Acid Base Disorders 2 Flashcards

1
Q

Differential diagnosis of metabolic alkalosis

A
  • Bartter Syndrome
  • Aldosteronism
  • NG suction
  • Gitelman Syndrome
  • Excess Akalai (antacids)
  • Renin
  • Emesis
  • Diuretics
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2
Q

increased serum HCO3 in metabolic alkalosis due to

A
  • GI hydrogen loss

- renal hydrogen loss

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3
Q

metabolic consequences of metabolic alkalosis

A
  • hypercarbia
  • hypoxemia
  • hypocalcemia
  • hypokalemia
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4
Q

two phases of metabolic alkalosis

A
  • generation phase

- maintenance phase

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5
Q

generation phase of metabolic alkalosis - loss of gastric acids

A
  • loss of HCl, Na and H2O from stomach and generation of Na and HCO3
  • reabsorb filtered chloride (prefer reabsorb Cl over HCO3) due to onset of hypovolemia and loss of excess HCO3 in urine with sodium and potassium
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6
Q

what would rapidly restore the situation to baseline in generation phase of metabolic alkalosis

A
  • renal excretion of alkali or retention of acid
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7
Q

maintenance phase of metabolic alkalosis - clinically evidence only when the elevated _________ concentration persists

requires impairment of

A
  • serum bicarbonate

- requires impairment of renal excretion of bicarbonate

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8
Q

causes of impaired renal bicarbonate excretion in metabolic alkalosis

A
  • kidney failure
  • secondary stimulation of collecting duct ion transport
  • primary stimulation of collecting duct ion transport
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9
Q

maintenance phase of metabolic alkalosis linked to - loss of gastric acids

A
  • chloride depletion
  • hypokalemia
  • greater degree of hypovolemia so enhanced reabsorption of filtered NaCl and all of the excess HCO3
  • increase in aldosterone which excretes more H+ in collecting duct
  • aciduria
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10
Q

maintenance phase of metabolic alkalosis- secondary stimulation of collecting duct ion transport due to

A
  • extra-renal losses of Cl with secondary renal K losses

- renal Cl losses with secondary K losses

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11
Q

renal Cl loses with secondary K loses due to

A
  • chloruretic diuretic drugs
  • recovery from chronic hypercapnia
  • inactivating mutation of Cl- linked Na+ cotransporters (Bartter and Gitelman syndromes)
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12
Q

maintenance phase of metabolic alkalosis - primary stimulation of collecting duct ion transport due to

A
  • mineralocorticoid induced or apparently mineralocorticoid excess syndromes
  • activating mutations of ENaC or signal pathway
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13
Q

up regulation of proximal tubule Na+/H+ exchanger and H+ ATPase results in

A
  • increased HCO3- reabsorption

- pump more hydrogen out which will absorb more HCO3 and bring it into the cell

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14
Q

impairment of LOH Na/K/2Cl results in

what causes this

A
  • increased Na+ delivery to distal nephron
  • loop diuretics
  • Bartter syndrome
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15
Q

impairment of early distal tubule Na/Cl transporter and late distal tubule HCO3/CL exchanger results in

what causes this

A
  • increased Na+ delivery to distal nephron
  • thiazide diuretics
  • Gitelman syndrome
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16
Q

activation of collecting duct ENaC, ROMK, H+ATPase, and H/K ATPase causes

due to

A
  • hypokalemia and chloride depletion

- primary/secondary hyperaldosteronism or mimics of aldosteronism

17
Q

relationship between plasma potassium and bicarbonate reabsorption

A
  • as plasma potassium increases, HCO3 reabsorbed goes down
18
Q

HCO3 reabsorption rises with what K+ levels

A
  • low
19
Q

secondary stimulation of collecting duct ion transport due to which syndromes

A
  • Cl depletion syndrome
  • renal Cl losses
  • Alkali intake or administration
20
Q

Cl depletion syndromes have what BP

A
  • BP normal or low
21
Q

extra-renal losses of Cl with secondary renal K losses due to

A
  • vomiting, nasogastric drainage
  • congenital chloridorrhea
  • high volume ileostomy drainage
  • cystic fibrosis
  • some villous adenomas

VCICV

22
Q

alkali intake or administration due to

A
  • kidney failure

- dietary Cl- restriction

23
Q

BP of appparent or for real mineralocorticoid excess syndromes

A
  • high
24
Q

conditions of apparent mineralcortcoid excess syndrome

A
  • liddle

- 11-hydroxysteroid dehydrogenase inhibition or deficiency

25
Q

conditions of mineralocorticoid excess syndromes

A
  • primary aldosteronism
  • glucocorticoid remediable aldosteronism
  • Cushing syndrome
  • congenital adrenal hyperplasia
  • renin secreting tumors or renal artery stenosis
  • fludrocortisone

PGCRFC
please get cush real fucking cool

26
Q

how loop and thiazide diuretics cause metabolic alkalosis

A
  • loss of Na+ and Cl- in urine
  • decrease ECF volume
  • activate SNS and RAAS
  • secondary hyperaldosteronism
  • ENaC activation (which reabsorbs Na)
  • negative charge in cortical collecting duct
  • loss of H+ (due to AGII and Aldo) and K+(due to Aldo) in urine
  • hypokalemia metabolic alkalosis
27
Q

what is natruiresis

A
  • excretion of sodium in the urine
28
Q

what mechanisms result in aldosterone escape

A
  • pressure natriuresis
  • atrial natriuretic peptide
  • down regulation of NaCl in DCT