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ED Primary Exam > Week 18 Physiology - Renal II + III > Flashcards

Week 18 Physiology - Renal II + III Flashcards

1
Q

List the ions that are either completely or almost completely reabsorbed in the kidneys?

A

Na+ (99%)
K+ (93.3%)
Cl (99%)
HCO3- (100%)
Urea (53%)

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2
Q

How much creatinine is reabsorbed?

A

<1%

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3
Q

Explain secondary active transport?

A

Process of maintaining low concentrations of intracellular sodium via Na/K ATPase, which then allows coupled transport against concentration gradient (i.e. glucose, amino acids etc)

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4
Q

What are the most important channels in each of the different segments of the nephron?

A

Na+/H+ exchanger in PCT
Na/K/2Cl Thick ascending limb
NaCl Cotransport Early DCT
ENaC Collecting Duct

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5
Q

What is the effect of aldosterone on the nephron?

A

Steroid which enters collecting duct principal cells –> increased insertion of ENaC and reabsorption of Na+, with exchange for K+

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6
Q

What effect does AT II have on proximal convoluted tubule?

A

Increased reabsorption of HCO3- and Na+

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7
Q

Define water diuresis:

A

The increase in urine output produced by increasing intake/large amounts of hypotonic solution –> decrease in ADH secretion

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8
Q

Why can water toxicity occur?

A

Maximum urine flow during water diuresis is 16mL/min –> if free water intake exceeds this, can lead to cellular swelling and overcoming ability to maintain ionic concentrations for cellular function

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9
Q

Where is the majority of K+ excreted/lost?

A

Mainly passive loss in the DCT –> dependent on amount of Na+ present in collecting ducts, due to Na+ being exchanged for K+ if being reabsorbed in large amounts.

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10
Q

What is the effect of H+ secretion in intercalated cells?

A

K+ reabsorption

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11
Q

What features of the loop of Henle allow the countercurrent multiplier exchange to work?

A

Complete permeability of descending limb to H20, and impermeability to solutes.

Complete impermeability of ascending to H20 and permeability to solutes.

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12
Q

What channels facilitate movement of H20 out of the descending LOH?

A

Aquaporin 1

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13
Q

How is the tonicity of the tubular fluid increased towards/into the renal medulla?

A

As isotonic fluid flows from PCT, H20 begins to move into intersitium from lumen in descending limb.

This is because it runs in close proximity to ascending limb, where Na+/K+/2Cl- channels are increasing the osmolality of the interstitium to create a concentration gradient that favours movement of water out of descending limb.

The net result is movement of water out into the interstitium as it descending down the descending limb.

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14
Q

What is the role of the vasa recta in conservation of water?

A

It runs parallel to the tubule, carrying blood in the opposite direction. As it passes

The effect is that it initially has blood that is very hypertonic due to passing next to the ascending limb, and picking up a lot of the sodium that is reabsorbed, so that there is a concentration that favours H20 reabsorption.

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15
Q

How does the vasa recta work to not remove solutes and ruin the concentration gradient set up by the loop of Henle?

A

The counter-current movement of peritubular blood has broadly 2 step process:

  1. Blood at the top of descending loop secretes water, and reaborbs solutes
  2. Blood heading to top of ascending loop, reabsorbs water, and secretes solutes.

The counter-current movement of blood vs tubular fluid prevents washout of the ionic concentration that enables water conservation in the kidney.

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16
Q

What is the role of urea in countercurrent mechanism?

A

Urea contributes to the hypertonicity of the renal medulla, freely passing into luminal fluid down its concentration gradient, and by reabsorption from the collecting ducts, via Urea transport - to allow for high concentrations of urea in medullary intersitium to aid in the counter-current exchange mechanism.

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17
Q

What is the overall effect of the movement of water and ions in the vasa recta?

A
  1. As DESCENDING vasa recta passes ASCENDING LOH, it takes the solutes from the ascending loop, and carries it back down into the medulla, so that solute content isn’t lost.
  2. As ASCENDING vasa recta passes DESCENDING LOH, which is soluble to water, it takes H20, as it is initially hypertonic. It also allows solutes to diffuse down concentration gradient to maintain hypertonicity.
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18
Q

What is the normal serum osmolality?

A

280-295 mOsm/kg

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19
Q

What is the effect of ADH on collecting duct? What receptor does it act on?

A

Increased permeability to water via increased apical expression of AQ-2 channels. Initiated via binding to V2 receptors on principal cells.

It allows more concentration of urine, and free water reabsorption back into plasma

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20
Q

What factors stimulate ADH secretion?

A

Increased osmolality of plasma
Pain, stress, exercise
Nausea/vomiting
Angiotensin II

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21
Q

What factors inhibit ADH secretion?

A

Decreased osmolality of plasma
Alcohol

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22
Q

Where is ADH secreted from? What receptors stimulate secretion?

A

Posterior pituitary

Low pressure receptors in great veins, RA, LA and pulmonary vessels –> send impulses via vagus nerve, as well as osmoreceptors within anterior pituitary (outside BBB)

23
Q

Outline the tonicity of filtrate as it passes along the nephron?

A

PCT = isotonic
Descending limb = hypertonic
Ascending limb = hypertonic
DCT = hypotonic
Collecting duct = hypertonic

24
Q

What is the role of tubuloglomerular feedback?

A

Mechanism by which the glomerulus gets feedback from the contents of the filtrate to help determine the rate of filtration to assist with regulation of solutes/fluid balance

25
Q

How does the glomerular feedback mechanism work?

A

Macula densa is the sensor apparatus.

Na+ and Cl- enter macula densa cells via Na/K/2Cl transporter in apical membrane –> and if increased levels of Na+, there is increased Na/K ATPase activity.

This increased activity leads to hydrolysis of ATP to form adenosine, acting as a paracrine hormone on A1 receptors of endothelial cells, cell signalling of increased intracellular calcium and constriction of afferent arterioles –> decreased GFR.

26
Q

How does the macula densa communicate with the juxtaglomerular cells?

A

Via release of prostaglandins, which stimulate secretion of renin by JG cells (PGE2) –> role is to increase blood volume and pressure

27
Q

What is renin? What is its action?

A

Enzyme secreted into plasma by JG cells, cleaves Angiotensinogen into ATI (angiotensinogen is a plasma protein that is synthesised in liver and always present in plasma)

28
Q

What stimulates renin secretion?

A

Na+ depletion
Beta adrenergic activation on JG cells

29
Q

What inhibits renin secretion?

A

Increased Na+ and Cl- reabsorption across macula densa
Increased afferent arteriole pressure
ADH
Angiotensin II

30
Q

Describe the process of ATI –> AT II

A

Angiotensin 1 circulates into capillaries, most notably in lungs, which express ACE, which cleaves to AT II

31
Q

What are the chief effects of ATII?

A

Ateriolar smooth muscle contraction –> increased BP
Action on afferent and efferent arterioles to stimulate increased

32
Q

What is the metabolism of AT II?

A

Rapid, t 1/2 1-2 mins in plasma, removed by amino peptidase

33
Q

What other vasoactive peptide does ACE cleave?

A

Bradykinin - role of bradykinin is to increase NO and cause vasodilation –> therefore ACEi can actually have a secondary vasodilator effect as bradykinin metabolism is slowed

34
Q

What stimulates secretion of ANP/BNP?

A

Atrial and ventricular stretch, marking an increase in blood volume –> causing increased Na+ and H20 excretion. Does this by dilating afferent arterioles, and increasing glomerular capillary permeability

35
Q

Where is EPO synthesised?

A

Interstitial cells of peritubular capillary bed in kidneys

36
Q

What is the function of EPO?

A

Circulates to bone marrow to increase number of committed stem cells that are converted to RBC precursors, as well as inhibiting apoptosis, stimulating growth and development of precursors

37
Q

What stimulates EPO?

A

Hypoxia
Alkalosis at high altitudes
Androgens

38
Q

Describe the process of H+ secretion in the proximal convoluted tubule?

A

Secondary active transport, where H+ is exchanged with Na+ (as there is less intracellular sodium due to Na/K ATPase activity).

39
Q

How is bicarbonate reabsorbed in the proximal convoluted tubule?

A

Cannot cross brush border due to being charged, instead forms carbonic acid in tubular lumen via carbonic anhydrase –> CO2 + H20.

These pass into tubular cells, and reverse reaction via CA occurs.

HCO3 - formed is then sequestered into plasma via Na+/HCO3- contransporter on basolateral surface, or via HCO3-/Cl- antiporter to allow almost 100% reabsorption of bicarbonate.

40
Q

How does H+ secretion in the distal tubule work?

A

Via primary active (ATP) driven transport, where it is actively secreted against its concentration gradient

41
Q

What is the maximal pH gradient that H+ can be actively secreted against?

A

pH of 4.5

42
Q

What are the 3 major urine buffering systems?

A
  1. Bicarbonate –> allows formation of CO2 + H20 in urine
  2. Ammonia –> NH3 binds H+ to become ammonium (NH4)
  3. Monohydrogen phosphate –> binds H+ to become H2PO4
43
Q

How does the kidneys generate ammonia to assist with buffering?

A

Through PCT and DCT, ‘glutaminase’ enzyme deaminates glutamine, causing byproduct of NH3 to form, which readily diffuses into tubular lumen. Rapidly binds to H+, maintaining concentration gradient of ammonia diffusing into lumen, as well as buffering hydrogen ion

44
Q

What effect does aldosterone have on acid secretion?

A

Via effect on late DCT/collecting duct, aldosterone enhances Na+ reabsorption via secretion of H+ and K+

45
Q

What are the most important buffer systems in b blood/plasma?

A

Plasma proteins (i.e. albumin) - Carboxyl and amine groups can function either as acid or base dependent on pH

RBCs/Hb have unique mechanisms:
- Hb binds H+ in acidic environments and releases O2 and the reverse of that in high O2 environments (H+ released to form CO2 and get blown off)

46
Q

What are the most important intracellular buffers?

A

Phosphate (ATP, G6P) - also important in the urine

47
Q

What are the two main mechanisms by which metabolic acidosis occurs?

A
  1. Gain of acid
  2. Loss of base
48
Q

What is the anion gap?

A

Basic principal is that blood needs to maintain electric neutrality.

Anion gap is the gap between measured cations and measured anions.

Na+ is the primary measured cation, and HCO3- and Cl- are the measured anions.

The difference between these represents the unmeasured ions (i.e. proteins)

49
Q

What is a high anion gap metabolic acidosis?

A

Where increased acid production/ingestion causes increased proton concentration in plasma.

The addition of acid to plasma causes dissociation of H+ from its organic anion. To maintain electroneutrality, this H+ binds to HCO3- and so bicarbonate is lost, but the negative charge is replaced by the organic acid anion. (i.e. lactate)

Where this occurs, there will be an elevated anion gap, as there will be an increased amount of unmeasured anions which are contributing to electroneutrality

50
Q

What are the causes of HAGMA?

A

Lactate
Toxins – methanol, metformin, phenformin, paraldehyde, propylene glycol, pyroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salicylates, solvents
Ketones

51
Q

What are the causes of NAGMA?

A

GI losses
Renal tubular acidosis
Addisons’/Carbonic Anhydrase inhibitors
Chloride

52
Q

What are the the commonest causes of metabolic alkalosis?

A

Vomiting –> loss of H+ from GI tract
Diuretics –> loss of H+ in urine
Hypokalaemia

53
Q

What is the mechanism of alkalosis with diuretics or hypokalaemia?

A

Increased HCO3- reabsorption due to volume contraction, or hypokalaemia - as it triggers the RAAS and actions of aldosterone on intercalated cells. This causes exchange of potassium for excretion of H+, and formation of new HCO3- ions in intercalated cells

54
Q
A

ED Primary Exam (46 decks)

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