Blood pressure and the kidneys Flashcards by Deleted Deleted

What is the major electrolyte of ECFV?

→ Na

How well did you know this?

Not at all

Perfectly

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

→ If Na+ increases

→ an equivalent amount of water is drawn with it

How well did you know this?

Not at all

Perfectly

Equation for BP?

→ CO x TPR

How well did you know this?

Not at all

Perfectly

What does an increase in blood volume lead to?

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

How well did you know this?

Not at all

Perfectly

What is long term control of blood pressure?

→ regulating Na levels

How well did you know this?

Not at all

Perfectly

What is short term control of blood pressure?

→ Baroreceptors

How well did you know this?

Not at all

Perfectly

Flow chart for changes in Na balance

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

How well did you know this?

Not at all

Perfectly

Why does resuscitation fluid not cause hypernatremia?

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

How well did you know this?

Not at all

Perfectly

What is the effect of retained sodium the same as?

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

How well did you know this?

Not at all

Perfectly

How is Na+ sensed in the body?

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

How well did you know this?

Not at all

Perfectly

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

→ Cardiac volume receptord
→ Baroreceptors
→ Renal arterial pressure

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

How is sodium taken in the body?

→ Diet 10 to > 400 mMol a day

How well did you know this?

Not at all

Perfectly

How is sodium removed from the body?

→ Sweat/faeces

→ Regulated renal excretion

How well did you know this?

Not at all

Perfectly

What are mammals designed to do with Na+?

→ Conserve sodium

How well did you know this?

Not at all

Perfectly

What is the Na+ conserving system called?

→ RAAS

How well did you know this?

Not at all

Perfectly

How does RAAS work?

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)

How well did you know this?

Not at all

Perfectly

Where is the macula densa?

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

How well did you know this?

Not at all

Perfectly

What are renin secreting juxtaglomerular cells?

→ Modified smooth muscle cells along the afferent arteriole

How well did you know this?

Not at all

Perfectly

What is renin secreted in response to?

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

How well did you know this?

Not at all

Perfectly

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

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

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

→ Decreased GFR

Where does aldosterone act?

→ Nuclear receptors mainly on DCT cells

Where is Na+ and water mainly reabsorbed?

→ PCT

How does aldosterone increase Na+ retention?

→ increases the expression of eNAC channels | → Increases activity of Na+/K+ pump

Where is the eNAC found?

→ Luminal side of the collecting duct

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

→ 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

What is Na+ absorption coupled with?

→ K+ excretion

What does excess aldosterone result in and why?

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

Where are ANP and BNP found?

→ Specialized cardiac myocytes

What are ANP and BNP released in response to?

→ Increased cardiac filling pressures

What are the renal effects of ANP?

→ Increased natriuresis ( Na+ excretion) | → Diuresis (H2O excretion)

What are the vasculature effects of ANP?

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

What are the hormonal effects of ANP?

→ Decrease renin secretion | → Decreased aldosterone secretion

What is the main effect of ANP?

→ opposes RAAS | → Na+ excreting system

What is pressure natriuresis?

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

What is the relationship between pressure and Na+ excretion?

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

How does pressure natriuresis occur?

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

Why is GFR not involved in pressure natriuresis?

→ Renal arterial pressure does not increase GFR | → Due to powerful renal auto-regulation

What are the criteria for hypertension?

→ Diastolic > 90mmHg | → Systolic > 140 mmHg

What are the classifications of hypertension?

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

What do secondary causes of hypertension involve?

→ Excess Na+ reabsorption and abnormalities in hormone secretion → Liddle's syndrome → Conn's syndrome → Renal artery stenosis

What can essential hypertension involve?

→ Abnormal handling of Na+ balance

What is Liddle's syndrome?

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

What are the effects of Liddle's syndrome?

→ Increased ECFV | → Increased BP

What is Conn's syndrome caused by?

→ Overproduction of aldosterone by the adrenal gland tumor

What are the consequences of raised aldosterone?

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

What are the consequences of Addisons disease?

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

How does renal artery stenosis cause Na+ retention?

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

How does congestive heart failure cause oedema?

``` 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 ```

What are environmental factors that can cause essential hypertension?

→ Life style → Diet → Diabetes