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Physiology / general Flashcards

1
Q

Where is aldosterone produced? What stimulates / inhibits its production?

A
  • Zona glomerulosa of the adrenal cortex
  • Stimulates: angiotensin II, hyperkalemia, ACTH
  • Inhibits: ANP, dopamine
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2
Q

What are the effects of ANP to stimulate natriuresis

A
  • Dilation of afferent arteriole and constriction of efferent arteriole -> increased GFR
  • Inhibition of sodium reabsorption in collecting ducts
  • Inhibition of renin secretion
  • Inhibition of aldosterone secretion
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3
Q

What is the effect of catecholamines on natriuresis

A

Catecholamines increase sodium reabsorption by:
- vasoconstriction the efferent arteriole (-> lower hydrostatic pressure in peritubular capillaries and increased reabsorption)
- stimulation of Na reabsorption in the proximal tubule (alpha1-adrenergic effect)
- stimulation of renin release (beta1-adrenergic effect)

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4
Q

What vasopressin receptors are found in the kidneys and where? What is their effect?

A

V2 receptors (Gs type of G protein coupled receptor), on the principal cells in the late distal convoluted tubule and collecting duct

Trigger expression of aquaporin 2 on the luminal membranes on the principal cells

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5
Q

Name causes of central and nephrogenic diabetes insipidus

A

Central:
- Congenital
- Traumatic
- Neoplastic
- Idiopathic

Nephrogenic:
- Congenital
- Glucocorticoids
- E Coli endotoxin
- Hypercalcemia
- Hyperthyroidism
- Liver insufficiency
- Hypoadrenocorticism
- Post-obstructive diuresis
- Polycystic kidney disease
- Chronic nephritis

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6
Q

What is the clearance of a substance

A

The volume of plasma that is cleared from the substance per unit of time

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7
Q

Formula for renal clearance of a substance

A

Clearance (mL/min) = [urine concentration (mg/mL) * urine output (mL/min)] / plasma concentration (mg/mL)

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8
Q

What fraction of CO is the renal blood flow? How is it separated between cortex and medulla?

A

22-25% of CO

Medullary blood flow is only 1-2% of entire blood flow (cortex gets most of it)

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9
Q

Name hormones / molecules causing vasoconstriction / vasodilation of renal arterioles. Indicate if there is a difference between afferent and efferent arterioles.

A

Vasoconstriction:
- Norepinephrine, epinephrine (both but slightly more efferent)
- Angiotensin II (more efferent)

Vasodilation:
- Dopamine
- Prostaglandins E2 and I2
- Bradykinin
- NO
- ANP (afferent only with slight vasoconstriction of efferent)

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10
Q

What are the 2 mechanisms of auto-regulation of renal blood flow

A
  • Myogenic (afferent arteriole contracts in response to stretch)
  • Tubuloglomerular feedback:
    –> decreased Cl in tubule is sensed by the cells of the macula densa in the thick ascending limb of the loop of Henle -> juxtaglomerular cells in the afferent arteriole trigger dilation of afferent arteriole and release of renin (-> angiotensin II -> constriction of efferent)
    –> increased renal arterial pressure –> increased delivery of fluid to macula densa –> constriction of afferent arterial
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11
Q

What is the renal filtration fraction? What is it normally?

A

Fraction of renal plasma flow that is filtered across the glomerular capillaries

FF = GFR / RPF = GFR / [RBF * (1 - Hct)]

with RPF = renal plasma flow and RBF = renal blood flow

Normal is 20% (varies for each solute)

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12
Q

What law determines glomerular filtration

A

Starling’s law

Jv = Kf*[(Pc-Pi) - s(pc-pi)]

where the interstitial space is the Bowman’s space here

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13
Q

How to calculate the reabsorption rate of a substance

A

Reabsorption rate = filtered load - excretion rate

Filtered load = GFR * plasma concentration of substance

Excretion rate = UOP * urine concentration of substance

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14
Q

At what urine pH will weak acids / weak bases be better excreted in urine

A
  • Weak acids in alkaline urine
  • Weak bases in acidic urine

Because they are in ionized form in the urine and cannot “back-diffuse” in the blood

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15
Q

Explain glomerulotubular balance

A

It means that the proximal tubular reabsorption rate of Na+ changes with the glomerular filtration rate to maintain a constant fractional reabsorption of Na and H2O.

When GFR increases, the oncotic pressure in the peri-tubular capillaries increases (proteins are more concentrated due to higher fluid filtration). Following Starling’s law, this increases reabsorption of water and solute in the peri-tubular capillary, which maintains the osmotic gradient between the peri-tubular space and the tubular cell, which promotes re-absorption of water and solutes.

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16
Q

In what tubular segments is Na reabsorbed? In what proportions and with which other solutes?

A
  • Proximal tubule: 2/3 (67%)
  • Early proximal tubule:
    Cotransport with glucose, amino-acids, HCO3-, and water (absorbed proportionately with water, no change in osmotic pressure)
    Countertranspport with H+
  • Late proximal tubule:
    Cotransport with Cl
  • Thick ascending limb of the loop of Henle: 25%
    Cotransport with K and Cl (Na-K-2Cl transporter)
    Absorbed without water
  • Distal tubule and collecting duct: 8%
  • Early distal tubule (5%):
    Cotransport with Cl
  • Late distal tubule and collecting duct (3%): Na channels under influence of aldosterone (Principal cells)
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17
Q

What is the excretion fraction of Na and K

A

Na: < 1% (freely filtered but almost fully reabsorbed)

K: variable (1-110%)

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18
Q

In what tubular segments is K reabsorbed/secreted? In what proportions?

A
  • Proximal convoluted tubule: reabsorbs 2/3 (67%)
  • Thick ascending loop of Henle: reabsorbs 20% (Na-K-2Cl transporter)
  • Late distal tubule:
  • secretion based on aldosterone and acid-base status (Principal cells)
  • or re-absorption (countertransport with H+ in intercalated cells) only in situations of K depletion
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19
Q

What factors influence K+ distal tubular excretion

A
  • Aldosterone (influences secretion from Principal cells)
  • Acid-base status (influences secretion in intercalated cell based on H+-K+ countertransport)
  • Dietary K+ (influences reabsorption in intercalated and principal cells based on intracellular K)
  • Diuretics:
  • loop / thiazide diuretics (due to increased tubular flow rate and Na delivery to distal tubule)
  • potassium sparing diuretics (decrease K secretion from Principal cells)
  • Luminal anions: increased tubular anions (HCO3) increase K secretion
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20
Q

Why does alkalosis increase renal K excretion

A
  • Decreased H+ secretion so decreased K+ reabsorption by H+-K+ transporter in intercalated cells of late distal convoluted tubule
  • Increased K+ secretion in distal convoluted tubule due to more negative tubular fluid (presence of HCO3)
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21
Q

What is the action of loop diuretics / thiazide diuretics on urinary Ca excretion

A
  • Loop diuretics: inhibit Ca reabsorption in the thick ascending loop of Henle
  • Thiazide diuretics: increase Ca reabsorption in early distal tubule
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22
Q

What are the 2 mechanisms required for establishment of the corticomedullary gradient? What hormone influences these mechanisms?

A
  • Countercurrent multiplier (loop of Henle, requires vasa recta)
  • Urea recycling (inner medullary collecting duct)

Both under the influence of ADH

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23
Q

What is the urine osmolality in the different tubular segments in the presence / absence of ADH?

A
  1. Without ADH:
    - Proximal convoluted tubule: 300 mOsm/L
    - Thick ascending limb of loop of Henle: 100
    - Late distal convoluted tubule: 100
    - Collecting duct: 50
  2. With ADH:
    - Proximal convoluted tubule: 300
    - Descending limb of loop of Henle: progressively increases to 1000-1200
    - Ascending limb of loop of Henle: progressively decreases to 300
    - Distal convoluted tubule: 100
    - Collecting duct: progressive increase up to 1200
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24
Q

What are the most important tubular segments for urine dilution / urine concentration

A
  • Urine dilution: thick ascending limb of loop of Henle +/- early distal convoluted tubule
  • Urine concentration: collecting ducts
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25
Q

What hormones act on the kidney? What are their actions?

A
  1. Aldosterone:
    - Increased Na reabsorption from distal tubule principal cells
    - Increased K secretion from distal tubule principal cells
    - Increased H+ secretion from distal tubule intercalated cells
  2. Angiotensin-II: increased Na reabsorption and H+ secretion (=HCO3 reabsorption) in proximal tubule
  3. ADH: increased water permeability in late distal tubule and collecting duct principal cells (V2 receptors)
  4. ANP: decreased NA reabsorption
  5. PTH: increases Ca reabsorption from distal convoluted tubule, decreases P reabsorption from proximal convoluted tubule (+ stimulates 1alpha-hydroxylase to produce calcitriol in proximal tubule)
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26
Q

Where is HCO3 reabsorbed? By what mechanism?

A

Proximal tubule

  • HCO3- + H+ -> CO2, H2O in tubular lumen
  • CO2 diffuses in tubular cell
  • CO2 + H2O -> HCO3- + H+ in cell
  • H+ gets excreted in exchange for Na+, HCO3- gets reabsorbed across baso-lateral membrane

/!\ allows HCO3 reabsorption but not H+ excretion

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27
Q

What is the renal mechanism of respiratory acidosis / alkalosis compensation

A

Respiratory acidosis:
- Increased pCO2 -> increased H+ in cells (including proximal tubular cells)
- Increased H+ excretion in proximal tubule (against Na+)
- H+ + HCO3- -> H2O + CO2 in tubular lumen
- CO2 diffuses in tubular cell, CO2 + H2O -> HCO3- + H+
- HCO3- reabsorbs at baso-lateral membrane of tubular cell -> metabolic alkalosis

Opposite for respiratory alkalosis

Also causes increased H+ secretion in distal convoluted tubule and collecting duct

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28
Q

What are the 2 mechanisms of H+ excretion in the distal tubule and collecting duct

A
  • Excretion as a titratable acid (H2PO4-)
  • Excretion as NH4+

In both cases H+ is secreted from intercalated cells by H+ ATPase (under control of aldosterone) while HCO3- is absorbed (“new” HCO3- for the body). H+ then combines with HPO4-2 or NH3 and is eliminated in urine (cannot diffuse back in cells)

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29
Q

What regulates H+ excretion in the distal tubule / collecting duct

A
  • Aldosterone (increases H+ ATPase activity)
  • Acidosis (increases NH3 production)
  • Kalemia (hyperkalemia inhibits NH3 synthesis, hypokalemia stimulates NH3 synthesis)
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30
Q

What is the normal GFR in cats and dogs

A

3 mL/kg/min

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31
Q

What is the normal urine osmolality in cats and dogs

A

Cats: 1250-2100 mOsm/kg

Dogs: 500-1400 mOsm/kg

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32
Q

What hormones are produced in the kidney

A
  • Renin
  • Erythropoietin
  • Calcitriol
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33
Q

What are the components of the renal vasculature

A
  • Renal artery
  • Lobar artery
  • Arcuate arteries
  • Interlobular arteries
  • Afferent arteriole
  • Efferent arteriole
  • Peritubular capillaries (vasa recta)
  • Venous system
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34
Q

What is the molecular size limit for glomerular filtration

A

70 kDa

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35
Q

What are the hydrostatic / oncotic pressures in the glomerular
capillaries, Bowman’s capsule, peritubular capillaries, and peritubular interstitium? Where does filtration / absorption happens

A
  • Filtration in glomerulus
  • Absorption in tubules

See picture (but oncotic pressure in glomerular capillary should be 25)

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36
Q

What is the transport maximum capacity? What is it for glucose?

A

Concentration of a solute at which transporters for tubular reabsorption become saturated

For glucose: 10 mmol/L in dogs, 13-16 mmol/L in cats

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37
Q

What is the range of BP for which renal auto-regulation is possible

A

MAP 80-180 mmHg

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38
Q

What part of the loop of Henle is permeable to water

A

Thin descending limb of the loop of Henle (thin ascending and thick ascending are impermeable)

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39
Q

Where is urea recycled in the nephron and under the influence of what hormone

A

Gets reabsorbed from the inner medullary collecting duct and joins the thin ascending loop of Henle (recycle)

Urea reabsorption stimulated by ADH (stimulates UT1 - transporter for urea)

(/!\ 50% of filtered urea is reabsorbed in proximal tubule, but recycling happens in the collecting duct)

40
Q

How is GFR measured

A

GFR = renal clearance of a substance that is not reabsorbed or secreted -> substance measured in urine for 24h to calculate clearance

Clearance = (concentration in urine * volume of urine in defined time) / plasma concentration

Theoretically should use inuline. In practice can estimate with creatinine at steady state.

41
Q

How is the relationship between GFR and creatinine

A

Logarithmic (when creatinine is low, an increase in creatinine indicates a major drop in GFR)

42
Q

Where is renin produced? Under what influence?

A
  1. Juxtaglomerular cells of the renal afferent arteriole
  2. Influence of:
    - Tubuloglomerular feedback (Cl delivery to the cells of the macula densa in the thick ascending limb of the loop of Henle)
    - Baroreceptors: carotid sinus, aortic arch, atrial stretch receptors (decrease in BP)
    - Decreased stretch in renal afferent arteriole
43
Q

What solute is preferentially reabsorbed in the loop of Henle

A

Magnesium

44
Q

What fraction of urea is reabsorbed in the proximal tubule

A

50%
(More can be reabsorbed in the medullary collecting duct for urea recycling)

45
Q

What fraction of phosphorus is reabsorbed in the proximal tubule

A

85%
(Not reabsorbed anywhere else - 15% gets excreted in urine)

46
Q

What is ammonium produced from and where

A

Glutamine, mostly in the proximal tubule cells

47
Q

Where can H+ be secreted in the nephron? Under which form?

A
  • Proximal tubule: excreted as NH4+
  • Cortical collecting duct (intercalated cells): secreted as H+ and complexed with NH3 or HPO4-2 in tubule
48
Q

Where is HCO3 mostly excreted in case of metabolic alkalosis

A

Intercalated cells (type B) of the cortical collecting duct. It is exchanged for Cl-

49
Q

Name 2 causes of refractory metabolic alkalosis

A
  • Hypoakalemia
  • Hypovolemia
50
Q

What are the 3 layers of glomerular capillaries

A
  • Endothelium + glycocalyx (with fenestrae)
  • Basement membrane
  • Epithelium (discontinuous podocytes)
51
Q

What is the USG of isosthenuric urine

A

1.007 - 1.015

52
Q

How can ultrasound be used to assess urine output

A

Measure bladder before and after urination

Urine volume = lengthwidthheight0.2pi

53
Q

What are the 3 determinants of urine output

A
  • Glomerular filtration rate
  • Tubular reabsorption of water and solutes
  • Impedance to flow
54
Q

How to differentiate hemoglobinuria from myoglobinuria (4 indicators)

A
  • Serum color: pink/red for Hb, colourless for Mb
  • Hyperbilirubinemia with hemoglobinuria
  • Increased AST / CK with myoglobinuria
  • Anemia (+/- Heinz bodies, agglutination, schistocytes) with hemoglobinuria
55
Q

What keto-acids are detected on urine dipstick

A
  • Aceto-acetate
  • Acetone
56
Q

What is the formula to measure urinary fractional excretion of a solute

A

Fractional excretion = (urine concentration of solute * plasma creatinine) / (urine creatinine * plasma concentration of solute)

It is the amount of filtered solute that ends up excreted in urine (/!\ different from filtration fraction)

A low fractional excretion = tubular reabsorption functions are working

57
Q

Where does renal glucose reabsorption happen? What are the transporters involved?

A

Proximal tubule

  • Cotransport with Na from tubule to tubular epithelial cell via SGLT transporters
  • Passive diffusion out of tubular cell towards interstitium and peritubular capillary via GLUT
58
Q

How is urea reabsorption determined in the proximal tubule

A

Reabsorbed by passive diffusion -> determined by tubular flow (urea is more reabsorbed if water is more reabsorbed)

59
Q

By what mechanisms does angiotensin II lead to renal sodium reabsorption

A
  • Stimulation of aldosterone (-> Na reabsorption in principal cells of distal tubule / collecting duct)
  • Direct stimulation of Na+/H+ transporter and Na/K ATPase in proximal tubule
  • Vasoconstriction of efferent arteriole -> decreased hydrostatic pressure in peritubular capillary -> increased reabsorption (Starling’s law)
  • Vasoconstriction of efferent arteriole ->increased GFR -> increased oncotic pressure in peritubular capillary -> increased reabsorption (Starling’s law)
60
Q

What is the difference between glomerulo-tubular balance and tubulo-glomerular feedback

A
  • Glomerulotubular balance = adjustment of reabsorption of solutes to the GFR (based on difference of oncotic pressure in peritubular capillaries)
  • Tubulo-glomerular feedback = adjustment of GFR to delivery of Cl in the distal tubule (based on regulation of tone of afferent and efferent arterioles)
61
Q

How do peri-tubular physical forces influence renal solute and water reabsorption

A
  • Hydrostatic pressure in peritubular capillaries depends on BP and vascular tone of efferent arteriole (constriction of arteriole(s) -> decreased hydrostatic pressure in capillary -> increased reabsorption OR increase in BP -> increased hydrostatic pressure -> decreased reabsorption)
  • Oncotic pressure in peritubular capillaries depends on proteinemia and filtration fraction (GFR / renal blood flow) (higher filtration fraction -> higher oncotic pressure -> increased reabsorption)
62
Q

Explain pressure natriuresis

A
  • Increased BP -> increased hydrostatic pressure in glomerular capillaries -> increased GFR (including increased filtered Na and water)
  • Increased BP -> increased hydrostatic pressure in peritubular capillaries -> decreased reabsorption of solutes (including Na and water)
  • Inhibition of angiotensin II release
63
Q

Explain mechanisms of urine dilution

A
  • Ascending limb of loop of Henle is impermeable to water -> solutes get reabsorbed (active transport) without movement of water -> dilution of urine in the tubule
  • In the absence of ADH, the distal tubule and collecting ducts are impermeable to water -> delivers dilute urine
64
Q

What are requirements to produce concentrated urine

A
  • Hyperosmotic inner medulla (thanks to countercurrent multiplier of the loop of Henle with the action of the vasa recta + urea recycling between medullary collecting duct and loop of Henle under the influence of ADH)
  • ADH to allow expression of aquaporins on principal cells of distal convoluted tubule and collecting duct to reabsorb water
65
Q

Why does BUN increase more than creatinine in pre renal azotemia?

A

Hypovolemia increases urea reabsorption in the proximal tubule

66
Q

True or false: if the filtered load is greater than the excretion rate, net reabsorption of the substance has occurred. If the filtered load is less than the excretion rate, net secretion has occurred

A

True

67
Q

What is the difference between Tm and threshold?

A

Tm: reabsorptive rate at which the carriers are saturated

Threshold: plasma concentration at which solute first appears in the urine

68
Q

What does it mean to have a high clearance, low clearance, clearance = to GFR?

Order the following substances from lowest clearance to highest clearance:

K+
inulin/creat
urea
Na+
glucose, amino acids, and HCO3-

A

High clearance: substances that are both filtered across the glomerular capillaries and secreted from the peritubular capillaries into urine

Low clearance: substances that either are not filtered (ex: protein) or are filtered and subsequently reabsorbed into peritubular capillary blood (ex: Na+, glucose, Cl-, HCO3-)

= to GFR: substances that are freely filtered, but not reabsorbed or secreted - biomarkers! (ex: creat)

glucose, amino acids, and HCO3- < Na+ < urea < inulin/creat < K+

69
Q

What is the mechanism of action of carbonic anhydrase inhibitors?

A

Diuretics that act in the early proximal tubule by inhibiting the reabsorption of filtered HCO3−

70
Q

How does ECF volume affect tubular reabsorption?

A

ECF volume contraction increases reabsorption
- Decreased Pc & increased pc

ECF volume expansion decreases reabsorption
- Increased Pc & decreased pc

71
Q

Which parts of the nephron are normally impermeable to water and are considered diluting segments?

A
  • Thick ascending limb of the loop of henle
  • Distal tubule and collecting duct
72
Q

How does ADH increase the principal cells’ permeability to H2O?

A

by directing the insertion of aquaporin 2 (AQP2) H2O channels in the luminal membrane.

In the absence of ADH, the principal cells are virtually impermeable to water.

73
Q

Where does secretion of K+ occur in the nephron?

A

Principle cells of the collecting ducts

74
Q

How does aldosterone increase K+ secretion by the principle cells?

A

Increased Na+ entry into the cells across the luminal membrane

–> Increased pumping of Na+ out of the cells by the Na+–K+ pump

–> Via the Na-K pump, increase in intracellular K+

–> Increased driving force for K+ secretion

*** Aldosterone also increases number of luminal K+ channels

75
Q

How do diuretics cause hypokalemia?

A
  1. Increase flow rate through the late distal tubules and collecting ducts –> dilution of luminal K+ –> increases driving force for K+ secretion
  2. Increase Na+ delivery to late distal tubule an collecting ducts –> increase intracellular K+ via Na-K pump –> increases driving force for K+ secretion
76
Q

What is the effect of fibroblast growth factor (FGF23)

A

Secreted by bone and inhibits Na+–phosphate cotransport in the early proximal tubule.

77
Q

What is the effect of PTH on phosphorus and calcium in the kidney?

A

Inhibits phosphate reabsorption in the early proximal tubule by activating adenylate cyclase, generating cyclic AMP (cAMP), and inhibiting Na+–phosphate cotransport

Increases Ca2+ reabsorption by activating adenylate cyclase in the distal tubule.

78
Q

Describe the relationship between magnesium and calcium in the nephron

A

In the thick ascending limb of the loop of henle, Mg and Ca compete for reabsorption

Hypercalcemia causes an increase in Mg2+ excretion

Hypermagnesemia causes an increase in Ca2+ excretion

79
Q

What is the role of the macula densa in the kidneys?

A

Constriction of the nearby afferent arteriole via the juxtaglomerula when it senses increased fluid load (via Cl-)

Dilation of afferent arteriole and release of renin (-> angiotensin II -> constriction of efferent) when it senses decreased Cl

80
Q

Name 5 functions of the kidneys

A
  • Removal of waste material and excretion in urine
  • Control volume and composition of body fluids
  • Production and secretion of hormones (renin, calcitriol, erythropietin)
  • Gluconeogenesis
  • Regulation of arterial BP
81
Q

What quantity of plasma volume is cleared/day?

A

60X

82
Q

3 factors that determine the filtering of molecules at the glomerular capillary

A
  • Size
  • Charge
  • Shape
83
Q

What are the 3 stimuli for ADH secretion?
Which is more sensitive?

A
  1. Increased osmolarity (more sensitive - responds to 1% change)
  2. Decreased ECV (more robust response)
  3. SIADH
84
Q

Which 3 receptors mediate ADH effects and how?

A
  1. V1 in vasculature - vasoconstriction
  2. V2 in the kidney - aquaporine-2 in the collecting ducts –> H2O reabsorption
  3. V1b hypothalamus/pituitary gland - facilitates ACTH release
85
Q

What are the mechanisms that lead to thirst?

A
  1. Increased osmolarity –> intracellular dehydration of osmoreceptors in the thirst centres
  2. Decreased ECV
  3. Dry mouth
  4. Angiotensin II
86
Q

What is the expected urinary Na+ concentration in the face of reduced ECV?

A

Urinary Na+ < 25 mEq/L

87
Q

In which non-pathological situation is auto-regulation of renal blood-flow lost?

A

General anesthesia

88
Q

What are the components of the juxtaglomerular apparatus?

A
  • Macula densa cells (thick ascending limb of the loop of henle)
  • Granule cells (aff. arteriole –> release renin)
  • Mesangial cells (relay signal between the 2 other cells)
89
Q

What part of the nephron is impermeable to NaCl?

A

Thin descending limb of the loop of henle

90
Q

For each tubular segment, what percentage of Na is reabsorbed,by what mechanism and what are the major regulatory factors?

A
91
Q

If protein is filtered in the proximal tubule, how will it be reabsorbed? (mechanism)

A

Pinocytosis

92
Q

What is the role of calcitriol in the kidney?

A
  • Increases calcium reabsorption in the distal tubule by increasing expression of transport proteins
  • Increases reabsorption of phosphate
93
Q

In what clinical scenario does urea recycling contribute to a large portion (40-50%) of creating a hyper osmotic renal medulla?

A

In a state of water deprevation

94
Q

Briefly explain medullary washout

A

Administration of large volumes of fluid –> increased medullary blood flow –> medullary washout –> inability of kidneys to concentrate urine

95
Q

What are the determinants of GFR?

A

Hydrostatic and osmotic forces across the glomerular membrane

Surface area + permeability of the membrane

Renal & urinary (4 decks)

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