Renal/GU Peer Teaching Flashcards
(72 cards)
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
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
3
Q
A
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.
5
Q
treatment of uncomplicated lower UTI
A
nitrofurantoin or trimethoprim
if this fails then MC&S urine and Tx according to sensitivities
6
Q
what is the treatement for pyelonephritis
A
broad spectrum antibiotics like co-amoxiclav
consider hospitalisation
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
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
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
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
11
Q
syphilis treatment
A
penicillin IM
12
Q
what is an important management point for all STIs
A
partner notification
13
Q
what are the Ix for GU malignancy
A
- Urine dip
- USS
- CT
- MRI
14
Q
what is nephrolithiasis
A
the presence of calculi in the urinary system
15
Q
what is the lifetime risk of renal stones
A
7-10%
then there’s >50% lifetime risk of recurrence
16
Q
what are the risk factors for nephrolithiasis
A
dehydration
diet
obesity
family history
medicine
metabolic abnormality
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)
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
- normally made of calcium oxalate
- uric acid stones
- risk factors are the same as for gout
- struvite stones
- infective stones
- klebsiella, pseudomonas and proteus infections
- NOT E.COLI
*
- NOT E.COLI
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
20
Q
management of renal colic and stones
A
- supportive
- analgesia
- IV diclofenac
- antibiotics
- IV cefuroxime/gentamicin
- analgesia
- If <5mm watchful waiting
- If <10mm
- medical expulsive therapy with alpha blocker like tamsulosin
- Lithotripsy
- Percutaneous nephrolithotomy if >10mm
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
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
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
24
Q
how does nephritic syndrome present
A
- haematuria
- proteinuria
- hypertension
- compensatory increase in BP due to reduced GFR
25
what is the commonest cause of nephritic syndrome? can you name some other causes?
IgA nephropathy is most common
post-streptococcal GN, anti-GMB (goodpastures), SLE
26
investigations and management of nephritic syndrome
* 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
27
presentation of nephrotic syndrome
proteinuria
hypoalbuminaemia
oedema
could lead to hyperlipidaemia
28
broadly nephrotic syndrome has two types of causes . what are they and what are some examples of each
* 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
29
complications of nephrotic syndrome
thromboembolism
infection
hyperlipidaemia
30
management of nephrotic syndrome
* 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
key differences between nephrotic and nephritic syndromes
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
in non-malignant scrotal disease examination: if you can't get above it what is it
hernia
33
in non-malignant scrotal disease examination: if it's seperate from the testis and cystic what is it
epididymal cyst
34
in non-malignant scrotal disease examination: if it's seperate from the testis and solid what is it
epididymitis or varicocele
35
in non-malignant scrotal disease examination: if it's testicular and cystic what is it
hydrocele
36
in non-malignant scrotal disease examination: if it's testicular and solid what is it?
a tumour, haematocele or orchitis
37
what is testicular torsion?
this is a twisted spermatic cord
it can cut off blood to the testis causing ischaemia
it is a urological emergency
38
presentation of testicular torsion
* sudden onset testicular pain
* hot, tender swollen testicle
* unilateral
* abdo pain
* N&V
* could occur at any age but commonly 11-30
*
39
treatment for testicular torsion
surgical exploration in \<6hrs
40
which zone of the prostate enlarges in BPH
the inner transitional zone
41
what are the risk factors for BPH
aging
family history
high levels of testosterone
42
which part of the prostate expands typically in prostatic carcinoma
the peripheral layer
43
clinical presentation of BPH
* LUTS symptoms - voiding and storage
* voiding (SHED)
* stream changes
* hesitancy
* emptying incomplete
* dribbling
* storage (FUND)
* frequency
* urgency
* nocturia
* dysuria
44
BPH investigations
DRE
PSA
Biopsy
Urinalysis
Urodynamics and cytoscopy
45
treatment of BPH
* 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
what type of tumour is prostate cancer, what zone of the prostate does it grow in and where do mets go
it's an adenocarcinoma that usually starts in the peripheral zone
mets go to the adjascent LN or to the bone or lungs
47
what is the medical treatment for overactive bladders
anti-cholinergic (oxybutynin)
48
prostate cancer risk factors
high levels of testosterone
hereditary/family risk
gene/oncogene fusion
increasing age
49
what is the clinical presentation of prostate cancer
non-specific weight loss
LUTS obstruction symptoms (SHED)
bone pains if there are mets
50
Investigation of suspected prostate cancer
* 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
treatment of prostate cancer
* if localised:
* prostatectomy
* if advanced/metastatic:
* androgen deprivation therapy
* GnRH agonist such as goserelin suppresses both GnRH and LH production
* chemo
52
how does the gleason score work
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
clinical presentation of AKI
* 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
ECG presentation of Hyperkalaemia
tall tented T waves, flattened P and broad QRS complexes
55
definition of AKI
* 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
what are the risk factors for AKI
sepsis
\>75yrs old
DM
cardiac failure
drugs
dehydration
57
pre-renal causes of AKI
* based on low renal perfusion
* volume depletion
* diarrhoea
* haemorrhage
* hypotension
* sepsis
* hypovolemia
* renal artery occlusion
58
three broad categories of causes of AKI
pre-renal
renal
post renal
59
renal causes for AKI
glomerulonephritis
SLE
acute tubular necrosis (e.g. due to nephrotoxic drugs like ACE-i, NSAIDs and gentamicin)
vascular disease like vasculitis
60
post renal causes of AKI
stones
tumour of ureter
other abdominal tumour
61
Ix for AKI
* urgent K+
* serum creatinine
* imaging
* renal US
* NCCT-KUB
* urinalysis (infection/glomerular disease)
* assess volume status
* BP, JVP, skin turgor, urine output
62
treatment of AKI
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
how do you manage hyperkalaemia
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
what is the definition of chronic kidney disease
abnormalities of kidney function or structure present for \>3 months with implications for health
65
causes of CKD
HTN
Diabetes
age
kidney diseases: PKD, GN, chronic pyelonephritis
long term NSAID use
66
CKD presentation
early: asymptomatic
normochromic normocytic anaemia (due to lack of EPO)
low calcium
HTN
Oedema due to fluid ovreload
Malaise, loss of appetite
67
investigation of CKD
* 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
what two modes of classification for CKD are there
* eGFR
* G1-5
* and albumin:creatinine ratio ACR
* A1-3
69
treatment for CKD
* 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
what are GnRH agonists indicated for and how do they work
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
what are GnRH antagonists indicated for and how do they work
prostate cancer
## Footnote
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
how is minimal change disease seen down the microscope
podocyte effacement seen with electron microscope
