Genitourinary tract

Question 1

what are the functions of the kidney?

Answer 1

• filter or secrete waste/excess substances
• maintains acid-base balance
• retains albumin and circulating cells
• reabsorbs glucose, amino acids and bicarbonates
• controls BP, fluid status and electrolytes
• activates 25-hydroxy vitamin D (by hydroxylating it to form 1,25 dihydroxy vitamin D)
• synthesises erythropoietin

Question 2

what is the GFR?

Answer 2

glomerular filtration rate

• the volume of fluid filtered from the glomeruli into Bowman’s space per unit time (minutes)
• 120ml/min = 7.2L/h = 170L/day

Question 3

what is the creatinine clearance rate?

Answer 3

• volume of blood plasma that is cleared of creatinine per unit time
• useful measure for approximating the GFR
• creatinine clearance exceeds GFR due to creatinine secretion, which can be blocked by cimetidine

Question 4

what is reabsorbed in the proximal tubule?

Answer 4

• 2/3rds of salt and water (via Na/K ATPase pump)
• 100% of organic solutes (glucose, amino acids, inorganic phosphate)
• 65% of potassium
• 50% of urea
• 80% of phosphate
• 70-90% of citrate

Question 5

what is Fanconi syndrome? what does it lead to?

Answer 5

• syndrome of inadequate reabsorption in the proximal renal tubules
• affects the PCT and proximal straight tubule
• glycosuria
• acidosis with failure of urine acidification
• phosphate wasting resulting in rickets/osteomalacia
• aminoaciduria

Question 6

what are some causes of Fanconi syndrome?

Answer 6

• cytinosis
• Wilson’s
• tenofovir
• congenital or acquired diseases
• toxicity
• ADRs

Question 7

what is reabsorbed in the loop of Henle?

Answer 7

• thin descending limb has low permeability to ions and urea, and is highly permeable to water
• thin ascending limb is impermeable to water but permeable to ions
• ascending limb reabsorbs sodium, potassium and chloride via NKCC2, and magnesium and calcium
• cortical thick ascending limb drains urine into the DCT

Question 8

what is reabsorbed in the DCT?

Answer 8

• regulates pH by absorbing bicarbonate and secreting protons, or by absorbing protons and secreting bicarbonate
• secretes potassium and absorbs sodium (mediated by aldosterone and WNK kinases)
• reabsorbs calcium (mediated by PTH)
• expresses arginine vasopressin receptor 2

Question 9

what is the function of the collecting duct?

Answer 9

• does salt handling; by this point, most of the salt has been reabsorbed
• tightly regulated by aldosterone (aldosterone increases the transcription of eNac channels which absorb Na+ in exchange for K+)
• secrete K+ and H+ into the urine
• water handling is also done here and water is absorbed via aquaporin 2 channels (regulated by vasopressin)

Question 10

what are features of renal potassium control?

Answer 10

• K+ is freely filtered and mostly reabsorbed in the proximal tubule/loop of Henle
• distal tubule secretion determines renal excretion
• insulin and catecholamines drive cellular K+ uptake, buffering acute changes

Question 11

what renal medication causes hypokalaemia?

Answer 11

• loop diuretics

- thiazide diuretics

Question 12

what renal medication causes hyperkalaemia?

Answer 12

• spironolactone (aldosterone antagonist)
• amiloride (acts on eNac channels)
• ACE inhibitors
• angiotensin receptor blockers (ARB)
• trimethoprim (acts on eNac channels but milder)

Question 13

how can diuretics affect kidney disease?

Answer 13

• diuretics are not nephrotoxic but hypovolaemia is (which they can cause)
• in advanced kidney disease you require huge amounts of diuretics to do the work
• thiazide and loop diuretics are extremely powerful and effective together resulting in profound diuresis

Question 14

what happens if plasma is too concentrated?

Answer 14

if things are too concentrated then ADH is released resulting in increased aquaporins in the collecting duct and thus more water is absorbed, thereby diluting plasma

Question 15

what are features of erythropoietin in the kidney? when is anaemia seen?

Answer 15

• the renal cortex acts as an oxygen sensor; blood flow and oxygen requirement (GFR) are matched
• anaemia is mainly seen after eGFR < 30
• erythropoietin is hormone that produces haemoglobin, it is produced in response to tissue hypoxia
• in advanced kidney disease and anaemia, erythropoietin will be given to help increase O2 transport

Question 16

what is the process of vitamin D hydroxylation in the kidneys?

Answer 16

it takes 25-hydroxy vitamin D and hydroxylates it to form 1,25-dihydroxy vitamin D (calcitriol) by the enzyme 1alpha hydroxylase - this is the active form of vitamin D

Question 17

what are the actions of calcitriol?

Answer 17

• increases Ca2+ and phosphate absorption from the gut
• increases phosphate absorption to a lesser extent
• suppresses parathyroid hormone (PTH)
• deficiency results in secondary hyperparathyroidism

Question 18

how does deficiency of calcitriol result in secondary hyperparathyroidism?

Answer 18

• low vitamin D results in low Ca2+ and phosphate resulting in increased PTH which causes Ca2+ and phosphate leeching out of the bones
• PTH also acts on osteoclasts by increasing their activity and thus increasing their turnover resulting in reduced bone quality

Question 19

what is the function of the lower urinary tract?

Answer 19

to convert the continuous process of excretion (urine production) to an intermittent, controlled volitional process (micturition)

Question 20

what are the essential features of the lower urinary tract?

Answer 20

• low pressure and insensible storage of urine of adequate capacity
• prevents leakage of the urine stored
• allows rapid, low-pressure voiding at an appropriate time and place

Question 21

what is the pressure like in the kidney?

Answer 21

• mean arterial pressure 60-70mmHg drives filtration in the Bowman’s capsule
• there is progressive reduction in pressure along the nephron due to reabsorption, until at the collecting system pressure is 3-10mmHg

Question 22

what is the neural control of voiding?

Answer 22

• pontine micturition centre stimulates excitatory control to detrusor nucleus and inhibits Onuf’s nucleus
• signal is transmitted from spinal root S3,4,5 via the parasympathetic nervous system and this results in contraction of detrusor muscles and relaxation of the urethra

Question 23

what is the neural control of storage?

Answer 23

• pontine storage centre stimulates and sends inhibitory signals to detrusor muscles and excitatory signals to Onuf’s nucleus
• signal is transmitted from spinal root T10, L1 and L2 via the sympathetic nervous system and this results in the relaxation of the bladder and contraction of the urethral sphincter

Question 24

what is the function of the sacral micturition centre?

Answer 24

at the sacral micturition centre there is a reflex that, when bladder is full it initiates voiding - this is inhibited by conscious parts of the brain:
• if the cord is cut above S2,3,4 then will only urinate when the bladder is full, but the descending pathway will not be able to inhibit this with the brain as descending pathway will be destroyed

Question 25

what occurs in voiding? is it parasympathetic or sympathetic?

Answer 25

- detrusor muscle contraction of bladder | - parasympathetic (cholinergic) - S3, S4, S5

Question 26

what occurs in storage? is it parasympathetic or sympathetic?

Answer 26

- urethral contraction - inhibition of detrusor muscle contraction of bladder - sympathetic (noradrenergic) - T10, L1, L2

Question 27

what is the histology of the bladder?

Answer 27

has urothelium (transitional epithelium): • highly specialised stratified, 3-7 cells thick • umbrella structure that is completely impermeable so cannot resorb urine • able to fold and unfold to increase volume

Question 28

what is the difference between women and men in urethras? what does this mean?

Answer 28

- men have a greater voiding pressure due to them having a longer urethra; more likely to develop retention - women have a shorter urethra with lower resistance and thus higher flow rates; more likely to develop incontinence

Question 29

what are renal stones?

Answer 29

* nephrolithiasis/urolithiasis * renal stones (calculi) consist of crystal aggregates; stones form in collecting ducts and may be deposited anywhere from the renal pelvis to the urethra

Question 30

where do renal stones classically occur?

Answer 30

occur classically at these 3 narrowings: - pelviureteric junction - pelvic brim - vesicoureteric junction

Question 31

what is the epidemiology of renal stones?

Answer 31

- incidence is increasing - 10-15% lifetime risk - peak age is between 20-40 yrs - more common in males than females - unusual in children - more than 50% lifetime risk of recurrence once you've had them - most stones are composed of calcium oxalate and phosphate

Question 32

what are risk factors and aetiology of renal stones?

Answer 32

- anatomical abnormalities that predispose to stone formation e.g. obstruction or trauma - chemical composition of urine that favours stone crystallisation - dehydration resulting in a concentrated urine - infection - hypercalcaemia, hyperoxaluria, hypercalciuria, hyperuricaemia - primary renal disease e.g. polycystic kidneys or renal tubular acidosis - drugs e.g. diuretics, antacids, acetazolamide, corticosteroids, aspirin, allopurinol, vitamin C and D - diet e.g. chocolate, tea, strawberries, rhubarb all increase oxalate levels - gout - family history

Question 33

what are types of renal stones?

Answer 33

renal stone/calculi form from crystals in supersaturated urine: • calcium oxalate are the most common stones (60-65%) • calcium phosphate stones are uncommon (10%)

Question 34

what are causes of hypercalcuria?

Answer 34

- hyperparathyroidism resulting in hypercalcaemia - excessive dietary intake of Ca2+ - idiopathic hypercalciuria - increased absorption in gut - primary renal disease such as polycystic kidneys or medullary sponge kidney

Question 35

what are causes of hyperoxaluria?

Answer 35

- high dietary intake of oxalate rich food e.g. spinach, rhubarb, chocolate and tea - low dietary Ca2+ resulting in decreased binding of oxalate (by Ca2+) so increased oxalate absorption and urinary excretion - increased intestinal resorption due to GI disease e.g. Crohn’s

Question 36

what are causes of uric acid stones?

Answer 36

* associated with hyperuricaemia with/without gout * dehydration * patients with ileostomies are at particular risk, both from dehydration and from bicarbonate loss from GI secretion resulting in the production of an acidic urine (uric acid is more soluble in alkaline than acidic) thereby stimulating stone formation

Question 37

what causes infection-induced kidney stones?

Answer 37

* mixed infective stones are composed of magnesium ammonium phosphate as well as calcium * these are often large * usually due to UTI with an organism such as Proteus mirabilis that hydrolyses urea forming ammonium hydroxide * the increased ammonium ions and the alkalinity both favour stone formation

Question 38

what are cystine stones caused by?

Answer 38

* caused by cystinuria | * this results in excessive urinary excretion and formation of cysteine stones

Question 39

what is clinical presentation of kidney stones?

Answer 39

- most are asymptomatic - renal colic - loin pain - if urinary tract is obstructed then fluid/diuretics make the pain worse as peristaltic flow increases - bowel sounds may be reduced - BP may be low - dysuria, strangury, frequency - recurrent UTI’s - haematuria - acute pyelonephritis

Question 40

what is the clinical presentation of renal colic?

Answer 40

* rapid onset - woken from sleep * pain that results from upper urinary tract obstruction * excruciating ureteric spasms * pain is from loin to groin and comes and goes in waves as the ureters peristalise * associated with nausea and vomiting * worse with fluid loading * radiates to groin and ipsilateral testis/labia * often cannot lie still (differentiates from peritonitis)

Question 41

what are differential diagnoses of kidney stones?

Answer 41

- vascular accident e.g. ruptured AAA if over 50 yrs until proven otherwise - bowel pathology e.g. diverticulitis or appendicitis - ectopic pregnancy or ovarian cyst torsion - testicular torsion can present with loin pain and nothing else

Question 42

what is used to diagnose kidney stones?

Answer 42

- history and examination - urine dipstick - mid-stream specimen of urine sent for microbiology culture and sensitivity - bloods - KUBXR - NCCT-KUB - ultrasound

Question 43

how is a urine dipstick used to diagnose kidney stones?

Answer 43

* usually positive for blood - haematuria | * also looks for red cells, protein and glucose

Question 44

how is KUBXR used to diagnose kidney stones?

Answer 44

Kidney Ureter Bladder X-ray • first line investigation • 80% sensitive • see stone in line of renal tract

Question 45

how is NCCT-KUB used to diagnose kidney stones?

Answer 45

non-contrast CT kidney ureter bladder • gold standard • very rapid • 99% sensitive for stones - diagnostic • no contrast so no renal damage or allergy • but no functional info and gives radiation dose equivalent to 18 months background radiation

Question 46

how is ultrasound used to diagnose kidney stones?

Answer 46

* shows kidney stones and renal pelvis dilatation well but ureteric stones can be missed * sensitive for hydronephrosis * very poor at visualising stones in ureter * useful in pregnant and younger recurrent stone-formers * rarely used acutely

Question 47

what is the treatment of kidney stones?

Answer 47

- strong analgesic - antibiotics if infection e.g. IV cefuroxime or IV gentamicin - antiemetics to prevent vomiting - observe for sepsis - stones less than 5mm in lower ureter 90% pass spontaneously - medical expulsive therapy (oral nifedipine or alpha blocker)

Question 48

what is the treatment if kidney stones are still not passing?

Answer 48

* extracorporeal shockwave lithotripsy; ultrasound fragments stone * endoscopy with YAG - laser for larger stones * percutaneous nephrolithotomy; keyhole surgery to remove stones that are large, multiple or complex

Question 49

how can kidney stones be prevented from recurring?

Answer 49

* overhydration * normal/low Ca2+ dietary intake * low salt diet * normal daIry intake * reduce BMI * reduction in animal proteins * active lifestyle

Question 50

how can uric acid stones be prevented from recurring?

Answer 50

- can be caused by long term allopurinol use - only form in acid urine - deacidification of urine e.g. oral sodium bicarbonate to alkalinise urine

Question 51

how can cysteine stones be prevented from recurring?

Answer 51

- overhydration - urine alkalisation - cysteine binders e.g. captopril

Question 52

what is the definition of acute kidney injury/acute renal failure?

Answer 52

an abrupt (over hours to days) sustained rise in serum urea and creatinine due to a rapid decline in GFR leading to a failure to maintain fluid, electrolyte and acid-base homeostasis - it is usually but not always reversible or self-limiting

Question 53

what is the RIFLE classification?

Answer 53

- old system that was used to define AKI - uses either an increase in serum creatinine (SCr) or a decrease in urine output - RIFLE describes three levels of renal dysfunction (RIF) and two outcome measures (LE) - these criteria indicate an increasing degree of renal damage and have a predictive value for mortality - risk, injury, failure, loss, end-stage renal disease

Question 54

what is the GFR and urine output criteria for the Risk category of RIFLE for AKI?

Answer 54

GFR criteria: 1.5 fold increase in creatinine or GFR decrease >25% urine output criteria: UO <0.5 ml kg^-1 h^-1 x6h

Question 55

what is the GFR and urine output criteria for the Injury category of RIFLE for AKI?

Answer 55

GFR criteria: 2 fold increase in creatinine or GFR decrease >50% urine output criteria: UO <0.5 ml kg^-1 h^-1 x12h

Question 56

what is the GFR and urine output criteria for the Failure category of RIFLE for AKI?

Answer 56

GFR criteria: 3 fold increase of GFR decrease >75% or creatinine >4mg per 100ml (acute rise of >0.5mg per 100ml dl) urine output criteria: UO <0.3 ml kg^-1 h^-1 x24h or anuria x12h

Question 57

what is the criteria for the Loss category of RIFLE for AKI?

Answer 57

persistent ARF = complete loss of kidney function >4hrs

Question 58

what is the criteria for the ESKD category of RIFLE for AKI?

Answer 58

end-stage kidney disease (>3 months)

Question 59

what is the KDIGO classification for AKI?

Answer 59

- staging system for AKI used currently | - also uses serum creatinine and urine output to assess severity

Question 60

what is the serum creatinine (sCr) criteria for AKI in the KDIGO classification?

Answer 60

1. increase >26umol/L in 48hrs OR increase >1.5 x baseline 2. increase 2-2.9 x baseline 3. increase >3 x baseline OR >354umol/L OR commenced on RRT irrespective of stage

Question 61

what is the urine output criteria for AKI in the KDIGO classification?

Answer 61

1. <0.5mL/kg/h for >6 consecutive hours 2. <0.5mL/kg/h for >12hrs 3. <0.3mL/kg/h for >24hrs or anuria for 12hrs

Question 62

what is the epidemiology of AKI?

Answer 62

- AKI is common, occurring in 18% of hospital patients - about 25% of patients with sepsis and 50% of patients with septic shock will have AKI - severe AKI (creatinine > 500μmol/L, often requiring dialysis) affects about 130-140 per million population per year - common in the elderly

Question 63

what is AKI associated with?

Answer 63

* diarrhoea * haematuria * haemoptysis * hypotension * urine retention

Question 64

what are the causes of AKI?

Answer 64

- commonest are ischaemia, sepsis and nephrotoxins - pre-renal (40-70%) - intrinsic renal (10-50%); required renal biopsy for diagnosis - post-renal (10-25%)

Question 65

what are causes of pre-renal (40-70%) AKI?

Answer 65

* renal hypoperfusion e.g. hypotension (due to hypovolaemia or sepsis) resulting in a drop in GFR * hypovolaemia of any cause - dehydration or haemorrhage * hypotension without hypovolaemia - cirrhosis or septic shock * low cardiac output - cardiac failure or cardiogenic shock * renal hypoperfusion - NSAIDs, ACE inhibitors

Question 66

what are the causes of intrinsic renal AKI (10-50%)?

Answer 66

* renal parenchyma damage * acute tubular necrosis - commonest renal cause of AKI, caused by pre-renal damage or nephrotoxins e.g. NSAIDs, radiological contrast, uric acid crystals, myeloma and increased Ca2+ * vascular * glomerular * interstitial

Question 67

what are vascular causes of intrinsic renal AKI?

Answer 67

- renal artery/vein thrombosis - cholesterol/thrombus emboli from angiography - vasculitis e.g. in SLE - haemolytic uraemic syndrome - thrombotic microangiopathy; haemolytic anaemia and reduced platelets - malignant hypertension

Question 68

what are glomerular causes of intrinsic renal AKI?

Answer 68

- glomerulonephritis or nephrotic syndrome | - autoimmune (SLE), drugs, infections

Question 69

what are interstitial causes of intrinsic renal AKI?

Answer 69

drugs, infiltration with e.g lymphoma, infection, tumour lysis syndrome following chemo

Question 70

what are causes of post-renal (10-25%) AKI?

Answer 70

* urinary tract obstruction at ureter, bladder or prostate * luminal: stones, clots or sloughed papillae * mural (wall) * extrinsic compression from malignancy especially from pelvis or due to retroperitoneal fibrosis

Question 71

what are causes of mural post-renal AKI?

Answer 71

- malignancy e.g. ureteric, bladder or prostate - benign prostate hyperplasia (BPH) - strictures

Question 72

what are risk factors for AKI?

Answer 72

- age > 75 yrs - heart failure - peripheral vascular disease - chronic liver disease - sepsis - poor fluid intake/increased losses - history or urinary symptoms - chronic kidney disease (CKD) especially if GFR < 60 - past history of AKI - hypovolaemia - haematological malignancy - diabetes - prostate cancer - nephrotoxic drugs - repeated use of radiological contrast

Question 73

what is the clinical presentation of AKI?

Answer 73

- depends on underlying cause or severity - on examination there may be palpable bladder, palpable kidneys, abdominal/pelvic masses, rashes - oliguria occurs in early sages - arrhythmias due to hyperkalemia - breathlessness occurs from a combination of anaemia and pulmonary oedema secondary to volume overload - pericarditis occurs with severe untreated uraemia and may be complicated by a pericardial effusion, tamponade or pericardial rub - impaired platelet function causes bruising and GI bleeding - infection due to immune suppression - postural hypotension - oedema - thirst - indicated fluid depletion and dehydration (possible cause of AKI)

Question 74

what are differential diagnoses of AKI?

Answer 74

abdominal aortic aneurysm, alcohol toxicity, alcoholic and diabetic ketoacidosis, chronic renal failure, dehydration, GI bleed, heart failure, metabolic acidosis

Question 75

when should you suspect chronic kidney disease?

Answer 75

small kidneys on ultrasound, anaemia, low Ca2+, high phosphate or high creatinine/low GFR

Question 76

how is a urine dipstick used to diagnose AKI?

Answer 76

can suggest infection (leucocytes + nitrites) and glomerular disease (blood + protein)

Question 77

how is blood count used to diagnose AKI?

Answer 77

anaemia and very high ESR suggests myeloma or vasculitis as underlying cause

Question 78

what is used to exclude infection in AKI?

Answer 78

- urine and blood cultures to exclude infection | - mid-stream-specimen of urine sent for microbiology culture and sensitivity

Question 79

how is ultrasound used to diagnose AKI?

Answer 79

* give assessment of renal size (very small indicates CKD) * can be used to distinguish obstruction and hydronephrosis and look for cysts, small kidneys (CKD), masses and corticomedullary differentiation (reduced in CKD)

Question 80

how is CT-KUB used to diagnose AKI?

Answer 80

* complete anuria is rare but if present it suggests obstructive cause * in elderly men this should be considered prostatic e.g BPH and can be relieved by catheterisation * if catheterisation does not relieve anuria then suspect obstruction above prostate

Question 81

what is done when catheterisation does not relieve anuria? what does this suggest? what is looked for?

Answer 81

- suspect obstruction above prostate - get an urgent ultrasound to look for hydronephrosis - get an urgent CT-KUB which can look for obstructing masses or calculi as well as retroperitoneal fibrosis

Question 82

how is ECG used to diagnose AKI?

Answer 82

to look for hyperkalaemic changes - tall tented T waves - prolonged PR interval - widening QRS complex

Question 83

how is CXR used to diagnose AKI?

Answer 83

to look for pulmonary oedema

Question 84

how is renal biopsy used to diagnose AKI?

Answer 84

* intrarenal causes of AKI | * perform for every patient with unexplained AKI and normal kidneys

Question 85

what is the treatment of pre-renal AKI?

Answer 85

- correct volume depletion with fluids | - treat sepsis with antibiotics

Question 86

what is the treatment of intrinsic renal AKI?

Answer 86

refer early to nephrology if concern over tubulointerstitial or glomerular pathology

Question 87

what is the treatment of post-renal AKI?

Answer 87

- catheterise and consider CT of renal tract (CTKUB) - if signs of obstruction and hydronephrosis then do cystoscopy and retrograde stents or nephrostomy insertion; this buys time to allows treatment of cause of obstruction

Question 88

what are some nephrotoxic drugs?

Answer 88

* NSAIDs * ACE-inhibitor * gentamicin * amphotericin

Question 89

what is the treatment of hyperkalaemia in AKI?

Answer 89

- calcium gluconate; cardioprotective - insulin to drive K+ into cells with glucose and dextrose to prevent hypoglycaemia - use dialysis or haemofiltration

Question 90

what is the treatment of AKI?

Answer 90

- hyperkalaemia treatment - diuretics or dialysis/haemofiltration for pulmonary oedema - sodium and potassium restriction and vitamin D supplied

Question 91

what are indications for dialysis in AKI?

Answer 91

- symptomatic uraemia including pericarditis or tamponade - hyperkalaemia not controlled by conservative measures - pulmonary oedema thats unresponsive to diuretics - severe acids - high potassium - tall T waves, low flat p waves, broad QRS or arrhythmias on ECG - metabolic acidosis - fluid overload that is resistant to diuretics

Question 92

what are components of renal replacement therapy?

Answer 92

haemofiltration and haemodialysis

Question 93

what are complications of RRT?

Answer 93

- cardiovascular disease due to combination of hypertension and calcium/phosphate dysregulation - infection - amyloid accumulates in long-term dialysis and may cause carpal tunnel syndrome, arthralgia and fractures - malignancy is commoner in dialysis patients; may be due to causes of end-stage renal failure e.g. urothelial tumours

Question 94

what is glomerulonephritis?

Answer 94

glomerulonephritis is a broad term that refers to a group of parenchymal kidney diseases that all result in the inflammation of the glomeruli and nephrons

Question 95

what does glomerulonephritis cause?

Answer 95

- damage to the filtration mechanism resulting in haematuria and proteinuria - damage to the glomerulus restricts blood flow, leading to compensatory hypertension - loss of the usual filtration capacity leads to AKI - causes 25% of end stage kidney failure

Question 96

how can glomerulonephritis present itself?

Answer 96

- acute nephritic syndrome (acute glomerulonephritis) - nephrotic syndrome - asymptomatic urinary abnormalities; haematuria, proteinuria or both - chronic kidney disease (CKD) - haematuria; visible or non-visible (red cell casts seen on microscopy) - proteinuria (usually < 2g in 24hrs) - hypertension and oedema (periorbital, leg, or sacral)

Question 97

what is acute nephritic syndrome often caused by?

Answer 97

often caused by an immune response triggered by an infection of other disease

Question 98

what is the commonest primary cause of acute nephritic syndrome?

Answer 98

IgA nephropathy

Question 99

what is the aetiology of acute nephritic syndrome?

Answer 99

- bacterial infection e.g. MRSA, typhoid or secondary syphilis - Hepatitis B and C - schistomiasis - malaria - post-streptococcal infection e.g. Strep. pyogenes - infective endocarditis - SLE - systemic sclerosis - ANCA associated vasculitis - Goodpastures disease - IgA nephropathy

Question 100

what are features of post-streptococcal infection as a cause of acute nephritic syndrome?

Answer 100

* occurs classically 2 weeks after tonsillitis | * bacterial antigen becomes trapped in the glomerulus leading to diffuse proliferative glomerulonephritis

Question 101

how can SLE cause acute nephritic syndrome? what is the clinical presentation of it?

Answer 101

* rash, arthralgia, kidney failure, neurological symptoms, pericarditis and pneumonitis * anti-nuclear antibody (ANA) positive and double stranded DNA positive * low complement C3 and C4

Question 102

what is the treatment of SLE as a cause of acute nephritic syndrome?

Answer 102

immunosuppression; steroids, cyclophosphamide, rituximab

Question 103

how does systemic sclerosis cause acute nephritic syndrome? what is the clinical presentation?

Answer 103

* ANA positive, Anti-Ro and Anti-La positive * severe hypertension * ‘onion skin’ changes on renal biopsy, raynauds phenomenon, fibrotic skin, oesophageal dysmotility

Question 104

what is the treatment of ANCA associated vasculitis as a cause of acute nephritic syndrome?

Answer 104

immunosuppression, steroids, cyclophosphamide, rituximab, plasma exchange

Question 105

what is Goodpastures disease?

Answer 105

- anti-glomerular basement membrane disease - rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs and kidney failure - attacks alpha-3 subunit of type IV collagen - the co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage and the presence of circulating antibodies directed against an intrinsic antigen to the basement membrane of both kidney and lung - antibodies against glomerular basement membrane - rapidly progressive kidney failure

Question 106

what is the treatment of Goodpastures disease?

Answer 106

- remove antibody via plasma exchange - immunosuppression - steroids/cyclophosphamide

Question 107

what is the commonest cause of nephritic syndrome in the developed world?

Answer 107

IgA nephropathy

Question 108

how does IgA nephropathy cause acute nephritic syndrome?

Answer 108

- form of glomerulonephritis - deposition of IgA antibody in the glomerulus - haematuria, IgA deposition in kidney mesangium (provides structural support to glomerulus) and kidney gets attacked - associated with tonsillitis and results in haematuria

Question 109

what is the treatment of IgA nephropathy?

Answer 109

BP control: ACEi/ARBs

Question 110

what is the clinical presentation of acute nephritic syndrome?

Answer 110

- haematuria (mild macrocytic) - proteinuria; usually less than 2g in 24 hours - hypertension (moderate-severe increase) and oedema (periorbital (around eyes), leg or sacral) caused by salt and water retention - oliguria (little urine) - uraemia and symptoms of it - deteriorating kidney function - moderate-severe decrease in GFR

Question 111

what are symptoms of uraemia?

Answer 111

* anorexia * pruritus i.e rash * lethargy and nausea

Question 112

how is acute nephritic syndrome diagnosed?

Answer 112

- take history to determine cause - measure eGFR, proteinuria, serum urea and electrolytes and albumin to determine current status and monitor progress - culture; swab from throat or infected skin - urine dipstick to detect proteinuria and haematuria - renal biopsy if necessary

Question 113

how is hypertension treated in acute nephritic syndrome?

Answer 113

salt restriction, loop diuretics, calcium channel blockers

Question 114

what is the triad of nephrotic syndrome?

Answer 114

- proteinuria > 3.5g/24 hours - hypoalbuminaemia - oedema - severe hyperlipidaemia is often present

Question 115

why is severe hyperlipidaemia often present in nephrotic syndrome?

Answer 115

liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and produces raised cholesterol

Question 116

what is nephrotic syndrome? what is it caused by? what is kidney function like?

Answer 116

- collection of symptoms due to kidney damage; includes protein in urine, low blood albumin levels, high blood lipids and significant swelling - don’t develop kidney failure but are leaking huge amounts of protein but kidney function remains the same - caused by structural and functional abnormalities of podocytes

Question 117

what is the epidemiology of nephrotic syndrome?

Answer 117

- relatively rare - diabetes is most common secondary cause - minimal change disease accounts for 10-25% of nephrotic syndrome in adults and is the commonest cause of nephrotic syndrome in children

Question 118

what are the primary causes of nephrotic syndrome?

Answer 118

* minimal change disease - seen in children and adults * membranous glomerulonephritis - adults * focal segmental glomerulosclerosis * membranoproliferative glomerulonephritis * rapidly progressive glomerulonephritis

Question 119

what is the most common cause of nephrotic syndrome in adults?

Answer 119

focal segmental glomerulosclerosis

Question 120

what is membranous nephropathy?

Answer 120

- asymptomatic proteinuria/nephrotic syndrome +/- microscopic haematuria, hypertension and renal impairment - deposition of IgG and C3 along outer aspect of glomerular basement membrane - treated with immunosuppression

Question 121

what are causes of membraneous nephropathy?

Answer 121

* drugs e.g. penicillamine, gold or NSAIDs * autoimmune - SLE, thyroiditis * infection e.g. hepatitis B or C, schistomiasis * neoplasia e.g. lung, colon, stomach and breast

Question 122

what is focal segmental glomerulosclerosis?

Answer 122

- unknown aetiology - scarring that is focal and only some glomeruli involved and segmental (only part of glomerulus affected) - CD80 deposited in podocytes resulting in increased permeability in glomeruli and thus proteinuria and haematuria

Question 123

what is clinical presentation of focal segmental glomerulosclerosis?

Answer 123

secondary hypertension and renal impairment

Question 124

what is treatment of focal segmental glomerulosclerosis?

Answer 124

corticosteroids and immunosuppressants

Question 125

what are secondary causes of nephrotic syndrome?

Answer 125

* diabetes mellitus - most common secondary cause * amyloid * infections e.g. Hep B or C and HIV * SLE, RA * drugs e.g. gold, penicillamine, NSAIDs and ACE-inhibitors * malignancy

Question 126

what is the most common secondary cause of nephrotic syndrome?

Answer 126

diabetes mellitus

Question 127

what are risk factors for nephrotic syndrome?

Answer 127

diabetes mellitus

Question 128

what is the pathophysiology of nephrotic syndrome?

Answer 128

- injury to podocyte appears to be the main cause of proteinuria - podocytes wrap around the glomerular capillaries and maintain the filtration barrier, preventing large molecular weight proteins from entering the urine - damage to podocyte foot processes or loss of podocytes can cause heavy protein loss

Question 129

what is the clinical presentation of nephrotic syndrome?

Answer 129

- normal-mild increase in BP - proteinuria > 3.5g/day - normal-mild decrease in GFR - hypoalbuniaemia - pitting oedema of ankles, genital, abdominal wall and sometimes face (periorbital) - frothy urine

Question 130

what are differential diagnoses of nephrotic syndrome?

Answer 130

- congestive heart failure | - cirrhosis

Question 131

how can congestive heart failure be distinguished from nephrotic syndrome?

Answer 131

* where there is oedema and raised JVP | * in nephrotic syndrome there is normal or low JVP (unless there is renal failure and oliguria)

Question 132

how can cirrhosis be distinguished from nephrotic syndrome?

Answer 132

* where there is hypoalbuminaemia and oedema | * but there are signs of chronic liver failure e.g. jaundice, fever and loss of body hair

Question 133

how is nephrotic syndrome diagnosed?

Answer 133

- establish cause - usually via renal biopsy - urine dipstick shows very high protein - CXR or ultrasound for pleural effusion or ascites - serum albumin is low - BP is usually normal or mildly increased - renal function is usually normal or mildly impaired - serum creatinine, eGFR, lipids and glucose - ANA, double-stranded DNA antibody, C3 and C4 indicates SLE - antiphospholipase A2 receptor antibody indicated membranous nephropathy - HepB surface antigen, HepC antibody or HIV

Question 134

what are metabolic/immunologic levels like in nephrotic syndrome?

Answer 134

- serum creatinine, eGFR, lipids and glucose - ANA, double-stranded DNA antibody, C3 and C4 indicates SLE - antiphospholipase A2 receptor antibody indicates membranous nephropathy - HepB surface antigen, HepC antibody or HIV

Question 135

what are complications of nephrotic syndrome?

Answer 135

- susceptibility to infection - thromboembolism - hyperlipidaemia

Question 136

what infections does nephrotic syndrome increase susceptibility to?

Answer 136

cellulitis, Streptococcus infections and spontaneous bacterial peritonitis

Question 137

why does nephrotic syndrome cause increased susceptibility to infections?

Answer 137

due to low serum IgG, decreased complement activity and reduced T-cell function due in part to loss of immunoglobulin in urine and also to immunosuppressive treatment

Question 138

how does nephrotic syndrome increase risk of thromboembolism?

Answer 138

hypercoaguable state due to increased clotting factors (produced by liver due to low albumin since liver goes into overdrive) and platelet abnormalities

Question 139

how does nephrotic syndrome increase risk of hyperlipidaemia?

Answer 139

increased cholesterol and triglycerides due to hepatic lipoprotein synthesis in response to low oncotic pressure due to low albumin

Question 140

what is the treatment of nephrotic syndrome?

Answer 140

- reduce oedema - reduce proteinuria - reduce risk of complications - treat underlying cause

Question 141

how is oedema reduced in nephrotic syndrome?

Answer 141

* loop diuretics e.g. IV furosemide - IV since gut oedema may prevent oral absorption * thiazide diuretics e.g. IV bendroflumethiazide * fluid and salt restriction while giving diuretics

Question 142

how is proteinuria reduced in nephrotic syndrome?

Answer 142

* ACE inhibitor e.g. ramipril * angiotensin receptor blocker e.g. candesartan * eat normal rather than high protein diet

Question 143

how is risk of complications reduced in nephrotic syndrome?

Answer 143

* prophylactic anticoagulation with warfarin, especially when albumin is low (<20g/l) * reduce cholesterol with statins e.g. simvastatin * treat infections promptly and vaccinate

Question 144

what is the most common cause of nephrotic syndrome in children?

Answer 144

minimal change disease

Question 145

what is minimal change disease?

Answer 145

disease affecting the kidneys which causes nephrotic syndrome

Question 146

what is the epidemiology of minimal change disease?

Answer 146

- commonest cause of nephrotic syndrome in children - occurs most commonly in boys under the age of 5 - accounts for 20% of adult nephritic syndrome

Question 147

what are risk factors and causes of minimal change disease?

Answer 147

- can be idiopathic - atopy is present in 30% of cases and allergic reactions can trigger nephrotic syndrome - drugs - Hep C, HIV and TB are rare causes - associated with Hodgkins lymphoma

Question 148

what are drugs that can cause minimal change disease?

Answer 148

* NSAIDs * lithium * antibiotics e.g. cephalosporins, rifampicin and ampicillin * bisphosphonates * sulfasalazine

Question 149

what is the pathophysiology of minimal change disease?

Answer 149

- glomeruli appear normal on light microscopy, but on electron microscopy, fusion of the foot processes of the podocytes is seen, consistent with a disrupted podocyte actin cytoskeleton - immature differentiating CD35 stem cells appear to be responsible for pathogenesis

Question 150

what is the clinical presentation of minimal change disease?

Answer 150

- proteinuria - oedema, predominantly around the face - fatigue - frothy urine

Question 151

how is minimal change disease diagnosed?

Answer 151

biopsy • normal under light microscopy • electron microscopy shows fused podocyte foot processes

Question 152

what is the treatment of minimal change disease?

Answer 152

- high dose corticosteroids can reverse proteinuria in 95% cases, however the majority relapse - frequent relapse or steroid-dependent disease is treated with cyclophosphamide or ciclosporin/tacrolimus

Question 153

what are asymptomatic urinary abnormalities? how is it diagnosed?

Answer 153

* incidental finding of dipstick haematuria +/- proteinuria * kidney function and blood pressure are normal * diagnosis is usually clinical, don’t biopsy unless kidney function abnormal or significant proteinuria

Question 154

what are causes of asymptomatic urinary abnormalities?

Answer 154

- IgA nephropathy | - thin membrane disease

Question 155

how does IgA nephropathy cause asymptomatic urinary abnormalities? what can it present as?

Answer 155

* abnormality in IgA glycosylation leads to deposition in mesangium (provides structural support for glomerulus) * can present as nephritic, nephrotic, asymptomatic or as progressive chronic kidney disease

Question 156

what is the commonest cause of glomerulonephritis worldwide?

Answer 156

IgA nephropathy

Question 157

what is IgA nephropathy associated with?

Answer 157

tonsillitis and macroscopic haematuria

Question 158

what is the treatment of IgA nephropathy?

Answer 158

treated with BP control and immunosuppression in aggressive disease

Question 159

how does thin membrane disease cause asymptomatic urinary abnormalities?

Answer 159

thin basement membrane so more likely to leak blood into urine

Question 160

what is chronic kidney disease? what is it defined as?

Answer 160

* CKD is longstanding, usually progressive impairment in renal function (haematuria, proteinuria or anatomical abnormality) for more than 3 months * defined as a GFR < 60mL/min/1.73 m2 for more than 3 months with/without evidence of kidney damage (haematuria, proteinuria or anatomical abnormality)

Question 161

what is the epidemiology of chronic kidney disease?

Answer 161

- between 6% - 11% of people can be defined as having CKD - risk of CKD increases with age; incidence rising as we are living longer - more common in females than males

Question 162

what is stage 1 CKD?

Answer 162

- GFR >90mL/min | - normal or raised GFR with other evidence of renal damage

Question 163

what is stage 2 CKD?

Answer 163

- GFR 60-89mL/min | - slight decreased GFR with other evidence of renal damage

Question 164

what is stage 3 CKD?

Answer 164

- 3A GFR: 45-59mL/min - 3B GFR: 30-44mL/min - moderate decreased GFR with or without evidence of other renal damage

Question 165

what is stage 4 CKD?

Answer 165

- GFR 15-29mL/min | - severe decreased GFR with or without evidence of other renal damage

Question 166

what is stage 5 CKD?

Answer 166

- GFR <15mL/min | - established renal failure

Question 167

what are signs of renal damage?

Answer 167

proteinuria, haematuria or evidence of abnormal anatomy or systemic disease

Question 168

what is the aetiology of CKD?

Answer 168

- diabetes mellitus - Type II > Type 1 - hypertension - atherosclerotic renal vascular disease - polycystic kidney disease - tuberous sclerosis - primary glomerulonephritides e.g. IgA nephropathy - SLE - amyloidosis - hypertensive nephrosclerosis (common in black africans) - small and medium-sized vessel vasculitis - family history of stage 5 CKD or hereditary kidney disease e.g. polycystic kidney disease - hypercalcaemia - neoplasma - myeloma - idiopathic - 20% cases

Question 169

what are risk factors for CKD?

Answer 169

- diabetes mellitus - hypertension - old age - CVD - renal stones or benign prostatic hyperplasia (BPH) - recurrent UTI’s - SLE - proteinuria - AKI - smoking - African, Afro-Caribbean or Asian origin - chronic use of NSAIDs

Question 170

what is the pathophysiology of CKD?

Answer 170

- in CKD, where many nephrons have failed, and scarred, the burden of filtration falls to fewer functioning nephrons - functioning (remnant) nephrons experience increased flow per nephron (hyperfiltration), as blood flow has not changed, and adapt with glomerular hypertrophy and reduced arteriolar resistance - increased flow, increased pressure and increased shear stress set in motion a vicious cycle of raised intraglomerular capillary pressure and strain, which accelerates remnant nephron failure - this increased flow and strain may be detected as new/increasing proteinuria

Question 171

what is the effect of reduced renal perfusion?

Answer 171

reduced renal perfusion - > decreased transglomerular pressure - > decreased GFR

Question 172

what is the response to reduced renal perfusion?

Answer 172

intrarenal activation of RAAS - > efferent arteriolar vasoconstriction - > increases transglomerular pressure - > restores GFR

Question 173

what are the effects of angiotensin II in CKD?

Answer 173

• produced locally, modulates intraglomerular capillary pressure and GFR, causing vasoconstriction of postglomerular arterioles, and increasing the glomerular hydraulic pressure and filtration fraction • by its effect on mesangial cells and podocytes, it increases the pore sizes and impairs the size-selective function of the basement membrane for macromolecules, resulting in increased proteinuria • also modulates cell growth by upregulating TGF-beta, increasing collagen synthesis and epithelial cell transdifferentiation to myofibroblasts, leading to excessive matrix formation • also up regulates plasminogen activator inhibitor-1, which inhibits matrix proteolysis by plasmin, resulting in the accumulation of excessive matrix and scarring in the glomeruli and interstitium

Question 174

what does the prognosis of CKD correlate with?

Answer 174

- hypertension - particularly if poorly controlled - proteinuria - degree of scarring in the interstitium on histology

Question 175

what is therapy for CKD aimed at?

Answer 175

aimed at inhibiting angiotensin II and reducing proteinuria mainly with ACE inhibitors or angiotensin receptor antagonists

Question 176

what is the clinical presentation of CKD?

Answer 176

- malaise - anorexia and weight loss - Insomnia - nocturia and polyuria (>40ml/kg/24hours) due to impaired concentrating ability - itching - nausea, vomiting and diarrhoea - symptoms due to salt and water retention; peripheral or pulmonary oedema - amenorrhea in women and erectile dysfunction in men - increased risk of peptic ulceration, acute pancreatitis, hyperuricaemia and incidence of malignancy

Question 177

what is used as surrogates of accumulating metabolites in CKD? why?

Answer 177

serum urea and creatinine are used as surrogates of accumulating metabolites (uraemic toxins) since their measurement is easy and there is a rough correlation between toxins and them

Question 178

when are symptoms of CKD common?

Answer 178

symptoms are common when the serum urea concentration exceeds 40mmol/L but many patients develop uraemic symptoms at lower levels of serum urea

Question 179

what does CKD increase the risk of?

Answer 179

peptic ulceration, acute pancreatitis, hyperuricaemia and incidence of malignancy

Question 180

what are blood complications of CKD?

Answer 180

normochromic normocytic anaemia: | • due to reduced erythropoietin production by diseased kidney

Question 181

what are bone complications of CKD?

Answer 181

• bone pain • renal osteodystrophy; osteomalacia, osteoporosis, hyperparathyroidism • renal phosphate retention and impaired 1,25-dihydroxy vitamin D production lead to a fall in serum Ca2+ and thus a compensatory increase in PTH which can result in skeletal decalcification leading to bone disease

Question 182

what are neurological complications of CKD?

Answer 182

* occurs in almost all patients with severe CKD * autonomic dysfunction presents as postural hypotension and disturbed GI motility * polyneuropathy resulting in peripheral paraesthesiae and weakness * in advanced uraemia there is depressed cerebral function, myoclonic twitching and seizures

Question 183

what are cardiovascular complications of CKD? why do they occur?

Answer 183

* highest mortality is from CVD particularly MI, cardiac failure, sudden cardiac death and stroke * occurs due to an increased frequency of hypertension, hyperlipidaemia and vascular calcification * pericarditis and pericardial effusion occurs in severe anaemia * pericardial friction rub * flow murmurs

Question 184

what are skin complications of CKD?

Answer 184

* pruritus due to nitrogenous waste products of urea; may be scratch marks * brown discolouration of nails

Question 185

what are differential diagnoses of CKD?

Answer 185

AKI

Question 186

how can CKD be differentiated from AKI?

Answer 186

* to differentiate it depends on history, duration of symptoms and previous urinalysis or measurement of serum creatinine * a normochromic anaemia, small kidneys on ultrasound and the presence of renal osteodystrophy favour CKD

Question 187

how is CKD diagnosed?

Answer 187

- ECG for high potassium signs - urinalysis - urine microscopy - serum biochemistry - bloods - immunology - imaging - biopsy and histology to diagnose condition causing renal failure

Question 188

what is seen in urinalysis in CKD?

Answer 188

* haematuria - indicates glomerulonephritis * proteinuria - if heavy suggestive of glomerular disease, can also be caused by infection * mid-stream urine sample sent for microscopy and sensitivity * albumin to creatinine ratio or protein to creatine ratio

Question 189

what is seen on urine microscopy in CKD?

Answer 189

* white cells - bacterial UTI * eosinophilia - allergic tubulointerstitial nephritis/cholesterol emboli * granular casts - active renal disease * red cells - glomerulonephritis

Question 190

what is seen on serum biochemistry in CKD?

Answer 190

* urea, electrolytes, bicarbonate and creatine - high urea and creatinine * low eGFR * raised alkaline phosphatase (renal osteodystrophy) * raised PTH if CKD stage 3 or more

Question 191

what is seen in bloods in CKD?

Answer 191

* raised phosphate * low Ca2+ * Hb low - normochromic normocytic anaemia * raised viscosity - myeloma or vasculitis * fragmented red cells indicate intravascular haemolysis

Question 192

what is seen on immunology in CKD?

Answer 192

* auto-antibody screening for SLE, scleroderma and Goodpastures * Hep B, C, HIV and streptococcal antigen tests

Question 193

how is ultrasound used in diagnosis of CKD? what is seen?

Answer 193

ultrasound to check renal size and exclude hydronephrosis: - in CKD kidneys tend to be small - can be large in infiltrative disorders e.g. amyloidosis

Question 194

how is CT used to diagnose CKD?

Answer 194

detect stones, retroperitoneal fibrosis and other causes of urinary obstruction and maybe cortical scarring

Question 195

what are the aims of treatment of CKD?

Answer 195

* therapy aimed at the underlying cause of renal disease * slow the deterioration of kidney function * reduce cardiovascular risk * identify and treat reversible causes * limit progression and complications

Question 196

how does CKD treatment identify and treat reversible causes?

Answer 196

* relieve obstruction * stop nephrotoxic drugs * stop smoking and achieve healthy weight to deal with cardiovascular risk * tight glucose control in diabetes

Question 197

what is the target BP in CKD?

Answer 197

< 130/80mmHg

Question 198

what is the treatment of BP in CKD?

Answer 198

- ACE-inhibitor - angiotensin receptor blocker - in diabetes start with ARB - diuretic to prevent hyperkalaemia and help reduce BP - calcium channel blocker if goals not met

Question 199

what is the treatment of bone disease in CKD?

Answer 199

- check PTH and treat if raised - restrict diet - give phosphate binders to decrease gut absorption and avoidance of phosphate-rich food e.g. milk, cheese, eggs - vitamin D e.g. calcitriol and Ca2+ supplements

Question 200

what is the treatment of CVD in CKD?

Answer 200

statins and aspirin

Question 201

what is the treatment of anaemia in CKD?

Answer 201

iron/folate/folic acid

Question 202

what is the treatment of acidosis in CKD?

Answer 202

- systemic acidosis accompanies the decline in kidney function and may contribute to increased serum potassium levels as well as dyspnea and lethargy - treat with sodium bicarbonate

Question 203

what is the best form of renal replacement therapy? what is another form?

Answer 203

* the ‘best’ form of renal replacement therapy is transplantation, since it can restore 100% renal function, but this involves surgery and it is not always successful * dialysis can maintain stability but has complications

Question 204

what are indications for dialysis?

Answer 204

- symptomatic uraemia including pericarditis or tamponade - hyperkalaemia not controlled by conservative measures - pulmonary oedema unresponsive to diuretics - severe acids - high potassium - tall T waves, low flat p waves, broad QRS or arrhythmias on ECG - metabolic acidosis - fluid overload that is resistant to diuretics

Question 205

what is haemofiltration? how is it done?

Answer 205

- most commonly used - achieves blood flow using a blood pump to draw and return blood from the lumen of a dual-lumen catheter placed in the jugular, subclavian or femoral vein - ultrafiltrate is continuously removed from patient combined with simultaneous infusion of replacement solution - has less haemodynamic instability than haemodialysis

Question 206

what is haemodialysis? how is it done?

Answer 206

- blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction, thus blood is always meeting a less-concentrated solution and diffusion of small solutes occurs down the concentration gradient - larger solutes do not clear as effectively - blood is taken from artery the and returned into a vein at an atrioventricular fistula (not suitable for atherosclerotic patients or those who have many fistulas) - allows good clearance of solutes in short periods but requires patient to be haemodynamically stable - time-consuming

Question 207

what are complications of haemodialysis?

Answer 207

* hypotension/cramps * nausea/headache * chest pain * fever/rigors * infected dialysis catheter

Question 208

what is peritoneal dialysis? how is it done?

Answer 208

- mainly used for CKD, rare in AKI - process uses patient's peritoneum in the abdomen as a membrane across which fluid and solutes are exchanged with blood - all peritoneal dialysis is done at home, at night

Question 209

what are complications of peritoneal dialysis?

Answer 209

* infection e.g. peritonitis * abdominal wall herniation * intestinal perforation * loss of membrane function over time

Question 210

what are complications of RRT?

Answer 210

- cardiovascular disease due to combination of hypertension and calcium/phosphate dysregulation - infection - amyloid accumulates in long-term dialysis and may cause carpal tunnel syndrome, arthralgia and fractures - malignancy is commoner in dialysis patients - may be due to the cause of end-stage renal failure

Question 211

what is a renal cyst? when can they occur? what can they cause?

Answer 211

- a renal cyst is a fluid collection in or on the kidney - solitary or multiple renal cysts are common, especially with advancing age; 50% of those over 50 have one or more such cysts - these cysts are often asymptomatic and are found incidentally on ultrasound examination - occasionally they may cause pain and/or haematuria if large, or bleeding may occur into the cyst

Question 212

what are the different types of kidney cysts?

Answer 212

- simple cysts - most common form; benign - polycystic; recessive or dominant - hydronephrosis is when ureter is blocked and kidney dilates and gets bigger - dysplasia – when not formed properly - medullary sponge – dilation of collecting ducts - acquired cystic disease – medullary uraemic, dialysis cystic

Question 213

what are features of congenital renal cysts?

Answer 213

- present at birth - uni/bilateral - isolated or multisystem disorder - inherited; autosomal or recessive

Question 214

how do congenital renal cysts develop?

Answer 214

* genetic mutation leads to predisposition for cyst formation * increased abnormal cell hyperproliferation → loss of planar polarity → cyst initiation → fluid secretion by epithelial cells → cyst

Question 215

what are features of acquired renal cysts?

Answer 215

- develop over time - no genetic mutation - bilateral/unilateral - isolated to kidneys - normal/small kidney size - associated with chronic kidney disease - route of development not clear

Question 216

what are causes of renal cysts?

Answer 216

- simple cysts develop over time - acquired cysts e.g. CKD - drugs e.g. lithium - autosomal dominant/recessive polycystic kidney disease - syndromic disease; tuberous sclerosis

Question 217

what is autosomal dominant polycystic disease?

Answer 217

* genetic disorder in which the renal tubules become structurally abnormal, resulting in the development and growth of multiple cysts within the kidney * cysts may begin in utero, infancy, childhood or adulthood * multiple cysts develop, gradually and progressively, throughout the kidney eventually resulting in renal enlargement and kidney tissue destruction

Question 218

what is the epidemiology of ADPKD?

Answer 218

- commonest inherited kidney disease - autosomal dominant inheritance with high penetrance - usually presents in adulthood (20-30) - more common in males than females - if one parent affected then 50% chance of transmission - if both parents affected then 50% chance being affected, 25% normal, 25% being homozygous for disease (these babies die in the womb)

Question 219

what is the aetiology/genetics of ADPKD?

Answer 219

- mutations in PKD1 (85%) gene on chromosome 16 | - mutations in PKD2 (15%) gene on chromosome 4

Question 220

what are risk factors for ADPKD?

Answer 220

family history of ADPKD, ESRF or hypertension

Question 221

what does PKD1 do?

Answer 221

PKD1 encodes polycystin 1 which is involved in cell-cell and/or cell-matrix interactions; regulates tubular and vascular development in the kidneys

Question 222

what does PKD2 do?

Answer 222

PKD2 encodes polycystin 2 which functions as a calcium ion channel

Question 223

what does disruption of the polycystin pathway due to genetic mutations lead to?

Answer 223

disruption of the polycystin pathway results in reduced cytoplasmic Ca2+, which, in principal cells of the collecting duct, causes defective ciliary signalling and disorientated cell division resulting in cyst formation

Question 224

what causes progressive loss of renal function in ADPKD?

Answer 224

- mechanical compression, apoptosis of healthy tissue and reactive fibrosis - rate of renal function decline is dependent on the growth and size of cysts; patients with rapidly growing cysts on MRI lose renal function more rapidly

Question 225

what is the clinical presentation of ADPKD?

Answer 225

- can be clinically silent for many years, so family screening is essential - symptoms tend to start to present from 20 yrs onwards - loin pain and/or haematuria from haemorrhage into a cyst, cyst infection or urinary tract stone formation - loin or abdominal discomfort as size of kidneys increase - excessive water and salt loss - nocturia - bilateral kidney enlargement - renal colic due to clots - hypertension - renal stones, mainly uric acid stones - progressive renal failure

Question 226

what is extrarenal clinical presentation of ADPKD?

Answer 226

* subarachnoid haemorrhage associated with berry aneurysm rupture * polycystic liver disease (70%) * pancreatitis * male infertility (rare) * mitral valve prolapse * ovarian cysts * diverticular disease

Question 227

what are differential diagnoses of ADPKD?

Answer 227

- acquired and simple cysts of the kidneys - autosomal recessive PKD - medullary sponge kidney - tuberous sclerosis

Question 228

how is ADPKD diagnosed?

Answer 228

- personal history - family history of ADPKD, ESRF, hypertension - BP may be raised - ultrasound - genetic testing for PKD1 and PKD2

Question 229

when is ultrasound diagnostic for at risk individuals?

Answer 229

- 15-39yrs ≥ 3 cysts (uni/bilateral) - 40-59yrs ≥ 2 cysts (each kidney) - 60yrs+ and ≥ 4 cysts (each kidney)

Question 230

when can ultrasound be used to exclude ADPKD?

Answer 230

≥ 40yrs with < 2 cysts

Question 231

when can ultrasound not be used to exclude ADPKD?

Answer 231

if <30yrs

Question 232

what is the treatment of ADPKD?

Answer 232

- no treatment shown to slow disease progression - blood pressure control with ACE-inhibitor - treat stones and give analgesia - laparoscopic removal of cysts to help with pain/nephrectomy - disease progression monitored by serial progression of serum creatinine - renal replacement therapy for ESRF - children and siblings of patients with the disease should be offered screening by renal ultrasound in their 20s - counselling and support

Question 233

what are indications for genetic testing?

Answer 233

* individual older case with no family history * atypical cystic disease * very early onset (<2 yrs) * prenatal/pre-implantation genetic diagnosis * to facilitate life choices/reproduction decisions * potential living related kidney donor (<40yrs with positive imaging)

Question 234

what is autosomal recessive polycystic kidney disease?

Answer 234

- recessive form of polycystic kidney disease - associated with a group of congenital fibrocystic syndromes - mutations in PKHD1 causes ARPKD - PKHD1 mutation on long arm (q) of chromosome 6

Question 235

what is the epidemiology of ARPKD?

Answer 235

- rarer than ADPKD with prevalence at 1 in 40,000 - autosomal recessive inheritance - disease of infancy

Question 236

what is the clinical presentation of ARPKD?

Answer 236

- variable - many present in infancy with multiple renal cysts and congenital hepatic fibrosis - enlarged polycystic kidneys - 30% develop kidney failure

Question 237

what are differential diagnoses of ARPKD?

Answer 237

- ADPKD - multicystic dysplasia - hydronephrosis - renal vein thrombosis

Question 238

how is ARPKD diagnosed?

Answer 238

- diagnosed antenatally or neonatally - ultrasound to see cysts - CT and MRI to monitor liver disease - genetic testing

Question 239

what is the treatment of ARPKD?

Answer 239

- currently no treatment available - genetic counselling for family members - laparoscopic removal of cysts to help with pain/nephrectomy - blood pressure control with ACE-inhibitor - treat stones and give analgesia - renal replacement therapy for ESRF - counselling and support

Question 240

what are different types of scrotal masses? how are they diagnosed?

Answer 240

• cannot get above - inguinoscrotal hernia or proximally extending hydrocele • separate and cystic - epididymal cyst • separate and solid - epididymitis or varicocele • testicular and cystic - hydrocele • testicular and solid - tumour, haematocele - orchitis

Question 241

what is an epididymal cyst?

Answer 241

smooth, extratesticular, spherical collection of fluid in the head of the epididymis

Question 242

what is the epidemiology of epididymal cysts?

Answer 242

- usually develop around the age of 40 - not uncommon - rare in children

Question 243

what is the clinical presentation of epididymal cysts?

Answer 243

- contain clear and milky fluid - lie above and behind the testis - normally present having noticed a lump - often are multiple and may be bilateral - small cysts may remain undetected and asymptomatic - once they get large then may be painful - well defined and will transluminate since fluid-filled - testis is palpable quite separately from the cyst (unlike hydrocele where the testis is palpable within the fluid filled swelling)

Question 244

what are differential diagnoses of epididymal cysts?

Answer 244

- spermatocele - hydrocele - varicocele

Question 245

what is a spermatocele? how is it differentiated from an epididymal cyst?

Answer 245

* retention cyst of a tubule of the rete testes or the head of the epididymis, distended with barely watery fluid that contains spermatozoa * fluid and sperm filled cyst in the epididymis * no way clinically to differentiate between a cyst of the epididymis and spermatocele * can be differentiated as sperm are present in the milky fluid aspirate of a spermatocele

Question 246

what is a hydrocele?

Answer 246

- accumulation of serous fluid in a body cavity - hydrocele testis is the accumulation of fluids around a testicle, within the tunica vaginalis - often caused by fluid secreted from a remnant piece of peritoneum wrapped around the testicle (tunica vaginalis)

Question 247

what is a varicocele?

Answer 247

an abnormal dilation of the testicular veins in the pampiniform venous plexus in the scrotum, caused by venous reflux

Question 248

how is an epididymal cyst diagnosed?

Answer 248

scrotal ultrasound

Question 249

how is an epididymal cyst treated?

Answer 249

- usually not necessary | - if painful and symptomatic then surgical excision

Question 250

what is the epidemiology of hydrocele?

Answer 250

- clinically apparent scrotal hydrocele are evident in 6% of term males beyond the newborn period - most paediatric hydroceles are congenital

Question 251

what is the aetiology of primary hydrocele?

Answer 251

* more common and larger * usually in younger men * associated with a patent processus vaginalis, which typically resolves during the 1st year of life

Question 252

what is the aetiology of secondary hydrocele?

Answer 252

rarer and present in older boys and men

Question 253

what is secondary hydrocele secondary to?

Answer 253

- testis tumour - trauma - infection - TB - testicular torsion - generalised oedema

Question 254

what is a simple hydrocele?

Answer 254

overproduction of fluid in the tunica vaginalis

Question 255

what is a communicating hydrocele?

Answer 255

processus vaginalis fails to close, allowing peritoneal fluid to communicate freely within the scrotal portion

Question 256

what is the clinical presentation of a hydrocele?

Answer 256

- scrotal enlargement with a non-tender, smooth, cystic swelling - pain is not a feature unless the hydrocele is infected - testis are usually palpable but may be difficult to palpate in large hydrocele - lies anterior to and below the testis and will transluminate

Question 257

what are differential diagnoses of hydrocele?

Answer 257

must differentiate from testicular torsion and strangulated hernia

Question 258

what is used to diagnose hydrocele?

Answer 258

- ultrasound - serum alpha-fetoprotein and human chorionic gonadotrophin to help exclude malignant teratomas or other germ cell tumours

Question 259

what is the treatment of hydrocele?

Answer 259

- resolve spontaneously - many of infancy resolve by 2 yrs - therapeutic aspiration or surgical removal

Question 260

what is the epidemiology of varicocele?

Answer 260

- left side more commonly affected - unusual in boys under 10yrs - incidence increases after puberty - associated with sub fertility

Question 261

what is the aetiology of varicocele?

Answer 261

- more common on the left - angle at which the left testicular vein enters the left renal vein - increased reflux from compression of the renal vein - lack of effective valves between the testicular and renal veins

Question 262

what is the clinical presentation of varicocele?

Answer 262

- often visible as distended scrotal blood vessels that feel like ‘a bag of worms’ - patient may complain of a dull ache or scrotal heaviness - scrotum hangs lower on the side of the varicocele

Question 263

what are differential diagnoses of varicocele?

Answer 263

secondary to other pathological processes blocking the testicular vein e.g. kidney tumours and other retroperitoneal tumours

Question 264

what is used to diagnose varicocele?

Answer 264

- venography | - colour doppler ultrasound (to see blood flow)

Question 265

what is treatment of varicocele?

Answer 265

surgery if there is pain, infertility or testicular atrophy

Question 266

what is testicular torsion?

Answer 266

torsion (twisting) of the spermatic cord resulting in occlusion of the testicular blood vessels which can rapidly lead to ischaemia and infarct and thus there is potential loss of the testis (germ cells are the most susceptible cell line to ischaemia)

Question 267

what is the aim of treatment of testicular torsion?

Answer 267

* aim is to recognise this condition before the cardinal symptoms fully manifest, as prompt surgery saves testes * if surgery is performed in < 6hrs the salvage rate is 90-100%; if > 24hrs it is 0-10%

Question 268

what is the epidemiology of testicular torsion?

Answer 268

- common urological emergency among adolescent boys and young men - typically occurs in neonates or post-pubertal boys but can occur in males of all ages, most common at 11-30yrs - left side is more commonly affected than right

Question 269

what is the aetiology of testicular torsion?

Answer 269

underlying congenital malformation (belt-clapper deformity) where the testis is not fixed to the scrotum completely, allowing for free movement leading to twisting

Question 270

what is the clinical presentation of testicular torsion?

Answer 270

- in any boy presenting with abdominal pain, the testes should be checked - sudden onset of pain in one testis, makes walking uncomfortable - pain often comes on during sport or physical activity - pain in abdomen, nausea and vomiting are common - inflammation of one testis; it is very tender, hot and swollen - testis may lie high and transversely - with intermittent torsion the pain may have passed on presentation, but if it was severe then prophylactic fixing may be wise

Question 271

what are differential diagnoses of testicular torsion?

Answer 271

- epididymo-orchitis (main one) - tumour, trauma and an acute hydrocele - torsion of testicular or epididymal appendage (remnant of Mullerian duct) - idiopathic scrotal oedema

Question 272

what are features of tosion of testicular or epididymal appendage as a differential diagnosis of testicular torsion?

Answer 272

* usually occurs in boys between 7-12yrs and causes less pain * small blue nodule under scrotum * due to the surge in gonadotrophins that signal the onset of puberty

Question 273

what are features of idiopathic scrotal oedema as a differential diagnosis of testicular torsion?

Answer 273

benign condition usually occurs between 2-10yrs and is differentiated from torsion by the absence of pain and tenderness

Question 274

what is used to diagnose testicular torsion?

Answer 274

- doppler ultrasound may demonstrate lack of blood flow to testis - urinalysis to exclude infection and epididymis - do not delay surgical exploration

Question 275

what is the treatment of testicular torsion?

Answer 275

- surgery: expose and untwist testis; 6 hour window to save testis - orchidectomy (removal of testis) and bilateral fixation

Question 276

what is BOO?

Answer 276

bladder outflow obstruction (urodynamic diagnosis) - urine is unable to flow from the kidneys through the ureters and out of the bladder through the urethra - decreased flow of urine leads to hydronephrosis

Question 277

what is hydronephrosis?

Answer 277

dilation of the renal pelvis and calyces as a result of obstruction to urine flow

Question 278

what is obstructive uropathy?

Answer 278

functional or anatomical obstruction of urine flow at any level of the urinary tract

Question 279

what is the normal function of the lower urinary tract?

Answer 279

- convert a continuous process of excretion (urine production) to an intermittent process of elimination - store urine insensibly - void urine when convenient

Question 280

what is the action of the detrusor muscles? what is the neural supply? is it parasympathetic or sympathetic?

Answer 280

• relaxes during storage (compliant) • contracts during voiding • parasympathetic cholinergic control via S3,S4 and S5: - drives detrusor contraction

Question 281

what is the distal sphincter mechansim? what is the neural supply? is parasympathetic or sympathetic?

Answer 281

``` • contracts during storage • relaxes during voiding • sympathetic noradrenergic control via T10,L1 and L2: - sphincter/urethral contraction - inhibits detrusor contraction ```

Question 282

what are storage symptoms in LUTS?

Answer 282

- urgency - nocturia (> 30% voided volume at night) - frequency - overflow incontinence (leaking urine during day/wetting bed)

Question 283

what are voiding symptoms in LUTS?

Answer 283

- poor intermittent stream - hesitancy - incomplete emptying - post micturition dribbling - straining - haematuria - dysuria

Question 284

what are red flags of LUTS?

Answer 284

haematuria and dysuria - warning symptoms of infection, stones or cancer

Question 285

what is PSA?

Answer 285

Prostate Specific Antigen - glycoprotein that is expressed by normal and neoplastic prostate tissue - small amounts in bloodstream normally

Question 286

when is PSA raised?

Answer 286

* BPH * prostate cancer * perianal trauma and mechanical manipulation of the prostate e.g. in cytoscopy (endoscopy of bladder), prostate biopsy or surgery * BMI < 25 * taller men * recent ejaculation * black africans * prostatitis * UTI

Question 287

what level of PSA confers an increased risk of LUTS progression?

Answer 287

PSA >1.4ng/ml

Question 288

what are flow rates and residual volume of the urine?

Answer 288

- how much urine being passed, how long for and flow rate - maximum flow rate is useful if more than 150ml voided - max flow rate < 10ml per second is suggestive of bladder outflow obstruction due to BPH

Question 289

what flow rate suggests BOO due to BPH?

Answer 289

max flow rate < 10ml per second is suggestive of bladder outflow obstruction due to BPH

Question 290

what are features of the frequency volume chart used in LUTS?

Answer 290

- measure volumes voided and time over minimum of 3 days - calculates whether polyuric (>40ml/kg/24hrs) - calculates whether nocturic (>30% voided volume at night)

Question 291

what characterises polyuria?

Answer 291

>40ml/kg/24hrs

Question 292

what characterises nocturia?

Answer 292

>30% voided volume at night

Question 293

what is acute urinary retention?

Answer 293

* sudden onset of painful inability to pass urine usually with over 500ml in the bladder * bladder is usually tender

Question 294

what are causes of acute urinary retention?

Answer 294

- prostatic obstruction e.g. due to BPH or prostate cancer - urethral strictures - anticholinergics - alcohol - constipation - post-op (pain/inflammation/anaesthetics) - infection - neurological (spinal compression - cauda equina syndrome)

Question 295

what is the examination of acute urinary retention?

Answer 295

abdomen, prostate (DRE), perineal sensation (to check for cauda equina syndrome)

Question 296

what is used to diagnose acute urinary retention?

Answer 296

- normal renal biochemistry, since not affected usually - renal ultrasound if abnormal biochemistry - PSA test to look for BPH/prostate cancer

Question 297

what is the treatment of acute urinary retention?

Answer 297

- catheter relieves pain - alpha-1 blocker which relaxes smooth muscle in bladder neck to aid voiding - prevent by giving 5-alpha-reductase inhibitor which reduces testosterone conversion to dihydrotestosterone and thus reduces prostate size

Question 298

what are features of chronic urinary retention?

Answer 298

* more insidious and may be painless * more difficult to define * incomplete bladder emptying * results in a increased risk of infection * can be low pressure with detrusor failure * can be high pressure with risk of interactive obstructive uropathy

Question 299

what can the pressures be like in chronic urinary retention?

Answer 299

* can be low pressure with detrusor failure | * can be high pressure with risk of interactive obstructive uropathy

Question 300

what are causes of chronic urinary retention?

Answer 300

- prostatic enlargement due to BPH/prostate cancer - pelvic malignancy or rectal surgery - diabetes

Question 301

what is the clinical presentation of chronic urinary retention?

Answer 301

- overflow incontinence; leaking urine during the day/wetting bed - loss of appetite - constipation - distended abdomen - UTI

Question 302

what is the management of chronic urinary retention?

Answer 302

only catheterise if there is pain, urinary infection or renal impairment

Question 303

what are features and types of urinary tract obstruction?

Answer 303

* common and should be considered in anyone with renal impairment * damage can be permanent if the obstruction is not treated properly * can be partial, complete, unilateral or bilateral

Question 304

what are causes of luminal urinary tract obstruction?

Answer 304

stones, blood, clot, sloughed papilla, tumour

Question 305

what are causes of mural urinary tract obstruction?

Answer 305

congenital or acquired stricture, neuromuscular dysfunction or schistomiasis

Question 306

what are causes of extra-mural urinary tract obstruction?

Answer 306

- abdominal or pelvic mass/tumour, retroperitoneal fibrosis, BPH, prostate cancer - pregnancy - inflammation e.g. peritonitis or diverticulitis

Question 307

what is the clinical presentation of urinary tract obstruction?

Answer 307

- acute upper tract (kidney and ureter) obstruction - chronic upper tract (kidney and ureter) obstruction - acute lower tract (bladder to urethra) obstruction - chronic lower tract (bladder to urethra) obstruction

Question 308

what is the clinical presentation of acute upper urinary tract (kidney and ureter) obstruction?

Answer 308

loin pain radiating to groin

Question 309

what is the clinical presentation of chronic upper urinary tract (kidney and ureter) obstruction?

Answer 309

flank pain, renal failure, infection and polyuria may occur due to impaired urinary concentration

Question 310

what is the clinical presentation of acute lower tract (bladder to urethra) obstruction?

Answer 310

* acute urinary retention with severe suprapubic pain, often preceded by symptoms of bladder outflow obstruction * distended, palpable bladder that's dull to percussion

Question 311

what is the clinical presentation of chronic lower tract (bladder to urethra) obstruction?

Answer 311

* urinary frequency, hesitancy, poor stream, terminal dribbling and overflow incontinence * distended, palpable bladder +/- large prostate on rectal exam * complications are UTI and urinary retention

Question 312

what is used to diagnose urinary tract obstruction?

Answer 312

* bloods: U+Es and monitor creatinine; this will be raised * mid-stream urinary sample; culture and sensitivity * ultrasound: if there is hydronephrosis then arrange CT

Question 313

what is the treatment of upper urinary tract obstruction?

Answer 313

- nephrostomy: artificial opening created between the kidney and the skin which allows for the urinary diversion directly from the upper tract - alpha-1 antagonist (bladder neck smooth muscle relaxer) improves flow - 5-alpha reductase inhibitor inhibits conversion of testosterone to active form and thus reduces prostate size

Question 314

what is the treatment of lower urinary tract obstruction? what should be monitored?

Answer 314

- urethral catheter - suprapubic catheter - beware of large diuresis after obstruction relief as can result in a temporary salt losing nephropathy resulting in weight loss; monitor weight and maintain fluid balance

Question 315

what are advantages/disadvantages of suprapubic catheters for lower urinary tract obstruction?

Answer 315

* less risk of urethral damage and thus UTI * requires general anaesthetic for insertion * small risk of bowel injury during insertion * less likely to be colonised by bacteria than with a long term urethral catheter * long term urethral catheter can lead to urethral erosion and damage to the urethral sphincter

Question 316

how is surgery used to treat urinary tract obstruction?

Answer 316

transurethral resection of the prostate | • less than 14% impotent, 1% incontinent and 10% erectile dysfunction

Question 317

what are indications for surgery for LUTS? (RUSHES)

Answer 317

RUSHES - Retention - UTI’s - Stones - Haematuria - Elevated creatinine due to bladder outflow obstruction - Symptoms deterioration

Question 318

what is benign prostatic enlargement/hyperplasia?

Answer 318

* increase in the size of the prostate without the presence of malignancy * prostate secretes 70% of the volume of seminal fluid and is hormone dependent * the prostate gland surrounds the urethra, the tube that carries urine from the bladder out of the body

Question 319

what is the epidemiology of benign prostatic enlargement/hyperplasia?

Answer 319

- common - 24% of men 40-64 and 40% of men over 60 - more common over 60 - unusual before the age of 45 - affects Afro-Caribbean's more severely than white men, probably due to the high levels of testosterone

Question 320

what are the risk factors for benign prostatic enlargement/hyperplasia?

Answer 320

- increases with age | - castration (removal of testicles) is protective

Question 321

why is castration protective against benign prostatic enlargement/hyperplasia?

Answer 321

* androgens do not cause BPH but are a requirement for BPH * BPH is not seen in those with castration prior to puberty, or those with genetic diseases that inhibit androgen action or production

Question 322

what is the pathophysiology of benign prostatic enlargement/hyperplasia?

Answer 322

- benign nodular or diffuse proliferation of musculofibrous and glandular layers of the prostate - inner (transitional) zone enlarges in contrast to the peripheral layer expansion that is seen in prostate carcinoma - as the prostate gets bigger, it may squeeze or partly block the urethra - this often causes problems with urinating

Question 323

what is the clinical presentation of benign prostatic enlargement/hyperplasia?

Answer 323

- LUTS - abdominal exam reveals enlarged bladder - acute urinary retention - in a small number of cases, BPH may cause the bladder to become occluded leading to anuria, resulting in acute urinary retention leading to UTI’s, bladder stones or kidney damage - BPH does not affect ability to father children - BPH does not cause prostate cancer or erection problems

Question 324

what are some LUTS that occur in benign prostatic enlargement/hyperplasia?

Answer 324

* nocturia (>30% voided volume at night) * frequency * urgency * post-micturition dribbling * poor stream/flow * hesitancy * overflow incontinence * haematuria * bladder stones * delay in initiation of micturition * incomplete emptying of bladder

Question 325

what are differential diagnoses of BPH?

Answer 325

- bladder tumour - bladder stones - trauma - prostate cancer - chronic prostatitis - UTI

Question 326

what is used to diagnose BPH?

Answer 326

- digital rectal exam; prostate would feel enlarged but smooth - serum electrolytes and renal ultrasound to exclude renal damage caused by obstruction - transrectal ultrasound to see size of prostate - serum PSA - biopsy and endoscopy - mid-stream urine sample to exclude infection - flow rates and residual volume (max flow rate < 10ml per second is suggestive of BOO due to BPH) - frequency volume chart (measure over 3 days)

Question 327

what lifestyle changes are made to treat BPH?

Answer 327

* avoid caffeine and alcohol to reduce urgency and nocturia * relax when voiding * void twice in a row to aid emptying * watchful waiting if minimal symptoms

Question 328

what first line drugs are used to treat BPH?

Answer 328

alpha1 antagonists e.g. oral tamsulosin

Question 329

what is the action of alpha 1 antagonists? give an example

Answer 329

- oral tamsulosin - relax smooth muscle in the bladder neck and prostate thereby producing increase in urinary flow rate and improvement in obstructive symptoms

Question 330

what are some side effects of alpha1 antagonists?

Answer 330

drowsiness, dizziness, depression, ejaculatory | failure, extra-pyramidal signs, weight increase and nasal congestion

Question 331

when should alpha1 antagonists be avoided?

Answer 331

postural hypertension

Question 332

what is second line treatment of BPH?

Answer 332

5-alpha-reductase inhibitor e.g. oral finasteride

Question 333

what is the action of 5-alpha-reductase inhibitor? give an example

Answer 333

- e.g. finasteride - blocks the conversion of testosterone to dihydrotestosterone (responsible for prostatic growth) - alternative to alpha-antagonist especially in men with very large prostate

Question 334

what are side effects of 5-alpha-reductase inhibitors?

Answer 334

impotence, decreased libido

Question 335

when is surgery used to treat BPH?

Answer 335

* usually reserved for those with a large prostate or failure to respond to an adequate trial of medical therapy * surgery is required if there is acute urinary retention, failed voiding trials, recurrent gross haematuria, renal insufficiency due to obstruction or failure of medical treatment

Question 336

what are types of surgery used to treat BPH?

Answer 336

transurethral resection of prostate (TURP): • gold standard • less than 14% impotent, 1% incontinent and 10% erectile dysfunction transurethral incision of prostate (TUIP): • less destruction than TURP and less risk to sexual function, best for smaller prostate

Question 337

what are complications of BPH if untreated?

Answer 337

- bladder calculi - UTI - haematuria - acute retention

Question 338

where does renal cell carcinoma arise from?

Answer 338

- also known as hypernephroma and Grawitz tumour - malignant - arises from PCT epithelium

Question 339

what is the epidemiology of renal cell carcinoma?

Answer 339

- most common renal tumour in adults - accounts for 2-3% of all malignancies - more common in males than females - usually present after 50 yrs of age - rare before 40 yrs - average age at presentation is 55 yrs - highest incidence is in the Czech republic

Question 340

what is the most common renal tumour in adults?

Answer 340

renal cell carcinoma

Question 341

what are risk factors and aetiology of renal cell carcinoma?

Answer 341

- smoking - obesity - hypertension - renal failure and haemodialysis (15% develop RCC) - polycystic kidneys - Von Hippel Lindau (VHL) syndrome

Question 342

how is VHL inherited? what are its effects? what can it predispose to?

Answer 342

* autosomal dominant * mutation of chromosome 3 on the short arm * loss of both copies or tumour suppressor gene * 50% develop RCC that is often bilateral and multifocal * renal and pancreatic cysts as well as cerebellar malignancy also arise

Question 343

what is the pathophysiology of renal cell carcinoma?

Answer 343

- malignant cancer of the proximal convoluted tubular epithelium - spread may be direct (renal vein), via lymph or haematogenous (bone, liver, lung) - 25% have metastases at presentation

Question 344

what is the clinical presentation of renal cell carcinoma?

Answer 344

- often asymptomatic and discovered incidentally - haematuria, loin/flank pain and abdominal mass - anorexia, malaise and weight loss - rarely, invasion of the left renal vein results in the compression of the left testicular vein causing a varicocele - polycythaemia in 5% - hypertension in 30% due to renin secretion by tumour - anaemia due to depression of erythropoietin - fever in around 20%

Question 345

what are differential diagnoses of renal cell carcinoma?

Answer 345

- transitional cell carcinoma - Wilms' tumour - renal oncocytoma - leiomyosarcoma

Question 346

what is used to diagnose a renal cell carcinoma?

Answer 346

- ultrasound (to distinguish cysts from tumour) - CT chest and abdomen with contrast - MRI (for tumour staging) - blood pressure (may be raised due to renin) - bloods - renal biopsy - bone scan (only if there are signs or serum Ca2+ raised)

Question 347

how is CT chest and abdomen with contrast used to diagnose renal cell carcinoma?

Answer 347

* more sensitive than ultrasound in detecting a renal mass and will show involvement of the renal vein of inferior vena cava, if present * using contrast demonstrates kidney function since in normal kidney should see it being taken up and excreted well

Question 348

what is seen in bloods in renal cell carcinoma?

Answer 348

* FBC to detect polycythaemia and anaemia due to EPO decrease * ESR may be raised * liver biochemistry may be abnormal

Question 349

how is localised renal cell carcinoma treated with surgery?

Answer 349

* nephrectomy, unless tumours are bilateral | * if bilateral involvement then partial nephrectomy

Question 350

what are ablative techniques used to treat renal cell carcinoma?

Answer 350

* cryoablation and radiotherapy are used in patients with significant comorbidities who would not tolerate surgery * can harm kidney function

Question 351

what is the treatment of malignant or locally advanced renal cell carcinoma?

Answer 351

* interleukin-2 and interferon alpha produce remission in 20% * biological angio-genesis targeted therapy: sunitinib, bevacizumab and sorafenib * temsirolimus (mTOR inhibitor) found to improve survival more than interferon * last 2 options given if patients do not respond to 1st

Question 352

what is Wilms' tumour?

Answer 352

* childhood tumour of the primitive renal tubules and mesenchymal cells * seen within the first 3 years of life; it is the chief abdominal malignancy in children

Question 353

what is the presentation of Wilms' tumour?

Answer 353

presents as an abdominal mass and less commonly with haematuria

Question 354

what is the diagnosis and treatment of Wilms' tumour?

Answer 354

* diagnosis is established by ultrasound, CT and MRI | * treated with a combination of nephrectomy, radiotherapy and chemotherapy

Question 355

what is bladder cancer? what is affected?

Answer 355

* type of transitional cell carcinoma (TCC) * TCCs are responsible for 3% of deaths from all forms of malignancy * the calyces, renal pelvis, ureter, bladder and urethra are all lined by transitional epithelium and are all susceptible to transitional cell carcinoma * bladder tumours are the most common TCC

Question 356

what is the epidemiology of bladder cancer?

Answer 356

- bladder tumours account for 50% of TCC’s - 4th most common cancer in men - 8th most common cancer in women - more common in males than females - incidence peaks in the 8th decade - most commonly occurs after the age of 40 yrs

Question 357

what are risk factors for bladder cancer?

Answer 357

- smoking - occupational exposure to carcinogens - exposure to drugs e.g. phenacetin and cyclophosphamide - chronic inflammation of urinary tract e.g. schistomiasis (usually associated with squamous carcinoma) or indwelling catheter - > 40 yrs - male - family history

Question 358

what carcinogens can cause bladder cancer?

Answer 358

* beta-napthylamine, benzidine, azo dyes | * workers in the petroleum, chemical, cable and rubber industries are at risk

Question 359

what is the tumour spread of bladder cancer?

Answer 359

* local → to pelvic structures * lymphatic → to iliac and para-aortic nodes * haematogenous → to liver and lungs

Question 360

what is the clinical presentation of bladder cancer?

Answer 360

- painless haematuria; most common symptom however, pain may result due to clot retention - any patient over 40 presenting with haematuria should be assumed to have a urothelial tumour until proven otherwise - recurrent UTI’s - voiding irritabiliity

Question 361

what are differential diagnoses of bladder cancer?

Answer 361

- haemorrhagic cystitis - renal cancer - UTI - urethral trauma

Question 362

what is used to diagnose bladder cancer?

Answer 362

- cytoscopy with biopsy; diagnostic - urine microscopy/cytology; cancers may cause sterile pyruria - CT urogram; provides staging and is diagnostic - urinary tumour markers - MRI/lymphangiography may show involved pelvic nodes - CT/MRI of pelvis

Question 363

what is the treatment of non-muscle invasive bladder cancer? what chemotherapy is used?

Answer 363

- surgical resection | - and/or chemotherapy: mitomycin, doxorubicin, cisplatin, to reduce recurrence

Question 364

what is the treatment of localised muscle invasive disease? what chemotherapy is used?

Answer 364

- radical cystectomy; gold standard - post-op chemotherapy: m-vac; methotrexate, vinblastine, adriamycin and cisplatin - radical radiotherapy if not fit for surgery - chemotherapy: CMV; cisplatin, methotrexate, vinblastine

Question 365

what is m-vac chemotherapy?

Answer 365

methotrexate, vinblastine, adriamycin and cisplatin

Question 366

what is CMV chemotherapy?

Answer 366

cisplatin, methotrexate, vinblastine

Question 367

what is the treatment of metastatic bladder cancer?

Answer 367

palliative chemotherapy and radiotherapy

Question 368

what are features of prostatic carcinomas?

Answer 368

* commonest male malignancy * the majority of prostate cancers are adenocarcinomas arising in the peripheral zone of the prostate gland * most are slow growing but some can be aggressive * most common site of metastases is the bone and lymph nodes * malignant change becomes more common with age

Question 369

what is the most common cancer in men?

Answer 369

prostatic carcinoma

Question 370

what is the epidemiology of prostatic carcinoma?

Answer 370

- accounts for 7% of all cancers in men and is the 6th most common in the world - incidence increases with age - by the age of 80 yrs, 80% of men have malignant foci within the gland but most of these appear to lie dormant - more common in black people due to higher testosterone

Question 371

what are risk factors for prostatic carcinoma?

Answer 371

- family history - genetics - increasing age - black - hormonal factors - if one first-degree relative has prostate cancer then risk is doubled (3 or more affected relatives or 2 relatives who have developed early onset)

Question 372

how does genetics act as a risk factor for prostatic carcinoma?

Answer 372

* HOXB13 is a predisposition gene | * BRCA2 confers a 5-7 times higher risk

Question 373

what is the spread of prostate cancer?

Answer 373

spread may be: • local → seminal vesicles, bladder and rectum • lymph • haematogenously; bone (sclerotic bony lesions) or less commonly brain, liver and lung

Question 374

what is the clinical presentation of prostate cancer? which ones suggest metastasis?

Answer 374

- LUTS if there is local disease: • nocturia • hesitancy • poor stream • terminal dribbling • obstruction - bladder outflow problems similar to BPH e.g. urinary retention - weight loss, bone pain and anaemia suggest metastasis

Question 375

what are differential diagnoses of prostate cancer?

Answer 375

BPH, prostatitis, bladder tumours

Question 376

what is used to diagnose prostate cancer?

Answer 376

- DRE (hard, irregular prostate) - raised PSA (can be normal in 30% cancers) - if metastatic then will be >16ng/ml - trans-rectal ultrasound and biopsy (diagnostic; uses Gleason score) - urine biomarkers e.g. PCA3 or gene fusion protein - endorectal coil MRI to locally stage tumour

Question 377

what is treatment of prostate cancer that's confined to the prostate?

Answer 377

* radical prostatectomy if <70yrs; excellent disease free survival * radiotherapy + hormone therapy; alternative to surgery * brachytherapy; implantation of radioactive material targeted at tumour * hormone therapy temporarily delays tumour progression * active surveillance if >70yrs and low risk

Question 378

what endocrine therapy is used to treat prostate cancer?

Answer 378

- prostate cancer is the most hormone-sensitive malignancy - binding at the androgen receptor stimulates tumour growth - androgen deprivation

Question 379

what are types of androgen deprivation treatments used for prostate cancer?

Answer 379

- orchidectomy (removal of testes) - LHRH agonists - androgen receptor blockers

Question 380

what are examples of LHRH agonists?

Answer 380

SC goserelin or SC leuprorelin

Question 381

what are features of LHRH agonists?

Answer 381

- they first stimulate and then inhibit the pituitary gonadotrophin, testosterone - due to this they can lead to an initial surge in testosterone which can lead to a tumour ‘flare’ and short worsening of symptoms and an anti-androgen e.g. oral cyproterone acetate is used

Question 382

what is an example of androgen receptor blocker?

Answer 382

bicalutamide

Question 383

what are the side effects of androgen receptor blockers?

Answer 383

weakness, nausea, hot flushes, weight changes

Question 384

what is the treatment of symptomatic prostate cancer?

Answer 384

- analgesia - treat hypercalcaemia - radiotherapy for bone metastases/spinal cord compression

Question 385

what is the epidemiology of testicular tumours?

Answer 385

- most common cancer in males aged 15-44 yrs - 10% occur in undescended testes - more than 96% arise from germ cells - 4% arise from non-germ cells

Question 386

what are testicular tumours that arise from germ cells?

Answer 386

* seminomas - 25-40 yrs and 60 yrs | * teratomas - infancy

Question 387

what are testicular tumours that arise from non-germ cells?

Answer 387

* leydig cell tumours * sertoli cell tumours * sarcomas

Question 388

what are risk factors for testicular tumours?

Answer 388

- undescended testis - infant hernia - infertility - family history

Question 389

what is the clinical presentation of testicular tumours?

Answer 389

- painless lump in testicle - testicular pain and/or abdominal pain - hydrocele - cough and dyspnoea is indicative of lung metastases - back pain is indicative of para-aortic lymph node metastasis - abdominal mass

Question 390

what are differential diagnoses of testicular tumours?

Answer 390

testicular torsion, lymphoma, hydrocele, epididymal cyst

Question 391

what is used to diagnose testicular tumours?

Answer 391

- ultrasound (differentiates between masses and swellings and tumours) - biopsy and histology - serum tumour markers (alpha-fetoprotein and/or beta-hCG) - CXR and CT to assess tumour staging

Question 392

what levels of serum tumour markers are seen in different testicular tumours?

Answer 392

- raised AFP and B-hCG in teratomas - B-hCG in minority of those with seminomas - AFP is not elevated in those with pure seminomas

Question 393

what is treatment of testicular tumours?

Answer 393

- radical orchidectomy via inguinal approach - seminomas with metastases below diaphragm are only treated with radiotherapy - more widespread tumours are treated with chemotherapy - teratomas treated with chemotherapy - sperm storage offered

Question 394

what is a urinary tract infection? what is it defined as?

Answer 394

* the inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriuria and pyuria * defined as > 10^5 organisms/ml or fresh mid-stream urine

Question 395

what 5 pathogens account for nearly all isolate from primary care for UTI? (KEEPS)

Answer 395

KEEPS: - Klebsiella spp. - E.coli (most common) - Entercocci - Proteus spp. - Staphylococcus spp

Question 396

how are UTIs classified?

Answer 396

- lower urinary tract vs upper - uncomplicated vs complicated - single/isolated vs unresolved - acute vs chronic

Question 397

what surface attachment molecules do UPECs have?

Answer 397

* fimbriae/pilli * afimbrial attachments e.g. glycocalix * acid polysaccharide coat that resists phagocytosis

Question 398

what do bacteria adhere to in UTIs?

Answer 398

* urothelium * vaginal epithelium * vaginal mucus

Question 399

when are there higher rates of adhesion of bacteria to cause UTIs?

Answer 399

* oestrogen depletion due to the loss of lactobacilli and pH change (seen post-menopause where pH rises and there is increased colonisation by colonic flora and reduction in vaginal mucus secretion) * those with HLA-A3 blood group antigen tend to have recurrent UTIs

Question 400

how do bacteria avoid host defences?

Answer 400

* capsule to resist phagocytosis, toxins (E.coli) and enzyme production (Proteus secretes urease) * adhere to urothelium, vaginal epithelium and vaginal mucus

Question 401

what are some Gram negative bacteria that secrete urease?

Answer 401

Proteus, Klebsiella and Pseudomonas

Question 402

what are some Gram positive bacteria that secrete urease?

Answer 402

Staphylococci and Mycoplasma

Question 403

what are host defence mechanism against UTIs?

Answer 403

- antegrade flushing of urine - Tamm-Horsfall protein has antimicrobial properties - low urine pH and high osmolarity - urinary IgA

Question 404

what are types of UTI?

Answer 404

* pyelonephritis * cystitis (bladder) * prostatitis * epididymo-orchitis * urethritis

Question 405

what is secreted by the proximal tubules?

Answer 405

- medications | - ammonium (via breakdown of glutamine to alpha-ketoglutarate, generating ammonium and bicarbonate ions)

Question 406

l

Answer 406

l

Question 407

what are features of chronic urine retention?

Answer 407

* more insidious and may be painless * more difficult to define * incomplete bladder emptying * results in a increased risk of infection * can be low pressure with detrusor failure * can be high pressure with risk of interactive obstructive uropathy

Question 408

what is a complicated UTI? what are features of treatment and complications?

Answer 408

- infection in patients with abnormal urinary tract e.g. stones, obstruction or systemic disease involving the kidney e.g. diabetes mellitus, sickle-cell, or virulent organism e.g. Staphylococcus Aureus - treatment failure is more likely - complications are more likely e.g. renal papillary necrosis and renal abscess - majority of UTI’s in men are considered complicated, associated with urological abnormalities such as bladder outlet obstruction

Question 409

what is the epidemiology of UTIs?

Answer 409

more common in women - affects 1/3rd in lifetime

Question 410

what are risk factors for UTIs?

Answer 410

- female - sex - pregnancy - menopause - decrease in host defence - urinary tract obstruction resulting in urine stasis - catheter

Question 411

what is the pathogenesis of UTIs?

Answer 411

- infection of urinary tract via the ascending transurethral route; sex and urethral catheter contribute - women are most susceptible due to shorter urethra and proximity to anus facilitates the transfer of bowel organisms to bladder - E.coli is the most common cause and arises from patients own flora

Question 412

what is pyelonephritis?

Answer 412

infection of the renal parenchyma and soft tissues of renal pelvis and upper ureter

Question 413

what are the main organisms causing pyelonephritis?

Answer 413

``` KEEPS • Klebsiella spp. • E.coli - majority • Enterococcus spp. • Proteus spp. • Staphylococcus spp - coagulase negative ```

Question 414

what is the epidemiology of pyelonephritis?

Answer 414

- predominantly affects females under 35 yrs - associated with significant sepsis and systemic upset - unusual in men - mainly caused by uropathogenic E.coli, typically with P pilli on surface to all ureteral ascent

Question 415

what are risk factors for pyelonephritis?

Answer 415

- structural renal abnormalities - calculi (stones) - catheterisation - pregnancy - diabetes - immunocompromised patient

Question 416

what is the pathophsyiology of pyelonephritis? how is it spread?

Answer 416

- infection is mostly due to bacteria (primarily E.coli) from own patients bowel flora - most commonly spread via the ascending transurethral route but can be via the bloodstream or lymphatics

Question 417

what are the adhesive factors of E. coli?

Answer 417

* P pilli to allow ureteral ascent * aerobactin - for Fe acquisition * haemolysin- for pore formation

Question 418

what is the triad of common symptoms in pyelonephritis?

Answer 418

loin pain, fever and pyuria

Question 419

what is the clinical presentation of pyelonephritis?

Answer 419

- triad of: loin pain, fever and pyuria - may have severe headache - rigors - significant bacteriuria - malaise, nausea, vomiting - oliguria (small amounts of urine) if it causes AKI

Question 420

what are differential diagnoses of pyelonephritis?

Answer 420

diverticulitis, abdominal aortic aneurysm, kidney stones, cystitis, prostatitis

Question 421

what is used to diagnose pyelonephritis?

Answer 421

- tender loin on examination - urine dipstick - midstream urine microscopy, culture and sensitivity; gold standard for diagnosis - bloods - urgent ultrasound

Question 422

what are features of pyelonephritis on urine dipstick?

Answer 422

* nitrites, released by bacteria breaking down nitrates * leucocyte elastase * foul-smelling urine * protein

Question 423

what is seen on bloods in pyelonephritis?

Answer 423

* FBC shows elevated white cell count | * CRP and ESR may be raised in acute infection

Question 424

what is the treatment of pyelonephritis?

Answer 424

- rest - cranberry juice and lots of water - analgesia - antibiotics - surgery to drain abscesses or relieve calculi that are causing infection

Question 425

what antibiotics are used to treat pyelonephritis?

Answer 425

- oral ciprofloxacillin or oral co-amoxiclav | - if severe then IV gentamicin or IV co-amoxiclav

Question 426

what is the epidemiology of cystitis?

Answer 426

urinary infection of the bladder - much more common in women - can occur in children - most common cause is E.coli

Question 427

what are risk factors for cystitis?

Answer 427

- urinary obstruction resulting in urinary stasis - previous damage to bladder epithelium - bladder stones - poor bladder emptying

Question 428

what is the clinical presentation of cystitis?

Answer 428

- dysuria - frequency - urgency - suprapubic pain - haematuria - offensive smelling/cloudy urine - abdominal/loin tenderness

Question 429

what is used to diagnose cystitis? what is seen in a urine dipstick?

Answer 429

- gold standard is microscopy and sterile midstream urine sample - dipstick urinalysis: positive leucocytes, blood and nitrites

Question 430

what are the first and second-line antibiotic treatments for cystitis?

Answer 430

1st: trimethoprim or cefalexin 2nd: ciprofloxacin or co-amoxiclav

Question 431

what is prostatitis?

Answer 431

* infection and inflammation of the prostate gland | * can be acute or chronic

Question 432

what is the epidemiology of prostatitis?

Answer 432

- common in men of all ages - most common UTI in men < 50 - usually presents > 35 yrs - associated with LUTS

Question 433

what are causes of acute and chronic prostatitis?

Answer 433

* bacterial e.g. Streptococcus faecalis, E.coli or Chlamydia | * non-bacterial e.g. elevated prostatic pressure, pelvic floor myalgia

Question 434

what are the risk factors for prostatitis?

Answer 434

- STI - UTI - indwelling catheter - post-biopsy - increasing age

Question 435

what is the clinical presentation of acute prostatitis?

Answer 435

* systemically unwell * fever, rigors, malaise * pain on ejaculation * significant voiding LUTS e.g. poor intermittent stream, hesitancy, incomplete emptying, post micturition dribbling, straining, dysuria * pelvic pain

Question 436

what is the clinical presentation of chronic prostatitis?

Answer 436

* acute symptoms for > 3 months * recurrent UTIs * pelvic pain

Question 437

what are the differential diagnoses of prostatitis?

Answer 437

cystitis, BPH, calculi, bladder neoplasia, prostatic abscess

Question 438

what is used to diagnose prostatitis?

Answer 438

- DRE - urine dipstick is positive for leucocytes and nitrites - mid-stream urine microscopy and sensitivity - blood cultures - sexually transmitted infection screen, for chlamydia in particular - trans-urethral ultrasound scan

Question 439

what is seen on DRE in prostatitis?

Answer 439

* prostate is tender or hot to touch | * hard from calcification

Question 440

what is the treatment of acute prostatitis? what drugs are given?

Answer 440

* IV gentamicin + IV coamoxiclav or IV tazocin or IV carbapenem * 2-4 weeks on a quinolone e.g. ciprofloxacin (antibiotic) once well * second line - trimethorpin * TRUSS guided abscess drainage if necessary

Question 441

what is the treatment of chronic prostatitis?

Answer 441

* 4-6 week course of quinolone e.g. ciprofloxacin (antibiotic) * but they don’t tend to respond as well to antibiotics * +/- alpha-blocker * NSAIDs

Question 442

what is urethritis?

Answer 442

* urethral inflammation due to infectious or non-infectious causes * primarily a sexually acquired disease

Question 443

what is the epidemiology of urethritis?

Answer 443

- most common condition diagnosed and treated in men at GUM clinics - non-gonococcal urethritis is the more common than gonococcal urethritis - chlamydia is the most common STI in young people aged 15-24 yrs

Question 444

what is the most common STI in young people aged 15-24?

Answer 444

Chlamydia

Question 445

what are the infective causes of urethritis?

Answer 445

- Neisseria gonorrhoea - Chlamydia trachomatis (most common cause) - Mycoplasma genitalium - Ureaplasma urealyticum - Trichomonas vaginalis

Question 446

what are non-infective causes of urethritis?

Answer 446

- trauma - urethral stricture - irritation - urinary calculi

Question 447

what are the risk factors for urethritis?

Answer 447

- sexually active - unprotected sex - male to male sex - being male

Question 448

what is the clinical presentation of urethritis?

Answer 448

- may be asymptomatic (90-95% with gonorrhoea, 50% of patients with chlamydia) - dysuria (painful urination) +/- discharge; blood or pus - urethral pain - penile discomfort - skin lesions - systemic symptoms

Question 449

what are differential diagnoses of urethritis?

Answer 449

Candida balantis, epididymitis, cystitis, acute prostatitis, urethral malignancy

Question 450

what is used to diagnose urethritis?

Answer 450

- nucleic acid amplification test - microscopy of gram-stained smears of genital secretions - blood cultures - urine dipstick to exclude UTI - urethral smear

Question 451

how is nucleic acid amplification test used to diagnose urethritis?

Answer 451

* female: self collected vaginal swab, endocervical swab, first void urine * male: first void volume * high specificity and sensitivity

Question 452

what is epididymo-orchitis? what is it mainly caused by?

Answer 452

- acute epididymo-orchitis is a clinical syndrome of pain, swelling and inflammation of the epididymis that can extend into the testis - caused mainly by the extension of infection from the urethra or bladder

Question 453

what is the epidemiology of epididymo-orchitis?

Answer 453

most common in male 15-30 yrs olds and those over 60

Question 454

what are the infective causes of epididymo-orchitis for those under 35 years?

Answer 454

* Chlamydia trachomatis | * Neisseria gonorrhoea

Question 455

what are the infective causes of epididymo-orchitis for those over 35 years?

Answer 455

UTI - KEEPS: - Klebsiella spp - E.coli (most common) - Enterococci - Pseudomonas - Staphylococcus - coagulase negative

Question 456

what are the non-infective causes of epididymo-orchitis?

Answer 456

- mumps - trauma - in elderly its predominantly catheter related

Question 457

what are risk factors for epididymo-orchitis?

Answer 457

- previous infection - indwelling catheter - structural/functional abnormality of urinary tract - anal intercourse

Question 458

what is the clinical presentation of epididymo-orchitis? what is seen on examination?

Answer 458

- subacute onset of unilateral scrotal pain and swelling - in STD epididymo-orchitis there may be urethritis or urethral discharge - mumps usually presents with headache, fever and unilateral or bilateral parotid swelling - sweats/fever - on examination there is tenderness and palpable swelling of the epididymis and testicles

Question 459

what are differential diagnoses of epididymo-orchitis?

Answer 459

testicular torsion, hydrocele, trauma, abscess formation

Question 460

how should testicular torsion be differentiated from epididymo-orchitis? what are features that are suggestive of tosion?

Answer 460

``` • must rule this out • if in any doubt then do surgical scrotal exploration • features suggestive of torsion: - short duration of pain - sudden onset - associated nausea/abdominal pain - high-riding/bell-clapper testis ```

Question 461

what is used to diagnose epididymo-orchitis?

Answer 461

- nucleic acid amplification test - mid-stream urine dipstick for UTI symptoms - ultrasound to rule out abscesses - STD screening - urethral smear and swab

Question 462

what is the treatment of epididymo-orchitis?

Answer 462

- chlamydia: oral doxycycline 7 days or stat azithromycin - gonorrhoea: IM ceftriazone and stat oral azithromycin - UTI: oral ciprofloxacin or oral ofloxacin - antibiotics should be used for 2-4 weeks - analgesia - NSAIDs e.g. ibuprofen - scrotal support - supportive underwear - abstain from sexual intercourse - partner notification and testing

Question 463

what organism causes Chlamydia?

Answer 463

Chlamydia trachomatis

Question 464

what organism causes Gonorrhoea?

Answer 464

Neisseria gonorrhoea

Question 465

what is the epidemiology of Chlamydia vs Gonorrhoea?

Answer 465

* Chlamydia is more common in women and 15-25yr olds * Gonorrhoea is more common in men and is less common than chlamydia * asymptomatic carriage of chlamydia is much more common than gonorrhoea

Question 466

where are sites of occurrence of Chlamydia and Gonorrhoea in the adult?

Answer 466

* urethra * endocervical canal * rectum * pharynx * conjunctiva

Question 467

where are sites of occurrence of Chlamydia and Gonorrhoea in the neonate?

Answer 467

* conjunctiva | * atypical pneumonia

Question 468

what are features and intubation of CT and GC in males?

Answer 468

- primary site of infection is urethra - dysuria and urethral discharge (mainly gonorrhoea) - CT: 7-21 days - GC: 2-5 days

Question 469

what are features of asymptomatic CT and GC in males?

Answer 469

* CT - at least 50% - more likely to be asymptomatic thus more likely to get complications since undetected and thus untreated for longer * GC - 10%; 90% men have symptoms

Question 470

what is the transmission of CT and GC from female to male?

Answer 470

* CT - 70% | * GC - 60-80% (20% if single encounter)

Question 471

what are features and intubation of CT and GC in females?

Answer 471

- primary site of infection is cervix - non-specific symptoms of dysuria, menstrual irregularity and discharge - CT: ill-defined - GC: up to 10 days

Question 472

what are features of asymptomatic CT and GC in females?

Answer 472

* CT - over 70% | * GC - 50%

Question 473

what is the transmission of CT and GC from males to females?

Answer 473

* CT - 70% | * GC - 50-90%

Question 474

what are complications of CT and GC in females?

Answer 474

- pelvic inflammatory disease - neonatal transmission - Fitz Hugh Curtis syndrome; peri-hepatitis but no decline in liver function

Question 475

what are features of pelvic inflammatory disease as a complication of CT and GC?

Answer 475

- infection spreads up to the fallopian tube leading to inflammation and scarring - tubular factor infertility - ectopic pregnancy - chronic pelvic pain

Question 476

how is Chlamydia diagnosed?

Answer 476

* often diagnosed in established relationships since there is a long asymptomatic carriage * Nucleic Acid Amplification Tests: high specificity and sensitivity, but negative test doesn't mean non-infection

Question 477

how is Gonorrhoea diagnosed?

Answer 477

* associated with recent partner change * near patient testing * culture on selective medium to confirm * antibiotic sensitivity testing * NAAT

Question 478

how is near patient testing used to diagnose Gonorrhoea?

Answer 478

- microscopy of gram stained smears of genital secretions, looking for gram negative diplococci - males; sample from urethra - females; sample from endocervix

Question 479

what is the treatment of Chlamydia? what drugs are used?

Answer 479

* partner management * test for other STIs * oral azithromycin stat (convenient - just 1 dose) or oral doxycycline for 7 days (less convenient, but more effective)

Question 480

what is the treatment of Chlamydia in pregnant women?

Answer 480

erythromycin for 14 days or azithromycin stat

Question 481

what is the treatment for Gonorrhoea? what drugs are given?

Answer 481

* partner notification * test for other STIs * continuous surveillance of antibiotic sensitivity * single dose treatment is preferred * IM ceftriaxone with azithromycin stat

Question 482

what is the neural control of the lower urinary tract?

Answer 482

- parasympathetic (cholinergic); S3 ,S4 and S5: • drives detrusor contraction - sympathetic (noradrenergic); T10, L1, L2: • urethral contraction (smooth muscle component but remember the main part of the sphincter is skeletal muscle) • inhibits detrusor contraction

Question 483

in which gender is urinary incontinence more common in?

Answer 483

females

Question 484

what is stress incontinence?

Answer 484

- caused by sphincter weakness | - small leak of urine when intra-abdominal pressure rises e.g. when coughing, laughing and standing up

Question 485

what are the causes of stress incontinence?

Answer 485

* women; secondary to birth trauma * men; post-prostatectomy * neurogenic or congenital

Question 486

what is the treatment of stress incontinence in females?

Answer 486

- pelvic floor exercises - duloxetine - surgery: sling, artificial sphincter

Question 487

what is the treatment of stress incontinence in males?

Answer 487

artificial sphincter or male sling

Question 488

what are the causes of urge incontinence?

Answer 488

* detrusor overactivity; rise in detrusor pressure on filling associated with urgency (most common in women) * less commonly by bladder hypersensitivity from local pathology e.g. UTI, bladder stones or tumour

Question 489

what is the treatment of urge incontinence?

Answer 489

* bladder exercises; gradually increasing the interval between voids * behavioural therapy; controlling caffeine, alcohol and frequency volume charts * drugs * surgery

Question 490

what drugs are used to treat urge incontinence?

Answer 490

- anticholinergic agents - beta3 agoinst e.g. mirabegron - botox of bladder

Question 491

what is an example of a beta3 agonist?

Answer 491

mirabegron

Question 492

what are surgical treatments of urge incontinence?

Answer 492

- detrusor myectomy | - cystoplasty

Question 493

how is cystoplasty used to treat urge incontinence?

Answer 493

- adding some bowel to bladder to increase surface area - gives increased bladder capacity and reduced detrusor overactivity - may have to self-catheterise due to muscle loss

Question 494

what spinal reflexes control the bladder?

Answer 494

- reflex bladder control from sacral micturition centre | - guarding reflex

Question 495

what is the guarding reflex?

Answer 495

proximal part of sphincter senses urine and sends impulse to spinal cord to tell Onuf’s nucleus to store urine

Question 496

what is the effect of a spastic spinal cord injury on the bladder?

Answer 496

* supra-conal (higher in spinal cord) lesion * loss of co-ordination and completion of voiding * reflexes work but are not controlled by the brain

Question 497

what are features of spastic spinal cord injury?

Answer 497

- reflex bladder contractions - detrusor sphincter dyssynergia; loss of completion of voiding - poorly sustained bladder contraction - potentially unsafe - puts kidneys at risk

Question 498

what is the effect of a flaccid spinal cord injury on the bladder?

Answer 498

conus lesion (lower spinal cord injury) - decentralised bladder

Question 499

what is lost in a flaccid spinal cord injury?

Answer 499

- reflex bladder contraction - guarding reflex - receptive relaxation

Question 500

what are the features of a flaccid spinal cord injury?

Answer 500

- areflexic bladder - stress incontinence - risk of poor compliance - potentially unsafe - puts kidneys at risk

Question 501

what are features of spastic paralysis vs flaccid paralysis?

Answer 501

spastic paralysis: - conus (lower end of spinal cord) functioning but not controlled by the brain - reflex bladder - involuntary urination (i.e. when senses full) - reflex bowel - involuntary defecation flaccid paralysis: - conus destroyed or non-functional - areflexic bladder - fills until it overflows - areflexic bowel - fills until it overflows

Question 502

what are features of autonomic dysreflexia caused by neuropathic bladder problems?

Answer 502

* commonly causes by over-distension of bladder * cccurs in lesions above T6 * overstimulation of sympathetic nervous system below the level of lesion in responses to a noxious stimulus * headache, severe hypertension and flushing

Question 503

what are features of maintaining bladder safety through treatment of neuropathic bladder problems? what could it lead to if not treated?

Answer 503

• an unsafe bladder is one that puts kidneys at risk • risk factors: - raised bladder pressure - vesico-ureteric reflux - chronic infection e.g. residual urine/stones

Question 504

what are features of symptom control of neuropathic bladder problems?

Answer 504

* harness reflexes to empty bladder into incontinence device, but may not keep bladder safe! * suppress reflexes converting bladder to flaccid type and then empty regularly

Question 505

what is the treatment of neuropathic bladder problems?

Answer 505

* alpha adrenergic blockers e.g. oral tamsulosin or sphincterotomy * cystoplasty * permanent catheterisation

Question 506

what is the sepsis 6?

Answer 506

* give high flow-oxygen via non-rebreathe bag * take blood cultures and consider source control * give IV antibiotics * start IV fluid resuscitation * check lactate * monitor hourly urine output and consider catheterisation * within 1 hour

Question 507

what is the use of saline?

Answer 507

* used to replace fluids and try to increase blood pressure | * normal saline is physiologically similar to the normal composition of extracellular fluid

Question 508

what does each litre of normal saline contain?

Answer 508

- around 150mmol of Na+ - around 150mmol of Cl- - around 300mmol of osmotically active ions - virtually no K+

Question 509

what are examples of alpha blockers?

Answer 509

tamsulosin, alfuzosin, doxazocin

Question 510

what are indications for alpha blockers?

Answer 510

- first line treatment for benign prostatic hyperplasia where lifestyle changes are insufficient - can be used alongside 5-alpha reductase inhibitors e.g. finasteride or surgery - can be used to aid passage of kidney stones

Question 511

what are the mechanisms of action of alpha blockers?

Answer 511

- highly selective for the alpha1 adrenoceptor found mainly in smooth muscle including blood vessels and the urinary tract (bladder neck and prostate) - stimulation induces contraction, blockage induces relaxation so thus causes vasodilatation and a fall in blood pressure and a reduced resistance to bladder outflow

Question 512

what are the adverse effects/contraindications of alpha blockers?

Answer 512

- can cause postural hypertension, dizziness and syncope - should not be used in existing hypotension - combining antihypertensives can provide profound effect so omitting doses of other medications when starting can help avoid first dose hypertension

Question 513

what is an example of 5-alpha reductase inhibitors?

Answer 513

finasteride

Question 514

what are indications for 5-alpha reductase inhibitors?

Answer 514

- used for treatment of benign prostatic hyperplasia as an add on to alpha blockers - provides less relief and takes longer for effect

Question 515

what are mechanisms of action of 5-alpha reductase inhibitors?

Answer 515

- 5-alpha reductase is the enzyme that converts testosterone to dihydrotestosterone (active form of testosterone), so blocking this conversion results in a dramatic decrease in serum dihydrotestosterone levels - this reduces prostate volume so improves symptoms of the enlarged prostate and reduces the risk of cancer

Question 516

what are adverse effects/contraindications of 5-alpha reductase inhibitors?

Answer 516

- since this treatment lowers PSA it may hide prostate cancer, there is a possible risk of sexual dysfunction - contraindicated for used in women

Question 517

what are examples of PDE type V inhibitors?

Answer 517

sildenafil

Question 518

what are indications for PDE type V inhibitors?

Answer 518

- erectile dysfunction | - primary pulmonary hypertension

Question 519

what are mechanisms of action of PDE type V inhibitors?

Answer 519

- sildenafil is selective for phosphodiesterase type 5 (PDE5) which is predominantly found in the smooth muscle of the corpus cavernous of the penis and the arteries of the lung - causes vasodilatation by inhibiting PDE5 which is responsible for the breakdown of cyclic GMP, thus increasing cyclic GMP concentrations which then causes arterial smooth muscle relaxation and vasodilation and penile engorgement

Question 520

what are adverse effects/contraindications of PDE type V inhibitors?

Answer 520

- flushing, headache, dizziness, nasal congestion and more seriously, hypotension, tachycardia and palpitations - increased risk of MI and stroke - should be avoided where vasodilatation is dangerous i.e. in recent stroke, acute coronary syndrome or other CVD and should be used with caution in hepatic and renal failure - contraindicated with other drugs that increase nitric oxide i.e. nitrates, since combined effect on cyclic GMP can cause severe vasodilation and cardiovascular collapse

Question 521

what are examples of anti-muscarinics?

Answer 521

oxybutynin, tolterodine

Question 522

what are indications for anti-muscarinics?

Answer 522

to reduce urinary frequency, urgency and urge incontinence in an overactive bladder

Question 523

what are mechanisms of action of anti-muscarinics?

Answer 523

- competitively inhibits acetylcholine, blocking the muscarinic receptors and promoting bladder relaxation to increase capacity - this reduces urgency and frequency of urination - these muscarinics are selective for M3 receptor which is the main receptor in the bladder

Question 524

what are adverse effects/contraindications of anti-muscarinics?

Answer 524

- dry mouth, tachycardia, constipation and blurred vision - contraindicated in UTI, use with care in the elderly as can cause drowsiness - use with care in angle closure glaucoma as can cause rise in intraocular pressure, and in patients with arrhythmias and those at risk of urinary retention

Question 525

what are examples of androgen receptor blockers?

Answer 525

flutamide, bicalutamide, cyproterone acetate

Question 526

what are indications for androgen receptor blockers?

Answer 526

used to treat prostate cancer

Question 527

what are mechanisms of action of androgen receptor blockers?

Answer 527

- anti-androgens decrease the body’s response to androgens so are beneficial in prostate cancer, as the cells require androgen for growth - drug competes with circulating androgens for receptors on prostate cells and promote apoptosis and inhibit growth - can be used as monotherapy or with surgery or chemotherapy

Question 528

what are adverse effects/contraindications for androgen receptor blockers?

Answer 528

- bicalutamide is better tolerated | - GI disturbance and possible liver injury

Question 529

causes of incontinence

Answer 529

* neurogenic detrusor overactivity * stress incontinence ( e.g. straining at the gym)

Question 530

urge incontinance caused by

Answer 530

* overactive bladder - * detrusor overactivity

Question 531

define “overactive bladder”

Answer 531

OAB is defined as urgency with frequency, with or without nocturia, when appearing in the absence of local pathology

Question 532

how is detrusor overactivity detected

Answer 532

using urodynamics

Question 533

why are anticholinergics used to treat an overactive bladder

Answer 533

they inhibit the parasympathetic pathway which is responsible for bladder contraction → relaxation

Question 534

why is mirabegron used in overactive bladder

Answer 534

it is a Beta3 agonist. B3 receptors in the bladder trigger relaxation thus mirabegron promotes relaxation

Question 535

effect of botox on the bladder

Answer 535

can cause urinary retention

Question 536

how is neuromodulation used in overactive bladder

Answer 536

it works on the afferent feedback system to the brain

Question 537

what are the spinal reflexes of the bladder

Answer 537

1. reflex bladder contraction: parasympathetic: S3 2. guarding reflex: rhabdosphincter tries to keep you dry by contracting: somatic innervation: brain control in Onulf's nucleus. 3. receptive relaxation: sympathetic nervous system: S3

Question 538

what happens to bladder in a supra-spinal cord injury

Answer 538

coordination is lost and loss of completion of voiding

Question 539

what is classed as an unsafe bladder

Answer 539

when the bladder puts the kidneys at risk due to: * high pressures in the bladder blocking the ureters preventing the kidneys from draining

Question 540

sacral spinal cord injury

Answer 540

loss of: * reflex bladder contraction * guarding reflex * receptive relaxation → poor compliance → prolonged high pressure in the bladder that can put kidneys at risk.

Question 541

features of sacral spinal cord injury

Answer 541

* areflexic bladder * stress incontinance * risk of poor compliance → risk to kidneys.

Question 542

how do brain conditions affect the bladder

Answer 542

* they maintain a coordinated void but they may still be incontinent

Question 543

what causes an unsafe bladder

Answer 543

prolonged high pressure

Question 544

what's the most common cause of autonomic dysreflexia

Answer 544

a full bladder - look for mechanism of this

Question 545

where does the spinal cord end

Answer 545

L1

Question 546

what are the main continence mechanisms

Answer 546

1. internal sphincter 2. external sprinter 3. pelvic floor muscles 4. prostate in men

Question 547

describe the micturition reflex

Question 548

why can't babies control their wee

Question 549

what surrounds the kidneys

Answer 549

* layers after the kidney are: * renal capsule * perirenal fat * renal fascia * pararenal fat

Question 550

the left kidney is slightly lower down than the right T/F

Answer 550

False the right is lower down due to being pushed by the kidney

Question 551

what vertebral levels are the kidneys found at

Answer 551

T12 - L3 they are ~ 3 vertebrae in length

Question 552

describe adrenal gland vasculature

Answer 552

* arteries x3 * superior artery = branch of the inferior phrenic artery * middle artery = branch of the abdominal aorta * inferior artery = branch of the renal artery * one vein drains the gland = the adrenal vein * the right adrenal vein drains directly into the IVC as its is in close proximity * the left adrenal vein drains into the left renal vein first

Question 553

describe the anatomy of the adrenal glands

Answer 553

* capsule * cortex * zona Glomerulosa * mineraolcorticoids synthesis * Zona Fascicularis * Glucocorticoids synthesis * Zona Reticularis * androgens synthesis * medulla * catecholamine synthesis

Question 554

what doe the renal hilum contain

Answer 554

* renal vein * renal artery * lymphatics * nerves * ureters

Question 555

describe the renal vasculature

Answer 555

* right and left renal arteries from the abdominal aorta * right and left renal veins that drain directly into the IVC * the right vein is shorter than the left

Question 556

where do the right and left gonadal veins drain into

Answer 556

right drains directly into IVC left drains into left renal vein first

Question 557

Describe the anatomy of the internal kidney

Answer 557

* cortex around the outside * medulla in the middle * arranged into pyramids * calyces * minor calyces → major calyces → renal pelvis → ureter

Question 558

what is a nephron

Answer 558

a functional unit of the kidney

Question 559

how is the nephron arranged within the kidney - where do the separate structure lie

Answer 559

* the glomerulus, Bowman's capsule, proximal and distal tubules and part of the collecting duct are in the cortex * the loop of henle and the rest of the collecting duct are in the renal pyramids

Question 560

what is the renal papilla and what is its function

Answer 560

the apex of the medulla it is the opening into a minor calyx for outflow of urine

Question 561

explain the pathway of the ureter

Answer 561

it passes from the kidney to the bladder and travels behind the numerous arteries including the uterine and ovarian arteries. “water under the bridge”

Question 562

urine is transported in the ureters by peristalsis T/F

Answer 562

True they have muscular walls

Question 563

describe the passage of blood in the kidneys starting from the abdominal aorta

Answer 563

Abdominal aorta → renal artery → segmental arteries → interlobular arteries → arcuate arteries → afferent arteriole → Glomerulus → efferent arteriole → peritubular capillaries → interlobular veins → Arcuate vein → interlobular vein → renal vein → IVC

Question 564

What are the functions of the kidney

Answer 564

A WET BED * Acid/base balance * Water removal * Erythropoietin * Toxins * Blood Pressure * Electrolyte * D - vitamin D activation

Question 565

how much of the cardiac output goes to the kidneys

Answer 565

20%

Question 566

what is glomerular filtration rate

Answer 566

The volume of fluid filtered through the from the glomerulus to the bowman's space Glomerulus = the collection of capillaries carrying blood to filtered bowman's capsule = the space into which filtrate is captured

Question 567

why is there no oncotic pressure of the Bowmas capsule

Answer 567

there are no proteins in bowmans space

Question 568

why is creatinine used as a marker substance

Answer 568

* it's freely filtered * not secreted or reabsorbed * not metabolised

Question 569

what factors affect GFR

Answer 569

1. Pressure 2. Size of the molecule 3. Charge of the molecule 4. Blood flow 5. Binding to plasma proteins

Question 570

describe the physiology of glomerular filtration and urine production

Answer 570

1. the glomerular capillaries are fenestrated, meaning they have gaps to allow molecules in the blood to be filtered out, everything except RBCs. * the endothelial cells have glycocaelyx - proteins - which are -vely charged to repel the passage of proteins [also -vely charged] through. 2. the afferent arteriole dilates while the efferent one constricts which raises the hydrostatic pressure exerted on the blood in the glomerulus → ultrafiltration. 3. the filtrate passes into Bowman’s capsule and is basically protein free plasma. 4. as the filtrate moves through the tubules, certain substances are **reabsorbed** either by diffusion or by mediated transport[ATP] 5. whats left enters the collecting duct into the calyces to form the urine

Question 571

how is GFR controlled

Answer 571

* To increase GFR; * Constrict the efferent arteriole (build up pressure before)•Dilate the afferent arteriole (builds up pressure after) * To decrease GFR; * Constrict the afferent arteriole (reduce blow flow)•Dilate the efferent arteriole (allows blood to escape easier)

Question 572

what is the glomerular filter layers made of

Answer 572

1. fenestrated endothelial cells 2. basement membrane * made from fusion of capillary and podocyte basement membrane. 3. podocytes

Question 573

what are the mechanisms of autoregulation within the glomerulus

Answer 573

* **Myogenic**; smooth muscle contraction in response to external stretching force, occurs in capillary walls, passive mechanism * **Tubuloglomerular feedback**; * constriction of afferent arteriole to increased sodium chloride concentration. * Dilation in response to decreased concentration. * Fast response via GFR and slow via RAAS

Question 574

explain tubuloglomerular feedback

Answer 574

1. GFR of individual nephron regulated by the rate at which filtered fluid reaches the distal tubule 2. Cells of **macula densa** (distal tubule) detect NaCl arrival 3. Macular densa cells release **prostaglandins** in response to reduced NaCl delivery. 4. This acts on **granular** cells, triggering **renin** release, activating the **renin-angiotensin system**

Question 575

protein is never found in the urine T/F

Answer 575

False * The only protein that is normally found in urine is Tamm– Horsfall protein (uromodulin) which is produced by the thick ascending limb * otherwise other proteins shouldnt be present in the urine and indicate leaky nephrons

Question 576

what is the filtration fraction

Answer 576

* **Filtration Fraction = GFR / Renal Plasma Flow** * i.e. the proportion that gets filtered.

Question 577

what is renal clearance

Answer 577

renal clearance is the volume of plasma completely cleared of a substance by the kidneys per unit time.

Question 578

main function of the proximal tubule

Answer 578

* **bulk reabsorption of essentials:** * Na+ * Cl- * water * glucose * bicarbonate * amino acids * phosphate * lactate * **⅔ of all filtrate reabsorbed here**

Question 579

how is glucose reabsorbed in the PCT

Answer 579

* via SGLT1 and SGLT2 transporters * these a co transporters that carry Na+ and glucose into the cell * SGLT1= 2Na+ and 1glucose * SGLT2=1Na+ and 1glucose * glucose reenters the blood passively via GLUT channels

Question 580

what is autoregulation in the kidneys and why is it important

Answer 580

**Pressure within afferent arteriole rises → stretches vessel wall → triggers contraction of smooth muscle → arteriolar constriction** * important because it prevents a rise in systemic arterial pressure reaching the capillaries in the nephron THUS it prevents damage and maintains constant level of filtration * revers happens in low pressure to maintain a constant rate of filtration

Question 581

main function of the loop of Henle

Answer 581

* Descending limb = H20 reabsorption * ascending limb = Na, Cl and K reabsorption

Question 582

function of the distal convoluted tubule

Answer 582

* “fine tuning” of sodium reabsorption, potassium and acid-base balance * impermeable to water * Macula densa located in juxtaglomerular apparatus which is in the DCT- * detects [Na+] and can activate RAAS.

Question 583

function os the collecting duct

Answer 583

* Collecting duct mediates water reabsorption and maintains acid base homeostasis * Principal cells - Na and water reabsorption and K excretion * site of ADH action * Intercalated cells (alfa and beta) – secrete H or HCO3 * •Essential for acid base homeostasis

Question 584

what is the normal pH range for blood

Answer 584

* 7.35-7.45 * Acidosis: pH\<7.35 * Alkalosis: pH\>7.45

Question 585

where is the juxtaglomerular apparatus located and what is it composed of

Answer 585

located in the distal convoluted tubule next to the glomerulus * macula densa cells * granular cells * afferent arteriole * distal convoluted tubule

Question 586

where are juxtaglomerular cells located

Answer 586

in the walls of the afferent arteriole

Question 587

what is RAAS

Answer 587

The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system within the body that is essential for the regulation of blood pressure and fluid balance

Question 588

what stimulates the RAAS

Answer 588

* decreased blood pressure * detected by little or no arteriolar stretch (from low blood volume due to low Na+ and thus H2O). * decreased NaCl detected in the macula densa cells * sympathetic innervation when any of these happens, then renin is released by the juxtaglomerular cells in the afferent arterioles

Question 589

what is renin and what does it do

Answer 589

an enzyme cleaves angiotensinogen → angiotensin1

Question 590

where is angiotensinogen produced

Answer 590

the liver

Question 591

where is ACE produced

Answer 591

in the pulmonary and renal endothelium

Question 592

what are the effects of angiotensin 2

Answer 592

1. **stimulates the adrenal gland → aldosterone secretion** * increases reabsotption of salt and water * increases K+ excretion 2. **stimulates the posterior pituitary gland → ADH secretion →** more conc. urine 3. **stimulates vasoconstriction of systemic arteries and arterioles** 4. **stimulates thirst in the hypothalamus** 5. **increases total peripheral resistance thus raises BP** 6. **stimulates sympathetic nervous system** to increase release of noradrenaline * Increase in cardiac output. * Vasoconstriction of arterioles. * Release of renin.

Question 593

where is ADH produced

Answer 593

hypothalamus

Question 594

which cells does ADH take effect in

Answer 594

principal cells of the collecting duct

Question 595

what effect does ADH have

Answer 595

1. it binds to the V2R receptors of the principal cells → 2. upregulation of aquaporin channels in the collecting tubule walls → 3. increased H2O reabsorption and less urine produced

Question 596

where is erythropoietin produced what is its function

Answer 596

in the kidneys increases production of RBCs in the bone marrow

Question 597

what hormones are produced in the adrenal glands

Answer 597

1. Aldosterone 2. cortisol 3. corticosterone 4. DHEA 5. androstenedione 1= glomerulosa 2+3=fasciculata 4+5 = reticularis

Question 598

what is the role of the adrenal medulla

Answer 598

* part of the autonomic nervous system * production of catecholamines * adrenaline 80% and noradrenaline20% * main site for adrenaline synthesis * production of catecholamines is dependent on cortisol levels [permissive effect]

Question 599

what is the role of the adrenal medulla

Answer 599

* part of the autonomic nervous system * production of catecholamines * adrenaline 80% and noradrenaline20% * main site for adrenaline synthesis * production of catecholamines is dependent on cortisol levels [permissive effect]

Question 600

TRUE or FALSE creatinine production is equivalent to creatinine excretion

Answer 600

True - this makes it a good marker of renal function

Question 601

what factors reduce GFR

Answer 601

Question 602

where do thiazide diuretics act give an example

Answer 602

* proximal convoluted tubule * bendroflumathiazide

Question 603

where do potassium sparing diuretics act give an example

Answer 603

* distal convoluted tubule * spironolactone [mineralocorticoid antagonist also] * amiloride

Question 604

where do loop diuretics act give an example

Answer 604

* loop of Henle * furosemide + bumetanide

Question 605

causes of hypokalaemia

Answer 605

* insulin * hyperaldosteronism: Conn's + Cushings * beta2 antagonists * alkalosis

Question 606

causes of hyperkalaemia

Answer 606

* insulin deficiency * aldosterone deficiency - Addison's * beta2 antagonists * exercise * acidosis * cell lysis * diet - lots of bananas

Question 607

how do NSAIDs → AKI

Answer 607

they reduce blood flow to the kidney by causing constriction of the afferent arteriole → reduced oxygen and cell death.

Question 608

causes of painful haematuria

Question 609

causes of painless haematuria

Question 610

triad of symptoms of nephrotic syndrome

Answer 610

* proteinuria * oedema - eye sockets, genital region + peripheral limbs * hypoalbuminaemia

Question 611

difference between nephrotic and nephritic syndrome

Question 612

**What cellular and structural changes in the glomerulus are responsible for nephrotic syndrome**

Answer 612

podocyte damage → widened gaps between them which allows the easy passage of substances through them such as proteins.