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ESA 3 > Urinary 4 > Flashcards

Urinary 4 Flashcards

1
Q

Describe the positive and negative ion composition of the 2 major compartments of the ECF

A

Plasma:

Positive:

Majority Na+

Some K+, Ca2+, Mg2+

Negative:

Cl- and protein are two biggest components

HCO3- and Pi also present

Interstial fluid:

Positive:

Same as Plasma

Negative:

Proteins mostly absent

Greater proportions of Cl- and Pi result

HCO3- also present

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2
Q

Give an outline of the Ion composition of the ICF

A

Positive:

Majority K+

Some Na+, Ca2+, Mg+

Negative:

Mostly Pi and Proteins

Some Cl- and HCO3-

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3
Q

What is the major factor affecting ECF volume?

A

Major osmotically effective ion is Na+

Thus water in ECF depends on Na+ content

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4
Q

What is the effect of Na+ conc change on ECF and BP?

A

Change in Na+ = change in volume of ECF (increase = increase and vice versa)

Therefore change in Na+ also results in change of the ‘effective circulating volume’

Which in turn is a factor in determining BP

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5
Q

How does the body deal with variable ingestion of Na+ in the diet?

Why is tight control necessary?

A

Sodium ingestion can vary day to day (0.5g to 20-25g_

Kidney sodium ion excretion rates must vary over a wide range to match ingestion to excretion and maintin Na+ balance

If Na+ ions in ECF where allowed to change with dietary intake:

    • Amount of water in ECF would change*
    • Thus ECV and BP would change*
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6
Q

Give the amount of Na+ ingested and excreted each day (on average) from different sources

A

Ingestion:

Food and drink - 10.5g

Excretion:

Urine - 10.0g

Sweat - 0.25g

Faeces - 0.25g

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7
Q

How is control of ECF volume achieved?

A

Isoosmotic solution must be added or removed to maintain osmolarity

However we have no active water pumps to move water

Therefore osmoles must be moved (E.g Na+) and water will follow

Therefore via manipulation of osmoles the body can add or remove isosmotic amounts of solution to/from the ECF

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8
Q

What proportion of total filtered load of water and Na+ are removed from the nephron at each segment?

A

Proximal tubule:

67% Na+

65% water

Descending limb of LoH:

0% Na+

10-15% water

Ascending thick and thin LoH:

25% Na+

0% water

DCT:

~5% Na+

0% water

CD:

3% Na+

5% water during water loading

>24% water during dehydration

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9
Q

How is Cl- absorption linked to Na+ absorption?

A

Cl- absorption dependent on Na+ absorption

Cl- absorption maintains electroneutrality

PCT reabsorption must balance anions and cations

(Na+ = Cl- + HCO3-)

60% of Cl- absorbed in PCT

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10
Q

How much Na+, Cl- and HCO3- does 1 litre of filtrate contain?

A

145mM Na+

110mM Cl-

24mM HCO3-

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11
Q

What is the basolateral membrane transporter responsible for driving Na+ absorption in the PCT?

A

Na+/K+ ATPase

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12
Q

In the PCT, what solutes:

  • Are preferentially reabsorbed?
  • Lag behind the rest?

Why does this occur?

A

Glucose, AAs and Lactate are preferentially reabsorbed first

Cl- reabsorption lags behind

Reabsorption in the early PCT must be isosmotic with the plasma

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13
Q

Describe the trasnporters present in the S1 segment of the PCT

A

Basolateral:

Na+/K+ ATPase

NaHCO3- cotransporter

Apical:

Na+/H+ exchange

Co-transporter of Na+ w/glucose

Co-transporter of Na+ w/AAs or carboxylic acids

Co-transporter of Na+ with Phosphate (NaPi channel number sensitive to PTH)

Aquaporins

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14
Q

Describe the involvement of Cl- in S1 of the PCT

A

S1 largely impermeable to Cl-

Increasing concentration helps maintain osmolarity

Also creates a conc. gradient of Cl- for reabsorption in S2-S3

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15
Q

Describe the transport of ions/water in the S2-3 segments of the PCT

A

Basolateral:

Na+/K+ ATPase

Apical:

Na+/H+ exchanger

Paracellular and transcellular Cl- absorption

Aquaporins

4mOsmol gradient favouring water reabsorption

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16
Q

Describe the driving forces behind reabsorption into the peritubular capillary

A

Osmotic gradient established by solute absorption (Increase in osmolarity of interstitium)

Increase in hydrostatic force in the interstitium

Increased oncotic force in the peritubular capillaries due to loss of 20% of plasma volume (increased proportion of proteins and blood cells)

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17
Q

What is glomerulotubular balance in the PCT?

A

2nd line of defense to prevent or reduce variation in reabsorption of solutes

In practical terms it means that the PCT will always endevour to remove a fixed percentage of solutes from the filtrate

Works to blunt the sodium excretion response to any GFR/Filtered load changes which do occur despite myogenic autoregulation and tubulo-glomerular feedback

E.g. If filtered load of solute rises by 100% then reabsorption rises by 67% of the additional 100% to compensate

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18
Q

Describe the function of the thick and thin descending Loop of Henle

A

Increase in intercellular concentration of Na+ as the tubule moves into the medulla drives paracellular uptake of water from the descending limb

This concentrates Na+ and Cl- ions in the lumen ready for active transport in the ascending limbs

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19
Q

How permeable is the ascending LoH to water?

A

Totally impermeable

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20
Q

What is the function of the thin ascending limb of the LoH?

A

Passive Na+ absorption via paracellular route

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21
Q

What are the transporters present in the thick ascending limb of the loop of henle?

A

Basolateral:

Na+/K+ ATPase

Cl- channels

Apical:

NaKCC2 transporter

(1Na+, 1K+, 2Cl-)

ROMK

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22
Q

Why is ROMK necessary to the function of the ascending limb of the loop of henle?

A

In the filtrate at this point there is a low conc of K+ ions so it is vital that K+ ins move back into the lumen to maintain activity of NaKCC2 transporter

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23
Q

Why is the thick ascending limb of the loop of henle particularly sensitive to hypoxia?

A

Uses more energy than any other region of the nephron

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24
Q

What is the key feature of soute leaving the thick ascending limb of the loop of henle?

A

Hypo-osmotic compared to plasma

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25
Q

Compare the permeability of the early and late DCT to water

A

Early - Almost copletely impermeable

Late - Veriable permeability based on ADH concentration

26
Q

What are the transporters that can be found in a typical DCT cell?

A

Basolateral:

Na+/K+ ATPase

NCX (Na+/Ca2+ exchange)

Cl- channels

Apical:

NCC transporter (Na+/Cl-)

Ca2+ channels

27
Q

How is Ca2+ reabsorption in the DCT controlled?

A

Parathyroid hormone stimulates

28
Q

What are the functions and cell types of the late DCT?

A

Responsible for fine tuning of filtrate

Responds to a variety of stimulants

Two types of cell:

Principal cells (70%)

- Reabsorption of Na+ via ENaC

Intercalated cells (30%)

    • Active reabsorption of Cl-*
    • Secrete H+/HCO3-* (More in acids/bases)
29
Q

Give the transporters found on principal cells and the relevance of principal cells to other functions in the late DCT/early CD

A

Basolateral:

Na+/K+ ATPase

Apical:

ENac

K+ channels

Aquaporins

Relevance:

Active uptake of Na+ without accompanying anion creates - luminal charge

Negative charge drives Cl- uptake paracellularly and has a role in K+ secretion into lumen

Aquaporins controlled by ADH (variable H2O absorption)

30
Q

How is PCT and DCT+CD reabsorption of Na+ controlled?

A

PCT:

Changes in osmotic pressures and hydrostatic pressure in peritubular capillaries alter PCT reabsorption of Na+ (and hence water)

If increased they inhibit Na+ (and hence water reabsorption) and vice versa

PCT Na+ reabsorption also stimulated by RAAS

DCT+CD:

Principle cells are targets for hormone aldosterone which increases Na+ reabsorption

31
Q

From CVS:

Give the equation to show mean arterial BP from first principles

A

Mean arterial BP = (Stroke volume x Heart rate) x TPR

Therefore

Mean arterial BP = Cardiac output x Total peripheral resistance

32
Q

What is the mechanism for short term regulation of BP?

A

Baroreceptor reflex

33
Q

Describe the baroreceptor reflex

A

Baroreceptor sensitive to stretch found in arch of aorta and carotid sinus

Stretch above threshold leads to afferent nerve stimulus to the medulla

Medulla then increases heart rate and contractility in the heart via increased sympathetic and reduced parsympathetic outflow

Also adjust/lower sympathetic input to peripheral vessels to lower resistance

When below threshold pressure for firing these effects not seen

BP = (SV x HR) x TPR

34
Q

Why can the baroreceptor reflex not be used to control medium/long term changes?

A

Threshold for baroreceptor firing is reset (higher) under conditions of long term increased blood pressure

35
Q

What are the 4 neurohumoral factors in medium/long term control of BP?

What is the common theme of all these methods of control?

A

RAAS

Sympathetic NS

ADH

Atrial Natriurectic peptide (ANP)

Common:

All act on Na+ levels and hence ECF volume

36
Q

Describe the factors contributing to the release of renin

A

Released from Granular cells (found in the afferent arteriole) of the juxtaglomerular apparatus

3 Factors:

Reduced NaCL at the macula densa

Reduced perfusion pressure registered by baroreceptors of afferent arteriole

Sympathetic stimulation of the JGA

37
Q

Give an overview of the renin-angiotension-aldosterone system (RAAS)

A

Angiotensinogen cleaved to Angiotensin I by Renin

Angiotensin I cleaved to Angiotensin II by ACE

Angiotensin II acts on AT I and AT II receptors over the body to perform a variety of actions

38
Q

What are angiotensin II receptors and where are they found?

What is their action at each site?

A

AT I + II recptors = GPCRs

Main actions via AT I receptors

Arterioles:

Vasoconstriction

Kidney:

Stimulate Na+ reabsorption

Sympathetic NS:

Increased release of NA

Adrenal cortex:

Stimulates release of aldosterone

Hypothalamus:

Increases thirst sensation (Stimulates ADH release)

39
Q

What are the direct actions of Angiotensin II on the kidney?

A

Vasoconstriction of the afferent and efferent arteriole (decrease GFR)

Enhaced Na+ absorption via stimulation of Na+/H+ Exchange in PCT

40
Q

What are the effects of increased aldosterone on the Kidney/

A

Stimulates water and Na+ reabsorption in the Late DCT and Early CD

Acts on principal cells

Increases expression of ENaC and Apical K+ channel

Also increases basolateral Na+ extrusion via upregulation Na+/K+ ATPase

41
Q

What are the actions of AE related to control of BP?

A

Cleaves Angiotensin I to Angiotensin II which has vasoconstricting effects

Also breaks down the vasodilator bradykinin

Double whammy of vasoconstriction

42
Q

How does the Sympathetic nervous system affect the kidney?

A

High levels of sympathetic stimulation lead to reduced renal blood flow (decreased GFR and hence Na+ excretion)

Activates apical Na+/H+ exchanger and basolateral Na+/K+ ATPase in PCT

Stimulates renin release from the JGA (RAAS activation)

43
Q

What are the effects of ADH on the Kidney?

A

Main role is formation of concentrated urine by retaining water and control of plasma osmolarity

Increases in ADH reduces permeability of the late DCT and early CD to water hence conserving it

Also acts on thick ascending limb of the Loop of Henle (stimulates apical NaKCC2 cotransporter)

44
Q

What causes the release of ADH?

A

Increase in plasma osmolarity or severe hypovolaemia

45
Q

Where is atrial natriuretic peptide synthesised, stored and released from?

Released in response to what?

What inhibits release?

A

Synthesised, stored and released from:

Atrial myocytes

Released in response to:

Atrial stretch (low pressure volume sensors in the atria)

Inhibition:

Reduced ECV reduces atrial stretch hence inhibits ANP release

46
Q

What are the effects of ANP on the kidney?

A

Vasodilation of the afferent arteriole (hence Increased GFR)

Inhibits Na+ reabsorption aong the nephron

47
Q

What is the importance of Prostaglandins in the kidney?

A

Release of prostaglandins from the macula densa leads to triggering of the RAAS system(renin release) and hence reduction in GFR and increase in Na+ reabsorption

However

Certain locally acting prostaglandins (Mainly PGE2) enhance GFR (vasodilation of afferent arteriole) and Decrease Na+ reabsorption

They may have an important protective function against overactive SNS and RAAS

48
Q

What is the clinical relation of prostaglandins and NSAIDs?

A

NSAIDs inhibit the Cyclo-oxygenase pathway involved in prostaglandin formation

Therefore administration of NSAIDs when renal perfusion is compromised can further decrease GFR and lead to acute renal failure

49
Q

How is hypertension graded and what are the criteria for each grade?

A

Mild hypertension:

140-159 systolic

90-99 diastolic

Moderate:

160-179 systolic

100-109 diastolic

Severe:

>180 systolic

>110 diastolic

50
Q

What are the causes of hypertension?

A

95% of cases cause unknown (essential hypertension)

When cause can be defined it is known as secondary hypertension

E.g. Renovascular disease, chronic renal disease, aldosteronism, Cushing’s

Important to treat primary cause of secondary hypertension

51
Q

Describe essential hypertension

A

No definable cause:

  • May be genetically linked (tends to run in families)

Environmental factors

Pathogenesis unclear

Must be above 140/90

52
Q

What is reno-vascular disease and how does it lead to hypertension?

A

Occlusion of renal artery leads to decreased perfusion in that kidney

This leads to increase in renin release and hence RAAS activation

Vasoconstriction and Na+ retention result, leading to increased BP

53
Q

What are the concequences of renal parenchymal disease

A

Earlier stage may be a loss of vasodilator substances

Late stage Na+ and water retention due to inadequate GFR (volume dependent hypertension)

54
Q

Give some adrenal causes of hypertension

A

Conn’s syndrome:

Aldosterone secreting adenoma

Hypertension and hyperkalaemia

Cushing’s:

Excess cortisol secretion

Cortisol at high Conc acts on aldosterone receptors due to high receptor homology (Na+ and water retention)

Phaeochromocytoma:

Tumour of adrenal medulla leading to increased NA and adrenaline relase

NA stimulates Renin release

55
Q

Why is it important to treat hypertension?

A

Can be asymptomatic however can have damaging effects on heart/vasculature

Increased afterload:

Heart failure and MI

Arterial damage:

Stroke

Aneurysm

Renal failure

Retinopathy

56
Q

How can we treat hypertension throught targetting the RAAS?

A

ACE inhibitors

Reduce Ang II

Therefore diuretic and vasodilator effects

57
Q

How can we treat hypertension through the use of diuretics?

A

Thiazide diuretics:

Reduce ECV

Inhibit Na/Cl contransport on apical cells of DCT

Other diuretics:

Aldosterone antagonists will also lower BP

58
Q

How can we treat hypertension through the use of vasodilators?

A

L-type Ca channel blockers:

Reduced Ca2+ influx into vascular smooth muscle cells hence relaxation

a1 receptor blockers:

Reduce sympathetic tone in vascular smooth muscle cells hence relaxation

59
Q

How can we treat hypertension with the use of Beta blockers?

A

Blocking B1 receptors in the heart will lead to reduced sympathetic effets

Reducing heart rate and contractility

Not a first line treatment

Would be used if there were other indications such as previous MI

60
Q

What are the non-pharmacological treatments for hypertension?

How eefective are these methods?

A

Exercise

Diet

Reduce Na+ intake

Reduced Alcohol intake

Effect:

Effects can be limited however failure to implement can limit the effectivness of other antihypertensive therapy

61
Q
A

ESA 3 (54 decks)

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