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P1: Ren > Blood Pressure And The Kidneys > Flashcards

Blood Pressure And The Kidneys Flashcards

1
Q

What is the major electrolyte of ECFV?

A

→ Na

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2
Q

If you add Na+ to the blood why doesn’t hypernatremia happen (Increase in Na+ concentration)?

A

→ If Na+ increases

→ an equivalent amount of water is drawn with it

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3
Q

Equation for BP?

A

→ CO x TPR

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4
Q

What does an increase in blood volume lead to?

A

→ ventricular filling and increased stroke volume (Starlings law)
→ Increase cardiac output
→ Increase blood pressure

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5
Q

What is long term control of blood pressure?

A

→ regulating Na levels

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6
Q

What is short term control of blood pressure?

A

→ Baroreceptors

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7
Q

Flow chart for changes in Na balance

A 
Changes in Na balance
↓
Changes in osmolarity
↓
ADH release
↓
H2O moves through ADH stimulated aquaporin channels in collecting duct
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8
Q

Why does resuscitation fluid not cause hypernatremia?

A

→ It is isotonic
→ Na+ cannot cross cell membranes
→ fluid will expand the ECFV

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9
Q

What is the effect of retained sodium the same as?

A

→ adding isotonic fluid
→ It draws an equivalent amount of water with it
→ Increase in blood pressure

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10
Q

How is Na+ sensed in the body?

A

→ Indirectly
→ A change in ECFV occurs (up or down)
→ Stretch and pressure receptors in CVS detect this

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11
Q

What are the afferent pathways for detecting indirect changes in Na+?

A

→ Cardiac volume receptord
→ Baroreceptors
→ Renal arterial pressure

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12
Q

What are the efferent pathways for responding to changes in Na+?

A

→ Neuronal : sympathetic nervous system
→ Hormonal : RAAS, ANP
→ Haemodynamic : + or - GFR, pressure natriuresis

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13
Q

How is sodium taken in the body?

A

→ Diet 10 to > 400 mMol a day

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14
Q

How is sodium removed from the body?

A

→ Sweat/faeces

→ Regulated renal excretion

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15
Q

What are mammals designed to do with Na+?

A

→ Conserve sodium

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16
Q

What is the Na+ conserving system called?

A

→ RAAS

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17
Q

How does RAAS work?

A

1) A loss of blood pressure stimulates the secretion of renin
2) Renin acts on a liver substrate called angiotensinogen and converts it to angiotensin I
3) Angiotensin I is converted to angiotensin II by angiotensin converting enzyme ( epithelial cells of the lung)
4) Angiotensin II acts on the AT1R receptor on the adrenal cortex and stimulates it to release aldosterone
5) Increases Na+ reabsorption in the nephron and increases K+ secretion
6) vascular smooth muscle contracts (vasoconstriction and BP increases)

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18
Q

Where is the macula densa?

A

→ The region of contact between the afferent arteriole and the distal tubule of the same nephron

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19
Q

What are renin secreting juxtaglomerular cells?

A

→ Modified smooth muscle cells along the afferent arteriole

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20
Q

What is renin secreted in response to?

A

1) decrease in BP and blood volume and renal blood flow detected by afferent arteriole mechanoreceptors
2) decrease Na levels at the macula densa
3) Sympathetic nerve activation of beta 1 adrenoceptors

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21
Q

What is aldosterone and where is it synthesized and what is it released by?

A

→ Steroid hormone
→synthesized in the zona glomerulosa of the adrenal gland
→ released by the action of angiotensin II

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22
Q

What does a decreased amount of Na+ at the macula densa mean?

A

→ Decreased GFR

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23
Q

Where does aldosterone act?

A

→ Nuclear receptors mainly on DCT cells

24
Q

Where is Na+ and water mainly reabsorbed?

A

→ PCT

25
Q

How does aldosterone increase Na+ retention?

A

→ increases the expression of eNAC channels

→ Increases activity of Na+/K+ pump

26
Q

Where is the eNAC found?

A

→ Luminal side of the collecting duct

27
Q

How does the Na+/K+ pump work to retain Na+?

A

→ Na+/K+ pump actively pumps sodium out
→ Low intracellular concentration of Na+
→ creates a diffusion gradient from the lumen of the tubule of the DCT
→ Na+ diffuses in via the eNAC
→ Na+ does not stay in the cell because the Na+/K+ pump is taking the Na+ out

28
Q

What is Na+ absorption coupled with?

A

→ K+ excretion

29
Q

What does excess aldosterone result in and why?

A

→ Hypokalaemia
→ K+ into the cell via Na+/K+ pump
→ K+ passively diffuses out of the cell into the lumen of tubule

30
Q

Where are ANP and BNP found?

A

Specialized cardiac myocytes

31
Q

What are ANP and BNP released in response to?

A

→ Increased cardiac filling pressures

32
Q

What are the renal effects of ANP?

A

→ Increased natriuresis ( Na+ excretion)

→ Diuresis (H2O excretion)

33
Q

What are the vasculature effects of ANP?

A

→ Vasodilation by stimulation of PKG in vascular smooth muscle cells
→ Decrease systemic BP

34
Q

What are the hormonal effects of ANP?

A

→ Decrease renin secretion

→ Decreased aldosterone secretion

35
Q

What is the main effect of ANP?

A

→ opposes RAAS

→ Na+ excreting system

36
Q

What is pressure natriuresis?

A

→ Increase in Na+ renal excretion due to a rise in renal arterial pressure

37
Q

What is the relationship between pressure and Na+ excretion?

A

→ The higher the pressure the higher the concentration of Na+ in the urine

38
Q

How does pressure natriuresis occur?

A

→ A rise in medullary capillary pressure
→ causes an increase in fluid filtration and interstitial pressure
→ Prevents tubular reabsorption

39
Q

Why is GFR not involved in pressure natriuresis?

A

→ Renal arterial pressure does not increase GFR

→ Due to powerful renal auto-regulation

40
Q

What are the criteria for hypertension?

A

→ Diastolic > 90mmHg

→ Systolic > 140 mmHg

41
Q

What are the classifications of hypertension?

A

→ Secondary - identifiable cause

→ Essential - unknown cause ( > 90% of cases)

42
Q

What do secondary causes of hypertension involve?

A

→ Excess Na+ reabsorption and abnormalities in hormone secretion

→ Liddle’s syndrome
→ Conn’s syndrome
→ Renal artery stenosis

43
Q

What can essential hypertension involve?

A

→ Abnormal handling of Na+ balance

44
Q

What is Liddle’s syndrome?

A 
→ Autosomal mutation that is rare
→ Genetic form of high blood pressure
→ Increases eNAC activity
→ Increases renal Na+ retention
→ Suppresses aldosterone/ renin
45
Q

What are the effects of Liddle’s syndrome?

A

→ Increased ECFV

→ Increased BP

46
Q

What is Conn’s syndrome caused by?

A

→ Overproduction of aldosterone by the adrenal gland tumor

47
Q

What are the consequences of raised aldosterone?

A

Acts on principal cells lining CD

→ Increase in ECFV
→ Renal sodium reabsorption increases
→ Increase eNAC / ATPase/ K+ excretion
→ decrease in renin secretion

48
Q

What are the consequences of Addisons disease?

A 
→ Insufficient release of aldosterone
→ Chronic Na+ loss
→ Decreased ECFV
→ Severe hypotension
→ Collapse and death
49
Q

How does renal artery stenosis cause Na+ retention?

A 
Decrease in renal artery pressure due to stenosis
↓
Decreased blood flow
↓
Renin secretion
↓
Angiotensin II production
↓
Increased aldosterone
↓
Increased vasoconstriction

This effect is systemic so it would affect the other kidney and the nonstenosic kidney will reduce renin production

50
Q

How does congestive heart failure cause oedema?

A 
LV failing to maintain enough pressure to maintain perfusion
↓
Arterial baroreceptors deactivated
↓
Body thinks blood volume is decreased
↓
Activates sympathetic output
↓
Increase RAAS system
↓
Stimulates Na+ retention
↓
ECFV expands
↓
Less arterial pressure
↓
Less hydrostatic pressure
51
Q

What are environmental factors that can cause essential hypertension?

A

→ Life style
→ Diet
→ Diabetes

52
Q

How is ECF volume sensed?

A

Change in amount of sodium in ECF

Atrial stretch receptors, Arterial baroreceptors
Afferent arteriole
NaCl delivery to DT

RAAS – sodium-retaining
ANP – sodium-excreting

Change in renal sodium and water excretion

53
Q

How is RAAS activated by? How is aldosterone secretion increased by?

A

Reduced renal perfusion
Increased sympathetic activity

Aldosterone secretion is increased by
RAAS
Increased plasma [K+]

54
Q

Describe the difference between aldosterone effect on principal and intercalated cells

A 
→Increases Na/K ATPase
→Increases expression of ENaC channels on luminal membrane 
→Resulting in
Increased Na+ reabsorption
Increased K+ secretion
Acts on intercalated cells of CD
→Increases H+ ATPase- which expells H+ into tubule
→Resulting in 
→Increased H+ secretion
→Increased HCO3- reabsorption
→Bicarbonate will move into the ECF
Metabolic alkalosis
55
Q

Defences against volume depletion

A

RAAS
Normal, continuous adjustment of Na excretion and ECF volume
→Can reduce Na excretion to very low levels in hypovolemia​ in distal tubule

ADH
→Last line of defence against volume depletion
→Non-osmotic ADH secretion if BP drops by ≈ 10-15%- ADH secretion is increased regardless of plasma osmolarity
→RAAS is already fully activated

P1: Ren (13 decks)

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