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Finals > Renal/Urology > Flashcards

Renal/Urology Flashcards

1
Q

what are the 3 classical locations for renal stones to get stuck?

A
  1. pelviureteric junction (PUJ)
  2. pelvic brim
  3. vesicoureteric junction (VUJ)

(the three places the ureters are narrowest)

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2
Q

what are most renal stones made up of? what are the other three substances?

A

*calcium oxalate.
- calcium phosphate
- urate
- struvite

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3
Q

give 3 predisposing factors for renal stones

A

hypercalcaemia, sarcoidosis, hyperparathyroidism, high uric acid, UTI, PKD, loop diuretics, antacids

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4
Q

why do renal stones form?

A

form when normally soluble material supersaturates the urine.
must also overcome the inhibitors of crystal formation present in normal urine.

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5
Q

what causes calcium renal stones?

A

hypercalciuria, due to hypercalcaemia - due to e.g. hyperparathyroidism, excess dietary clacium, excessive bone resorption (prolonged immobilisation)

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6
Q

who’s particularly at risk of uric acid stones?

A

those with clinical gout - hyperuricaemia.
those with ileostomies - loss of bicarbonate from GI secretions leads to acid urine, reducing solubility of uric acid.

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7
Q

how might frequent UTIs put you at risk of renal stones?

A

some infecting organisms produce urease

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8
Q

how do ureteric/renal calculi present? how does the pattern of pain relate to innervation of ureters?

A

renal colic - excruciating spasms, ‘loin to groin’.
restlessness, dysuria, desire but inability to void. not normally actually colicky pain.

might get macroscopic haematuria. if N&V, fever - worry about secondary pyelonephritis/pyonephrosis.

loin to groin pain as innervated by ilioinguinal and genitofemoral nerves.

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9
Q

what is the best investigation to visualise renal stones with?

A

KUB/abdo XR (kidney, ureter + bladder) - 50% of stones are radio-opaque. if they do turn up it’s helpful cos it’s easy to do follow up abdo XRs in clinic.
CT-KUB - for radio-lucent stones

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10
Q

what other investigations might you perform in renal colic (apart from imaging)?

A

urine dipstick - 90% +ve for blood, also white cells for secondary infection (MSU for MC&S if present)
calcium and urate levels - 24h urine.

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11
Q

how would you treat a patient with renal stones?

A

depends on size and material of stone. <7mm leave to pass naturally with LOTS OF ANALGESIA (diclofenac)

if >7mm:
- lithotripsy
- lithoplapaxy
- percutaneous nephrolithotomy

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12
Q

give some examples of steps to be taken to prevent recurrence of renal stones

A

drink plenty, normal dietary calcium intake, reduce salt intake

allopurinol for urate stones, pyridoxine for oxalate stones.

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13
Q

define hydronephrosis. what can it lead to?

A

dilatation of renal pelvis - compression and thinning of renal parenchyma - decrease in kidney size.

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14
Q

what happens to the urinary tract proximal to a point of obstruction?

A

dilates

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15
Q

give 3 possible causes of urinary tract obstruction

A

prostatic obstruction - hypertrophy or tumour.
gynaecological cancers (but also other gynae stuff like ovarian cysts/endometriosis - most common kind of cause in young women)
hypercalcaemia.
caliculi (stones).
renal tubular acidosis.
primary hyperoxaluria.
medullary sponge kidney.
TB.

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16
Q

how would acute upper urinary tract obstruction present?

A

loin to groin pain.
superimposed infection ± loin tenderness.
enlarged kidney.

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17
Q

how would chronic upper urinary tract obstruction present?

A

flank pain, renal failure, superimposed infection, polyuria (due to impaired urine concentration).

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18
Q

how would acute lower urinary tract obstruction present?

A

severe suprapubic pain.
symptoms of bladder outflow obstruction.
distended, palpable bladder, dull to percussion.

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19
Q

how would chronic lower urinary tract obstruction present?

A

urinary frequency, hesitancy, poor stream, terminal dribbling, overflow incontinence.
distended palpable bladder.

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20
Q

how would you treat upper urinary tract obstruction?

A

nephrostomy or ureteric stent.
alpha blockers - decrease ureteric spasm, help with stent pain.

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21
Q

how would you treat lower urinary tract obstruction?

A

urethral/suprapubic catheter.
treat underlying cause.
possible large diuresis on relief of obstruction - watch for salt loss!

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22
Q

give 2 pre-renal causes of AKI

A

renal hypoperfusion, sepsis, CCF, cirrhosis, renal artery stenosis, NSAIDs, ACE inhibitors

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23
Q

give 2 renal causes of AKI

A

acute tubular necrosis, PKD, SLE, renal cell carcinoma, myeloma, diabetic nephropathy, drugs, vasculitis, thrombus, HUS, TTP, infections.

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24
Q

give 2 post-renal causes of AKI

A

urinary tract obstruction by stones/clots, blocked catheter, retroperitoneal fibrosis, benign prostatic hypertrophy/prostatic carcinoma

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25
Q

what would be the most worrying investigation result in AKI?

A

hyperkalaemia

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26
Q

what is used as a way to estimate kidney function? why is it good for this?

A

serum creatinine, used to calculate eGFR.
produced by body at pretty steady rate and is excreted by kidneys through glomerular filtration - no reabsorption.
if filtration is impaired, this is shown by high serum creatinine.

serum urea also rises in AKI.

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27
Q

give 3 risk factors for AKI

A

age >75yrs, CKD, cardiac failure, peripheral vascular disease, chronic liver disease, diabetes, drugs, sepsis, poor fluid intake/increased losses

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28
Q

explain the staging of CKD

A

1 - GFR >90, other renal damage
2 - 60-89, other renal damage
3a - 45-59 ± renal damage
3b - 30-44 ± renal damage
4 - 15-29 ± renal damage
5 - less than 15 - established renal failure

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29
Q

give 3 causes of CKD

A

diabetes (type 2»type 1).
glomerulonephritis (IgA nephropathy, SLE, vasculitis).
idiopathic, hypertension, renovascular disease, pyelonephritis, reflux nephropathy, PKD.

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30
Q

give 3 risk factors for CKD

A

diabetes, hypertension, heart disease, smoking, obesity, age >65yrs, FHx

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31
Q

give 3 symptoms of CKD

A

fatigue, weakness, anorexia, vomiting, metallic taste, pruritus, restless legs, bone pain, impotence

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32
Q

give 3 signs of CKD you might find on examination

A

uraemic flab, leuconychia, scratch marks, raised JVP, anaemia, ascites, peripheral neuropathy, AV fistula

usually presents as incidental finding in hypertensive diabetic >50yrs

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33
Q

what lifestyle measures would you ask a CKD patient to take?

A

stop smoking, lose weight, exercise, sodium restriction, increase fluid intake

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34
Q

explain how haemodialysis works

A

blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction - small solutes diffuse down this concentration gradient into the dialysis fluid.

access required via AV fistula, CVC or synthetic graft.
3x hosp trips per week, 4hrs at a time - or at home 5x/week for 2-3hrs.
good for - live alone/frail/elderly or unsuitable for PD e.g. surgery

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35
Q

how can haemodialysis be used to clear excess fluid?

A

ultrafiltration, to create a negative transmembrane pressure, clearing fluid from the blood

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36
Q

give 2 problems with haemodialysis

A

risk of *disequilibration syndrome, hypotension, time consuming.
access problems - need AV fistula or tunnelled venous access line.

complications:
- *access - infection, thrombosis, aneurysm, endocarditis, stenosis
- *hypotension (common), cardiac arrhythmias, air emboli
- N&V, headache, cramps
- *anaphylaxis to sterilising agents
- *disequilibration synd.

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37
Q

explain how haemofiltration works

A

blood is filtered across a highly permeable membrane, allowing movement of small and large solutes by convection.
ultrafiltrate is replaced with an equal volume of fluid.

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38
Q

what is the main problem with haemofiltration?

A

takes a lot longer than haemodialysis - useful in critically ill patients, but impractical long term

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39
Q

explain how peritoneal dialysis works

A

uses the peritoneum as a semi-permeable membrane - catheter is inserted into the peritoneal cavity and fluid infused. sits in the cavity, allowing solutes to diffuse across.

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40
Q

what are the main positives and negatives of peritoneal dialysis?

A

positives - can be carried out at home, ‘ambulatory’ PD can be used, or overnight, so patient leads normal life.

negatives - peritonitis, exit site infection, loss of membrane function over time, herniation at exit site.

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41
Q

give 2 contraindications to renal transplantation

A

active infection, cancer, severe comorbidity

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42
Q

give 2 possible complications of renal transplantation

A

surgical - bleed, thrombosis, infection, hernia.
delayed graft function, drug toxicity, infection, malignancy, rejection.

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43
Q

how would you manage acute rejection of a kidney transplant?

A

high dose IV methylprednisolone + intensify immunosuppression regime.

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44
Q

what 2 genes are associated with ADPKD and what is the difference between them?

A

PKD1 and PKD2.
PKD2 renal cysts develop more slowly - ESRF comes later.

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45
Q

give 3 signs of ADPKD

A

renal enlargement with cysts.
abdo pain ± haematuria (haemorrhaging cyst).
cyst infection, renal caliculi, hypertension, progressive renal failure.

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46
Q

name 2 extra-renal features of ADPKD

A

liver cysts, intra-cranial aneurysm leading to subarachnoid haemorrhage, mitral valve prolapse, ovarian cysts, diverticular disease

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47
Q

how would you treat a patient with ADPKD?

A

aggressive BP management (less than 130/80)

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48
Q

how would you diagnose ADPKD?

A

renal USS.
screen family members using USS too.

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49
Q

what is the difference between ADPKD and ARPKD?

A

autosomal recessive is an infancy disease with renal cysts and congenital hepatic fibrosis

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50
Q

define glomerulonephritis

A

group of disorders where damage to the glomerular filtrating apparatus causes leaking of protein/blood into the urine.
3rd most common cause of ESRF (in adults usually FSGN in nephrotic synd)
changes most likely immune mediated.

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51
Q

give 3 causes of glomerulonephritis

A

SLE, infections (strep throat, HIV), vasculitis, gold, penicillamine, malignancy of breast/bone/myeloma, diabetes, hypertension

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52
Q

what investigation would you perform in glomerulonephritis?

A

renal biopsy

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53
Q

what lung disease is associated with a type of glomerulonephritis?

A

Goodpasture’s syndrome aka anti-glomerular basement membrane disease

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54
Q

explain the pathology of IgA nephropathy

A

patient starts with sore throat/UTI due to streptococcus - triggers an immune reaction, leading to deposition of IgA complexes in the glomeruli

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55
Q

what would a biopsy show with rapidly progressive glomerulonephritis?

A

crescents

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56
Q

how does IgA nephropathy usually present?

A

with macroscopic/microscopic haematuria (occasionally with nephritic syndrome)

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57
Q

what are the features of nephrotic syndrome?

A

normal/mildly high BP.
urine = proteinuria.
GFR = normal to mildly low.
peripheral oedema
hypoalbuminaemia
hyperlipidaemia.

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58
Q

what are the features of nephritic syndrome?

A

BP = moderately/severe high.
urine = haematuria.
GFR = moderate to severely low.

oliguria/AKI
HTN
haematuria - active urinary sediment
it’s an AKI with rapid deterioration in function.

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59
Q

what is seen on renal biopsy in IgA nephropathy?

A

mesangial proliferation, IgA and C3 deposits

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60
Q

what is Henoch-Schonlein purpura? how does it present?

A

systemic variant of IgA nephropathy - causes small vessel vasculitis.
purpuric rash on extensor surfaces, flitting polyarthritis, abdo pain, nephritis.

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61
Q

how would you diagnose Henoch-Schonlein purpura?

A

IgA and C3 deposits seen in renal or skin biopsy

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62
Q

what parts of the kidney are damaged in SLE?

A

vascular, glomerular and tubulointerstitial components

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63
Q

how would you diagnose anti-GBM disease (Goodpasture’s)?

A

serum anti-GBM - autoantibodies to type IV collagen (in GBM)

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64
Q

give some different causes of rapidly progressive glomerulonephritis. what do they all have in common?

A

all show crescents affecting most glomeruli at biopsy.

immune complex disease e.g. post infection, SLE, IgA/HSP.
Pauci-immune disease (ANCA+ve) - granulomatosis with polyangitis (Wegener’s), microscopic polyangitis.
Goodpasture’s.

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65
Q

what specific features would you see on inspecting the urine in acute tubular necrosis?

A

muddy brown casts

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66
Q

what are the 2 most common causes of acute tubular necrosis?

A

renal tubular cell death by ischaemia (renal hypoperfusion) or by nephrotoxins (drugs - tetracycline)

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67
Q

what is the classical triad of clinical features of nephrotic syndrome? explain each one

A

hypoalbuminaemia - due to increased catabolism of reabsorbed albumin in proximal tubules.
proteinuria - due to injury to podocytes - filtration barrier no longer maintained, proteins leak into urine.
oedema - due to lowered plasma oncotic pressure and sodium retention.

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68
Q

name 2 primary causes of nephrotic syndrome

A

minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis (FSGS), mesangiocapillary GN (MCGN)

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69
Q

name 2 secondary causes of nephrotic syndrome

A

hepatitis B/C, SLE, diabetic nephropathy, amyloidosis, paraneoplastic or drug related

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70
Q

how might nephrotic syndrome present?

A

pitting oedema.
urine dipstick massive +ve for protein.

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71
Q

what do the glomeruli of a patient with minimal-change glomerulonephritis look like on light microscopy and electron microscopy?

A

look normal on light microscopy.
on EM - fusion of podocytes.

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72
Q

give 2 things associated with minimal-change glomerulonephritis

A

Hodgkin’s lymphoma, steroids, immunosuppressive drugs, asthma, eczema

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73
Q

how would you treat minimal change glomerulonephritis?

A

high dose prednisolone.
if relapse - ciclosporin/cyclophosphamide.

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74
Q

give 2 causes of membranous nephropathy

A

idiopathic, malignancy, hep B, gold, penicillamine, NSAIDs, autoimmunity.

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75
Q

what would you see on immunofluorescence of a renal biopsy in membranous nephropathy?

A

diffusely thickened GBM with IgG and C3 subepithelial deposits.

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76
Q

explain the difference between immune complex mediated and complement mediated mesangiocapillary GN

A

IC mediated - driven by circulating immune complexes, deposit in kidney and activate complement via classical pathway. SLE/hepC etc.
complement mediated - persistent activation of the alternative complement pathway e.g. due to C3 nephritic factor.

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77
Q

what would you seen on a renal biopsy of a patient with mesangiocapillary GN?

A

mesangial and endocapiallary proliferation.
thickened capillary BM.
tramline capillary walls.
immunofluorescence - Ig staining, complement staining or light chains.

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78
Q

how does focal segmental glomerulosclerosis (FSGS) present?

A

nephrotic syndrome or proteinuria

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79
Q

what would you see on renal biopsy of a patient with focal segmental glomerulosclerosis?

A

scarring of certain segments of some glomeruli.
immunofluorescence shows IgM and C3 deposits.

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80
Q

what is the main cause of urinary incontinence in men?

A

enlarged prostate - urge incontinence or dribbling resulting from partial retention of urine.

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81
Q

define functional incontinence

A

not really to do with physiology - patient is too slow in finding toilet due to immobility, unfamiliar surroundings etc

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82
Q

define stress incontinence

A

leakage from incompetent sphincter e.g. when intra-abdominal pressure rises (coughing, laughing)

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83
Q

who is commonly affected by stress incontinence?

A

pregnant women and following birth.
elderly women - weak pelvic floor.

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84
Q

define urge incontinence (aka overactive bladder syndrome)

A

urge to urinate is quickly followed by uncontrollable emptying of bladder as detrusor muscle contracts

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85
Q

what can precipitate urgency/leakage in urge incontinence?

A

arriving home (latchkey incontinence - conditioned reflex), cold, sound of runnning water, coffee/tea, obesity.

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86
Q

what can cause urge incontinence?

A

detrusor overactivity - malfunction of central inhibitory pathway, or a bladder muscle problem.

also - UTI, diabetes, diuretics, atrophic vaginitis, urethritis.

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87
Q

how could you manage stress incontinence?

A

pelvic floor exercises, surgery or duloxetine

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88
Q

how could you manage urge incontinence?

A

bladder training and weight loss. absorbent pads.
condom catheter for males.
tolterodine (antimuscarinic).

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89
Q

explain the physiology of erections

A

result from NO induced cGMP build up.
cGMP dependent protein kinase activates calcium/potassium channels, hyperpolarising and relaxing vascular and trabecular smooth muscle cells - allows engorgement

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90
Q

how would you identify that a case of erectile dysfunction was due to psychological causes alone?

A

morning erections still occur

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91
Q

name 3 (non-pharmacological) causes of erectile dysfunction

A

smoking, diabetes, alcohol.
hypogonadism, hyperthyroidism, cord lesions, MS, bladder neck/prostate surgery, radiotherapy, atheroma, renal or hepatic failure prostatic hyperplasia, post-priapism.

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92
Q

name 3 drugs that can cause erectile dysfunction

A

digoxin, beta blockers, diuretics, antipsychotics, antidepressants, oestrogens, finasteride, narcotics, alcohol.

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93
Q

what are the treatment options available for erectile dysfunction?

A

counselling.
sildenafil - phosphodiesterase (PDE5) inhibitor - increases cGMP.
vacuum aids.
intracavernosal injections.
transurethral pellets.
prostheses - inflatable or malleable.

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94
Q

list some common side effects of phosphodiesterase inhibitors (e.g. sildenafil)

A

headache, flushing, dyspepsia, stuffy nose

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95
Q

in what layer of the scrotum does a hydrocele form in?

A

tunica vaginalis

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96
Q

give a primary and a secondary cause of hydroceles

A

primary - patent processus vaginalis, resolves in first year.
secondary - trauma, tumour, infection.

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97
Q

what causes a varicocele?

A

dilated veins of the pampiniform plexus

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98
Q

what are epididymal cysts? where do they lie?

A

smooth, extravesical, spherical cysts in the epididymis, containing clear or milky fluid.
live above and behind the testis.

99
Q

what is a hydrocele? how would you treat it?

A

fluid within the tunica vaginalis.
aspiration/surgery.

100
Q

how might a varicocele present?

A

patient complains of dull ache.

visible as distended scrotal blood vessels - feels like bag of worms.

101
Q

how might a patient with testicular torsion present?

A

sudden onset of pain in one testis making walking uncomfortable, pain in abdomen, nausea and vomiting.

102
Q

what causes testicular torsion?

A

spermatic cord twists, cutting off blood supply to testis

103
Q

what would you find on examining the scrotum of a man presenting with testicular torsion?

A

inflammation of one testis - tender, hot and swollen.
testis may lie high and transversely.

104
Q

how must testicular torsion be treated?

A

prompt surgery - expose and untwist the testis, fix both testis to scrotum to prevent recurrence.

105
Q

which layer of the prostate is enlarged in benign prostatic hyperplasia?

A

inner transition zone - layer closest to urethra

106
Q

give 3 symptoms of benign prostatic hyperplasia

A

Storage symps - frequency, nocturia, urgency

Voiding symps - terminal dribbling, poor stream, hesitancy, incomplete voiding

107
Q

what might you feel on PR exam of a man with benign prostatic hyperplasia?

A

enlarged and smooth prostate

108
Q

what investigations should be performed in benign prostatic hyperplasia?

A

Key triad = DRE, TRUSS (± biopsy), PSA
Others:
- bloods - U&E, PSA (be careful with this!)
- urine dip for concurrent UTI
- abdo XR
- bladder scan - how much are they leaving each time they empty
- USS KUB - for hydronephrosis secondary to bladder outflow obstruction

109
Q

how would you manage benign prostatic hyperplasia?

A

for all = behavioural management = avoid caffeine and alcohol, review meds (e.g. diuretics take in morning, or switch to alternative antiHTN), underwear pads, limit pads, bladder training, double voiding

if mild, but not bothered = watch and wait

mild, but bothered about it, or mod/severe = alpha blocker or 5a-reductase, or COX-2 inhibitor (NSAID) e.g. celecoxib

abnormal DRE or elevated PSA = surgical referral. prostate < 80g do TURP. prostate >80g might need open prostatectomy.

110
Q

what type of carcinoma are prostatic carcinomas, usually? which layer of the prostate is affected?

A

adenocarcinoma of peripheral zone - arise from glandular cells.

can present as picked up on PSA testing, or with symps of bony mets (back pain) or generic wt loss, anorexia.

111
Q

how will the prostate feel on PR exam, if it is prostatic carcinoma?

A

“hard and craggy”, irregular/nodular.
when doing PR comment on whether or not prostate gland is still mobile (helps with staging)

112
Q

what essential investigations should be carried out in prostatic carcinoma?

A
  • bloods = FBC, U&E, LFTs (mets), PSA
  • transrectal ultrasound and needle biopsy - for Gleason score
  • CT or MRI ± bone scan for staging
113
Q

name 2 types of testicular tumour

A

seminoma, non-seminomatous germ cell tumour, mixed germ cell tumour, lymphoma

114
Q

name 2 risk factors for testicular tumours

A

undescended testis, infant hernia, infertility

115
Q

how might a testicular tumour present?

A

painless testis lump, secondary hydrocele, may be painful, dyspnoea (lung mets), abdo mass (lymph nodes)

116
Q

which lymph nodes would a testicular malignancy spread to?

A

para-aortic

117
Q

give 3 differential diagnoses of a testicular lump

A

tumour.
inguinoscrotal hernia, epididymal cyst, varicocele, haematocele, orchitis.

118
Q

what 3 tumour markers would you test for in testicular cancer?

A

alpha-fetoprotein, beta-human chorionic gonadotrophin, lactase dehydrogenase

119
Q

how would you treat a testicular tumour?

A

radical orchidectomy.
seminoma = orchidectomy + radiotherapy.

120
Q

give 2 possible causative organisms of acute prostatitis

A

S faecalis, E coli, chlamydia

121
Q

how would acute prostatitis present? what is the difference between this and chronic prostatitis?

A

UTIs, retention, pain, haematospermia, swollen/boggy prostate on PR exam.
chronic = as above, but for 3+ months.

122
Q

how would you treat prostatitis?

A

analgesia, oral levofloxacin

123
Q

give 2 possible causes of epididymo-orchitis

A

if young think STIs (chlamydia, gonorrhoea) or mupms

if >35 UTI more likely (e coli, enterococcus) - esp if bladder outlet obstruction, instrumentation of urinary tract

catheter

124
Q

how would epididymo-orchitis present?

A

unilateral painful swelling (develops over days) - associated with LUTS, sweats/fever, urethral discharge

rule out torsion!!!!!!

125
Q

how would you manage epididymo-orchitis?

A

Ix - first catch urine sample to look for discharge, or NAAT for chlam/gon. urine dip + microscopy/culture. colour duplex USS, surgical exploration (if concerned re torsion)

Rx:
- likely STI? = single dose ceftriaxone IM + 2wks doxycycline PO.
- likely UTI? = levofloxacin for
- supportive measures = rest, scrotal elevation/supportive underwear, NSAID/paracetamol

126
Q

what part of the kidney do renal cell carcinomas arise from and what are they like histologically?

A

80% clear cell/adenorenal carcinoma (renal cortical parenchyma) - large cells with clear cytoplasm.
15% papillary tumour.

RCCs can contain high levels of multiple drug resistance protein P-glycoprotein so CHEMORESISTANT.

127
Q

give 3 clinical features of renal cell carcinoma

A

haematuria, loin pain, mass in flank, anorexia, malaise, weight loss, hypertension

often asymptomatic, incidental diagnosis.

128
Q

what is the Mayo prognostic risk score? what does it take into account?

A

score used to predict prognosis for renal cell carcinoma - SSIGN.
Stage
Size
Grade
Necrosis.

129
Q

what investigation would you use to stage renal cell carcinoma, and what staging system would you use?

A

CT abdo/pelvis, MRI.
Robson score:
I - confined to kidney and <7cm
II - involves perinephric fat/confined to kidney but >7cm

III - spread to renal veins or adrenals
IV - spread to adjacent/distant organs

LNs = para-aortic and hilar.

130
Q

how would you treat renal cell carcinoma?

A

usually either partial nephrectomy, laparoscopic nephrectomy or sometimes just local ablation. radical nephrectomy if stage 3+/

RCC = radio/chemo resistant.

targeted molecular therapy for unresectable tumours = tyrosine kinase inhibitor - first line e.g. sunitinib +/- palliative local radiation and bisphosphonates for bone mets.

131
Q

what is a nephroblastoma?

A

childhood tumour of renal tubules and mesenchymal cells

Wilm’s tumour - abdo mass + haematuria.

132
Q

where can urothelial tumours arise from and what are they also known as? what other kinds of tumour might be found in bladder cancer?

A

bladder, ureter and renal pelvis.
aka transitional cell tumours.

other, rarer forms of bladder cancer = SSC, adenocarcinomas

133
Q

give 3 risk factors for bladder cancers

A

for general bladder Ca - increasing age, being male, smoking,
specific to TCC - dye factories (exposure to aromatic amines)
SCC - schistosomiasis, long term indwelling catheter, recurrent bladder stones

134
Q

what significant presenting feature would make you suspect a bladder cancer?

A

painless haematuria!!

other features - if large clots, might get stuck = acute retention.
15% of bladder Ca presents with urinary frequency.

135
Q

how would you investigate a bladder cancer?

A

cystoscopy + biopsy - either rigid or flexible, any painless haematuria should be referred for this really.
- bloods: FBC (anaemia), U&E (poss ureteric obstruction)
- MSU: for any associated UTI
- CT/MRI for staging

136
Q

explain the staging and grading system for bladder cancers

A

Tis - carcinoma in situ, Ta - confined to epithelium, T1 - in lamina propria
= transurethral resection.

T2 - superficial muscle involved, T 3 - deep muscle/perivesical fat involved
= radical cystectomy.

T4 - beyond bladder
= palliative chemo/radiotherapy.

Grades 1-2 = low grade, Grade 3 = high grade

137
Q

how might gonorrhoea present in a male?

A

urethral pus ± dysuria.
tenesmus.
proctitis ± discharge PR.

138
Q

how might gonorrhoea present in a female?

A

usually asymptomatic.
vaginal discharge, dysuria, proctitis.

139
Q

how would you manage gonorrhoeal urethritis?

A

encourage safe sex. contact tracing.
ceftriaxone IM (+ azithromycin oral for chlamydia)

140
Q

give 3 organisms that can cause non-gonorrhoeal urethritis

A

C trachomatis, ureaplasma urealyticum, mycoplasma genitalium, trichomonas vaginalis, gardnerella, Gram -ve anaerobic bacteria, candida

141
Q

how would you treat non-gonorrhoeal urethritis?

A

azithromycin oral or doxycyline.
contact tracing.

142
Q

when are UTIs considered complicated?

A

when occurring in men and children

143
Q

what is the organism that causes most UTIs?

A

E coli

144
Q

name 3 organisms that can cause a UTI

A

*E coli.
proteus mirabili
Klebsiella penumonia.
pseudomonas

145
Q

give risk factors for UTI
what about for pyelonephritis?

A

female gender.
sexual intercourse, exposure to spermicide in females (diaphragm/condom), pregnancy, menopause, immunosuppression.
urinary tract - obstruction, stones, catheter

risks for pyelonephritis - structural abnormalities, calculi, catheters, pregnancy, diabetes

146
Q

how would acute pyelonephritis present (kidney infection)?

A

high grade/swinging fever, rigors, N&V, loin pain, oliguria
O/E - febrile, renal angle tenderness, dehydration
renal angle = between last rib and lateral border of erector spinae muscle

147
Q

how would cystitis present (bladder infection)?

A

frequency, dysuria, urgency, haematuria, suprapubic pain

148
Q

how would you investigate a UTI?

A

dipstick urine - nitrites, WCC. maybe blood too if pyelonephritis
bloods - FBC, U&E, blood cultures (esp if pyelonephritis - risk fo sepsis)
if pyelonephritis consider US KUB for horeshoe kidneys/other kidney abnormalities. can also see if there’s a stone that’s caused the infection.

imaging mandatory in recurrent pyelonephritis = renal uss, contrast ct, ?DMAS for renal scarring.

149
Q

how would you treat a UTI?

A

drink plenty of fluids, urinate often.
trimethoprim, amoxicillin.

if pyelonephritis - admit for IV abx (gentamicin used in Sheffield - but only if adequate renal function)

150
Q

give 3 causes of sterile pyuria

A

TB, appendicitis, PKD, calculi, bladder tumour

151
Q

what drugs can cause AKI and why?

A

aspirin/NSAIDs - prostgalandins normally cause vaosdilation of the afferent arterioles of the glomeruli, so using NSAIDs restricts the blood flow through the glomeruli - causes hypoperfusion.
ACEi - normally angiotensin II causes vasoconstriction of the efferent arterioles which increases the GFR so the inhibition the production of ATII causes vasodilation of the efferent arterioles causing more blood to flow out, loweringthe GFR and leading to damage.

152
Q

when suffering from chronic renal failure, many patients develop anaemia - why is this, and how is it treated?

A

Epo is produced by the kidneys and controls the rate of RBC production by acting on EPO receptors.
in CKD, the specialised cells that produce Epo are destroyed, leading to decreased red cell production - use recombinant Epo to treat the anaemia.

153
Q

how do gonadotrophin-releasing analogues help treat prostatic carcinoma?

A

acts as agonist of pituitary GnRH receptors - interrupts normal secretion levels and indirectly downregulates secretion of gonadotrophins, leading to hypogonadism and dramatic reduction in testosterone.
testosterone causes prostatic growth, so when blocked, the carcinoma stops proliferating.

154
Q

name 2 alpha blockers. what are they used for?

A

doxazosin, tamsulosin, alfuzosin.
used for benign prostatic hyperplasia, and to aid passage of kidney stones.

155
Q

how do alpha blockers work?

A

highly selective for alpha1 adrenoreceptor found mainly in smooth muscle (including blood vessels, bladder neck and prostate).
stimulation induces contraction, blockage induces relaxation - causes vasodilation and a fall in BP, and a reduced resistance to bladder outflow.

156
Q

what class of drug is finasteride and what is it used to treat?

A

5 alpha reductase inhibitors.
treats benign prostatic hyperplasia as an add on to alpha blockers.

157
Q

how does finasteride work?

A

5 alpha reductase is an enzyme converting testosterone to dihydrotestosterone - blocking this conversion results in a dramatic decrease in serum dihydrotestosterone levels - reduces prostatic volume so improves symptoms of the enlarged prostate and reduces risk of cancer.

158
Q

what is important to note, when giving a patient finasteride?

A

it lowers prostate specific antigen, so there’s a risk it will hide prostatic cancer

159
Q

what class of drug is sildenafil, and how does it work against erectile dysfunction?

A

phosphodiesterase V (PDE5) inhibitor.
PDE5 is found mainly in the smooth muscle of the corpus cavernosum of the penis - sildenafil causes arterial vasodilation by inhibiting PDE5, leading to increased cGMP concentrations.
this causes arterial smooth muscle relaxation, vasodilation and penile engorgement.

160
Q

give some possible SEs of sildenafil

A

flushing, headache, dizziness, nasal congestion.
hypotension, tachycardia and palpitations.

161
Q

give 2 antimuscarinics with GU uses, and what they are used for.

A

oxybutin, tolterodine, solifenacin.
to reduce urinary frequency, urgency and urge incontinence in overactive bladder.

162
Q

name 2 androgen receptor blockers. what are they used for?

A

flutamide, bicalutamide, cyproterone acetate.
used to treat prostate cancer.

163
Q

how do androgen receptor blockers work?

A

they decrease the body’s response to androgens, so are beneficial in prostate cancer, as the cells require androgen for growth.

164
Q

give an example of a vasopressin receptor antagonist. what are they used for?

A

lixivaptan, mozavaptan, satavaptan.
used to treat PKD.

165
Q

describe where the kidneys are - what surrounds them?

A
  • retroperitoneal organs
  • spinal levels T12 to L3
  • R sits lower than L due to the liver
  • adrenal gland sits on top of each one
  • adrenal glands + kidneys are surrounded by paranephric fat
  • paranephric fat is then enclosed in layer of fascia (renal/Gertoa’s fascia)
166
Q

describe blood supply to/from kidney

A
  • each kidney has a renal artery + a renal vein
  • artery divides into segmental arteries, each supply separate segment of the kidney
167
Q

describe the flow of urine through the kidney

A

main job of kidney = produce/concentrate urine!
- occurs at nephron
- urine produced by each nephron drains into minor calyces of kidney
- these drain into major calyces –> into renal pelvis
- renal pelvis narrows and descends to form ureters

168
Q

what hormone concentrates urine? where is it produced? what cells of the kidney does it act on?

A

ADH (antidiuretic hormone)
secreted by posterior pituitary gland
synthesied by supraoptic + paraventricular nuclei in hypothalamus
- acts on distal convoluted tubule, collecting ducts

169
Q

briefly outline the steps involved in concentration of urine

A

glomerular filtration –> tubular resorption –> countercurrent multiplication

170
Q

apart from producing and concentrating urine, list some other functions of the kidneys

A
  • electrolyte regulation
  • renin production/BP regulation
  • erythropoietin production
  • conversion of vit D to active hydroxylated form
  • acid-base regulation
171
Q

briefly describe pathway leading to angiotensin II production

A

renin production in juxtaglomerular apparatus is stimulated by reduced NaCl to distal tubule, reduced perfusion pressure to kidney, and/or sympathetic stimulation.

renin used in conversion of angiotensinogen to angiotensin I.
ACE converts angiotensin I to II.

172
Q

what are the key functions of angiotensin II?

A
  • vasoconstriction of arterioles
  • reabsorption of Na+ by kidneys
  • release of aldosterone
  • thirst stimulation + ADH release
173
Q

how do ACE inhibitors work?

A

inhibit ACE - prevents conversion of angiotensin I to II
=> reduced vasconstriction
=> reduced BP

174
Q

what are the main functions of hydroxylated vitamin D?

A

prehormone that gets metabolised in kidneys into calcitriol (active vitamin D).
this increases level of Ca2+ in blood by increasing gut absorption, kidney reabsorption and resorption from bone.

175
Q

describe the course of the ureters

A

ureteropelvic junction –> descends medial to psoas muscle –> over pelvic prim + into pelvis –> descends along pelvis’ lateral wall –> joins back wall of bladder forming vesicoureteric junction

176
Q

describe the innervation of the ureters?

A

autonomic nervous system
nerve fibres from SNS originate from T10-L1; never fibres from PNS come from S2-S4

177
Q

briefly describe anatomy of bladder, including innervation for voiding etc

A

sits behind pubic synthesis.
main muscle layer = detrusor muscle.
detrusor innervated by autonomic nervous system:
- parasympathetic NS causes detrusor contract (PNS makes you Pee) - nerves for this come from sacral spinal cord.
- sympathetic NS causes detrusor relaxation (SNS makes you Stop peeing) - nerve fibres for this come from lumbar spinal cord.

ureters join bladder at oblique angle which closes off when detrusor contracts, preventing reflux of urine.

178
Q

what neurotransmitter is needed for bladder contraction? how does this relate to what drugs can be used for urge incontinence?

A

acetylcholine (acts on M3 muscarinic ACh receptors)

so anticholinergics/antimuscarinics e.g. oxybutynin.

179
Q

what are the four parts of the male urethra?

A
  • prostatic = bit that goes through middle of prostate
  • membranous = bit surrounded by external urethral sphincter
  • bulbar = first part of the anterior urethra (which is the bulbar + penile sections), lined with stratified epithelium. site of most idiopathic strictures.
  • penile = bit going through penis to external urethral meatus.
180
Q

describe the path of the female urethra

A

internal urethral sphincter of bladder –> vestibule enclosed by labia minora
lives in front of vagina

181
Q

briefly describe anatomy of the prostate gland

A

relations:
- ant = pubic symphysis
- post. = seminal vesicles + rectum
- distal = pelvic floor and external urethral sphincter
- proximal = bladder

through middle = prostatic urethra
surrounded by fascia capsule.
drained by venous plexus –> internal iliac veins

182
Q

red flag symptoms for a pt with LUTS?

A
  • back pain
  • wt loss
  • haematuria
  • recurrent UTI
  • new renal impairment
  • palpable bladder
  • high PSA
183
Q

what receptors does doxazosin act on? how does this link to the SEs a patient should watch out for?

A

alpha1 adrenoceptors - also found in bronchioles, iris dilator muscles, seminal tract, salivary gland, heart muscle.

SEs therefore incl - low BP, dizziness, SOB, diarrhoea etc

184
Q

what’s the clinical difference between acute and chronic urinary retention?

A

acute = sudden, painful inability to pass urine
chronic = gradual, painless increase in vol. residual urine

185
Q

list some causes of acute vs chronic urinary retention

A

acute = prostatic obstruction, urethral strictures, anticholinergic, “holding”, cauda equina, post-op (pain/inflammation/anaesthetics), UTI, constipation, cancer

chronic = BPH or prostate Ca, pelvic malignancy, rectal surgery, DM, CNS disease (e.g. MS).

186
Q

give some causes of raised PSA apart from prostate Ca

A
  • UTI
  • BPH
  • prostatitis
  • acute retention
  • TURP
  • catheterisation
187
Q

explain Gleason grading

A

used for histology of prostate Ca, runs from 1-5.
1 = low grade
5 = severely high grade
for the Gleason score, the Gleason grade of the two most common histological patterns are added together.
therefore score is /10 (min. 2 - but practically you don’t get <6 on needle biopsy).

188
Q

how does TNM staging influence management of prostate Ca?

A

T1-2 = active surveillance, radical prostatectomy, radical radiotherapy, brachytherapy
T3-4 = combination of androgen deprivation therapy (ADT) w/ external beam radiotherapy, OR watchful waiting

189
Q

what’s the difference between active surveillance and watchful waiting?

A

active surveillance = using PSA + DRE every 6/12 to closely monitor. will aim for cure when Rx commenced.

watchful waiting = fewer tests, used when you reckon something else will kill them first, any Rx will be palliative.

190
Q

what is brachytherapy?

A

internal radiotherapy - radioactive seed/rod thing inserted and left in there to do the therapy.

191
Q

how does androgen deprivation therapy work? what’s second line if/when this doesn’t work?

A

growth of mets driven by testosterone, therefore to Rx metastatic prostate Ca you need to androgen deprive either medically or surgically (orchidectomy).
medically = course of LH releasing hormone (LHRH) analogues. after a while all this extra LH downregulates the LH receptors on testes, so they stop making testosterone.

second line = taxane-based chemo, abiraterone or oestrogens.
± palliative radiotherapy for bony pain.

192
Q

what is the initial affect of LHRH therapy on testosterone levels?

A

initial testosterone surge - can worsen symptoms.
started on an oral anti-androgen initially before switching to injection to help counter the effect of this.

193
Q

what is pyonephrosis?

A

specifically an infection of the collecting system

194
Q

ig a patient has developed pyelonephritis or pyonephrosis secondary to a stone what needs doing urgently?

A

need a nephrostomy sited urgently - allows infected urine sitting in renal pelvis to drain (prevents further complications)

195
Q

how is bladder cancer treated, according to stages/grades?

A
  • low-grade non-invasive cancers = G1-2, Ta tumours = TURBT, then intravesical chemotherapy (curative intent, surveillance F/U)
  • high-grade invasive cancer = G3 T2-3 tumours = radical cystecomty + lymphadenectomy, OR radical radiotherapy w/ (neo)adjuvant systemic chemo (can be curative intent)
  • metastatic bladder cancer = T4 tumours = symptom control and palliation
196
Q

give examples of intravesical chemo agents, how is it given?

A

e.g. BCG, mitomycinc
3 way catheter put in - chemo injected through the third tube into the bladder (tube 1 = urine, tube 2 = balloon)

197
Q

what are the different reconstructive options after a radical cystectomy?

A
  • bladder reconstruction (orthoptic bladder)
  • ileal conduit w/urinary diversion (ureters are plugged into piece of isolated ileum, which is made into a stoma which drains urine)
  • continent urinary diversion
198
Q

name a scoring system that might be used in BPH

A

IPSS (international prostate symptom score) - 0-35, incl. QOL rating.
mild = 0-7, mod = 8-19, severe = 20+

199
Q

list some possible complications of BPH

A
  • progression (reduced by alpha blockers)
  • sexual dysfunction (due to alpha blockers/5a-reductase or surgical management)
  • acute urinary retention
  • TURP syndrome
200
Q

what is TURP syndrome? Rx?

A

rare but life threatening.
due to absorption of irrigating fluids into prostatic venous sinuses.
- fluid overload, disturbed electrolytes (esp hyponatraemia), hypothermia

Rx 0 supportive, 100% O2 NRBM, arterial line for BP monitoring, correct hyponatraemia

201
Q

management for acute urinary retention?

A

immediate + complete bladder decompression with catheter.
offer men an alpha blocker prior to removal

then - TWOC, ?prostate surgery etc (all depends on cause)

poss. complications retention = UTI, AKI

202
Q

what genes have a role in prostate Ca?

A

BRCA
HPC-1 (hereditary prostate cancer)

203
Q

list some possible causes of haematuria

A

medical:
- UTI
- anticoagulation
- coagulopathies
- “pseudocontamination” menstrual blood
- pyelonephritis
- trauma/instrumentation

surgical:
- stones
- urological malignancy
- BPH

204
Q

what is prostatitis? how does it feel on examination? causes etc

A

infection of prostate - mostly e.coli, also enterococcus/pseudomonas
O/E - warm/soft, “boggy” prostate.
present with lower abdo/ejaculatory/rectal/perineal PAIN.

acute prostatitis = painful inflammation w/ evidence of recent/current infection
chronic = lasting 3+ months, may or may not be bacterial

205
Q

how do you Ix and Rx prostatitis?

A

Ix- urinalysis/culture, culture of prostatic secretions (“by massage” - grim), blood cultures if febrile, PSA, STI screen, TRUSS if ?abscess

Rx:
- ?sespis = sepsis six, NSAID, SPC to relieve obstruction, drain abscess
- no sepsis = 2-4 weeks ciprofloxacin + NSAID + relieve obstruction + drain any abscess
- chronic = 4-6 weeks cipro ± NSAID ± alpha blocker

206
Q

what is a normal GFR? what actually is eGFR?

A

normal = 120 ml/min/1.73msq
20% of cardiac output.

eGFR = predicted using blood creatinine and age, gender, race, sex

creatinine = chemical waste product from muscle metabolism. gets secreted as well as filtered! so Cr clearance is > GFR.
inhibitors of secretion will make Cr rise and function look worse e.g. trimethoprim.

207
Q

what systems in the kidneys help with volume control and pressure control?

A

RAAS = responds to low blood pressure (detected as decreased renal perfusion)

aldosterone = decreased excretion
angiotensin II = decreased excretion
ANP released by heart in response to high pressure increases excretion

208
Q

how are the kidneys involved in blood pressure control?

A

via combo of volume control and vasoconstriction.

decreased BP at afferent arteriole –> juxtaglomerular apparatus –> renin
prostaglandin - dilates afferent arteriole
angiotensin II - constricts efferent arteriole (to maintain GFR)

209
Q

where does sodium reabsorption take place?

A

70% is in proximal tubule
25% loop of Henle
5% distal convoluted tubule
2% collecting duct
there’s different channels etc

water follows sodium.

watch youtube vids on nephron function…

210
Q

briefly outline potassium control by kidneys

A
  • freely filtered at proximal tubule and loop of Henle
  • distal secretion determines rate of renal excretion (driven by Na and aldosterone)
211
Q

give examples of drugs that can cause hypo or hyperkalaemia

A

hypoK+ = loop diuretics, thiazide diuretics
hyperK+ = spironolactone, amiloride, ACEi, ARB

212
Q

how does erythropoietin work in terms of kidneys?

A

erythropoietin stimulates RBC production
renal cortex acts as an O2 sensor - blood flow and O2 requirement are matched.

therefore at low GFR, can become anaemic (GFR <30) as Epo not being stimulated.

213
Q

give some brief info on what gets reabsorbed etc at proximal convoluted tubule

A

70% of filtrate reabsorbed - most essential things get reabsorbed here!
incl:
nutrients - glucose, amino acids
ions - Na, K, Cl
small plasma proteins
some urea and uric acid

move by either active or passive transport.

214
Q

what happens in the loop of Henle?

A

thin descending limb absorbs water, thick ascending limb does other jobs.

concentrates or dilutes fluid by countercurrent multiplication.
key transport = NKCC2: Na K Cl Cotransporter (energy dependent)

furosemide = loop diuretic.

215
Q

what happens in distal convoluted tubules and collecting ducts?

A

sodium reabsorption = 5% @ early DCT, 3% @ late DCT and CD determining how much sodium is excreted

transporters = sodium/potassium ATPase drives reabsorption of calcium and chloride.

hormones = sodium reabsorption regulated by aldosterone and ADH

216
Q

what is the function of the distal convoluted tubules?

A
  • reabsorb Na through coupled secretion of H+ or K+ ions into tubular fluid via aldosterone
  • acidifies urine through secretion of hydrogen or ammonium (late) - acid-base balance
  • electrolyte homeostasis - Ca reabsorption via Vit D dependent process
  • part of juxtaglomerular apparatus that regulates renin release

main channel - passive Na/Cl co-transporter - prevents reabsorption of sodium and water

217
Q

what hormones act on distal convoluted tubule? what diuretic?

A

1) PTH - Ca reabsorbed and phosphate excreted
2) *aldosterone - more Na absorbed (ENaC), more K excreted (ROMK) - mainly at collecting ducts though
3) ANP - causes DCT to excrete Na

diuretics - thiazides (+amiloride/potassium sparing)

218
Q

what is the function of collecting duct? what are the major cell types and channels?

A
  • concentration of urine and regulation of acid/base balance
  • principle cells - respond to aldosterone and vasopressin affecting sodium/potassium
  • also: alpha intercalated cells, beta intercalated cells (secrete H+)
  • channels = ENaC and ROMK in principle cells
219
Q

what are the important hormones that act on collecting duct and what’s the mechanism?

A

aldosterone and ADH/vasopressin
- aldosterone increases expression of ENaC in apical membrane and N+/K+ antiporters
- vasopressin binds V2 channels and insert aquaporin 2 channel to apical membrane allowing free movement of water
- alpha intercalated cells secrete acid to urine
- beta intercalated cells secrete bicarbonate to urine

220
Q

how do aldosterone antagonoists work?

A

work at collecting duct - spironolactone (weak, useful in cirrhosis when aldosterone is increased).
spare K+.
competitive binding of aldosterone receptor.

effects - hypotension, hypoNa, hyperK, gynaecomastia (compliance issues!)

drugs that work at collecting duct (K+ sparing diuretics) shouldn’t be used with other K+ sparing drugs like ACEis or ARBs

221
Q

how do potassium sparing diuretics work?

A

e.g. amiloride (weak but can use in combo with other diuretic to counteract potassium loss e.g. co-amilofruse).

work at DCT on ENaC to inhibit absorption of sodium and water.

effects - hypotension, hypoNa, hyperK+

drugs that work at collecting duct (K+ sparing diuretics) shouldn’t be used with other K+ sparing drugs like ACEis or ARBs

222
Q

what is renal tubular acidosis?

A
  • numerous disorders in which excretion of acid or reabsorption of bicarbonate is disproportionate to GFR.
  • results in hyperchloraemic metabolic acidosis + hypobicarbonataemia + decreased arterial pH + normal anion gap

may be hypo or hyper K+ depending on exact defect.

mainly due to Fanconi syndrome or drug induced - all rare.
there are different types but this seems a bit niche?

223
Q

what is Fanconi syndrome?

A

myeloma proteins and various drugs cause proximal tubule injure so you get a proximal RTA, or can be AD inherited.
bicarb <18

224
Q

how does RTA (renal tubular acidosis) present?

A
  • growth retardation/failure to thrive
  • muscle weakness (if Fanconi)
  • hypoglycaemia after fructose
  • rickets (persistent phosphate loss in some types of RTA)
  • distal RTA with deafness = inherited
  • Kussmaul breathing if severe
  • RFs = childhood, urinary tract obstruction, DM, adrenal insufficiency
225
Q

what would investigations show in renal tubular acidosis?

A
  • low serum bicarb
  • high serum chloride
  • variable potassium
  • arterial pH low
  • serum anion gap normal (12-18)
  • urine pH >5.5
226
Q

management of RTA?

A

depends on type.
sodium or potassium alkali e.g. Shohl’s solution +/- potassium supplementation +/- thiazide diuretics
etc

227
Q

list the possible complications of renal tubular acidosis

A

1) volume depletion - loss of sodium etc at proximal tubule dysfunction
2) nephrocalcinosis
3) osteoporosis - secondary to bone buffering of acidosis –> demineralisation
4) growth retardation - acidosis assoc. w/ muscle catabolism
5) renal rickets - in Fanconi as can’t reabsorb phosphate

228
Q

list some possible causes of end stage renal failure

A

1) glomerulonephritis
2) pyelonephritis
3) diabetes
4) polycystic kidney disease

229
Q

give some risk factors making an individual more susceptible to getting complicated pyelonephritis

A

1) age - infants and older people
2) structural abnormalities - VUR, PKD, horseshoe, double ureter
3) foreign body - stone, catheter
4) impaired renal function
5) immunocompromised e.g - DM, sickle cell, transplant, malignancy, radio/chemo, alcohol, HIV, steroids
6) instrumentation - cystoscopy
7) male (less likely to get lower UTI though)
8) obstruction - BPH, stone etc
9) pregnancy

230
Q

management of pyelonephritis

A

if mild/mod + uncomplicated = ciprofloxacin (500mg PO BD 7-14 days) or cefixime

if severe/complicated/pregnant - admit, IV ceftriaxone or ciprofloxacin or gentamicin (not if pregnant), IV fluids, IV paracetamol. consider catheterisation.

231
Q

how would you investigate a RCC?

A
  • BP - increased from renin secretion
  • percutaneous renal biopsy
  • FBC - polycythaemia (EPO)
  • LDH - raised = poor prognosis
  • corrected calcium = >2.5 poor prognosis
  • LFT = raised AST/ALT = mets
  • *Cr = elevated if reduced clearance
  • urinalysis = haematuria and/or proteinuria

imaging:
- abdo/pelvis USS and/or CT
- MRI
- CXR = cannonball mets, might also do bone scan, MRI brain/spine

232
Q

what is AKI?

A

= acute decline in GFR from baseline/increase in Cr with or without oliguria (<0.5ml/kg/hr)/anuria (<50ml/day)

results in impaired clearance and regulation of metabolic homeostasis, impaired acid-base, electrolyte and vol. reduction.
due to impaired renal perfusion, nephrotoxic drugs, outflow obstruction or intrinsic renal disease.

233
Q

list the main nephrotoxic drugs according to prerenal/intrarenal/postrenal

A

Pre-renal= drugs causing GI loss, NSAIDs (hypoperfusion), ACEi (if compromised perfusion, mustn’t prescribe w/NSAIDs)

Intrarenal =
- glomerulonephritis - captopril, penicillamine, gold, penicillins, rifampicin
- interstitial nephritis - penicillins, cephalosporins, thiazide, furosemide, NSAIDs, rifampicin
- ATN = aminoglycosides, amphotericine, ciclosporin

Post-renal = anticholinergics (TCA) + alcohol –> retention

CANT DAMAG:
Contrast, Abx (penicillin/ceph), NSAIDs, Therapeutic index (narrow), Diuretics, ACEi, Metformin, ARB, Gentamicin/gold

234
Q

how is AKI classified into stages?

A

1) Stage 1:
- Cr: 1.5-1.9 x baseline
- ≥26.5 micromol/L increase in Cr
- Urine output <0.5mL/kg for 6h
2) Stage 2
- Cr: 2.0-2.9 x baseline
- Urine output <0.5mL/kg for 12h
3) Stage 3
- Cr: ≥3 x baseline
- Cr: ≥ 354
- RRT started
- Urine output < 0.3mL/kg for 24hr or anuria for 12 hrs

235
Q

how can AKI present?

A

usually vague/nondescript - depends a lot on cause, often just routine U&E monitoring:

  • Decreased urine
  • Vomiting (early could be causative, late could be uraemia)
  • Dizziness (orthostatic suggests pre-renal)
  • Orthopnoea (fluid overload)
  • Altered mental status (uraemia)
  • Signs of uraemia (asterixis)
  • Peripheral oedema
  • Hypertension
  • Hypotension
  • Muscle tenderness (rhabdomyolysis)
236
Q

Ix for AKI?

A

1) U+E+Cr:
*Elevated creatinine, *high serum potassium (or on *VBG), *metabolic acidosis

2) Urine dip, MC + S - Infection -> leukocytes/nitrates
Glomerular disease -> blood/protein
3) FBC - Anaemia (CKD/blood loss), leukocytosis (infx), thrombocytopenia (HUS, TTP)
4) Imaging *priority if anuric
Renal USS -> obstruction, cysts, mass
5) *ECG - for *hyperkalaemia - increased PR, widened QRS, peaked T, sine wave
6) Ratio serum urea:creatinine + other tests of cause (20:1 -> pre-renal cause)

237
Q

outline basic approach to managing AKI

A

1) stop nephrotoxic drugs
2) ABCDE - incl. fluid challenge if hypotensive, diuretic if hypertensive
3) catheterise for accurate UO
4) urgent VBG/ABG for K+ and ECG
5) urgent USS KUB if ?obstruction - ?nephrostomy
6) urine dip for glomerulonephritis/infection
7) if uraemia, severe metabolic acidosis or severe hyperkalaemia - dialysis.

238
Q

give some possible complications of CKD

A
  • anaemia - due to diminished EP
  • renal osteodystrophy
  • CVD (CKD is RF)
  • protein malnutrition due to loss in urine
  • hyperkalaemia
  • metabolic acidosis
  • pulmonary oedema
239
Q

what would Ix show in CKD?

A
  • Serum creatinine elevated
  • Urinalysis: haematuria or proteinuria
  • Urine microalbumin: microalbuminuria
  • Renal USS: small kidney, obstruction/hydronephrosis, large kidney (infiltration myeloma, amyloidosis)
  • eGFR < 60
  • Blood sugar
  • FBC - anaemia, normochromic normocytic
  • Osteodystrophy: hypocalcaemia, hyperphosphataemia and hyperparathyroidism, high alkaline phosphatase
  • Antibodies: autoantibodies, antibodies to streptococcal antigens of hep B/C antibodies
240
Q

management of CKD?

A
  • ID and Rx all reversible causes, tight glycaemic/BP control
  • treat complications:
    anaemia - EPO +/- ferrous sulfate if needed
  • treat renal bone disease - diet, phosphate binding drugs, calcitriol
  • oedema - loop diuretics, sodium restriction
  • high potassium - low K+ diet
  • Stage 5 or uraemia = RRT (dialysis or transplant)
241
Q

give indications for RRT (dialysis) in AKI

A

1) Uraemia (pericarditis, gastritis, encephalopathy)
2) Pulmonary oedema (fluid retention) unresponsive med Rx
3) Severe hyperkalaemia (>6.5) unresponsive to med Rx
4) Severe hypo/hypernatramia
5) Severe metabolic acidosis (<7.0) unresponsive to bicarb
6) Severe renal failure (urea > 30)

242
Q

list some possible complications of nephrotic syndrome

A
  • susceptibility to infection (increased urinary loss of IgG) or 2ndary to steroids
  • hypercoagulable/thromboembolism
  • hypercholesterolaemia
  • hypervolaemia
  • AKI
  • HTN
243
Q

how does glomerulonephritis tend to present?

A

with RFs + haematuria + oedema + oliguria

other features hint at cause:
- Anorexia/nauseas -> vasculitic
- Weight loss -> systemic
- Fever -> infectious aetiology
- Skin rash -> vasculitic
- Arthralgia -> vasculitic
- Abdo pain -> HSP and post-streptococcal glomerulonephritis
- Haemoptysis -> in anti-glomerular basement membrane disease and Wegener’s

244
Q

management of glomerulonephritis?

A

mild = treat cause and supportive measures e.g. abx, antivrials, withdraw drug, limit salt + fluid

mod/severe = oral meds:
- ACEi/ARB reduce proteinuria, + abx + furosemide + prednisolone w/immunosuppressant

rapidly progressive - IV meds = plasma exchange, IV methypred, IV cyclophos etc

depends on cause

Finals (15 decks)

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