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Phase 2a - Systems > Genitourinary > Flashcards

Genitourinary Flashcards

1
Q

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

A
  1. pelviureteric junction
  2. pelvic brim
  3. vesicoureteric junction
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2
Q

what are most renal stones made up of? give some other possible constituents

A

*calcium oxalate.

phosphate, urate, hydroxyapatite, mixed.

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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 are 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

describe the pain of renal colic

A

excruciating spasms, ‘loin to groin’.

often with nausea, comes and goes in waves, restlessness, dysuria, desire but inability to void.

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9
Q

what is the best investigation to visualise renal stones with?

A

KUBXR (kidney, ureter + bladder) or spiral CT

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10
Q

what other investigations might you perform in renal colic?

A

urine dipstick - 90% +ve for blood.
MSU for MC&S.
24h urine for calcium, oxalate, urate, citrate sodium, creatinine, stone biochemistry

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11
Q

how would you treat a patient with renal stones?

A

analgesia - diclofenac.

if 5mm - shock wave lithotripsy - US waves shatter stone.

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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, 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.
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

how would you investigate AKI?

A 
ABCs - asses volume status for C! urgent potassium check for hyperkalaemia.
urine dipstick + MC&S.
renal USS, CT KUB.
renal biopsy.
FIND CAUSE basically.
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29
Q

how would you manage a patient with AKI?

A

IV fluids.
hyperkalaemia - calcium, glucose and insulin.
stop nephrotoxic drugs - NSAIDs, ACEis etc.
treat cause.

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30
Q

explain the classification 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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31
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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32
Q

give 3 risk factors for CKD

A

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

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33
Q

give 3 symptoms of CKD

A

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

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34
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

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35
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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36
Q

how would you medically manage CKD?

A

stop nephrotoxic drugs, tight glucose control.

ACEi or ARB to target BP less than 140/90

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37
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.

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38
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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39
Q

give 2 problems with haemodialysis

A

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

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40
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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41
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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42
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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43
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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44
Q

give 2 contraindications to renal transplantation

A

active infection, cancer, severe comorbidity

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45
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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46
Q

how would you manage acute rejection of a kidney transplant?

A

high dose IV methylprednisolone + intensify immunosuppression regime.

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47
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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48
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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49
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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50
Q

how would you treat a patient with ADPKD?

A

aggressive BP management (less than 130/80)

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51
Q

how would you diagnose ADPKD?

A

renal USS.

screen family members using USS too.

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52
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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53
Q

define nephritic syndrome/glomerulonephritis

A

group of disorders where damage to the glomerular filtrating apparatus causes leaking of protein/blood into the urine.
common cause of ESRF.

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54
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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55
Q

what investigation would you perform in glomerulonephritis?

A

renal biopsy

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56
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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57
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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58
Q

what would a biopsy show with rapidly progressive glomerulonephritis?

A

crescents

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59
Q

how would you treat a glomerulonephritis, other than treating the underlying cause?

A

methylprednisolone + cyclophosphamide.

control BP with ramipril + losartan.

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60
Q

how does IgA nephropathy usually present?

A

with macroscopic/microscopic haematuria (occasionally with nephritic syndrome)

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61
Q

what are the features of nephrotic syndrome?

A

normal/mildly high BP.
urine = proteinuria.
GFR = normal to mildly low.

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62
Q

what are the features of nephritic syndrome?

A 
BP = moderately/severe high.
urine = haematuria.
GFR = moderate to severely low.
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63
Q

what is seen on renal biopsy in IgA nephropathy?

A

mesangial proliferation, IgA and C3 deposits

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64
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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65
Q

how would you diagnose Henoch-Schonlein purpura?

A

IgA and C3 deposits seen in renal or skin biopsy

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66
Q

what parts of the kidney are damaged in SLE?

A

vascular, glomerular and tubulointerstitial components

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67
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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68
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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69
Q

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

A

muddy brown casts

70
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)

71
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.

72
Q

name 2 primary causes of nephrotic syndrome

A

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

73
Q

name 2 secondary causes of nephrotic syndrome

A

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

74
Q

how might nephrotic syndrome present?

A

pitting oedema.

urine dipstick massive +ve for protein.

75
Q

how would you treat nephrotic syndrome?

A

reduce oedema - loop diuretic (furosemide) - IV, high dose.
reduce proteinuria - ACEi or ARBs.
reduce risk of complications - anticoagulate, statins, vaccinate.
treat underlying cause.

76
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.

77
Q

give 2 things associated with minimal-change glomerulonephritis

A

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

78
Q

how would you treat minimal change glomerulonephritis?

A

high dose prednisolone.

if relapse - ciclosporin/cyclophosphamide.

79
Q

give 2 causes of membranous nephropathy

A

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

80
Q

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

A

diffusely thickened GBM with IgG and C3 subepithelial deposits.

81
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.

82
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.

83
Q

how does focal segmental glomerulosclerosis (FSGS) present?

A

nephrotic syndrome or proteinuria

84
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.

85
Q

what is the main cause of urinary incontinence in men?

A

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

86
Q

define functional incontinence

A

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

87
Q

define stress incontinence

A

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

88
Q

who is commonly affected by stress incontinence?

A

pregnant women and following birth.

elderly women - weak pelvic floor.

89
Q

define urge incontinence (aka overactive bladder syndrome)

A

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

90
Q

what can precipitate urgency/leakage in urge incontinence?

A

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

91
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.

92
Q

how could you manage stress incontinence?

A

pelvic floor exercises, surgery or duloxetine

93
Q

how could you manage urge incontinence?

A

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

94
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

95
Q

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

A

morning erections still occur

96
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.

97
Q

name 3 drugs that can cause erectile dysfunction

A

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

98
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.
99
Q

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

A

headache, flushing, dyspepsia, stuffy nose

100
Q

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

A

tunica vaginalis

101
Q

give a primary and a secondary cause of hydroceles

A

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

102
Q

what causes a varicocele?

A

dilated veins of the pampiniform plexus

103
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.

104
Q

what is a hydrocele? how would you treat it?

A

fluid within the tunica vaginalis.

aspiration/surgery.

105
Q

how might a varicocele present?

A

patient complains of dull ache.

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

106
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.

107
Q

what causes testicular torsion?

A

spermatic cord twists, cutting off blood supply to testis

108
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.

109
Q

how must testicular torsion be treated?

A

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

110
Q

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

A

inner transitional layer

111
Q

give 3 symptoms of benign prostatic hyperplasia

A

frequency, nocturia, terminal dribbling, poor stream, hesitancy, overflow incontinence, haematuria

112
Q

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

A

enlarged and smooth prostate

113
Q

what investigations should be performed in benign prostatic hyperplasia? what must be excluded?

A

transrectal ultrasound (±biopsy) and PSA - exclude cancer

114
Q

how would you manage benign prostatic hyperplasia?

A 
avoid caffeine and alcohol.
alpha blockers (tamsulosin) - relaxes smooth muscle.

finasteride - 5 alpha reductase inhibitor - stops conversion of dihydrotestosterone to testosterone (which is what drives prostate growth).

transurethral resection/incision of prostate.

115
Q

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

A

adenocarcinoma of peripheral layer

116
Q

if a patient presents with symptoms of benign prostatic hyperplasia, what additional features would make you think of malignancy?

A

weight loss, back pain

117
Q

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

A

hard, irregular

118
Q

what essential investigations should be carried out in prostatic carcinoma?

A

trasrectal ultrasound and prostate biopsy.

± PSA (raised)

119
Q

how would you treat prostatic carcinoma?

A

radical prostatectomy/radiotherapy.

hormonal treatment - gonadotrophin-releasing analogues - goserelin, lueprolide

120
Q

name 2 types of testicular tumour

A

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

121
Q

name 2 risk factors for testicular tumours

A

undescended testis, infant hernia, infertility

122
Q

how might a testicular tumour present?

A

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

123
Q

which lymph nodes would a testicular malignancy spread to?

A

para-aortic

124
Q

give 3 differential diagnoses of a testicular lump

A

tumour.

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

125
Q

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

A

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

126
Q

how would you treat a testicular tumour?

A

radical orchidectomy.

seminoma = orchidectomy + radiotherapy.

127
Q

give 2 possible causative organisms of acute prostatitis

A

S faecalis, E coli, chlamydia

128
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.

129
Q

how would you treat prostatitis?

A

analgesia, oral levofloxacin

130
Q

give 2 possible causes of epididymo-orchitis

A

chlamydia, E coli, mumps, N gonorrhoea, TB

131
Q

how would epididymo-orchitis present?

A

sudden onset tender swelling, dysuria, sweats/fever, urethral discharge

132
Q

how would you manage epididymo-orchitis?

A

take urine sample - 1st catch, to look for discharge.
STI screen.
doxycyline (if 25yo or younger, to cover chlamydia)
if >35 - ciprofloxacin for associated UTI.
IM ceftriaxone stat if gonorrhoea suspected.

133
Q

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

A

proximal tubular epithelium.

large cells with clear cytoplasm.

134
Q

give 3 clinical features of renal cell carcinoma

A

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

135
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.
136
Q

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

A 
MRI.
Robson score:
I - confined to kidney
II - involves perinephric fat
III - spread to renal vein
IV - spread to adjacent/distant organs
137
Q

how would you treat renal cell carcinoma?

A

nephrectomy unless there are bilateral tumours.
RCC = radio/chemo resistant.
angio-genesis targeting agents (sunitinib) for unresectable tumours.

138
Q

what is a nephroblastoma?

A

childhood tumour of renal tubules and mesenchymal cells

139
Q

where can urothelial tumours arise from and what are they also known as?

A

bladder, ureter and renal pelvis.

aka transitional cell tumours.

140
Q

give 3 risk factors for urothelial tumours (+ thus bladder cancer)

A

smoking, dye factories, schistosomiasis, chronic cystitis

141
Q

what significant presenting feature would make you suspect a urothelial tumour?

A

painless haematuria

142
Q

how would you investigate a urothelial tumour?

A

cystoscopy + biopsy

CT for staging

143
Q

explain the staging system for urothelial tumours, and how different stages are treated

A

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

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

T4 - beyond bladder
= palliative chemo/radiotherapy.

144
Q

how might gonorrhoea present in a male?

A

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

145
Q

how might gonorrhoea present in a female?

A

usually asymptomatic.

vaginal discharge, dysuria, proctitis.

146
Q

how would you manage gonorrhoeal urethritis?

A 
encourage safe sex. contact tracing.
ceftriaxone IM (+ azithromycin oral for chlamydia)
147
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

148
Q

how would you treat non-gonorrhoeal urethritis?

A

azithromycin oral or doxycyline.

contact tracing.

149
Q

when are UTIs considered complicated?

A

when occurring in men and children

150
Q

what is the organism that causes most UTIs?

A

E coli

151
Q

name 3 organisms that can cause a UTI

A

*E coli.
proteus mirabili
Klebsiella penumonia.
Staphylococcus saprophyticus

152
Q

give 2 risk factors for UTI

A

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

153
Q

how would acute pyelonephritis present (kidney infection)?

A

high fever, rigors, vomiting, loin pain and tenderness, oliguria

154
Q

how would cystitis present (bladder infection)?

A

frequency, dysuria, urgency, haematuria, suprapubic pain

155
Q

how would you diagnose a UTI?

A

dipstick urine.

if dipstick shows nitrites or leucocytes, do MC&S of MSU

156
Q

how would you treat a UTI?

A

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

(upper UTI - co-amoxiclav).

157
Q

give 3 causes of sterile pyuria

A

TB, appendicitis, PKD, calculi, bladder tumour

158
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.

159
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.

160
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.

161
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.

162
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.

163
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.

164
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.

165
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

166
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.

167
Q

give some possible SEs of sildenafil

A

flushing, headache, dizziness, nasal congestion.

hypotension, tachycardia and palpitations.

168
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.

169
Q

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

A

flutamide, bicalutamide, cyproterone acetate.

used to treat prostate cancer.

170
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.

171
Q

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

A

lixivaptan, mozavaptan, satavaptan.

used to treat PKD.

Phase 2a - Systems (18 decks)

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