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11. Urinary > 4. Plasma Volume > Flashcards

4. Plasma Volume Flashcards

1
Q

What are the two compartments for water in the body?

A

Intracellular fluid, and extracellular fluid.

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2
Q

What separates intracellular from extracellular fluid?

A

Cell membrane.

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3
Q

Which concentration largely determines ECF volume?

A

NaCl.

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4
Q

What is sodium balance?

A

The kidneys balancing the amount of Na+ excretion with ingestion.

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5
Q

What happens with ECF expansion?

A

Na+ excretion is less than intake so is retained in the ECF, water is drawn out from the nephron into the ECF so its volume increases.

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6
Q

What are the possible consequences of ECF expansion?

A

Blood volume and arterial pressure rise as well as oedema.

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7
Q

What happens with ECF contraction?

A

Na+ excretion is greater than intake so the Na+ content of ECF decreases. Less water is drawn out of the nephron so ECF volume decreases.

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8
Q

How can Na+ content in ECF change without affecting osmolarity?

A

Water moves to compensate for Na+ amount changes.

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9
Q

Where is Na+ mostly reabsorbed?

A

In the proximal convoluted tubule.

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10
Q

What proportion of Na+ is reabsorbed by the PCT?

A

67%.

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11
Q

How does glomerular tubular balance blunt Na+ excretion response?

A

Autoregulation prevents the GFR from changing too much.

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12
Q

What drives Na+ reabsorption?

A

3Na-2K-ATPase on the basolateral membrane drives movement of Na+ across the apical membrane.

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13
Q

How is Na+ reabsorbed in section 1 of the PCT?

A

It is co-transported with glucose. Na-H exchange is used. Co-transported with amino acids/ carboxylic acids, also with phosphate. Transport using aquaporin.

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14
Q

How is Na+ reabsorbed in section 2 and 3 of the PCT?

A

Using the Na-H exchanges. Also paracellular Cl- reabsorption, and transcellular Cl- reabsorption. Also aquaporin.

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15
Q

What is the gradient across the lumen for water?

A

4mOsmol favouring uptake from the lumen.

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16
Q

What is the consequence of the PCT being highly water permeable?

A

Allows reabsorption to be isosmotic with plasma.

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17
Q

What drives reabsorption of water across the PCT?

A

Osmotic gradient established by solute reabsorption. Hydrostatic force in the interstitium. Oncotic force in peritubular capillary due to loss of 20% filtrate at the glomerulus but cells and proteins remaining in blood.

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18
Q

What is the glomerulotubular balance?

A

The balance between glomerular filtration rate and the rate of reabsorption of solutes.

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19
Q

How does rate of reabsorption of solutes respond to increased GFR?

A

It increases too.

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20
Q

How does reabsorption of the loop of Henle differ between the descending and ascending limbs?

A

Descending limb reabsorbs water but not NaCl. Ascending limb reabsorbs NaCl but not water.

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21
Q

Why is the ascending limb of the loop of Henle known as the diluting segment?

A

It reabsorbs NaCl but not water so dilutes NaCl in the filtrate.

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22
Q

What is the osmolarity of tubule fluid leaving the loop compared to plasma?

A

Hypo-osmotic.

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23
Q

How is Na+ and Cl- concentrated in the lumen of the descending limb?

A

Paracellular reuptake of water from the descending limb due to increased intracellular concentration of Na+ from the PCT.

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24
Q

Why is the ascending limb of the loop of Henle impermeable to water?

A

Tight junctions instead of loose junctions.

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25
Q

How is NaCl transport in the thick ascending limb?

A

From the lumen into cells by NaKCC2 channel.

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26
Q

What happens to Na, K, and Cl ions after action of the NaKCC2 channel in the thick ascending limb?

A

Na+ moves into the intersticium due to action of Na-K-ATPase. K+ diffuse back into lumen via ROMK. Cl- ions move into intersticium.

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27
Q

What do loop diuretics target?

A

The NaKCC2 channel.

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28
Q

What is the effect of loop diuretics on K+?

A

Increased loss of K+ in urine so hypokalaemia.

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29
Q

Why does fluid leave the distal convoluted tubule more hypo-osmotic?

A

Hypo-osmotic fluid enters loop and Na+ is actively transported. The DCT is not very water permeable so the filtrate is more hypo-osmotic.

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30
Q

How do thiazide diuretics work?

A

They act on the NaCC transporter in the distal convoluted tubule.

31
Q

What are the two cell types of the collecting duct?

A

Principal cells and intercalated cells.

32
Q

What is the role of principal cells in the collecting duct?

A

Reabsorb Na+ via ENaC and produces lumen charge - electrical gradient for paracellular Cl- reabsorption and potassium secretion into the lumen. Variable water uptake through aquaporin 2 channels, depends on ADH.

33
Q

What is the role of intercalated cells in the collecting duct?

A

Active reabsorption of Cl- and secretes H+ or HCO3-.

34
Q

What are the four neurohormonal factors controlling blood pressure?

A

Renin-angiotensin-aldosterone system, sympathetic nervous system, antidiuretic hormone, atrial natriuretic peptide.

35
Q

How do neurohormonal factors control blood pressure generally?

A

In part work by controlling sodium balance and ECF volume.

36
Q

How does the sympathetic nervous system control blood pressure?

A

Vasoconstriction by a1-adrenoceptors. Increased force/ rate of heart contraction by B1-adrenoceptors.

37
Q

How does the sympathetic nervous system respond to decreased renal blood flow?

A

Decreased GFR and Na+ excretion, activated NaH exchanger in PCT. Renin release stimulated by juxtaglomerular cells to increase angiotensin II and aldosterone levels.

38
Q

What is the effect of atrial natriuretic peptide?

A

Opposite direction to the rest of the neurohormonal responses, acts to lower BP.

39
Q

Where is ANP synthesised and stored?

A

Atrial myocytes.

40
Q

How does ANP affect Na+ excretion?

A

It promotes it, causing vasodilation of afferent arterioles.

41
Q

How does ANP respond to high BP?

A

The atrial myocyte cells are stretched so more ANP is released. This increases Na+ excretion, volume decreases so BP decreases.

42
Q

How does ANP respond to low BP?

A

The atrial myocyte cells are stretched less so release is reduced. Reduced Na+ excretion so volume and BP increase.

43
Q

How does ANP affect Na+ reabsorption in the nephron?

A

It inhibits it.

44
Q

How do the kidneys respond to reduced perfusion pressure?

A

It is detected by baroreceptors in the afferent arteriole, this causes release of renin from granular cells of the juxtaglomerular apparatus. Renin cleaves angiotensinogen to angiotensin I which is cleaved to angiotensin II by angiotensin converting enzyme. Angiotensin raises BP.

45
Q

How does sympathetic stimulation of the juxtaglomerular apparatus happen?

A

Decreased NaCl concentration at macula densa cells causes it, so more renin is released.

46
Q

What are the actions of angiotensin II?

A

Vasoconstriction, aldosterone, sympathetic activity, increase Na+ reabsorption, thirst, breaks down bradykinin.

47
Q

How does angiotensin II cause vasoconstriction?

A

It works on vascular smooth muscle cells to increase TPR and therefore BP. Also causes vasoconstriction of afferent and efferent arterioles.

48
Q

How does angiotensin II affect aldosterone?

A

It stimulates the adrenal cortex to synthesise and release aldosterone.

49
Q

What is the affect of aldosterone on Na+ movement?

A

It stimulates Na+ reabsorption so water follows. It acts on principal cells of the collecting ducts to activate ENaC and apical K+ channels. This increases Na+ extrusion via Na-K-ATPase.

50
Q

How does angiotensin II cause increased Na+ reabsorption?

A

Stimulates Na-H exchanger in the apical membrane of the proximal convoluted tubule.

51
Q

How does angiotensin II cause thirst?

A

It stimulates ADH release at the hypothalamus.

52
Q

How does angiotensin II breaking down bradykinin affect BP?

A

Bradykinin is a vasodilator, so if it is broken down, there is less vasodilation and BP is kept from dropping and effectively rises.

53
Q

How do the baroreceptors in the atria and pulmonary vasculature respond to a 5-10% drop in blood pressure?

A

Low-pressure baroreceptors send signals to the brainstem via the vagus nerve. This modulates sympathetic nerve outflow and secretion of ADH and reduction of ANP release.

54
Q

How do the baroreceptors in the atria and pulmonary vasculature respond to a 5-10% rise in blood pressure?

A

High-pressure baroreceptors send impulse via the vagus and gloospharyngeal nerves.

55
Q

What are the actions of ADH?

A

Addition of aquaporin to collecting duct so more reabsorption of water so urine is more concentrated. The Na/K/Cl co-transporter in the thick ascending limb is stimulated so less Na+ moves out into the medulla and there is less osmotic gradient for water to exit the lumen.

56
Q

What are prostaglandins?

A

Vasodilators. They enhance glomerular filtration and reduce Na+ reabsorption.

57
Q

How do NSAIDs affect prostaglandins?

A

They inhibit cyclo-oxygenase pathway that is involved in formation of prostaglandins so less made.

58
Q

What is hypertension?

A

A sustained increase in blood pressure.

59
Q

What is essential hypertension?

A

Where the cause of hypertension is unknown.

60
Q

What is secondary hypertension?

A

Where the cause of hypertension is known.

61
Q

What are the key causes of secondary hypertension?

A

Renovascular disease, chronic renal disease, aldosteronism, Cushing’s syndrome.

62
Q

What is renovascular disease caused by?

A

Occlusion of the renal artery, causing a fall in perfusion pressure in that kidney.

63
Q

What adrenal causes lead to secondary hypertension?

A

Conn’s syndrome, Cushing’s syndrome, pheochromocytoma.

64
Q

How does Conn’s syndrome cause hypertension?

A

It’s a aldosterone secreting adenoma. This leads to hypertension and hypokalaemia.

65
Q

How does Cushing’s syndrome cause hypertension?

A

Excess cortisol release so act on aldosterone receptor and lead to Na+ and water retention.

66
Q

How does pheochromocytoma cause hypertension?

A

It’s a tumour of the adrenal medulla that secretes noradrenaline and adrenaline.

67
Q

What groups of drugs can treat hypertension?

A

ACE inhibitors, thiazide diuretics, vasodilators, beta blockers.

68
Q

How do ACE inhibitors treat hypertension?

A

The prevent the production of angiotensin II from angiotensin I.

69
Q

How do thiazide diuretics treat hypertension?

A

They inhibit NaCC co-transporter on the apical membrane of the DCT.

70
Q

What is a side effect of thiazide diuretics?

A

Can cause hypokalaemia.

71
Q

How do vasodilators treat hypertension?

A

Ca2+ channel blockers so reduce Ca2+ entry into smooth muscle cells. Also a1 receptor blockers reduce sympathetic tone.

72
Q

How do beta blockers treat hypertension?

A

Block B1-receptors in the heart to reduce heart rate and contractility.

73
Q

What non-pharmacological approaches can help treat hypertension?

A

Diet, exercise, reduced Na+ intake, and reduced alcohol intake.

11. Urinary (12 decks)

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