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2A content- Sameera > 10. GU > Flashcards

10. GU Flashcards

1
Q

what r nephroliathiasis and what are they made of and where do they form

A

kidney stones
calcium oxolate
collecting duct

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2
Q

explain the pathophysiology of nephroliathiasis

A
  1. excess solute in collecting ducts leads to crystallisation of urine
  2. these obstruct the outflow of urine
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3
Q

what is a complication of nephroliathiasis and explain what this is and how this this treated

A

hydronephrosis- dilation of the renal pelvis in response to obstruction
surgical decompression

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4
Q

what 2 risks increase with obstruction and dilation of the renal pelvis

A
  1. infection risk
  2. obstruction causes prostaglandin release which results in natural diuresis risk
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5
Q

what r the 3 most common obstruction sites for nephroliathiasis

A
  1. PUJ pelvo-ureteric junction
  2. pelvic brim (where ureter crosses over iliac blood vessels)
  3. VUJ vesico-urethral junction
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6
Q

presentation of nephroliathiasis 4

A
  1. unilateral, colicky pain from loin to groin which comes in peristaltic waves
  2. patient cannot lie still
  3. haematuria
  4. dysuria
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7
Q

1st line and GS/ diagnostic for nephroliathiasis and give their pros and cons (2, 3)

A

1st line: kidney, ureter and bladder X ray
-> 80% specific for stones
-> cheap and easy
GS: Non contrast CT KUB -> 90% specific for stones
-> rapid
-> background radiation

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8
Q

with urinary symptoms what test is important to take if the presenting patient is female

A

pregnancy test

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9
Q

treatment of nephrothialiasis 4

A
  1. watch and wait for stones smaller than 5mm as they spontaneously pass
  2. medium stones require either endoscopic sound wave lithotripsy (breaks up the stones)
  3. large stones require percutaneous nephrolitherectomy (keyhole surgery)
  4. analgesia- IV diclofenac
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10
Q

what is acute kidney injury and what 3 things characterise it

A

abrupt decline in kidney function (hours-days)
1. increased serum creatinine
2. increased urea
3. decreased urine output

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11
Q

explain the classification criteria for acute kidney injury 3

A

KDIGO:
1. serum creatinine above 26 micromol/L within 48 hours - needs a baseline
OR
2. 1.5 times the baseline in 7 days (increase of 50%)
3. urine output <0.5ml/kg/hour for 6 or more consecutive

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12
Q

how to determine the type of acute kidney injury 1 and what value determines each type 3

A

urea: creatinine ratio
>100:1= pre renal
<40:1= renal
40-100= post renal

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13
Q

what is the staging method for acute kidney injury, what r the stages and what does a higher stage mean

A

AKIN
stage 1-3
higher stage= decreased likelihood of kidney recovery

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14
Q

what r the top 3 causes of AKI

A

sepsis, cardiogenic shock, MAJOR SURGERY

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15
Q

what are the 4 pre renal causes of AKI and what is the general trend

A
  1. decrease in CO: heart failure or shock
  2. liver failure
  3. renal artery stenosis
  4. drugs: NSAIDs, ACEi, IV contrast
    -> all to do with hypoperfusion
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16
Q

what are the 4 renal causes of AKI and what is the general trend

A
  1. tubular (acute tubular necrosis)
  2. interstitial
  3. glomerular (inflammation)
  4. toxins (sepsis)
    -> nephron and parenchyma damage
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17
Q

what r the 3 post renal causes of AKI and what is the general trend

A
  1. stones (ureteral, bladder or urethra)
  2. BPH
  3. drugs (ANTICHOLINERGICS, calcium channel blockers)
    -> obstructive uropathy
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18
Q

risk factors of AKI 2

A

elderly
nephrotoxic drugs

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19
Q

which substances accumulate due to AKI 4 and what do they lead to 4

A

K+= arrythmias
H+= acidosis
urea= pruritis due to urea deposites in the skin
fluid= odema

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20
Q

symptomatic presentation of AKI 3

A
  1. oedema- swelling of limbs and abdomen
  2. oligouria/ haematuria/ proteinuria (changes to urine)
  3. ENCEPHALOPATHY/ MENTAL CONFUSION
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21
Q

investigations for AKI 1 AND 2 WAYS OF DETERMINING CAUSES

A
  1. establish cause with urea: creatinine ratio
  2. FBC: K+, H+, urea and creatinine
  3. RENAL CAUSE- RENAL BIOPSY
  4. POST RENAL- KUB US
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22
Q

treatment of AKI 3 and what is the last resort treatment

A

treat complications:
1. high K+- calcium gluconate
2. metabolic acidosis- sodium bicarbonate
3. oedema= diuretics
last resort= renal replacement therapy

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23
Q

what indicates haemo-dialysis in AKI 5

A

Acidodid (pH <7.1)
Fluid overload (odema)
Uremia (symptomatic)
K+ >6.4
ECG changes due to K+
AFUKE

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24
Q

what is CKD

A

eGFR of <60mL/min/1.73m2 for 3 or more months

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25
Q

what r the best readings to quantify CKD 2

A

eGFR and albumin: creatinine ratio

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26
Q

what r the stages of CKD 5 and their values

A

stage 1: >90mL/min eGFR
stage 2: 60-89 mL/min eGFR
stage 3A: 45-59mL/min eGFR
stage 3B: 30-44mL/min eGFR
stage 4: 15-29mL/min eGFR
stage 5: less than 15mL/min eGFR (end stage CKD)

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27
Q

what r the 2 most common risk factors for CKD

A
  1. diabetes mellitus
  2. hypertension
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28
Q

what is the pathophys of CKD 4 and explain why proteins and blood can get into urine

A
  1. low GFR due to damaged nephrons
  2. this increases burden on remaining nephrons
  3. this also increases RAAS activation to increase GFR but this increases pressure
  4. this causes loss of basement membranes selective permeability= blood and protein in urine
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29
Q

why is CKD initially asymptomatic 1 and why does CKD become symptomatic 1

A

asymptomatic- lots of nephrons as a reserve
symptomatic- due to substance accumulation

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30
Q

what r the investigations for CKD 3

A

FBC and U&Es Creatinine, albumin, anaemia
Urinalysis - haematuria, proteinuria, glycosuria
Renal ultrasound

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31
Q

treatment for CKD 4
(what is the aim of treatment, example, when to refer and last resort treatment)

A

Irreversible so treat to prevent progression of disease and symptom control:

eg Oedema - fluid and sodium restriction furosemide

  1. Referral to nephrology if eGFR < 30 (stage 4) or A:CR>70

last resort- renal replacement therapy

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32
Q

compare AKI and CK presentation time

A

AKI: shorter symptom onset
CKD: 3+ months presentation

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33
Q

compare if there is anaemia or no anaemia in CKD and AKI

A

AKI: no anaemia
CKD: anaemia of chronic kidney disease

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34
Q

compare ultrasound results for AKI and CKD

A

AKI: USS is normal
CKD: USS shows bilateral small atrophied kidneys

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35
Q

what is benign prostatic hyperplasia and when is this classified as normal

A

non malignant prostate hyperplasia
normal with ageing

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36
Q

risk factors for BPH 2

A

age
African caribbean origin

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37
Q

what is protective against BPH

A

castration (removal of testicles)

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38
Q

pathophysiology of BPH

A

inner transitional zone of prostate (muscular and gland) proliferate and narrows the urethra

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39
Q

what r the two issues caused by BPH, which is more common

A

issues with storage and voiding
voiding more common

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40
Q

name 4 aspects of storage

A

frequency, urgency, nocturia, incontinence
FUNI

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41
Q

name 4 aspects of voiding

A

poor stream, dribbling, incomplete emptying, hesitency
SHID

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42
Q

what r the symptoms of retention 4 and when does this occur

A

anuria, UTI, stones, hydronephrosis
when the urethra is completely occluded

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43
Q

what r the two investigations for BPH and what is an issue with one of them

A

DRE (rectal exam)- smooth enlarged mass
prostate specific antigen (used rule out prostate cancer but can be raised in both)

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44
Q

treatment for BPH 3 approaches, 4

A
  1. lifestyle- reduce caffeine intake
  2. medications
    -> 1st line tamsulosin alpha blocker which relaxes bladder neck
    -> 2nd line finasteride alpha reductase inhibitor which decreases testosterone production
  3. surgery
    transurethral resection of prostate
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45
Q

complication of transurethral resection of prostate

A

retrograde ejaculation

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46
Q

what r the 5 GU cancers

A

-> renal cell carcinoma
-> wilms tumour
-> bladder cancer
-> prostate cancer
-> testicular cancer

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47
Q

what is renal cell carcinoma and what age does it occur in

A

proximal convoluted tubule epithelium carcinoma
over 40s

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48
Q

risk factors of renal cell carcinoma 2

A

smoking
hereditary

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49
Q

presentation of renal cell carcinoma 3

A

often asymptomatic (25%)
triad- flank pain, haematuria, abdominal mass

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50
Q

1st line and GS investigation for renal cell carcinoma and what is the advantage of the GS

A

1st line: USS
GS: CT chest/ abdo/ pelvis (more sensitive)

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51
Q

treatment for renal cell carcinoma 1

A

nephrectomy (full/ partial depending if bilateral)

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52
Q

what is wilms tumor and what ages does it occur

A

renal mesenchymal stem cell tumour
seen in children under 3

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53
Q

what is bladder cancer

A

transitional cell carcinoma of bladder

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54
Q

unique risk factor for bladder cancer 1

A

occupational exposure to dyes/paint/rubber (painter, hairdressers, mechanic working with tyres)

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55
Q

presentation of bladder cancer 1

A

painless haematuria

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56
Q

investigation for bladder cancer 1

A

flexible cystoscopy GS

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57
Q

treatment for bladder cancer 3 approaches (4)

A

conservative= support eg specialist nurse
medical= chemo/radiotherapy
surgery= TURBT (transurethral resection of bladder tumour) or last resort CYSTECTOMY

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58
Q

what is prostate cancer

A

proliferation of outer peripheral zone of prostate (adenocarcinoma)

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59
Q

risk factors for prostate cancer 4

A

genetic BRCA1/2 and HOXB13 and lynch syndrome
elderly
family history
A/C origin

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60
Q

presentation of prostate cancer 2

A

LUTS like BPH (voiding and storage issues) but with systemic cancer symptoms eg weight loss, fatigue, night pain and bone pain

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61
Q

where does prostate cancer typically metastasise to and what is the effect of this

A

typically metastasises to bone= sclerotic lesions, typical lumbar back pain
also metastasises to liver, lung and brain

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62
Q

investigations for prostate cancer (community 2, GS/ diagnostic)

A

DRE is hard and irregular and PSA in community
GS/ diagnostic:
transrectal USS and biopsy

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63
Q

how is prostate cancer staged 1 and what is a higher score indicative of 1

A

use GLEASON score to grade- based on biopsy (the higher it is, the worse the prognosis)

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64
Q

4 treatment approaches for prostate cancer

A
  1. prostatectomy
  2. radio/chemotherapy
  3. hormone therapy Gonadotrophin receptor agonist- goserelin
  4. bilateral orchidectomy/ castration
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65
Q

explain hormone therapy treatment for prostate cancer (example name, how does it work and 2 side effects)

A

GnRH receptor agonist eg goserelin
increases LH and FSH but results in suppression of HPG axis= less testosterone
side effects= libido loss, erectile dysfunction

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66
Q

what r the two categories of testicular cancer

A

germ cell (90%) or non germ cell (10%) tumour

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67
Q

what r the causes of germ cell testicular cancer 2

A

seminoma, teratoma

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68
Q

what r the causes of non-germ cell testicular cancer 3

A

sertoli, leydig, sarcoma

69
Q

what is the most common cancer in young men and what age is this

A

testicular cancer
20-45

70
Q

risk factors for testicular cancer 3

A

undescended testes
infertility
family history

71
Q

presentation for testicular cancer 2

A

painless lump in testicle which doesn’t transilluminate (often self found)
may show lung metastases signs eg cough (consider chest x ray)

72
Q

investigations for testicular cancer 2

A

urgent doppler USS testes (90% diagnostic)
tumour marks AFP and BhCG (+ LDH which is raised non specifically in tumours)

73
Q

when r the 2 tumour markers raised in testicular cancer and what do they indicate 1 each

A

AFP- raised in teratoma
BhCG- raised in seminomas

74
Q

treatment for testicular cancer 2 and what should always be offered

A

always 1st line: urgent radical orchiectomy
adjacent chemo or radio
offer sperm storage

75
Q

what r the two locations for UTIS and what is each called

A

upper- kidney
lower- bladder and down

76
Q

what r the upper UTIs 1

A

pyelonephritis

77
Q

what r the lower UTIs 4

A

cystitis, prostatitis, urethritis, epididymo-orchiditis

78
Q

what r the organisms of UTI

A

KEEPS
klebsiella, enterbacter, E.coli, proteus, s. saphrophyticus

79
Q

what is the main cause of UTIs and in how many of the cases

A

UPEC- uropathogeinc E coli
80

80
Q

why r females more likely to get a UTI

A

they have a shorter urethra, therefore closer to anus which makes it easier for bacteria to colonise

81
Q

explain the investigations for all UTIs (1st, GS) and results

A

1st line: urine dipstick
-positive leukocytes
-positive nitrites
-haematuria
GS: midstream MC + S

82
Q

what is the purpose of midstream MC and S and what does it stand for

A

confirms UTI and IDs pathogen
midstream microscopy, culture and sensitivity

83
Q

what is obstructive uropathy

A

block of urine flow
can affect one or both kidney depending on the level of obstruction

84
Q

what is obstruction of one kidney

A

obstructive nephropathy

85
Q

what is the pathophys of obstructive uropathy and how it leads to hydronephrosis 3

A
  1. obstruction leads to retention
  2. causes urine backlog in renal pelvis
  3. hydronephrosis= dilated renal plexus which is more infection prone
86
Q

what is the treatment for obstructive uropathy 2

A
  1. relieve kidney pressure- catherise urethra, urethral stent
  2. treat cause of obstruction eg BPH/ stones
87
Q

what is pyelonephritis and what organism usually causes it

A

infection of renal parenchyma and upper ureter
usually UPEC caused, can be other KEEPS

88
Q

how is pyelonephritis acquired and who does it affect

A

most commonly acquired via ascending transurethral spread
affects females under 35

89
Q

2 things that increase your risk of getting pyelonephritis 2

A

urine stasis ie stones
catheters

90
Q

presentation of pyelonephritis 3

A

triad: loin pain, fever and pyuria (pus in urine)

91
Q

investigation for pyelonephritis 1 and what is the reasoning behind this 1

A

midstream urine sample and do MC+S
to ID the pathogen for the most appropriate antibiotic regime

92
Q

treatment for pyelonephritis 3 one contraindication

A
  1. analgesia- paracetamol
  2. antibiotics: cefalexin or co-amoxiclav if results form culture are back and the pathogen IDed is susceptible (CO-AMOXICLAV IS TETAROGENIC)
93
Q

what is cystitis by what organism

A

UPEC infection of the bladder

94
Q

risk factors for cystitis 3

A

urine stasis
bladder lining damage
catheters

95
Q

presentation of cystitis 4

A

suprapubic tenderness and discomfort
increased frequency
urgency
visible haematuria

96
Q

treatment for cystitis 2

A

antibiotics: trimethoprim or nitrofurantoin

97
Q

what is urethritis and main cause

A

urethral inflammation with or without infection
main cause is a sexually acquired condition

98
Q

non infective causes of urethritis 1

A

trauma

99
Q

infective causes of urethritis split into 2 subcategories

A

gonococcal= neisseria gonorrhoea, less common (gram -ve diplococcus)
non-gonococcal= chlamydia tractiomatis, more common (gram -ve aerobe bacilli)

100
Q

risk factors for urethritis 2

A

male-male sex
unprotected sex

101
Q

presentation of urethritis 2

A

dysuria with or without urethral discharge (blood or pus)
urethral pain

102
Q

investigation for urethritis 1

A

NAAT (nucleus acid amplification test) which detects STIs (NG or CT cause)

103
Q

treatment for urethritis 2

A

NG: IM ceftriazone and azithromycin
CT: azithromycin (or doxycycline)

104
Q

what is Epididymo-orchitis

A

inflammation of epididymis, extending to testes

105
Q

what causes epididymo-orchitis 2

A

STI or UTIs

106
Q

presentation of epididymo-orchitis 3

A

unilateral scrotal pain and swelling
pain relieved with elevating testes
cremaster reflex is intact

107
Q

investigation for epidiymo-orchitis 1

A

Nucleic Acid Amplification Tests

108
Q

treatment for epididymo-orchitis 2

A

depends on infectious cause
NG: IM ceftriazone and azithromycin
CT: azithromycin (or doxycycline)

109
Q

differential for epididymo-orchitis 1 and what r the 3 symptoms for this

A

testicular torsion
nausea and vomiting and bell clapper sign

110
Q

what can present as both nephrotic and nephritic 2

A

diffuse proliferative glomerulonephritis
membrano-proliferative glomerulonephritis

111
Q

What is the major clinical difference between nephritic and nephrotic syndrome?

A

Inflammation (Nephritic) vs Oedema (Nephrotic)

112
Q

if a patient presents with frothy urine and oedema, what syndrome do they have and what is their treatment

A

nephrotic
ACEi/ARB and loop diuretics

113
Q

what are the characteristics of nephrotic syndrome 5

A

proteinuria (more than 3.5g/day)= frothy appearance
low serum albumin (<30g/L)
Oedema
Hyperlipidemia
hypertension

114
Q

what are the characteristics of nephritic syndrome 4

A

Haematuria
Oliguria
hypertension
mild proteinuria (less than 3.5g/day)

115
Q

what is the pathophysiology of nephrotic syndrome 2

A

podocyte injury= protein leaks into urine

116
Q

pathophysiology of nephritic syndrome 2

A

inflammation of the kidney= blood leaks into urine

117
Q

what are the causes of nephritic syndrome (systemic 4, 1 renal) and what type of reaction are these

A

systemic:
SLE
post strep glomerulonephritis
goodpastures
small vessel vasculitits
renal:
IgA nephropathy
ALL examples of type 3 hypersensitivity, except good pastures which is type 2

118
Q

investigation for nephritic and nephrotic syndrome 2

A

urinalysis: haematuria (nephritic), proteins (nephrotic)
biopsy= DIAGNOSTIC

119
Q

treatment for nephritic syndrome 2

A

1st line: BP control with ACEi
12 week corticosteroids if continuous haematuria

120
Q

what are the causes of nephrotic syndrome (3 primary, 5 secondary)

A

primary:
-minimal change disease
-focus segmental glomerulosclerosis
-membranous nephropathy

secondary: DDANI
-diabetes
-drugs
-autoimmune
-neoplasia
-infection

121
Q

investigation results for all causes of nephrotic syndrome

A

biopsy and microscopy for all
minimal change: podocyte effacement and fusion
focal segmental glomerulosclerosis: segmental sclerosis
membranous nephropathy: subpodocyte immune complex deposition

122
Q

specific test for membranous nephropathy (nephrotic syndrome) 1

A

anti phospholipase A2 receptor antibody

123
Q

treatment for nephrotic syndrome conditions 2

A

prednisolone
treat symptoms specifically eg oedema with loop diuretics

124
Q

what is the most common cause of nephritic syndrome in developed countries

A

IgA nephropathy

125
Q

What is IgA nephropathy and what does it cause

A

deposition of IgA into the mesangium of the kidney
this causes inflammation and damage

126
Q

presentation of IgA nephropathy 2

A

asymptomatic
haematuria (ribena/coke)

127
Q

investigation for IgA nephropathy 1

A

diagnostic= biopsy (IgA complex deposition)

128
Q

treatment for IgA nephropathy 2

A

1st line: BP control with ACEi
corticosteroids if continuous inflammation

129
Q

differential for IgA nephropathy 1 and how to differentiate 1

A

Henloch Schonlein purpura
systemic immune complex deposition, not isolated to kidneys

130
Q

what is post strep glomerulonephritis and what doe it cause 1

A

deposition of strep antigens 3-6 weeks post infection
this causes inflammation

131
Q

presentation of post strep glomerulonephritis 1 and what is this after

A

visible haematuria (ribena/coke) 3-6 weeks after group A beta haemolytic strep (Strep. pyogenes) infection

132
Q

diagnosis of post strep glomerulonephritis

A

strep infection evidence

133
Q

treatment for post strep glomerulonephritis 2

A

antibiotics and supportive care

134
Q

what is often found secondary to SLE and what does it involve

A

lupus nephritis
ANA deposition in endothelium

135
Q

investigation for SLE 2

A

ANA positive, anti dsDNA positive

136
Q

treatment for SLE 2

A

steroids- hydroxycholorquine
immunosuppressants eg cyclophosphamide

137
Q

what is goodpastures 3

A

anti glomerular basement membrane antibodies (anti GBM) attacks BM in lungs and the kidneys

138
Q

treatment for goodpastures 2

A

steroids and plasma exchange

139
Q

what is polycystic kidney disease 1 and what does this cause

A

cyst formation throughout renal parenchyma
enlargement and damage

140
Q

risk factor for polycystic kidney disease 1

A

family history

141
Q

causes of PKD 2 and which is more common

A

auto recessive inheritence or auto dominant inhertence
auto dom is more common

142
Q

who is affected in auto recessive and dominant PKD

A

recessive= infants/ babies
dominant= males 20 year olds

143
Q

name the two mutations and their percentage for auto dom PKD

A

mutated PKD1 (85%) or PKD (15%)

144
Q

presentation of PKD 3

A
  1. bilateral flank/ back/ abdominal pain
  2. with or without hypertension and haematuria
  3. extra renal cysts (particularly in circle of Willis)
145
Q

investigation of PKD 2

A

kidney ultrasound- shows enlarged bilateral kidneys with multiple cysts
genetic testing

146
Q

treatment for PKD 3

A
  1. non curative
  2. manage symptoms eg hypertension with ACEi
  3. end stage renal failure with renal replacement therapy/ transplant
147
Q

what are scrotal diseases 1 and what is important to note about them clinically 1

A

non cancerous
BUT assumed to be cancer unless proved otherwise

148
Q

4 types of scrotal diseases

A

epididymal cyst
hydrocele
varicocele
testicular torsion

149
Q

what is epididymal cyst and does it transilluminate

A

extratesticular cyst (above and behind testes)
will transilluminate

150
Q

how are scrotal diseases diagnosed 1

A

USS of scrotum

151
Q

what is hydrocele 2 and does it transilluminate

A

fluid collection in tunica vaginalis
cyst that testicle sits within
will transilluminate

152
Q

what is variocele 1, why does it occur 1

A

distension of veins in pampiniform plexus in spermatic cord
due to increased left renal vein pressure

153
Q

presentation of variocele 2

A

bag of worms
typically painless

154
Q

complication of veriocele 1

A

infertility

155
Q

what is testicular torsion 1, what does it cause 1 and what does it lead to if not treated 2

A

spermatic cord twists on itself
causing occlusions of testicular artery
leads to ischaemia and gangrene of testes if not dealt with

156
Q

risk factor of testicular torsion 1

A

bell clapper deformity (“horizontal lie” of the testes)

157
Q

presentation of testicular torsion 5

A

server unitesticular pain (hurts to walk)
abdominal pain
nausea and vomitng
cremasteric reflex lost (stroke winner thigh- ipsilateral testicle should elevate and retract upwards)
no pain relief with elevating testes (prehn sign)

158
Q

investigation for testicular torsion 2 what if there is increased risk?

A

physical exam
USS to check testicular bloodflow
1st physical exam during surgery

159
Q

treatment for testicular torsion 2 and what about if the testicle is non viable

A
  1. urgent surgery bilateral orchiplexy (fixing of testes to scrotal sac to overcome bell clapper deformity)
    -> non viable= orchidectomy
160
Q

what gender does incontinence occur mostly in

A

females

161
Q

two types of incontinence and what are they

A

stress (sphincter weakness eg post pregnancy trauma)
urge (detrusor muscle overactivity)

162
Q

treatment of incontinence 2

A

surgery
anticholinergic drugs eg oxybutinin

163
Q

what is retention and what volume does this involve

A

inability to pass urine even when bladder is full (500+ mls)

164
Q

who does retention affect the most

A

men

165
Q

causes of retention 2

A
  1. obstruction (stones, BPH, neurological flaccid paralysis)
  2. hypotonia of detrusor, as LMN
166
Q

treatment for retention 1

A

catheter

167
Q

when do storage symptoms occur

A

occur when bladder should be storing urine and therefore need to pee

168
Q

when do voiding symptoms occur

A

occurs when bladder outlet is obstructed making it hard to pee

169
Q

what are urinary red flags 2

A

haematuria
dysuria

2A content- Sameera (21 decks)

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