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Functions of the urinary system

Regulation of concentrations of key substances in ecf
By virtue of above effecting icf
Excretion of waste products
Endocrine
Metabolism

1

What are the hormones synthesised in the kidneys?

Epo
Renin
Prostaglandins

2

What is the metabolic activity of the kidney?

Activation of vit D
Catabolism of insulin

3

What proportion and amount of body mass is fluid?

60%
42L

4

What proportion and amount of body fluid is ECF

1/3rd
14L

5

What proportion and amount of ECF is plasma?

20%
3L

6

What is the difference between osmolarity and osmolality?

Osmolarity - number of osmoles of solute per litre solvent
Osmolality - number of osmoles of solute per kilogram solvent

7

How much ultrafiltrate is produced by the kidneys each day? Hw much is reabsorbed?

180 L produced
178.5 L reabsorbed

8

What are the vertebral levels of the kidneys?

Left T11-L2
Right T12-L3

9

What are the layers surrounding the kidney from inside out?

Capsul
Perinephric fat
Renal facia (anterior and posterior)
Paranephric fat (posteriorly)
Parietal peritoneum (anteriorly)

10

How does the kidney attach to the diaphragm? What is the consequence for the kidney position?

Via the renal fascia to the diaphragmatic fascia
Moves with respiration

11

How can the renal medulla be subdivided?

Renal pyramids containing nephrons
Renal columns carrying blood flow from hilum to cortex

12

How many major and minor calices are in each kidney

2 or 3 major calices each with 2 or 3 minor calices

13

Which vessel, artery or vein, is anterior as it enters the kidney?

Vein

14

What is the medical consequence of the segmental arteries not anastamosing in the kidney?

Each segment is surgically resectable

15

What are the autonomic nerves to the kidney?

The splanchnic nerves

16

Where do the ureters origionate? What is their abdominal course?

Uretopelvic junction posterior to artery and vein.
Pass down just anterior to the tips of the transverse processes of the spine

17

Where do the ureters enter the pelvis?

By the bifurcation of the common iliac artery (by the sacroiliac joint)

18

What is the course of the ureters in the pelvis?

Turn anteriomedially at the level of the ischial spines

19

How is backflow prevented from bladder to ureters?

They enter obliquely. Increased bladder pressure and constriction of the muscle on voiding close the lumen

20

What is the only thing that passes between the peritoneum and the ureter in males?

The vas defrans

21

Is the ureter anterior or posterior to the uterine artery in females?

Posterior

22

What is the arterial supply of the ureter?

Branches of the renal, gonadal, aorta, common iliac arteries snd internal iliac arteries
Many anastamoses

23

What nerves innervate the ureters?
Where do pain fibres travel?

Adjacent autonomic plexuses
Pain follows sympathetics back to T11 to L1

24

What is the space between the pubic bone and the bladder?

He potential reteropubic space

25

What supports the neck of the bladder?

Puboprostatic ligament (males) and pubovesicular ligament (females)

26

What is the triangle between the ureters and urethra termed?

Trigone

27

What is the arterial supply to the bladder?

Superior and inferior vesicular arteries

28

What are the three stages of urinary development?

Pronephros
Mesonephros
Metanephros

29

When and where does the pronephros form?
What does it do?

In the cervical region creating a duct to the cloaca
Beginning of week 4, regresses after several days

30

Where does the mesonephros develop? What is formed?

Caudal to the pronephros in the intermediate mesoderm.
Excretory tubules appear associated with capillary tufts. As they develop the urogenital ridge is formed

31

What happens to urine produced by the mesonephros?

Drains to the cloaca (not ruptured until week 7) so passes up the alantois into the umbilical cord

32

How does the mesonephros degenerate

Starting cranially even as the caudal end is still developing

33

How does the metanephros form?

Formation of the uteric bud by the mesonephros
Drives development of the metanephric blastema from the surrounding intermediate mesoderm
When the uteric bud contacts the metanephric blastema it branches forming the collecting system up to the collecting ducts of the nephrons

34

How does the metanephros reach its adult position?
What is the consequence?

Ascends from the pelvis
Partely due to cranial movement, partly done by remaining still as the trunk elongates.
Sequential ascending blood supply, usually degenerates but can create accessory vessels either into the hilum or into poles

35

What is renal agenesis?

Uteric bud fails to stimulate metanephric blastema
If bilateral not compatible with life?

36

What is duplication defect of the kidney?

The uteric bud splits forming two collection systems, these can open atopically eg. into the vagina causing incontinance

37

What are the two cyctic kidney diseases? What is different about them?

Multicystic kidney disease is a developmental disease where there is failed recanalisation of the ureter

Polycystic kidney disease is a genetic diaorder that causes renal failure, it has a poor prognosis

38

What is the consequence of failure of the kidneys in utero called? What is it?

Potters sequence:
Oligourea
Oligohydraminos
Hypoplastic lung disease

39

What is the urachus in healthy adult life?

Median umbilical ligament

40

How is the urogenital sinus formed?

Decent of the urorectal septum forms the rectum anteriorly and the urogenital sinus posteriorly

41

What are the three parts of the urogenital sinus? What do they form?

Upper part - future bladder
Pelvic and phallic part - future urethra

42

Where does the uteric bud open? How does this change during development?

Into the mesonephric duct
As the bladder expands it absorbs this junction and the uteric bud then opens directly into the bladder

43

What is the fate of the mesonephric duct in men?

As the bladder expands its opening is pushed further caudally into the developing prostate

44

What is the renal corpuscle?

The glomerulus within bowmans capsule

45

How does bowmans capsule form?

Blind ended tube of the metanephric blastema contacts and envelopes the glomerulus creating a double layered space with a visceral and parietal layer.
Viceral layer develops into podocytes wrapping around the glomerular capillaries.

46

What does the plasma have to cross to become ultra filtrate in the kidneys?

Fenestrated capillary endothelium
Basement membrane
Filtration slits between podocytes

47

Where is the PCT found? How does it appear in section?

Mainly in the cortex, though does dip into the medulla
Simple ciliated cuboidal

48

What are the four parts of the loop of henle?

Pars recta
Thin descending
Thin ascending
Thick ascending

49

How does the thin limbs of the loop of henle appear histologically?

Simple squamous, no blood cells (distinguish from capillaries), no brush border

50

How does the thick ascending limb of the loop of henle appear?

Simple cuboidal with no brush border

51

How does the dct appear histologically? Where is it found?

In the cortex
A squashed simple cuboidal epithelial tube. No cilia

52

How does the collecting duct appear histologically?

Non ciliated simple cuboidal epithelium. Appears very similar to thick loop of henle but slightly larger and more irregular

53

What are the components of the juxtaglomerular apparatus?

Dct - macular densa cells
Afferent arteriole - juxtaglomerular cells
Between - lacis cells

54

Hw many layers of muscle does the ureter have?

2/3rds bilayered
1/3rd trilayered

55

Where is transitional epithelium found?

Ureters, bladder, proximal urethra

56

What is then structure and function of transitional epithelium?

Stratified cells that are distensible. Covered in umbrella cells that are impermiable even at full stretch.
Function to protect from urine but also prevent tissue fluid entering the hypertonic urine

57

What is the charge on the basement membrane of the renal corpuscle?

Negative

58

Which are filtered more at the renal corpuscle anions or cations?

Cations are filtered more redily ( more end up in ultrafiltrate)

59

What effects filtration rate?

Capillary hydrostatic pressure vs ultrafiltrate hydrostatic pressure and osmotic gradient (outwards due to oncotic pressure)

60

What two methods of autoregulation exist to ensure constant filtration?

Myogenic response (contraction of smooth muscle on stretch)
Tubular glomerular feedback

61

How does tubular glomerular feedback work?

High gfr causes high na+ and cl- at dct
This is detected by macula densa cells causing release of adenosine resulting in afferent arteriole vasoconstriction
Low gfr causes reverse with macula densa releasing prostaglandins dilating afferent arteriole.

62

How is glucose reabsorbed in the pct?
Right the way into the blood please!

Na/k atpase sets up gradient of na+
Glucose and na+ reabsorbed using SGLT2 channels
This moves it against conc gradient into cell
It then moves down conc gradient into ecf then into blood

63

What substances are secreted into the tubule? Why?

Only 20% of plasma filtered therefore secretion necessary if more is needed to be removed
K+
H+
Anions and cations
Drugs (adrenaline, morphine, penicillin)

64

What is normal gfr for males and females?

Males 115-125ml/min
Females 90-100ml/min

65

What is renal plasma flow?

1.1 L/min of blood, 55% plasma thus 605ml/min plasma

66

What is the filtration fraction? How is it calculated?

20%
GFR/renal plasma flow x 100

67

What is clearance in the kidney?

The volume of plasma from which a substance is completely removed by the kidneys/minute

Clearance = ([substance in urine] x urine flow)/[substance in plasma]

68

What properties does a substance need in order to apply its clearance to calculate gfr?

Not secreted or reabsorbed
Filtered freely
Not metabolised in the urine

69

What does egfr account for when measuring serum creatinine?

Age sex mass

70

What is the ideal substance for calculating gfr?

Inulin

71

What is filtered load of a substance?

Plasma concentration x gfr
(amount of substance filtered per minute)

72

What is the transport maximum?

The amount of substance the tubule can reabsorb

73

What is the renal threshold?

The plasma concentration of a substance that will exceed the filtered load that would exceed the renal threshold!

74

Why must the kidneys be able to vary sodium excretion?

To deal with varied dietary absorption
To allow BP control

75

What drives na reabsorption in the kidneys?
What ion comes with it? What is the exception to this rule?

Na/k atpase on basal membrane
Cl but in early pct hco3

76

What is the effect of the early pct reabsorbing hco3- alongside na rather than chlorine?

Increases cholorine tubular concentration allowing paracellular reabsorption

77

Where is most sodium and water reabsorbed? How much?

PCT
65% water
67% sodium

78

What are the sodium channels in the PCT
Which one is under regulation of hormone? Which hormone?

Na/glucose, Na/aa, Na/phosphate, Na/H exchanger
Na/Phosphate under PTH control

79

How do ion channels differ along the PCT?

All present in the first segment
Latter two segments only have Na/H exchanger

80

Why is the reabsorptionin the PCT described as isoosmotic?

Fully permeable to water so no change in osmolarity

81

What is the degree of reabsorption of na and water in the loop of henle?

Decending - 10-15% water
Ascending - 25% na

82

How is na reabsorbed in the ascending loop of henle?

In thin limb passive paracellular due to high osmolarity in tubule
In thick limb Na/k atpase driving NKCC2

83

In the thick ascending limb where do the cl- and k+ ions go after reabsorption?

Cl into ecf
K through romk back into tubule

84

What is the character of the fluid found at the top of the ascending limb?

Hypoosmotic

85

What cell type is found in the early DCT?what does it absorb and how?

Tubular cells
Na/KATPase drives Na/Cl synporter with the Cl being extruded basally

86

Where is calcium reabsorption controllable? How?

Tubular cells of Early DCT
NCX on basal membrane allows apical reabsorption from tubule under PTH influence

87

Where is most calcium reabsorbed? Where else?

PCT
Ascending loop by lumen positive potential

88

Explain the principle of glomerulotubular balance

By reabsorbing by percentage rather than amount any increase of decrease in gfr is compensated for

89

How much water and na is reabsorbed in the early dct? What happens to the osmolarity of the filtrate?

5-8% sodium
No water
Becomes more hyposmotic

90

How much sodium and water is reabsorbed in the late dct and cd?

3% sodium
5-25% water depending on adh

91

What are the two cell types in the late dct / cd

Principal cells
Intercalated cells

92

What is the function of principal cells? What are they sensitive too? What is the effect on the lumen?

Na/K atpase sets up na gradient
Enac uniporter for sodium reabsorption
Romk uniporter for K secretion
Sensitive to aldosterone
More na absorption than k secretion so lumen becomes -ve driving the k secretion and Cl reabsorption

93

What are the general functions of the intercalated cells of the dct?

Acid base balance
Active cl reabsorption

94

What systems influence long term blood pressure control?

RAAS
SNS
ADH
ANP

95

What stimulates renin release?

SNS
Low perfusion of afferent arteriole detected by baroreceptors
Low Na/Cl in DCT thus low GFR detected by macula densa

96

Actions of angiotensin II

Stimulates aldosterone release
Vasoconstriction
Increased Na/H in PCT

97

Effect of SNS on BP

Stimulates renin release
Decreases renal bloodflow decreasing GFR
Activates Na/H and Na/KATPase in PCT

98

How does ADH influence blood pressure?

Increased osmolarity or hypovolemia stimulate ADH release resulting in water retention
Also stimulates NKCC2

99

Role of ANP in blood pressure regulation?

Released by atria in response to excessive stretch
Causes vasodilation of afferent arteriole increasing GFR and inhibits Na reabsorption in nephron

100

Why do NSAIDs cause renal failure?

If GFR decreases tubuloglomerular feedback results in prostaglandin release from juxtaglomerular apparatus to dilate afferent arteriole. NSAIDs block the prostaglandin synthesis

101

What are the physiological consequences of HTN?

Increased afterload:
LVH
Myocardial ischemia due to increased demand

Arterial damage (athereosclerosis and weakened vessels):
Aneurysm
Thrombus (Cerebrovascular disease)
Retinopathy
Kidney damage


102

How are changes in osmolarity detected?
How does this occur?

Swelling or shrinkage of hypothalmic osmoreceptors
Surrounding capillaries have fenstrated epithelium exposing the receptor to the plasma osmolarity directly

103

What occurs if plasma osmolarity increases?

Stimulation of osmoreceptors stimulates ADH release and increases thirst.

104

What is the thirst pathway?

Large increased osmolarity or decreased plasma volume increases thirst
Induces drinking behaviour
Immediately pathway is sated - anticipation of water being absorbed once drunk

105

Where is ADH released from?

Posterior pituitary

106

What is the structure of ADH?

Small peptide hormone

107

What are the actions of ADH on the kidney generally?

Vasoconstriction of glomerulus reducing GFR
Increased NKCC2
Activates Gs GPCR on late DCT and CD with increased PKA causing insertion of aquaporin 2 into the apical membrane

108

How does water travel through the basal membrane of the late DT and CD?

Through aquaporin 3 and 4

109

If there is no ADH what happens to urine? Condition?

Large volumes of dilute urine
Diabetes insipitus

110

What takes priority in a case of low blood volume (low BP) and low osmolarity?

The low volume - ADH will be secreted in spite of low osmolarity

111

What is the corticopapillary osmotic gradient? How is it formed?

The gradient of increasing interstitial osmolarity in the interstitium from the top of the cortex (low osmolarity) to the renal papilla (high osmolarity)
- countercurrent multiplying and exchange from the loop of henle and the vasa recta respectively
- recycling of urea

112

How does urea cycling effect the corticopapillary osmotic gradient?

Urea is at high concentration in the collecting duct
It is reabsorbed through aquaporin 2 thus reabsorption increases when ADH is high
It is then reabsorbed into the ascending limb

113

How is a corticopapillary osmotic gradient set up using Na/Cl and water?

The loop of Henle acts as a countercurrent multiplier - the ascending limb reabsorbs Na into interstitium decreasing filtrate osmolarity and increasing interstitial osmolarity by up to 200momol/l

Water leaves descending limb and is reabsorbed by vasa recta due to high oncotic pressure and counter current exchanger giving it high osmolarity. This concentrates the descending limb fluid

Water from the descending limb moves into the ascending limb, as it is now a higher osmolarity it can have more na reabsorbed concentrating the interstitium further still and so on!

114

What are the actions of PTH?

Increases osteoblasts decreases osteoclasts
Increases DCT reabsorption of calcium
Decreases PCT Pi reabsorption
Activates vitamin d

115

What is the half life of PTH? What causes its release?

4 minutes so can respond quickly to changes in calcium
Released as low calcium increases mRNA transcription and stability

116

Where is PTH produced and degraded?

Chief cells of the parathyroid gland

117

What are the two precursors to vit D? How do they differ?

Cholecalciferol (from light)
Ergocalciferol (from diet)

118

What are the steps of activation of vit d? Where?

Cholecalciferol
LIVER - 25hydroxycholecalciferol
KIDNEY - 1.25dihydroxycholecalciferol (calcitriol)

119

Which step of vit. D synthesis is controlled by pth?

25hydroxyvitd to 1.25dihydroxyvitd

120

What is another name for 1.25dihydroxycholecalciferol?

Calictriole

121

When sufficient calcitriol has been produced where is excess 25.hydroxycholecalciferol diverted too?

24.25dihydroxycholecalcifeole

122

What increases risk of vit d deficiency?

Non-caucasian
Lack of sunlight (indoors, clothes, sunscreen, climate)
Lack of fish oil (ergocalciferol)
Elderly/obese
Cyp450 inducers

123

Actions of calcitriol

Increased gi calcium absorption
Cell differentiation and proliferation
Decreased cell growth
Increase insulin
Decreases renin

124

What is primary hyperparathyroidism?
Biochemical presentation

Adenoma of parathyroid gland
High PTH driving high Ca

125

What is secondary hyperparathyroidism?
Biochemical presentation

Low calcium driving raised PTH to return to normal
Low (uncompensated) or normal (compensated) calcium
High PTH

126

What is malignant hyperparathyroidism?

Release of PTHrP causing high calcium
Calcium very high, PTH low as supressed

127

What is tertiary hyperparathyroidism?
Biochemical presentation?

Long term secondary hyperparathyroidism causing autonomous pth release and thus hypercalcaemia
High pth and high calcium

128

What type of hyperparathyroidism is more likely to be present in raised calcium on investigation of renal calculi. Which one is unlikely?

Primary hyperparathyroidism is likely
Malignant hyperparathyroidism is unlikely

129

What type of hyperparathyroidism is characterised by a rapid onset?

Malignant

130

What are signs and symptoms of hypercalcaemia?

Stones
Moans (constipation)
Grones (depression)
Short QT
HTN
Drowsiness
Polyurea / polydipsia

131

What is the treatment of hypercalceamia?

Underlying condition
Hydration to increase excretion
Loop diuretics
Bisphosphonates
Calcitonin

132

What diuretics can worsten hypercalcemia? Why?

Thiazides
Block na/cl = decreased na reabsorption = low sodium in cells = increased basal NCX = low calcium in cells = increased calcium absorption

133

What are the four most common types of renal calculi?

Calcium (70%)
Magnesium ammonium phosphate
Urate
Cystine

134

What sort of renal calculi is radiolucent

Urate

135

If you have had one renal stone what is your chance of having another?

50%

136

Which gender is more likely to get renal stones?

2:1 males:females

137

What increases risk of renal stones?

Male, dehydrated, previous stone, infection, hypercalcemia/hypercalciurea
Drugs
Loop diuretics - calcium stones
Thiazides - urate stones

138

How do renal calculi present?

Asymptomatic
Haematuria
Pain

139

General treatment options of renal calculi

Surgery
Lithotripsy
Fluid

140

What is used in uric acid stones

Allopurinol

141

What tests in renal calculi?

Blood screen
Urine screen
Radiography

142

What are the effects of alkalaemia?

Increases calciums affinity for albumin lowering serum free calcium. Low free calcium increases NCX, increasing intracellular sodium causing depolarisation - tetany

143

What are the systemic effects of academia

H excreted in exchange for K reabsorption in the kidneys - similar in cells - h taken in extruding k all causing hyperkalaemia.
Damage to enzymes causing decreased muscle contractility, glycolysis and hepatic function

144

What do the kidneys do to compensate or correct pH disturbance. Which type of does the kidney do each for?

Changes HCO3- excretion and creation
Compensates for respiratory
Corrects metabolic

145

What is the general response of the kidney to acidosis?

Recover all filtered HCO3-, secretes H+ and create new HCO3-

146

How does the kidney reabsorb HCO3-?

Secretes H+ through Na/H antiporter
H+HCO3- to CO2 and water
Reabsorb CO2
Recombine with water in cell
excrete H again
NOTE there is no net H+ excretion by this method

147

What is it that triggers bicarbonate reabsorption in the kidneys?
Not just acidosis - what about it and what else!

High CO2 in PCT cells increases H for secretion
Volume depletion increases reabsorption of Na+ thus excretion of H and also increases RAAS and Ang 2 increases NHE

148

Where and how does the kidney make hco3- in acidosis?

Alpha intercalated cells
H2O and CO2 to H and HCO3-
H actively secreted into lumen in exchange for K (uses ATP)
HCO3- enters ECF

Also secretes NH3 from aa breakdown to buffer H+ in urine to NH4+

149

What buffers H+ in urine, why is this necessary?

Phosphate and ammonia
Prevents damage and maintains concentration gradient

150

How do the kidneys increase H+ secretion? Where from?

H/K exchange in alpha intercalated cells as HCO3- is produced

151

What is the anion gap?

The difference between principle cations (Na+ and K+) and principle anions (HCO3- and Cl-). A high gap means a large number of unusual anions suggesting high acid production (e.g. lactate ions) rather than increased loss of HCO3- (e.g. renal tubular acidosis)

152

How do the kidneys aim to correct or compensate for alkalosis? What may stop this occurring?

Increase HCO3- excretion
But if volumed depleted unable to do this as Na reabsorption also stimulates HCO3- reabsorption
Thus fix by rehydration

153

Why do small changes in the. Balance of K have huge effects on the body?

98% k is in icf thus little change in balance will dramatically shift extracellular concentration

154

How does the body respond to rapid fluctuations in k? Why?

Intracellular buffering
Kidneys cant respond fast enough

155

What is internal k balance

Stabilising ecf K by moving in and out of icf

156

What is external k balance?

Matching excretion to intake

157

What increases K uptake into cells?

Increased ecf K
Hormones (insulin, aldosterone, catacholamines)
Alkalosis (shunt K in for H out)

158

What increases K release from cells?

Low ecf k
Exercise (repolarisation and muscle damage)
Cell lysis (rhabdomyolysis, haemolysis)
Increased ECF osmolarity (relative decreases as water moves out)
Acidosis (K out to allow H in)

159

Where and how in the kidney is K reabsorbed?

PCT - paracellular diffusion
Thick ascending limb - NKCC2
Alpha intercalated cells - K/H antiporter

160

Where and how in the kidney is K secreted?

Principal cells
Apical ROMK

161

How is K reabsorption and secretion controlled in the kidney?

By altering secretion amounts from 15-120%
Responsive to aldosterone

162

What factors cause K secretion in principal cells?

High intracellular K
High intracellular Na (through ENaC) creating electrical gradient with negative luminal and positive cellular potential

163

What increases secretion of k from principal cells?

Increased ecf k activating na/k atpase
Increased na reaching them in lumen
Increased flow in lumen removing secreted k increasing gradient
Increased aldosterone
Alkalosis (stimulates na/k atpase)

164

How does acidosis result in hyperkalaemia?

Increased H/K atpase in alpha intercalated cells
Decreased na/k atpase in principal cells lowering k secretion

165

What can cause hyperkalaemia?

Increased intake (needs renal dysfunction OR IV dose)
Decreased excretion (kidney disease, adrenal disease)
Internal shift (acidosis, cell lysis, exercise)

166

How should hyperK be treated?

Calcium gluconate
Glucose and insulin
Salbutamol
Dialysis

167

Causes of hypokalaemia

Increased loss (diarrhoea, vomiting, diuresis, high aldosterone)
Internal shift (alkalosis, aldosterone, adrenaline)

168

Treatment of hypok

K replacement
Block aldosterone

169

What diseases result in high aldosterone secretion?

Conns syndrome (aldosterone secreting adenoma)

170

What is the lifetime risk of uti in women?
When are they most likely?

50%
Children, sexually active (honeymoon), pregnancy, elderly

171

Risk factors for uti

Short urethra (women)
Obstruction (calculi, prostate, tumour, pregnancy)
Neuro problems (unable to empty bladder fully)
Ureteric reflux (especially children)

172

What adaptations to bacteria aid them in surviving to cause uti

Fimbriae for attachment
Polysaccharide capsule to avoid immune system
Urease production to increase ph

173

How does a lower uti present?

Cystitis
Increased urinary frequency
Mild fever
Dysuria

174

How does an upper uti present

Loin pain
High fiver

175

Who is more at risk of asymptomatic uti?

Elderly
Catheters

176

Define complex uti?

Treatment resistant
Male
Pregnancy
Children
Elderly
Pyleonephritis

177

What urine dip sign is very sensitive for uti? What is very specific?

Leucocyte esterase very sensitive
Nitrites very specific

178

What. Is the negative predictive value of turbidity in urine for uti?

97%

179

When would you culture a uti? What specific test is applied to it?

Complicated uti
Fermenting lactose to dx ecoli

180

What proportion of females with uti symptoms have significant bacteriuria? What may cause this?

50%
Sti urethritis, vaginal infection, mechanical cause, on abx, tb, fastidious organism (complex requirements so hard to grow)

181

When is microscopy of urine indicated?

Kidney disease
Endocarditis
Children under 6

182

What could squames visible on microscopy of urine indicate?

Contaminationn

183

Tx for simple, complex and pylonephritis uti

Simple 3 days
Complex 7 days
Nitrofurantoin or trimethoprim

Pylo 14 days
Ciprofloxacin or ceftrioxone or gentamicin

184

What can be done for frequently reoccurring utis?

More than three a year, prophylactic nitrofuritoin or trimethoprim

185

Which uti patients need imaging?

Children
Suspicion of problem with posterior urethral valve (men)
Suspicion of vesicouteric reflux (women)

186

What is the somatic, sympathetic and parasympathetic innervation to the bladder?

Som - pudendal
Symp - hypogastric nerve
Para - pelvic nerve

187

What does parasympathetic stimulation to the bladder do on a cellular level?

Stimulates M3 Ach receptors causing activation of GalphaQ to IP3 and DAG causing detrusor muscle contraction

188

What does sympathetic stimulation to the bladder do on a cellular level?

Detrusor muscle
Stimulates Beta3 receptors triggering GalphaS resulting in K efflux and hyperpolarisation thus muscle relaxation
Internal sphincter
Stimulates Alpha1 receptors triggering GalphaQ resulting in IP3 and DAG thus contraction and sphincter closure

189

What are the two phases of the bladder?

Storage
Voiding

190

What is the reflex involved in storing urine?

Low levels of stretch stimulate pelvic afferents
These activate the spinal continence centre
1) causing pudendal to close sphincter
2) causing hypogastric to stimulate detrusor relaxation and internal sphincter contraction

191

How can higher centers influence urinary storage?

Cerebral storage centre activates pontine storage centre which bilaterally activates the spine continence centre to activate the pudendal nerve closing the external sphincter.

192

What is the effect of detrusor relaxation during bladder filling?

Very little change in pressure

193

How does the micturition reflex occur?

Stretch of bladder detected by pelvic afferents, triggers stimulation of parasympathetic pelvic nerve and inhibition of the pudendal and sympathetic hypogastric nerve. This promotes voiding.

194

How do higher centres influence micturition?

Also recieve afferents informing them of stretch.
Cerebral micturition centre stimulates pontine micturition centre which in turn causes the increased parasympathetic and decreases symp and somatic. If urination not desirable can consciously activate storage centres promoting contraction of the external sphincter.

195

What would happen to the bladder in a spine injury above S2?

Lack of conscious control
On filling sacral spine reflex will cause detrusor contraction but lack of stimulation from pontine micturition centre will mean:
1) incomplete voiding
2) dyssynergia - external sphincter will not relax in time with contraction causing retention

196

What would happen to the voiding of the bladder in a sacral or peripheral nerve damage?

Flaccid bladder - overfilling with overflow incontinence

197

4 types of incontinance

Stress (SUI) - leakage on effort, sneezing, cough, exertion
Urge (UUI) - leakage preceded by urgency
Mixed (MUI) - SUI and UUI
Overflow (OUI) - dribbling of urine secondary to LMNL

198

What is overactive bladder syndrome?

Polyuria, nocturia and urge +/- UUI

199

What are non modifiable risk factors for incontinance?

Family hx
Anatomical abnomalities
Neurological abnormalities
Age

200

Modifiable risk factors for incontience

Drugs, uti, chronic cough, obesity, preggo, childbirth, pelvic surgery, dementia

201

Examinations in incontinent patients?

Bmi
Abdo
DRE
Vaginal
Urine dipstick
Frequency volume chart/diary

202

Advanced investigations for incontinace

Invasive urodynamics
Pad test
Cystoscopy

203

SUI management

Stop smoking (decrease cough)
Pelvic floor training
Duloxetine (NA/5HT reuptake inhibitor)
Vaginal tape
Fascial sling
Intermurial bulking

204

UUI Management

Decrease caffine
Scheduled voiding with gradual increase in duration over months
Anticholinergics e.g. Oxybutynin
Beta 3 agonists
Botulinum toxin
Sacral nerve neuromodualtion
Urinary diversion into a bag

205

Management of overflow incontinance

Treat compression
Avoid constipation

206

Ways of mitigating incontinance?

Catheters
Sheaths
Incopads

207

What is AKI?

Clinical syndrome causing acute decline in GFR over days to weeks

208

Diagnostic criteria of AKI

Raise in serum creatining greater than 26.5mmol/l in 48 hrs or 1.5x baseline in 7 days
Maybe low urine volume (<0.5ml/kg/hr) for 6 hours

209

What can AKI cause?

Changes to ecf volume
Electrolyte abnormalities
Ph abnormalities

210

What is the in hospital incidence of. AKI

5%

211

Cause of prerenal AKI

Decreased renal perfusion
- volume depletion, chf, systemic vasodilation, preglomerular vasoconstriction (NSAID), postglomerular vasodilation (ACEi/ARB)

212

What is the effect of pre renal aki on sodium excretion?

Active reabsorption of na and h2o thus fractional na excretion less than 1%

213

Treatment of pre renal aki

Fluids
Underlying cause
Stop offending meds

214

What different pathologies can cause renal aki?

ATN
Glomulonephritis
Interstitial disease
Intrarenal obstruction

215

Causes of ATN

Sepsis
Nephrotoxins
Ischemia
Continum from pre renal AKI

216

What effect does ATN have?

Damage to tubular cells impaired salt and water reuptake with expulsion of excess water.

217

Examples of endogenous nephrotoxins

Bilirubin
Myoglobin
Urate

218

Examples of exogenous nephrotoxins

Xray contrast
Nsaids
Animoglycosides
Lithium
Antifreeze
Weedkiller

219

What can cause a low fractional excretion of sodium that isn't pre renal AKI.

Glomerulonephritis
Early rhabdomyolitis
Hypercalcemia
Vasoconstrictive drugs (e.g. NA)
Hepatorenal syndrome
Contrast nephropathy

220

Signs that an AKI is. Prerenal?

Postural hypotension
Low JVP
Sepsis/CHF
Rapid weak pulse
Low CVP

221

Why does ATN cause decreased GFR and thus fluid overload if aggressively resuscitated

Increased sodium - tubularglomerular feedback - afferent constriction
Back leak of filtrate in pct
Obstruction of tubule by debris from dying tubular cells

222

What can cause tubulointersitial nephritis?

Pyleonephritis
Toxins

223

What causes post renal AKI?

Obstruction if bilateral or effecting a sole functioning kidney

224

Examples of. Obstruction causing post renal aki

Luminal - calculi, blood clots,
Wall - neuromuscular dysfunction, neurogenic bladder, stricture
External - tumour, prostate, AAA, ligation
BLOCKED CATHETER

225

Tests in AKI?

Dipstick
Culture
Microscopy
Biochemistry (U+E, FENa+)
Imaging in post renal or non refractory prerenal/renal
CVP and CXR if risk of fluid overload
Histology in renal if not clear ATN

226

When would dialysis be considered in AKI?

HyperK not responsive to medical tx
Non refractory metabolic acidosis
Fluid overload not refractory to diuretics
Dialysable nephrotoxin (eg aspirin OD)
Uremia

227

Signs of uremia

Pericarditis
Lowered GCS
N+V

228

What different dysfunctions can renal disease present with?

Excretion - hyperK, fluid overload, acidosis
Glomerular - proteinuria, haematuria
Tubular - nocturia, polyuria, glycosuria
Hormonal - osteomalacia, anaemia, htn

229

Causes of microscopic haematuria

Uti
Polycystic kidneys
Renal stones
Tumours
AV malformations
Glomerular disease

230

At what age should all haematuria cases receive a cystoscopy?

>45

231

Differentiate haematuria from glomerular disease and lower urinary tract

Glomerular - smoky brown +\- protein, painless
LUT - red, clots, pain, no protein

232

Non blood causes of red/brown urine

Myoglobinuria
Beetroot

233

At what point in GFR do CKD symptoms present?

<30ml/min

234

Presentation of proteinuria

Frothy urine
Oedema due to low oncotic pressure
Infection due to low plasma immunoglobulin
Thrombus risk due to imbalanced coagulation factors

235

Types of protienuria

Glomerular - increased permiability
Tubular - decreased reabsorption of filtered small proteins
Overflow - filtration of small proteins above transport maximum

236

Cause of overflow proteinuria

Multiple myeloma

237

What is nephrotic syndrome. How does it feed back on itself? What random thing does it cause?

Proteinuria with oedema 2ndry to hypoalbuminia
Decreases circulating volume increases RAAS increases sodium retention, increases oedema
High cholesterol

238

What is nephritic syndrome?

Rapid onset oligouria, low GFR, HTN, oedema, haematuria, normal albumin.

239

How can the renal capsule result inpathology?

Blockage
Leakage

240

What 4 points of the glomerulus are vulnerable to damage?

Subepithelial
Basement membrane
Subendothelial
Mesangial

241

Glomerular causes of nephrotic syndrome

Minimal change glomerulonephritis
Membranous glomerulonephtitis
Diabetes mellitus

242

Age distribution of minimal change glomerulonephritis?
Treatment?
Consequence of this

Most common nephrotic syndrome in children
Very good response to steroids
Treat and if responds no need to biopsy

243

Changes of minimal change glomerulonephritis on biopsy?

None to light microscopy
On electron loss of podocyte foot processes

244

Prognosis of minimal change glomerulonephritis?

Responds well to steroids. May progress to renal focal segmental glomerulosclerosis and renal failure. If so often returns post transplantation.

245

What is the commonest adult glomerular nephrotic syndrome?
What causes it?

Membranous glomerulonephritis
Immune complexes forming and damaging subepithelial layer - autoimmune or secondary to SLE or plasmodium malariae

246

How does membranous glomerulonephritis appear histologically?
What is the treatment?

Masses of immunoglobulin deposition
Immunosuppressants

247

How does diabetes cause glomerular disease?

Microvascular glomeruli disease causing progressive proteinuria
Basement membrane thickens
Podocytes detach
Scarring and nodules form

248

Primary causes of nephritic syndrome

IgA nephropathy
Thin glomerular basement membrane disease
Alports syndrome
Goodpastures syndrome

249

When does IgA nephropathy tend to occur?
What does it cause?

Post mucosal infection
Immune complex deposition in mesangium
Haematuria

250

What is the prognosis of IgA nephropathy?

Progression to renal failure with transplant as the only option

251

What is the prognosis of thin glomerular basement membrane disease?

Benign

252

What is alports syndrome?

X linked inherited disease causing split basement membrane
Progresses to renal failure

253

What is goodpastures syndrome?

Rapidly progressing nephritic syndrome with autoantibodies against basment membrane
Treatable with immunosupression and plasmaphoresis if caught early

254

What is. Goodpastures syndrome associated with?

Pulmonary haemorrhage in smokes

255

What is a secondary cause of nephritic syndrome? What marker will be raised?

Vasculitis e.g. Wegners
Antineurtophil cytoplasmic antibody ANCA

256

What is the epidemiology of prostate cancer?

Most common male cancer
Second most common cause of male cancer death

257

What is the prognosis of prostate cancer?

Most people diagnosed are unlikely to die of the cancer

258

What increases the risk of prostate cancer?

Age
Family history
Black ethnicity

259

Why is the fact that prostate cancer incidence increases with age problematic?

Urinary symptoms and benign enlargement also increase with age so harder to detect

260

What can cause a raised prostate specific antigen? What does this mean for screening?

Malignant cancer
Prostatic hypertrophy
Benign cancer
Prostatic inflammation

Massive overdiagnosis

261

What are the risks involved with prostate cancer treatment?

1/3 risk LUT symptoms
1/3 risk erectile dysfunction
5% risk incontinence

262

What is the prevalence of prostate cancer in 80 year old males

80%!

263

What are symptoms of prostate cancer?

Asymptomatic
Bladder overactivity
Metastatic bone pain
Urinary tract obstruction
Uncommonly weight loss and haematuria

264

What investigations are warranted in diagnosing prostate cancer (two routes)

DRE and PSA - transrectal ultrasound guided biopsy
LUT symptoms - TURP

265

How is prostate cancer graded?

Gleason grade - two numbers
First - grade of the most common area of the biopsy
Second - grade of the least differentiated area that is not the first

266

What treatments are available for prostate cancer?

Surveillance
Radical prostatectomy
Radiotherapy (external or brachytherapy)

267

What hormone treatment is used in metastatic prostate cancer?what complication does this have?

Surgical or chemical castration to reduce testosterone (as cancer is testosterone sensitive)
Flare - initial surge in testosterone

268

What non hormonal treatments are available for metastistied prostate cancer?

Targeted radio and chemo therapy for the bone mets
Bisphosphonates

269

What is the normal type of bladder cancer?

Transitional cell carcinoma

270

What are risk factors for bladder cancer?

Smoking
Occupational exposure to rubber, plastic, oil
Schistosomiasis causing metaplasia

271

How are bladder tumours staged?

Superficial (most)
In situ
Invading muscle

272

How are superficial bladder tumours treated?

Transureathral resection of bladder tumour

273

Hw are bladder tumours that have invaded muscle treated?

Radical cystectomy
Palliative

274

Risks for renal cell carcinoma

Smoking
Obesity
Dialysis

275

How can renal tumours spread?

Perinephric
Lymph nodes
Into IVC to right atrium

276

How can upper tract transitional cell carcinomas spread?

Pelvis to bladder NOT reverse usually due to urine. Flow

277

How are renal cell carcinomas treated

Radical or partial nephrectomy

278

How are upper tract transitional cell carcinomas treated

Nephrouterectomy (kidney, fat, ureter, cuff of bladder)

279

What is ckd

Irreversible and sometimes progresive loss of renal function over months to years

280

Cuases of ckd

Glomerulonephritis
Pyelonephritis
Obstruction
Htn
Vascular disease
Dm

281

How is ckd. Detected?

Opportunistic testing of at risk groups

282

How id ckd graded?

g1-G5 based on GFR
A1-A3 based on protein:creatinin ratio in urine

283

What. Grade of ckd is kidney failure?

G5

284

What. Is the main cause of death in CKD

Cvd

285

What does proteinuria mead diagnostically in ckd?

Increased risk of need of dialysis

286

When should a biopsy be performed in ckd?

Normal sized kidney with no obvious diagnosis

287

Complications of CKD

Acidosis
Anaemia
Bone disorders.
Non bone calcification
Cvd

288

What are the bone disorders of ckd?

Osteomalacia due to low active vit d thus low calcium absorption
Ostitis fibrosa cystica due to high PTH resulting in areas of reabsorbed bone replaced with fibrous cysts

289

Benefits and costs of haemodialysis

Benefits - others to talk to, low responsibility, days off

Costs - disruption to life, see others get ill, time consuming, high diet restrictions, high fluid restrictions, large number of meds

290

Contraindications and side effects of haemodialysis

Contraindications - failed vascular access, heart failure (relative - can it cope with extra 300ml)

Complications - infection of central line, thrombus at fistual, steal syndrome, cvs instability, bleeding

291

Benefits and costs of peritoneal dialysis

Benefits - convinience, independence, low diet and fluid reatrictions, initially better renal preservation

Costs - high responsibility, frequent bag changes or on every night

292

Contraindications and complications of peritoneal dialysis

Contraindications - adhesions, hernias, extensive abdo surgery, unable to do at home by pt or carer

Complications - peritonitis, infection, leaks into scrotum, hernia, failure of ultrafiltration due to scarring

293

When is the largest risk post kidney transplant?

3 months

294

What are the risks post kidney transplant?

Infection
Cancer
HTN

295

What type of donor provides best chance?
What is ave. life expectancy

Related live
12 years

296

What meds are used to prevent kidney donor rejection?

Mycophenolate
Tacrolimus