Session 4 - Changes in plasma volume Flashcards Preview

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Flashcards in Session 4 - Changes in plasma volume Deck (23):
1

What is the intracellular and extracellular conc of: a) sodium b) potassium c) calcium d) Chloride

a) i - 15             e - 140

b) i - 140          e - 5

c) i - 0.0001    e - 2.5

d) i - 5              e - 100

 

mM units

2

Does osmolarity in the PCT change? Explain.

• Osmolarity remains the same throughout the PCT

• Chloride ion reabsorption lags behind in order to ensure osmolarity remains the same.

• Water is taken with the glucose, AA, and lactate to prevent changes in osmolarity.

3

What happens to the concentration of the solute as it moves from the PCT to the loop of Henle

Goes from isomotic to hypotonic

4

What does the ascending and descending limb of the loop of henle do?

• Descending limb absorbs water making the solution very hypertonic

• Ascending limb absorbs ions making solution hypotonic (Thick ascending limb impermeable to water)

5

How does the thin ascending limb reabsorb sodium ions

via paracellular route

6

How does the thick ascending limb reabsorb sodium ions?

Luminal side:

1) NAKCC2 - na, k and 2 Cl into cell

2) ROMK - potassium out of cell

 

Apical side:

1) Cl transporters

2) Na - k - ATPase

7

How does the descending limb reabsorb water?

paracellularly

8

How does the early and late DT reabsorb sodium and calcium ions?

luminal:

1) NCC transporter - Na and Cl symporter

2) Calcium transporter

 

Apical:

1) Cl transporter

2) NCX - Calcium into ECF and sodium into cell

3) Na - k - ATPase

9

What ion is the DCT a major site for reabsorption of?

calcium

10

What are the 2 cell types in the late DCT and CD? What are their functions?

1) Intercalated cells - active reabsorption of chloride and secretion of H+ or HCO3 to make urine acidic or basic

2) Principal cells - Variable water uptake through aquaporin dependent on the actions of ADH

11

Give the equation for BP

BP = CO x TPR

12

Give the equation for CO

CO = SV x HR

13

How is the BP regulated in the short term? How does this mechanism regulate BP?

Short term regulation – baroreceptor reflex, nerve endings in the carotid sinus and aortic arch sensitive to stretch:

o Adjusts sympathetic and parasympathetic inputs to the heart to alter CO

o Adjusts sympathetic input to peripheral resistance vessels to alter TPR.

14

Describe the function of the RAAS and how it works. What factors affect the release of renin? Where is it released from?

Renin released from granular cells of Juxtaglomerular apparatus (JGA) 3 factors affect release from JGA:

1. Reduced NaCl delivery to distal tubule – achieved by decreased circulating volume

2. Reduced perfusion pressure in the kidney causes release of renin – sensed by baroreceptors in afferent arterioles of glomerulus

3. Sympathetic stimulation to JGA increases release of renin

 

Process of the RAAS:

Angiotensinogen – produced by liver circulates in blood and becomes angiotensin I, cleaved by renin 2.

Angiotensin I becomes angiotensin II by ACE 3.

Angiotensin II: ---> Vasoconstricts afferent and efferent arterioles, decreasing GFR --> Stimulates sodium reabsorption at PCT, stimulates NA-H exchanger in apical exchanger --> Increases thirst sensation, --> Stimulates aldosterone release from adrenal cortex.

Aldosterone activates ENaC, apical K channels, and Na/K/ATPase, stimulating Na and therefore water reabsorption. Hormone crosses intracellular membrane and increases expression of these channels.

15

What are the 2 types of angiotensin 2 receptors available?

AT1 and AT2

16

What are the actions of bradykinin? What breaks it down?

Bradykinin has vasodilator actions and is broken down by ACE

17

How can the sympathetic nervous system autoregulate renal blood flow?

• High levels of sympathetic stimulation reduce renal blood flow by vasodilating blood vessels to muscles, decreasing GFR and Na excretion.

• This activates apical NaCl cotransporter and basolateral Na/K ATPase in DCT

• This stimulates renin release from JG cells, leading to increased Ang II levels and increased aldosterone levels.

18

How does ADH autoregulate BP? Where does it act?

• Forms concentrated urine by retaining water and increasing sodium reabsorption and controlling plasma osmolarity

• ADH release stimulated by increase in plasma osmolarity or severe hypovolaemia.

• Acts on thick ascending limb to stimulate apical Na/K/Cl co transporter.

19

What is the function of natriuretic peptides (ANPs)?

• ANP (atrial NPs) promotes sodium excretion and is released from atrial cells in response to stretch

• Low pressure volume sensors in the atria inhibit ANP if there is a reduced effective circulating volume.

 

• ANP actions:

o Vasodilates the afferent arteriole and increases blood flow, therefore increasing GFR o Inhibits Na reabsorption

20

Why should NSAIDs be avoided if someone has compromised renal blood flow?

Prostaglandins:

• Act as vasodilators and enhance GFR, and reduce Na reabsorption.

• Helps to maintain renal blood flow and GFR in presence of vasoconstrictors

• NSAIDs inhibit COX pathway involved in forming prostaglandins and therefore giving NSAIDs when renal perfusion is compromised can further decrease GFR and lead to acute renal failure.

21

What are the 2 types of hypertension?

Essential and secondary

22

How can you treat hypertension? Give 3 methods

1) Treating the cause in secondary hypertension,

2) ACE inhibitors,

3) Diuretics (decrease circulating volume)

4) L-type calcium channel blockers – relaxes vascular smooth muscle

5) Beta blockers to reduce effects of sympathetic output on heart

6) Exercise, diet, reduced alcohol and na intake

23