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Semester 3: Urinary > Session 4 > Flashcards

Session 4 Flashcards

1
Q

How is pressure measured?

A

Flow X Resistance

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2
Q

What is the short term regulation of blood pressure?

A

Baroreceptor reflex

  • Adjust sympathetic and parasympathetic inputs to the heart to alter the cardiac output
  • Adjust sympathetic input to peripheral resistance vessels to alter TPR
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3
Q

What is the long term regulation of blood pressure?

A

Neurohormonal resposes to affect salt and water balance

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4
Q

What are the hormonal responses to low renal perfusion?

A
  • Renin-angiotensin aldosterone system
  • Sympathetic nervous system
  • Prostaglandins
  • ADH
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5
Q

What factors stimulate the renin release?

A
  • Reduced NaCl delivery to the distal tube
  • Reduced perfusion pressure in the kidney causes the release of renin
  • Sympathetic stimulation of the juxtaglomerular increases release of renin
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6
Q

Where is renin released from?

A

Juxtagomerular cells of the afferent arteriole in repose to reduced perfusion pressure and stimulation by the sympathetic nervous system

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7
Q

What triggers the release of renin?

A
  • Decreased NaCl delivery to the macula densa is detected
  • Decreased renal perfusion pressure
  • Sympathetic stimulation of the beta 1 receptors
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8
Q

What are the direct actions of angiotensin 2 on the kidney to control blood pressure?

A
  • Vasocnstrciton of the efferent and to a lesser extend the afferent arteriole
  • Enhanced sodium reabsorption at the proximal collecting tubule by stimulation of Na-H(NHE3) exchanger in the apical membrane
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9
Q

What are some indirect effects of angiotensin 2 on the kidney to control blood pressure?

A
  • Release of aldosterone

- Release of ADH

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10
Q

What are the actions of aldosterone on the kidney?

A

Acts on principal cells of collecting ducts to:

  • Stimulate Na+ and therefore water reabsorption
  • Activates apical Na+ channel and apical K+ channel
  • Increases basolateral Na+ extrusion via Na/K/ATPase
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11
Q

What are the actions of the sympathetic nervous system in response to high blood pressure?

A
  • Reduction of the renal blood flow by vasocontrcitin of arterioles and decrease in the GFR
  • Activates apical Na/H exchanger and basolateral Na/K ATPase in proximal collecting tubule
  • Stimulates renin release from JG cells
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12
Q

What are effects of prostaglandins in the kidney?

A

Causes vasodilation of the afferent arteriole

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13
Q

What riggers the release of prostaglandins in the kidney?

A
  • Angiotensin 2
  • Noradrenaline
  • Anti diuretic hormone
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14
Q

What is the effect of prostaglandins released locally on renin release?

A

Enhances renin release

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15
Q

What is the net effect of the interaction of prostaglandins and the RAAS system?

A
  • Systematic vasoconstrinon
  • Vasoconstriction of the efferent artriole
  • Vasodilation of the afferent arteriole
  • The GFR is preserved as a result
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16
Q

What is action of ADH?

A
  • Formation of concentrates urine by retaining water to control the plasma osmolarity. Reabsorption of water is increased at the distal nephron
  • Vasoconstriiton
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17
Q

What stimulate release of ADH?

A
  • Increase in plasma osmolarity

- Sever hypovolaemia

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18
Q

What is involved in renal autoregulation?

A
  • Myogenic reflex

- Tubuloglomerular feedback

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19
Q

What are the 2 major actions for atrial natriuretic peptide?

A
  1. Causes vasodialtion

2. Inhibits Na+ reabsorption especially in the collecting duct causing natriuresis

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20
Q

What triggers the release of ANP?

A

Low circulating volume. It acts to support the blood pressure

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21
Q

What is pressure natriuresis?

A

Increasing blood pressure gradually resents the kidneys for salt concentrations and water volume and this means the regulatory mechanisms aren’t working as well. It is thought to be one of the causes of hypertension

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22
Q

What is hypertension?

A

-Persistent increase in blood pressure

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23
Q

What are some causes of secondary hypertension?

A
  • Reno-vascular hypertension
  • Coarctation of the aorta
  • Primary hyperaldosteronism (Conn’s syndrome)
  • Cushing’s syndrome
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24
Q

What are the 2 main types of renovascualr disease?

A
  • Atheroma

- Fobromuscular dysplasia

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25
Q

What causes renovascular disease?

A

-Renal artery stenosis which is narrowing of the renal artery

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26
Q

Why does renovascular disease lead to hypertension?

A
  • Lack of blood supply to the kidney causes the kidney to sense hypovolaemia in the body
  • This means that it triggers changes in order to increase the blood pressure
  • This causes hypertension because the mechanism are constantly trying to increase blood pressure even though the blood is normotensive
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27
Q

What happens with unilateral renal artery stenosis?

A
  • One kidney triggers mechanism to increase blood pressure by activating the RAAS system because it senses hypovolaemia
  • One kidney works normally and sense the increase in sodium so acts to excrete the sodium. It suppresses the RAAS system.
  • Net effect is hypertension with no fluid overload and salt as the kidney that works normally excrete the extra salt and water
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28
Q

What happens with bilateral renal artery stenosis?

A
  • RAAS system is activated
  • Kidney does not get rid of the extra salt and water and hypertension persists
  • Risk of acute pulmonary oedema
29
Q

What is coarctation of aorta?

A

Stenosis in the aorta vessels

30
Q

What is the mechanism that causes hypertension due coarctation of the aorta?

A
  • Less renal blood flow

- Kidney triggers the RAAS system as it senses hypovolaemia wrongly

31
Q

What are the circulating levels of renin and AT2?

A

Low

32
Q

What is primary hyperaldosteronism and the causes?

A

Excess secretion of aldosterone

  • Adrenal adenoma
  • Adrenal hyperplasia
33
Q

What are the features of primary hyperaldosteronism?

A
  • Hypertension

- Can cause hypokalemia

34
Q

What is used in the diagnosis of the the primary hyperaldosteronism?

A
  • Aldosterone:renin ratio is high
  • Look for adenoma with a CT scan and remove if present
  • If no adenoma treat by blockage of aldosterone
35
Q

What is the effect of excess liquorice on the blood pressure?

A
  • Blocks an enzyme
  • Cortisol can’t be converted to cortisone
  • Cortisol instructs with mineralocorticoid receptor triggering the same effect as aldosterone
  • Blood pressure increase
  • Simular mechanism as Cushing’s
36
Q

What causes oedema?

A

-Kidney are involved when generalised

37
Q

What are some causes of generalised oedema?

A
  • Heart failure
  • Chronic kidney disease
  • Nephrotic disease
  • Liver disease
  • Pregnancy
38
Q

What is chronic kidney disease?

A

inability to exert excess salt and water due to reduced kidney function.
Leads to hypertension and fluid overload (oedema)

39
Q

What is nephrotic syndrome?

A

Mixture of

  • Reduced oncotic pressure causing reduced perfusion pressure and activation of RAAS/SNS/ADH
  • Alteration in sodium and water excretion due to reduced kidney function
40
Q

What are the indications of nephrotic syndrome?

A
  • Proteinuria
  • Hyperalbuminaemia
  • Oedema
41
Q

Which ion primarily affects the effective circulating volume?

A
  • Sodium ions

- Water in the extracellular fluid compartment depends on the sodium ion content.

42
Q

What would be the effect of changing the amount of sodium that is ingested (without kidney action)?

A
  • Amount of water in the extra cellular fluid would change
  • Effective circulating volume would also change
  • Blood pressure also changes as a result
43
Q

Why does the kidney Na+ excretory rates have to vary over a wide range?

A
  • The kidney needs to match excretion of sodium to ingestion to remain sodium balance.
  • Urinary water excretion can be varied physiologically
44
Q

Why can you not add or remove water to change the plasma volume?

A

-Plasma osmolarity would change

45
Q

What can you do to increase the plasma volume?

A

Add an isosmotic solution

46
Q

How can we add or remove an isosmotic solution?

A
  • Movement of osmoles

- Water will follow

47
Q

What Can affect the proximal tubule Na+ reabsorption?

A
  • Changes in osmotic pressure and hydrostatic pressure

- RAAS system can stimulate proximal tubule Na+ reabsorption

48
Q

What are the targets of hormone aldosterone

A

Principle cells of the distal collecting tubule and collecting duct

49
Q

What causes pressure natriuresis and pressure diuresis when renal blood pressure increases?

A
  • Increased renal artery blood pressure
  • Reduced number of Na-H and reduced Na-K ATPase activity in proximal tubule
  • Causes reduction in sodium and water reabsorption in proximal tubule
  • Leads to pressure natriuresis and pressure diruresis together in order for the ECF volume to be decrease and diminish the BP rise.
50
Q

What are aqua porin channels in the kidney?

A

-Holes in the membrane through which water can move down a concentration gradient

51
Q

What are the sodium channels in the proximal tubule?

A

Na-H antiporter
Na-Glucose symporter
Na-AA co-transporter
Na-Pi

52
Q

What are the sodium channels in the loop of henle?

A

NaKCC symporter

53
Q

What are the sodium channels found in the early distal tubule?

A

NaCl symporter

54
Q

What are the sodium channels found in the late distal tubule and collecting tubule?

A

ENaC (epithelial Na channels)

55
Q

What are the histological features of the proximal tubule?

A
  • Brush border
  • Large outside diameter
  • Lots of mitochondria (incredibly active)
56
Q

What are the solutes transported in the 1st segment of the proximal tubule?

A 
-Apical
Na-H exchange 
Co-transport with glucose
Co-transport with amino acid or carboxylic acids
Co-transprt with phosphate

-Basolateral
3 Na-2K ATPase
NaHCO3- co transporter for acids and bases

  • Aquaporin channels
  • Chloride concentration increases
57
Q

What are the solutes transported in the 2nd segment of the proximal tubule?

A

Basolateral
3Na-2K ATPase

Apical
Na+ is reabsorbed via Na-H exchanger

Paracellular and transcellular transport of Cl-

58
Q

What is the overview of the function of the proximal collecting tube?

A
  • Highly water permeable so bulk transport of water reabsorption
  • Reabsorption is isosmotic with plasma
  • Reabsorbs 65% water, 100% glucose and amino acids, 67% of sodium
  • Driving force for reabsorption is osmotic gradient established by solute absorption, hydrostatic force in the interstitum, oncotic force in peritubular capillary due to loss of 20% filtrate at glomerulus but cells and proteins left in blood
59
Q

What are the features of the thin descending limb?

A
  • Lots of aqua porin channels
  • No mitochondria
  • Loose junctions
  • No brush border
  • Thin
  • Flattened
  • Passive in nature
60
Q

What are the features of the thick segment of the ascending limb?

A
  • Impermeable to water
  • Many mitochondria
  • No aqua porin
  • Lots of active transport
61
Q

What is the function of the thick and thin descending limb?

A
  • Paracellular reuptake of water due to increased intercellular concentrations of sodium
  • Concentrate sodium and chloride ions in the lumen of the descending limb ready for active transport in the ascending
62
Q

What is the function of the thin ascending limb?

A

Passive sodium reabsorption due the actions of the descending limb. Epehtelium permits passive reabsorption by paracellular route

63
Q

What is the function of the thick ascending limb?

A
  • NKCC2 transrptoer that transports sodium, (2)chloride and potassium from lumen to cells
  • Na+ ions move into the interstitum due to the action of 3Na-2K-ATPase
  • ROMK channels move potassium from the cell into the lumen to allow the NKCC2 channels to work
64
Q

What is the clinical significance of the thick ascending limb?

A

Sensitive to hypoxia due to the amount of energy use

65
Q

Give an overview of the loop of henle reabsorption.

A
  • Descending limb reabsorbs water and not NaCl
  • Ascending limb reabsorbs NaCl but not water
  • The tubule fluid leaving the loop is hypo-osmotic compared to plasma
66
Q

Outline features of reabsorption in the distal convoluted tubule

A
  • Hypo-osmotic fluid enters
  • Active transport of 5-8% of Na+
  • Water permeability is low
  • Has 2 regions DCT1 and DCT1
67
Q

What are the channels present in DCT1?

A

Apical

  • NaCl enters across apical membrane via electro-neutral NCC transporter
  • NCC transporter is sensitive to thiazides diuretics

Basolateral

-3Na-2K-ATPase

68
Q

What are the channels present in the distal convoluted tubule 2?

A

Apical

  • Na+ enter via ENaC
  • NaCL enters by the NCC

Basolateral

  • 3Na-2K-ATPase
  • KCC4
69
Q

Which channels are affected by a milo ride diuretics?

A

ENaC channels

Semester 3: Urinary (5 decks)

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