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VIVA > Physiology: Renal > Flashcards

Physiology: Renal Flashcards

1
Q

Define GFR

A

Volume of fluid filtered from glomerular capillaries into Bowman’s capsule per unit time.

125ml/min (180L/24 hours) 10% less in women

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2
Q

Factors controlling GFR?

A
  1. Hydrostatic pressure in capillaries and tubules
  2. Osmotic pressure gradient (oncotic)
  3. Size of capillary bed
  4. Permeability of capillary bed (Mesangial cells contract/relax)
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3
Q

Starling Forces

A

Starling Forces = K(Hydrostatic pressure of capillaries – hydrostatic pressure of tubules) – (osmotic pressure of capillaries – osmotic pressure of tubules)

K = GF coefficient altered by mesangial cell contraction.

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4
Q

Clinical factors that affect Starling forces

A
  1. Renal blood flow
  2. Systemic BP
  3. Ureteric obstruction
  4. Renal parenchymal oedema
  5. Afferent and efferent arteriolar contraction
  6. Plasma proteins
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5
Q

Role of Mesangial cells

A

Contraction decreases area for filtration

Contraction: Noradrenaline and Histamine, ADH, ATII

Relaxation: Prostaglandins, Atrial Natriuretic Peptide, Dopamine

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6
Q

Kidney regulation of urine

A
  1. Filtration
  2. Secretion
  3. Reabsorption
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7
Q

Measuring GFR

A

Measure the excretion of a substance, which is freely filtered through the glomeruli – neither secreted nor reabsorbed by the tubule.

Non toxic and not metabolized e.g. insulin

GFR = Ux X V/Px

Ux = concentration of X in urine

V = urine flow/time

Px = Arteriolar concentration of X

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8
Q

How do kidneys deal with K+?

A

Freely filtered at glomerulus

Actively reabsorbed in PCT

Secreted in distal tubule – rate proportional to flow

Secreted in CT – aldosterone excreted

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9
Q

Factors influence ATII production

A

ATII is the effector protein in the RAAS – integral to the control of volume regulation

So principally those that influence renin secretion:

Increased secretion

  1. Increased sympathetic activity
  2. Increased circulating catecholamines
  3. Prostaglandins
    (from Na+ depletion, diuretics, hypovolaemia, CCF, dehydration, upright posture, renal artery/aortic constriction)

Decreased secretion

  1. Increased Cl– and Na+ re-absorption
  2. Increased afferent arteriolar pressure
  3. Vasopressin (ADH)
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10
Q

Physiological affects of ATII

A
  1. Arteriolar constriction
  2. Directly on adrenal cortex to release aldosterone
  3. Contraction of mesangial cells causing decreased GFR
  4. Direct effect on renal tubules to increase Na+ reabsorption
  5. On the brain to decrease sensitivity to baroreceptors
  6. Reflex to increase water and increase secretion of ADH and ACTH
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11
Q

Essential feature of the loop of Henle countercurrent multiplex

A

High permeability of their descending limb to water and active transport of Na+ and Cl– out of thick ascending limb which is not permeable to H2O.

Role

Contributes to osmotic gradient in the medullary pyramids

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12
Q

How does urea reach interstitium?

A

Transported by urea transporters by facilitated diffusion.

Amount of urea depends on amount filtered which depends on dietary protein.

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13
Q

Describe the way kidneys handle glucose

A
  1. Freely filtered
  2. Reabsorbed in the early part of PCT (by secondary active transport)
  3. Na+ dependent co-transportation
  4. Excreted in urine if renal threshold is exceeded.
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14
Q

Potential consequences of glycosuria

A

Osmotic diuresis = dehydration, electrolyte loss.

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15
Q

What factors influence clearance of substances by the kidneys?

A
  1. Amount of substance excreted = amount filtered and net amount transferred
  2. Changes in renal blood flow and systemic blood pressure
  3. Active transport (primary and secondary(
  4. Hormones (aldosterone, angiotensin, endothelial growth factor)
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16
Q

Describe the renal response to acidosis

A

Kidneys aim to return serum pH to normal by increasing H+ :

  1. Kidneys retain HCO3– by actively secreting H+
  2. Renal tubule cells secrete carbonic anhydrase converting CO2 to H+ and HCO3 , then tubule cells secrete H+ in exchange for Na+
  3. Amount of secreted H+ limited by pH>4.5 but buffering in tubular fluid pH with HCO2, HPO4 and NH3 allows greater H+ secretion

a) Carbonic anhydrase converts CO2 to H+ and HCO3
b) Renal to actively secrete H+ in exchange for Na+
c) HCO3– actively reabsorbed

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17
Q

Urinary buffers:

A

Bicarbonate (proximal tubule) – HCO3–->CO2 + H2O

Phosphate (distal tubule) – HPO42–> H2PO4–

Ammonia (both) – NH3->NH4+

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18
Q

Metabolic acidosis compensation?

A
  1. Respiratory system: Increased ventilation & Decreased PCO2
  2. Glutamine synthesis in liver in chronic metabolic acidosis -> increased to provide additional source of NH4+ as well as NH3 secretion to increase over days.
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19
Q

By what mechanism is H+ secreted in the distal tubules and collecting ducts of the kidneys?

A

ATP driven proton pump

Aldosterone acts on this pump to increase H+ secretion

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20
Q

Principal buffering systems in the body?

A

Blood – Bicarbonate, Protein, Hb

Intracellular – Protein and phosphate

Urine – also uses ammonia

Interstitium – bicarbonate

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21
Q

Body’s response to metabolic acidosis?

A
  1. Buffering : in blood, intracellular and interstitial space
  2. Respiratory response: increased ventilation and excretory CO
  3. Renal response : Linked to Na+/K+/ATPase
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22
Q

Is there a difference between proximal and distal tubules?

A

PCT/DCT/CT secrete H+

PCT via Na+/H+ exchange and Na+/K+/ATPase

DCT/CD H+ secretion by ATP driven proton pump.

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23
Q

Factors that increase acid secretion

A

Increased PCO2, increased PaCO2

Increased aldosterone

Increased calcium concentration, decreased K+ (Increased K+ decreases H+ secretion)

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24
Q

How does the kidney handle K+?

A

Filtered, reabsorbed and secreted

  1. Freely filtered at glomeruli (600mEq/day)
  2. Mostly/largely reabsorbed in proximal tubule by active transport
  3. K+ is then secreted by passive diffusion in distal tubule.
  4. Passively secreted in collecting duct
  5. Total K+ excretion is approximately equal to K+ intake = 90mmol
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25
Q

Factors influencing this? (Kidney handling of K+)

A
  1. Rate of K+ secretion is proportional to flow of tubular flow
  2. Aldosterone increases Na+ reabsorption (primarily in the collecting duct) and therefore promotes K+ secretion
  3. In distal nephron, K+ and H+ compete for secretion in association with Na+ reabsorption therefore in acidosis, when H+ excretion is increased, K+ secretion decreases
  4. Inhibition of K+ reabsorption in proximal nephron (e.g. osmotic/loop diuretic) promotes excretion of K+.
26
Q

How is ascending and descending loops of Henle different?

A

Thin descending limb is water permeable (due to presence of aquapores) and tubular fluid becomes hypertonic. Thick ascending limb is impermeable to H2O and Na+ is actively transported out, so fluid is more hypotonic (K+ diffuses back passively)

27
Q

Describe the process of tubuloglomerular feedback in the nephron

A

This process occurs to maintain the constancy of the load delivered to the distal tubule. The macula densa in the ascending limb of the loop of henle sense the rate of flow and feeds back to either increase of decrease the rate of filtration in the glomerulus.

28
Q

Please outline the structure of the LOH

A
  1. Thin/descending, Thick/Ascending – situated mostly in the medulla
  2. Origin from PCT
  3. Short and long loops
  4. Macula densa at distal end, where it joins the DCT.
29
Q

Can you draw a nephron and describe functions of each part

A

Glomerulus – Filtration (afferent and efferent arterioles)

PCT – reabsorption of sodium, glucose, amino acids and bicarbonate

Descending limb – then, H2O permeable

Ascending limb – site of the Na+K+2Cl – generates concentration gradient

DCT – Na+K+Cl– pump–

CD: under control of ADH and aldosterone

Cell types in Glomerulus – cap endothelial cells fenestrated with 70-90nm pores

Epithelial cells of Bowman’s capsule – Podocytes possess pseudopodia that form filtration slits once capillary epithelium

30
Q

What properties of substances in blood prevent free passage across glomerular membrane?

A
  1. Large diameter >8nm

2. Lack of neutrality (charged)

31
Q

How does RAS respond to hypotension?

A

Decreased BP leads to renin being released from the JG cells to form angiotensin I -> AT I converted to ATII in lungs by ACE. ATII causes vasoconstriction and decreased secretion of both salt and water.

32
Q

Other systems affected by RAS

A
  1. Sodium and water retention
  2. Stimulate aldosterone secretion
  3. Facilitate secretion of noradrenaline
  4. Downgrade- baroreceptors
  5. Increase secretion of vasopressin
33
Q

Major physiological features of acute intrinsic renal failure?

A
  1. Loss of urine concentrating and diluting capacity: Polyuria->oliguria->Anuria
  2. Uraemia : Increased buildup of urine, creatinine and toxins
  3. Acidosis, anaemia
  4. Sodium retention, oedema and heart failure
34
Q

Common finding in urinalysis of intrinsic renal failure

A
  1. Leucocytes
  2. Proteinuria
  3. Red cells
  4. Casts
35
Q

What are urinary casts?

A

Proteinaceous material precipitated in tubules washed into the bladder.

36
Q

Neurological pathways in normal micturition

A
  1. Spinal reflex: S2+S3+S4 roots. Facilitated/inhibited higher centers; subject to voluntary control (first urge to void at 150ml. Marked fullness at 400ml)
  2. Micturition reflex – stretch receptors in bladder wall
  3. Parasympathetic efferent nerves – mediate contractions of detrusor muscle
  4. Pudendal Nerve (S2,3,4) – voluntary contraction of perineal and external urethral sphincter.
37
Q

Muscles involved in micturition

A
  1. Bladder: Smooth muscle in spiral, longitudinal and circular bundles (Circular bundle = detrusor muscle whose contraction results in involuntary emptying)
  2. External urethral sphincter – Skeletal muscle: relaxes during voluntary micturition
  3. Perineal muscles
  4. In males – urine left in urethra expelled by several contractions of bulbocavernous muscle
  5. Abdominal wall muscle – contraction aids urine expulsion. NB -> internal sphincter (SM) plays no role.
38
Q

What prevents vesico-ureteric reflux?

A

Oblique passage of ureters through bladder wall (i.e. keeps ureters closed during peristaltic waves)

39
Q

What factors increase renin secretion?

A

Catecholamines

Sympathetic activity – via renal nerves

Prostaglandins

40
Q

Role of vasopressin in dehydration

A

Promotes water reabsorption in CD via aquaporin. It causes vasoconstriction.

41
Q

Hormones involved in ECF volume maintenance

A
  1. Renin
  2. ATII
  3. Aldosterone
  4. Vasopressin
42
Q

Response of atrial naturetic peptide in response to fluid overload?

A

Diuresis -> mesangial cells relaxation -> increased GFR -> Increased Na+ secretion from kidneys -> H2O follows

43
Q

Normal Renal Blood Flow

A

= 25% of CO (1250ml)

= 1.2-1.3L/min at rest

44
Q

Mechanisms that determine Renal Blood Flow

A
  1. Perfusion pressure (systemic MAP)
  2. Renal arterial flow – Na+ ATII = constriction, Ach, prostaglandin
  3. Renal nerves – Sympathetic -> noradrenaline -> decreased renal blood flow
  4. Autoregulation – duct smooth muscle contraction, MO
  5. Regional differences in renal blood flow
45
Q

How do blood flow and O2 extraction vary in different parts of the kidney?

A
  1. Cortical flow = high (and O2 extraction low)
  2. Medullary blood flow = low O2: extraction higher
  3. Medullary is vulnerable to hypoxic damage = if flow is reduced, increased O2 usage
46
Q

Consequence of sustained reduction of RBF

A

Renal blood flow maintained at MBP>70

Medulla is vulnerable to hypoxia (high Metabolic Rate)

ATN

Uraemia

47
Q

Renin INCREASE

A

1) Sympathetic activity
2) Catecholamines
3) Prostaglandins

48
Q

Renin DECREASE

A

1) Increase Na+ and Cl– reabsorption
2) Increased afferent and efferent pressure
3) ATII and vasopressin

NB: Afferent and efferent pressures detected at intrarenal baroreceptors

49
Q

What conditions increase renin secretion?

A
  1. Dehydration, haemorrhage, hypotension, diuretics
  2. Upright position, psychological stimuli
  3. CF, hepatic cirrhosis
  4. Constriction of renal artery, constriction of aorta
  5. Sodium depletion
50
Q

How is Na+ handled in the kidney?

A
  1. Glomerular filtration
  2. Actively transported out except in the descending limb of the loop of henle
  3. Active reabsorption 99% (influenced by aldosterone and ADH)
51
Q

Mechanisms involved in reabsorption and secretion at renal tubules

A

Endocytosis

Passive diffusion

Facilitated diffusion

Active transport

52
Q

Where does Na+ reabsorption occur in the nephron?

A

All parts except the descending limb of the loop of Henle.

60% PCT primarily

30% thick ascending limb of loop of Henle

7% DCT

3% CT

53
Q

Mechanisms involved in Na absorption

A

Na/K ATPase active transport

54
Q

Mechanisms that decrease sodium excretion:

A
  1. Decreased GFR
  2. Increased tubular reabsorption
    – Increased aldosterone
    – AT II (PCT)
    – Decreased AMP
55
Q

Vasopressin action on kidneys

A

Collecting duct -> ADH binds to aquaporin 2 channel inserted to increased H2O permeability

56
Q

Vasopressin - Drink large amounts of H2O

A

Begins 15 minutes post and maximum effect in about 45 minutes

Drinking decreases ADH = diuresis

Most inhibition is because of decrease in plasma osmolality

57
Q

Thirst: An appetite under hypothalamic control

What causes it?

A
  1. Increased plasma osmolality – osmoreceptors in anterior hypothalamus
  2. Hypovolaemia: RAS, barocreptors in heart and blood vessels
  3. Prandial
    Habit, GI, hormone effects
  4. Psychogenic
    Dry pharyngeal mucous membranes
58
Q

Vasopressin actions

A

1) Retention of H2O
2) Decreased CO
3) Glycogenolysis
4) ACTH secretion from anterior pituitary

59
Q

Vasopressin secretion is increased by:

A

1) Osmolality increase
2) ECF volume decrease
3) Pain, nausea, surgical stress, emotion, vomiting, standing, drugs (carbamazepine)

60
Q

Vasopressin secretion is decreased by:

A

1) Alcohol
2) Decreased osmolality
3) Increased ECF volume

61
Q

Water re-absorption:

A
  1. 60-70% in PCT
  2. 15% loop of henle
  3. 5% DCT
  4. Up to 10% in CD, depending on presence of ADH

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