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Urinary System > Handling Sodium And Hypertension > Flashcards

Handling Sodium And Hypertension Flashcards

1
Q

What is the most osmotically effective solute in the ECF?

A

Na+

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2
Q

The input and output of Na+ is approximately how much per day?

A

10.5 g/day

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3
Q

How is Na+ lost from the body?

A

Urine (10g)
Sweat (0.25g)
Faeces (0.25g)

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4
Q

What is the osmotic status of sweat?

A

Hypo-osmotic

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5
Q

In which part of the nephron can we control how much Na+ is reabsorbed?

A

DCT

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6
Q

What percentage of sodium is reabsorbed in the PCT?

A

67%

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7
Q

How will changes in the peritubular capillaries affect the PCT Na+ reabsorption?

A

Decreased pressure in capillaries = increased reabsorption

Increased pressure in capillaries = decreased reabsorption

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8
Q

Describe what happens to Na+ reabsorption when renal BP increases

A 
Decreased Na-H antiporter and reduced ATPase activity 
Decreased Na+ reabsorption in PCT 
Decreased water reabsorption in PCT 
ECF volume decreases 
BP decreases
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9
Q

How is Cl- reabsorbed?

A

Transcellular (active)
Paracellular (passive)
Coupled to pumps and dependent of Na+

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10
Q

What percentage of bicarbonate is reabsorbed in the PCT?

A

90%

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11
Q

What percentage of Cl- is reabsorbed in the PCT?

A

60%

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12
Q

Which sodium transporters are present in the PCT?

A

Na-H antiporter
Na-glucose symporter
Na-AA cotransporter
Na-Pi

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13
Q

Which sodium transporter is present in the loop of Henle?

A

NaKCC symporter

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14
Q

Which sodium transporter is present in the early DCT?

A

NaCl symporter

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15
Q

Which sodium transporter is present in the late DCT and CD?

A

ENaC

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16
Q

Which molecules are reabsorbed up to 100% in the PCT?

A

Glucose
Amino acids
Lactate

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17
Q

What is the order of molecules reabsorbed as you travel down the PCT?

A 
First = glucose, amino acids, lactate
Second = bicarbonate 
Third = phosphate 
Fourth = chloride
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18
Q

How is the PCT divided?

A

3 segments

S1, S2, S3

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19
Q

Describe the glomerulotubular balance

A

Autoregulation - blunts Na+ excretion in response to GFR changes
Always try to take 67% of whatever is filtered
Higher GFR -> more reabsorption

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20
Q

How come the PCT can regulate how much Na+ it reabsorbs?

A

Because the PCT has flexibility due to not using all of its transporters all of the time

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21
Q

What is the equation for filtered load?

A

Filtered load = GFR x concentration

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22
Q

What is the osmotic status of the filtrate at the bottom of the loop?

A

Hypertonic in comparison to plasma

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23
Q

How does Na+ reabsorption occur in the thin ascending limb?

A

Relies on the steep gradient of Na+ conc to drive passive reabsorption of Na+

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24
Q

How does Na+ reabsorption occur in the thick ascending limb?

A

Active (pumped)

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25
Q

What does NKCC2 move?

A

Na+, K+ and 2Cl- from filtrate into cells

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26
Q

What happens to the ions that pass through NKCC2?

A

Na+ pumped into interstitium via ATPase
K+ diffuses via ROMK back into the tubule
Cl- diffuses into the interstitium

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27
Q

Which region of the nephron is particularly sensitive to hypoxia?

A

Thick ascending limb of loop of Henle

Uses the most energy

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28
Q

What is the osmotic status of filtrate leaving the loop of Henle?

A

Hypo-osmotic in comparison to plasma

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29
Q

Why is the filtrate further diluted in the DCT?

A

Because active Na+ reabsorption can occur but the water permeability of the DCT is fairly low so water cannot follow

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30
Q

In the late DCt and CD, what does water permeability depend on?

A

ADH

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31
Q

Describe the ion movement occurring in the early DCT

A 
NaCl enters across apical membrane via NCC transporter 
(Driven by ATPase in basolateral)
Leakage of K+ into interstitium 
KCC4 transporter moves Cl- into blood 
Leakage of Cl- into interstitium
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32
Q

Which transporter is sensitive to thiazide diuretics?

A 
NCC transporter 
(Moves NaCl into cells from filtrate)
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33
Q

Describe the ionic movement in the late DCT

A

NaCl enters cells via NCC and ENaC
Driven by ATPase in basolateral
(Still has the K+ and Cl- leakage seen in the early DCT)

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34
Q

Which diuretics are ENaC sensitive to?

A

Amiloride diuretics

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35
Q

Is movement through ENaC electroneutral?

A

No

The difference drives paracellular Cl- reuptake

36
Q

Where is the major site for Ca2+ reabsorption?

A

DCT

37
Q

How is Ca2+ reabsorbed in the DCT?

A

Apical calcium transport - Ca2+ enters cell, bound by calbindin, shuttles to basolateral membrane
Transporter across basolateral via NCX

38
Q

Why is only a small amount of calcium filtered at the glomerulus?

A

Ca2+ in the blood is usually bound

39
Q

What are the 2 regions of the collecting duct?

A

Cortical region and the medullary region

40
Q

What are the 2 distinct cell types in the CD?

A

Principle cells

Intercalated cells

41
Q

What is the role of the principle cells of CD?

A

Reabsorption of Na+ via ENaC

42
Q

What is the role of the intercalated cells of CD?

A

Active reabsorption of Cl-

43
Q

What are the 2 types of intercalated cells in the CD and what are their roles?

A 
A-IC = secretion of acid
B-IC = secretion of bicarbonate
44
Q

What is the equation for pressure in blood vessels?

A

Pressure = flow x resistance

45
Q

What is the equation for mean arterial BP?

A

MaBP = CO x TPR

46
Q

What is the equation for cardiac output?

A

CO = SV x HR

47
Q

Describe the short term regulation of blood pressure

A

Baroreceptor reflex - nerve endings in the carotid sinus and th aortic arch are sensitive to stretch
Adjusts sympathetic and parasympathetic nervous stimulation to alter the CO
Adjust sympathetic output to peripheral resistance vessels to alter TPR

48
Q

Which 2 nerves may be stimulated in the baroreceptor reflex?

A

Glossopharyngeal nerve

Vagus nerve

49
Q

Why can’t we use the baroreceptor reflex for sustained BP increases?

A

The threshold for baroreceptor firing resets

Gets used to the sustained increase

50
Q

Which responses control medium/long term changes in BP?

A

Neurohumoral responses

51
Q

What do the neurohumoral responses try to control?

A

Na+ balance (ECF volume)

52
Q

Describe Starling’s law of the heart

A

More blood volume returning to the heart
Increased stretch
Increased cardiac output

53
Q

What are the 4 parallel neurohumoral pathways?

A

RAAS
Sympathetic NS
ADH
Atrial natriuretic peptide (ANP)

54
Q

What is renin?

A

A proteolytic enzyme released from granular cells JGA

55
Q

What factors stimulate the release of renin?

A

Reduced NaCl to DCT
Reduced perfusion pressure in kidneys (afferent arteriole)
Sympathetic stimulation to JGA

56
Q

How is angiotensin II made?

A

Angiotensinogen converted to angiotensin I by renin
Angiotensin I converted to angiotensin II by ACE
(ACE = angiotensin converting enzyme)

57
Q

What are the effects of angiotensin II?

A

Aldosterone release from adrenal cortex
Vasoconstriction
Na+ reabsorption in kidneys

58
Q

What are the 2 types of angiotensin II receptor and which is the main one?

A

AT1 and AT2

AT1 is the main action

59
Q

What type of receptor is the ATI receptor?

A

GPCR

60
Q

What are the main sites of the AT1 receptor?

A 
Arterioles
Kidney 
Sympathetic NS
Adrenal cortex 
Hypothalamus (increased thirst and ADH release)
61
Q

What are the direct effects of AngII on the kidneys?

A

Vasoconstriction of afferent and efferent arterioles

Enhanced Na+ reabsorption at PCT via stimulation of Na-H exchanger in apical membrane

62
Q

How does aldosterone affect the kidneys?

A

Acts on principle cells of collecting duct - stimulate Na+ and water reabsorption
Activates apical ENaC and K+ channels (increased expression of ENaC)
Increased basolateral extrusion of Na+ via ATPase

63
Q

Why might ACE inhibitors lead to a dry cough?

A

ACE usually breaks down bradykinin and substance P
Bradykinin is increased
Gives a dry cough

64
Q

What is the major effect of bradykinin?

A

Vasodilation

65
Q

What are the end results of ACEi?

A

Prevent production of AngII
Prevent breakdown of bradykinin
Enhance vasodilation

66
Q

How does the sympathetic NS act to increase BP?

A

Vasoconstriction of arterioles (decreased GFR and Na+ excretion)
Directly activates apical Na-H exchanger and basolateral pump in PCT
Stimulates renin release from JG cells

67
Q

What is the main role of ADH?

A

Formation of concentrated urine by retaining water to control plasma osmolarity

68
Q

What stimulates ADH release?

A

Increased plasma osmolarity

Severe hypovolaemia

69
Q

What are the effects of ADH?

A

Increase water reabsorption in CD via AQP 2 channels
Increased Na+ reabsorption in thick ascending limb
Causes vasoconstriction

70
Q

Describe natriuretic peptides

A

Act to decrease BP
Synthesised and stored in atrial myocytes
Released in response to stretch (volume sensors)
Promotes natriuresis - loss of blood volume

71
Q

What are the actions of ANP?

A

Vasodilation in afferent arteriole increases GFR
More sodium filtered out of the blood
Inhibits some Na+ reabsorption along the nephron

72
Q

Describe the role of prostaglandins

A

Local mediators
Act as vasodilators
Enhance GFR and reduce Na+ reabsorption - decrease BP
Buffer excessive vasoconstriction (important when AngII levels are high)

73
Q

How do NSAIDs work?

A

Inhibit to COX pathway which is involved in the formation of prostaglandins

74
Q

Why don’t we give NSAIDs when renal perfusion is compromised?

A

Can further decreased GFR

Lead to acute renal failure

75
Q

How does dopamine act in the kidney?

A

Causes vasodilation to increase renal blood flow

Reduced reabsorption of NaCl (inhibits NH exchanger and Na pump)

76
Q

What are the stages of hypertension and their boundaries?

A

Stage 1: greater than or equal to 140/90
Stage 2: greater than or equal to 160/100
Severe: greater than or equal to 180/110

77
Q

What is primary hypertension?

A

The cause of the hypertension is unknown

95% of cases

78
Q

What is secondary hypertension and give some examples?

A

Where the cause of the hypertension can be defined
Eg. Renovascular disease
Aldosteronism
Cushing’s syndrome

79
Q

High dose of dopamine causes: vasodilation or constriction?

A

Vasoconstriction

Even though a lower dose will cause vasodilation

80
Q

What is Conn’s syndrome?

A

Aldosterone secreting adenoma

Leading to hypertension and hypokalaemia

81
Q

Give 2 types of vasodilators used for hypertension.

A

L type Ca2+ channel blockers

Alpha 1 receptor blockers

82
Q

How do L type Ca2+ channel blockers work?

A

Reduced calcium entry to vascular smooth muscle cells
Relaxation of vessel walls
Reduced BP

83
Q

Why don’t we tend to use alpha 1 adrenoceptor blockers?

A

They cause postural hypotension

84
Q

Give 2 diuretics commonly used for hypertension and how they work

A

Thiazide - inhibit NaCl contransporter in DCT, increased loss of Na+ and water
Spironolactone - aldosterone antagonist

85
Q

What are the actions of beta blockers?

A

Block Beta 1 receptors
Decreased SNS to heart
Decreased heart rate and contractility

86
Q

When do we give beta blockers?

A

Only used in hypertension if there is also another reason to give them eg. Previous MI

Urinary System (14 decks)

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