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Flashcards in LSS - Urinary Deck (111):
1

Describe the structure and formation of ureters

Structure: muscular tubes transporting urine from kidneys to bladder using peristalsis Formation: continuous with renal pelvis and formed by condensation of 2/3 major calices

2

Describe the course of the ureters and state the locations of constrictions

Course: descend retroperitoneally on the medial aspect of Psoas major to the pelvic brim, where they cross the common iliac/proximal end of the external iliac artery to enter the pelvic cavity and enter the bladder (at the level of the ischial spine) Constrictions: 1) Ureteropelvic junction 2) Point of crossing the common iliac vessels at the pelvic brim 3) Entrance to the bladder

3

Describe the vasculature and innervation of the ureters

Vasculature: renal arteries, abdominal aorta and internal iliac arteries all branch to supply Innervation: renal, aortic and sup/inferior hypogastric plexuses all innervate

4

Describe where urinary stones will cause pain in the ureters and the mechanism of referred pain

Pain: when reach the three constrictions Mechanism: visceral afferents return to T11-L2 leading to referred pain at those dermatomes e.g. posterolateral abdominal wall pain

5

Describe the structure of the bladder

Apex: most anterosuperior point Base: inverted triangle and points posteriorly; ureters enter at upper corners, with the urethra draining inferiorly from the lower corner of the base Trigone: smooth area between openings of ureters and urethra

6

Describe the attachments of the apex and inferolateral surfaces of the bladder

Apex: directed towards the top of the pubic symphysis and attached to the umbilicus via the medial umbilical ligament Inferolateral surfaces: cradled by pelvic muscles

7

Describe the lining/wall of the bladder

Lined by the urothelium (3-layered membrane with slow cell turnover and large, impermeable luminal cells)

8

Describe the anchoring of the neck of the bladder in men and women

Men: puboprostatic ligaments - blend with fibrous capsule of the prostate which surrounds the neck Women: pubovesical ligaments - supported by peritoneum and associated muscles

9

Describe the reflexive response of the bladder to filling

Filling activates sensory PSNS stretch fibres, leading to S2-4 motor neurones to signal detrusor muscle to cause contraction and open internal sphincter

10

State the location, muscle type and innervation of sphincter vesicae of the urethrae

Location: neck of the bladder Muscle type: internal smooth muscle Innervation: PSNS relax, SNS contract

11

State the location, muscle type and innervation of sphincter urethrae of the urethrae

Location: perineum Muscle type: external striated muscle Innervation: tone maintained by somatic nerves (S2-4; leading to voluntary control)

12

Describe the length and course of the urethra in males

Longer urethra, passes inferiorly through the prostate, through the deep perineal pouch and perineal membrane and enters the root of the penis (divided to preprostatic, prostatic, membranous and spongy parts)

13

Describe the length and course of the urethra in females

Short urethra, travelling inferiorly through the pelvic floor and deep perineal pouch/membrane to open into the vestibule between the labia minora;

14

Describe the macroscopic structure of the kidneys and associated glands

Kidneys: bean-shaped organs located retroperitoneally in the posterior abdomen, surrounded by a fascial pouch containing peri-renal adipose tissue Suprarenal glands: also enclosed within the renal fascia and separated by a thin septum, with the fused layer connecting with the transversalis fascia on the lateral abdominal wall

15

State the superior relations of the kidneys

Diaphragm (and spleen for left kidney)

16

State the posterior relations of the kidneys

medial to laterally Psoas major, quadratus lumborum, transversus abdominis Neurovascular: top half has ilio-inguinal nerve, ilio-hypogastric nerve and subcostal vessels passing posteriorly

17

State the anterior relations of the kidneys

Left: stomach, pancreas, spleen and splenic flexure Right: liver and hepatic flexure

18

State the height of the kidneys and their hilums

Left kidney: apex = 11th rib posteriorly Right kidney: apex = 11th ICS posteriorly Both: hilum = L1

19

Describe the appearance and role of the renal cortex and medulla in kidneys

Renal cortex: outer layer of the kidney - continuous band of place tissue, with projections called renal columns into the inner aspect to divide the medulla to discontinuous aggregations [Granular] Renal medulla: pyramid shaped regions of the kidneys where nephrons are present [Striated]

20

Describe the structure and roles of the minor calices, major calices and hilums of the kidneys

Minor calices: apical projections of the renal pyramids Major calices: unity of several minor calices - multiple major calices unite to form the renal pelvis Hilum: deep vertical slit through which the renal vessels, lymphatics and nerves enter/leave (continuous internally with the renal sinus)

21

Describe the arterial supply of the kidneys including at the hilum

Renal arteries: lateral branches of the abdominal aorta that supply each kidney; arise inferior of the SMA origin at L2/3, with the left renal artery shorter and higher At the hilum: the renal arteries divide to anterior and posterior branches to supply the parenchyma

22

Describe the venous drainage of the kidneys, including the relations to the arterial supply

Renal veins: are formed by multiple smaller veins, and run anterior to the arteries; left renal vein crosses anterior to aorta but posterior to the SMA, and can be compressed by aneurysms in either vessel

23

Recall what proportion of cardiac output normally perfuses the kidney

20-25% CO to generate pressure for ultrafiltration (achieved due to direct branching from the aorta)

24

Define the renal filtration fraction and state the normal value

Ratio of renal plasma flow to amount of filtrate filtered by the glomerulus - normally 20%

25

Define renal plasma flow, state how it can be calculated and how it may be used to calculate the GFR

RPF: volume of plasma passing through the kidneys per unit time - usually approx 0.6L min-1 Calculation: renal blood * (100 - haematocrit [%]) GFR = RPF x Filtration Fraction

26

Define the terms freely filtered and primary urine

"Freely filtered": solute found at same concentration in filtrate and plasma Primary urine: clear ultrafiltrate fluid free from blood and proteins (produced before secretion/absorption occurs)

27

Describe the process of glomerular filtration and the barriers in place

Process: passively occurs as fluid driven through semipermeable walls of glomerular capillaries into Bowman's capsule by cardiac hydrostatic pressures Filtration barrier: fenestrated capillary endothelia and semipermeable Bowman's capsule (due to podocyte foot processes) highly permeable to fluids and small solutes but not cells, proteins and drugs carried by proteins

28

Form an equation to determine the amount of a substance excreted by the kidneys

Amount secreted = amount filtered + amount secreted - amount absorbed

29

Define the glomerular filtration rate and state the normal value

Amount of fluid filtered from the glomeruli into the Bowman's capsule per unit time (ml min-1) - sum of rate of all functioning nephrons Normal value: 120ml min-1

30

State and explain the equation for glomerular filtration rate

GFR = Puf x Kf Kf: ultrafiltration coefficient and represents membrane permeability and surface area available for filtration (changes lead to imbalance, and kidney disease may reduce number and hence SA)

31

Describe the glomerular filtration pressures and form an equation for Puf

Glomerular filtration pressures: driving force is the hydrostatic pressure in glomerular capillaries (Pgc) but is opposed by the hydrostatic pressure of the tubule (Pt) and osmotic pressure of glomerular plasma proteins (πgc) Puf = Pgc - Pt - πgc; usually creates a net ultrafiltration pressure of 10-20mmHg

32

State the factors that affect GFR and how these may be controlled

Pgc: Pressure in the capillaries πgc: Osmotic pressure of glomerular plasma proteins Pt: Pressure in the tubules Kf: ultrafiltration coefficient All can be hormonally or neurally controlled

33

State the effects of arterial blood pressure, plasma protein concentration and uretal obstruction on GFR

Arterial blood pressure: if increases, will increase Pgc and hence Puf and GFR Plasma protein concentration: if increases, will increase πgc and hence decrease Puf and GFR Ureteral obstruction: will increase Pt, hence decreasing Puf and GFR

34

Describe myogenic autoregulation of blood flow in the kidneys

VSMCs contract when smooth muscle stretched, so when afferent arterial pressures rise, vessel resistance does too, reducing the blood flow to keep the GFR constant

35

Define renal clearance and form an equation

Renal clearance: extent to which substances passing through the kidneys are removed from the blood - no. Litres plasma that are completely cleared of the substance per unit time Clearance = (urine concentration x rate of urine production)/concentration in plasma ml min-1

36

Describe how GFR may be estimated using clearance, stating the two substances used

Estimation: use freely filtered not secreted/reabsorbed molecules (filtered = excreted) Inulin: non-toxic plant polysaccharide that can be measured in plasma and urine - must be transfused Creatinine: endogenous waste product from muscle metabolism of creatine - constant amount in blood and hence urine - if high/low then renal failure

37

Describe how renal plasma flow may be estimated using renal clearance

PAH (para aminohippurate) filtered and actively secreted in one pass of the kidney and should be 625ml min-1

38

List the regions of the nephron and type lining seen in each

Afferent arteriole: simple squamous Corpuscle: fenestrated capillary endothelium, specialised basal lamina, podocytes with foot processes Proximal tubule: cuboidal epithelium and brush border Loop of Henle: simple squamous (thinner on dLoH) Distal tubule: cuboidal epithelium and no brush border Collecting duct: epithelial

39

List the arteries supplying a nephron in order from aorta to glomerulus

Aorta > Renal Artery > Segmental Artery > Interlobal Arteries > Arcuate Arteries > Afferent Arterioles

40

Describe the functional significance of the efferent arteriole and glomerulus

Efferent: smaller diameter than afferents to increase glomerular pressure Glomerulus: fenestrated walls for ultrafiltration

41

Describe the distribution of body fluids

Intracellular: 65% Extracellular: 35% including interstitial, plasma and transcellular

42

List the processes that lead to water loss and the volume lost in each per day

Sweating: variable; approx 450ml Faeces: approx 100ml Respiration: approx 350ml Urine: approx 1500ml

43

State the percentage of filtered water that reaches the dLoH, DCT and Bladder

dLoH: 30% DCT: 20% Urine: 1-10%

44

State the locations of low pressure and high pressure baroreceptors

Low pressure baroreceptors: right atria, right ventricle and pulmonary circulation High pressure baroreceptors: carotid sinus, aortic arch and juxtaglomerular apparatus

45

Describe the response of low-pressure baroreceptors to hypo- and hyper-tension

Hypotension: afferent fibres to brainstem increase ADH release and SNS discharge Hypertension: atrial stretch releases ANP/BNP

46

Describe the response of high-pressure baroreceptors to hypotension

Hypotension: causes afferent fibres to brainstem to increase ADH release and SNS discharge; JGA causes renin release

47

Describe the release and functions of ANP

ANP: atrial natiuretic peptide; release in atria in response to stretch Functions: - Renal vessel vasodilation - Inhibition of sodium reabsorption - Inhibition of renin/aldosterone release - Blood pressure reduction

48

Describe the response of the heart, brain and kidneys to changes in volume

Heart: hypervolaemia leads to ANP/BNP to inhibit sodium reabsorption and renin release Brain: increases ADH to increase aldosterone/sodium reabsorption if hypovolaemic Kidneys: hypovolaemia leads to renin secreiton to produce more AGTII/aldosterone

49

Recall the homeostatic, endocrine and exocrine functions of the kidneys

Homeostatic: controlling electrolyte reabsorption to affect volume state Endocrine: produces erythropoietin and hydroxylates hydroxycholecalciferol to produce calcitriol Exocrine: removes urea, metabolites and toxins from blood

50

Recall the changes in processes after kidney failure

Loss of excretory functions - Loss of homeostatic function - Loss of endocrine - Abnormality of glucose homeostasis

51

Describe the appearance of hypokalaemia and hyperkalaemia on an ECG

Hypokalaemia: risk of VF (sigmoid T-waves) Hyperkalaemia: risk of asystole (pointed T waves, QRS broadening and loss of P waves)

52

Describe the effect of kidney disease on electrolytes, renal function and cardiovascular disease

Electrolytes: hyperkalaemia and hyponatraemia (leading to volume depletion) Renal function: high plasma urea and creatinine CVD: increased risk of MI

53

Describe the effects of kidney failure on the endocrine system

Anaemia: results due to reduced erythropoietin synthesis Hyperparathyroidism: lower level of hydroxylation of cholecalciferol leading to increased PTH

54

Describe the effect of chronic kidney disease on acid-base balances and attempts at compensation

Acidosis: decreased proton excretion and base rentention leads to acidaemia and Kussmahl's respiration (air hunger - rapid/deep breathing to attempt to compensate)

55

State how acute and chronic loss of kidney function may be distinguished

Acute loss: previously normal creatinine and renal size unchanged Chronic loss: previously abnormal creatinine, renal size reduced and chronic uraemic symptoms

56

Recall methods of estimating renal function, stating the disadvantages of each

Urea: poor indicator and confounded by GI bleeding, drugs and diet Creatinine: affected by muscle, age, sex and race Creatinine clearance: overestimates low GFR Inunlin clearance: labour intensive

57

Describe how renal function may be estimated clinically

eGFR: estimated GFR - uses equations to calculate GFR from serum creatinine and patient factors such as age, ethnicity and sex

58

Explain the MoA of Loop diuretics

Blocks the Na+/K+/Cl- transporter on the aLoH, reducing movement into the lining so water and electrolytes are retained in urine E.g. furosemide

59

Explain the MoA of Thiazide diuretics

Block the Na+/Cl- exchanger in the DCT, reducing sodium uptake but also allowing the Na+/Ca2+ exchanger to dominate, so more calcium is reabsorbed

60

Explain the MoA of Osmotic diuretics

Glucose/mannitol act as solutes to reduce osmotic gradient and decrease water reabsorption

61

Explain the MoA of Potassium sparing diuretics

Amiloride: blocks sodium channels Spironolactone: aldosterone antagonist

62

Explain the MoA of carbonic anhydrase inhibitor diuretics

Inhibit carbonic anhydrase to reduce sodium reabsorption as fewer protons are available for the Na+/H+-ATPase pump

63

List the normal tests on a urine dipstick, and what abnormalities each may represent

Blood and protein: kidney damage Urobilinogen and bilirubin: liver disease Nitrite: produced by bacteria - indicate infection Ketones: disruption to carbohydrate metabolism Glucose: diabetes pH Leukocytes: infections

64

Recall options available for renal replacement therapy

Haemodialysis: blood extracted from fistula and extra-corporeally filtered to remove waste and water Peritoneal dialysis: dialysate fluid pumped to peritoneal cavity, with capillaries as blood source; ultrafiltration controlled by altering osmolality of dialysate Transplantation: provides best long term outcomes; placed extraperitoneally in the iliac fossa

65

Recall the dietary modifications advised for kidney disease

Avoidance of high salt food as sodium will not be removed - Low potassium foods - Consideration of phosphate intake (not usually a problem in early CKD) - Do not restrict protein - Fluid restriction in advanced CKD VitD supplementation - Iron tablets if anaemic

66

Recall the normal blood and urine pH ranges, stating the percentages of acid clearance performed by the lungs and kidneys

Blood: 7.35-7.45 Urine: 5-8 Acid clearance: 99% by lungs and 1% by kidneys

67

State the function of bicarbonate in the plasma and amount reabsorbed in the PCT, aLoH, DCT and CD

Function: high capacity chemical buffer that can rapidly respond to volatile acid production PCT: 80% aLoH: 10% DCT: 6% CD: 4%

68

Recall the Henderson-Hasselbach equation and normal values

HH: pH = pK + log10([HCO3-]/[CO2]) pK: constant at 6.1 [HCO3-] = 24mmol/L [CO2] = 1.2 mmol/L

69

Describe the role of the Davenport diagram

Graphical representation of assocation between pH, bicarb and CO2

70

Describe the regions of a Davenport diagram occupied by a metabolic acidosis and alkalosis

Metabolic alkalosis: curves up and right as pH increases and bicarbonate does too Metabolic acidosis: curves down and left as pH decreases and bicarbonate does too

71

Describe the regions of a Davenport diagram occupied by an acute and chronic respiratory acidosis

Respiratory acidosis: curves up and left as pH decreases but CO2 increases Chronic respiratory acidosis: long slower disorder that steadily increases CO2 and decreases pH

72

Describe the regions of a Davenport diagram occupied by an acute and chronic respiratory alkalosis

Respiratory alkalosis: curves down and right as pH increases but CO2 decreases Chronic respiratory alkalosis: long slower disorder that steadily decreases CO2 and increases pH

73

Recall how the concentration of bicarbonate inside cells lining the nephron tubule is increased

1) Carbonic anhydrase catalyses the reaction of HCO3- and protons to form CO2 and water 2) CO2 diffuses into the cell over the membrane 3) Carbonic anhydrase catalyses the reaction of CO2 and water to produce H+ and HCO3-

74

Recall the mechanisms to reabsorb bicarbonate into the blood in the kidneys

First enters cells using carbonic anhydrase Chloride-bicarb exchangers: remove bicarbonate from the lining in exchange for chloride ions (diffuse to blood via CFTRs) Sodium-bicarb cotransporters: symport 3 HCO3- ions for one Na+ into the blood (requires sodium proton antiporter to increase cellular [Na+]

75

Describe the role of intercalating cells in the nephron

Either exist as alpha acid-secreting cells or beta bicarbonate-secreting cells

76

Recall the mechanisms to secrete acid in alpha intercalated cells

Carbonic anhydrase increases plasma [HCO3-] and [H+] Acid secretion: protons secreted to filtrate using sodium-proton antiporters, H+/K+-ATPases or H+-ATPases Bicarb saving: chloride bicarb exchangers move HCO3- to blood to buffer remaining acid

77

Recall the mechanisms to secrete bicarb in beta intercalated cells

Carbonic anhydrase increases plasma [HCO3-] and [H+] Bicarb secretion: chloride bicarb exchangers move HCO3- to filtrate and CFTRs allow chloride to diffuse back out Acid saving: protons secreted to blood using sodium-proton antiporters, H+/K+-ATPases or H+-ATPases

78

Describe how bicarbonate may be generated in the kidneys

1) Glutamine split into ammonium and bicarbonate 2) Ammonium exchanged for sodium, entering the filtrate 3) Chloride bicarbonate exchangers remove bicarbonate from the cell to the blood in exchange for chloride ions (which diffuse out the cell via CFTRs)

79

Describe acute and chronic compensation for respiratory acid-base disturbances

Acute: intracellular buffering Chronic acidosis: bicarb generation and increased ammonium excretion Chronic alkalosis: decreased bicarb reabsorption and decreased ammonium secretion

80

Explain the meaning of transcellular and paracellular transport

Transcellular transport: through the renal tubular cell walls Paracellular transport: via the tight junctions between cells

81

Describe methods of passive movement of molecules in the nephron, and rate limits

Protein independent transport: for lipophilic molecules (rate increases linearly with concentration) Protein dependent transport: for hydrophilic molecules (rate limited by number of protein transporters)

82

Contrast primary and secondary active transport

Primary: directly coupled to hydrolysis Secondary: indirectly coupled to ATP hydrolysis (ATP used to establish concentration gradient for symport/antiport)

83

Describe how protein is reabsorbed from the urine

Some protein enters primary urine, and low specificity/high affinity receptors on the tubular wall lead to endocytosis Endosome pH decreases to allow detachment and recirculation of receptors to the membrane

84

Describe how glucose is reabsorbed in the nephrons

Up to 10-15mmol/L can be reabsorbed by co-transport of sodium (after this maxima, all channels saturated)

85

List the substances passively and actively reabsorbed in the PCT

Passive: urea and water Active: glucose, amino acids, sodium, potassium, calcium, VitC and uric acid

86

Describe the structure and role of the proximal convoluted tubule

Structure: cuboidal epithelium, sealed with tight junctions, and a brush border Role: Na+/K+-ATPase used to establish sodium concentration gradient for co-transport of solutes

87

Describe the composition of tubular fluid

Glucose, small proteins, urea, electrolytes, water and filtered molecules

88

Contrast the luminal and basolateral membranes

Luminal: faces the lumen and contains many co-transporters that use sodium to facilitate reabsorption Basolateral: faces peritubular capillaries and contains protein channels to allow molecules to enter capillaries, Na+/K+-ATPase and a Cl-/HCO3- exchanger

89

Recall examples of ion-selective channel transport and co/counter-transport of solutes in the renal tubules

Ion-selective channels: potassium diffuses from lining to lumen of aLoH Co-transport: Na+/Cl- co-transporter in DCT Counter-transport: Na+/K+-ATPase in DCT

90

Recall mutations in tubular transporters causing renal dysfunction

Renal Tubular Acidosis: faulty carbonic anhydrase/proton pumps mean protons accumulate in blood Bartter Syndrome: Na+/Cl-/K+ mutation = excessive electrolyte loss (hypokalaemia) Fanconi Syndrome: PCT disease associated w/RTA leading to uric acid and protein secretion

91

Recall the proportions of solute reabsorbed in the PCT compared to distal nephron

PCT: 60-70% all solutes reabsorbed (100% glucose and 65% sodium) Distal nephron: LoH absorbs 25% sodium and DCT 8%

92

Describe the mechanism of reabsorption in the PCT

Na+/K+-ATPase pumps sodium from the lining to the peritubular capillaries to establish a concentration gradient Co-transporters reabsorb molecules using sodium ions in the lumen (secondary active transport)

93

Describe the mechanism of reabsorption in the aLoH

Na+/K+-ATPase establishes sodium concentration gradient Na+/K+/Cl- transporter moves Na+, 2 Cl- and K+ from lumen to lining Chloride ion channels on basolateral membrane and potassium channels on the apical membrane allow facilitated diffusion out the lumen, and a K+/Cl- co-transporter is present on the basolateral membrane

94

Describe the mechanism of reabsorption in the DCT

Na+/K+-ATPase establishes concentration gradient Chloride ions co-transported with sodium on the apical surface, and then enters blood using basolateral ion channels 3Na+/Ca2+ exchanger establishes calcium gradient, encouraging facilitated diffusion over the apical membrane using an ion channel

95

Contrast principal and intercalated cells

Principal cells: aldosterone sensitive; tight junctions limit paracellular transport Intercalated cells: ATP dependent proton pump to regulate acid base balance

96

Describe the effects of modifying dietary sodium

Increasing sodium = increasing blood osmolarity and BP Increased: ANP decreases reabsorption Decreased: SNS/AGTII/Aldosterone stimulates nephron to reabsorb more

97

Define osmolarity and state the normal osmolarity of plasma and urine

Osmolarity: measure of osmotic pressure exerted by a solution across a semi-permeable membrane (depends on number of particles in solution) Plasma: 285-295 mosmol/L Urine: 50-1200 mosmol/L

98

Describe the interstitial osmolarity

Exists in gradient, highest at base and lowest at top (300-1200 mosmol/L)

99

Describe how a gradient is established in the LoH

1) salt actively pumped out aLoH, generating an osmotic gradient to the interstitium 2) water leaves the dLoH via osmosis, concentrating the filtrate 3) dLoH filtrate enters the aLoH and salt actively removed, decreasing concentration as rises so less removed at the top

100

Describe the process of urea recycling

AQPs in the CD allow water but not urea to diffuse out the lumen, concentrating urea down the CD At the base of the CD, urea permeability increases due to UT-A1 and UT-A3, causing diffusion to the interstitium to generate an osmotic gradient

101

Describe the role of the vasa recta

Permeable to water and solutes, allowing oxygen and nutrients to be delivered without loss of gradient

102

Describe the mechanism of vasopressin and the effect of EtOH on release

Mechanism: causes insertion of AQP2 to luminal CD membrane to increase water permeability and stimulates UT-A1/UT-A3 fusion at the base to allow urea movement Ethanol: inhibits release causing dehydration

103

Describe the macula densa mechanism in the RAAS

Macula densa cells shrink due to hyperosmolar environment leading to PGE2/NO production/release that stimulate renin release

104

Describe the effects of AGTII on the adrenal gland, PCT and vascular system

Adrenals: aldosterone synthesis PCT: increased sodium uptake (increasing water reabsorption and hence BP) Vascular: increased vasoconstriction (and hence BP)

105

Describe the effects of aldosterone

- Increased sodium reabsorption: induces apical Na+ channel expression - Increased potassium secretion: induces Na+/K+-ATPase pump formation - Increased proton secretion

106

Describe the effects of hypo- and hyper-aldosteronism

Hypoaldosteronism: reduced DCT sodium reabsorption leads to urinary loss and BP decrease - increasing renin, AGTII and ADH (causes dizziness, salt craving and palpitations) Hyperaldosteronism: increased DCT sodium reabsorption leads to reduced urinary loss, increased ECF volume and reduced renin/AGTII/ADH (and increased A/BNP) - (causes muscle weakness, polyuria and thirst)

107

Recall the effect of the SNS in response to blood volume changes

SNS activity stimulates renin release and arteriolar vasoconstriction to decrease GFR

108

Describe the immediate response to potassium intake

Enters cells using Na+/K+-ATPase, and insulin/aldosterone/adrenaline increase rate of uptake

109

Describe the secretion of potassium by principal cells

Na+/K+-ATPase pump moves potassium into principal cells, allowing it to leak out to tubule via apical channels

110

Describe the effect of cilia and aldosterone on renal potassium handling

Cilia: stimulate PDK1 to cause cascade to increase intracellular Ca2+ and activate potassium channels Aldosterone: stimulates uptake to principal cells so more enters the lumen

111

Recall the frequency and causes of hypo- and hyper-kalaemia

Hypokalaemia: 20% patients; diuretics and vomiting/diarrhoea Hyperkalaemia: 1-10% patients; potassium sparing diuretics, ACE inhibitors and elderly