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ACEM Primary Written > Renal: Physiology - Regulation of extracellular fluid composition, volume and acid-base balance > Flashcards

Renal: Physiology - Regulation of extracellular fluid composition, volume and acid-base balance Flashcards

1
Q

What is the normal plasma osmolality?

A

280-295mOsm/kg of H2O

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2
Q

At what osmolality is vasopressin maximally inhibited at?

A

285mOsm/kg of H2O

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3
Q

What happens to vasopressin secretion and thirst response when the effective plasma osmotic pressure increases?

A

Vasopressin secretion increases
Thirst response stimulated

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4
Q

What is total body osmolality proportional to?

A

[(total body Na+) + (total body K+)] / TBW

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5
Q

Where are the osmoreceptors located?

A

Outside the blood-brain barrier in the anterior hypothalamus
Primarily in the organum vasculosum of lamina terminalis (OVLM), one of the circumventricular organs

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6
Q

How many vasopressin receptors are there? What are their effects?

A

Three:
V1A and V1B increase intracellular Ca2+
V2 increases cAMP

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7
Q

Which vasopressin receptor mediates the antidiuretic effect of vasopressin in the kidneys? How is this achieved?

A

V2 activation increases cAMP and promotes rapid translocation of aquaporin-2 channels (stored in endosomes inside collecting duct cells) to the apical membrane of principal cells of the collecting ducts

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8
Q

What are the three effects of V1A receptor activation?

A
  1. Vasoconstriction - however relatively large amounts of vasopressin are needed to raise BP in vivo because vasopressin also acts centrally to reduce CO
  2. Glycogenolysis
  3. Also found in brain where vasopressin functions as a neurotransmitter
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9
Q

What is the role of V1B receptors? Where are they found?

A

Found in the anterior pituitary where it stimulates ACTH release

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10
Q

What is the area postrema and what is vasopressin’s effect here?

A

Brainstem structure and one of the seven circumventricular organs
When stimulated by vasopressin causes sympathoinhibition (reduces CO, part of baroreflex)

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11
Q

Biologic half-life of vasopressin

A

18mins

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12
Q

Where is circulating vasopressin inactivated?

A

Primarily in liver and kidneys
Occurs rapidly (short biologic half-life)

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13
Q

Eight factors that increase vasopressin secretion

A
  1. Increased effective plasma osmotic pressure (>285mOsm/kg of H2O)
  2. Decreased ECF volume
  3. Pain, emotion, stress
  4. Exercise
  5. Nausea and vomiting
  6. Standing
  7. Drugs: clofibrate and carbamazepine
  8. Angiotensin II
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14
Q

Three factors that decrease vasopressin secretion

A
  1. Decreased effective osmotic pressure of plasma
  2. Increased ECG volume
  3. Alcohol
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15
Q

Where is vasopressin stored?

A

Posterior pituitary

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16
Q

What is the relationship between vasopressin secretion and discharge rate of stretch receptors?

A

Inversely proportional: when stretch receptor discharge rate increases (due to increased ECF), rate of vasopressin secretion decreases

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17
Q

Where are the low-pressure stretch receptors located? Where are the high-pressure stretch receptors located?

A

Low-pressure: great veins, right and left atria, pulmonary vessels
High-pressure: carotid sinuses, aortic arch

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18
Q

Is vasopressin secretion responsive to venous or arterial pressure?

A

Both: low-pressure stretch receptors are responsive to moderate decreases in blood volume that reduce CVP without affecting arterial pressure

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19
Q

What are the primary mediators of volume effects on vasopressin secretion: low- or high-pressure stretch receptors?

A

Low

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20
Q

How does angiotensin II increase vasopressin secretion?

A

By acting on the circumventricular organs

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21
Q

Describe the pathway involved in transmitting impulses from low-pressure stretch receptors to the hypothalamus

A

Low-pressure stretch receptor activation (increased CVP) -> nucleus of tractus solitarius (NTS) -> inhibitory pathway from NTS to caudal ventrolateral medulla (CVLM) -> inhibits excitatory pathway from CVLM to hypothalamus

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22
Q

What is the effect of hypovolaemia and hypotension in massive haemorrhage on vasopressin release? What is the effect on the osmotic response curve?

A

Large amounts of vasopressin released
In presence of hypovolaemia, results in water retention and reduced plasma osmolality (with hyponatraemia)
Osmotic response curve shifts to the left and the slope is increased

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23
Q

Volume stimuli can override osmotic stimuli in increasing vasopressin secretion: true or false?

A

True

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24
Q

What is diabetes insipidus? What are the two types?

A

Syndrome resulting either from vasopressin deficiency (central DI), or failure of the kidney to respond to vasopressin (nephrogenic DI)

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25
Q

Causes of central diabetes insipidus

A
  1. Pituitary neoplasm (primary or metastatic) 30%
  2. Posttraumatic (including post surgical removal of posterior pituitary) 30%
  3. Idiopathic 30%

Remaining 10%:
4. Vascular lesions
5. Infections
6. Systemic diseases affecting the hypothalamus (e.g. sarcoidosis)
7. Genetic (e.g. mutations in gene for prepropressophysin)

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26
Q

Is central DI as a result of surgical removal of the posterior pituitary permanent or temporary?

A

May be temporary if distal ends of supraoptic and paraventricular fibres are only damaged because they can recover and make vasopressin again

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27
Q

Symptoms of diabetes insipidus

A

Polyuria
Polydipsia (if not maintained, can become fatally dehydrated)

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28
Q

What are the two causes of nephrogenic diabetes insipidus?

A

Both genetic:
1. X-linked recessive V2 receptor mutation
2. Autosomal AQP2 gene mutation

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29
Q

What is SIADH?

A

Syndrome of inappropriate antidiuretic hormone
Occurs when vasopressin is inappropriately high relative to serum osmolality
Causes water retention and dilutional hyponatraemia
Loss of salt in urine also results in decreased secretion of aldosterone

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30
Q

Describe vasopressin escape

A

Prolonged exposure to elevated levels of vasopressin results in down-regulation of AQP2 production

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31
Q

Five broad causes of SIADH with specific examples

A
  1. Primary brain injury (e.g. meningitis, SAH)
  2. Drugs (e.g. carbamazepine, SSRIs, amitriptyline, morphine)
  3. Malignancy (e.g. SCLC)
  4. Infective causes (e.g. pneumonia, cerebral abscess)
  5. Hypothyroidism
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32
Q

What drug may be used to treat SIADH?

A

Demeclocycline
Antibiotic that reduces renal response to vasopressin

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33
Q

What is the most important determinant of ECF volume?

A

[Na+]

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34
Q

Four mechanisms by which angiotensin II acts to maintain BP

A
  1. Stimulates aldosterone release
  2. Stimulates vasopressin and ACTH release
  3. Stimulates NA release
  4. Vasoconstricts
  5. Mesangial cell contraction to decrease GFR
  6. Increases thirst
  7. Direct tubular effect to increase Na+ reabsorption
  8. Acts on brain to decrease sensitivity of baroreflex
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35
Q

What stimulates ANP and BNP release? What effect does this have?

A

Increased ECF volume
Induces natriuresis and diuresis

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36
Q

Describe the response of the kidney to reduced ECF volume in terms of Na+ reabsorption?

A

ECG volume decreases -> BP falls -> decreased glomerular capillary pressure -> decreased GFR -> decreased Na+ filtration
Aldosterone release -> increased Na+ reabsorption

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37
Q

Three hormones produced by the kidney

A

Renin
EPO
1,25-dihydroxycolecalciferol

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38
Q

What does endogenous oubain do?

A

Inhibits Na K ATPase

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39
Q

What other organs produce prorenin?

A

Ovaries (however very little prorenin is converted to renin in the circulation; active renin is primarily a product of the kidney)

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40
Q

Half-life of active renin

A

80mins

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41
Q

Function of renin

A

Cleaves angiotensin I from the amino terminal end of angiotensinogen (renin substrate)

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42
Q

Where is angiotensinogen produced?

A

In the liver

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43
Q

Five substances that increase the circulating level of angiotensinogen

A
  1. Glucocorticoids
  2. Thyroid hormones
  3. Oestrogens
  4. Cytokines
  5. Angiotensin II
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44
Q

Role of angiotensin-converting enzyme

A

Converts angiotensin I to angiotensin II
Inhibits bradykinin (called kininase II in this context)

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45
Q

Mechanism of cough side effect seen in ACEIs

A

Increased bradykinin acting on B2 receptors

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46
Q

Where does conversion of angiotensin I to II predominantly take place?

A

In the lungs

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47
Q

Two forms of ACE

A

Somatic: found throughout the body
Germinal: found solely in spermatogenic cells and spermatazoa

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48
Q

Drugs reducing renin secretion or activity

A

Reduced renin secretion: indomethacin, B-blockers (e.g. propranolol)
Direct renin inhibitor: enalkiren, pepstatin

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49
Q

Half-life of angiotensin II

A

1-2mins

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50
Q

How is plasma renin activity measured?

A

Sample is incubated and an immunoassay is used to measure the amount of angiotensin I produced
Exogenous angiotensinogen may be added to prevent falsely low PRAs due to low angiotensinogen: this effectively measures plasma renin concentration (PRC)

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51
Q

Normal PRA

A

1ng/ml/hr of angiotensin I generated

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52
Q

What is more potent: angiotensin II or NA?

A

Angiotensin II 4-8x more potent that NA

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53
Q

Why is angiotensin II activity decreased in the setting of Na+ depletion and in cirrhosis?

A

There is increased circulating angiotensin II in these conditions, which causes downregulation of vascular AT1 receptors (but upregulation of adrenocortical AT1 receptors)

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54
Q

Two classes of angiotensin II receptors and their cellular effects

A
  1. AT1: increased cytosolic free Ca2+
  2. AT2: K+ channel opening, increased NO and cGMP
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55
Q

Which cells of the kidney produce renin? Where are they found?

A

Juxtaglomerular cells, found in media of afferent arterioles
Also found in lacis cells but significance unknown

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56
Q

Three factors increasing renin secretion

A
  1. Increased sympathetic activity via renal nerves
  2. Increased circulating catecholamines
  3. Prostaglandins
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57
Q

Four factors decreasing renin secretion

A
  1. Increased Na+ and Cl- reabsorption across macula densa
  2. Increased afferent arteriolar pressure
  3. Angiotensin II
  4. Vasopressin
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58
Q

How does angiotensin II decrease renin secretion?

A

Acts directly on juxtaglomerular cells

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59
Q

Ten conditions that increase renin secretion

A
  1. Na+ depletion
  2. Diuretics
  3. Hypotension
  4. Haemorrhage
  5. Upright posture
  6. Dehydration
  7. Cardiac failure
  8. Cirrhosis
  9. Constriction of renal artery or aorta
  10. Various psychological stimuli

Most increase renin secretion due to decreased CVP triggering sympathetic response, some also decrease renal arteriolar pressure
Psychological stimuli increase activity of renal nerves

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60
Q

Which receptors are involved in sympathetically mediated renin secretion?

A

B1-adrenergic receptors on juxtaglomerular cells

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61
Q

Where is BNP predominantly produced?

A

In the heart (also found in brain)

62
Q

Five mechanisms by which ANP and BNP produce natriuresis and lower BP

A
  1. Relax mesangial cells and dilate afferent arterioles to increase GFR
  2. Act on tubules to inhibit Na+ reabsorption
  3. Increase capillary permeability causing fluid extravasation and decreased BP
  4. Relax vascular smooth muscle in arterioles and venules
  5. Inhibit renin secretion
63
Q

Which natriuretic peptide is found in the brain and what is its role here?

A

ANP found in neurons in the brain
Has opposite central effects to angiotensin II

64
Q

How many natriuretic peptide receptors are there?

65
Q

What stimuli promote ANP and BNP secretion?

A

Increased ECF volume -> atrial (ANP) and ventricular (BNP) stretch

66
Q

What is the role of EPO?

A

Increases number conversion of EPO-sensitive haemopoietic stem cells to RBC precursors

67
Q

Where is EPO inactivated?

68
Q

Half-life of EPO

69
Q

How long does it take for an increase in circulating RBCs to be observed post EPO?

A

2-3 days (takes time for RBC maturation)

70
Q

Sources of endogenous EPO

A

Kidneys 85%
Liver 15%

71
Q

Which cells in the kidney are responsible for EPO production? What receptor is involved?

A

Interstitial cells in the peritubular capillary bed
Via catcholamines acting on B-adrenergic receptors

72
Q

Two uses for epoetin alfa

A
  1. Treatment of anaemia in ESRF
  2. Stimulation of RBC production for blood banking for autologous transfusions
73
Q

What is the typical stimulus for EPO release, and what other factors can induce release?

A

Hypoxia
Other factors which increase secretion include cobalt salts, androgens and respiratory alkalosis (seen in high-altitude conditions)

74
Q

What drug can be used to treat central DI? What receptors does it act on?

A

Desmopressin (dDVAP)
Acts via V2 receptors

75
Q

What plasma Na+ and osmolality, and urinary Na+ and osmolality are suggestive of SIADH?

A

Euvolaemic hyponatraemia <135mmol/L
Plasma osmolality <280mOsm/L
Urine osmolality >100mOsm/L
Urine sodium >20mmol
Urine osmolality > serum osmolality

76
Q

In what parts of the nephron is H+ secreted?

A

Proximal tubule
Distal tubule
Collecting ducts

77
Q

What transporter is responsible for H+ secretion in the proximal tubules? What type of transport is this?

A

Na-H exchanger (primarily NHE3)
Secondary active transport (Na K ATPase on basolateral membrane creates gradient for Na-K exchanger)

78
Q

What % of filtered HCO3- is reabsorbed in the proximal tubule?

79
Q

Describe the process of H+ secretion and HCO3- reabsorption in the proximal tubule. What is the effect on pH of the tubular fluid?

A

Na K ATPase on the basolateral membrane actively transports Na+ out of the cell into the interstitium
Low intracellular Na+ sets up a gradient driving Na+ into the cell from the tubular lumen via the Na-H exchanger on the apical membrane, with H+ secreted into the lumen
Secreted H+ combines with filtered HCO3- to form H2CO3
Carbonic anhydrase on the apical membrane catalyses formation of H2O and CO2 from H2CO3
Proximal tubule is permeable to H2O and CO2
Intracellular carbonic anhydrase then catalyses formation of H2CO3 from CO2 and H2O
H2CO3 dissociates into H+ and HCO3- intracellularly: H+ is again secreted in tubular lumen via Na-H exchanger, and HCO3- diffuses into interstitium
Little effect on pH of tubular fluid (main function is HCO3- reabsorption)

80
Q

Describe the process of H+ secretion and HCO3- reabsorption in the distal tubule

A

Occurs in intercalated cells
H+ is secreted by ATP-drive proton pump (H+ ATPase; i.e. is independent of Na+, conversely to proximal tubule)
Also by H-K+ ATPase
Abundant carbonic anhydrase within I cells
Anion exchanger 1 (AE1) in basolateral membrane may function as Cl/HCO3 exchanger to transport HCO3- to interstitium

81
Q

What is the effect of aldosterone on H+ secretion?

A

Increases H+ secretion in intercalated cells of the distal tubule by acting on H+ ATPase

82
Q

How is H+ secretion increased in acidosis?

A

Number of H+ ATPase pumps in apical cell membrane of intercalated cells is increased (via insertion of tubulovesicles into membrane)

83
Q

What is the limiting pH of urine?

84
Q

What three buffer reactions occurring within the tubular fluid remove free H+ to enable the secretion of more acid?

A
  1. Bicarbonate: H+ + HCO3- -> H2CO3 (carbonic acid) -> H2O + CO2
  2. Dibasic phosphate: H+ + HPO4(2-) -> H2PO4- (titratable acids)
  3. Ammonia: H+ + NH3 (ammonia) -> NH4+ (ammonium)
85
Q

What % of nonvolatile acids are excreted as titratable acid each day? What is this in mEq?

86
Q

What % of nonvolatile acids are excreted as ammonium each day? What is this in mEq?

87
Q

What is a nonvolatile acid?

A

Nonvolatile acid is an acid produced in the body from sources other than carbon dioxide, and is not excreted by the lungs
All acids produced in the body are nonvolatile except carbonic acid, which is the sole volatile acid

88
Q

pKa of the bicarbonate buffer system

89
Q

pKa of the dibasic phosphate buffer system

90
Q

pKa of the ammonia buffer system

91
Q

Concentration of bicarbonate and phosphate in the plasma and therefore the glomerular filtrate (in mEq)

A

HCO3-: 24mEq/L
PO4-: 1.5mEq/L

92
Q

How many mEq of HCO3- are filtered and reabsorbed each day?

93
Q

Where does secreted H+ react with dibasic phosphate? Why?

A

To greatest extent in the distal tubules and collecting ducts
Reabsorption of water in the distal tubules and collecting ducts means that phosphate that escaped proximal reabsorption is greatly concentrated

94
Q

Where does secreted H+ react with NH3?

A

Proximal and distal tubules

95
Q

Where is NH3 made?

A

Proximal tubule

96
Q

How is the urine titratable acidity measured?

A

By determining the amount of alkali that must be added to the urine to return its pH to 7.4 (glomerular filtrate pH)

97
Q

Why does the titratable acidity only measure a fraction of the acid secreted?

A

It doesn’t take into account H2CO3 that has been converted to H2O and CO2

98
Q

How does the kidney replenish the body with new HCO3 ions?

A

When H+ is removed from the body as NH4+ or titratable acid
New HCO3- forms within the cells (i.e. these HCO3- ions are not those originally filtered)

99
Q

How much does ammonia contribute to the titratable acidity? Why?

A

Very little
pKa is 9.0 and ammonia system is titrated only from urinary pH to pH 7.4
When pKa > pH, environment is considered relatively basic and compound will exist primarily in its protonated form (i.e. will be unable to “buffer” further H+)

100
Q

What is the ratio of NH3 to NH4+ at pH 7.0?

A

1:100

pH = pKa + log(NH3:NH4+)
7.0 = 9.0 + log(NH3:NH4+)
-2 = log(NH3:NH4+)
10^(-2) = NH3:NH4+
NH3:NH4+ = 1/(10^2) = 1/100

101
Q

How does NH3 move out of the tubular cells into the interstitium and urine? How does it become “trapped” in the urine?

A

Lipid soluble, moves down concentration gradient
Reacts with H+ in the urine to form NH4+
This process is more important in the collecting duct (in proximal tubule NH4+- can be secreted)

102
Q

What is the principle reaction producing NH4+ in tubular cells?

A

Conversion of glutamine to glutamate, catalysed by glutaminase (abundant in renal tubular cells)
Glutamate is then converted to a-ketoglutarate by glutamate dehydrogenase, producing again more NH4+
Metabolism of a-ketoglutarate utilises 2H+, freeing 2HCO3-

103
Q

What is the effect of chronic acidosis on NH4+ excretion at any given urine pH? What is the effect on phosphate buffer system?

A

Increases because more NH3 enters the tubular urine
Enhances H+ secretion

Limited urinary excretion of acid via phosphate buffer system as the amount of phosphate filtered at the glomerulus cannot be increased

104
Q

How is NH4+ secreted into the urine in the proximal tubule vs collecting ducts?

A

Proximal tubule: NH4+ can be secreted into the urine, often by replacing H+ on the Na-H exchanger (nonionic diffusion less importantly)
Collecting duct: nonionic diffusion of NH3 which is then converted to NH4+ in the urine (maintains concentration gradient for further NH3 diffusion)

105
Q

Describe the pH changes that occur along the nephron

A

Moderate drop in pH occurs in proximal tubular fluid, but most secreted H+ has little effect on pH due to bicarbonate buffer system
Distal tubule has decreased H+ secreting capacity but more effect on urinary pH (as this is where reactions with titratable acid buffer system occurs)

106
Q

4 factors influencing renal acid secretion, their effect and the mechanism

A

Changes in intracellular:
1. P(CO2): increased P(CO2) (i.e. respiratory acidosis) increases formation of H2CO3 and enhances H+ secretion
2. K+ concentration: decreased K+ causes intracellular acidosis (even if plasma pH is elevated) which increases H+ secretion
3. Carbonic anhydrase level: increased CA increases H2CO3 formation to increase H+ secretion
4. Adrenocortical hormone concentration: aldosterone increases tubular reabsorption of Na+ and secretion of H+ and K+

107
Q

Give an example of a weak acid secreted by nonionic diffusion. What is the effect of urine pH?

A

Salicylate
Rate of diffusion is dependent on urinary pH (urinary alkalinisation enhances secretion)

108
Q

What is the effect of plasma concentration of HCO3- on urinary pH?

A

When [HCO3-] exceeds the renal threshold for HCO3- (>26-28mEq/L), it is excreted in the urine which becomes alkaline
When [HCO3-] is below the renal threshold for HCO3- (<26mEq/L), there is more free H+ available (as it is not all being used for HCO3- reabsorption) which can combine with other buffer anions including NH3 to form NH4+, increasing the acidity of the urine

109
Q

What is the renal threshold for HCO3-?

A

26-28mEq/L

110
Q

What is the effect of ECF expansion on HCO3- reabsorption?

A

HCO3- reabsorption is decreased with ECF volume expansion

111
Q

What is true plasma?

A

Plasma that has been in equilibrium with red cells

112
Q

What is the difference in plasma H+ concentration at normal pH vs in extreme acidosis and extreme alkalosis?

A

Normal (pH 7.4): 4x10^(-8)mol/L (0.00004mEq/L)
Extreme acidosis (pH 7.0): 1x10^(-7)mol/L (0.0001mEq/L)
Extreme alkalosis (pH 7.7): 2x10^(-8)mol/L (0.00002mEq/L)

113
Q

What is the urinary H+ concentration at maximal urine acidity?

A

Maximal urine acidity (pH 4.5): 3x10^(-5)mol/L (0.03mEq/L)

114
Q

What is the pH and H+ concentration of gastric HCl?

A

pH 0.8
H+ concentration 0.15mol/L (150mEq/L)

115
Q

What is the pH and H+ concentration of pancreatic juice?

A

pH 8.0
H+ concentration 1x10^(-8)mol/L (0.00001mEq/L)

116
Q

Is venous plasma pH higher or lower than arterial?

117
Q

What variation in plasma pH can occur without untoward effects?

118
Q

What is the definition of pH?

A

Negative log10 of H+ concentration

119
Q

Four sources of extra acid load

A
  1. Exercise (lactic acidosis)
  2. Diabetic ketosis (acetoacetic acid and B-hydroxybutyric acid)
  3. Ingestion of acidifying salts (e.g. NH4Cl, CaCl2) which in effect add HCl to the body
  4. Failure of diseased kidneys to excrete normal amounts of acid
120
Q

Three sources of extra alkali load

A
  1. Fruits (contain Na+ and K+ salts of weak organic acids; anions of these salts are metabolised to CO2, leaving NaHCO3 and KHCO3)
  2. Ingested NaHCO3
  3. Loss of acid from body due to vomiting of gastric juice rich in HCl
121
Q

Describe the role of liver and kidneys in handling metabolically produced acid loads

A

Amino acids are used for gluconeogenesis in the liver, producing NH4+ and HCO3- as byproduct (or H2SO4 if sulfur-containing AAs, and H3PO4 is phosphorylated AAs)

NH4+ and HCO3-: NH4+ and HCO3- are used to produce urea and glutamine in the liver, urea is excreted directly by the kidneys, and glutamine is converted to NH4+ and a-ketoglutarate in the kidneys as previously described
H2SO4 and H3PO4: major H+ load to buffers in ECF, SO4(2-) is excreted by the kidneys, HPO4(2-) enables H+ secretion in the kidneys in the form of H2PO4-

122
Q

Principal buffer system in the interstitium

A

Bicarbonate: H2CO3 -> H+ + HCO3-

122
Q

Three principal buffer systems in the blood

A
  1. Bicarbonate: H2CO3 -> H+ + HCO3-
  2. Protein: HProt -> H+ + Prot-
  3. Haemoglobin: HHb -> H+ + Hb-
123
Q

Two principal buffer systems in the intracellular fluid

A
  1. Protein: HProt -> H+ + Prot-
  2. Phosphate: H2PO4 -> H+ + HPO4(2-)
124
Q

In what cells is carbonic anhydrase found in high concentrations?

A
  1. Gastric acid-secreting cells (parietal cells)
  2. Renal tubular cells
125
Q

Three compounds that inhibit carbonic anhydrase

A
  1. Cyanide
  2. Azide
  3. Sulfide
126
Q

Two principal buffer systems in CSF and urine

A
  1. Bicarbonate: H2CO3 -> H+ + HCO3-
  2. Phosphate: H2PO4- -> H+ + HPO4(2-)
127
Q

What % of acid load is buffered by the bicarbonate system in the ECF during metabolic acidosis? Where is the remainder buffered?

A

15-20% buffered by bicarbonate system in ECF
Remainder buffered intracellularly

128
Q

What % of OH- load is buffered intracellularly during metabolic alkalosis?

129
Q

Where does most of the buffering occur in respiratory acidosis and alkalosis: intracellular or extracellular?

A

Intracellular

130
Q

Where does most of the buffering occur in metabolic acidosis and alkalosis: intracellular or extracellular?

A

Metabolic acidosis: predominantly intracellular
Metabolic alkalosis: predominantly extracellular

131
Q

What are the principal regulators of intracellular pH?

A

HCO3- transporters

132
Q

Three kinds of HCO3- transporters

A
  1. CL–HCO3- exchanger (AE1)
  2. Na+-HCO3- cotransporter (three subtypes)
  3. K+-HCO3- cotransporter
133
Q

Describe the body’s response to strong acid load. What is the difference when the acid load is CO2?

A

Major buffer reactions are driven to the left
Blood levels of the three “buffer anions” (Hb-, Prot-, HCO3-) drop
Anions of the added acid are filtered into renal tubules, accompanied by cations (predominantly Na+) to maintain electrochemical neutrality
Tubules replace Na+ with H+ and in doing so reabsorb equimolar amounts of Na+ and HCO3- to conserve cations, eliminate acid, and restore supply of buffer anions

When acid load is CO2, H2CO3 is formed and plasma HCO3- is increased rather than decreased

134
Q

What is the effect on plasma Cl- of renal compensation in chronic respiratory acidosis?

A

Cl- falls as HCO3- increases (Cl- exchanged for HCO3-)

135
Q

What changes occur in chronic metabolic acidosis?

A

Glutamine synthesis increases to provide extra NH4+ to the kidneys for buffering and additional HCO3-

136
Q

What is the effect of respiratory compensation to metabolic acidosis on the renal response?

A

Renal response to metabolic acidosis is partially inhibited by respiratory compensation, due to it causing a drop in P(CO2) which hinders acid secretion
However respiratory compensation also decreases filtered load of HCO3- so the net inhibitory effect is not great

137
Q

HCO3-:H2CO3 ratio at pH 7.4, 6.0, 7.1 and 7.3

A

7.4 = 20
6.0 = 0.9
7.1 = 10
7.3 = 16

138
Q

Causes of HAGMA

A

L TKR:

Lactic acidosis
Toxins
Ketoacidosis
Renal failure

Normal anion gap – GIT losses, renal loss of bicarb, renal dysfunction(RTA), azetozolamide, TPN, Addisons
Compensated by :Increase resp rate and Increase renal secretion of H+

139
Q

Four examples of toxins causing HAGMA

A
  1. Aspirin
  2. Ethylene glycol
  3. Cyanide
  4. Isoniazid
140
Q

Causes of normal anion gap metabolic acidosis

A

CAGE ABCD

Chloride excess
Acetazolamide/Addisons
GI causes: diarrhea/vomiting, fistulae (pancreatic, ureters, billary, small bowel, ileostomy)
Extra – RTA

Addisons (adrenal insufficiency)
Bicarbonate loss (GI or Renal)
Chloride excess
Diuretics (Acetazolamide)

141
Q

What calculation can be used to differentiate between GI and renal causes of normal anion gap acidosis? How is this interpreted?

A

Urinary anion gap: (Na+ + K+) – Cl-
Remaining significant unmeasured ions are NH4+ and HCO3-

Renal causes will have increased urinary AG due to increased urinary HCO3- excretion
GI causes will have decreased urinary AG due to increased NH4+ excretion

142
Q

What does the anion gap mainly consist of?

A

Proteins, HPO4, SO4 and organic acids

143
Q

What is the Siggaard-Andersen curve nomogram and what is it used to interpret?

A

Nomogram with P(CO2) plotted on a log scale on vertical axis and pH on horizontal axis
Used to plot acid-base characteristics of arterial blood

144
Q

Normal base excess

145
Q

Formula for expected CO2 in metabolic acidosis

A

CO2 = (1.5 x HCO3-) + 8

146
Q

What is the standard bicarbonate?

A

What the plasma bicarbonate would be once the respiratory component is eliminated (measure of the alkali reserve of the blood; index of the degree of metabolic acidosis or alkalosis present)

147
Q

What is the buffer base? What is the normal value of the buffer base?

A

Equal to the total number of buffer anions (principally Prot–, HCO3–, and Hb–) that can accept H+ in the blood
Normal value is 48mEq/L

148
Q

What is the base excess? What is its value in acidosis vs alkalosis?

A

The amount of acid or base that would restore 1L of blood to normal acid–base composition at a PCO2 of 40mm Hg
Positive in alkalosis, negative in acidosis

149
Q

What amount of bicarbonate must be added to correct a base deficiency?

A

~1.2x the standard bicarbonate deficit (difference between normal standard bicarbonate 24mEq/L and actual standard bicarbonate)

150
Q

What is the effect of NaHCO3 on CO and BP?

A

Decreases CO
Lowers BP

151
Q

What is the anion gap and how is it calculated?

A

Difference between the measured cations minus anions
(Na+ + K+) – (Cl-+ HCO3-)

ACEM Primary Written (150 decks)

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