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Guyton > Unit 5 > Flashcards

Unit 5 Flashcards

1
Q

How is water added to the body?

A

Ingestion
Oxidation of CHO

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2
Q

What % of bodyweight is water?

A

60%

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3
Q

What % of bodyweight is intracellular fluid?

A

40%

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4
Q

What % of bodyweight is extracellular fluid?

A

20%

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5
Q

How do plasma and interstitial fluid differ?

A

Higher protein in plasma
Higher cations in plasma (Donnan effect)
Higher anions in interstitial fluid

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6
Q

Ddx hyponatraemia

A

Dehydration - adrenal insufficiency, diuretic overuse, v/d
Overhydration - ADH excess, bronchogenic tumours

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7
Q

Ddx hypernatraemia

A

Dehydration - DI
Overhydration - HAC, hyperaldosteronism

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8
Q

What are the causes of intracellular oedema?

A

Hyponatraemia
Depression of metabolic systems
Lack of cellular nutrition

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9
Q

Which part of the LOH is the ‘thin’ segment?

A

Descending and lower end of ascending

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10
Q

Where is the macula densa located?

A

At the end of the thick, ascending LOH

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11
Q

What are cortical and juxtaglomerular nephrons? How are they different?

A

Cortical nephron - glomeruli in outer cortex, short LOH than penetrate a short distance into medulla
Juxtaglomerular nephron - glomeruli deeper in cortex, long LOH
JG nephrons have vasa recta

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12
Q

Describe the neuroanatomy of the bladder

A

Supplied by pelvic nerves via the sacral plexus (S2-3)
Contains sensory + motor fibres
Motor n - parasympathetic fibres
Pudendal nerve - external sphincter (skeletal)
Hypogastric nerves - sympathetic - blood vessels

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13
Q

What innervates the a)detrusor, b)internal sphincter, c)external sphincter

A

a)pelvic n
b)pelvic n
c)pudendal n

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14
Q

What is the structure of the glomerular capillary membrane?

A

1 - endothelium
2 - basement membrane
3 - epithelial cells (podocytes)

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15
Q

How does efferent arteriolar constriction affect GFR?

A

Biphasic
Mild/moderate - slight increase in GFR
Severe - reduces GFR

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16
Q

How does afferent arteriolar constriction affect GFR?

A

Reduces

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17
Q

What is anatomy of the juxtaglomerular complex?

A

Macula densa cells in proximal distal tubule
Juxtaglomerular cells in afferent/efferent arteriole

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18
Q

Describe tubuloglomerular feedback

A

Reduced GRF => slow flow in LOH => increased Na/Cl reabsorption => reduced Na/Cl at macula densa => afferent arteriolar dilation + ^ renin release => efferent arteriolar constriction

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19
Q

What substances are found in higher quantities in plasma than glomerular filtrate?

A

Albumin
Calcium
Fatty acids

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20
Q

Describe the structure of the glomerular capillary membrane and how they alter filtration

A

Endothelium (with fenestrate). Endothelial proteins negatively charged - repeals plasma proteins
Basement membrane - mesh of collagen and proteoglycans. PGs negatively charged
Podocytes (with slit pores) - epithelium negatively charged

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21
Q

What conditions are associated with a reduction in glomerular capillary filtration coefficient?

A

CKD (reduced number of glomerular capillaries)
Systemic hypertension

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22
Q

How if filtration fraction calculated?

A

FF = GFR/RBF

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23
Q

What factors influence the glomerular capillary colloid osmotic pressure?

A

Arterial plasma osmotic pressure
Filtration fraction (affected by GFR and RBF)

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24
Q

How does efferent arteriolar constriction affect GFR?

A

Biphasic
If mild/moderate, slight increase
If severe, decreases (due to increased FF and glomerular colloid oncotic pressure)

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25
Q

How is renal blood flow regulated?

A

Tubuloglomerular feedback
Myogenic autoregulation

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26
Q

How do dietary protein and hyperglycaemia affect renal blood flow and GFR?

A

Increase both
Amino acids/glucose reabsorbed with sodium => reduced sodium delivery to macula densa => afferent arteriolar dilation

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27
Q

What are the main primary active transport pumps in the renal tubules?

A

Na-K ATPase
H+ ATPase
H-K ATPase
Ca ATPase

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28
Q

Describe the renal tubular Na-K ATPase pump

A

Na exchanged for K at basolateral membrane using ATPase
Na+ passively diffuses across luminal membrane along concentration and electrical gradient

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29
Q

How is the proximal tubule adapted for Na reabsorption?

A

Brush border - ^ surface area
Carrier proteins for facilitated diffusion
^Mitochondria
Intercellular + basal channels

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30
Q

Describe glucose reabsorption in the proximal tubule

A

Na-K ATPase in basolateral membrane creates Na concentration gradient
SGLT 1 and 2 in brush border absorb glucose up concentration gradient
Glucose diffuses out of cell using glucose transporters GLUT1 and GLUT2

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31
Q

What are the sodium glucose cotransporters in the proximal tubule and where are they located? Which is more active?

A

SGLT2 in early PT
SGLT1 in latter PT
90% reabsorbed by SGLT2

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32
Q

What are the glucose transporters in the proximal tubule? Where are they located?

A

GLUT2 in early PT
GLUT1 in latter PT

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33
Q

What is an example of counter transport?

A

Na - H+ exchanger in PT

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34
Q

Where are AQO-1 channels found?

A

Proximal tubule

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35
Q

How does water permeability vary in different parts of the nephron?

A

PT - high
Descending LOH - high
Ascending LOH - low
Distal tubule, collecting tubules, collecting ducts - low/high (ADH dependent)

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36
Q

How is chloride reabsorbed?

A

Transported with sodium due to electrical potential, along paracellular pathway
Na reabsorption = H20 reabsorption = ^ Cl concentration = concentration gradient
Secondary active transport - Na-CL cotransporter

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37
Q

How is urea reabsorbed

A

Na reabsorption = H2O reabsorption = ^ urea concentration
Urea transporters - inner medullary collecting ducts

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38
Q

How much Na/H2O is reabsorbed in the PT?

A

65%

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39
Q

How is sodium reabsorbed in different regions of the PT?

A

First half - cotransport with glucose + amino acids
Second half - reabsorbed with Cl-

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40
Q

What is secreted in the PT?

A

Bile salts, oxalate, urate, catecholamines
PAH
Drugs/toxins

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41
Q

What are the 3 segments of the LOH?

A

Thin descending
Thin ascending
Thick ascending

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42
Q

How much water is resorbed in the LOH?

A

20%

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43
Q

How permeable is the LOH to water?

A

Descending highly permeable
Ascending impermeable

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44
Q

What is the function of the LOH?

A

Descending - simple diffusion
Thick ascending - active reabsorption of Na/K/Cl

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45
Q

How is sodium reabsorbed in the thick ascending LOH?

A

Diffusion gradient maintained by Na-K ATPase in basolateral membrane
Na movement mediated by luminal NKCC2 contransporter (Na + K + 2xCl) - drives K+ reabsorption against concentration gradient

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46
Q

What is the site of action of frusemide?

A

NKCC2 cotransporter

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47
Q

What substances are absorbed/secreted in the thick ascending LOH?

A

Na, K, Cl reabsorbed vis NKCC2 cotransporter
Na reabsorbed, H+ secreted via Na-H exchanger
Mg, Ca, Na and K - paracellular absorption - encouraged by positive charge in luminal fluid

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48
Q

What is the reason for the positive charge of luminal fluid in the LOH?

A

Backless of K+ into lumen

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49
Q

How does the distal tubule function?

A

First portion - macula densa
Second portion - similar function to thick ascending LOH - diluting segment
Second half - principal cells - Na reabsorption/K secretion
Intercalated cells - secrete or reabsorb H+, HCO3, K

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50
Q

How is sodium chloride absorbed in the distal tubule?

A

Na-Cl cotransporter on luminal surface

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51
Q

Where do thiazide diuretics act?

A

Na-Cl cotransporter in distal tubule

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52
Q

What is the action of principal cells and where are they located?

A

Second half distal tubule
Basolateral Na-K ATPase maintains low Na concentration
Na/K channels facilitate diffusion along concentration gradient (Na in, K+ out)

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53
Q

Where does spironolactone act?

A

Principle cells of distal tubule

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54
Q

Where does amiloride and triamterene act?

A

Na channel blockers
Block luminal Na channel in principal cells, reduced activity of basolateral Na-K ATPase

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55
Q

What is the function of type A/B intercalated cells?

A

A - H+ secretion
B - HCO3 secretion

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56
Q

How do type A intercalated cells act?

A

Secrete H+ into lumen by H-ATPase and H-K ATPase transporter
H+ generated by carbonic anhydrase, liberating HCO3
HCO3 reabsorbed with HCO3-Cl exchanger
K/Cl leave cell via channels (pg 353)

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57
Q

How do type B intercalated cells act?

A

Secrete HCO3 into lumen using pendrin - HCO3/Cl exchanger
H+ transported across basolateral membrane with H-ATPase or H-K ATPase cotransporter

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58
Q

Which intercalated cells are involved in K+ reabsorption/secretion?

A

A - reabsorption
B - secretion

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59
Q

Summarise the function of the late distal and cortical collecting tubule

A

Impermeable to urea
Reabsorb Na in principal cells under aldosterone control
Type A intercalated cells secrete H+ in acidosis
Type B intercalated cells secrete HCO3 in alkalosis
Permeability to water controlled by ADH

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60
Q

Summarise the function of the medullary collecting duct

A

Permeability to water controlled by ADH
Permeable to urea + urea transporters - important for formation of concentrated urine
Capable of H+ secretion

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61
Q

How is tubular reabsorption regulated?

A

Glomerulotubular balance
Peritubular capillary and renal interstitial fluid physical forces
Pressure natriuresis/diuresis
Hormonal - aldosterone, angiotensin, ADH, ANP, PTH
SNS

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62
Q

What is glomerulotubular balance?

A

Proximal tubular reabsorption increased with GFR - percentage of GFR remains stable at approx 65%
Also happens to smaller degree in LOH
Prevents overload of distal segments at high GFR

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63
Q

How do peritubular capillary and renal interstitial fluid physical forces regulate reabsorption?

A

Increased arterial pressure = increased peritubular capillary pressure = reduced reabsorption
Increased afferent/efferent arteriole resistance = reduced peritubular capillary pressure = increased reabsorption
Osmotic pressure - higher FF = higher osmotic pressure in peritubular capillaries = more reabsorption
Higher interstitial pressure (due to increased capillary hydrostatic or decreased capillary osmotic pressure) = increased backleak

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64
Q

What is pressure diuresis/natriuresis?

A

Increased ABP =
1) ^GFR
2) v tubular reabsorption (mechanisms not fully understood)
3) v AngII => v Na reabsorption
4) Internalisation of Na transporters

65
Q

Where does aldosterone exert its effects on tubular reabsorption? What are they?

A

Collecting tubule/duct
Increased NaCl + H2O reabsorption
Increased K + H secretion

66
Q

Where does angII exert its effects on tubular reabsorption? What are they?

A

Proximal tubule, thick ascending LOH, distal tubule, collecting tubule
Increased NaCl + H2O reabsorption
Increased H+ secretion

67
Q

Where does ADH exert its effects on tubular reabsorption? What are they?

A

Distal tubule/collecting tubule and duct
Increased H2O reabsorption

68
Q

Where does ANP exert its effects on tubular reabsorption? What are they?

A

Distal tubule/collecting tubule and duct
Reduced NaCl reabsorption

69
Q

Where does PTH exert its effects on tubular reabsorption? What are they?

A

Reduced PO4- reabsorption
Increased Ca++ reabsorption

70
Q

On which cells does aldosterone act? How does it act?

A

Principal cells of collecting duct
Stimulates Na-K ATPase on basolateral membrane + increased Na permeability of luminal membrane by inserting Na channels

71
Q

What is the main stimulus for aldosterone secretion?

A

Increased extracellular K+
Increased angII - (usually associated with sodium/volume depletion or low BP)

72
Q

What is the body’s main Na-retaining hormone?

A

AngII

73
Q

What stimulates AngII formation?

A

Low BP

74
Q

What are the actions of angII?

A

Aldosterone secretion
Efferent arteriole constriction - increases reabsorption, raises filtration fraction => further reabsorption
Directly stimulates Na reabsorption in PT, LOH, DT and CT

75
Q

How does angII act to stimulate Na reabsorption?

A

Stimulates basolateral Na-K ATPase pump
Stimulates Na-H exchange on luminal surface (especially proximal tubule)
Stimulates basolateral Na-HCO3 cotransport

76
Q

Where does ADH bind? How does it act?

A

V2 receptors in late distal tubule, collecting tubules and collecting ducts
Increases formation of CAMP and protein kinase - stimulates movement of AQP-2 to luminal membrane

77
Q

Where are AQP 1, 2, 3 and 4 found? Which are controlled by ADH?

A

AQP -1 - proximal tubular lumen, proximal LOH, not ADH controlled
AQP-2 - luminal - ADH controlled
AQP-3/4 - basolateral, not ADH controlled

78
Q

What are the effects of chronic ADH increase?

A

Formation of AQP-2 protein through unregulated gene transcription

79
Q

What stimulates ANP release? What are it’s actions?

A

Atrial stretch
Inhibits Na/H20 reabsorption + renin secretion

80
Q

How does the SNS act to control sodium reabsorption?

A

If severe - constricts arterioles => reduced GFR
Low levels - act on alpha-adrenergic receptors in tubular epithelium => increased Na reabsorption

81
Q

What is renal clearance?

A

The volume of plasma cleared of a substance by the kidneys per unit time

82
Q

What is the main hormone responsible for controlling urine concentration?

A

ADH

83
Q

Describe how osmolality of fluid in the renal tubule changes

A

Proximal tubule - isosmotic (300)
Descending LOH - very hypertonic (600)
Ascending LOH - hypo osmotic (100)
Distal/collecting tubule
- ADH absent - further dilution (50)
- ADH present - concentration (~600)

84
Q

What is USG? How does it compare to osmolarity?

A

Measure of weight of solutes in given volume of urine - determined by number and size of molecules
Osmolarity - number of solute molecules

85
Q

Describe the steps involved in causing a hyper osmotic renal medullary interstitium

A

Guyton page 369

86
Q

Where are the urea transporters located?

A

UT-A1 + UT-A3 - medullary collecting duct
UT-A2 - thin loop of henle

87
Q

How is plasma osmolarity estimated?

A

= 2x(Na) + glucose + urea

88
Q

Describe the osmoreceptor-ADH feedback system

A

Water deficit => ^extracellular osmolarity
Osmoreceptor cells in anterior hypothalamus shrink => impulse => posterior pituitary => ADH release => reduced water excretion

89
Q

Where is ADH synthesised?

A

Hypothalamus (supraoptic/paraventricular nuclei)

90
Q

What areas detect osmolarity?

A

Osmoreceptors - anterior hypothalammus
AV3V region - third ventricle

91
Q

What are the stimuli for ADH release?

A

Increased osmolarity
Decreased arterial blood pressure
Decreased blood volume

92
Q

What stimulates thirst?

A

Increased extracellular fluid osmolarity
Decreased extracellular fluid volume
Angiotensin II
Dry mouth
GI/pharyngeal stimuli

93
Q

What factors shift K+ into cells?

A

Insulin
Aldosterone
B-adrenergic stimulation
Alkalosis

94
Q

What factors shift K+ out of cells?

A

Diabetes mellitus
Hypoadrenocorticism
B-adrenergic blockade
Acidosis
Cell lysis
Exercise
Increased extracellular fluid osmalality

95
Q

Why dp patients with hypoadrenocorticism develop hyperkalaemia?

A

Reduced cellular K+ uptake
Reduced renal excretion

96
Q

Summarise renal tubular handling of potassium

A

65% reabsorbed in proximal tubule
25-30% reabsorbed in LOH (especially thick ascending)
Collecting tubules/ducts - variable, depending on intake

97
Q

Which cells are most important for regulating potassium excretion?

A

Principal cells

98
Q

How do the principal cells secrete K+?

A

Uptake into cell from Na-K ATPase on basolateral membrane
Passive diffusion into tubular fluid via ROMK and BK channels

99
Q

What cells are involved in potassium reabsorption/secretion in the distal tubule? Do they reabsorb or secrete?

A

Principal cells - secrete
Intercalated cells - reabsorb or secrete

100
Q

Which intercalated cells secrete/reabsorb K+?

A

Type A - reabsorb
Type B - secrete

101
Q

What acid-base complication can occur secondary to severe prolonged hypokalaemia

A

Alkalosis
K reabsorption in Type A intercalated celly - H-K ATPase

102
Q

What factors increase/decrease tubular secretion of K+?

A

Increase - increased extracellular potassium, increased aldosterone, increased tubular flow rate
Decrease - acidosis

103
Q

How do increased ECF K+ levels directly stimulate K+ excretion?

A

1 - stimulates Na K ATPase activity
2 - increased K gradient to interior of epithelial cell
3 - stimulates synthesis of K channels
4 - stimulates aldosterone secretion

104
Q

How does aldosterone increase K+ secretion?

A

Activates Na K ATPase on principal cells
Increases K channels

105
Q

How is normal potassium excretion preserved during increased sodium excretion?

A

Increased Na excretion = reduced aldosterone secretion + increased tubular flow
Increased tubular flow => K concentration gradient
=> increased BK channels

106
Q

How is plasma calcium found?

A

50% ionised
40% protein bound
10% complexed with anions

107
Q

How does acid-base status influence plasm calcium?

A

Acidosis - less bound
Alkalosis - more bound

108
Q

What is the main method of removal of calcium from the body?

A

Faeces

109
Q

How does PTH act to increase serum calcium?

A

Increases bone resorption
Increases activation of vitamin D and intestinal absorption
Increases tubular reabsorption

110
Q

Where is calcium reabsorbed in the kidneys?

A

65% PT
25-30% LOH
4-9% distal/collecting tubules

111
Q

How is calcium absorbed in the proximal tubules?

A

Mostly paracellular
20% transcellular - flows into cell down electrochemical gradient (cell has slight negative charge)
Exits cell via basolateral Ca ATPase or Ca-3Na countertransporter

112
Q

How and where is calcium reabsorbed in the LOH and distal tubule?

A

Thick ascending loop
50% paracellular
50% transcellular - PTH controlled

Distal tubule - all active transport. Similar process to proximal tubule

113
Q

What regulates active transport of calcium in the LOH and distal tubule?

A

Mostly PTH
Vitamin D and calcitonin
Direct action of calcium on CSRs in LOH

114
Q

What factors increase/decrease renal calcium excretion?

A

PTH - decrease
Extracellular volume expansion/increased arterial pressure - increase
Increased serum phosphate - decrease
Acidosis - increase

115
Q

How is renal phosphate excretion regulated?

A

Overflow mechanism - renal transport maximum for excretion

116
Q

How does PTH effect phosphorus levels?

A

Promotes bone resorption => increased phosphorus
Reduces reabsorption => decrease phosphorus

117
Q

What factors increase renal phosphate excretion?

A

High dietary phosphate
PTH
Acidosis
Hypertension

118
Q

What factors decrease renal phosphate excretion?

A

Low dietary phosphate
1, 25 D3
Alkalosis
T4

119
Q

How is magnesium distributed in the body?

A

> 50% bones
49% intracellular
<1% in extracellular fluid

> 50% plasma Mg protein bound

120
Q

Where is Mg reabsorbed in the kidney?

A

25% proximal tubule
65% LOH

Mechanism of regulation poorly understood

121
Q

What factors increase Mg excretion?

A

High extracellular Mg concentration
High extracellular Ca
Low PTH
High extracellular fluid volume
Acidosis

122
Q

What factors decrease Mg excretion?

A

Low extracellular Mg concentration
Low extracellular Ca
PTH
Low extracellular fluid volume
Alkalosis

123
Q

What are the effects of acute and chronic increases in BP on urinary sodium?

A

Increases
Efficiency increased with chronic due to suppression of renin release

124
Q

What actions take place following an increase in sodium intake?

A

Low pressure reflex receptors - inhibit SNS
Suppression of RAAS
ANP
Pressure natriuresis

125
Q

What 3 systems defend against changes in H+ concentration? Which is the most powerful?

A

Buffer systems
Respiratory system
Kidneys***

126
Q

Where is carbonic anhydrase found?

A

Alveoli and renal tubules

127
Q

Describe the bicarbonate buffer system

A

CO2 + H20 <= => H2CO3
Carbonic anhydrase

H2CO3 <= => H+ + HCO3-
+
Na

128
Q

With regards to acid base - what is K?

A

Dissociation constant of an acid

129
Q

When is a buffer system most efficient?

A

At pH close to it’s pK

130
Q

Where is the phosphate buffer system most important?

A

Intracellular fluid and renal tubular fluid

131
Q

What are the main elements of the phosphate buffer system?

A

H2PO4- and HPO4–

132
Q

What are nonvolatile acids?

A

Not H2CO3
Cannot be removed by lungs

133
Q

Where does hydrogen iron secretion and HCO3 reabsorption occur?

A

All parts of the tubules except depending and ascending thin limbs of LOH

134
Q

Where is the main site of bicarbonate reabsorption?

A

80-90% in proximal tubule
10% thick ascending LOH
Remainder distal tubule and collecting duct

135
Q

How is H+ secreted in the early tubular segments?

A

Na-H counter transport using Na gradient

136
Q

What is the net change in H/HCO3 in the early tubular segments?

A

For every H+ secreted one HCO3 reabsorbed

137
Q

How is bicarbonate reabsorbed in the proximal tubule/LOH/distal tubule/collecting ducts?

A

Early proximal tubule - HCO3 - Na cotransporter
Late proximal tubule, thick LOH, distal tubule/collecting duct - Cl - HCO3 exchange

138
Q

Which cells secrete H+ in the distal and collecting tubules? How do they do it?

A

Type A intercalated cells
Primary active transport - H-ATPase and H-K ATPase

139
Q

What facilitates excretion of large amounts of H+ in the urine?

A

Phosphate and ammonia buffer systems

140
Q

Describe the phosphate buffer system

A

Once all bicarbonate in tubules reabsorbed, H+ combines with HPO4–
Excreted as NaH2PO4

141
Q

How does H+ excretion via the phosphate buffer system differ from the bicarbonate buffer system?

A

Reflects net gain of HCO3-, rather than replacement of filtered HCO3
Net effect of addition of new HCO£-

142
Q

Describe the ammonia buffer system

A

Proximal tubule
Glutamine transported into epithelial cells of proximal tubule, metabolised to 2x NH4+ + 2x HCO3-
NH4+ exchanged for sodium on luminal membrane

Collecting duct
H+ actively secreted, combines with NH3 => NH4

143
Q

What is the dominant mechanism for H+ excretion during chronic acidosis?

A

Excretion of NH4+

144
Q

What factors increase H+ secretion and HCO3 reabsorption?

A

^PCO2
^H+ / v HCO3
v ECFV
^ AngII
^Aldosterone
v K+

145
Q

What factors decrease H+ secretion and HCO3 reabsorption?

A

v PCO2
v H+ / ^ HCO3
^ ECFV
v AngII
v Aldosterone
^ K+

146
Q

What acid-base abnormality is associated with diuretics and why?

A

Metabolic alkalosis
1 - Diuretics increase flow in distal and collecting tubules => increased sodium reabsorption in exchange for H+
2 - RAAS stimulation

147
Q

How long does it take for respiratory compensation to an acid-base abnormality?

A

6-12 hours

148
Q

How long does it take for metabolic compensation to an acid-base abnormality?

A

3-5 days

149
Q

How is AG calculated? What is considered normal?

A

Na - HCO3 - Cl
8-16

150
Q

Where do loop diuretics act? How does this increase urine output?

A

1-Na, 2-Cl, 1-K co-transporter in thick ascending LOH
Increase quantities of solutes delivered to distal nephron
Disrupt countercurrent multiplier system

151
Q

Where do thiazide diuretics act>

A

Na Cl cotransporter in early distal tubule

152
Q

Where does acetylzolamide act?

A

Carbonic anhydrase inhibitor
Proximal tubule

153
Q

Where do mineralocorticoid receptor antagonists act?

A

Collecting tubule/duct

154
Q

Where does amiloride act?

A

Na channel blocker
Inhibit sodium reabsorption and potassium secretion in collecting tubules

155
Q

What are the potassium sparing diuretics?

A

Spironolactone - MRA
Amiloride - Na channel blocker

156
Q

Describe the mechanisms behind the development of bone demineralisation in CKD

A

Reduced renal conversion of vit D into 1,25- vit D = reduced intestinal calcium absorption
Increased serum PO4 => increased binding of PO4 and Ca => reduced serum ionised calcium => ^PTH

157
Q

How does Fanconi syndrome manifest?

A

Increased excretion of amino acids, glucose and PO4
In severe cases - metabolic acidosis, increased excretion of K/Ca, NDI

158
Q
A

Guyton (10 decks)

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