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gu Flashcards

1
Q

What is the innervation of bladder relaxation?

A
  • Autonomic sympathetic (noradrenergic)
  • T10-L2 nuclei
  • Urethral contraction (smooth muscle component but remember the main part of the sphincter is skeletal muscle)
  • Inhibits detrusor contraction
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2
Q

Spinal reflexes for bladder

A
  • Reflex bladder contraction - sacral micturition centre
  • Guarding reflex - onuf’s nucleus (rhabdosphincter - skeletal muscle so somatic)- the guarding reflex occurs to prevent voiding of the bladder caused by unexpected abdominal pressure.
  • Receptive relaxation - sympathetic - the smooth muscles of the proximal part of the stomach relax and dilate when food enters the stomach. This receptive relaxation enables a large amount of food to amass in the stomach with a minimal rise in intragastric pressure.
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3
Q

What is the function of the proximal convoluted tubule?

A

Reabsorption of:
- some water and Na+
- some other ions
- all glucose and amino acids

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4
Q

What is the function of the distal convoluted tubule?

A
  • Regulating acid-base balance
  • By secreting H+ and absorbing HCO3-
  • Also regulates Na+ level
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5
Q

What is the structure of the collecting duct in the kidney?

A

Principal cells:
- Regulate Na+ reabsorption and K+ excretion
- Respond to aldosterone and ADH

Intercalated cells:
- Exchange H+ for HCO3-

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6
Q

What is the structure of urothelium?

A
  • Complex stratified epithelium
  • Can stretch in 3 dimensions
  • Layer of umbrella cells - make it urine proof
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7
Q

What is the innervation of bladder contraction?

A
  • Autonomic parasympathetic (cholinergic)
  • S3-S5 nuclei
  • Drive detrusor contraction
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8
Q

What is the innervation of A-δ fibres (bladder stretch) and C fibres (bladder pain)?

A
  • Sensory autonomic
  • S2-S4 nuclei
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9
Q

Functions of the prostate

A
  • Produces testosterone and dihydrotestosterone (5x more potent)
  • Produces PSA (prostate specific antigen)- liquefies semen
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10
Q

Storage lower urinary tract symptoms (LUTS)

A

Occur when bladder should be storing urine -> need to pee
Frequency
Urgency
Nocturia
Incontinence

More common in females

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11
Q

Voiding lower urinary tract symptoms (LUTS)

A

Occur when bladder outlets obstructed -> hard to pee
Poor Stream
Hesitancy
Incomplete emptying
Dribbling after finishing urination

More common in males

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12
Q

What is Prehn’s sign?

A
  • Used to determine the cause of testicular pain
  • Performed by lifting the scrotum and assessing the consequent changes in pain
  • Prehn’s sign positive = pain relief upon elevation
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13
Q

What is the cremasteric reflex?

A

Stroke inner thigh, ipsilateral testicle should elevate

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14
Q

What is an unsafe bladder?

A

One that puts the kidneys at risk - caused by prolonged high pressure

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15
Q

What is erectile dysfunction?

A
  • Persistent inability to attain amd maintain an erection sufficient to permit satisfactory sexual performance
  • Commonly found in men over 40
  • Up to 10% of men are affected
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16
Q

Pathophysiology of erectile dysfunction

A
  • Neurogenic - failure to initiate
  • Arteriogenic - failure to fill (mc)
  • Venogenic - failure to store

prolactin

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17
Q

Innervation of the penis

A
  • Sympathetic - T11 - L2
  • Parasympathetic - S2-S4
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18
Q

Aetiology of erectile dysfunction

A
  • Atherosclerosis
  • Diabetes
  • Age
  • Hypogonadism
  • Trauma to pelvic plexus
  • Iatrogenic - surgery that damages pelvic plexus, drugs
  • Psychosomatic
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19
Q

Treatment of erectile dysfunction

A
  • Treat underlying cause
  • oralphosphodiesterase type 5 inhibitor drugs- increase blood flow
  • Psychosexual counselling if necessary
  • Intracavernosal injection
  • Vaccuum assisted device
  • Implant
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20
Q

Pathophysiology of acute kidney injury

A

Accumulation of usually excreted substances:
- K+ (arrhythmias)
- Urea (pruritis + uremic frost, confusion if severe)
- Fluid (pul + peripheral oedema)
- H+ (acidosis)

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21
Q

Pre-renal AKI

A

Due to hypoperfusion of the kidneys, leading to decreased GFR
- Hypovolaemia
- Reduced cardiac output (cardiac failure, liver failure, sepsis, drugs)
- Drugs that reduce blood pressure (ACE-i, ARBs, NSAIDs, loop diuretics)

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22
Q

Renal AKI

A

A consequence of structural damage to the kidney, eg: tubules, glomeruli, interstitium, bvs. May result from persistent pre-renal and post-renal causes, damaging renal cells
- Toxins and drugs (eg: antibiotics, contrast agent, chemo)
- Vascular causes (eg: vasculitis, thrombosis, etc)
- Glomerular, tubular (MC) or interstitial causes

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23
Q

Post-renal AKI

A

Least common (10%) - due to acute obstruction of the flow of urine -> increased intratubular pressure and decreased GFR
- Renal stones
- Blocked catheter
- Enlarged prostate
- GU tract tumours
- Neurogenic bladder

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24
Q

Diagnosis of AKI

A
  • Establish cause (pre, intra, post) w KDIGO classification
  • Check K+, H+, urea, creatining w U+E
  • FBC + CRP check for infection
  • Renal biopsy will confirm intrarenal cause, ultrasound for post renal
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25
Q

Treatment for AKI

A
  • Treat complications
  • Fluid rehydration with IV fluids for pre-renal AKI
  • Stop nephrotoxic medications
  • Relieve obstruction in post-renal AKI
  • Last resort = Renal replacement therapy
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26
Q

What is acute kidney injury?

A

Abrupt decline in kidney function (hours-days) characterised by high serum creatinine + urea and low urine output

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27
Q

NICE criteria for acute kidney disease (any one)

A
  • Rise in serum creatinine of > 25μmol/L within 48 hours
  • 50% or greater rise in serum creatinine over 7 days
  • A fall in urine output to less than 0.5ml/kg/hour for more than 6 consecutive hours
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28
Q

Risk factors for acute kidney injury

A
  • 65+
  • Comorbidities
  • Cognitive impairment (less water intake)
  • Hypovolaemia of any cause
  • Oliguria
  • Nephrotoxic drug use including contrast agents
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29
Q

Best way to establish cause of AKI

A

Urea:Creatinine
> 100:1 = Prerenal
< 40:1 = Renal
40-100:1 = Postrenal

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30
Q

When would haemodialysis be given for AKI

A

Acidosis (pH<7.1)
Fluid overload (oedema)
Uremia
K+ >6.5 /ECG change

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31
Q

Complications of AKI

A
  • Hyperkalaemia (most important)
  • Rhabdomyolysis
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32
Q

Risk factors for benign prostatic hyperplasia

A
  • Age (50+)
  • Men (obviously)
  • Afrocarribean = high testosterone
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33
Q

Pathophysiology of benign prostatic hyperplasia

A
  • Inner transitional zone of prostate (muscular, gland) proliferates
  • Causes narrowing of the urethra
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34
Q

Presentation of benign prostatic hyperplasia

A

LUTS

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35
Q

What happens in benign prostatic hyperplasia if the urethra is totally occluded?

A

Anuria
- Retention
- Hydronephrosis
- UTI
- Stones

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36
Q

Diagnosis of benign prostatic hyperplasia

A

Digital rectal examination (DRE) - Smooth, enlarged
Prostate-specific antigen (PSA) - To rule out prostate cancer (but unreliable as it can be raised in both, but more in cancer)

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37
Q

Treatment for benign prostatic hyperplasia

A
  • First line: Alpha blocker (tamsulosin)
  • Second line: 5 alpha reductase inhibitor (finasteride) - decreases testosterone production and therefore prostate size
  • Last resort, surgery - TURP - transurethral resection of the prostate (SE = retrograde ejaculation)
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38
Q

Pathophysiology of CKD

A
  • Many nephrons damaged, increased burden on the remaining nephrons
  • Compensatory RAAS but this increases transglomerular pressure -> shearing and loss of BM selective permeability -> proteinuria/haematuria
  • Angiotensin 2 upregulates TGF-beta and plasminogen activator-inhibitor-1 -> mesangial scarring
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39
Q

Normal eGFR

A

120mL/min/1.73m2

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40
Q

When is metformin contraindicated?

A

When eGFR < 30

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41
Q

CKD G scores (eGFR)

A

G1. ≥ 90ml/min/1.73m2
G2. 60-90ml/min/1.73m2
G3a. 45-59ml/min/1.73m2
G3b. 30-44ml/min/1.73m2
G4. 15-29ml/min/1.73m2
G5. <15ml/min/1.73m2

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42
Q

Best clinical readings to quantify CKD

A
  • eGFR
  • Albumin:Creatinine (more sensitive measurement of proteinurea than PCR)
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43
Q

Aetiology of CKD

A
  • T2DM
  • Hypertension
  • Glomerulonephritis
  • PKD
  • Nephrotoxic drugs
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44
Q

Risk factors for CKD (other than diseases)

A
  • Older age
  • Family history
  • Smoking
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45
Q

Presentation of CKD

A
  • Asymptomatic early on (lots of nephrons = reserve supply)
  • Symptoms due to substance accumulation + renal damage (diabetic nephropathy)
  • Pruritis, loss of appetite, nausea, oedema, muscle cramps, pallor
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46
Q

Complications of CKD

A
  • Anaemia (Low EPO)
  • Osteodystrophy (low vit D activation)
  • Neuropathy and encephalopathy
  • CVD and hypertension
  • Haematuria and proteinuria
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47
Q

Diagnosis of CKD

A
  • FBC for anaemia
  • U+E for eGFR
  • Early morning urine dipstick for haematuria and albumin:creatinine (>70mg/mmol = significant proteinuria)
  • Ultrasound shows bilateral renal atrophy
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48
Q

Treatment for CKD

A

No cure so treat complications:
- Anaemia: Fe + EPO
- Osteodystrophy: Vit D supplements
- CVD: ACE-i and statins
- Oedema: diuretics
- Stop NSAIDs
- Stage 5 (end stage renal failure) -> RRT (dialysis)
- Ultimately if ESRF, cure is renal transplant

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49
Q

CKD A scores (albumin:creatinine)

A

A1. < 3mg/mmol
A2. 3-30mg/mmol
A3. >30mg/mmol

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50
Q

A patient has a score of A1 combined with G1 or G2. Can they be diagnosed with CKD?

A

No. They need at least an eGFR of <60 or proteinuria

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51
Q

What type of cancer is bladder cancer?

A
  • Transitional cell carcinoma of bladder (mc, and mc subtype is transitional urothelium)
  • If patient has schistosomiasis, they are more likely to have squamous cell carcinoma
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52
Q

Risk factors for bladder cancer

A
  • Smoking
  • Age 55+
  • Males
  • Occupational exposure to aromatic amines, eg: painter, hairdresser (dyes), mechanic working with tyres (rubber)
  • Chemo/radiotherapy (cyclophosphamide)
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53
Q

Presentation of bladder cancer

A
  • Painless visible haematuria
  • LUTS
  • Recurrent UTIs
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54
Q

Diagnosis of bladder cancer

A

Gold standard: flexible cystoscopy + upper tract imaging

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55
Q

NICE 2 week wait referral criteria for bladder cancer

A

Age 45 or above with:
- Unexplained visible haematuria
- or visible haematuria that persists after UTI treatment
Age 60 or above with:
- Unexplained non-visible haematuria
- and either: dysuria or raised white cell count

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56
Q

Treatment for bladder cancer

A

T1: Transurethral resection of bladder tumour
T2-3: Cystoprostatectomy in men, anterior extentoration in women
T4: Palliative or chemo/radiotherapy

Intravesical therapy: mitomycin and BCG to reduce recurrence

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57
Q

Transitional cell carcinoma of the upper tract

A
  • Less common
  • Same risk factors as bladder cancer
  • Haematuria, loin pain, “clot colic”
  • Managed by nephroureterectomy
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58
Q

Risk factors for renal cell carcinoma

A
  • > 40
  • Smoking
  • Obesity
  • Male
  • Hypertension
  • Haemodialysis (15% chance)
  • Von-Hippel Lindau syndrome (also tuberous sclerosis, Burt Hogge Dube and hereditary papillary RCC)
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59
Q

What is Von-Hippel Lindau syndrome?

A
  • Autosomal dominant loss of tumour suppressor gene
  • RCC (50%) bilaterally
  • Renal + pancreas cysts
  • Cerebellum cancers, pheochromocytomas
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60
Q

Presentation of renal cell carcinoma

A
  • Often asymptomatic and found incidentally, 25% metastasised cases at presentation
  • Triad: loin pain, haematuria, abdo mass
  • May have left sided varicocele- rare block of test. vein
    -malaise, anorexia, weight loss, pyrexia
  • Anaemia (low EPO)
    -can secrete renin- hypertension
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61
Q

Diagnosis of renal cell carcinoma

A
  • First line: Ultrasound
  • Gold standard: CT chest/abdo/pelvis
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62
Q

Renal cell carcinoma metastases

A
  • Spreads to the tissues around the kidney, within Gerota’s fascia
  • Often spreads to the renal vein, then IVC
  • “Cannonball metastases” in the lungs are a classic feature of renal cell carcinoma
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63
Q

Staging of renal cell carcinoma

A

1 - confined to renal capsule

2- through capsule, confined to Gerota’s fascia

3- renal vein or vena cava involvement and/ or regional node involvement

4- direct organ invasion or distant metastases

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64
Q

Treatment for renal cell carcinoma

A
  • Sometimes watch and wait
  • Radiofrequency ablation or cryotherapy (only if tumour is <4cm)
  • Gold standard: Partial nephrectomy- if both kidneys affected
  • Radical (full) nephrectomy (most common)
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65
Q

What type of cancer is renal cell carcinoma?

A

PCT epithelial carcinoma

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66
Q

NICE two week wait referral criteria for renal cancer

A

45 or over with:
- Unexplained visible haematuria without UTI
- or visible haematuria that persists after treated UTI

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67
Q

What is a Wilms tumour?

A
  • Renal mesenchymal stem cell tumour found via us/ct and treated with chemo/radio
  • Seen in children (<3 years)
  • Much rarer. 90% survival
  • Aka: nephroblastoma
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68
Q

What type of cancer is prostate cancer?

A

Adenocarcinoma of outer peripheral prostate

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69
Q

Risk factors for prostate cancer

A
  • Genetic: BRCA1, BRCA2, HOXB13
  • Increased age
  • Afrocaribbean ethnicity
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70
Q

Presentation of prostate cancer

A
  • LUTS
  • Systemic cancer symptoms (weight, loss, fatigue, night pain)
  • Bone pain
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71
Q

Prostate cancer metastases

A
  • Typically to bone (thick sclerotic lesions)
  • Typically lumbar back pain
  • Also liver, lung, brain
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72
Q

Diagnosis of prostate cancer

A
  • DRE + PSA (3-10ng/ml= benign hyperplasia or cancer, >10 usually cancer) in community
  • Gold standard: Transrectal ultrasound, multiparametric mri
  • transperineal ultrasound guided Biopsy

all gives Gleason score - higher = worse

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73
Q

Treatment of metastatic prostate cancer

A
  • Hormone therapy
  • Bilateral orchidectomy (best)
  • GNRH receptor agonist eg: goserelin
  • Survielance in early disease
  • External beam radiotherapy directed at prostate
  • Barchytherapy
    • Radiotherapy done via seeds inside prostate
  • Bicalutamide
  • Surgery to remove prostate
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74
Q

Treatment of localised prostate cancer

A
  • Radical prostatectomy
  • Radiotherapy - external beam, bachytherapy
  • Watchful waiting
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75
Q

What type of cancer is testicular cancer?

A

Germ cell (90%+) or non germ-cell (<10%) tumour

Germ = seminoma (mc) or teratoma
Non germ = sertoli, leydig, sarcoma

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76
Q

Risk factors for testicular cancer

A
  • Most common cancer in young men 20-45 (more common in caucasians)
  • Cryptorchidism (undescended testes)
  • HIV
  • Previous testicular cancer
  • Infertility
  • Family history
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77
Q

Presentation of testicular cancer

A
  • Painless, hard, irregular lump in testicle
  • Does not transilluminate
  • May show lung metastasis signs, eg: cough -> consider chest x-ray
  • Gynaecomastia (breast enlargement) if it is a Leydig cell tumour (rare)
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78
Q

Diagnosis of testicular cancer

A
  • Examination including lymph nodes, testes and scars from previous orchidopexy
  • Urgent (Doppler) ultrasound of testes (90% diagnostic)
  • Bloods for tumour markers
  • CXR if resp symptoms
  • Staging: CT chest/abdo/pelvis
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79
Q

Tumour markers for testicular cancer

A
  • beta hCG - raised in seminomas
  • AFP - raised in teratomas
  • LDH raised non-specifically
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80
Q

Royal Marsden staging system for testicular cancer

A
  1. Isolated to testicle
  2. Spread to retroperitoneal lymph nodes
  3. Spread to lymph nodes above diaphragm
  4. Metastasised to other organs (mc: lymphatics, lungs, liver, brain)
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81
Q

Treatment of testicular cancer

A
  • Urgent inguinal orchidectomy (+ offer sperm banking)
  • Adjuvant chemotherapy
    Or radiotherapy
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82
Q

Classification of incontinence

A
  • Stress incontinence (sphincter weakness)
  • Urge incontinence (detrusor or bladder overactivity)
  • Mixed incontinence
  • Overflow incontinence
  • Spastic paralysis (neurological UMN lesion)
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83
Q

Suprapontine incontinence

A
  • Mid brain functioning but not controlled by cortex (will present with neuro problems like dementia or cerebral palsy)
  • Reflex bladder and bowel - involuntary urination and defaecation
  • Coordinated sphincter

Complete emptying

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84
Q

Spastic SCI incontinence- spinal cord injury

A
  • Conus functioning but not controlled by brain (sphincter isn’t being told to relax by pons)
  • Reflex bladder and bowel - involuntary urination and defaecation
  • Dyssynergic sphincter

Incomplete emptying

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85
Q

Flaccid SCI incontinence

A
  • Conus destroyed or non-functional
  • Areflexic bladder and bowel - fill until they overflow
  • Non-functional sphincter
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86
Q

Management of stress incontinence

A

Women:
- Pelvic floor re-education/physiotherapy
- Duloxetine (caution)
- Surgery (last line)

Men:
- Artifical urinary sphincter

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87
Q

Stress incontinence causes

A

Women:
- Post-pregnancy trauma

Men:
- Neurogenic
- Iatrogenic (prostatectomy)

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88
Q

Management of overactive bladder

A
  • Behavioural therapy or physiotherapy
  • Anticholinergic therapy
  • Mirabegron (b3 agonist)
  • Botox
  • Neuromodulation
  • Bladder augmentation
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89
Q

What diseases can present as both nephrotic and nephritic?

A
  • Diffuse proliferative glomerulonephritis
  • Membranoproliferative glomerulonephritis
90
Q

Aetiology of nephritic syndrome

A
  • IgA nephropathy/Berger’s disease - mc
  • Post strep glomerulonephritis
  • SLE
  • Goodpasture’s syndrome
  • Haemolytic uraemic syndrome
  • All examples of Type 3 hypersensitivity, except for Goodpasture’s which is Type 2
91
Q

General presentation of nephritic syndrome

A
  • Visible/non-visible haematuria (+little proteinuria)
  • Oliguria (little urine, salt + water retention)
  • Hypertension
  • Oedema
92
Q

Difference in pathophysiology of nephrotic vs nephritic syndromee

A

Nephrotic
- Podocyte injury
- Scarring
Nephritic
- GBM breaks
- Inflammation
- Bowman crescents

93
Q

Pathophysiology of Goodpasture’s syndrome

A
  • Presence of autoantibodies (anti-GBM) to alpha-3 chain of Type 4 collagen in glomerular and alveolar membrane
  • Pulmonary and alveolar haemorrhage, lung fibrosis and glomerulonephritis
94
Q

Treatment for Goodpasture’s syndrome

A
  • Corticosteroids
  • Plasma exchange (to get rid of anti-GBM antibodies)
  • Cyclophosphamide (for immune suppression)
95
Q

Presentation of Goodpasture’s syndrome

A
  • Dyspnoea
  • Coughing problems
  • Oliguria
  • Haematuria
96
Q

Diagnosis of Goodpasture’s syndrome

A
  • Lung and kidney biopsy - damage and Ig deposition
  • Serology - anti-GBM positive
97
Q

Pathophysiology of Henoch Schoenlein purpura

A
  • Small vessel vasculitis
  • Affects kidney and joints due to IgA deposition
  • IgA nephropathy only in kidneys
  • HSP everywhere

Do biopsy

98
Q

Presentation of Henoch Schoenlein purpura

A
  • Purpuric rash on legs
  • Nephritic symptoms
  • Joint pain due to IgA deposition
99
Q

Diagnosis of Henoch Schoenlein purpura

A
  • Diagnosed clinically
  • Confirmed with renal biopsy
100
Q

Treatment of Henoch Schoenlein purpura

A
  • Corticosteroids
  • ACE-i/ARB
101
Q

Risk factors for IgA nephropathy

A
  • Asian populations
  • Associated with HIV
  • Teenagers or young adults
102
Q

Presentation of IgA nephropathy

A
  • Visible haematuria (ribena/coke)
  • 1-2 days after tonsilitis
  • Viral infection (or gastroenteritis viral infection)
103
Q

Diagnosis of IgA nephropathy

A
  • Immunofluorescence microscopy shows IgA complex deposition
  • Biopsy
104
Q

Treatment of IgA nephropathy

A
  • Non-curative
  • 30% progress to ESRF
  • First line: BP control (ACE-i)
105
Q

Diagnosis of post strep glomerulonephritis

A
  • Light microscope - hypercellular glomeruli
  • Electron microscope - subendothelial immune complex deposition
  • Immunoflorescence - starry sky appearance

biopsy???

106
Q

Presentation of post-strep glomerulonephritis

A
  • Visible haematuria
  • 2 weeks after pharyngitis from Group A, beta-haemolytic strep (S.pyogenes)
107
Q

Complications of post strep glomerulonephritis

A
  • Self limiting usually
  • Sometimes may progress to rapidly progressing glomerulonephritis
108
Q

Treatment of post-strep glomerulonephritis

A
  • Antibiotics to clear the strep
  • Supportive care
109
Q

What is RPGN?

A

Subtype of glomerulonephritis that progresses to ESRF very fast (weeks to months)

110
Q

Diagnosis of RPGN

A

Biopsy shows Inflammatory cresents in Bowman’s space

111
Q

Causes of RPGN

A
  • Wegener’s granulomatosis (c-ANCA +ve)
  • MPA (pANCA +ve)
  • Goodpasture’s
112
Q

Pathophysiology of SLE nephropathy

A
  • Lupus nephritis secondary to SLE
  • ANA deposition in endothelium
113
Q

Diagnosis of SLE nephropathy

A
  • ANA positive
  • Anti-ds DNA positive

how??? bloods???

114
Q

Treatment of SLE nephropathy

A
  • Steroids
  • Hydroxychloroquine
  • plus immunosuppressants, eg: cyclophosphamide
115
Q

Aetiology of nephrotic syndrome

A

Primary:
- Minimal change disease (mc in children)
- Focal segmental glomerulosclerosis (mc in adults)
- Membranous nephropathy (caucasian adults)
Secondary:
- Mc to diabetes

116
Q

Presentation of nephrotic syndrome

A
  • Proteinuria (frothy apple juice🧃) (>3.5g/24hours)
  • Hypoalbuminaemia (<30g/L)
  • Oedema (eg: puffy face)
  • Hyperlipidemia + weight gain
117
Q

Diagnosis of minimal change disease

A

On biopsy:
- Light biopsy = no change
- Electron biopsy = podocyte effacement + fusion

118
Q

Diagnosis of focal segmental glomerulosclerosis

A

On biopsy:
- Light microscopy -> segmental sclerosis
- < 50% glomeruli affected

119
Q

Diagnosis of membranous nephropathy

A

On biopsy:
- Light microscopy - thickened GBM
- Electron microscopy - subpodocyte immune complex deposition, spike + dome appearance

120
Q

Treatment of nephrotic syndrome

A
  • Steroids for 12 weeks with variable response
  • Minimal change = responds well to them
  • Focal segmental glomerulosclerosis + membranous nephropathy = less well :(
121
Q

Supportive treatment of nephrotic syndrome

A
  • Control fluids - diuretics, ACE-i/ARB, spironolactone
  • Statins
  • Anticoagulation (espesh when albumin <20g/L)
  • Abx in children
122
Q

Aetiology of calcium oxalate stones

A
  • Low urine volume
  • Hypercalciuria
  • Hyperuricosuria
  • Hyperoxaluria
  • Hypocitraturia
123
Q

Aetiology of calcium phosphate stones

A
  • Low urine volume
  • Hyperclciuria
  • Hypocitraturia
  • High urine pH
  • Hyperparathyroidism
  • Renal tubular acidosis
124
Q

Drugs that impair urine composition

A
  • Acetazolamide
  • Allopurinol
  • Aluminium magnesium hydroxide
  • Ascorbic acid
  • Calcium
  • Furosemide
  • Laxatives
  • Vit D
  • Topiramate
125
Q

Drugs that crystallise in urine

A
  • Allopurinol/oxypurinol
  • Amoxicillin/ampicillin
  • Ceftriaxone
  • Ephedrine
  • Indinavir
  • Magnesium trisilicate
  • Quinolones
  • Sulphonamides
  • Triamterene
  • Zonisamine
126
Q

Methods of surgery for kidney stones

A
  • Extracorporeal shock wave lithotripsy (ESWL) - non-invasive, smaller stones
  • Percutaneous nephrolithotomy (PCNL) - larger stones, 20mm+
  • Uteroscopy (URS) - energy sources including lasers break up stones
  • Open surgery (last resort when all else fails)
127
Q

What are kidney stones made from?

A

Calcium
- Calcium oxalase (80%)
- Calcium phosphate (20%)
Other types:
- Struvite (RF = UTI) (1-5%)
- Uric acid (10-20%)
- Cystine (1%)
- Drug induced (1%)

128
Q

Aetiology of cystine stones

A

Cystinuria, a genetic disorder that causes cystine to leak through the kidneys into the urine

129
Q

Epidemiology of kidney stones

A
  • M:F about 2:1
  • Uncommon in children
  • Age 30-50 but decreasing
130
Q

Pathophysiology of kidney stones

A
  • Excess solute in collecting duct
  • Supersaturated urine, favours crystallisation
  • Stones cause regular outflow obstruction
  • Hydronephrosis -> dilation + obstruction of renal pelvis
131
Q

Presentation of kidney stones

A
  • Unilateral loin to groin pain that is colicky (fluctuating)
  • Patient can’t lie still (DDx = peritonitis)
  • Haematuria and dysuria
  • UTI symptoms/recurrent UTIs
132
Q

Three common obstruction sites for kidney stones

A
  • Pelvoureteric junction
  • Pelvic brim (where ureter crosses over iliac vessels)
  • Vesicoureteral junction
133
Q

Diagnosis of kidney stones

A

First line: KUBXr - 80% specific for renal stones, cheap + easy
Gold standard: Non-contrast CT KUB - 99% specific for stones
Bloods: FBC (raised Calcium and Phosphate) U+E (haematuria)

Ultrasound if pregnant

134
Q

Treatment for kidney stones

A
  • Symptomatic -> hydrate, non-opiate analgesia or NSAIDs
  • Antibiotics if UTI present
  • Alpha blocker to help stones pass (up to 10mm)
  • Surgical elective treatment if stones are too big to pass (5mm<)
135
Q

Why shouldn’t you use contrast agent when kidney disease is suspected?

A

Contrast would need to be excreted by the kidney

136
Q

Prevention of uric acid stones

A

Deacidification of urine to pH 7-7-5

137
Q

Prevention of cystine stones

A
  • Excessive overhydration
  • Urine alkalinisation
  • Cysteine binders
138
Q

Pathophysiology of obstructive uropathy

A
  • Obstruction
  • Retention and increased kidney ureter bladder (KUB) pressure
  • Refluxing/backlogged urine in renal pelvis
  • Hydronephrosis - dilated renal pelvis, more infection prone
139
Q

Most common causes of obstructive uropathy

A
  • Benign prostatic hyperplasia
  • Kidney stones
140
Q

Treatment of obstructive uropathy

A
  • Relieve kidney pressure -> catheterise urethra, urethral stent
  • Treat cause/infection
141
Q

Autosomal recessive PKD

A
  • Much less common
  • Mutated PKHD1 gene on chromosome 6
  • Infancy or prebirth
  • High mortality
  • Congenital abnormalities
  • eg: Potter’s sequence: flattened nose + clubbed feet
142
Q

Autosomal dominant PKD

A
  • Most common
  • Mutated PKD1 (85%) or PKD2 (15%)
  • More males
  • Presentation at 20-30 years
143
Q

Pathophysiology of polycystic kidney disease

A

Normally
- PKD 1+2 codes for polycystin (Ca2+ channels)
- Usually, cilia move and polycystin open
- Ca2+ influx inhibits excessive growth
PKD
- PKD gene mutated
- Lack of Ca2+ influx
- Excessive growth of cilia
- Results in polycysts

144
Q

What is PKD?

A
  • Cyst formation through renal parenchyma
  • Bilateral enlargement and damage
145
Q

Presentation of PKD

A
  • Bilateral flank/back or abdo pain
  • Hypertension
  • Haematuria (when cysts rupture), resolves within a few days
  • Renal stones more common
  • End stage renal failure at around 50 years
146
Q

Extrarenal cysts

A
  • Particularly in Circle of Willis
  • Berry aneurysm if rupture -> subarachnoid haemorrhage
147
Q

Diagnosis of PKD

A
  • Kidney ultrasound shows enlarged bilateral kidneys with multiple cysts
  • Also genetic testing
148
Q

Treatment of PKD

A
  • Non-curative
  • Manage symptoms
149
Q

What is a consequence of autosomal dominant PCKD?

A

IBS

150
Q

What is retention?

A

Inability to pass urine even when bladder is full (500+mL)

151
Q

Causes of retention

A
  • Obstruction
  • Stones
  • BPH
  • Neurological flaccid paralysis
    (hypotonia of detrusor, as LMN)
152
Q

Treatment of retention

A

Catheterise

153
Q

What does a scrotal mass indicate?

A

Cancer until proven otherwise

154
Q

What is an epididymal cyst?

A
  • Extratesticular cyst above and behind testis
  • Transilluminates
  • Diagnosed by scrotal ultrasound
  • Dissolves in 10 days
155
Q

Presentation of epididymitis

A
  • Acute unilateral pain
  • Sometimes following previous infection
  • Prehn’s sign positive
156
Q

Treatment of epididymitis

A
  • Stat IM ceftriaxone (if organism unknown)
  • Plus doxycyline
157
Q

What is hydrocele?

A
  • Cyst that testicle sits within
  • Transilluminates
  • Diagnosed with scrotal ultrasound
158
Q

Pathophysiology of hydrocele

A

Fluid collection in tunica vaginalis

159
Q

Pathophysiology of testicular torsion

A
  • Spermatic cord twists on itself
  • Occlusion of testicular artery
160
Q

Risk factor for testicular torsion

A

Bell clapper deformity (“horizontal lie” of testes)

161
Q

Presentation of testicular torsion

A
  • Severe unitesticular pain - hurts when walking
  • Abdo pain
  • Nausea and vomiting
  • Cremastering reflex lost
  • Prehn’s negative
162
Q

Diagnosis of testicular torsion

A
  • First, surgical exploration
  • Then, ultrasound to check testicular blood flow
163
Q

Treatment of testicular torsion

A
  • Urgent surgery within 6 hours (90-100% successful)
  • All cases require bilateral orchiplexy (fixing of scrotal sac to overcome biclapper deformity)
  • If testes non-viable = orchidectomy
164
Q

Pathophysiology of varicocele

A
  • Distended pampiniform plexus
  • Due to increased left renal vein pressure causing reflux
165
Q

Complication of varicocele

A

Infertility

166
Q

Presentation of varicocele

A
  • Bag of worms (on left hand side mostly)
  • Typically painless, painful when more severe
  • Diagnosed clinically
167
Q

Presentation of chlamydia and gonorrhoea

A
  • Vaginitis and cervicitis
  • Proctitis
  • Epididymo-orchitis
  • Pelvic inflammatory disease
  • Pharyngitis
  • Reactive arthritis
168
Q

What do GUM clinics screen for?

A
  • Chlamydia
  • Gonorrhoea
  • Syphilis (blood test)
  • HIV (blood test)
169
Q

How do nucleic acid amplification tests work?

A
  • Check if a gonococcal infection is present or not
  • By looking at gonococcal RNA or DNA
170
Q

Reactive arthritis (Reiter’s triad)

A
  • Can’t see - conjunctivitis
  • Can’t pee - urithritis
  • Can’t climb a tree - arthritis
171
Q

Treatment for chlamydia

A
  • First line: doxycycline
  • If CI or not tolerated: azithromycin
  • If CI: erythromycin…or ofloxacin but this is CI in pregnancy
  • Sexual intercourse should be avoided until treatment is complete
  • Partner must also be treated
172
Q

What is chlamydia caused by?

A

Chlamydia trachomatis, a gram negative intracellular bacillus

173
Q

Epidemiology and risk factors for chlamydia

A
  • Most common STI in the UK
  • Under 25 and sexually active
  • New sexual partner or more than one sexual partner in the last year
  • Lack of consistent condom use
  • Unprotected sex
174
Q

Symptoms of lymphogranuloma venereum (a type of chlamydia)

A
  • Tenesmus
  • Anorectal discharge (often bloody) and discomfort
  • Diarrhoea or altered bowel habits
175
Q

Diagnosis of chlamydia

A

Nucleic acid amplification testing

  • Women - vulvovaginal or endocervical swab
  • Men - first-void urine
176
Q

Symptoms in chlamydia

A

70% of women and 50% of men are asymptomatic

177
Q

Treatment for gonnorrhoea

A
  • IM ceftriaxone 1g
  • Refer to GUM clinic
178
Q

What is gonorrhoea caused by?

A
  • Gram-negative diplococcus Neisseria gonorrhoeae
  • Spread by penetretive sexual intercourse most commonly
179
Q

Risk factors for gonorrhoea

A
  • Frequent or unprotected sexual intercourse
  • Multiple sexual partners
  • MSM
  • Chlamydial infection
180
Q

Symptoms in gonorrhoea

A

50% of women and 90% of men are symptomatic

181
Q

Symptoms of rectal and pharyngeal gonorrhoea infection

A
  • Rectal infection is usually asymptomatic but may cause anal discharge and pain or discomfort
  • Pharyngeal is asymptomatic in most cases but is occasionally associated with a sore throat
182
Q

Diagnosis of gonorrhoea

A
  • Nucleic acid amplifiction testing
  • Microscopy shows gram negative diplococci
  • Swab infected areas
183
Q

Treatment for early syphilis

A
  • Single deep intramuscular dose of benzathine benzylpenicillin
  • Refer to GUM clinic
  • Notify all partners in the last 3 months
184
Q

Pathophysiology of syphilis

A
  • Spirochete bacteria called Treponema pallidumial
  • Gets in through skin or mucous membranes, replicates and then disseminates through the body
185
Q

Risk factors for syphilis

A
  • MSM
  • IVDU
  • Sex workers
  • Multiple or unprotected sexual partners
186
Q

Primary syphilis

A
  • Painless ulcer called a ‘chancre’ at the original site of infection (usually genitals)
  • Femoral lymphadenopaty
  • Presents 9-90 days after exposure
  • Usually resolves spontaneously over 3-10 weeks
187
Q

Secondary syphilis

A
  • Systemic features, skin lesions, alopecia, mucous patches and early neurosyphilis
  • Presents 4-12 weeks after initial chancre
  • Untreated symptoms slowly resolve over 3-12 weeks but may recur
188
Q

Latent syphilis

A
  • Asymptomatic
  • Less than 2 years duration from initial infection
  • Late latent - more than 2 years
189
Q

Tertiary syphilis

A
  • Gummatous, cardiovascular and neuro syphilis
  • Presents 15-40 years after initial infection
190
Q

Diagnosis of syphilis

A
  • Antibody testing for T.pallidum
  • Samples from site of infection can be tested to confirm the presence of T.pallidum with dark field microscopy and PCR
191
Q

Five most common UTI pathogens

A

Klebsiella
E.coli
Enterobacter
Proteus
S.saphrophyticus

MC is uropathogenic e.coli

192
Q

Why are females more affected by UTIs?

A
  • Shorter urethra
  • Closer to anus
  • Easier for bacteria to colonise
193
Q

Diagnosis of all types of UTI

A

First line:✨Urine dipstick✨
+ve leukocytes
+ve nitrites (bc bacteria break down nitrates into nitrites)
+/- haematuria

Gold standard: Midstream MC + S
- Confirms UTI
- Identifies pathogen

194
Q

Complicated vs uncomplicated UTIs

A

Uncomplicated - non pregnant women
Complicated - everyone else

195
Q

Teatment of asymptomatic bacteruria

A

Do not treat if they’re over 65 (???)

196
Q

What to do while waiting UTI test results

A

First line (trimethroprim) if patient is symptomatic

197
Q

Diagnosis of urethritis, epididymo-orchitis and prostatitis

A
  • Normal diagnosis for UTIs
  • As well as NAAT (nucleuc acid amplification testing) to detect STI
198
Q

Treatment of urethritis and epididymo-orchitis

A

Dependent on cause

199
Q

What is pyuria?

A

The presence of leukocytes in the urine

200
Q

What is cystitis?

A
  • UPEC infection of the bladder
  • Most common in young sexually active women
201
Q

Aetiology of cystitis

A
  • Urine stasis
  • Bladder lining damage
  • Catheters
202
Q

Presentation of cystitis

A
  • Suprapubic tenderness and discomfort, worse with a full bladder
  • High frequency and urgency
  • Visible haematuria
203
Q

Treatment for cystitis

A
  • Trimethroprim (avoid in pregnancy) or nitrofurantoin (avoid in 3rd trimester)
  • If pregnant, take amoxicillin instead
204
Q

What is epididymo-orchitis?

A
  • Inflammation of the epididymis, extending to the testes
    Usually due to:
  • Urethritis (<35 years)
  • Cystitis extension (>35 years)
  • Can also be caused in the elderly from a catheter
205
Q

Presentation of epididymo-orchitis

A
  • Unilateral scrotal pain and swelling
  • Prehn’s sign positive
  • Cremaster reflex intact
  • DDx = rule out testicular torsion
206
Q

Treatment for epididymo-orchitis

A

Depends on if it’s caused by an STI (NG/CT) or UTI - treat either appropriately

207
Q

Acute vs chronic prostatitis

A
  • Acute bacterial prostatitis - more rapid onset of symptoms
  • Chronic prostatitis - symptoms lasting for at least 3 months, can be subdivided.

Types of chronic prostatitis:
- Chronic pelvic pain syndrome - no infection
- Chronic bacterial prostatitis - infection

208
Q

Most common cause of prostatitis

A

E.Coli

209
Q

Presentation of prostatitis

A
  • Perineal, penile or rectal pain
  • Acute urinary retention, obstructive voiding symptoms
  • Low back pain, pain on ejaculation
  • Tender, swollen warm prostate on examination
210
Q

Infective vs non-infective urethritis

A

Infective: Gonococcal (LC) and non-gonococcal (MC, chlamydia)
Non-infective: Trauma

211
Q

Risk factors for urethritis

A

MSM and unprotected sex

212
Q

Presentation of lower urinary tract infections

A
  • Dysuria
  • Frequency

+/- urethral discharge, urethral pain (Urethritis)

213
Q

Treatment for urethritis

A
  • N.Gonorrhoea - IM ceftriaxone or azithromycin
  • C.Trachomatis - azithromycin (or doxycycline)
214
Q

Investigations for upper UTI

A
  • Midstream urine
  • Blood cultures
215
Q

Treatment for pyelonephritis

A
  • Analgesia: Paracetamol
  • Antibiotics: Ciprofloxacin or co-amoxiclav
    (if pregnant, give cefalexin)
  • Refer to hospital if there are signs of sepsis
216
Q

What is pyelonephritis?

A

Infection of the renal parenchyma and upper ureter, ascending transurethral spread

217
Q

Most common causative pathogens of pyelonephritis (most to least common)

A
  • Uropathogenic E.Coli
  • Kleblsiella
  • Proteus
  • Pseudomonas
  • Enterobacter
218
Q

Presentation of pyelonephritis

A

Triad: loin pain, fever, n+v

219
Q

Patients who have significant symptoms or do not respond to treatment w pyelonephritis

A
  • Renal abscess
  • Kidney stones
220
Q

Complication of pyelonephritis

A

Hydronephritis from dilated renal pelvis

Haroon flashcards (10 decks)

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