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ESA 3 Callum's Cards > Urinary S4 (Done) > Flashcards

Urinary S4 (Done) Flashcards

(61 cards)

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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
Compare the permeability of the early and late DCT to water
Early - Almost copletely impermeable Late - Veriable permeability based on ADH concentration
26
What are the transporters that can be found in a typical DCT cell?
**Basolateral:** Na+/K+ ATPase NCX (Na+/Ca2+ exchange) Cl- channels **Apical:** NCC transporter (Na+/Cl-) Ca2+ channels
27
How is Ca2+ reabsorption in the DCT controlled?
Parathyroid hormone stimulates
28
What are the functions and cell types of the late DCT?
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
Give the transporters found on principal cells and the relevance of principal cells to other functions in the late DCT/early CD
**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
How is PCT and DCT+CD reabsorption of Na+ controlled?
**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
From CVS: Give the equation to show mean arterial BP from first principles
Mean arterial BP = (Stroke volume x Heart rate) x TPR Therefore Mean arterial BP = Cardiac output x Total peripheral resistance
32
What is the mechanism for short term regulation of BP?
Baroreceptor reflex
33
Describe the baroreceptor reflex
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
Why can the baroreceptor reflex not be used to control medium/long term changes?
Threshold for baroreceptor firing is reset (higher) under conditions of long term increased blood pressure
35
What are the 4 neurohumoral factors in medium/long term control of BP? What is the common theme of all these methods of control?
RAAS Sympathetic NS ADH Atrial Natriurectic peptide (ANP) **Common:** All act on Na+ levels and hence ECF volume
36
Describe the factors contributing to the release of renin
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
Give an overview of the renin-angiotension-aldosterone system (RAAS)
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
What are angiotensin II receptors and where are they found? What is their action at each site?
**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
What are the direct actions of Angiotensin II on the kidney?
Vasoconstriction of the afferent and efferent arteriole (decrease GFR) Enhaced Na+ absorption via stimulation of Na+/H+ Exchange in PCT
40
What are the effects of increased aldosterone on the Kidney/
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
What are the actions of AE related to control of BP?
Cleaves Angiotensin I to Angiotensin II which has vasoconstricting effects Also breaks down the vasodilator bradykinin Double whammy of vasoconstriction
42
How does the Sympathetic nervous system affect the kidney?
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
What are the effects of ADH on the Kidney?
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
What causes the release of ADH?
Increase in plasma osmolarity or severe hypovolaemia
45
Where is atrial natriuretic peptide synthesised, stored and released from? Released in response to what? What inhibits release?
**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
What are the effects of ANP on the kidney?
Vasodilation of the afferent arteriole (hence Increased GFR) Inhibits Na+ reabsorption aong the nephron
47
What is the importance of Prostaglandins in the kidney?
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
What is the clinical relation of prostaglandins and NSAIDs?
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
How is hypertension graded and what are the criteria for each grade?
**Mild hypertension:** 140-159 systolic 90-99 diastolic **Moderate:** 160-179 systolic 100-109 diastolic **Severe:** \>180 systolic \>110 diastolic
50
What are the causes of hypertension?
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
Describe essential hypertension
**No definable cause:** - May be genetically linked (tends to run in families) Environmental factors Pathogenesis unclear **Must be above 140/90**
52
What is reno-vascular disease and how does it lead to hypertension?
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
What are the concequences of renal parenchymal disease
Earlier stage may be a loss of vasodilator substances Late stage Na+ and water retention due to inadequate GFR (volume dependent hypertension)
54
Give some adrenal causes of hypertension
**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
Why is it important to treat hypertension?
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
How can we treat hypertension throught targetting the RAAS?
ACE inhibitors Reduce Ang II Therefore diuretic and vasodilator effects
57
How can we treat hypertension through the use of diuretics?
**Thiazide diuretics:** Reduce ECV Inhibit Na/Cl contransport on apical cells of DCT **Other diuretics:** Aldosterone antagonists will also lower BP
58
How can we treat hypertension through the use of vasodilators?
**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
How can we treat hypertension with the use of Beta blockers?
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
What are the non-pharmacological treatments for hypertension? How eefective are these methods?
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

ESA 3 Callum's Cards (55 decks)

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