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Physiology B2 & B3 > Renal > Flashcards

Renal Flashcards

1
Q

What are the determinants of Glomerular filtration?

A

Effective filtration pressure = ~20 torr

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2
Q

What are the determinants of renal blood flow?

How is capillary pressure maintained despite fluctuating arterial BP?

A
  • RBF maintaining by matching of pressure and renal vascular resistance
  • Autoregulation occurs via two mechanisms
    • The vascular response: myogenic (bayliss reflex); contracting of SMC in response to stretch
    • Glomerular-vascular:
      • change in [NaCl] @ thick ascending limb
      • ↑ [NaCl] -> afferent constriction
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3
Q

What percentage of Na+ is reabsorbed at each of the 4 key areas in the nephron?

A
  • PCT – 67%
  • TAL – 25%
  • DCT – 5%
  • CD – 3%

-> 0.4% filtered load remaining

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4
Q

How is sodium handled at the PCT, TAL, DCT and CD? (images)

A
  • PCT
  • TAL
  • DCT
  • CD
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5
Q

What are the two types of glucose transporters in the apical membrane of the PCT?

A
  • SGLT2- not very saturable, low affinity
  • SGLT1- (late PCT) – low saturability, very high affinity (mops up remaining glucose)
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6
Q

What are the primary mechanisms that regulate [K+] in the ECF?

A

PCT

TAL

CD.

  • Intercalated cells in late distal tubules and CD
  • Principal cells in late distal tubules and CD - aldosterone mediated
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7
Q

Explain the counter current multiplier in respect the development of a hyperosmotic medullary insterstitium.

A

Descending limb: only permeable to water

Ascending limb: only permeable to Na+ (diluting segment)

  • Active pump in TAL pumps Na+ into interstitium, establishing a 200 mOsm/L gradient between tubular fluid and interstitial fluid.
  • The TDL then equalibriates (400mosm/L) with the increase interstitial osmolarity, as water leaves into the interstitium (interstitium osmolarity maintain dt. constant active transport of Na+ from TAL).
  • New fluid is then pushed through from TDL, causing hyperosmolar fluid from TDL to flow into the TAL, this fluid then again establishes the 200mOsm/L gradient, but now at the higher osmolarity of 500mOsm/L
  • -> this repetition is the counter current multiplier – allows a very high osmolarity to be established despite only a 200mOsm/L gradient being capable of being established between lumen and interstitium at the loop of henle
  • A very dilute tubular fluid is delivered to DCT and CD -> allows for modulation of fluid balance.
  • Vasa recta also run in similar counter current pathway -> prevents washing out of establishing medullary gradient.
  • Urea also contributes about 50% of medullary osmolarity,
    • very high delivery of urea to medullary CD
    • -> urea diffuses into interstitium -> horizontal transfer to Loop of Henle where it is secreted into luminal fluid, and urea recirculates each time contributing to higher osmolarity of interstitium.
    • Therefore, low protein diets -> less ability to concentrate urine.
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8
Q

How does ADH promote H20 reabsoprtion?

A
  • Increase in ADH = Increase in number of aquaporins open.
  • Aquaporins are the channels that H20 use for osmosis
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9
Q

How does ADH promote urea recycling?

A

Increase levels of ADH in CD, promotes UT-A1 transporters to open so urea can be reabsorbed into the interstitial fluid.

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10
Q

How does the counter current exchanger maintain gradient

A
  • Vasa recta is freely permeable to NaCl and H20.
  • Therefore passive diffusion out of solute and passive diffusion in out H20 is easily performed.
  • This ensures the blood and the surrounding fluid are in equilibrium.
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11
Q

How does the countercurrent multiplier achieve its role

A
  • (1) In TAL: Active transport pumps NaCl out into interstitial fluid. Creating a concentration gradient of 200mosm between the tubule and interstitial fluid.
  • (2) The TDL equilibrates with the new increase osmolality of the interstitial fluid by pumping H20 out via passive diffusion.
  • (3) New fluid arrives in TDL, this moves the hyperosmolality fluid up into in the TAL, which then again promotes the active pumping of Nacl out. This fluid again establishes a 200mosm gradient but just at a higher osmolarity of 500mosmol/L.
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12
Q

How is ADH stimulated

A

Plasma osmolality >300mosm

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13
Q

Osmolality

A

The number of dissolved solutes in 1kg of fluid

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14
Q

Role of ADH

A

Promotes the reabsorption of H20. Thus contributes to urine being more concentrated.

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15
Q

Structures responsible for diluting or concentrating urine

A
  • Vasa Recta
  • Loop of Henle
  • Collecting Duct
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16
Q

Two mechanisms of countercurrent

A
  • Countercurrent Multiplier: Loop of Henle
  • Countercurrent exchanger: Vasa Recta
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17
Q

What is important to remember about Counter current exchanger

A

Vasa recta does not contribute to gradient but rather it protects it.

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18
Q

What is the role of the countercurrent exchanger

A

The vasa recta ensures the concentration gradient is maintained so the counter current multiplier can continue to dilute/concentrate urine

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19
Q

What is the role of the countercurrent mechanism

A

Keep solute of body fluid ~300mosm by regulating urine concentration and volume

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20
Q

What is the role of the countercurrent mulitpier

A

Main goal is to concentrate urine

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21
Q

What is the role of urea

A

Urea enhances urine to be concentrated.

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22
Q

What are the different classes of diuretics

A

REMEMBER: Over Caffeinated Ladies Talk Intensely After Midnight

  • Osmotic diuretic
  • Carbonic anhydrase
  • Loop diuretics
  • Thiazides
  • Inhibitors of ENaCs
  • Aldosterone antagonist
  • Methlyxandithine
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23
Q

Give an example of Osmotic diuretic and where it acts long the nephron

A
  • E.g. Mannitol
  • PT and TAL
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24
Q

What are the mechanism, contraindications and side effects of osmotic diuretics

A
  • M: Osmotic receptors attach onto H20 preventing it from reabsorbing.
  • C: Anuria and Heart Failure
  • S/E: Mg2+ loss
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25
Q

What are osmotic diuretics used for

A

Brain odema

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26
Q

Give an example of Carbonic anhydrase and where it acts long the nephron

A
  • E.g. Acetazolamide
  • PT and CD
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27
Q

What are the mechanism, contraindications and side effects of carbonic anhydrase

A
  • M: Prevents Na+/H+ exchanger and HCO3- reabsorption
  • C: Acidosis
  • S/E: Metabolic acidosis
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28
Q

What are carboinc anhydrase use for

A

Glaucoma

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29
Q

Give an example of Loop diuretics and where it acts long the nephron

A
  • E.g. Frusemide
  • TAL
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30
Q

What are the mechanism, contraindications and side effects of Loop diuretics

A
  • M: Inhibits the NKCC2 transporter by binding onto the Na+ site. Prevents the reabsorption of Na+, K+ and Cl-.
  • C: Anuria
  • S/E: Loss of electrolyte and uric acid secretion
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31
Q

What are loop diuretics use for

A

Oedema

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32
Q

Give an example of a thiazide and where it acts long the nephron

A
  • E.g. Cholorthiazide
  • DT
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33
Q

What are the mechanism, contraindications and side effects of Thiazides

A
  • M: Blocks the NCC (Na+, Cl-) co-transporter. Binds onto the Cl-, therefore more Na+ arrives at the CD
  • C: Anuria and Hypokalemia
  • S/E: Hypokalemia and retention of uric acid
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34
Q

What are thiazides use for

A
  • HT
  • Oedema with good GFR
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35
Q

Give an example of a inhibitor of ENaCs and where it acts long the nephron

A
  • E.g. Amiloride
  • Principal cells of CD
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36
Q

What are the mechanism, contraindications and side effects of Inhibitors of ENaCs

A
  • M: Amiloride competes with Na+ site on the ENaC. This blocks Na+ absorption and K+ secretion
  • C: Hyperkalemia and Anuria
  • S/E: Hyperkalemia and N/V
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37
Q

What are Inhibitors of ENaCs used for

A
  • HT (in conjunction with other diuretics)
  • Reduced the K+ loss of Loop diuretics
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38
Q

What is the special feature of Inhibitors of ENaCs

A

K+ sparing diuretics

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39
Q

Give an example of a Aldosterone antagonist and where it acts long the nephron

A

E.g. Spironolactone

CD

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40
Q

What are the mechanism, contraindications and side effects of Aldosterone antagonist

A
  • M: Inhibits aldosterone from binding thus inhibiting Na+ reabsorption and K+ secretion
  • C: Hyperkalemia
  • S/E: Acidosis and Hyperkalemia
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41
Q

What are Aldosterone antagonist used for

A

HT and Hyperaldosteronism

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42
Q

What is the special feature of Aldosterone antagonist

A

K+ sparing diuretics

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43
Q

Give an example of methylxanithines and discuss its function

A

E.g. caffeine

No clinical use, increases GFR via pre renal mechanism

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44
Q

Normal pH

A

7.4 tightly regulated

45
Q

Acidosis

A

<7.35

46
Q

Alkalosis

A

>7.45

47
Q

What are the three layers of protection from acids

A

(1) Chemical Buffering
(2) Respiratory response
(3) Kidney response

48
Q

chemical buffering

A

Looks after excess H+ by binding it to body’s buffer bases

49
Q

Respiratory response

A

Excess H+ is breathed out in the form of CO2

50
Q

Kidney Response

A

Deals with acid load by dividing the acid (H2Co3-) into H+ and HCO3-. H+ gets excreted out in the urine and HCO3- re-enters the blood stream

51
Q

How does kidney reabsorption and secretion of HCO3- and H+ work

A

Direct response: Involves secretion and reabsorption of H+

Indirect response: Involves secretion and reabsorption of HCO3-

52
Q

Kidney’s during acidosis

A

(1) Secrete H+ by primary and secondary active transport

(2) Buffer H+ with ammonia or phosphate
(3) Make new HCO3- from CO2 and H20

53
Q

Transporters involved with H+ and HCO3-

A
  • Na+/K+ ATPase
  • Na+/H+ antiporter
  • Na+/HCO3-symporter
  • Na+/NH4+ antiporter
  • H+ ATPase channel
  • H+/K+ ATPase
  • HCO3-/Cl- antiporter
54
Q

Titratable Acid

A
  • Represents the amount of H+ bound to phosphate which is present in significant concentration.
  • Primary urinary buffer is considered to be a titratable acid
55
Q

Which part of the nephron absorbs the largest amount of HCO3-

A

PT followed by LOH (TAL) and DT

56
Q

What’s the relationship between plasma [HCO3-] and urine [HCO3-]

A

Once the plasma [HCO3-] gets to it’s threshold point there is a increase in urine [HCO3-]

57
Q

When is HCO3- secreted

A

During metabolic alkalosis

58
Q

Why is HCO3- secreted during metabolic alkalosis

A

Want to reabsorb the H+ rather than excrete to help deal with the alkalosis. Therefore there is a decrease in new HCO3- being formed

59
Q

How is new HCO3- formed

A

Two mechanisms:

(1) Secretion of H+ produces new HCO3-
(2) Secretion of NH4+ produces new HCO3-

60
Q

Discuss the process in which secretion of H+ produces new HCO3-

A
61
Q

Discuss the process in which secretion of NH4+ produces new HCO3-

A
62
Q

What is the role of making NH4+

A

Increase the synthesis of new HCO3-

63
Q

WHy is NH4+ secretion important

A

If NH4+ wasn’t secreted it would re-enter the blood stream and end up at the liver where it would be metabolised to make urea. Formation of urea requires two HCO3-

64
Q

Urine Anion Gap

A

Gives a rough indication of how much NH4+ is in the body.

65
Q

What are the types of renal tubular acidosis

A
  1. (1) Proximal RTA: Decrease H+ secretion –> Decrease HCO3- reabsorption
  2. (2) Distal RTA: Decreases H+ secretion –> Decrease excretion of titratable acid
  3. (3) Other RTA: Decrease in NH4+ production –> Decrease NH4+ urinary production
66
Q

What does a high plasma anion gap indicate

A

Metabolic acidosis

67
Q

What is paradoxical aciduria and which condition does it occur in

A

When there is a low urine pH even though the body is in metabolic alkalosis. Commonly occurs in vomiting

68
Q

How does paradoxical aciduria occur

A
  • Increase Na+ reabsorption due to volume loss
  • This stimulates increase HCO3- reabsorption and H+ secretion.
  • Also, increase in aldosterone, leads to increase H+ secretion
69
Q

Ultrafilter

A

Semipermeable membrane that is used as a filter to separate small molecules and water from large molecules

70
Q

Ultrafiltration

A

High hydrostatic pressure that forces small molecules into the filter.

71
Q

Three properties of an ultra filter

A

Three properties of an ultra filter

    1. Endothelial fenestrations: “Gaps”
    1. Basal membrane composed of collagen and elastic: Importnat to GN
    1. Podocytes: Prevents large molecules going into filtrate
72
Q

How does the filtrate remain clean

A
  1. Podocytes
  2. Mesangial macrophages
73
Q

Determinants of filtration

A
  1. Pcap: Pressure that pushes fluid out of the capillaries
  2. Oncotic pressure: Pressure that is exerted on the fluid by proteins in the blood
  3. Pinterst: Compels fluid to be pushed back into the capillaries
74
Q

Effective Filtration Pressure (Peff)

A
  • Considered the net pressure of the filtration. Composed of force out - force in.
  • Pcap - (osmotic + PInterst)
  • Around 25 torr
75
Q

What provokes auto-regulation of RBF

A
    1. [NaCl] DT - detected by the macula densa cells
    1. Changes in MAPr (Mean arterial pressure of kidney)
76
Q

What is auto-regulation of RBF

A

Essentially, autoregulation stops the RBF drastically changing in response to changes in MAPr between the pressure ranges of 80-170mmHg. This is achieved due to Pcap remaining ~60 torr irrespective of changes in MAPr

77
Q

Discuss how changes in MAPr evoke auto-regulation

A
  • Tendency of SM to contract when stretched.
  • increase in vessel diameter –> Leads to non selective cation channel to open –> Depolarisation occurs which leads to influx of Ca2+ and contraction
78
Q

Discuss how changes in [NaCl] evoke auto-regulation

A

Increase in [NaCl] on DT is picked up by macula Densa cells. The rise causes the afferent arteriole in vasoconstrict.

79
Q

Function of RBF

A
  • Determines GFR
  • Delivers substrates for excretion
  • Delivers O2 and nutrients to renal cells
  • Assist in urine concentration
80
Q

In terms of GFR, RBF and Pgc, what happens with afferent vasoconstriction

A
    • Decrease GFR
    • Decrease Pgc
    • Decrease RBF
81
Q

In terms of GFR, RBF and Pgc, what happens with afferent vasodilation

A
    • Increase GFR
    • Decrease in Pgc
    • Increase RBF
82
Q

In terms of GFR, RBF and Pgc, what happens with efferent vasconstriction

A
    • Increase GFR
    • Increase Pgc
    • Decrease RBF
83
Q

In terms of GFR, RBF and Pgc, what happens with efferent vasodilation

A
    • Decrease GFR
    • Decrease Pgc
    • Increase RBF
84
Q

Vasoconstrictors

A
  • Remember: Never Attempt Absailing Naked
    • NSAIDs
    • ANP
    • AG II
    • Noradrenaline
85
Q

Vasodilators

A
  • Remember: April Pascoe Never Associated with Assholes
    • ANP
    • Prostaglandin
    • NO
    • Ace1
    • ARB
86
Q

What two components determine homeostatic control

A

Fluid Volume

Fluid Osmolality

87
Q

What is fluid osmolality

A

H20 reabsorption (Diluting and concentrating of urine)

88
Q

What is fluid volume

A

NaCl reabsoprtion

89
Q

What controls fluid osmolality

A

ADH

90
Q

What controls fluid volume

A

RAA system

91
Q

What stimulates ADH

A

Plasma osmolality > 300mosmol

92
Q

Osmoregulation

A

Regulation of osmotic pressure of fluid to maintain homeostasis of H20 content

93
Q

How is thirst stimulated

A

Stimulated with ~2-3% increase in osmolality

94
Q

What stimulates the RAA system

A

Effective volume control (CVe)

95
Q

Identify the sensors of CVe

A
  1. (1) Vascular * most important
  2. (2) Hepatic
  3. (3) CNS
96
Q

What are the different responses to CVe

A
  1. (1) Local response - Response of a single nephron. Fast acting
  2. (2) Systemic response - Response of entire kidney. Slower acting
97
Q

What is the function of Juxtaglomerular Appratus

A

Control the renal blood flow and glomerular filtration rate

98
Q

Identify the cells of the JGA

A

Glomerular cells

Macula Densa cells

99
Q

What is the role of glomerular cells

A

control the release of renin

100
Q

What is the role of macula densa cells

A

respond to [NaCl] changes in nephron

101
Q

Why do we have a systemic response to CVe

A

Allows our body to change the systemic volume and BP

102
Q

What is the role of RAA system

A

Regulates the body’s BP and Volume via the action of angiotensin II and aldosterone.

103
Q

What organs are involved in RAA system

A
  • Kidney -> Makes Renin
  • Adrenal Gland –> Makes aldosterone
  • Liver –> Makes angiotensin
  • Lung and Kidney –> Express ACE
  • ACE targets –> Vessels, CNS, Kidneys and Adrenal gland
104
Q

How does the RAA system work

A
105
Q

What mechanisms are used to maintain Na+ delivery to CD

A
    • Auto-regulation of GFR
    • Glomerular tubular balance (GTB)
    • Load dependency of Na+ reabsorption
106
Q

Changes with hypervolumic state

A
  • Increase ANP
  • Decrease ADH
  • Decrease Symp. acitivity
  • Decrease renin
  • Decrease Angiotensin II
  • Decrease Aldosterone
107
Q

Changes with hypovolumic state

A
  • Decrease ANP
  • Increase ADH
  • Increase Symp.activity
  • Increase Renin
  • Increase Angiotensin II
  • Increase Aldosterone
108
Q

What prevails osmotic control or volume control

A
  • Osmotic control > volume control
  • Quicker and stronger response

Physiology B2 & B3 (5 decks)

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