ‘flare’ initially

Usually take for 3yrs, once stopped PSA will rise slightly but usually settle around 1 or 2

90
Q

Which drug might you prescribe alongside GnRH agonists in the treatment of prostate cancer?

A

Bicalutamide

91
Q

What are the initial and maintenance immunosuppressive regimes in kidney transplant?

A

initial: ciclosporin/tacrolimus with a monoclonal antibody
maintenance: ciclosporin/tacrolimus with MMF or sirolimus
add steroids if more than one steroid responsive acute rejection episode

92
Q

What should you monitor for in patients taking immunosuppressive therapy for renal transplant?

A

CVS disease
Renal failure - drugs have nephrotoxic effects
Malignancy - immunosuppression can make more at risk, e.g. skin cancers

93
Q

What are the complications of nephrotic syndrome?

A

HIT
Hyperlipidaemia (increased risk of CVS disease/strokes), infection, thromboembolism

94
Q

What causes the increased chance of thrombosis in nephrotic syndrome?

A

Loss of antithrombin-III (+ proteins C and S) and an associated rise in fibrinogen levels predispose to thrombosis

95
Q

Marker of good prognosis in IgA nephropathy?

A

Frank haematuria

96
Q

Which UTI bacteria predisposes to which type of stone formation?

A

Proteus mirabilis infection predisposes to struvite kidney stones

97
Q

What causes acute interstitial nephritis?

A

Accounts for 25% of drug induced AKI
- penicillin, rifampicin, NSAIDs, allopurinol, furosemide
Also systemic disease (SLE) and infections

98
Q

Symptoms of acute interstitial nephritis?

A

Causes an ‘allergy’-type reaction
Features: fever, rash, arthralgia
Mild renal impairment

99
Q

Investigations for acute interstitial nephritis?

A

Sterile pyuria
Urine: eosinophils + white cell casts

100
Q

When might you give someone erythropoietin?

A

Tx of anaemia associated with CKD + associated with cytotoxic therapy

101
Q

SEs of erythropoietin?

A

Accelerated HTN potentially leading to encephalopathy + seizures
Bone aches
Flu-like symptoms
Urticaria
Pure red cell aplasia (d/t Abs against erythropoietin)
Secondary iron deficiency (iron needed for RBC, may not be enough if more are created quickly)

102
Q

Indications for plasma exchange?

A

Guillain-Barre syndrome
myasthenia gravis
Goodpasture’s syndrome
ANCA positive vasculitis
TTP/HUS
cryoglobulinaemia
hyperviscosity syndrome e.g. secondary to myeloma

103
Q

How long might it take for Finasteride to take effect?

A

Finasteride treatment of BPH may take 6 months before results are seen

104
Q

What is AL amyloidosis and what can it cause?

A

Most common type
Associated with a clumping of abnormal light chain fragments

Due to myeloma, Waldenstrom’s, MGUS

features include: nephrotic syndrome, cardiac and neurological involvement, macroglossia, periorbital eccymoses

105
Q

What is AA amyloidosis and what does it usually occur with it?

A

associated with the deposition of amyloid AA fibrils
Usually occurs with chronic infection/inflammatory disease e.g. TB, RA, osteomyelitis or Crohn’s
Also occurs in Hodgkin’s/non-Hodgkin’s lymphoma

renal involvement most common feature

106
Q

Investigations in amyloidosis?

A

Tissue biopsy - amyloid fibrils stain with Congo red and show apple-green birefringence in polarised light

107
Q

What percentage of children who present with UTIs suffer from VUR?

A

30%

108
Q

What is the best investigation for VUR?

A

micturating cystourethrogram

109
Q

Grading of VUR?

A

I - Reflux into the ureter only, no dilatation
II - Reflux into the renal pelvis on micturition, no dilatation
III - Mild/moderate dilatation of the ureter, renal pelvis and calyces
IV - Dilation of the renal pelvis and calyces with moderate ureteral tortuosity
V - Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity

110
Q

What is the triad of symptoms in HUS?

A

AKI
Microangiopathic haemolytic anaemia
Thrombocytopaenia

111
Q

What is the most common cause of HUS?

A

Classically Shiga toxin-producing E. coli (STEC) 0157:H7 – accounts for >90%

112
Q

How do you manage HUS?

A

Supportive - fluids, blood transfusion/dialysis if required
No role for antibiotics
Eculizumab/plasma exchange may have a role

113
Q

What percentage change in creatinine and eGFR would be acceptable when starting an ACEi?

A

NICE suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, although any rise should prompt careful monitoring and exclusion of other causes

114
Q

If commencing an ACEi causes a more than acceptable rise in creatinine, what would you worry about?

A

Something causing hypoperfusion to the kidneys e.g. RAS

115
Q

What is the most common cancer found in the kidney?

A

Renal cell carcinoma (90%)

116
Q

What are the RFs for RCC?

A

Smoking
Tuberous Sclerosis
von Hippel-Lindau syndrome

117
Q

What percentage of people with RCC have mets at diagnosis?

A

25%

118
Q

What is a common site for metatastes from RCC?

A

Cannon ball mets in chest

119
Q

How do you measure prognosis in RCC?

A

Predicted by the Mayo prognostic risk score (SSIGN) – tumour stage, size, grade and necrosis

120
Q

What is the most common type of cancer in the bladder?

A

Transitional cell carcinoma

121
Q

What are the RFs for bladder cancer?

A

Transitional cell:

Aromatic amines (dyes)
Chronic cystitis

Smoking, rubber, cyclophosphamide

Squamous cell:
Schistosomiasis, smoking (more common RFs for squamous cell carcinomas)

122
Q

Early management of TCC (80% of patients) and 5yr survival?

A

Diathermy or TURBT
Need regular cystoscopies
5yr survival = 95%

123
Q

Management options for TCC if some delay in diagnosis?

A

Radical cystectomy - gold standard
Radiotherapy/chemo - may be palliative
Very late - chronic cauterisation and urinary diversions

124
Q

What is a Wilms tumour?

A

Nephroblastoma - childhood tumour primitive renal tubules and mesenchymal cells
Presents with abdo mass and haematuria

125
Q

What is the most common organism to cause peritonitis in patient with peritoneal dialysis?

A

Staph epidermidis

126
Q

Indications for dialysis?

A
  • Refractory pulmonary oedema (Pulm. oedema not responding to dietary Na restriction + diuretics)
  • Persistent hyperkalaemia
  • Severe metabolic acidosis
  • Uraemic symptoms e.g. pericarditis/encephalopathy
  • Drugs – BLAST (barbituates, lithium, alcohol, salicylates, theophylline)
127
Q

When should you refer a renal patient to a nephrologist?

A

Renal tranplant
ITU patient with unknown cause of AKI
Vasculitis/glomerulonephritis/tubulointerstitial nephritis/myeloma
AKI with no known cause
Inadequate response to treatment
Complications of AKI
Stage 3 AKI (see guideline for details)
CKD stage 4 or 5
Qualify for renal replacement hyperkalaemia/metabolic acidosis/complications of uraemia/fluid overload (pulmonary oedema)

128
Q

What condition causes haematuria without kidney disease, in a patient with a FH of haematuria?

A

Thin Basement Membrane Disease

T4 collagen disorder

129
Q

What is the mechanism of action of Tolvaptan?

A

A vasopressin receptor 2 antagonist

130
Q

RF for testicular cancer?

A

Undescended testis, infertility, FH, mumps

131
Q

Commonest age for testicular tumour?

A

15-44yo

132
Q

Types of testicular tumour?

A

Seminoma 55%
Non-seminomatous germ cell tumour 33% (previously called teratoma)
Mixed germ cell tumour 12%
Lymphoma

133
Q

Tumour markers for testicular cancer?

A

seminomas: hCG elevated in around 20%
non-seminomas: AFP and/or b-hCG elevated in 80-85%
LDH elevated in around 40% of germ cell tumours

134
Q

First line investigation for testicular cancer?

A

ultrasound

135
Q

Management of testicular cancer?

A

Radical orchidectomy
Radiotherapy and chemotherapy also have a place
5 year survival is >90%
Seminomas have a better prognosis

136
Q

What is the mechanism of action of loop diuretics?

A

Blocks Na/K/Cl co-transporter in the thick ascending limb of the loop

137
Q

What is the mechanism of action of thiazide diuretics?

A

Inhibit the NaCl transporter in the distal convoluting tubule

138
Q

What is the mechanism of action of potassium-sparing diuretics?

A

Two types – aldosterone antagonists (inhibit the sodium retaining action of aldosterone)
Epithelial sodium channel blockers in the collecting ducts

139
Q

SEs of loop diuretics?

A

Ototoxicity, electrolyte abnormalities, dehydration, met alkalosis, gout

140
Q

SEs of potassium-sparing diuretics?

A

met acidosis, anti-androgenic effects (e.g. gynaecomastia, impotence)

141
Q

What type of vasculitis is HSP?

A

an IgA mediated small vessel vasculitis

142
Q

What non-renal factors might affect your eGFR?

A

pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being taken

143
Q

Biopsy findings in Goodpasture’s?

A

linear IgG deposits along the basement membrane

144
Q

ECG changes in hyperkalaemia?

A

peaked or ‘tall-tented’ T waves (occurs first)
loss of P waves
broad QRS complexes

145
Q

What is the difference between Alport’s and Goodpasture’s syndrome?

A

Mutations in genes corresponding to the building blocks of type IV collagen cause Alport’s syndrome, whereas autoantibodies against structures that are usually within collagen IV cause Goodpasture’s syndrome

146
Q

Biopsy findings in Goodpastures?

A

linear IgG deposits along the basement membrane

147
Q

Which type of paraneoplastic syndrome can occur in RCC?

A

paraneoplastic hepatic dysfunction syndrome. Also known as Stauffer syndrome. Typically presents as cholestasis/hepatosplenomegaly. It is thought to be secondary to increased levels of IL-6

148
Q

What is fibromuscular dysplasia?

A

a disease that causes one or more arteries in the body to have abnormal cell development in the artery wall. As a result, areas of stenosis, aneurysms, or dissection may occur

149
Q

What are the two most common causes of renal vascular disease?

A

1) Renal artery stenosis (90%)
2) Fibromuscular dysplasia (10%)

150
Q

What are the symptoms of fibromuscular dysplasia?

A

HTN
CKD or more AKI e.g. secondary to ACE-inhibitor initiation
‘flash’ pulmonary oedema

151
Q

What would you see on USS in renal vascular disease?

A

Asymmetric kidneys with the affected side being smaller. Doppler USS would also show disturbance in renal blood flow.
MR angiography - string of bead appearance

152
Q

What is cryoglobulinaemia?

A

Cryoglobulinemia is characterized by the presence of cryoglobulins in the blood. Cryoglobulins are abnormal proteins that thicken and clump together at cold temperatures.
When these proteins clump together, they can restrict blood flow to joints, muscles, and organs.

153
Q

Drugs causing calcium stones?

A

SALT
S - steroids
A - Acetazolamide
L - Loop diuretics
T - Theophylline

154
Q

Endocrine effects of RCC?

A

may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH

155
Q

What would happen to Na in pre-renal AKI as opposed to renal AKI?

A

In pre-renal, kidneys try to hold on to Na to increase the water retention, therefore there will be low URINE Na

156
Q

What is Fanconi’s syndrome?

A

Inadequate reabsorption in the proximal convoluting tubules - multiple causes, results in electrolyte abnormalities

157
Q

At which stage of CKD do you become symptomatic?

A

stage 4 (GFR 15-30)

158
Q

Definition of CKD?

A

impaired renal function for >3 months based on abnormal structure or function, or GFR<60mL/min/1.73m2 with/without evidence of kidney damage

159
Q

Which antihypertensives should be used in CKD?

A

ACEi, then furosemide

160
Q

How should you protect against bone disease in CKD?

A

i. Restrict high phosphate foods (milk/cheese/egg) + give phosphate binders (calcium carbonate) to decreased gut absorption
ii. Vitamin D analogies (alfacalcidol) and Ca supplements decrease the resorption of calcium from the bone

161
Q

How to manage the following symptoms in CKD - anaemia, acidosis, oedema, restless legs/cramps?

A

a. Anaemia – usually d/t reduced erythropoietin levels, check haematocrit and replace iron/B12/folate if necessary -> If still anaemic consider recombinant human erythropoietin
b. Acidosis – Consider sodium bicarbonate supplements for patients with low serum bicarbonate (also may slow progression of CKD)
c. Oedema – high doses of loop diuretics may be needed and restriction on fluid and sodium intake
d. Restless legs/cramps – check ferritin, clonazepam or gabapentin may help. Quinine sulfate can help with cramps

162
Q

When should you refer to a nephrologist in CKD?

A

Refer to a nephrologist if the eGFR falls below 30 or drops by >5 in a year

163
Q

How does CKD cause an increase in phosphate, decrease in calcium and drop in vitamins D?

A

Kidney’s produce vitD -> in CKD vit D levels fall
Kidney’s normally excrete phosphate -> in CKD phosphate levels rise
The low vit D causes low calcium (as vit D is needed to allow Ca absorption)
This causes Ca to be ‘dragged’ out of bone, which causes Osteomalacia and secondary hyperparathyroidism

164
Q

What is the most common cause of death in patients requiring dialysis and why?

A

Ischaemic heart disease
Various factors:
- DM + HTN = leading causes for CKD and also contribute to IHD
- chronic volume overload + anaemia = L vent hypertrophy
- myocardial stunning while undergoing dialysis treatment
- multiple other contributing factors

165
Q

Complications of haemodialysis?

A

Infection/stenosis at the site
Endocarditis
Hypotension
Cardiac arrhythmias
Disequilibrium syndrome – caused by cerebral oedema

166
Q

What causes AR PKD?

A

Due to defect on Chr 6 which encodes for fibrocystin (impt for normal tubular development)

167
Q

When do you normally diagnosis AR PKD and what additional features do you find?

A

Diagnosis can be made on prenatal USS/in early infancy with abdo mass/renal failure
ESRF develops in childhood
Patients also typically have liver involvement

168
Q

What are the causes of sterile pyuria?

A
  • Treated UTI < 2 weeks before
  • Inadequately Tx UTI
  • Appendicitis, prostatitis, bladder tumour etc
169
Q

In which group of patients would you treat asymptomatic pyuria?

A

Pregnant women - at risk of PYELONEPHRITIS, preterm labour, anaemia

170
Q

Advice to prevent UTIs?

A

 Regular voiding/double voiding
 Increased fluids
 Pre + post-sexual intercourse voiding
 Reduced spermatocides (diaphragm/condoms)
 Increased vaginal oestrogens
 Antibiotic prophylaxis (continuously or post-coital)
 Cranberry juice

171
Q

What are the possible causes of testicular lumps that are:
Separate and cystic?
Separate and solid?
Testicular and cystic?
Testicular and solid?
Can’t get above it?

A

Cannot get above it: Inguinoscrotal hernia or hydrocele extending proximally
Separate and cystic: epididymal cyst
Separate and solid: Epididymitis/varicocele
Testicular and cystic: hydrocele
Testicular and solid: tumour, haematocele, granuloma etc

172
Q

Causes of epididymo-orchitis?

A

chlamydia, E. coli, mumps, N. gonorrhoea, TB

173
Q

Symptoms of epididymo-orchitis?

A

Sudden-onset tender swelling, dysuria, sweats/fever

174
Q

Treatment of epididymo-orchitis?

A

warn of possible infertility and symptoms worsening before improving
If <35 (more likely d/t STI) = azithromycin/doxycycline, if gonorrhoea suspected add ceftriaxone
If >35 (more likely d/t UTI) = ciprofloxacin
Also: analgesia, scrotal support, drainage of abscess

175
Q

What is varicocele?

A

Dilated veins of pampiniform plexus

176
Q

What are the symptoms and clinical findings of a varicocele?

A

Left side more commonly affected
Often visible as distended scrotal blood vessels, feels like ‘a bag of worms’
Patients may complain of dull ache

177
Q

How do you treat a varicocele?

A

Associated with sub-fertility, repair via surgery/embolization

178
Q

RF/causes of ED?

A

Multiple
Common = smoking, alcohol and diabetes
Common in >50s

179
Q

What is Buerger’s disease, who is it common in, what do you find on investigation and how is it treated?

A
  • Thrombotic occlusions in the lower limbs (affects large + medium sized vessels)
  • © young male smokers
  • Proximal pulses present, pedal pulses lost
  • Angiography – tortuous corkscrew collateral vessels
  • Tx – smoking cessation
180
Q

What post-void volumes are acceptable and at what age?

A

Post-void volumes of <50 ml are considered physiological in patients aged < 65 years old.
Post-void volumes of < 100ml are considered physiological in patients aged > 65 years old.

MRCP (14 decks)

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