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Phase 2a Peer Teaching > Renal/GU Peer Teaching > Flashcards

Renal/GU Peer Teaching Flashcards

1
Q

what are the three types of urinary incontinence

A

urgency incontinence

stress incontinence

overflow incontinence

female preponderance in all but overflow where it is male

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2
Q

what us OAB, what is the commonest cause, what is the investigation and what is the management

A

Overactive bladder is urgency with frequency, with or without nocturia when it is in the ABSENCE of local pathology

cause is usually detrusor muscle overactivity

Ix is bladder diary and urodynamics

1st line Mx is bladder retraiing and exercises. can also advise limit to caffeine and alcohol

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3
Q
A
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4
Q

what is stress incontinence usually due to and what is the usual management

A

usually due to pelvic floor weakness secondary to birth trauma. in this case the usual treatment is pelvic floor strengthening exercises.

note that there can be a neuro cause so look for other neuro signs.

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5
Q

treatment of uncomplicated lower UTI

A

nitrofurantoin or trimethoprim

if this fails then MC&S urine and Tx according to sensitivities

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6
Q

what is the treatement for pyelonephritis

A

broad spectrum antibiotics like co-amoxiclav

consider hospitalisation

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7
Q

what is the treatment for a complicated UTI

A

if pregnant seek extra help

if male give 7 days Abx

if catheterised send MSU if symptomatic only

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8
Q

suspected pyelonephritis Ix and Mx

A
  • Ix
    • dipstick will show pyuria
    • MSU M,C&S
    • Bloods - FBC, U&E, CRP, Blood culture
    • Imaging - USS
  • Mx
    • Fluid resuscitation
    • Empirical - broad spec like co-amoxiclav & gentamicin together
    • then based on MC&S
    • Fluids analgesia and catheter if in hosp
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9
Q

chlamydia presentation, diagnosis, investigation and management

A
  • CT is often asymptomatic but symptoms sometimes
    • women: dyspareunia, dysuria, post-coital bleeding, increased discharge
    • men: dysuria, discharge
  • diagnosis in women: NAAT of self-collected vaginal swab
  • diagnosis in men: NAAT of first-pass urine
  • treatment:
    • azithromycin once
    • doxycycline 7 days
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10
Q

gonorrhoea symptoms, Ix, Mx

A
  • symptoms
    • discharge, dysuria,
    • asymptomatic in 50% women and 10% men
  • male Ix:
    • NAAT of FPU
  • female Ix:
    • NAAT of self-collected vaginal swab
  • Mx
    • IM ceftrioxone with oral azithromycin
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11
Q

syphilis treatment

A

penicillin IM

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12
Q

what is an important management point for all STIs

A

partner notification

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13
Q

what are the Ix for GU malignancy

A
  • Urine dip
  • USS
  • CT
  • MRI
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14
Q

what is nephrolithiasis

A

the presence of calculi in the urinary system

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15
Q

what is the lifetime risk of renal stones

A

7-10%

then there’s >50% lifetime risk of recurrence

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16
Q

what are the risk factors for nephrolithiasis

A

dehydration

diet

obesity

family history

medicine

metabolic abnormality

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17
Q

what are the three common sites for kidney stones to get stuck?

A

pelvi-ureteric junction (PUJ)

pelvic brim

vesico-ureteric junction (VUJ)

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18
Q

what are the common compositional elements of renal stones

A
  • calcium stones (80% of renal stones)
    • normally made of calcium oxalate
      • oxalate rich food e.g. spinach
  • uric acid stones
    • risk factors are the same as for gout
  • struvite stones
    • infective stones
    • klebsiella, pseudomonas and proteus infections
      • NOT E.COLI
        *
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19
Q

Investigations for renal colic

A
  • urine dipstick may show haematuria
  • NCCT KUB - 99% sensitive and is the gold standard
    • no contrast as this can cause renal damage
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20
Q

management of renal colic and stones

A
  • supportive
    • analgesia
      • IV diclofenac
    • antibiotics
      • IV cefuroxime/gentamicin
  • If <5mm watchful waiting
  • If <10mm
    • medical expulsive therapy with alpha blocker like tamsulosin
  • Lithotripsy
  • Percutaneous nephrolithotomy if >10mm
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21
Q

what are the DDs for renal colic

A
  • ruptured AAA - if >50 then this is what it is until proven otherwise
  • diverticulitis
  • appendicitis
  • ectopic pregnancy
  • ovarian cyst torsion
  • testicular torsion
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22
Q

prevention of renal stones

A

adequate hydration with 2-3L per day

reduce sodium fat and protein in the diet

reduce oxalate rich food

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23
Q

what is glomerulonephritis, what can it cause and how is it diagnosed

A
  • on a spectrum from nephritic (inflamed) to nephrotic (protein in urine)
  • diagnosed on renal biopsy
  • can progress to renal failure unless it’s minimal change disease
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24
Q

how does nephritic syndrome present

A
  • haematuria
  • proteinuria
  • hypertension
    • compensatory increase in BP due to reduced GFR
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25
Q

what is the commonest cause of nephritic syndrome? can you name some other causes?

A

IgA nephropathy is most common

post-streptococcal GN, anti-GMB (goodpastures), SLE

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26
Q

investigations and management of nephritic syndrome

A
  • Ix
    • dipstick - protein and blood
    • blood - FBC, U&E, LFT, CRP, Ig, Complements
    • urine - MC&S, RBC cast
    • it’s renal biopsy for diagnosis
  • Mx
    • treat the underlying cause
    • ACE-i/ARB reduce proteinuria and protect the rena function
    • use corticosteroids
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27
Q

presentation of nephrotic syndrome

A

proteinuria

hypoalbuminaemia

oedema

could lead to hyperlipidaemia

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28
Q

broadly nephrotic syndrome has two types of causes . what are they and what are some examples of each

A
  • Primary
    • minimal change disease (most common cause for child)
    • membranous nephropathy
    • focal segmental glomerulosclerosis
  • Secondary (DDANI)
    • diabetes
    • drugs (e.g. NSAIDs)
    • autoimmune (e.g. SLE)
    • Neoplasia
    • Infection
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29
Q

complications of nephrotic syndrome

A

thromboembolism

infection

hyperlipidaemia

30
Q

management of nephrotic syndrome

A
  • reduce oedema
    • fluid and salt restriction, daily weight, loop diuretic furosemide
  • treat the underlying cause
    • e.g. corticosteroid for minimal change disease
  • reduce proteinuria
    • ARB/ACE-i
  • prevent thromboembolism
    • LMWH and warfarin
  • Prevent infection
    • with vaccines
  • statins for hyperlipidaemia
31
Q

key differences between nephrotic and nephritic syndromes

A

nephrotic the proteinuria is more extreme than in nephritic

hypoalbuminaemia and hyperlipidaemia in nephrotic only

oedema is more profound in nephrotic

visible/nonvisible haematuria is only in nephritic

32
Q

in non-malignant scrotal disease examination: if you can’t get above it what is it

A

hernia

33
Q

in non-malignant scrotal disease examination: if it’s seperate from the testis and cystic what is it

A

epididymal cyst

34
Q

in non-malignant scrotal disease examination: if it’s seperate from the testis and solid what is it

A

epididymitis or varicocele

35
Q

in non-malignant scrotal disease examination: if it’s testicular and cystic what is it

A

hydrocele

36
Q

in non-malignant scrotal disease examination: if it’s testicular and solid what is it?

A

a tumour, haematocele or orchitis

37
Q

what is testicular torsion?

A

this is a twisted spermatic cord

it can cut off blood to the testis causing ischaemia

it is a urological emergency

38
Q

presentation of testicular torsion

A
  • sudden onset testicular pain
  • hot, tender swollen testicle
  • unilateral
  • abdo pain
  • N&V
  • could occur at any age but commonly 11-30
    *
39
Q

treatment for testicular torsion

A

surgical exploration in <6hrs

40
Q

which zone of the prostate enlarges in BPH

A

the inner transitional zone

41
Q

what are the risk factors for BPH

A

aging

family history

high levels of testosterone

42
Q

which part of the prostate expands typically in prostatic carcinoma

A

the peripheral layer

43
Q

clinical presentation of BPH

A
  • LUTS symptoms - voiding and storage
    • voiding (SHED)
      • stream changes
      • hesitancy
      • emptying incomplete
      • dribbling
    • storage (FUND)
      • frequency
      • urgency
      • nocturia
      • dysuria
44
Q

BPH investigations

A

DRE

PSA

Biopsy

Urinalysis

Urodynamics and cytoscopy

45
Q

treatment of BPH

A
  • watchful waiting and conservative managemen e.g. with pads
  • medical
    • alpha blocker like tamsulosin or doxazosin
    • 5-alpha reductase inhibitor like finasteride
    • anticholinergics for an overactive bladder
    • surgical
      • trans urethral resection of prostate (TURP)
46
Q

what type of tumour is prostate cancer, what zone of the prostate does it grow in and where do mets go

A

it’s an adenocarcinoma that usually starts in the peripheral zone

mets go to the adjascent LN or to the bone or lungs

47
Q

what is the medical treatment for overactive bladders

A

anti-cholinergic (oxybutynin)

48
Q

prostate cancer risk factors

A

high levels of testosterone

hereditary/family risk

gene/oncogene fusion

increasing age

49
Q

what is the clinical presentation of prostate cancer

A

non-specific weight loss

LUTS obstruction symptoms (SHED)

bone pains if there are mets

50
Q

Investigation of suspected prostate cancer

A
  • DRE/PR exam will find hard, irregular, craggy/nobbly, enlarged prostate
  • high PSA (this is not specific)
  • TRUSS + biopsy
  • gleason grading
  • TNM staging
  • Bone scan
  • CXR
  • Serum Ca2+
51
Q

treatment of prostate cancer

A
  • if localised:
    • prostatectomy
  • if advanced/metastatic:
    • androgen deprivation therapy
      • GnRH agonist such as goserelin suppresses both GnRH and LH production
    • chemo
52
Q

how does the gleason score work

A

pathologist gives two scores (higher is worse) based on how abnormal the cells are. the first score is based on the most commonly seen cell type in the tumour. the second grade is given to describe the cells with the most abnormal appearance.

these are then added together

each score is out of five

so the maximum gleason score is 5+5=10

53
Q

clinical presentation of AKI

A
  • oliguria or anuria
  • systemic symptoms like nausea vomiting and confusion
  • high pulse
  • fluid overload with increased JVP, peripheral oedema and HTN
  • emergencies
    • no urine production
    • pulmonary oedema
    • hyperkalaemia
54
Q

ECG presentation of Hyperkalaemia

A

tall tented T waves, flattened P and broad QRS complexes

55
Q

definition of AKI

A
  • it is the rapid reduction in kidney function over hours-days
  • any one of the following = Dx AKI
    • rise in creatinine >26micromol/L in 48hrs
    • rise in creatinine >50% above baseline within 7 days
    • urine output <0.5ml/kg/h for >6 consecutive hrs
56
Q

what are the risk factors for AKI

A

sepsis

>75yrs old

DM

cardiac failure

drugs

dehydration

57
Q

pre-renal causes of AKI

A
  • based on low renal perfusion
    • volume depletion
      • diarrhoea
      • haemorrhage
    • hypotension
      • sepsis
      • hypovolemia
    • renal artery occlusion
58
Q

three broad categories of causes of AKI

A

pre-renal

renal

post renal

59
Q

renal causes for AKI

A

glomerulonephritis

SLE
acute tubular necrosis (e.g. due to nephrotoxic drugs like ACE-i, NSAIDs and gentamicin)

vascular disease like vasculitis

60
Q

post renal causes of AKI

A

stones

tumour of ureter

other abdominal tumour

61
Q

Ix for AKI

A
  • urgent K+
  • serum creatinine
  • imaging
    • renal US
    • NCCT-KUB
  • urinalysis (infection/glomerular disease)
  • assess volume status
    • BP, JVP, skin turgor, urine output
62
Q

treatment of AKI

A

if pre-renal give IV fluid and abx if sepsis

stop any nephrotoxic drugs

manage hyperkalaemia if present

manage pulm oedema with furosemide and O2

dialysis if underlying pathology cannot be corrected

63
Q

how do you manage hyperkalaemia

A

insulin and dextrose

calcium gluconate is cardioprotective but doesn’t reduce K+

salbutamol inhaler - like insulin it causes an intracellular K+ shift but tachycardia may limit use

64
Q

what is the definition of chronic kidney disease

A

abnormalities of kidney function or structure present for >3 months with implications for health

65
Q

causes of CKD

A

HTN

Diabetes

age

kidney diseases: PKD, GN, chronic pyelonephritis

long term NSAID use

66
Q

CKD presentation

A

early: asymptomatic

normochromic normocytic anaemia (due to lack of EPO)

low calcium

HTN

Oedema due to fluid ovreload

Malaise, loss of appetite

67
Q

investigation of CKD

A
  • assess renal function: low GFR
  • U&E
    • high urea
  • FBC - Normochromic, normocytic anaemia
    • high creatinine
    • low calcium due to less activated vit D so less absorption
    • high PTH to compensate
      • bones therefore lose Ca2+
    • high phosphate
    • high K+
  • urine dipstick
    • haematuria/proteinuria suggest glomerulonephritis
  • US
  • Renal biopsy
68
Q

what two modes of classification for CKD are there

A
  • eGFR
    • G1-5
  • and albumin:creatinine ratio ACR
    • A1-3
69
Q

treatment for CKD

A
  • maintain blood pressure
    • ACEi/ARB if CKD not caused by these drugs
  • control DM
  • lifestyle: exercise, smoking, diet, weigth
  • stop nephrotoxic drugs
  • give Vit D
  • for end stage kidney disease (Stage 5)
    • peritoneal dialysis or haemodialysis
    • transplant
      • cyclosporin for immunosuppression
      • malignancy risk increase
70
Q

what are GnRH agonists indicated for and how do they work

A

prostate cancer

Gonadotropin-releasing hormone (GnRH) agonists (such as buserelin) suppress LH production through down-regulation (after an initial stimulatory effect that causes increased LH and testosterone production, making the tumour briefly grow). Despite this initial increase in LH production, the constant supply quickly outmatches the body’s natural production rhythm and soon both LH and GnRH production falls.

71
Q

what are GnRH antagonists indicated for and how do they work

A

prostate cancer

GnRH antagonists (such as abarelix) suppress LH production by the anterior pituitary. This prevents stimulation of testosterone production in the testes and thus reduced DHT production. This reduces proliferation of the cells of the prostate and may cause it to shrink, rather than to grow.

72
Q

how is minimal change disease seen down the microscope

A

podocyte effacement seen with electron microscope

Phase 2a Peer Teaching (10 decks)

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