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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
What does NKCC2 move?
Na+, K+ and 2Cl- from filtrate into cells
26
What happens to the ions that pass through NKCC2?
Na+ pumped into interstitium via ATPase K+ diffuses via ROMK back into the tubule Cl- diffuses into the interstitium
27
Which region of the nephron is particularly sensitive to hypoxia?
Thick ascending limb of loop of Henle | Uses the most energy
28
What is the osmotic status of filtrate leaving the loop of Henle?
Hypo-osmotic in comparison to plasma
29
Why is the filtrate further diluted in the DCT?
Because active Na+ reabsorption can occur but the water permeability of the DCT is fairly low so water cannot follow
30
In the late DCt and CD, what does water permeability depend on?
ADH
31
Describe the ion movement occurring in the early DCT
``` 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 ```
32
Which transporter is sensitive to thiazide diuretics?
``` NCC transporter (Moves NaCl into cells from filtrate) ```
33
Describe the ionic movement in the late DCT
NaCl enters cells via NCC and ENaC Driven by ATPase in basolateral (Still has the K+ and Cl- leakage seen in the early DCT)
34
Which diuretics are ENaC sensitive to?
Amiloride diuretics
35
Is movement through ENaC electroneutral?
No | The difference drives paracellular Cl- reuptake
36
Where is the major site for Ca2+ reabsorption?
DCT
37
How is Ca2+ reabsorbed in the DCT?
Apical calcium transport - Ca2+ enters cell, bound by calbindin, shuttles to basolateral membrane Transporter across basolateral via NCX
38
Why is only a small amount of calcium filtered at the glomerulus?
Ca2+ in the blood is usually bound
39
What are the 2 regions of the collecting duct?
Cortical region and the medullary region
40
What are the 2 distinct cell types in the CD?
Principle cells | Intercalated cells
41
What is the role of the principle cells of CD?
Reabsorption of Na+ via ENaC
42
What is the role of the intercalated cells of CD?
Active reabsorption of Cl-
43
What are the 2 types of intercalated cells in the CD and what are their roles?
``` A-IC = secretion of acid B-IC = secretion of bicarbonate ```
44
What is the equation for pressure in blood vessels?
Pressure = flow x resistance
45
What is the equation for mean arterial BP?
MaBP = CO x TPR
46
What is the equation for cardiac output?
CO = SV x HR
47
Describe the short term regulation of blood pressure
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
Which 2 nerves may be stimulated in the baroreceptor reflex?
Glossopharyngeal nerve | Vagus nerve
49
Why can't we use the baroreceptor reflex for sustained BP increases?
The threshold for baroreceptor firing resets | Gets used to the sustained increase
50
Which responses control medium/long term changes in BP?
Neurohumoral responses
51
What do the neurohumoral responses try to control?
Na+ balance (ECF volume)
52
Describe Starling's law of the heart
More blood volume returning to the heart Increased stretch Increased cardiac output
53
What are the 4 parallel neurohumoral pathways?
RAAS Sympathetic NS ADH Atrial natriuretic peptide (ANP)
54
What is renin?
A proteolytic enzyme released from granular cells JGA
55
What factors stimulate the release of renin?
Reduced NaCl to DCT Reduced perfusion pressure in kidneys (afferent arteriole) Sympathetic stimulation to JGA
56
How is angiotensin II made?
Angiotensinogen converted to angiotensin I by renin Angiotensin I converted to angiotensin II by ACE (ACE = angiotensin converting enzyme)
57
What are the effects of angiotensin II?
Aldosterone release from adrenal cortex Vasoconstriction Na+ reabsorption in kidneys
58
What are the 2 types of angiotensin II receptor and which is the main one?
AT1 and AT2 | AT1 is the main action
59
What type of receptor is the ATI receptor?
GPCR
60
What are the main sites of the AT1 receptor?
``` Arterioles Kidney Sympathetic NS Adrenal cortex Hypothalamus (increased thirst and ADH release) ```
61
What are the direct effects of AngII on the kidneys?
Vasoconstriction of afferent and efferent arterioles | Enhanced Na+ reabsorption at PCT via stimulation of Na-H exchanger in apical membrane
62
How does aldosterone affect the kidneys?
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
Why might ACE inhibitors lead to a dry cough?
ACE usually breaks down bradykinin and substance P Bradykinin is increased Gives a dry cough
64
What is the major effect of bradykinin?
Vasodilation
65
What are the end results of ACEi?
Prevent production of AngII Prevent breakdown of bradykinin Enhance vasodilation
66
How does the sympathetic NS act to increase BP?
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
What is the main role of ADH?
Formation of concentrated urine by retaining water to control plasma osmolarity
68
What stimulates ADH release?
Increased plasma osmolarity | Severe hypovolaemia
69
What are the effects of ADH?
Increase water reabsorption in CD via AQP 2 channels Increased Na+ reabsorption in thick ascending limb Causes vasoconstriction
70
Describe natriuretic peptides
Act to decrease BP Synthesised and stored in atrial myocytes Released in response to stretch (volume sensors) Promotes natriuresis - loss of blood volume
71
What are the actions of ANP?
Vasodilation in afferent arteriole increases GFR More sodium filtered out of the blood Inhibits some Na+ reabsorption along the nephron
72
Describe the role of prostaglandins
Local mediators Act as vasodilators Enhance GFR and reduce Na+ reabsorption - decrease BP Buffer excessive vasoconstriction (important when AngII levels are high)
73
How do NSAIDs work?
Inhibit to COX pathway which is involved in the formation of prostaglandins
74
Why don't we give NSAIDs when renal perfusion is compromised?
Can further decreased GFR | Lead to acute renal failure
75
How does dopamine act in the kidney?
Causes vasodilation to increase renal blood flow | Reduced reabsorption of NaCl (inhibits NH exchanger and Na pump)
76
What are the stages of hypertension and their boundaries?
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
What is primary hypertension?
The cause of the hypertension is unknown | 95% of cases
78
What is secondary hypertension and give some examples?
Where the cause of the hypertension can be defined Eg. Renovascular disease Aldosteronism Cushing's syndrome
79
High dose of dopamine causes: vasodilation or constriction?
Vasoconstriction | Even though a lower dose will cause vasodilation
80
What is Conn's syndrome?
Aldosterone secreting adenoma | Leading to hypertension and hypokalaemia
81
Give 2 types of vasodilators used for hypertension.
L type Ca2+ channel blockers | Alpha 1 receptor blockers
82
How do L type Ca2+ channel blockers work?
Reduced calcium entry to vascular smooth muscle cells Relaxation of vessel walls Reduced BP
83
Why don't we tend to use alpha 1 adrenoceptor blockers?
They cause postural hypotension
84
Give 2 diuretics commonly used for hypertension and how they work
Thiazide - inhibit NaCl contransporter in DCT, increased loss of Na+ and water Spironolactone - aldosterone antagonist
85
What are the actions of beta blockers?
Block Beta 1 receptors Decreased SNS to heart Decreased heart rate and contractility
86
When do we give beta blockers?
Only used in hypertension if there is also another reason to give them eg. Previous MI

Urinary System (14 decks)

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