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PPE > Urinary > Flashcards

Urinary Flashcards

0
Q

What are the hormones synthesised in the kidneys?

A

Epo
Renin
Prostaglandins

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1
Q

Functions of the urinary system

A 
Regulation of concentrations of key substances in ecf
By virtue of above effecting icf
Excretion of waste products
Endocrine 
Metabolism
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2
Q

What is the metabolic activity of the kidney?

A

Activation of vit D

Catabolism of insulin

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3
Q

What proportion and amount of body mass is fluid?

A

60%

42L

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4
Q

What proportion and amount of body fluid is ECF

A

1/3rd

14L

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5
Q

What proportion and amount of ECF is plasma?

A

20%

3L

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6
Q

What is the difference between osmolarity and osmolality?

A

Osmolarity - number of osmoles of solute per litre solvent

Osmolality - number of osmoles of solute per kilogram solvent

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7
Q

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

A

180 L produced

178.5 L reabsorbed

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8
Q

What are the vertebral levels of the kidneys?

A

Left T11-L2

Right T12-L3

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9
Q

What are the layers surrounding the kidney from inside out?

A 
Capsul
Perinephric fat
Renal facia (anterior and posterior)
Paranephric fat (posteriorly)
Parietal peritoneum (anteriorly)
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10
Q

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

A

Via the renal fascia to the diaphragmatic fascia

Moves with respiration

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11
Q

How can the renal medulla be subdivided?

A

Renal pyramids containing nephrons

Renal columns carrying blood flow from hilum to cortex

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12
Q

How many major and minor calices are in each kidney

A

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

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13
Q

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

A

Vein

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14
Q

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

A

Each segment is surgically resectable

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15
Q

What are the autonomic nerves to the kidney?

A

The splanchnic nerves

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16
Q

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

A

Uretopelvic junction posterior to artery and vein.

Pass down just anterior to the tips of the transverse processes of the spine

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17
Q

Where do the ureters enter the pelvis?

A

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

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18
Q

What is the course of the ureters in the pelvis?

A

Turn anteriomedially at the level of the ischial spines

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19
Q

How is backflow prevented from bladder to ureters?

A

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

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20
Q

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

A

The vas defrans

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21
Q

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

A

Posterior

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22
Q

What is the arterial supply of the ureter?

A

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

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23
Q

What nerves innervate the ureters?

Where do pain fibres travel?

A

Adjacent autonomic plexuses

Pain follows sympathetics back to T11 to L1

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24
Q

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

A

He potential reteropubic space

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25
Q

What supports the neck of the bladder?

A

Puboprostatic ligament (males) and pubovesicular ligament (females)

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26
Q

What is the triangle between the ureters and urethra termed?

A

Trigone

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27
Q

What is the arterial supply to the bladder?

A

Superior and inferior vesicular arteries

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28
Q

What are the three stages of urinary development?

A

Pronephros
Mesonephros
Metanephros

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29
Q

When and where does the pronephros form?

What does it do?

A

In the cervical region creating a duct to the cloaca

Beginning of week 4, regresses after several days

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30
Q

Where does the mesonephros develop? What is formed?

A

Caudal to the pronephros in the intermediate mesoderm.

Excretory tubules appear associated with capillary tufts. As they develop the urogenital ridge is formed

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31
Q

What happens to urine produced by the mesonephros?

A

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

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32
Q

How does the mesonephros degenerate

A

Starting cranially even as the caudal end is still developing

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33
Q

How does the metanephros form?

A

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

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34
Q

How does the metanephros reach its adult position?

What is the consequence?

A

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

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35
Q

What is renal agenesis?

A

Uteric bud fails to stimulate metanephric blastema

If bilateral not compatible with life?

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36
Q

What is duplication defect of the kidney?

A

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

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37
Q

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

A

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

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38
Q

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

A

Potters sequence:
Oligourea
Oligohydraminos
Hypoplastic lung disease

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39
Q

What is the urachus in healthy adult life?

A

Median umbilical ligament

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40
Q

How is the urogenital sinus formed?

A

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

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41
Q

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

A

Upper part - future bladder

Pelvic and phallic part - future urethra

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42
Q

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

A

Into the mesonephric duct

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

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43
Q

What is the fate of the mesonephric duct in men?

A

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

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44
Q

What is the renal corpuscle?

A

The glomerulus within bowmans capsule

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45
Q

How does bowmans capsule form?

A

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.

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46
Q

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

A

Fenestrated capillary endothelium
Basement membrane
Filtration slits between podocytes

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47
Q

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

A

Mainly in the cortex, though does dip into the medulla

Simple ciliated cuboidal

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48
Q

What are the four parts of the loop of henle?

A

Pars recta
Thin descending
Thin ascending
Thick ascending

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49
Q

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

A

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

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50
Q

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

A

Simple cuboidal with no brush border

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51
Q

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

A

In the cortex

A squashed simple cuboidal epithelial tube. No cilia

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52
Q

How does the collecting duct appear histologically?

A

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

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53
Q

What are the components of the juxtaglomerular apparatus?

A

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

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54
Q

Hw many layers of muscle does the ureter have?

A

2/3rds bilayered

1/3rd trilayered

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55
Q

Where is transitional epithelium found?

A

Ureters, bladder, proximal urethra

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56
Q

What is then structure and function of transitional epithelium?

A

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

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57
Q

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

A

Negative

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58
Q

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

A

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

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59
Q

What effects filtration rate?

A

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

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60
Q

What two methods of autoregulation exist to ensure constant filtration?

A 
Myogenic response (contraction of smooth muscle on stretch)
Tubular glomerular feedback
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61
Q

How does tubular glomerular feedback work?

A

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.

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62
Q

How is glucose reabsorbed in the pct?

Right the way into the blood please!

A

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

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63
Q

What substances are secreted into the tubule? Why?

A 
Only 20% of plasma filtered therefore secretion necessary if more is needed to be removed
K+
H+
Anions and cations 
Drugs (adrenaline, morphine, penicillin)
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64
Q

What is normal gfr for males and females?

A

Males 115-125ml/min

Females 90-100ml/min

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65
Q

What is renal plasma flow?

A

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

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66
Q

What is the filtration fraction? How is it calculated?

A

20%

GFR/renal plasma flow x 100

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67
Q

What is clearance in the kidney?

A

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]

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68
Q

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

A

Not secreted or reabsorbed
Filtered freely
Not metabolised in the urine

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69
Q

What does egfr account for when measuring serum creatinine?

A

Age sex mass

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70
Q

What is the ideal substance for calculating gfr?

A

Inulin

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71
Q

What is filtered load of a substance?

A

Plasma concentration x gfr

amount of substance filtered per minute

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72
Q

What is the transport maximum?

A

The amount of substance the tubule can reabsorb

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73
Q

What is the renal threshold?

A

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

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74
Q

Why must the kidneys be able to vary sodium excretion?

A

To deal with varied dietary absorption

To allow BP control

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75
Q

What drives na reabsorption in the kidneys?

What ion comes with it? What is the exception to this rule?

A

Na/k atpase on basal membrane

Cl but in early pct hco3

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76
Q

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

A

Increases cholorine tubular concentration allowing paracellular reabsorption

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77
Q

Where is most sodium and water reabsorbed? How much?

A

PCT
65% water
67% sodium

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78
Q

What are the sodium channels in the PCT

Which one is under regulation of hormone? Which hormone?

A

Na/glucose, Na/aa, Na/phosphate, Na/H exchanger

Na/Phosphate under PTH control

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79
Q

How do ion channels differ along the PCT?

A

All present in the first segment

Latter two segments only have Na/H exchanger

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80
Q

Why is the reabsorptionin the PCT described as isoosmotic?

A

Fully permeable to water so no change in osmolarity

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81
Q

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

A

Decending - 10-15% water

Ascending - 25% na

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82
Q

How is na reabsorbed in the ascending loop of henle?

A

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

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83
Q

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

A

Cl into ecf

K through romk back into tubule

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84
Q

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

A

Hypoosmotic

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85
Q

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

A

Tubular cells

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

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86
Q

Where is calcium reabsorption controllable? How?

A

Tubular cells of Early DCT

NCX on basal membrane allows apical reabsorption from tubule under PTH influence

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87
Q

Where is most calcium reabsorbed? Where else?

A

PCT

Ascending loop by lumen positive potential

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88
Q

Explain the principle of glomerulotubular balance

A

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

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89
Q

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

A

5-8% sodium
No water
Becomes more hyposmotic

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90
Q

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

A

3% sodium

5-25% water depending on adh

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91
Q

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

A

Principal cells

Intercalated cells

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92
Q

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

A 
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
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93
Q

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

A

Acid base balance

Active cl reabsorption

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94
Q

What systems influence long term blood pressure control?

A

RAAS
SNS
ADH
ANP

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95
Q

What stimulates renin release?

A

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

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96
Q

Actions of angiotensin II

A

Stimulates aldosterone release
Vasoconstriction
Increased Na/H in PCT

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97
Q

Effect of SNS on BP

A

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

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98
Q

How does ADH influence blood pressure?

A

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

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99
Q

Role of ANP in blood pressure regulation?

A

Released by atria in response to excessive stretch

Causes vasodilation of afferent arteriole increasing GFR and inhibits Na reabsorption in nephron

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100
Q

Why do NSAIDs cause renal failure?

A

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

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101
Q

What are the physiological consequences of HTN?

A

Increased afterload:
LVH
Myocardial ischemia due to increased demand

Arterial damage (athereosclerosis and weakened vessels):
Aneurysm
Thrombus (Cerebrovascular disease)
Retinopathy
Kidney damage
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102
Q

How are changes in osmolarity detected?

How does this occur?

A

Swelling or shrinkage of hypothalmic osmoreceptors

Surrounding capillaries have fenstrated epithelium exposing the receptor to the plasma osmolarity directly

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103
Q

What occurs if plasma osmolarity increases?

A

Stimulation of osmoreceptors stimulates ADH release and increases thirst.

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104
Q

What is the thirst pathway?

A

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

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105
Q

Where is ADH released from?

A

Posterior pituitary

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106
Q

What is the structure of ADH?

A

Small peptide hormone

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107
Q

What are the actions of ADH on the kidney generally?

A

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

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108
Q

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

A

Through aquaporin 3 and 4

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109
Q

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

A

Large volumes of dilute urine

Diabetes insipitus

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110
Q

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

A

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

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111
Q

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

A

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
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112
Q

How does urea cycling effect the corticopapillary osmotic gradient?

A

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

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113
Q

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

A

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!

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114
Q

What are the actions of PTH?

A

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

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115
Q

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

A

4 minutes so can respond quickly to changes in calcium

Released as low calcium increases mRNA transcription and stability

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116
Q

Where is PTH produced and degraded?

A

Chief cells of the parathyroid gland

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117
Q

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

A

Cholecalciferol (from light)

Ergocalciferol (from diet)

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118
Q

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

A

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

119
Q

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

A

25hydroxyvitd to 1.25dihydroxyvitd

120
Q

What is another name for 1.25dihydroxycholecalciferol?

A

Calictriole

121
Q

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

A

24.25dihydroxycholecalcifeole

122
Q

What increases risk of vit d deficiency?

A 
Non-caucasian
Lack of sunlight (indoors, clothes, sunscreen, climate)
Lack of fish oil (ergocalciferol)
Elderly/obese
Cyp450 inducers
123
Q

Actions of calcitriol

A 
Increased gi calcium absorption
Cell differentiation and proliferation
Decreased cell growth
Increase insulin
Decreases renin
124
Q

What is primary hyperparathyroidism?

Biochemical presentation

A

Adenoma of parathyroid gland

High PTH driving high Ca

125
Q

What is secondary hyperparathyroidism?

Biochemical presentation

A

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

126
Q

What is malignant hyperparathyroidism?

A

Release of PTHrP causing high calcium

Calcium very high, PTH low as supressed

127
Q

What is tertiary hyperparathyroidism?

Biochemical presentation?

A

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

128
Q

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

A

Primary hyperparathyroidism is likely

Malignant hyperparathyroidism is unlikely

129
Q

What type of hyperparathyroidism is characterised by a rapid onset?

A

Malignant

130
Q

What are signs and symptoms of hypercalcaemia?

A 
Stones
Moans (constipation)
Grones (depression)
Short QT
HTN
Drowsiness
Polyurea / polydipsia
131
Q

What is the treatment of hypercalceamia?

A 
Underlying condition
Hydration to increase excretion
Loop diuretics
Bisphosphonates
Calcitonin
132
Q

What diuretics can worsten hypercalcemia? Why?

A

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

133
Q

What are the four most common types of renal calculi?

A

Calcium (70%)
Magnesium ammonium phosphate
Urate
Cystine

134
Q

What sort of renal calculi is radiolucent

A

Urate

135
Q

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

A

50%

136
Q

Which gender is more likely to get renal stones?

A

2:1 males:females

137
Q

What increases risk of renal stones?

A

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

138
Q

How do renal calculi present?

A

Asymptomatic
Haematuria
Pain

139
Q

General treatment options of renal calculi

A

Surgery
Lithotripsy
Fluid

140
Q

What is used in uric acid stones

A

Allopurinol

141
Q

What tests in renal calculi?

A

Blood screen
Urine screen
Radiography

142
Q

What are the effects of alkalaemia?

A

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

143
Q

What are the systemic effects of academia

A

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
Q

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

A

Changes HCO3- excretion and creation
Compensates for respiratory
Corrects metabolic

145
Q

What is the general response of the kidney to acidosis?

A

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

146
Q

How does the kidney reabsorb HCO3-?

A 
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
Q

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

A

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
Q

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

A

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
Q

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

A

Phosphate and ammonia

Prevents damage and maintains concentration gradient

150
Q

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

A

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

151
Q

What is the anion gap?

A

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
Q

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

A

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

153
Q

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

A

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

154
Q

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

A

Intracellular buffering

Kidneys cant respond fast enough

155
Q

What is internal k balance

A

Stabilising ecf K by moving in and out of icf

156
Q

What is external k balance?

A

Matching excretion to intake

157
Q

What increases K uptake into cells?

A

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

158
Q

What increases K release from cells?

A

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
Q

Where and how in the kidney is K reabsorbed?

A

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

160
Q

Where and how in the kidney is K secreted?

A

Principal cells

Apical ROMK

161
Q

How is K reabsorption and secretion controlled in the kidney?

A

By altering secretion amounts from 15-120%

Responsive to aldosterone

162
Q

What factors cause K secretion in principal cells?

A

High intracellular K

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

163
Q

What increases secretion of k from principal cells?

A 
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
Q

How does acidosis result in hyperkalaemia?

A

Increased H/K atpase in alpha intercalated cells

Decreased na/k atpase in principal cells lowering k secretion

165
Q

What can cause hyperkalaemia?

A 
Increased intake (needs renal dysfunction OR IV dose)
Decreased excretion (kidney disease, adrenal disease) 
Internal shift (acidosis, cell lysis, exercise)
166
Q

How should hyperK be treated?

A

Calcium gluconate
Glucose and insulin
Salbutamol
Dialysis

167
Q

Causes of hypokalaemia

A 
Increased loss (diarrhoea, vomiting, diuresis, high aldosterone)
Internal shift (alkalosis, aldosterone, adrenaline)
168
Q

Treatment of hypok

A

K replacement

Block aldosterone

169
Q

What diseases result in high aldosterone secretion?

A

Conns syndrome (aldosterone secreting adenoma)

170
Q

What is the lifetime risk of uti in women?

When are they most likely?

A

50%

Children, sexually active (honeymoon), pregnancy, elderly

171
Q

Risk factors for uti

A 
Short urethra (women)
Obstruction (calculi, prostate, tumour, pregnancy)
Neuro problems (unable to empty bladder fully)
Ureteric reflux (especially children)
172
Q

What adaptations to bacteria aid them in surviving to cause uti

A

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

173
Q

How does a lower uti present?

A

Cystitis
Increased urinary frequency
Mild fever
Dysuria

174
Q

How does an upper uti present

A

Loin pain

High fiver

175
Q

Who is more at risk of asymptomatic uti?

A

Elderly

Catheters

176
Q

Define complex uti?

A 
Treatment resistant
Male 
Pregnancy 
Children 
Elderly 
Pyleonephritis
177
Q

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

A

Leucocyte esterase very sensitive

Nitrites very specific

178
Q

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

A

97%

179
Q

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

A

Complicated uti

Fermenting lactose to dx ecoli

180
Q

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

A

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

181
Q

When is microscopy of urine indicated?

A

Kidney disease
Endocarditis
Children under 6

182
Q

What could squames visible on microscopy of urine indicate?

A

Contaminationn

183
Q

Tx for simple, complex and pylonephritis uti

A

Simple 3 days
Complex 7 days
Nitrofurantoin or trimethoprim

Pylo 14 days
Ciprofloxacin or ceftrioxone or gentamicin

184
Q

What can be done for frequently reoccurring utis?

A

More than three a year, prophylactic nitrofuritoin or trimethoprim

185
Q

Which uti patients need imaging?

A

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

186
Q

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

A

Som - pudendal
Symp - hypogastric nerve
Para - pelvic nerve

187
Q

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

A

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

188
Q

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

A

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
Q

What are the two phases of the bladder?

A

Storage

Voiding

190
Q

What is the reflex involved in storing urine?

A

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
Q

How can higher centers influence urinary storage?

A

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

192
Q

What is the effect of detrusor relaxation during bladder filling?

A

Very little change in pressure

193
Q

How does the micturition reflex occur?

A

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
Q

How do higher centres influence micturition?

A

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
Q

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

A

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
Q

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

A

Flaccid bladder - overfilling with overflow incontinence

197
Q

4 types of incontinance

A

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
Q

What is overactive bladder syndrome?

A

Polyuria, nocturia and urge +/- UUI

199
Q

What are non modifiable risk factors for incontinance?

A

Family hx
Anatomical abnomalities
Neurological abnormalities
Age

200
Q

Modifiable risk factors for incontience

A

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

201
Q

Examinations in incontinent patients?

A 
Bmi
Abdo
DRE
Vaginal 
Urine dipstick
Frequency volume chart/diary
202
Q

Advanced investigations for incontinace

A

Invasive urodynamics
Pad test
Cystoscopy

203
Q

SUI management

A 
Stop smoking (decrease cough)
Pelvic floor training
Duloxetine (NA/5HT reuptake inhibitor) 
Vaginal tape 
Fascial sling
Intermurial bulking
204
Q

UUI Management

A 
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
Q

Management of overflow incontinance

A

Treat compression

Avoid constipation

206
Q

Ways of mitigating incontinance?

A

Catheters
Sheaths
Incopads

207
Q

What is AKI?

A

Clinical syndrome causing acute decline in GFR over days to weeks

208
Q

Diagnostic criteria of AKI

A

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
Q

What can AKI cause?

A

Changes to ecf volume
Electrolyte abnormalities
Ph abnormalities

210
Q

What is the in hospital incidence of. AKI

A

5%

211
Q

Cause of prerenal AKI

A

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

212
Q

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

A

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

213
Q

Treatment of pre renal aki

A

Fluids
Underlying cause
Stop offending meds

214
Q

What different pathologies can cause renal aki?

A

ATN
Glomulonephritis
Interstitial disease
Intrarenal obstruction

215
Q

Causes of ATN

A

Sepsis
Nephrotoxins
Ischemia
Continum from pre renal AKI

216
Q

What effect does ATN have?

A

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

217
Q

Examples of endogenous nephrotoxins

A

Bilirubin
Myoglobin
Urate

218
Q

Examples of exogenous nephrotoxins

A 
Xray contrast
Nsaids
Animoglycosides 
Lithium
Antifreeze 
Weedkiller
219
Q

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

A 
Glomerulonephritis
Early rhabdomyolitis 
Hypercalcemia 
Vasoconstrictive drugs (e.g. NA)
Hepatorenal syndrome 
Contrast nephropathy
220
Q

Signs that an AKI is. Prerenal?

A 
Postural hypotension
Low JVP
Sepsis/CHF
Rapid weak pulse 
Low CVP
221
Q

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

A

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

222
Q

What can cause tubulointersitial nephritis?

A

Pyleonephritis

Toxins

223
Q

What causes post renal AKI?

A

Obstruction if bilateral or effecting a sole functioning kidney

224
Q

Examples of. Obstruction causing post renal aki

A

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

225
Q

Tests in AKI?

A 
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
Q

When would dialysis be considered in AKI?

A 
HyperK not responsive to medical tx
Non refractory metabolic acidosis 
Fluid overload not refractory to diuretics 
Dialysable nephrotoxin (eg aspirin OD)
Uremia
227
Q

Signs of uremia

A

Pericarditis
Lowered GCS
N+V

228
Q

What different dysfunctions can renal disease present with?

A

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

229
Q

Causes of microscopic haematuria

A 
Uti
Polycystic kidneys
Renal stones
Tumours
AV malformations
Glomerular disease
230
Q

At what age should all haematuria cases receive a cystoscopy?

A

> 45

231
Q

Differentiate haematuria from glomerular disease and lower urinary tract

A

Glomerular - smoky brown +- protein, painless

LUT - red, clots, pain, no protein

232
Q

Non blood causes of red/brown urine

A

Myoglobinuria

Beetroot

233
Q

At what point in GFR do CKD symptoms present?

A

<30ml/min

234
Q

Presentation of proteinuria

A

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

235
Q

Types of protienuria

A

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

236
Q

Cause of overflow proteinuria

A

Multiple myeloma

237
Q

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

A

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

238
Q

What is nephritic syndrome?

A

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

239
Q

How can the renal capsule result inpathology?

A

Blockage

Leakage

240
Q

What 4 points of the glomerulus are vulnerable to damage?

A

Subepithelial
Basement membrane
Subendothelial
Mesangial

241
Q

Glomerular causes of nephrotic syndrome

A

Minimal change glomerulonephritis
Membranous glomerulonephtitis
Diabetes mellitus

242
Q

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

A

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

243
Q

Changes of minimal change glomerulonephritis on biopsy?

A

None to light microscopy

On electron loss of podocyte foot processes

244
Q

Prognosis of minimal change glomerulonephritis?

A

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

245
Q

What is the commonest adult glomerular nephrotic syndrome?

What causes it?

A

Membranous glomerulonephritis

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

246
Q

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

A

Masses of immunoglobulin deposition

Immunosuppressants

247
Q

How does diabetes cause glomerular disease?

A

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

248
Q

Primary causes of nephritic syndrome

A

IgA nephropathy
Thin glomerular basement membrane disease
Alports syndrome
Goodpastures syndrome

249
Q

When does IgA nephropathy tend to occur?

What does it cause?

A

Post mucosal infection
Immune complex deposition in mesangium
Haematuria

250
Q

What is the prognosis of IgA nephropathy?

A

Progression to renal failure with transplant as the only option

251
Q

What is the prognosis of thin glomerular basement membrane disease?

A

Benign

252
Q

What is alports syndrome?

A

X linked inherited disease causing split basement membrane

Progresses to renal failure

253
Q

What is goodpastures syndrome?

A

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

254
Q

What is. Goodpastures syndrome associated with?

A

Pulmonary haemorrhage in smokes

255
Q

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

A

Vasculitis e.g. Wegners

Antineurtophil cytoplasmic antibody ANCA

256
Q

What is the epidemiology of prostate cancer?

A

Most common male cancer

Second most common cause of male cancer death

257
Q

What is the prognosis of prostate cancer?

A

Most people diagnosed are unlikely to die of the cancer

258
Q

What increases the risk of prostate cancer?

A

Age
Family history
Black ethnicity

259
Q

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

A

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

260
Q

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

A

Malignant cancer
Prostatic hypertrophy
Benign cancer
Prostatic inflammation

Massive overdiagnosis

261
Q

What are the risks involved with prostate cancer treatment?

A

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

262
Q

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

A

80%!

263
Q

What are symptoms of prostate cancer?

A 
Asymptomatic
Bladder overactivity
Metastatic bone pain
Urinary tract obstruction
Uncommonly weight loss and haematuria
264
Q

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

A

DRE and PSA - transrectal ultrasound guided biopsy

LUT symptoms - TURP

265
Q

How is prostate cancer graded?

A

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
Q

What treatments are available for prostate cancer?

A

Surveillance
Radical prostatectomy
Radiotherapy (external or brachytherapy)

267
Q

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

A

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

268
Q

What non hormonal treatments are available for metastistied prostate cancer?

A

Targeted radio and chemo therapy for the bone mets

Bisphosphonates

269
Q

What is the normal type of bladder cancer?

A

Transitional cell carcinoma

270
Q

What are risk factors for bladder cancer?

A

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

271
Q

How are bladder tumours staged?

A

Superficial (most)
In situ
Invading muscle

272
Q

How are superficial bladder tumours treated?

A

Transureathral resection of bladder tumour

273
Q

Hw are bladder tumours that have invaded muscle treated?

A

Radical cystectomy

Palliative

274
Q

Risks for renal cell carcinoma

A

Smoking
Obesity
Dialysis

275
Q

How can renal tumours spread?

A

Perinephric
Lymph nodes
Into IVC to right atrium

276
Q

How can upper tract transitional cell carcinomas spread?

A

Pelvis to bladder NOT reverse usually due to urine. Flow

277
Q

How are renal cell carcinomas treated

A

Radical or partial nephrectomy

278
Q

How are upper tract transitional cell carcinomas treated

A

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

279
Q

What is ckd

A

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

280
Q

Cuases of ckd

A 
Glomerulonephritis
Pyelonephritis
Obstruction
Htn
Vascular disease 
Dm
281
Q

How is ckd. Detected?

A

Opportunistic testing of at risk groups

282
Q

How id ckd graded?

A

g1-G5 based on GFR

A1-A3 based on protein:creatinin ratio in urine

283
Q

What. Grade of ckd is kidney failure?

A

G5

284
Q

What. Is the main cause of death in CKD

A

Cvd

285
Q

What does proteinuria mead diagnostically in ckd?

A

Increased risk of need of dialysis

286
Q

When should a biopsy be performed in ckd?

A

Normal sized kidney with no obvious diagnosis

287
Q

Complications of CKD

A 
Acidosis
Anaemia
Bone disorders. 
Non bone calcification
Cvd
288
Q

What are the bone disorders of ckd?

A

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
Q

Benefits and costs of haemodialysis

A

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
Q

Contraindications and side effects of haemodialysis

A

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
Q

Benefits and costs of peritoneal dialysis

A

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

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

292
Q

Contraindications and complications of peritoneal dialysis

A

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
Q

When is the largest risk post kidney transplant?

A

3 months

294
Q

What are the risks post kidney transplant?

A

Infection
Cancer
HTN

295
Q

What type of donor provides best chance?

What is ave. life expectancy

A

Related live

12 years

296
Q

What meds are used to prevent kidney donor rejection?

A

Mycophenolate

Tacrolimus

PPE (12 decks)

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