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URI > Renal endocrinology > Flashcards

Renal endocrinology Flashcards

1
Q

What is the action of parathyroid hormone?

A

Increase blood concentrations of calcium

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2
Q

How does parathyroid hormone carry out its function?

A
  • Stimualtes production of calcitriol in kidney
  • Facilitates mobilisation of calcium and phosphate from bone
  • Maximise tubular reabsorption of calcium within teh kidney
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3
Q

What is the action of calcitonin?

A

Decrease blood calcium

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4
Q

How does calcitonin carry out its function?

A
  • Suppress renal tubular reabsorption of calcium

- Inhibits bone resorption

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5
Q

Why are calcium and phosphorous considered together?

A
  • Ratio
  • React in opposite ways
  • As calcium increases, phosphate falls and vice versa
  • Can bind together
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6
Q

How are calcium and phosphorous linked to iron?

A
  • Are all divalent ions, so need ion transported in order to be absorbed from GI tract
  • Compete for these transporters
  • I.e. excess calcium in diet leads to iron deficiency
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7
Q

Describe the actions of magnesium in the body

A
  • Enzyme cofactor
  • Needed for regulation of blood glucose, production of energy and protein, nerve transmission, muscle contraction, bone and cel formation
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8
Q

What is unusual about magnesium in ruminants?

A
  • Is absorbed from rumen

- In otehers is absorbed from small and large intestine

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9
Q

What condition is caused by low magnesium intake? What are the signs?

A
  • Hypomagnesaemic tetany
  • Aka Grass Staggers
  • Often cows
  • Weakness, muscle cramps, tremors
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10
Q

Why does renal failure often lead to derangements of calcium and phosphorous?

A
  • Calcitriol synthesised in kidney
  • No calcitriol = no absorption of calcium from intestine = deficiency
  • Tubular reabsorption of calcium in the kidney
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11
Q

Why does bone demineralisation occur in renal failure?

A
  • Increased PTH to increase blood calcium
  • No calcitriol to feedback to stop PTH production
  • PTH continues to be produced, causes bone resorption
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12
Q

What is RAAS?

A

Renin angiotensin aldosterone system

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13
Q

What are the mechanisms of autoregulation of renal blood flow?

A
  • Myogenic feedback

- Tubuloglomerular feedback

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14
Q

Describe myogenic feedback in high bood pressure

A
  • Increased renal blood flow
  • Stretch vascular smooth muscle in afferent arteriole
  • Calcium entry, release of more Ca from internal stores
  • Automatic constriction of afferent arteriole to reduce glow to glomerulus and decrease GFR
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15
Q

Describe myogenic feedback low blood pressure

A
  • Reduced renal blood flow
  • Reduced stretch of vascular smooth muscle
  • Automatic vasodilation of afferent to increase flow to glomerulus (increase GFR)
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16
Q

Why is the renal myogenic response considered to be pre-renal?

A

Controls the blood going into the renal corpuscle

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17
Q

Describe the mechanisms of tubuloglomerular feedback

A
  • Signal from distal tubule to glomerulus to reciprocally alter filtration
  • Decrease flow rate in ascending LoH = increase GFR in same nephron
  • Also related to NaCl levels in tubular fluid
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18
Q

Describe the effect of NaCl in tubuloglomerular feedback

A
  • NaCl low, cells at macula densa generate less adenosine
  • Stimulates decreased intracellular Ca in VSMC = afferent vasodilation
  • Reverse with high NaCl
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19
Q

What is the action of prostaglandins and nitric oxide on the afferent arteriole?

A

Vasodilate (to protect against severe vasoconstriction)

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20
Q

What occurs in acute heamorrhage?

A
  • Intrinsic mechanisms of kidney (myogenic and tubuloglomerular feedback)
  • Extrinsic mechansms e.g. sympathetic system, angiotensin II, endothelin, prostaglandins, nitric oxide
  • Main aim is to maintain pressure to brain, massive total peripheral vasoconstricton
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21
Q

How does the kidney control blood pressure?

A
  • Water balance (blood volume directly impacts blood pressure)
  • Hormonal (stimulation of RAAS)
  • Macula densa
  • Acts to monitor blood pressure and stimulate hormonal systems, since recevies 20% of cardiac output and has high perfusion
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22
Q

What are the components of the RAAS and where are these produced what is their stimulation?

A
  • Renin: kidney, low perfusion
  • Angiotensin: liver, in response to renin
  • Aldosterone: adrenal gland cortex in response to Ang II
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23
Q

Describe how the RAAS works

A
  • Low perfusion sensed by kidney
  • Release of renin
  • Catalyses conversion of angiotensinogen to angiotensin I
  • Angiotensin I to angiotensin II using ACE from lungs and endothelial cells
  • Angiotensin II to adrenal cortex to stimulate aldosterone secretion
  • Aldosterone acts on kidney to increase Na retention
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24
Q

What are the actions of angiotensin II?

A
  • Increase sympathetic activity
  • Increase Na, Cl reabsorption, K_ excretion and thus H2O retention
  • Stimulate aldosterone secretion
  • Arteriolar vasoconstriction to increase blood pressure
  • Stimulate ADH secretion to increase collecting duct reabsorption of H2O
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25
Q

What is the action of RAAS in relation to blood pressure?

A
  • Stabilise blood pressure rapidly

- Enables variable salt intake whilst maintaining ECF volume and thus arterial pressure

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26
Q

What is the function of the macula densa?

A
  • Senses distal tubule and afferent/efferent arterioles

- Increase or decrease nerve firing and flow rate in response

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27
Q

Describe the overall effect of RAAS

A
  • Loss of blood volume > redcued ECF > BP falls > renal flow falls > tubular flow decreased > less NaCl to macula densa > stimualtes renin from juxtaglomerular apparatus > increased intrarenal and systemic Ang II > increase systemic and intrarenal resistance > support continued filtration despite reduced RBF adn increased peripheral vascular resistance
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28
Q

How does angiotensin II exert its actions in the renal tubules as a whole?

A

Insertion of Na+ channels in renal tubules via AT1 receptors

-

29
Q

How does angiotensin II exert its actions in the proximal tubule?

A
  • Inserts apical Na+/H+ exchanger

- Inserts basolater Na+3(HCO3-) and Na+/K+ ATPase

30
Q

How does angiotensin II exert its actions in the thick ascending limb?

A
  • Inserts apical Na+/H+ exchanger

- Na+K+2Cl- pump

31
Q

How does angiotensin II exert its actions in the collecting duct?

A

Inserts epithelial Na+ channel (ENaC)

32
Q

What is the function of ACE?

A
  • Angiotensin converting enzyme

- Converts angiotensin I to angiotensin II

33
Q

What are the actions of AngII in cardiac disease?

A
  • Contraction of vascular smooth muscle produces vasoconstriction
  • Stimulates aldosterone secretion from adrenal cortex
  • Increases sodium reabsorption in proximal tubule
  • Stimulates hypertrophy of myocardiac and vascular smooth muscle
  • Stimulates thirst receptors in brain
  • Enhanced adrenergic tone and increased release of noradrenaline from sympathetic nerve terminals
  • increases endothelin release, may cause vasoconstriction
  • Increased BP, furhtering heart disease
34
Q

What is the role of AngII in renal disease?

A
  • Increased glomerular capillary pressure (efferent vasoconstriction)
  • Increased glomerular protein loss
  • Activaton of inflam cells
  • Development of systemic hypertension associated with some renal disease, can contribute to progressive renal damage
35
Q

What is the function of ACE inhibitors?

A
  • Inhibit ACE

- Thus reduce activity of AngII

36
Q

What are the systemic actions of ACE inhibitors

A
  • Inhibits Ang-II production
  • Lack of vasoconstriction
  • Reduced aldosterone production
  • Inhibit hypertrophy of myocardium and smooth muscle
  • Decrease water intake
  • Decrease sympathetic activation
  • Decrease vasopressin release
37
Q

Why are ACE inhibitors considered balanced vasodilators?

A

Dilate arteries and veins equally

38
Q

What is the significance of ACE inhibitors?

A

Are the only vasodilators to counteract RAAS

39
Q

What are the ocal actions of ACE inhibitors?

A
  • Local RAAS exist in various tissues (cardiac, vascular, renal) and can be inhibited
  • Inhibit hypertrophy and fibrosis (chornic activation by Ang-II) in heart and blood vessels
  • Reduce glomerular capillary hypertension in kidney
40
Q

What is the importance of reducing glomerular capillary hypertension using ACE inhibitors?

A
  • Reduces proteinuria
  • Reduce nephron loss and thus replacemet with collagen
  • Would lead to glomerulosclerosis and intersitial fibrosis, thus loss of renal function
41
Q

Describe the beneficial actions of ACE inhibitors in congestive heart failure

A
  • Balanced vasodilation (decrease in systemic, pulmonary and atrial pressures decreasing venous ceongestion and excessive load on myocardium)
  • Decreased sodium and water retention reducing circulating fluid and decreasing venous congestion
  • Decreasing myocardial (and vascular) hypertrophy and fibrosis
42
Q

Describe the beneficial actions of ACE inhibitors in renal failure

A
  • Decreased efferent renal arteriolar resistance, increase coefficient of glomerular ultrafiltration
  • Reduction in glomerular hypertension
  • Decreased magnitude of proteinuria (hyperproteinuric renal disease)
  • Decreased blood pressure (hypertensive renal diseae)
43
Q

Give examples of ACE inhibitors

A

Enalapril, benazapril, ramipril, imidapril

44
Q

What are the risks of using ACE inhibitors?

A
  • Teratogenic
  • May tip some dogs/cats with pre-existing renal disease and proteinuria into acute renal crisis due to effects on tubular perfusion
45
Q

List the factors influencing RAAS

A
  • Hypertension
  • ACE inhibitors
  • Angiotensin receptor blockers
  • Beta-blockers (inhibit renin)
  • Low sodium diets
  • Diuretics
  • Ca2+ channel antagonists
  • Alpha-1 blockers
  • SNS activity
46
Q

Explain the nephrotoxic action of NSAIDs

A
  • Inhibit afferent arteriole vasodilators
  • Less blood to nephron
  • NO perfusion
  • No glomerular filtrate
  • Injury cannot be repaired
47
Q

Give examples of alternatives to ACEi

A
  • ANG-II receptor blockers

- Ca channel blockers

48
Q

What is the role of the kidney in the production of new red blood cells?

A
  • Kidneys produce EPO

- EPO stimulates proliferation and terminal differentiation of red blood cells

49
Q

Where in the kidneyis EPO produced?

A
  • Interstitial fibroblasts

- In association with peritubular capillary and proximal convoluted tubule

50
Q

Which region of the kidney is particulary vulnerable to ischaemic damage?

A

Renal medulla

51
Q

Why is the kidney particularly vulnerable to ischaemic damage?

A
  • High oxygen consumption in outer medulla
  • Major recipient of cardiac output
  • High metabolic activity (high impact by hypertension)
  • Multiple complex enzyme pathways
52
Q

Why might EPO be beneficial as a drug for renal failure?

A
  • Prevents anaemia
  • Prevents reception of low perfusion
  • Hypertension will not increase, limits damage
53
Q

Why are older cats susceptible to renal disease?

A
  • Toxins, infections, hypertension, high protein diet
  • Physiological cahnges when aging
  • Vulnerable to ibuprofen and antifreeze
54
Q

Describe calcium uptake in the proximal tubules and thick ascending limb of LoH

A
  • Passive, driven largely by Na uptake

- Ca leak channels, paracellular as tubular Ca increases down tubules due to isosmotic water uptake

55
Q

Describe calcium uptake in the distal tubule

A
  • Active, transcellular
  • Epithelial apical ca channels
  • Intracellular transport by Ca-binding proteins
  • Basolateral Ca-ATPase (PMCA) pumps Ca back to body
  • Basolateral 3Na/Ca antiporter (NCX) pumps Ca back to body
56
Q

Explain the action of PTH and vit D in increasing Calcium reabsorption in the distal tubule

A
  • Epithelial apical channels activated by PTH
  • Intracellular transport proteins upregulated by vit-D
  • Basolateral Ca-ATPase stimulated by vit-D and PTH
57
Q

How can secondary hyperparathyroidism occur?

A
  • In response to hypocalcaemia
  • e.g. excess plasma P binding to Ca, perceive low Ca = release of PTH
  • Also excess exercise/sweating in horses
58
Q

How can secondary hypoparathyroidism occur?

A
  • Renal disease, Ca and P excreted less

- Increase plasma Ca and P therefore increase in PTH

59
Q

Describe phosphate in the kidney

A
  • Non-protein bound freely filtered
  • 80% reabsorbed in proximal tubule, transcellular with Na (NPT2)
  • No significant uptake in loop
  • DT and CD similar to PT
60
Q

What is the effect of PTH on phosphate reabsorption?

A

Inhibits reabsorption

61
Q

How does hyperphosphataemia occur?

A
  • Increased dietary intake
  • Decreased renal excretion (e.g. urinary tract obstruction, rupture, renal failure)
  • Cell lysis releasing P
  • Hyperthyroidism
62
Q

How does hyperphosphataemia occur in chronic kidney disease?

A
  • Increase in blood PTH from CKD
  • Stimualtes increased renal excretion of Pa, decreased Ca excretion
  • Inadequate in late CKD, hyperphosphataemia
  • PTH high, bone resorption, more P present
  • Inhibition of calcitriol production so reduced Ca absorption
63
Q

What may reduce P excretion in acute kidney disease?

A

Decreased GFR

64
Q

Describe the renal handling of Mg

A
  • Non-protein bound freely filtered
  • 30% reabsorbed in PT (passive, trans-epithelial gradietn)
  • 65% in TAL
  • 5% in DT (active uptake)
65
Q

Describe the reabsorption of MG in the distal tubule

A
  • Active
  • Apical Mg channel (TRPM6)
  • Open state of channel influenced by intracellular [Mg]
  • Basolateral Mg-ATPase
66
Q

What is the effect of PTH and calcitonin on Mg reabsorption?

A

Increase passive reabsorption

67
Q

Describe the mechanisms behind changes in body calcium and phosphorous levels in renal failure

A
  • Renal failure = reduced excretion of P and decreased reabsorption of Ca
  • P and Ca bind, lead to hypocalcaemia and hyperphosphataemia
68
Q

Explain how secondary hyperparathyroidism occurs

A
  • Renal failure, decreased P excretion, increase in serum P
  • Increased serum P binds to Ca
  • Decrease in free Ca
  • PTH secretion
  • Decreased calcitriol formation due to renal failure, decreased Ca uptake from gut, further increase in PTH (no negative feedback)
69
Q

What can be done to treat secondary hyperparathyroidism?

A
  • Dietary phosphate restriction
  • Phosphate binders
  • Calcitriol therapy
  • Treat underlying cause

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