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Urology Flashcards

1
Q

How do we calculate osmolarity?

A

Osmolarity = Concentration x No. of dissociated particles

   = Osm/L OR mOsm/L
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2
Q

Describe the steps for positive/negative water balance

A

Positive:
High water intake –> ECF increases, plasma osmolality decreases, sodium concentration increases –> Hypoosmotic urine production –> Osmolarity normalises

Vise versa

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3
Q

What happens to urea after being filtered through Bowman’s capsule and how does vasopressin affect this?

A

Vasopressin boosts UTA1 and UTA3 numbers which is located in the collecting duct. Urea leaves collecting duct –> increases interstitial osmolarity. UTA2 receptor along thin descending limb leads to uptake of urea. UT B1 uptakes urea back into blood

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4
Q

Factors influencing ADH production and release (2 broad categories)

A

Stimulatory:
Nicotine
Hypovolaemia
Hypotension
High plasma osmolarity
Angiotensin II

Inhibitory:
Ethanol
ANP
Hypervolaemia
Hypertension
Low plasma osmolarity

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5
Q

How does Atrial natriuretic peptide affect ADH production?

A

Inhibitory

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6
Q

Describe how ADH works at the collecting duct

A

Binds to V2 receptor on basolatoral membrane –> cyclic AMP –> protein kinase A –> upregulation of AQP2 & 3 –> increased water reabsorption

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7
Q

At a cellular level how is NaCl reabsorbed in thick ascending limb?

A
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8
Q

What does ADH do in terms of Na+ reabsorption?

A

Thick ascending limb: ↑Na+ - K+ - 2Cl- symporter

Distal convoluted tubule: ↑Na+ - Cl- symporter

Collecting duct: ↑Na+ channel

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9
Q

TReatment for nephrogenic diabetes insipidus

A

Very hard to treat - try diuretics + NSAIDS

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10
Q

Symptom of inappropriate ADH secretion (SIADH) clinical features and treatment

A

Hyperosmolar urine
Low urine volume
Hypoosmolar blood
Low plasma osmolarity

Treat the cause

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11
Q

What does the Henderson-Hasselbalch equation help us study?

A
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12
Q

What part of the brain centrally controls regulation of sodium intake?

A

Lateral parabrachial nucleus at the junction of the midbrain and pons

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13
Q

What does the parabrachial nucleus do under normal conditions of euvolemia (normal sodium levels)

A

A set of cells in parabrachial nucleus that respond to serotonin, glutamate suppress basal Na+ intake

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14
Q

What happens under conditions of Na+ deprivation?

A
  • There is an increased appetite for Na+
  • This is driven by GABA and opioids
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15
Q

How is GFR linked to renal plasma flow rate and blood pressure?

A
  • RPF rate is proportional to mean arterial pressure
  • Approx 20% of renal plasma enters tubular system so GFR = RPF * 0.2 therefore GFR is also proportional to mean arterial pressure
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16
Q

What happens at a certain threshold of high blood pressure to GFR and RPF?

A

It plateus; dont want to excrete excess salt while exercising etc

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17
Q

Describe the nephron’s system to limit sodium loss through kidney excretion

A

HIgh sodium in filtrate so high sodium in DCT
detected by the macula densa in juxtaglomerlular apparatus.
Increased NaCl means greater NaCL absorbption by macula densa triple transport.
Releases adenosine which has two functions:
1. Acute reduction of renin production
2. detected by extramesangial cells which interact with afferent arteriole leading to vasodilation. Reduced blood flow so lower perfusion pressure so reduced eGFR

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18
Q

Describe the various systems in the nephron to increase Na+ reabsorption/retention

A

Sympathetic activity (3)
- contracts SMC of afferent arteriole
- stimulates Na+ uptake of PCT cells
- stimulates JGA cells to produce renin which leads to Ang II production

  • Ang II (3)
    • stimulates PCT cells to take up Na+
    • stimulates adrenal glands to produce aldosterone which stimulates Na+ uptake in distal part of DCT and collecting duct
    • Vasoconstriction

Low tubular Na+ itself will stimulate production of renin from JGA and therefore Ang II

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19
Q

Now describe the system in the nephron for decreasing Na+ reabsorption

A

Atrial natriuretic peptide:

  • Acts as vasodilator
  • Reduces Na+ uptake in PCT, DCT and collecting duct
  • Suppresses production of renin by JGA
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20
Q

How does the body react when we have low sodium levels?

A

1) Low sodium means lower blood pressure and low fluid volume

2) This increases beta1-sympathetic activity which stimulates afferent arteriole SMC to contract and reduce glomerular filtration pressure

3) Stimulates renin production which cleaves angiotensinogen into Ang I which is cleaved by ACE into Ang II

4) Ang II stimulates zona glomerulosa of adrenal gland to release aldosterone which increases Na+ reabsorption

5) Ang II also promotes vasoconstriction and Na+ reabsorption

6) This all reabsorbs more Na+ and reduces water output

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21
Q

How does the body react when we have high sodium levels?

A

) High sodium means higher fluid volume meaning higher blood pressure

2) This suppresses beta1-sympathetic activity and causes production of ANP

3) This reduces renin which reduces Ang I which reduces Ang II which reduces aldosterone

4) This promotes vasodilation and decreases Na+ and water reabsorption

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22
Q

What stimulates aldosterone release?

A

Ang II promotes synthesis of aldosterone synthase which causes last 2 enzymatic steps in production of aldosterone from cholesterol

  • Also released when there’s a decrease in blood pressure via baroreceptors
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23
Q

What does aldosterone do to the kidneys?

A
  • Stimulates Na+ reabsorption (35g per day)
  • Increased K+ secretion
  • Increased H+ secretion
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24
Q

What kind of renal cancers are there?

A
  • 85% are renal cell carcinomas (adenocarcinomas)
  • 10% are transitional cell carcinomas
  • 5% are sarcoma/Wilms tumour/other types
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25
Q

Common causes of Renal Cancer

A
  • Smoking
    -Obesity
  • Hypertension
  • Renal failure and dialysis
  • Genetic predisposition with Von Hippel-Lindau syndrome (50% of individuals will develop RCC)
    -Having hepatitis C
  • Abstestos
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26
Q

Clinical features of renal cancer and explanation
and what is the most common

A
  1. Mass - if there’s a mass there would be anaemia, weight loss, hypercalcaemia
  2. If no mass
    - Loin pain
    - Haemorrhage
    - Varicocele- why?
    • left sided renal tumours
    • You get compression of renal vein due to tumour thrombus
      -Metastatic disease symptoms like bone pain, haemoptysis, shortness of breath
  3. Most common= painless haematuria
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27
Q

Investigation for kidney cancer following Painless visible Haematuria

A

Flexible cystoscopy

CT urogram

Renal function

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28
Q

Investigation for kidney cancer following Persistent non visible haematuria

A

Flexible cystoscopy

US KUB

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29
Q

Suspected kidney cancer Investigation

A

CT renal triple phase
- staging CT chest
- bone scan if symptomatic

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30
Q

Two features of Kidney cancer staging and grading with their breakdown

A

Fuhrman grade - differentiation ( 1 well - 3/4 poor)
TNM staging of RCC - Tumour size greater or less than 7, outside kidney a bit, outside kidney a lot
N1 – Met in single regional LN
N2 – met in ≥2 regional LN
M1- distant met

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31
Q

Kidney Cancer management

A

Gold standard:
Partial nephrectomy (single kidney, bilateral tumour, multifocal RCC in patients with VHL, T1 tumours (up to 7cm)

Radical Nephrectomy

In patents with small tumours unfit for surgery – Cryosurgery

Metastatic disease
- Receptor Tyrosine Kinase inhibitors, Immunotherapy

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32
Q

Types of bladder cancer

A

transitional cell carcinoma
squamous cell carcinoma - schistosomiasis is endemic
Adenocarcinoma

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33
Q

Aetiology of bladder cancer

A

Smoking, Occupational exposure, Chronic inflammation of bladder (including long term catheter use), Drugs, Radiotherapy

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34
Q

Clincial features of bladder cancer

A

Painless haematuria/persistent microscopic haematuria

Suprapubic pain

Lower urinary tract symptoms and UTI

Metastatic disease symptoms –bone pain, lower limb swelling

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35
Q

Investigation for bladder cancer following Painless visible Haematuria

A

Flexible cystoscopy

CT urogram

Renal function

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36
Q

Investigation for bladder cancer following Persistent microscopic haematuria

A

Flexible cystoscopy

US KUB

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37
Q

Two features of bladder cancer staging and grading with their breakdown

A

TNM
Ta – non invasive papillary carcinoma
Tis – carcinoma in situ
T1 – invades subepithelial connective tissue
T2 – invades muscularis propria
T3 – invades perivesical fat
T4 – prostate, uterus, vagina, bowel, pelvic or abdominal wall

N1 – 1 LN below common iliac birufication
N2 - >1 LN below common iliac birufication
N3 – Mets in a common iliac LN

M1- distant mets
Who classification ( G1 well - G3 poorly differentiated)

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38
Q

Management of bladder cancer

A

Non Muscle Invasive

  • If low grade and no CIS then consideration of cystoscopic surveillance +/- intravesicular chemotherapy/BCG

Muscle Invasive

Cystectomy
Radiotherapy
+/- chemotherapy
Palliative treatment

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39
Q

Type of prostate cancer

A

adenocarcinoma

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40
Q

Aetiology of prostate cancer

A

Increasing age, Western nations(Scandinavian countries), Ethnicity(African Americans

41
Q

Normal levels of PSA

A

<50 years old – PSA levels 0–2.5 ng/ml.

50–59 years old– PSA levels 0–3.5 ng/ml. 60–69 years old – PSA should be 0–4.5 ng/ml
70–79 years old – PSA levels of 0–6.5 ng/ml

42
Q

Prostate cancer investigations

A

Blood tests – PSA is prostate-specific but no prostate-cancer specific (can be elevated in — UTI, prostatitis, Benign prostatic hyperplasia)

MRI- done before biopsy

Biopsy - Trans perineal prostate biopsy

43
Q

Two features of prostate cancer staging and grading with their breakdown

A

TNM -
palpable or not
outside capsule a little (fat)
or a lot (adjacent structures)
T3 – beyond prostatic capsule into periprostatic fat
N1 – regional LN (pelvis)
M1a- non regional LN
M1b- bone
M1x- other sites
Gleason Score 2-6 well to 8 poorly differentiated. Grade 1 low to grade 5 high risk

44
Q

Prostate cancer management

A

If young and fit + High grade cancer Radical prostatectomy/Radiotherapy/Focal

                         \+   Low grade cancer                                           Active surveillance ( Regular PSA, MRI and Bx)

Post prostatectomy – monitor PSA ( should be undetectable or <0.01ng/ml). If >0.2ng/ml then relapse

If old/unfit + high grade cancer/Metastatic disease Hormone therapy

                          \+ Low grade cancer                                        Watchful waiting (regular PSA testing)
45
Q

What happens to the homeostatic function of the kidney in Chronic Kidney Disease

A
  • Potassium increases
  • Phosphate increases
  • Bicarbonate decreases
  • pH decreases (metabolic acidosis)
  • Salt and water imbalance
46
Q

What happens to the excretory function of the kidney in kidney disease?

A
  • Increase in urea
  • Increase in creatinine
  • Decrease in insulin requirement (due to low insulin clearance so more stays in system)
47
Q

What happens to the endochrine function of the kidney in CKD?

A
  • Decrease in calcium (1-alpha hydroxylase for vitamin D)
  • Anaemia (erythropoeitin)
  • Increase in parathyroid hormone (to compensate for low calcium)
48
Q

Glucose metabolism of the kidney (2)

A
  • Gluconeogenesis
  • Insulin clearance
49
Q

What are the normal ranges for:
Urea
Creatinine
Sodium
Potassium
Haemoglobin
pH
pCO2
pO2
Bicarbonate
Base excess

A

Urea 3 - 7
Creatinine 50-110
Sodium 135-145
Potassium 3.5-5.0
Haemoglobin 12-16
pH 7.35-7.45
pCO2 4.67-7.00
pO2 10.0 -13.3
Bicarbonate 25 - 30
Base excess < 5

50
Q

For CKD what features suggest hypo- volemic status

A

Hypo:
- Low bp
- Reduced capillary refill
- JVP not visible
- No pulmonary oedema

51
Q

Kidney failure tends to reduce secretion of salt and water leading to:

A
  • Hypertension
  • Oedema
  • Pulmonary oedema
52
Q

In what kind of circumstances can salt and water loss be seen though? (3)

A
  • In tubulointerstitial disorders- damage to concentrating mechanism of urine
  • kidney transplant
  • after kidney obstruction is relieved
53
Q

What may be a cause of AKI?

A

Hypovolemia

54
Q

What does hyponatremia mean and what does it not mean?

A
  • It does not mean reduced total body sodium
  • It’s to do with how much free water you have- you’ll have more in hyponatremia
55
Q

Describe how acidosis happens in renal failure

A
  • Reduced secretion of H+ ions which means you become acidotic
  • Cells take up this H+
    -The cells taking up the H+ also forces K+ out of the cells leading to hyperkalaemia
56
Q

What are the symptoms of hyperkalaemia? (3)
What are the signs?
What are the consequences?

A
  • Cardiac arrhythmias
  • Neural and muscular activity
  • Vomiting

Signs:
- Peaked T waves
- P waves broaden, have reduced amplitude and disappear
- QRS widening
- Heart block
- Asystole
- VT/VF (ventricular tachycardia/ventricular fibrillation)

Consequences:
- Anorexia
- Muscle catabolism

57
Q

What effect does reduced vitamin D have in CKD?

A
  • Reduced 1-25 Vit D levels:
    • Reduced intestinal calcium absorption
    • Hypocalcaemia
    • Hyperparathyroidism
    • There’s also phosphate retention in chronic renal failure (phosphate usually excreted by kidneys)
    • This contributes to low levels of 1-25 vit D and hypocalcaemia and therefore hyperparathyroidism
58
Q

What is the initial management plan of CKD?

A
  • Fluid balance
    • Hypovolaemia- give fluids
    • Hypervolaemia- trial of diuretics/dialysis

Hyperkalaemia
- Drive it into cells
- sodium bicarbonate
- insulin dextrose (fatalities associated with it due to hypoglycaemia)
- We only use it when potassium >6.5 or there are ECG changes

  • Drive it out of the body
    diuretics/dialysis
  • Reduce gut absorption- how?
    Potassium binders
59
Q

Kidney failure risk equation (KFRE)

A

Validated risk prediction tool for kidney replacement therapy in the next two or five years for adults with STABLE chronic kidney disease (CKD) Stages 3A to 5

Calculated from:
Age in years
Sex
CKD-EPI eGFR
Urine albumin creatinine ratio (ACR)

60
Q

Kidney failure – Long-term management

A

Conservative treatment
- erythropoietin injections to correct anaemia
- diuretics to correct salt water overload
- phosphate binders
- 1.25 vit d supplements
- symptom management

Home therapy
- haemodialysis
- peritoneal dialysis/assisted programmes

In Centre therapy
- haemodialysis, 4 hours 3 times a week

61
Q

Avoiding transfusions in transplantable patients with kidney disease.- Why?

A

Increase risk of rejecting transplant

When adding central line, use the back of their hand, avoid the cephalic vein of the wrist and the median cubital vein of the anterior cubital fossa

62
Q

Traditional methods of calculating eGFR and their problems

A

UREA -
Poor indicator
Confounded by diet, catabolic state, GI bleeding (bacterial breakdown of blood in gut), drugs, liver function etc.

CREATININE-
Affected by muscle mass, age, race, sex etc.
Need to look at the patient when interpreting the result. TREND helpful.

RADIONUCLIDE STUDIES-
EDTA clearance etc
Reliable but expensive

CREATININE CLEARANCE-
Difficult for elderly patients to collect an accurate sample
Overestimates GFR at low GFR (as a small amount of creatinine is also secreted into urine)

INULIN CLEARANCE-
Laborious - used for research purposes only

63
Q

What patient factors influence CKD Epidemiology Collaboration (CKD-EPI)

A

Age
Female
Black

64
Q

What features are measured in the NICE guidelines for chronic kidney risk?

A

Kidney function
Albumin to creatinine ratio

65
Q

What is the way to filter less blood in the kidney?

A

Reduce eGFR by vasoconstriction of afferent arteriole or vasodilation of efferent arteriole

66
Q

Pathophysiology of hypoaldosteronism

A

Reduced reabsorption of sodium in the distal nephron
Increased urinary loss of sodium
ECF volume falls
–> Increased renin, Ang II and ADH

67
Q

Symptoms of hypoaldosteronism

A

Dizziness

Low blood pressure

Salt craving

palpitations

68
Q

Pathophysiology of hyperaldosteronism

A

Increased reabsorption of sodium in the distal nephron
Reduced urinary loss of sodium

ECF volume increases (hypertension)
reduced renin, Ang II and ADH
Increased ANP and BNP

69
Q

Symptoms of hyperaldosteronism

A

High blood pressure
Muscle weakness
Polyuria
thirst

70
Q

Liddle Syndrome

A

An inherited disease of high blood pressure.

mutation in the aldosterone activated sodium channel.
-channel is always ‘on’
-Results in sodium retention, leading to hypertension

71
Q

What part of the cardiovascular system monitors blood pressure; low and high

A

Low: Atria, Right ventricle, Pulmonary vasculature

High: Carotid sinus, Aortic arch, JGA

72
Q

Action of ANP

A

-Stimulates the production of cyclic GMP and activates protein kinase G —> Vasodilatation of renal (and other systemic) blood vessels

-Inhibition of Sodium reabsorption in proximal tubule and in the collecting ducts

-Inhibits release of renin and aldosterone

-Reduces blood pressure

Released in response to atrial stretch (i.e. high blood pressure)

73
Q

ACE inhibitors function

A

Reduced Angiotensin II
vasodilation - increased vascular volume – decreased blood pressure

Direct Renal Effects:
Na+ reuptake in the PCT
Na+ in the distal nephron

Adrenal Effects:
Reduced aldosterone

74
Q

Carbonic anhydrase inhibitors function

A

Carbonic anhydrase activity leads to Na+ re-absorption and increased urinary acidity

reduced Na+ reuptake in the PCT
Increased Na+ in the distal nephron
Reduced water reabsorption

75
Q

Loop diuretics (furosemide) function

A

Triple transporter Inhibitors

reduced Na+ reuptake in the LOH
Increased Na+ in the distal nephron
Reduced water reabsorption

76
Q

Thiazides function

A

reduced Na+ reuptake in the DCT
Increased Na+ in the distal nephron
Reduced water reabsorption
Increased Calcium reabsorption

77
Q

Potassium sparing diuretics function

A

Inhibitors of aldosterone function (e.g. spironolactone)

78
Q

Immediate response to dietary K+

A

Insulin stimulates the activity of the sodium proton exchanger which increases intracellular sodium.
This increase in intracellular sodium activates the sodium potassium ATPase increasing potassium uptake.

79
Q

Potassium secretion by principal cells

A

Increased plasma potassium leads to increased activity of the sodium potassium ATPase and reduce return of potassium into the plasma so increased potassium excretion

80
Q

Tubular flow and potassium excretion

A

Tubular flow regulates potassium by activating cilia that activate PDK1. –> This increases Ca++ in the cell which stimulates the opening of potassium channels on the apical membrane.
increased plasma pH increases potassium secretion

81
Q

Causes of hypokalaemia

A

Inadequate dietary intake
Diuretics ( due to increase tubular flow rate)
Surreptitious vomiting
Diarrhea
Genetics

82
Q

Causes of hyperkalaemia

A

Kidney disease
K+ sparing diuretics
ACE inhibitors
Elderly
Severe diabetes

83
Q

Blood supply of ureter

A

renal/lumbar/gonadal/common iliac, internal iliac and superior vesical arteries with corresponding venous drainage.

84
Q

Lymphatics of ureter

A

left ureter drains into left para-aortic nodes, right ureter drains into right paracaval and interaortocaval lymph nodes

85
Q

At what points along the ureter can urinary stones form?

A

Where the renal pelvis joins the top of the ureter- pelvic ureteric junction (PUJ, or UPJ)

Pelvic brim, crossing the iliac vessels

As it passes through the bladder wall; uretero-vesical junction (UVJ, or VUJ)

86
Q

Blood supply and lymphatics of urinary bladder

A

Blood supply: superior and inferior vesical branches of internal iliac artery. Drained by vesical plexus which drains into internal iliac vein

Lymphatics: internal iliac nodes and then paraaortic nodes

87
Q

Blood supply, Lymphatics and Nerve supply of female urethra

A

Blood supply: internal pudendal arteries and inferior vesical branches of the vaginal arteries with corresponding venous drainage.

Lymphatics: proximal urethra into internal iliac nodes, distal urethra to superficial inguinal lymph nodes.

Nerve Supply: vesical plexus (proximal), pudendal nerve (distal).

88
Q

Blood supply, Lymphatics and Nerve supply of male urethra

A

Blood supply: prostate- inferior vesical artery, urethra- bulbourethral artery and internal pudendal artery with corresponding venous drainage.

Lymphatics: prostatic and membranous urethra drain to obturator and internal iliac nodes, spongy urethra to deep and superficial inguinal nodes.

Nerve supply: vesical plexus (proximal), pudendal nerve (distal).

89
Q

Neural control of micturition

A

Prefrontal cortex permits the pontine micturition centre in the brainstem to change from storage mode to voiding.

This activates the parasympathetic nucleus (bladder contraction), and inhibits Onuf’s nucleus (sphincter relaxation)

90
Q

Autonomic receptor drug targets of pelvic organs

A

Bladder neck: α-adrenergic (α-1)- alpha blocker

Detrusor:
Cholinergic M3/ M2. Antimuscarinic
β-adrenergic β-3 agonist

Erectile: nitrergic. PDE5 inhibitor

91
Q

Stress urinary incontinence:

Definition
Risk factor
Pathology

A

Complaint of involuntary leakage on effort or exertion, or on sneezing or coughing

aging, obesity, smoking, pregnancy and route of delivery

impaired bladder and urethral support and impaired urethral closure

92
Q

Stress Urinary incontinence
Signs & Symptoms

Investigation

Management

A

Involuntary leakage from urethra with exertion/effort or sneezing or coughing

Descent of pelvic floor on vaginal examination, positive stress test
Urodynamics test in the storage phase, showing stress incontinence

Non-surgical: physiotherapist teaching pelvic floor muscle exercises.

Surgical: a sling placed to support the urethra, using the anterior vaginal wall to support the urethra (colposuspension), periurethral bulking injection.

93
Q

Overactive bladder (urgency, ± urgency incontinence)

Definition
Risk factors
Pathology

A

urinary urgency, usually with urinary frequency and nocturia, with or without urgency urinary incontinence

age, prolapse, increased BMI, bladder irritants (caffeine, nicotine)

not well understood. Involuntary “overactive” detrusor (bladder wall) muscle contractions. Cause can be idiopathic or neurogenic (loss of central nervous system inhibitory pathways)

94
Q

Overactive bladder (urgency, ± urgency incontinence)

Signs & Symptoms
Investigation

A

urgency, frequency, nocturia and urgency incontinence. Impact on QOL due to sleep disruption, anxiety and depression.

Assess for enlarge prostate in males and prolapse in women

exclude infection with urine dip/MSU
Bladder diary
Bladder scan (post void residual)
[Urodynamics - detrusor overactivity (detrusor should be inactive) with incontinence ]

95
Q

Management of overactive bladder

A

Behavioural/lifestyle changes
Bladder retraining
Antimuscarinic drugs
Beta-3 agonist
Bladder injections with botox
Neuromodulation
Augmentation cystoplasty

96
Q

Benign prostatic hyperplasia
Definition
Aetiology
Pathology

A

non malignant growth or hyperplasia of prostate tissue, common cause of lower urinary tract symptoms in men. Outward enlargement can be felt with rectal exam.

hormonal effects of testosterone on prostate tissue

hyperplasia of both lateral lobes and the median lobe, leading to compression of the urethra and therefore bladder outflow obstruction. See hyperplasia of the stroma (smooth muscle and fibrous tissue) and glands

97
Q

Benign prostate hyperplasia

Signs & Symptoms

A

hesitancy in starting urination
poor stream
dribbling post micturition
can present with acute retention

98
Q

Benign prostate hyperplasia

Investigation

A

Investigations: urine dipstick/ culture, post void residual, bladder diary
Bloods: PSA
Imaging: ultrasound to assess upper renal tracts
Urinary flow studies/urodynamics
Cystoscopy if concerned about bladder cancer

Exclude other causes for above symptoms Abdominal and rectal examination

Bladder cancer (haematuria)

Prostate cancer (raised prostate specific antigen (PSA))

Urinary tract infections/ Prostatitis

Urethral stricture

Could lead to chronic renal disease if not detected early

99
Q

Benign prostate hyperplasia

Management

A

Lifestyle: weight loss, reduce caffeine and fluid intake in evening, avoid constipation

Medical:

α blocker- prostate stromal smooth muscle and bladder neck. Blocking the receptor relaxes muscle tone

5-α reductase inhibitor-prevents conversion of testosterone into di-hydro-testosterone (which promotes prostate growth) so slowly results in shrinkage

Surgery: transurethral resection of the prostate (TURP)-debulks occluding part to produce adequate channel for urine to flow. Can also be done with laser. This is not the same as radical prostatectomy for cancer

BRS missed out (10 decks)

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