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Block 1 > Tubular Processing & Electrolyte Balance > Flashcards

Tubular Processing & Electrolyte Balance Flashcards

1
Q

What is the key process in the kidneys to fine tune volume/composition of urine and to avoid high fluid and solute losses?

A

Tubular processing

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2
Q

What is more important for most substances; reabsorption or secretion?

A

Reabsorption

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3
Q

What are the 2 properties of tubular reabsorption?

A
  1. Quantitatively large

2. Highly selective; allows independent regulation of solute excretion

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4
Q

What 2 types of transport does tubular reabsorption utilise to move fluid/solutes from tubule lumen to peritubular capillary?

A

Passive

Active

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5
Q

What do luminal and basal surfaces of tubule epithelial cells have on them and what does this achieve?

A

Transporters -> establish concentration gradients e.g. Na+/K+ ATPase

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6
Q

How is water reabsorbed in the nephron?

A

Linked closely to Na+ (main osmotically active substance) reabsorption and permeability of the different parts of the nephron

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7
Q

Where does the majority of reabsorption occur?

A

Proximal convoluted tubule

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8
Q

Where does fine tuning of water and solute excretion occur and via what?

A

More distal parts of nephron under hormonal control

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9
Q

What occurs in the Proximal Convoluted Tubule (PCT) and what characteristics does it have to do this?

A

Roles:
Majority of Na+ and water (~65%) & glucose and AA reabsorption
Site of secretion of metabolic acids/bases, drugs etc.
Characteristics:
Fluid leaving PCT is isosmotic as epithelium freely permeable to water
Brush border increases SA
Mitochondria provide energy

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10
Q

How are glucose and amino acids reabsorbed in the PCT?

A
  • Secondary active transport linked to Na+ reabsorption -> Na+ glucose co-transporters (SGLT2 mainly) on luminal side move glucose against concentration gradient into cell -> glucose transporters (GLUT) on basal side allow facilitated diffusion into interstitial fluid
  • Similar process for AAs but different transporters used to move them from tubular lumen to interstitial fluid
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11
Q

What happens if the amount of glucose appearing in the filtrate increases?

A

Finite number of SGLT transporters on proximal tubule cells and because glucose should all be reabsorbed, if too much glucose gets into filtrate they reach a transport maximum (Tm) where reabsorption cannot go faster -> glucose lost in urine + water retained in tubule lumen getting excreted too (osmotic diuresis)

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12
Q

How are H+ ions secreted?

A

Na+ reabsorption linked to secondary active transport of H+ into tubular lumen using a Na+/H+ exchanger (NHE) where Na+ goes into tubular cells and H+ is secreted into tubular lumen (important for HCO3- reabsorption in proximal tubule)

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13
Q

What are the 3 main parts of the Loop Of Henle and there functional characteristics?

A
  1. Thin descending limb: water permeable + no active reabsorption/secretion of solutes
  2. Thin ascending limb: water impermeable + barely any reabsorption/secretion of solutes
  3. Thick ascending limb: water impermeable, active reabsorption of Na+/others + dilutes luminal fluid (hypo-osmotic)
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14
Q

How does reabsorption + dilution of luminal fluid occur in the thick ascending limb of the Loop Of Henle?

A

Reabsorption from tubule lumen occurs primarily by Na+K+2Cl- co-transporters (all 3 move into tubular cells)
+ve charge in lumen encourages paracellular reabsorption of cations e.g. Ca2+, Mg2+
Water cannot solutes into tubular cells as it is impermeable to water so tubular lumen fluid becomes diluted + hypo-osmotic (solution with lesser concentration of solutes)

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15
Q

What occurs in the early distal tubule?

A

Macula densa cells in 1st portion -> part of JGA involved with feedback control of GFR/BP + sensitive to [NaCl]
Impermeable to water so contributes to filtrate dilution
Active reabsorption of Na+ utilising Na+Cl- co-transporter on luminal side further diluting tubular luminal fluid

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16
Q

What happens in the late distal & cortical collecting tubule?

A

Water permeability under hormonal control by ADH i.e. water permeable when ADH present and vice versa
2 main cell types:
1. Principal cells: Na+ reabsorption & K+ secretion
2. Intercalated cells: K+ reabsorption & H+ secretion

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17
Q

What do principal cells do?

A

Na+ enter cells through epithelial Na+ channels (ENaC) on luminal side -> transported out of tubular cells via Na+/K+ ATPase to maintain concentration gradient - no. of ENaC channels & Na+/K+ activity controlled by aldosterone hormone e.g. high aldosterone = increase in channels -> more ion movement - as Na+ is reabsorbed, water follows + K+ is secreted in collecting tubule & duct

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18
Q

What happens in the medullary collecting duct?

A

Final site for urine processing; key role in regulating degree of [urine]
Water permeability controlled by ADH i.e. ADH increases water reabsorption
Surrounded by medullary interstitium with a high [solutes]
Urea permeability allows medullary interstitium to remain concentrated
Close relationship to Loop Of Henle aids these processes

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19
Q

How are tubular processes regulated?

A

Local feedback & hormonal/neural mechanisms
Reabsorption of individual solutes can be adjusted independently via hormones acting on different parts of nephron (unlike GFR regulation)

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20
Q

Where/how is Atrial Natriuretic Peptide (ANP) produced and what does it do?

A
  • Released by atrial muscle fibres in response to increased stretch of atria as a result of excessive blood volume (also pathologically raised e.g. in cardiac failure when there is increase in ECV)
  • Decreases NaCl reabsorption in the distal tubule/collecting tubule and duct
  • Causes small increases in GFR and decreases renal reabsorption
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21
Q

What does parathyroid hormone do?

A

Decreases phosphate (PO4) reabsorption and increases Ca2+ reabsorption in the proximal tubule, thick ascending loop of Henle/distal tubule

22
Q

What does angiotensin II do?

A
  • Increases NaCl + water reabsorption and H+ secretion in the proximal tubule, thick ascending loop of Henle/distal tubule + collecting duct (directly on renal tubule cells increasing activity of Na+ transporters & indirectly via increased aldosterone in adrenal gland)
  • Vasoconstriction
  • Indirectly increases thirst & ADH release in posterior pituitary
  • > increase arterial BP
23
Q

Where does ADH have its affects?

A

Distal tubule/collecting tubule + duct

24
Q

Describe the 2 mechanisms via which receptors can detect high or low levels of electrolytes to keep levels balanced.

A
  1. Direct e.g. ECF [K+] has a direct effect on release of aldosterone
  2. Indirect e.g. baroreceptors indicate ECF volume so are a marker of Na+ levels as water tends to follow Na+ (however serum ECF samples do not necessarily reflect body content of any electrolyte due to water)
25
Q

How is Na+ levels regulated?

A

Major EC electrolyte + determinant of ECF volume so kidneys help to maintain ECF volume by regulating amount of Na+ excreted in urine e.g. if Na+ is lot, water will follow + be lost decreasing ECF volume (normally reabsorb most Na+ filtered so only small amount excreted) - regulated by local, hormonal + neural factors

26
Q

What is pressure diuresis/natriuresis?

A

Ability of kidney to increase urine output/Na+ excretion in response to increased arterial BP/volume - helps maintain blood volume over a wide range of fluid & Na+ intake

27
Q

What do granular cells of the afferent arteriole of the JGA do?

A

Secrete an enzyme called renin in response to falls in ECV/low Na+ by utilising baroreceptors that detect a decrease in ECF volume and increase Na+ reabsorption and thus, water reabsorption

28
Q

What are the 3 main triggers of renin release?

A
  1. Low afferent arteriole pressure
  2. Activation of sympathetic nerves that supply JGA
  3. Low [NaCl] in distal tubule
    - > renin released by granular cells of afferent arteriole
29
Q

What happens in the renin angiotensin aldosterone system (RAAS)?

A

Angiotensinogen (liver) -> converted to angiotensin I (produced due to decreased arterial BP which releases renin in kidneys to produce this) -> Angiotensin Converting Enzyme (ACE) in the lungs converts this to angiotensin II

30
Q

What is the aim of the RAAS process?

A

Helps maintain ECV and arterial BP despite wide variations in dietary intake of Na+ e.g. if Na+ intake reduced decreasing ECF, RAAS activity increases and vice versa (also responds to situations where ECF and BP falls independently of salt intake)

31
Q

What would happen in the RAAS system step-by-step if there was an increase in salt/Na+ intake?

A

Increased ECV -> increased arterial BP -> decreased renin + angiotensin -> decreased renal retention of salt + water -> return of ECV almost to normal + arterial BP almost to normal

32
Q

Where is aldosterone produced + what does it do?

A
  • Secreted by zona glomerulosa of adrenal cortex in response to increased angiotensin II or EC [K+]
  • Increases Na+ reabsorption by acting on principal cells in late distal/cortical collecting tubule by binding to nucleus + increasing production of proteins e.g. ENaC & Na+/K+ ATPase which increases ability of cells to reabsorb Na+
33
Q

Why does K+ levels need to be regulated?

A

K+ is the major determinant of resting membrane potential so small changes can cause life-threatening cardiac arrhythimas - most K+ is located IC so need rapid ways to regulate EC levels (performed mainly by kidneys)

34
Q

Why is serum [K+] not a good reflection of total body K+?

A

Because there is only a small amount in the EC so a lot of it could be IC e.g. in diabetic ketoacidosis levels initially appear high but the amount in the body might actually be low

35
Q

What 4 factors decrease the blood levels of K+ by driving it into cells decreasing EC [K+]?

A
  1. Insulin increases Na+/K+ ATPase activity (why it is used as part of emergency treatment of hyperkalaemia)
  2. Aldosterone acts in the same way to effect urinary excretion of K+
  3. B-adrenergic sympathetic stimulation increases Na+/K+ ATPase activity too (why salbutamol for e.g. can cause low blood levels of K+ if used in excess)
  4. Alkalosis i.e. low EC [H+] possibly due to exchange of IC H+ for EC K+
36
Q

What 7 factors decrease blood levels of K+ by shifting it out of cells increasing EC [K+]?

A
  1. Insulin deficiency e.g. DM
  2. Aldosterone deficiency e.g. Addisons disease
  3. B-adrenergic blockade
  4. Acidosis i.e. high EC [H+] reduces Na+/K+ ATPase activity possibly to exchange of IC K+ for extracellular H+
  5. Cell lysis releases IC K+ via damaged cell membrane
  6. Strenuous exercise via damaged cell membranes too
  7. Increased EC fluid osmolarity causing cellular dehydration - increases IC [K+] resulting in a larger concentration gradient to promote movement out of the cell
37
Q

What is responsible for most of the variation in K+ excretion?

A

The amount of secretion in late distal tubule/cortical collecting tubule (controlled by aldosterone)

38
Q

How is K+ secreted/excreted?

A

Na+/K+ ATPase moves K+ into principal cells from the renal interstitial fluid creating a high IC concentration -> K+ then passes through channels in luminal membrane into tubular lumen

39
Q

What are the 3 factors that determine the rate of K+ secretion?

A
  1. Activity of Na+/K+ ATPase
  2. [K+] gradient between blood, principal cell + tubular lumen
  3. Permeability of luminal membrane to K+ e.g. number/amount in an open state of K+ transporters
40
Q

What cells can reabsorb K+ during K+ depletion?

A

Intercalated cells

41
Q

What are the 4 factors that regulate K+ secretion?

A
  1. Plasma K+ concentration
  2. Aldosterone
  3. Tubular flow rate
  4. [H+]
42
Q

How does plasma [K+] affect rate of K+ excretion?

A
  • Increases Na+K+ ATPase activity
  • Increases [K+} gradient from blood to lumen
  • Increases permeability of luminal membrane to K+ via increased no. of transporters
  • Increase aldosterone release
    = increased rate of K+ secretion/excretion
43
Q

How does aldosterone affect rate of K+ excretion?

A
  • Increases Na/K+ ATPase activity
  • Increases permeability of luminal membrane to K+ via increased no. of transporters
    = Increased K+ secretion in cortical collecting tubules + thus, excretion
44
Q

How does tubular flow rate occur and how does it affect rate of K+ excretion?

A
  • Can occur with volume expansion, high Na+ intake or some diuretics (loop/thiazide so side effect is hypokalaemia)
  • Increases [K+] gradient from principal cell to tubular lumen (low levels in lumen)
  • Increases permeability of luminal membrane to K+
    = increased rate of K+ secretion/excretion
    (useful mechanism as K+ excretion occurs independently of aldosterone which can be suppressed by high Na+ intake)
45
Q

What happens if there is increased Na+ intake in terms of K+ secretion/excretion in a healthy person?

A

Aldosterone is suppressed which is trying to decrease K+ secretion in cortical collecting duct
GFR is increased + proximal tubular Na+ reabsorption is decreased increasing distal tubular flow rate which causes increased K+ secretion in cortical collecting duct
Thus, there is unchanged K+ excretion

46
Q

How does [H+] concentration affect the rate of K+ excretion?

A

Increased [H+] acutely decreases Na+/K+ ATPase activity, lowering the concentration gradient + decreasing rate of K+ excretion

47
Q

What is the normal range for EC [K+]?

A

3.5 - 5.3 mmol/L

48
Q

What is hypokalaemia? Describe the signs/symptoms, general approach to causes & treatment.

A

EC [K+] below normal range with signs/symptoms including muscle weakness + cardiac arrhythimas (often asymptomatic though)
You should consider causes such as reduced intake, excessive losses (e.g. diuretics, severe diarrhoea, aldosterone excess) + altered body distribution
Thus, should address underlying cause and perhaps give K+ supplements

49
Q

What is hyperkalaemia? Describe the signs/symptoms, general approach to causes & treatment.

A

EC [K+] above normal range with signs/symptoms including cardiac arrhythimas (tall T waves in ECG) (often asymptomatic though)
Should consider causes such as excessive intake, inadequate losses (e.g. kidney disease, aldosterone deficiency) + altered body distribution (e.g. acidosis)
Thus, should address underlying cause, restrict intake, give Ca gluconate (stabilise myocardium), give insulin (+ glucose, maybe salbutamol) (drive K+ into cells) & aid excretion via fluids, ion-exchange resins or dialysis (treatment depends on severity)

50
Q

Why can altered body distribution affect the blood levels of K+?

A

The body may have distributed K+ into the cells which may make the blood result abnormal however, if you do more bloods, K+ may start to appear again

Block 1 (54 decks)

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