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ACVIM Generals Revision > Renal Physiology COPY > Flashcards

Renal Physiology COPY Flashcards

1
Q

What are the sources of insensible fluid loss and its approximate rate in dogs?

A

Respiratory tract
Skin (independent of sweating)

1ml/kg/d in the dog

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2
Q

What are the main water in’s and outs in animals?

A

In:
- Ingestion
- Carbohydrate oxidation
OUT:
- Insensible losses
- Faecal
- Urinary

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3
Q

What is the fluid composition of a typical animal?

A

TBW = 60%

  • ICF = 40%
  • ECF = 20%
  • Interstitial = 15%
  • Plasma = 5%

Alternative memory aid = 60:40:20 rule

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4
Q

What is the trans cellular fluid compartment?

A

Specialised ECF e.g. pericardium, synovial fluid etc.

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5
Q

What is the main difference between fluid composition of the plasma and interstitial fluid?

A

Protein content of the plasma => otherwise the substance make up is pretty much the same so can be considered as the ECF.

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6
Q

What is the Donnan effect and what is its relevance to bodily fluid composition?

A

= uneven distribution of ionic compounds across a semi-permeable membrane

The plasma has a slight positive charge compared to the IF. This is due to plasma proteins having a slightly negative charge and therefore they retain cations more readily than the IF.

n.b. this effect is usually ignored when considering bodily fluid compartments

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7
Q

What is the difference in membranes between plasma + intestitial fluid vs. ECF + ICF?

A
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8
Q

Which fluid compartment does the kidney control?

A

ECF

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9
Q

Name the main:

1) ECF cations
2) ICF cations
3) ECF anions
3) ICF anions

A

1) Sodium
2) Potassium, magnesium, calcium
3) HCO3, Chloride
4) Phosphates, proteins

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10
Q

What is the main extracellular cation?

A

Sodium

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11
Q

What is the main extracellular anion?

A
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12
Q

What is the main intracellular cation?

A
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13
Q

What is the main intracellular anion?

A

Protein, closely followed by phosphates

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14
Q

What is osmolality?

A
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15
Q

What is osmolarity?

A

The number of osmoles per volume of a solution e.g. mOsm/L

(n.b. osmolarity and osmolality are often equivalent in bodily fluids)

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16
Q

Effective vs. ineffective osmoles

A 
Effective = do not cross the membrane and therefore retain water in a particular compartment
Ineffective = cross the membrane and therefore do not retain water in a particular compartment (as they just equilibirate)
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17
Q

Tonicity

A

The effective osmolality of a solution

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18
Q

Osmolol gap

A

The difference between calculated and measured osmoles

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19
Q

Serum osmolality calculation

Serum tonicity calculation

A
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20
Q

What is the approximate canine osmolality?

A

300mOsm/kg

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21
Q

What is the real meaning of a isotonic/hypotonic/hypertonic fluid?

A

Refers to what the fluid will do to the intracellular fluid.

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22
Q

Explain what would happen to ECF and ICF volume and osmolarity with the addition of the following fluids:
1) Isotonic fluid

2) Hypertonic fluid
3) Hypotonic fluid
4) Pure water

A
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23
Q

What is the overally safety factor against oedema in the interstitium expressed as a pressure?

A

17mmHg

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24
Q

How do changes in pressure in the efferent arteriole of the kidney impact GFR and tubular reabsorption?

A

Increased efferent pressure –> increased glomerular pressure (thus increased GFR)
Decreased peritubular capillary pressure (thus increased resorption as there is less hydrostatic pressure in these capillaries)

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25
Q

Which section of the LoH is thick vs. thin?

A

Thin is the first part and is descending. The TAL is the second part.

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26
Q

What are the main differences between cortical and juxtamedullary nephrons?

A

Cortical - only penetrate a small section of the medulla.

Juxtamedullary - deep into the medulla. Also surrounded by the vasa recta

n.b. the collecting duct penetrates deep into the medulla.

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27
Q

What are the three basic process by which urine forms?

A
  1. Glomerular filtration
  2. Reabsoprtion
  3. Secretion
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28
Q

What are the main anatomical components of the glomerular filtration barrier and how does this affect molecule movement?

A
  1. Capillary endothelium - fenestrations to allow easy movement.
  2. Basement membrane consisting of negatively charged collagenous proteins
  3. Podocyte epithelium with slit pores. Sialoglycoprotein coating is also negatively charged.

Summary = protein filtration is prevented by the size of the membrane but also the presence of lots of negative charges that will prevent movement of protiens (size selectivity and charge selectivity).

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29
Q

What is the equation that determines GFR?

A
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30
Q

What are the forces (and approximate values if you know them) that favour and oppose GFR?

A

Forces Favouring Filtration

  • Glomerular capillary hydrostatic pressure (60mmHg)
  • Bowman’s space oncotic pressure (0mmHg)

Forces Opposing Filtration

  • Glomerular capillary oncotic pressure (32mmHg)
  • Bowmans space hydrostatic pressure (18mmHg)
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31
Q

By what pathologic mechanims might the glomerular filtration coefficient (Kf) be affected?

A
  1. Change in the surface area avaible for filtration
  2. Change in the thickness of the capillary membrane

These are, in turn, the two components of the Kf

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32
Q

Why does urinary tract obstruction reduce GFR?

A

It increased Bowman’s capsule hydrostatic pressure.

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33
Q

What is the effect of constriction of the afferent or efferent arteriole on renal blood flow?

A

Both will decrease renal blood flow.

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34
Q

Change in the diameter of which blood vessel will likely have the biggest impact on GFR?

a) afferent arteriole
b) efferent arteriole

A

Constriction of the afferent arteriole as this reduces both renal blood flow and the glomerular capillary pressure

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35
Q

What is meant by the biphasic effect of efferent arteriolar pressure on GFR?

A

Small constrictions will increase GFR due to increased glomerular capillary pressure.
Large constrictions will also restrict renal blood flow and therefore decrease GFR.

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36
Q

What are the main deteriminants of renal blood flow (at a basic level)?

A
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37
Q

Which arteriole does angiotensin II preferentially vasoconstrict?

A

The efferent arteriole

The efferent arterioles seem to be protected due to endogenous production of nitric oxide and prostaglandins.

38
Q

Why is ANG II such a powerful hormone in cases of low arterial pressure (reference to its renal action)

A

It contricts the efferent arteriole therefore increasing capillary hydrostatic pressure to preserve GFR but this subsequently reduces peritubular blood flow and so allows greater sodium and water reabsorption to preserve circulating fluid volume.

39
Q

Where are the following structures located:

1) Macula densa cells
2) Juxtaglomerular cells

A

1) The very initial portion of the distal tubule in direct contact with the mesangium that is close to the juxtaglomerular cells
2) These are present on the afferent and efferent arterioles in close proximity to the macula densa.

40
Q

What is the stimulus for the macula densa mechanism and what is its impact?

A
  • Decreased NaCl delivery to the macula densa cells
  • Immediate dilation of the afferent arteriole (MoA unknown)
  • Release of renin from juxtaglomerular cells, then end result of which is the production of ANGII and therefore constriction of the afferent arteriole.
41
Q

What is the proposed mechanism of the myogenic reflex?

A

Increased vascular wall stretch increases permeability to calcium ions thus the smooth muscle will contract.

42
Q

Why might a high protein meal or hyperglycaemia increase GFR?

A

Both amino acids and glucose are co-transported with sodium => reducing delivery of NaCl to the macula densa and initiation of juxtaglomerular feedback.

43
Q

Where in the tubular epithelial cell is Na/K+ ATPase located?

A

The basolateral membrane.

44
Q

Which carrier proteins are responsible for glucose transport from the tubular lumen into the epithelial cell in the:

  1. Initiial proximal tubule
  2. Late proximal tubular

What are the % of glucose resorbed in these segments?

A
  1. SGLT2 - 90% of glucose
  2. SGLT1 - 10% of glucose
45
Q

How does glucose diffuse across the basolateral membrane in:

  1. S1 segment of the PCT
  2. S3 segment of the PCT
A
  1. Through GLUT 2
  2. Through GLUT 1
46
Q

What is the most prominant aquaporin in the prozimal convuluted tubule?

A

AQ1

47
Q

What is solvent drag?

A

The process by which water draws dissolved components with it when it is being re-absorbed.

48
Q

Name three mechanisms by which chloride is re-absorbed by the tubules

A
  1. Follows the electrochemical gradient created by sodium transport
  2. Follows the concentration gradient created by water reabsorption (H2O movement out of the lumen creates a high luminal Cl concentration)
  3. Facilitated transport in combination with sodium (NaCl co-transporter) present on the luminal membrane.
49
Q

What percentages of water are reabsorbed by the different segments of the nephron?

A
  1. 65% in the proximal tubule
  2. 20% in the thin limb of the LoH
  3. 15% in the collecting duct
50
Q

What transporter is responsible for luminal sodium transport in the thick ascending limb of the LoH?

A

NKCC2 co-transporter

Site of action of loop diuretics

51
Q

Site of action of loop diuretics

A

NKCC2 transporter on the luminal membrane of the thick ascending limb of the LoH.

52
Q

How is H+ secreted by the thick ascending limb of the LoH?

A

Na-H exchanger (luminal)

53
Q

What is the site of action of thiazide diuretics?

A

NaCl co-transporter in the early distal tubule.

54
Q

Potassium exretion by XXX cells

  • name the cell
  • location
  • mechanism of secretion
A
  • Principle cells
  • Distal tubule (late)
  • Na/KATPase is important in producing a concentration gradient. Potassium then diffuses down this into the tubule lumen.
55
Q

MoA of spironolactone

A

Competes with aldosterone for binding sites on the mineralocorticoid receptor in principle cells in the late distal tuble.

56
Q

MoA of amiloride

  • What class of drug is this
A

Sodium channel blocker on principle cells of the late distal tubule

57
Q

What are the two sub-types of potassium sparing diuretics?

A
  1. MCR blockers
  2. Na channel blockers
58
Q

How does the function of type A and type B intercalated cells differ?

A

Type A secretes H+ whilst generating HCO3-

Type B secretes HCO3- whilst generating H+

59
Q

What are the transporters that are present in intercalated cells, how do these differ between cells.

A

H+ transporters

  • H+ ATPase
  • H+/K+ Atpase (exchanger)

Present on the luminal surface in type A cells and the basolateral surface in type B cells.

HCO3 transporters

  • HCO3-/Cl- exchanger

Present on the basolateral surface of type A cells and the luminal surface in type B cells. It is in the form of pendrin in the type B cells only.

60
Q

Where in the nephron does ADH and aldosterone act?

A

The late distal tubule and cortical and medullary collecting duct.

61
Q

What are the main factors that lead to aldosterone release?

A

ANG II and potassium concentration

62
Q

What are the main cellular effects of aldosterone on principle cells?

A
  1. Increased activity of Na/KATPase
  2. Increases luminal sodium permeability
63
Q

What are ANGII main effects on the kidneys

A
  1. Stimulates aldosterone secretion
  2. Constriction of the efferent arteriole
  3. Direct effects on renal tubular cells with resorptive/secretory activity:
    a) Increased Na/KATPase activity
    b) Increased activity of the H/Na exchanger
    c) Increased activity of Na/HCO3 co-transporter
64
Q

What are the effects of ADH, which receptor, which channels are where?

A

Activates V2 receptor which increases cAMP and leads to AQ2 channels on the luminal membrane. It will also increase gene transcription for AQ2.

AQ3&4 are on the basolateral surface

65
Q

What are ANPs effects on renal sodium and fluid balance?

A

Increase naturesis
Inhibits renin secretion

66
Q

Described the changes in renal tubular fluid tonicity through the following structures:

  • PCT
  • Descending LoH
  • Ascending LoH
  • DCT
  • Collecting duct
A

PCT: isoosmotic

DLoH: becomes hypertonic as impermeable to solutes

ALoH: becomes hypotonic as impermeable to water

DCT: further dilution

CD: this is where ADH can exert its effect.

67
Q

How much of the osmolality of the medullary interstitium can urea contribute when forming a maximally concentrated urine?

A

40-50%

68
Q

Where can urea leave the tubular fluid, through which channels and under the influence of which hormone?

A

The medullary collecting duct, UT-A1 & UT-A3, ADH influence

69
Q

Where are the following urea transporters located and what are their roles?

  1. UT-A1
  2. UT-A2
  3. UT-A3
A
  1. & 3 = urea transport out of the medullary collecting duct
  2. Urea transport into the thin segments of the LoH.
70
Q

What is the formula for estimating plasma osmolarity?

A
71
Q

Where, neuroanatomically, are the osmoreceptors located?

A

In the anteroventral region of the third ventricle (AV3V region) of the hypothalamus.

72
Q

What stimuli can result in ADH secretion?

A
  1. Increased serum osmolality
  2. Reduced arterial blood pressure (through baroreceptor and cardiopulmonary reflexes).
  3. Nausea
  4. Some drugs (e.g. nicotine)
73
Q

Which of the following hormones contributes the most to changes in serum osmolality?
Aldosterone, ADH or ANG II

A

ADH

74
Q

What are the main channels involved in sodium and potassium cells in the principle cells?

A

ENaC = sodium comes in

BK = potassium leaves the luminal surface

ROMK = potassium leaves the luminal surface

75
Q

What membrane protein is though to be involved in type A intercalated cells role in potassium balance?

A

H+/K+ ATPase. This exchanged hydrogen (out of cell, into tubular fluid) for potassium (in to cell)

76
Q

How is calcium reabsorbed in the proximal tubule?

A
  1. Solvent drag accounts for the majority.
  2. Transcellular:
    i) calcium enters the epithelial cell due to the electrochemical gradient (negative inside cell)
    ii) calcium leaves the cell through either calcium ATPase or the 3Na1Ca exchanger.
77
Q

What mechanism prevents excessive fluid or sodium retention when there are high levels of ANGII or aldosterone?

A

Pressure diuresis and pressure naturesis. This is a result of the hormones increasing arterial blood pressure. These mechanisms may be compromised in heart failure, for example.

78
Q

What are the different bodily buffers and where are they important?

A
  1. HCO3-
  2. Phosphate (more important in the kidneys and intracellular fluid) (H2PO4- and HPO4=)
  3. Proteins (also intracellular but has a major effect on the ECF)
79
Q

Why is respiratory compensation for alkalosis less effective than for acidosis?

A

In alkalosis the alveolar ventillation may decrease but this will lead to decreased PaO2 which will then increase alveolar ventillation again.

80
Q

What are the fundamental processes by which the kidney’s regulate acid-base physiology?

A
  1. Secretion of H+
  2. Reabsorption of HCO3-
  3. Generation of ‘new’ HCO3-
81
Q

Where in the kidney does hydrogen ion secretion and HCO3 reabsorption NOT occur?

A

The thin parts of the LoH

82
Q

Where does urine become acidic?

A

In the late distal tubules and collecting duct

83
Q

What is the lower limit of urine pH that can be achieved in a normal kidney?

A

4.5

84
Q

What is the predominant mechanism for H+ excretion in chronic acidosis?

A

Upregulation of renal glutamine metabolism and therefore increased ammonium ion excretion in the urine.

85
Q

What is the mechanism of action and site of action of osmotic diuretics?

A

Increases tubular osmolality thus affecting water and solute absorption

Mostly proximal tubules.

86
Q

What is the mechanism of action and site of action of loop diuretics?

A

The NKCC2 luminal co-transporter
TAL of the LoH

87
Q

What is the mechanism of action and site of action of thiazide diuretics?

A

Na/Cl co-transporter

Early distal tubule

88
Q

What is the mechanism of action and site of action of carbonic anhydrase inhibitors? What is an example?

A

e.g. acetalzolamide

inhibits carbonic anhydrase which will reduce hydrogen excretion and HCO3 reabsorption. This also reduces sodium reabsorption (since the Na/H+ exchanger will be less effective). Main effect is on the PCTs.

89
Q

What type of diuretic is spironolactone, its mechanism and main site of action?

A

Aldosterone antagonist (antagonises the MCR). Its main effects are therefore in the principle cells of the late tubules and collecting duct.

90
Q

What type of diuretic are triamterine and amelioride, their mechanism and main site of action?

A

Sodium channel blockers (block inward luminal sodium channels)

Late distal tubule and collecting duct principle cells.

ACVIM Generals Revision (32 decks)

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