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Phase 2a Flashcards > GU and renal > Flashcards

GU and renal Flashcards

1
Q

Ureters cross iliac vessels at what and insert into what? How long? Reflux prevented by valvular mechanism at what junction?

A

Pelvic brim and insert into trigone of bladder
25-30cm
Vesicoureteric junction

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2
Q

4 nerves involved in bladder and sphincter control? Nerve levels, neurotransmitter and what role?

A

Parasymp (pelvic)= S2-S4, ACh, involuntary control
Symp (hypogastric)= T11-L2, NAd NT, involuntary
Somatic (pudendal)- S2-S4(Onuf’s nucleus), ACh
Afferent pelvic- sensory, signals from detrusor muscle

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3
Q

Neural centres involved with urinary tract?

A

Cortex= voluntary control, pontine micturition centre/ periaqueductal grey= coordination of voiding
Sacral centre= micturition reflex, Onuf’s nucleus: guarding reflex

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4
Q

Micturition reflexes and storage phase= %? Normal storage volume in adult? 1st sensation at what volume? As volume increases, pressure reduces due to what?

A

Inappropriate to void= guarding reflex–> micturition reflex, 98%
400-500ml
100-200ml
Receptive relaxation and detrusor muscle compliance

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5
Q

Nerve actions during filling phase of bladder? Micturition is a what reflex? High volume sends fast signals to where? Other nerves stim?

A

Afferent pelvic= slow firing signals to pons
Symp stim= detrusor relaxation, somatic= urethral contraction

Autonomic
Sacral centre
Parasymp= detrusor contacts, pudendal inhibited and external sphincter relaxes

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6
Q

Nerves during guarding reflex of bladder?

A

Voluntary control in adults, afferent from PMC/ PAG and transmitted–> higher cortical centres, symp= detrusor relaxes, pudendal= contraction of external sphincter

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7
Q

LUT symptoms divided into what 2 types? Definition of BPH? BPE? BOO? LUTS?

A

Storage- frequency, nocturia, urgency, urgency incontinence
Voiding- hesitancy, straining, poor/ intermittent stream, incomplete emptying, post mic dribbling, haematuria, dysuria
Benign prostatic hyperplasia, benign prostatic enlargement, bladder outflow obstruction, lower symptoms- neither gender/ disease specific

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8
Q

BPH found on what? What is it? This may be due to increase/ decrease of what?

A

Histology= increase in epithelial and stromal cell numbers in periurethral area of prostate, increase in cell number/ decrease in apoptosis or due to combination of both

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9
Q

Assessment of BPH? Needs what? Management?

A

Urine dipstick- exclude infection as major differential
PSA before DRE- assess for prostate cancer
Rectal exam- size, shape and characteristics
Androgens
Reassurance and monitoring
Medications: alpha blockers- relax smooth muscle e.g. tamsulosin 400mg once daily
5- alpha reductase inhibitors- block testosterone, help reduce size of prostate e.g. finasteride
Surgery: TURP, TUVP, HoLEP, open prostatectomy via abdo/ perineal incision

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10
Q

What is TURP? Aim? Major complications? Alternatives?

A

Accessing prostate through urethra and ‘shaving’’ off prostate tissue from inside using diathermy
Create wider space for urine to flow through, improving symptoms
Bleeding, infection, incontinence, retrograde ejaculation, urethral strictures, failure to resolve symptoms, erectile dysfunction, sepsis, haemorrhage, clot retention
TUVP- prostate tissue removed with a laser
HoLEP- prostate tissue removed using an electrical current

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11
Q

What leads to benign prostatic obstruction? It is the what component? What accounts for 40% of area of density of hyperplastic prostate? What happens when prostate is sufficiently large? Resistance to urine flow may lead to what?

A

Bladder outflow obstruction- BOO
Dynamic- alpha 1 adrenoceptor mediated prostatic SM contraction
Smooth muscle
Nodules impinge on urethra and increase resistance to flow of urine from bladder= obstruction

Progressive hypertrophy, instability/ weakness (atony) of bladder muscle

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12
Q

Relation between prostatic enlargement and hyperplasia? Complications? Pain relieved by what? How much residual urine? Caused by what?

A

Can’t get hyperplasia w/o enlargement but can get enlargement w/o hyperplasia, can be due to hypertrophy
Symptom progression, infections, stones, haematuria, acute urinary retention
Catheterisation, 600ml- 1L
Obstruction, urethral strictures, anticholinergics, alcohol, constipation, postop, infection, carcinoma

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13
Q

Features of chronic urinary retention? Interactive obstructive uropathy? Should observe for what?

A

May be painless, incomplete bladder emptying, increased risk of infections/ stones, can be low pressure w/ detrusor failure or high pressure w/ risk of interative obstructive uropathy, caused by prostatic enlargement rectal malignancy

Structural/ functional hindrance of normal urine flow, sometimes–> renal dysfunction, nocturnal enuresis
Diuresis- increased urine, may need indwelling catheter

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14
Q

Patient evaluation and history of LUTS? Examination? Investigations?

A

Establish symptoms that are bothersome to pt, objective documentation of LUT function, exclusion of serious urological pathology
Symptoms and duration, storage, voiding/ mixture? PMH, DH, allergies, symptoms score- 20-35= severe
General, abdo exam, external genitalia, DRE, focused neurological exam, urinalysis

Renal biochem, imaging, PSA, flow rates- normal in men<40= 21ml/s, >60= 13ml/s, should peak then go back down again , at least 125ml for representative flow, reduced due to LUT obstruction/ detrusor underactivity, PVR<12ml in ALL normal men, freq volume chart, trans-rectal USS, flexible cytoscopy- infection, haematuria/ onset storage symptoms, urodynamics

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15
Q

Tx of BPE? Mild symptoms?

A

Improve urinary symptoms/ QoL, reduce complications of BOO
Observation/ watchful waiting, lifestyle changes- avoid caffeine, alcohol, relax when voiding, void twice in row to aid emptying, practise emptying methods e.g. breathing exercises
Moderate- severe= reducing prostatic SM tone/ size of prostate

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16
Q

Indications for surgery with LUTS and BPH? Procedures?

A

Retention, UTIs, stones, haematuria, elevated creatinine due to BOO, symptom deterioration

Bladder neck incision, TURP, bipolar, greenlight laser, Thullium laser, Holmium enucleation, Millius retro-pubic prostatectomy, TUMA, TUMT, HIFV, stents

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17
Q

What is the major cause of incontinence in men? What or what may occur as a result from partial retention of urine? What may weaken the bladder sphincter and cause incontinence? What needs specialist assessment?

A

Enlarged prostate
Urge incontinence or dribbling
TURP and other pelvic surgery
Troublesome incontinence

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18
Q

What is urge incontinence/ overactive bladder syndrome? Urgency/ leaking is precipitated by what? Causes?

A

The urge to urinate quickly followed by uncontrollable and sometimes complete emptying of the bladder as the detrusor muscle contracts
Arriving home- latchkey incontinence= a conditioned reflex; cold; sound of running water; caffeine and obesity
Detrusor overactivity= on urodynamics
Detrusor overactivitye.g. from central inhibitory pathway malfunction/ sensitisation of peripheral afferent terminals in the bladder; or bladder muscle problem
Organic brain damage- stroke, Parkinson’s, dementia
Urinary infection, diabetes, diuretics, atrophic vaginitis, urethritis

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19
Q

What is functional incontinence? Stress incontinence?

A

When physiological factors are relatively unimportant, patient is ‘caught short’ and too slow in finding the toilet because of immobility or unfamiliar surroundings

Usually from incompetent sphincter, intra-abdominal pressure rises, increase age and obesity= RFs, examine for pelvic floor weakness/ prolapse/ pelvic masses, cough leak on standing and with full bladder= common in pregnancy and following birth

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20
Q

Methods of overactive bladder management?

A

Behavioural therapy- vol chart, caffeine, alcohol, bladder drill
Anti-muscarinic agents= decrease parasymp activitty by blocking M2/3 receptors, SE= dry mouth
B3 agonists= increase symp activity
Botox- blocks NM junction for ACh release, SE= incomplete emptying, catheterise in 15%, daycase
Sacral neuromodulation- electrode–> S3 modulate afferent signals from bladder
Surgery- augmentation cytoplasty- small bowel, colon, stomach

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21
Q

Management for stress incontinence? Urge incontinence?

A

Pelvic floor exercises, intravaginal electrical stimulation, ring pessary for uterine prolapse, surgical- stabilise mid-urethra, urethral bulking, med= duloxetine 40mg/12h PO, SE= nausea

Incontinence chart for 3d, spinal cord and CNS signs?, vaginitis?- topical oestrogen therapy for limited period, bladder training and weight loss, drugs- reduce night-time incontinence, aids- absorbent pad, condom catheter
Urodynamic asses before surgical- exclude detrusor overactivity or sphincter dyssynergia

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22
Q

What is mixed incontinence? 2 types of voiding problems? Txs?

A

Stress and urgency incontinence- continuous= due to fistula, overflow= due to full bladder, social= in dementia
Obstructive- BPE, urethral stricture, prolapse/ mass, BPE= alpha-blockers =/- 5 alpha reductase inhibitor, TURP if all else fails
Non-obstructive- long-term catheterisation to empty- ISC/ LTC/ SPC

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23
Q

What can you lose with spastic spinal cord injury (supra-conal lesion)? Effects?

A

Coordination, voiding completion, reflex bladder contractions, detrusor sphincter dyssynergia, poorly sustained bladder contraction
Potentially unsafe, DSD

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24
Q

What is lost with a flaccid spinal cord injury (conal lesion)? Effects?

A

Reflex bladder contraction, guarding reflex, receptive relaxation
Areflexic bladder, stress incontinence, risk of poor compliance, potentially unsafe, DCPP, poor compliance

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25
Q

Aims of spinal lesion management? What can autonomic dysreflexia result in?

A

Bladder safety, continence/ symptom control, prevent AN dysreflexia
Lesions above T6, overstim of symp below level of lesion in response–> noxious stimulus
Headache, severe HTN, flushing

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26
Q

What bladder risk factors puts kidneys at risk of damage? What causes raised bladder pressure? Results in what?

A

Raised bladder pressure, vesico-ureteric reflux, chronic infection- residual urine, stones
Prolonged detrusor contraction, loss of compliance
Issues with drainage of urine from kidneys, hydronephrosis and renal failure

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27
Q

2 ways of achieving a reflex bladder? What is a paraplegic bladder? Management?

A

1) Harness reflexes to empty bladder into incontinence device 2) Suppress reflexes converting bladder–> flaccid type and empty regularly

Paralysed from waist down, normal upper body function, can do ISC, transfers, causes spasm, reflex bladder

Suprapubic catheter, conveen or suppress reflexes/ poorly compliant bladder converting bladder—> safe type, empty regularly using ISC

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28
Q

What is convene drainage? What makes the sphincter safe? Features of suprapubic catheter? How are bladder contractions suppressed?

A

No indwelling catheter, needs monitoring, incomplete bladder emptying developed long term
Sphincterectomy

Under anaesthetic, infections, stones, use clip and release is possible
Anticholinergics, mirabegron, botulinum toxin, posterior rhizotomy(spinal nerves cut,) cystoplasty

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29
Q

Flaccid and low spinal lesions? Complete loss of distal cord function causes? In neurogenic stress incontinence, ensure what before treating? Men and women tx?

A

Spina bifida, sacral fracture, transverse myelitis, ischaemic injuries, cauda equina
Flaccid paraplegia, areflexic bladder, stress incontinence, loss of reflex erections

Bladder safety, men= artificial sphincter, women= autologous sling, artificial sphincter, synthetic vaginal tapes

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30
Q

Bladder issues in MS?

A

Overactive bladder syndrome, incomplete bladder emptying, upper tract issues secondary to high pressure bladders, reduction in general mobility/ spasticity including hand function, cognitive impairment

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31
Q

Risk factors for prostate cancer? Staged using what system? Graded? Majority are what type histologically?

A

Increasing age, family history- x2-3 1st degree relative, being black, tall and use of anabolic steroids
TNM system, Gleason
Peripheral zone (70%) adenocarcinoma (90%), 20%= transitional zone, 10%= central zone

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32
Q

What prostate cancer grades are 2x prominent? Spreads locally through what and metastasises into what? Can directly spread into what things?

A

1-5 grades
Prostate capsule, into lymph nodes and bone, occasionally–> lung, liver and brain
a) Direct- Intrinsic= rest of prostate, extrinsic: upward–> UB, ureter, downward= urethra, laterally= sciatic nerve and iliac vessels,, forward–> pubic bone, backward–> rectum= rare and late
b) Lymphatic- external iliac, internal iliac, presacral nodes c) Haematogenous- to lymph nodes and bone occassionally to lung, liver and brain

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33
Q

Symptoms of prostate cancer? Red flags?

A

Asymp or nocturia, poor stream, hesitancy, terminal dribbling or obstruction, weight loss +/- bone pain suggests mets
Anorexia, loss of appetite, fever, lethargy

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34
Q

When to do PSA test? Also elevated in what conditions? Other diagnostics? How Gleason grades gotten by pathologist?

A

Before DRE- avoid stimulate release of PSA
BPE, UTI and prostatitis- prostate specific not cancer specific, best for monitoring progress and success of tx, normal= <3ng/ml
DRE= may show hard, irregular prostate
Transrectal USS and biopsy= suspicious DRE and MRI lesion, Xray- bone scan; CT/ MRI for mets, staging= MRI
Analysing histology from 2 separate areas of tumour specimen and adding= 2-10

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35
Q

Prostate cancer tx depends on what? For and against confined to prostate tx? Tx options?

A

Grade, stage, co-morbidities, life expectancy and preference
Radical prostatectomy- fit with localised cancer, urinary incontinence and impotence
Radical radiotherapy- localised and locally advanced, causes impotence and urinary issues
Hormone therapy- delays progression, refractory disease eventually develops, in elderly unfit with high-risk disease
Active surveillance- if >70y/o and low-risk

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36
Q

Other tx for prostate cancer?

A

Orchiectomy- remove testicles, LH agonists e.g. leuprolide, gosrelin, buserelin= block at testes level, can get tumour flare, urinary issues, depression, flushes= issues
Antiandrogens= block testosterone e.g. flutamide
Chemo- adds 3-6 months
Bisphosphonates
Radio for bone pain
TURP- after obstruction
Nephrastomies- ureteric obstruction

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37
Q

Prognosis for prostate cancer? Reasons against screening? Benefits and risks?

A

Localised- 60-90% 10y disease, locally advanced non metastatic, metastatic= median- 2-3y
Uncertain natural history, overtreatment, morbidity of tx

Early diagnosis, early tx of advanced
Overdiagnosis of insig disease, harm from invest/ tx

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38
Q

Complications of radical tx with prostatectomy and radiotherapy?

A

Erectile dysfunction, urinary incontinence, radiation induced enteropathy, urethral strictures

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39
Q

Focused history for renal, bladder and testicular cancer? Diff diagnosis?

A 
Smoking, associated symptoms, instrumentation, catheters, travel, exposure carcinogens, chemo/ cyclophosphamide
Infection: UTI, pyelonephritis, TB
Malignancy- anywhere in tract 
Stones- bladder, kidney, ureteric
Trauma: penetrating, blunt
Nephrological: diabete, nephropathy
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40
Q

Haematuria may be what or what? Other causes of discoloured urine?

A

Visible (macroscopic), non visible (dipstick is based on peroxidase like activity of Hb- haem catalysed reaction and causes oxidation of indicator used)- microscopic> 3 RBC/ power field, symptomatic, asymptomatic

Myoglobinuria, haemoglobunuria, beeturia(unmetabolised pigments- Betanin- absorbed in colon), drugs- Rifampicin

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41
Q

When may transient (short-term) microscopic haematuria be seen? What things may produce a false +ve? False -ve?

A

After vigorous exercise, sexual intercourse, menstrual contamination
Myoglobinuria, bacterial peroxidases, povidone, hypochilorite, dehydration, exercise
Rare reducing agents- ascorbic acid

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42
Q

Significant haematuria is what? Causes?

A

ALL visible haematuria, symptomatic in absence of UTI, persistent asymptomatic (2/3 +ve dipsticks)
Urological/ nephrological, (usually young adults/ children, check renal function and urine proteinuria, ask about FH renal disease, recent infections, rashes and arthritis)–> malignancy, stones, infection, truma, BPE/ BPH, renal cystic disease

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43
Q

Investigations from haematuria? Emergency if what?

A

Urine MC&S, U&E, upper tract imaging–> USS/ KUB XR, CT urogram, flexible cytoscopy
Concerns re blood loss/ risk of clot retention, IV access, bloods, 3 way catheter w/ irrigation, investigations

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44
Q

Bladder cancer found in who? % are transitional and SCC? Rarer causes? Arises from what lining?

A

3:1 men to women, cancer of ageing, 90% and 10%
Adenocarcinoma, sarcoma, small cell
Endothelial lining (urothelium)

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45
Q

Risk factors for bladder cancer?

A

Paraplegia= x20, smoking= x3, occupational- rubber, cable, textile, printing- maybe latent period 15-20 years, drugs- aspirin, phenacetin, cyclophosphamide, schistosomiasis- bladder stones, pelvic irradiation, age, family history= x2 1st degree relative

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46
Q

Presentation of bladder cancer? Examination and tests?

A

Painless haematuria, recurrent UTIs, voiding irritability
General, abdominal, external genitalia, DRE, BMI
Cystoscopy, urine: microscopy/ cytology- may cause pyuria, CT urogram both diagnostic and provides staging, bimanual examination under anaesthetic helps assess spread, MRI/ lymphangiography- may show pelvic node involvement

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47
Q

Grading for bladder cancer? Prognosis?

A

1= well diff, low grade, 2= intermediate, medium grade, 3= poorly diff, high grade, 80%= confined to bladder mucosa, only 20% penetrates muscles
10 yr survival= 50%, based on grade/ stage and cystoscopy

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48
Q

Tx options for bladder cancer- non-muscle invasive and muscle-invasive?

A

G1 Tis or Ta/ G2 T1 (non muscle invasive)- 80% patients= heat using high-freq electric currents via TURBT, intravesical chemotherapeutic agents- multiple small tumours or high-grade, regimen of mitomycin C, doxorubicin and cisplatin to prevent recurrence

Radical cystectomy= gold standrd, radiotherapy= worse 5yr survival rates than surgery, ‘salvage cystectomy’, post-op chemo, neoadjuvant chemo with CMV, orthotopic reconstruction is neck not involved rather than urostoma

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49
Q

Tx for metastatic bladder cancer- G3 T4? Follow-up? Tumour spread?

A

Palliative chemo/radiotherapy, chronic catheterisation to relieve pain
History, examination and cystoscopy: high-risk= every 3 months for 2 yrs then every 6 months, low-risk= first after 9 months, then yearly
Local–> pelvic structures, lymphatic–> iliac and para-aortic nodes; haem–> liver and lungs

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50
Q

Complications of bladder cancer tx?

A

Sexual and urinary malfunction, bladder haemorrhage may complicate tx, consider solution bladder irrigation for intractable haematuria in advanced malignancy= in-patient procedure

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51
Q

Most common renal cancer? Staged using what? Prognosis? What metastases are typical? Arises from where?

A

RCC- 95%, TNM system, 50% alive at 10 years
‘Cannon ball metastases’
Proximal convoluted tubule- is an adenocarcinoma of the renal cortex

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52
Q

Risk factors for renal cancer? Symptoms and spread?

A

Smoking, obesity, renal failure/ dialysis, polycystic and horseshoe kidneys, VHL
50%= found incidentally, haematuria, loin pain, abdominal mass, anorexia, malaise, weight loss, pyrexia
Direct via renal vein, lymph or haem (bone, liver, lung), 25%= metastases at pres

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53
Q

Investigations for RCC? Management?

A

Bloods- FBC–> polycythaemia, U&E, LFT, Ca2+, urine, imaging
T1/ localised= radical nephrectomy, metastatic= biological therapies: mTOR inhibitors(temsirolimus,) TKI- sunitinib, sorafenib, MAbs- bevacizumab
Can be quite chemo/radio resistant

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54
Q

What to assess with a testicular mass? Acutely painful scrotum is what until proven otherwise?

A

Look, feel, move, sign of scrotal mass- possible to get above it, cystic masses can be transilluminated, solid masses do not
Torsion of testes

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55
Q

Epididymitis is mostly who? What organisms? Organsism may go to epididymis by what? Risk from what x3?

A

Young males, E.coli, chlamydia, by retrograde spread from prostatic urethra and seminal vesicles, less common= blood stream,
UTI urethral instrumentation and STIs

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56
Q

What is a hydrocele? It is what and has no what?Causes?

A

Excessive fluid in tunica vaginalis, irreducible, bowel sounds
Primary, large and tense, more common in young boys, secondary to tumours, infections, torsion, hytadid of Morgagni torsion

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57
Q

Symptoms of epididymo-orchitis? Tx?

A

Gradual onset over minutes/ hours, usually unilateral, test pain and tenderness, dragging/ heavy sensation, urethral discharge, tender on palpation, particularly over epididymis, swelling of testicle and epididymis, erythema to scrotum

Admit and treat sepsis otherwise as outpatient, antibiotics as per local guidelines, tight underwear for scrotal support during illness, abstain from intercourse, US of scrotum= diagnosis

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58
Q

Testicular tumours are the commonest malignancy in who? Risk factors? Presentation of testicular cancer?

A

In 20-40 y/o males, crytorchidism, previous tumour, poorly understood
Non tender, hard without fluctuance or transillumination, irregular, age 15-40, dyspnoea(lung mets,) abdominal mass (enlarged nodes)
25% seminomas and 50% NSGCTS= metastases

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59
Q

Tests for testicular cancer? Staging?

A

CXR- lung mets, CT, excision biopsy, alpha-FP and Beta-hCG= useful tumour markers and monitor treatment
1= no evidence metastasis, 2= infradiaphragmatic node involvement, 3= supradiaphragmatic node involvement, 4= lung involvement (haematogenous)

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60
Q

Types of testicular cancer? Tx seminomas are sensitive to? Non-seminomatous? What is a teratoma?

A
  1. Seminomas= 55%- radiation and respond well–> chemo
  2. Non-seminomatous germ cell tumour= 33%- well to chemo, teratomas, grow faster, earlier mean age at time of diagnosis and lower 5 yr survival rate
  3. Mixed germ cell tumour- 12%
    Tumour w/ tissue/ organ components resembeling normal derivatives of germ layer- meso, endo and ectoderm
  4. Lymphoma
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61
Q

Signs of testicular cancer? Risk factors?

A

Painless testis lump, after trauma/ infection+/- haemospermia(blood in semen,) secondary hydrocele, pain, dyspnoea, abdo mass, effects of secreted hormones
Undescended testis, infant hernia, infertility

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62
Q

Tx for testicular cancer?

A

Radical orchidectomy- removal of 1/2 testicles, seminomas= radiosensitive, stage 1= orchidectomy and radiotherapy- cures 95%, close follow-up to detect relapse
NSGCT= 3 cycles of chemo- bleomycin, etoposide and cisplatin= 5yr survival=>90% in all groups, even with mets

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63
Q

What is an epididymal cyst? Tx for hydroceles?

A

Soft, fluctuant lump at top of testicle, clear/ milky fluid, remove is symptomatic, appear in adulthood

Aspiration- may need repeating, surgery- plicating (reducing) tunica vaginalis(Lord’s repair)/ inverting the sac (Jaboulay’s repair), doubt= do USS

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64
Q

What is a varicocele? Haematocele?

A

Dilated veins of pampniform plexus, left side= more common, ‘bag of worms,’ may complain of dull ache
Ass with subfertility- repair= seems to have little effect on subsequent pregnancy rates

Blood in tunica vaginalis- follows trauma, may need drainage/ excision

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65
Q

Aim with testicular torsion? Symptoms? Signs? Most common age?

A

Recognise before the cardinal signs and symptoms are fully manifested, surgery<6hrs= salvage rate is 90-100%
Sudden onset of pain in one testis, which makes walking uncomfortable, pain in the abdomen, nausea and vomiting= common
Inflammation of one testis- very tender, hot and swollen, testis may lie high and transversely
11-30 years

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66
Q

Diff diagnosis for testicular torsion? Tests and tx?

A

Epididymo-orchitis= tends to be older, may be symptoms of urinary infection and more gradual onset of pain
Tumour, trauma and acute hydrocele
Idiopathic scrotal oedema= benign condition usually between 2-10 years and is diff from torsion by absence of pain and tenderness

Doppler USS- lack of blood flow+ isotope scanning
Possible orchidectomy and bilateral fixation, surgery= expose and untwist testis, colour looks good= return it to the scrotum and fix both to the scrotum

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67
Q

What is a ‘Bell-Clapper’ deformity? Management?

A

Fixation posteriorly–> tunica vaginalis= absent, can rotate within tunica, twists–> cuts off blood supply
Urgent urology assessment, immediate surgical scrotal exploration, untwist testicle, both fixed in correct position to prevent further episodes= orchiplexy, possible orchiectomy if delayed surgery/ necrotic testicle present

68
Q

Kidneys filters how much fluid a day? Retains what substances? Other functions? GFR value? % of CO?

A

180L/day, secrete waste/ excess substances
Albumin, circulating cells, reabsorb glucose, amino acids, HCO3, control BP, fluid status, electrolyts, activate vit D, synthesis erythropoietin
120ml/ min and 20% of CO

69
Q

Complications of kidneys? eGFR predicts what? What can be misleading? eGFR value between what meaning need for dialysis and ‘end stage renal disease’?

A

Anaemia, bone disease, symptoms
Creatinine generation from age, gender and race
Extremes of muscle mass- cachexia(wasting due to chronic illness,) body builders, amputees, liver disease etc- requires a steady state
7-10

70
Q

What is creatinine clearance higher than? More prominent at what? Inhibitors of this will make what rise? e.g.?

A

GFR
At low GFR
Serum creatinine and function will look worse
Trimethoprim, cimetidine, ritonavir

71
Q

Albumin below what is normal in mg? Above what in g means nephrotic range? Proximal tubule filters what % Na+? What else? Vulnerable to what?

A

30mg
3g
70%, glucose, amino acids, phosphate
Ischaemic injury, acute tubular necrosis

72
Q

What is Fanconi syndrome? Due to what? Causes?

A

Rare, proximal tubular insult due to glycosuria, acidosis with failure of urine acidification, phosphate wasting; rickets/ osteomalacia, aminoaciduria
Cystinosis, tenofovir, paraprotein disease, Wilson’s disease, glycogen storage diseases

73
Q

The collecting regulates absorption of what? Increased by what hormone? What 2 drugs affects it? What drug affects the loop of Henle? Distal convoluted tubule?

A

Na+, aldosterone
Vasopressin antagonists= aquaporins, aldosterone antagonist
Loop diuretics
Thiazides

74
Q

K+ is what and mostly reabsorbed by what? Distal secretion determines renal excretion and is governed by what?

A

Freely filtered and mostly reabsorbed in proximal tubule/ loop of Henle
Distal delivery of Na, aldosterone, insulin and catecholamines drive cellular K+ uptake, buffering acute changes
K-modifying renal medication; hypokalaemia(loop diuretics, thiazide diuretics- ineffective with low GFR but together are very effective), hyperkalaemia(spironolactone, amiloride, ACE inhibitors, ARBs)

75
Q

Excretion of sodium regulated by reduced but increased what? BP control occurs via what? In renal artery stenosis, get what 2 things? What happens in CKD if you constrict the blood vessels further? Aim to prevent HTN by giving what or what? Should be stopped in the setting of what? Increase of what?

A

Reduced aldosterone and angiotensin II, increased atrial natriuretic peptide
Volume and vasoconstriction
Resistant HTN and flash pulmonary oedema
GFR will increase but damage will increase too
Giving ACEi/ ARB- initially reduce GFR, use indicated in glomerular HTN
Acute insults (sepsis,) renovascular disease and HTN elsewhere

76
Q

In CKD the ability to respond to what is preserved so what are not common features of kidney disease? Prostaglandin preferentially dilates what? Angiotensin II preferentially constricts what?

A

ADH- hypo/ hypernatraemia
Afferent arteriole
Efferent arteriole

77
Q

What is nephrogenic diabetes insidious? It is caused by what, leading to a decrease in what? This improper response may be due to what? S&S?

A

A disorder in which a defect in the tubules in the kidneys causes a person to pass a large amount of urine and lose too much water
Response of kidney to ADH–> decrease in ability of kidney to concentrated urine by removing free water
Electrolyte imbalance, kidney disease, chronic lithium ingestion, genetic
Excessive thirst, excretion of large amounts of urine, dehydration, incontinence- secondary to chronic bladder distension

78
Q

What 2 things that lead to stiff vessels is bad? Net renal excretion of what things? Build up will lead to what?

A

Phosphate retention and vascular calcification

Na+, K+, phosphate, acid, uraemic toxins–> nausea, pruritus, fatigue, confusion, pericarditis

79
Q

Calcitriol actions? Role of erythropoietin? Produce primarily in what? Circulates in what? What is seen after eGFR<30 as there is a deficiency in EPo? Exacerbated by what deficiency?

A

Increases uptake of Ca2+ and phosphate from the gut, suppresses PTH, deficiency–> secondary hyperparathyroidism
Controls RBC production by regulating the differentiation and proliferation of erythroid progenitor cells in the bone marrow, produced primarily in the kidney
In the plasma–> target cells in bone marrow
Anaemia and reduced haemopoiesis
Iron deficiency

80
Q

Calcitriol (circulating vit D) is produced by what in the proximal tubule? What is increased in CKD? This inhibits what? Get what in calcitriol deficiency?

A

1-alpha hydroxylation
FGF-23
Alpha hydroxyls
Secondary hyperparathyroidism- Rugger jersey spine, brown tumours, radial border of phalanges, salt and pepper skull

81
Q

Pressure in glomerulus compared to peripheral capillary beds? Net hydrostatic pressure due to capsule pressure of what? Colloid pressure of what due to proteins in blood? Overall pressure?

A

50mmHg compared to 35mmHg
35mmHg, 15 mmHg
25mmHg
10 mmHg–> solute in direction of tubules

82
Q

What is glomerulonephritis? Can cause what? Presents as what?

A

Group of parenchymal diseases- inflammation and damage
Weakly glomeruli, high BP, reduce function, 25% end stage kidney failure
Often treatable and reversible
Acute nephritic syndrome, nephrotic syndrome, asymptomatic urinary abnormalities, CKD

83
Q

Primary and secondary causes of glomerulonephritis?

A

Primary= no underlying drive to disease, secondary= infection, autoimmunity, malignancy, tend to present w/ similar syndromes

84
Q

Tests for glomerulonephritis?

A

Degree of damage and potential cause, blood: FBC, U&E, LFT, ESR, CRP; immunoglobulins, serum and urine electrophoresis, complement, autoantibodies: ANA, ANCA, anti-dsDNA, anti-GBM; blood culture, anti-streptolysin O titre, HBsAg, anti-HCV. Serum albumin, creatinine, lipids, glucose
Urine: RBC casts, MC&S, protein: creatinine ratio, ACR
Imaging: CXR, renal USS
Renal biopsy: what is affected, how much of kidney, how much of glomerulus, what is seen on immunofluorescence and electron microscopy

85
Q

General management of glomerulonephritis?

A

Early referral–> nephrologist, keep BP< 130/80 or <125/75 if proteinuria >1g/d
Include ACE-i, ARB as these have proven benefits in reducing proteinuria and preserving renal function; no additional from dual therapy

86
Q

What is nephritic syndrome due to? Nephrotic syndrome–> what triad?

A

Damage to glomerulus, damage to filtration mechanism- leaky glomeruli/ active dipstick–> Haematuria and proteinuria, loss of filtration capacity–>AKI, deteriorating kidney function and ESKD

Injury to podocyte= main cause–> proteinuria, hypoalbuminaemia, hyperlipidaemia often present

87
Q

Symptoms of nephritic syndrome? Causes- primary?

A

Haematuria- on urine dipstick (macro/ micro,) proteinuria- urine dipstick, HTN, low urine volume <300ml/ day
Primary= IgA nephropathy- commonest in high-income countries, present= asymptotic non-visible Haematuria, proteinuria<1g, prognosis if male, HTN, proteinuria or renal failure
Mesangiocapillary GN- primary= immune mediated, secondary= SLE, hep, usually–> ESRF

88
Q

Secondary causes of nephritic syndrome?

A

Post-strep GN- antigen on glomerulus causing host reaction, IgG and C3 deposits in kidney on immunofluorescence, serology= increased ASOT, C3, Tx= supportive- >95% recover renal function and antibiotics
ANCA vasculitis- Tx= immunosuppression- steroids, cyclophosphamide, rituximab, plasma exchange
SLE- serology= ANA positive, ds-DNA +ve, low complement, tx= immunosuppression
Systemic sclerosis- ANA, anti-Ro and anti-La antibodies
Anti-glom basement membrane disease- Goodpastures= autoantibodies to type IV collagen

89
Q

What is rapidly progressive GN a collection of? 3 categories? Clinically? Commonest cause of death in ANCA +ve patients?

A

AKI, active dipstick, oliguria, HTN, fluid overload, potential–> ESRF
1. Immune complex disease 2. Pauci-immune disease 3. Anti-GBM disease
AKI +/- systemic disease
Pulm haemorrhage- aggressive immunosuppression, high-dose IV steroids and cyclophosphamide +/- plasma exchange, prognosis= 5-yr survival= 80%

90
Q

Assessing nephrotic syndrome? Diff diagnosis?

A

Pitting oedema- severe and rapid onset, in dependent areas and of low tissue resistance e.g. periorbitally
History- acute/ chronic infections, drugs, allergies, systemic symptoms= autoimmunity or malignancy, dipstick= +++ protein, low albumin, BP= normal/ mildly increased, renal function= normal/ mildly impaired
CCF/ liver disease- increased albumin –> nephrologist and renal biopsy

91
Q

Tx of nephrotic syndrome?

A

Reduce oedema= Loop diuretics, daily weight and U&Es, fluid restrict to 1L/ day and salt restrict while giving diuretics
Reduce proteinuria= ACE-i, ARB
Reduce comp risk= anticoagulant if nephrotic range proteinuria, statin, infections= antibiotics and vaccinate- pneumovax II, flu
Treat underlying cause- infections, malignancy, systemic disease
Stop causative drugs

92
Q

Primary causes nephrotic syndrome?

A

Membranous nephropathy- thickening of glomerular capillary wall, secondary= drugs, hep B, tumours
Biopsy= C3 and IgG sub epithelial deposits on immunofluorescence
Minimal change- commonest in children, electron microscopy= fused podocyte processes, remission= steroids, relapse= cyclophosphamide
Focal segmental glomerulosclerosis= biopsy- part of glomeruli= scarring of certain segments, steroids help
Mesangiocapillary glomerulonephritis- immune complex and complement mediated

93
Q

Secondary causes of nephrotic syndrome? Complications?

A

Diabetic nephropathy, SLE, amyloidosis, paraneoplastic, drug-related, hep B/C
Infections, thromboembolism(increased clotting factors and platelet abnormalities,) hypercholesterolaemia (increased synthesis to counteract reduce oncotic pressure)

94
Q

What is chronic kidney disease defined as? What does it mean by ESRF?

A

Impaired renal function> 3 months based on abnormal structure/ function/ GFR< 60ml/ min/1.73 squared for > 3 months with/ without evidence of kidney damage
Irreversible but can be slowed down
Death is imminent without renal replacement therapy- eGFR<15ml/min/1.73m2

95
Q

Kidney functions? What is creatinine?

A

Fluid management, ePO production, actively excretes H+, absorbs HCO3-, excrete waste, vit D metabolism
Waste product muscle metabolism, sarcopaenic= lower as getting rid of waste

96
Q

Presentation of CKD?

A

Most useful= bilaterally small kidneys on USS
Malaise, loss of appetite, insomnia, nocturia and polyuria due to unable to conc urine, itching= high urea, anaemia, peripheral and pulm oedema, bruising, bone pain
Advanced= CNS- mental slowing, seizures, or myoclonus
Eventually may be oliguria- in ARF and late stages of CRF

97
Q

Causes of CKD?

A

Congenital/ inherited e.g. polycystic KD, renal artery stenosis, HTN, glomerular diseases- IgA nephropathy, granulomatosis, interstitial diseases- reflux nephropathy, multiple myeloma, systemic inflam disease- SLE, vasculitis, diabetes- racial and regional differences, more type II, unknown= 5-20%

98
Q

How many stages of CKD? Check for what in level 1? Level 2-3 involves what action? Prepare for what in stage 4-5 if appropriate?

A

5
Proteinuria, Haematuria
Renoprotection- control BP, modify diet- low protein
Dialysis

99
Q

Albumin in urine can be diluted/ concentrated depending on what? Creatinine is excreted in urine at what rate? Ratio should be constant irrespective of what?

A

Urine volume
Constant rate
Urine volume

100
Q

Screening is recommended in who for CKD?

A

At-risk patients: diabetes mellitus, HTN, IHD, PVD, structural renal disease, recurrent UTIs, CH history of vesicoureteric reflux, multi system disorders e.g. SLE, FH of ESRF or hereditary disease, Haematuria/ proteinuria

101
Q

Examination for CKD? Tests?

A

Pallor, uraemic tinge to skin, purpura, excoriations, increased BP, cardiomegaly, signs of fluid overload and possible cause

Blood: Hb= normal, glucose= DM, decreased Ca2+, increased phos/ alk phos/ PTH
Urine: dipstick, MC&S, albumin, creatinine ratio/ protein: creatinine ratio
Imaging: USS
Renal biopsy- rapidly progressive/ unclear cause, normal sized kidneys

102
Q

6 aspects of CKD management?

A
  1. Investigation- identify and tx of reversible causes
  2. Limiting progression/ complications- BP, renal bone disease, statins and aspirin w/ raised lipids, diet by dietician
  3. Symptom control- of anaemia, acidosis- HCO3- supplements, oedema, restless legs/ cramps- gabapentin, quinine sulphate
  4. Prep renal replacement therapy- create AV fistula
  5. Renal transplantation- medically stable ESRF
  6. Fluid management
103
Q

3 methods renal replacement therapy? Method, comps and unsuitability of haemodialysis?

A
  1. Haemodialysis 2. Haemofiltration 3. Peritoneal dialysis

Double lumen catheter through IJV–> RA, over semi-permeable membrane against dialysis fluid in opposite direction, small solutes diffuse = 3-5 hrs, 3x week
Hypotension, cramps, nausea, headache, chest pain, fever, rigors, blocked catheter, infected dialysis catheter/ fistula, aneurysmal fistula
Full-time workers, lack of access, severe HF

104
Q

Method of haemofiltration? Peritoneal? Comps and unsuitable?

A

Blood across highly perm membrane, small and large solutes across- in ITU, impractical as long-term

Uses peritoneum as membrane, catheter into cavity and fluid infused, water removed by varying conc of osmotic agents, can be done via continuous ambulatory peritoneal dialysis
Infection–> PD peritonitis, catheter exit site/ tunnel line infection, herniation, perforation
Previous abdo surgery, abdo hernia, recurrent PD peritonitis, lack adequate space at home

105
Q

Contraindications for renal transplantation? HLA matched via what, determined by how many antigens? HLA gene on short arm of what chromosome? Then tested via what? Class I antigens expressed on surface of most what cells? Class II antigens?

A

Absolute–> severe vascular disease, systemic/ recent malignancy, chronic infection, severe CV disease, neuropsych disorder, extremes of age, HIV+, active/ fungal/ bacterial/ viral infection
Tissue typing- 6 antigens, chromosome 6
Cross matching
Nucleated cells, APC and activated lymphocytes

106
Q

Features of a cadaver donor? Issues? Evaluation of kidney function in potential donor?

A

Irreversible brain damage, normal renal function for age, no evidence pre-existing renal disease/ transmissible disease, ABO compatible, best HLA match possible

Limited organ survival, decreased availability, HLA protein match, ischaemia- re perfusion injury
Serum creatinine, creatinine clearance, radionucleotide GRF, urine analysis/ culture, GFR> 70ml/min

107
Q

Fluid intake in CKD? Losses? Assessment of fluid status? Complications?

A

Food, drink, IVI, blood transfusion
D&V, burns, NG tube, heat/ evaporation

BP, pulse, skin turgor, jugular venous pressure, central venous pressure
3rd space- fluid doesn’t normally collect–>large amounts e.g. pleural effusion, ascites, bowel obstruction, massive intra-abdominal bleed or in v obese pt

108
Q

What is crystalloid when giving oral/ IV fluid? Colloid e.g. Gelofusine? Special considerations for oliguric/ anuric CKD patients?

A

5% dextrose, 0.9% NaCl- small molecules through cell membrane and move from intra to extravascular space
Large molecules don’t pass through membrane- remains in intravascular compartment
How much urine passed/ day? Next dialysis? Fluid restriction? Careful assess and don’t give lots IV w/o regular fluid assess/ Hartmann’s solution- 5mmol K+

109
Q

What is acute kidney injury? Risk factors?

A

Sudden, sustained decline in renal function, based on changes in serum creatinine and urea, eGFR, urine output

Age>75 y/o, CKD, cardiac failure, PVD, chronic liver disease, diabetes, drugs- NSAIDs and ACEi, sepsis, poor fluid intake/ increases losses, history of urinary symptoms

110
Q

3 types of renal failure causes and examples?

A
  1. Pre-renal= due to reduced renal perfusion- hypotension, renal artery stenosis, and infrarenal haemodynamics- ACEi, NSAIDs, HF
  2. Intrinsic renal- leading to reduce filtration of blood, may be due to: GN, interstitial nephritis, acute tubular necrosis, vascular- vasculitis, malignancy, HTN, thrombus
  3. Post-renal- by urinary tract obstruction= obstructive uropathy: kidney stones, masses in abdomen/ pelvis, ureter/ urethral strictures, enlarged prostate/ cancer
111
Q

Investigations for AKI? 3 criteria often used?

A

Urinalysis for protein, blood, leucocytes, nitrites and glucose: leucocytes and nitrites= infection, protein and blood= acute nephritis, glucose= diabetes
USS= for obstruction

Rise in creatinine>26micromol in 48 hours
Rise in creatinine>1.5 x baseline
Urine output< 0.5ml/kg/h for >6 consecutive hours

112
Q

Presentation of AKI? What do ACEi do to the kidneys? NSAIDs?

A

Depends on underlying cause and severity, oliguria or anuria, polyuria may occur due to reduce fluid reabsorption
Nausea, vomiting
Dehydration, confusion, HTN, urinary retention, dehydration, postural hypotension

Dilates efferent arterioles decreasing GFR
Inhibits cycloxygenase, causes excess vasoconstriction of afferent arteriole

113
Q

Management for AKI? Complications?

A

Aim for euvolaemia, stop nephrotoxic drugs, check and adjust doses of renal excreted drugs, aim for normal calorie intake and protein, if oral intake poor, consider NG nutrition early
1) Pre-renal- fluids, sepsis= ABs, ICU if signs of shock
2) Post-renal= catheterise and consider CT of renal tract and urology referral if obstruction= likely cause, cystoscopy if obstruction/ stents
3) Intrinsic renal- refer to nephrologist if concern over interstitial/ glomerular pathology, systemic disease, multi-organ involvement/ dialysis indications
Hyperkalaemia, give insulin/ dextrose or salbutamol neb with calcium gluconate (cardio-protective)

114
Q

2 types inherited polycystic kidney disease?

A

Autosomal dominant- 85% mutation in PKD1- reach ESRF by 50s, 15%= mutation in PKD2, reach ESRF by 70s, family screening- MRI important
Autosomal recessive= rarer, variable signs, may present in infancy with multiple renal cysts and congenital hepatic fibrosis
No specific tx

115
Q

Presentation of ADPKD?

A

Excessive water and salt loss, nocturia, loin pain, HTH, bilateral kidney enlargement, gross Haematuria following trauma, renal colic due to clots, UTI and pyelonephritis may be presenting features, renal stones= x2 common general population

116
Q

Investigations for ADPKD? Management?

A

US diagnostic criteria: at least 2 unilateral/ bilateral renal cysts at age<30 years, at least 2 cysts in each kidney between ages 30-59, at least 4 in each kidney at age>60 years, diagnosis= supported by hepatic or pancreatic cysts

No cure, counselling, monitor for progression, treat HTN, UTIs, stones, give analgesia, dialysis for ESRF

117
Q

Causes of simple and acquired cysts?

A

Simple= unknown, acquired= CKD, drugs= lithium, congenital

118
Q

Erectile function? Flaccid state is due to what tone? Erect state due to what stimulation?

A

Neurovascular phenomenon under hormonal control= vascular event, balance between inflow and outflow of blood
Sympathetic tone- arterioles constricted
Parasympathetic stimulation- arteriolar dilatation, trabecular smooth muscle relaxation

119
Q

Anatomy of the penis?

A

Corpus cavernosa covered by tunica albuginea, fused by septum and contains spongy vascular erectile tissue (SM lined by endothelial cells,) corpus spongiosum (thinner tunica contains urethra) Also glans penis, bulb of penis

120
Q

Arterial supply and venous daring of penis? Nerve supply?

A

Internal iliac–> internal pudendal artery—> dorsal penile artery(glans penis,) cavernosal artery (supplies spongy tissue of corpora,) bulbar arteries (supplies bulb, spongiosum and glans)

Sinusoids- drains to subtunical plexus–> circumflex vein–> deep dorsal vein
Corpora cavernosum= drains to cavernous veins–> crucial veins–> internal pedundal veins

Parasymp- erectile= S2-4, sympathetic- T11-L2, cavernous nerve- carried both fibres and possess posterolateral to prostate

121
Q

Hormone needed for normal erectile function? Primary, secondary and congenital causes of low levels? Physiology of erection- higher stimuli and peripheral control?

A

Testosterone
Pituitary/ hypothalamus failure, testes (tumour, injury, drugs)
Kleinfeldern syndrome, Noonans syndrome

Hypothalamus, oxytocin pro-erectile pathways
Smooth muscle mediated- arteriolar dilatation, trabecular relaxation, NO release by cavernous nerves and endothelium causes smooth muscle relaxation (ischiocavernous muscle)

122
Q

What is erectile dysfunction? Causes? Risk factors?

A

Persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance
Organic- vasculogenic, hormonal, neurogenic, anatomical, drug induced, psychogenic

Similar to CVS disease- lack exercise, obesity, smoking, hypercholesterolaemia, metabolic syndrome, DM, MI, liver disease and alcohol, renal failure, trauma, iatrogenic

123
Q

Non-organic causes erectile dysfunction? Diagnosis?

A

Sudden onset, relationship difficulties, performance anxiety, morning and non-coital erections= normal

History of psych cause= sudden onset, good nocturnal and early morning erections, situational ED, younger pt, sexual history–> erectile function, orgasmic function, sexual desire, ejaculation, intercourse and overall satisfaction

124
Q

Examination and tests for erectile dysfunction?

A

BP, HR, hepatosplenomegaly, genitalia, prostatic enlargement/ cancer, hypogonadism

Fasting glucose, lipid profile, morning testosterone- low–> perform pro-lectin, FSH, LH, specialised= nocturnal penile tumescence- spontaneous during sleep or when waking up, intra-cavernosal infection test, duplex USS of penile arteries, arteriography

125
Q

Tx of erectile dysfunction? 1st line SEs of PDE5 inhibitors? CIs?

A

Lifestyle and risk factor modification, testosterone replacement, psychosexual counselling- gives variable results
1st line= phosphodiesterase inhibitors–> sildenafil (viagra,) cialis, vardenafil- PDE5 breaks down cGMP–> arterial SM relax, vasodilation and penile enlargement= need sexual stimulation
Headaches, flushing, nasal congestion, impaired colour vision, priapism
Vasodilators, cytochrome p450 inhibitors

126
Q

2nd line med for erectile dysfunction? Intracavernous injections, SEs?

A

Sublingual apomorphine- centrally acting dopamine agonist, not CI w/ nitrates, lower efficiency than 1st line and limited to mild-moderate ED
Caverject into shaft, SE= pain, priapism(not back to flaccid state after sexual event>4hrs, risk perm isch damage to corpora) and fibrosis

127
Q

Intraurethral therapy? SEs? CI? What is penile prosthesis? Risks?

A

Alprostadil, MUSE pellet= increases cAMP, activates secondary pathway for erection
Urethral pain, hypotension, dizziness, urethral bleeding
In urethral stricture

2 cylinders with reservoir and pump, malleable
Urethral perforation, cold glans ‘‘Concorde glans”, malfunction, infection, erosion

128
Q

What is a premature ejaculation? Due to what? Tx?

A

Ejaculation always/ nearly prior to within 1 minute of vaginal penetration and inability to delay, frustration, avoidance of sexual intimacy
Psychological, endocrine, Parkinson’s, opioid withdrawal
Counselling, “quiet vagina,” squeeze technique, topical local anaesthetic, SSRIs

129
Q

What is Peyronie’s disease? Causes? Tx? What is a vacuum constriction device? Can causee what? CI?

A

Fibrotic plaque–> bend on erection
Dupytren’s contracture, alcohol excess, diabetes
Photos in dorsal and lateral view
Initially conservative management, Nesbit’s plication/ Lue’s procedure, penile prosthesis

Passive engorgement w/ constriction ring to force erection–> pain, inability to ejaculate, ptechiae- red/ purple spots on skin, bruises and numbness
Those on anticoags/ bleeding disorders

130
Q

Sites of chlamydia trachoma’s and neisseria gonorrhoea? Symptoms of chlamydia- men, women and complications?

A

Adult- urethra, endocervical canal, rectum, pharynx, conjunctiva
Neonate= conjunctiva
Atypical pneumonia also in neonatal
Men= pain when urinating, discharge from tip of penis, burning/ itching in urethra, pain in testicles can–> epididymis-orchitis, reactive arthritis
Women= discharge, menstrual irregularity, dysuria can–> PID, ectopic pregnancy and infertility

131
Q

Diagnosing chlamydia? Tx?

A

NAAT- high spec and send, female= self collected vaginal swab, first void urine- lower mens, sometimes= in community asymptomatic screening, male= first void urine

Partner management, tests for other STIs, doxycycline 100mg bd for 7 days, erythromycin 500mg bd for 14 days/ azithromycin in pregnancy, AB resistance= clinical important issue

132
Q

Diagnosing gonorrhoea? Tx?

A

Near patient test- microscopy of gram stained smears of genital secretions looking for gram negative diplococci within cytoplasm of polymorphs, male urethra, female endocervix, rectum
Culture on selective medium to confirm diagnosis, sensitivity testing, NAAT

Partner notification, test for other STIs, continuous survival of antibiotic sensitivity, single dose tx preferred
Aim to cure at least 95% of people at first, current regime= ceftriaxone 1g IMI

133
Q

2 types of syphilis? Types of early infectious and late syphilis? Highly transmissible by what?

A 
Early infectious (within 2 years infection)
Late syphilis
Primary, secondary and early latent 
Late latent, CNS, CVS, gummatous 
Oral sex
134
Q

Primary chancre where for primary syphilis? Incubation period? What else? Any what is syphilis until proven otherwise?

A 
95% genital skin, also nipples, mouth
9-90 days 
Dusky macule-papule- indurated clean based non-tender ulcer
Regional nodes= 1-2/52 after chancre 
Untreated- heals without scarring 4-8/52
Any genital ulcer
135
Q

Secondary syphilis how many days after infection? % with skin rash? Other manifestations?

A

6-8 days- primary chancre may be present, may have no history
70%
Mucous membrane lesions, generalised lymphadenopathy, alopecia, hoarseness, bone pain, hepatitis, nephrotic syndrome, deafness, iritis, meningitis, cranial and palsies, constitutional

136
Q

Diagnosing syphilis? Serological tests? Tx?

A

Early moist lesions- may be able to identify motile spirochetes on wet mount using dark ground microscopy
Genital ulcer- serology usually +ve if ulcer >2 weeks, repeat at 6 and 12 weeks to exclude diagnosis

Screening EIA, confirmatory tests for samples which screen positive- TPPA test
Non-treponemal test to assess disease activity

Penicillin by injection, efficient follow up and partner notification essential

137
Q

Men who have sex with men (MSM) are disproportionately affected by what 2 things? STI/ HIV transmission model (RBCD)? What is sexual health?

A

Syphilis and gonorrhoea
Reproductive rate, B= infectivity rate, C= partners over time, D= duration of infection

State of physical, emotional, mental and social wellbeing in relation to sexuality- not just absence of disease, dysfunction or infirmity

138
Q

6x factors of sexual health? Primary prevention strategies?

A

Services, individual factors, social relationships, emotions and emotional intelligence, social groups, external and political factors
STI awareness campaigns to reduce personal risk behaviour, one to one risk reduction discussion, vaccination- hep B, HPV, pre and post exp prophylaxis

139
Q

Post-ex prophylaxis available where? Pre-expo prophylaxis reduces HIV risk by what %? Treatment as prevention known as what? Secondary prevention methods? Tertiary prevention?

A

A&E and sexual health services
86%
TasP
Easy access to STI tests, partner notification, targeted screening- antenatal for HIV and syphilis, national chlamydia, HIV home-testing

Anti-retrovirals for HIV, prophylactic antibiotics for PCP, acyclovir for suppression of genital herpes

140
Q

Why trace sexual partners? How are partners traced?

A

Break chain of transmission, prevent re-infection of index patient, prevent complications of untreated infection
Patient referral, provider referral, conditional or contract referral, emphasis on patient choices and confidentiality

141
Q

Online outreach for preventing STIs? At Public Sex Environment (PSE) sites?

A

GPS based mobile apps, x2 weekly online outreach sessions using profile, information nationally and locally, signposting to sexual health services

Providing info, advice and signposting, providing condoms and lube on-site, 1x2 hr bi-weekly session

142
Q

What is bacteriuria? What is pyuria? What is a UTI? Lower and upper UTIs known as?

A

Bacteria in the urine- can be symptomatic or asymptomatic
Pus/ leucocytes in the urine- w/ infection, may be sterile
Inflam response of urothelium to bacterial invasion, usually ass with bacteriuria and pyuria

Urethritis, cystitis, prostatitis, epididymitis
Pyelonephritis

143
Q

What is uncomplicated UTIs? Given what as 1st one? Also tell patient what?

A

Normal renal tract and function–> empirical tx, trimethoprim/ nitrofurantoin as 1st line
Increase fluid intake, regularly void (pre and post intercourse,) keep good hygiene, avoid spermicides etc.

144
Q

What does complicated UTIs involve? Tx? Further investigations?

A

Abnormal structural/ functional abnormality in renal/GU tract, voiding difficult, decreased renal function, impaired host defences, virulent organisms- s.aureus, male, pregnant, child, recurrent UTI- >2eps in 6 months or >3 in 12m with same bacteria or unresolved infection, immunocompromised, nosocomial infection, urosepsis
Longer course antibiotics

MSU, DRE, post void bladder scan, USS of renal tract/ pelvis, CT if stones suggested, flexible cystoscopy

145
Q

What is bacteriuria? What is pyuria? What is a UTI? Lower and upper UTIs known as?

A

Bacteria in the urine- can be symptomatic or asymptomatic
Pus/ leucocytes in the urine- w/ infection, may be sterile
Inflam response of urothelium to bacterial invasion, usually ass with bacteriuria and pyuria

Urethritis, cystitis, prostatitis, epididymitis
Pyelonephritis

146
Q

What is uncomplicated UTIs? Given what as 1st one? Also tell patient what?

A

Normal renal tract and function–> empirical tx, trimethoprim/ nitrofurantoin as 1st line
Increase fluid intake, regularly void (pre and post intercourse,) keep good hygiene, avoid spermicides etc.

147
Q

What does complicated UTIs involve? Tx? Further investigations?

A

Abnormal structural/ functional abnormality in renal/GU tract, voiding difficult, decreased renal function, impaired host defences, virulent organisms- s.aureus, male, pregnant, child, recurrent UTI- >2eps in 6 months or >3 in 12m with same bacteria or unresolved infection, immunocompromised, nosocomial infection, urosepsis
Longer course antibiotics

MSU, DRE, post void bladder scan, USS of renal tract/ pelvis, CT if stones suggested, flexible cystoscopy

148
Q

RFs for UTIs? Pathogenesis?

A

Female, sex, exposure to spermicide in females, pregnancy, menopause, decreased host defence, obstruction, reflux, Tamm-Horsfall protein, low urine pH and high osmolarity, commensal flora, urinary obstruction

5 pathogens= e.coli, s.saphrophyticus, proteus, Klebsiella pneumoniae, enterococci- broader in hospital/ catheterised patients
Colonic flora colonise vagina, in urethral meatus, ascent via vaginal mucus

149
Q

Diagnosis of UTIs? Tx?

A

Symptoms and urinalysis- nitrates, WBC, blood-often present, pH- in urea splitting infections, SG raised, protein may be present, glucose- diabetes increases risk, ketones

Antibiotics IV/PR/ oral- be aware of allergies, resistance= due to enzymes, DNA changes, complications- risk of c.diff, colonising flora

150
Q

Prevention of catheter-ass UTIs?

A

Intermittent, suprapubic catheterisation, prevent bacteriuria- keep closed, remove ASAP, prevent comps- don’t treat if asymptotic catheter replacement
Culture rather than dipstick, +ve confirmed with 2nd sample, asymptotic should be treated, test of cure should be sent 1 week after tx

151
Q

Majority of pyelonephritis caused by what? Presents? Investigation and tx? Comps?

A

UPEC- due to P pilli
Loin pain, fever and pyuria
Regular obs, examination, PV, bloods/ cultures, urgent USS to rule out obstruction
IV antibiotics- Gentamicin, Coamoxiclav, drain obstructed kidney and catheter if compromised, fluid replacement, analgesia

Renal abscess, more common in diabetics, emphysematous pyelonephritis

152
Q

Symptoms of cystitis? 4 classifications of prostatitis? Investigation and tx?

A

Dysuria, frequency, urgency +/- supra, pubic pain, Haematuria, offensive/ cloudy urine

1= acute bacterial prostatitis, 2= chronic bacterial, 3= chronic pelvic pain syndrome (CPPS)- inflammatory, non-inflammatory, 4= asymptomatic inflame prostatitis

Urinalysis and MSU, segmented urine/ semen cultures, bloods, STI screen, transracial US +/- CT abdo and pelvis
IV gentamicin and coamoxiclav w/ long course quinolone once well

153
Q

What does urethritis present with?

A

Urethral pain, dysuria+/- discharge, predominant an STI/ non specific (gonorrhoea, chlamydia, ureaplasma urealyticum)

154
Q

Epidemiology of stone disease (urolithiasis in urinary tract)? Where can you get stones?

A

Increasing incidence, M>F, commonest age= 30-50, lifetime risk= 10-15%, w/ 50% lifetime risk of recurrence

Anywhere from collecting duct–> external urethral meatus
Upper= renal and ureteric stones, lower= bladder, prostate and urethral stones

155
Q

Causes of stone disease?

A

Anatomical factors- congenital (horseshoe, duplex, PUJO, spina bifida,) acquired- obstruction, trauma, reflux, urinary factors- metastable urine, promoters and inhibitors, calcium, oxalate, urate, cystine, dehydration, infection

156
Q

Mechanism of stone formation?

A

‘Nucleation theory’- from crystals in supersaturated urine, of normal urinary contents- 80% calcium oxalate, 10% uric acid- usually glowing on Xray, 5-10% magnesium ammonium phosphate- infection stones, 1% cystine- congenital–> excessive secretion of 4 AA; cystine, ornithine, lysine and arginine–> COLA

157
Q

General prevention of stone formation? Specific prevention?

A

Overhydration- 2.5-3L/ 24hr urine output, low salt diet, normal dairy, healthy protein intake, reduce BMI, active lifestyle, regular checks of calcium level
Uric acid- only in acid urine, de-acidify urine, cystine stones- excessive overhydration, urine alkalinisation, cysteine binders- captopril, penicillamine +/- genetic counselling

158
Q

Asymptomatic symptoms of stone disease? Renal colic? Renal obstruction? Obstruction of mid-ureter? Lower ureter?

A

Loin pain
Unilateral loin pain/ spasms, rapid onset, unable to get comfortable, radiates to groin and ipsilateral testis/ labia, associated nausea/ vomiting, colicky- worse w/fluid loading, classically severe, UTI symptoms= dysuria, strangury, urgency, frequency, recurrent UTIs, haematuria
Loin between rib 12 and lateral edge lumbar muscles
May mimic appendicitis/ diverticulitis
Bladder irritability and pain in scrotum, penile tip or labia majora

159
Q

Obstruction in bladder/ urethra symptoms? Pyonephrosis?

A

Pelvic pain, dysuria, strangury

Infected hydronephrosis, proteinuria, sterile pyuria, anuria(no urine production)

160
Q

Investigations for stone disease?

A

ABG, analgesia, history and examination, urinalysis, FBC, U&E, calcium, uric acid, imaging- non contrast computerised tomography of kidney, ureter and bladder- one breath hold, shows 99% stones, shows if pathological organs
Radiation used and no functional info given
KUB Xray- if visible- 80% are, aids follow up and may be able to avoid repeat CTs, USS- sensitive for hydronephrosis but not visualising stones in ureter- useful in pregnant and younger recurrent stone formers, intravenous urogram- almost as good as NCCT

161
Q

Diff diagnosis for stone formation?

A

Vasc accident- AAA ruptured until proven otherwise, bowel path- diverticulitis, appendicitis, gynae- ectopic pregnancy, ovarian torsion, testicular torsion, MSK

162
Q

Management of ureteric colic? What is pyonephrosis? Consequences of urosepsis?

A

Analgesia- NSAID= diclofenac, opiaites, antiemetics, observe- for sepsis, can–> septic shock
Pus in renal pelvis and can cause failure of kidney within 24hrs, need IV ABs/ oxygen escalation, URGENT drainage via nephrostomy or ureteric stent to relieve

Infection in urinary tract–> bloodstream, needs 10 days in ITU, 5 weeks in hospital, tracheostomy and 20 digit gangrene

163
Q

Tx of ureteric colic?

A

Depends on site/ size of stones and pt factors/ comps/ risks
Allow 2 weeks to pass, majority<4mm will pass, only 10% >7mm
Drainage if sepsis
Extracorporeal shock wave lithotripsy- destroy via US waves for stones <1cm
Open/ laparoscopic surgery
Utereoscopy- any stone, laser, basket extraction, lithoclast

164
Q

Small kidney stones (calculi) can do what? Larger stones? If stone infected can cause what?

A

Can migrate into ureter or if <1cm, can be observed, only 1/3 will progress
Can occlude the calyces +/- pelviureteric junction acutely obstructing and causing renal/ ureteric colic
Chronic renal damage/ abscess/ fistulae/ xanthogranulomatous pyelonephritis- foamy macrophages cluster with other cells

165
Q

Tx for renal colic?

A

Conservative for small in safe location, asymptomatic, of static size
Extracorporeal shock wave lithotripsy- stones up to 1-2cm, issues with fragment passage
Ureteroscopic- flexible, laser for stones <2 cm
Precut nephrolithotomy- key hole for larger
Nephrectomy- if split function <10-15%
Open/ laparoscopic surgery- rare

166
Q

Tx of bladder stones?

A

Conservative- if asymptomatic/ unfit
Endoscopic- can be accompanied by tx of BOO
Open / laparoscopic- ideal for larger stones/ if other open procedures required

Phase 2a Flashcards (14 decks)

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