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Renal Exam 2 > Renal Control of Acid-Base Balance > Flashcards

Renal Control of Acid-Base Balance Flashcards

1
Q
  • Volatile reactions that occur in the body
A
  • Aerobic glucose metabolism
  • Fat metabolism
  • Aerobic glucose metabolism
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2
Q
  • Fixed reactions that occur in the body
A
  • Cysteine metabolism
  • Phosphoprotein metabolism
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3
Q
  • An increase in 0.3 pH _ H+ concentration
A
  • Halves (pH and concentration of H+ are inversely related)
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4
Q
  • Arterial blood H+ concentration
  • Arterial blood H+
A
  • 4.0 x 10-5
  • 7.40
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5
Q
  • Venous blood H+ concentration
  • Venous blood pH
A
  • 4.5 x 10-5
  • 7.35
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6
Q
  • Interstitial fluid H+ concentration
  • Interstitial fluid pH
A
  • 4.5 x 10-5
  • 7.35
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7
Q
  • Intracellular fluid H+ Concentration
  • Intracellular pH
A
  • 1 x 10-3 to 4 x 10-5
  • 6.0-7.4
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8
Q
  • Urine H+ Concentration
  • Urine pH
A
  • 3 x 10-2 to 1 x 10-5
  • 4.5-8.0
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9
Q
  • What are the buffer systems of the body?
A
  • Bicarbonate
  • Hemoglobin
  • Phosphate
  • Plasma Proteins
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10
Q
  • What is the pK of the bicarbonate buffer system?
  • What does this represent?
A
  • 6.1
  • Half of the solution is H+ and half is H2CO3
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11
Q
  • What organs play a role in the buffer system?
A
  • Lungs
  • Kidney
  • Bone
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12
Q
  • H+ ions can be buffered by
A
  • Plasma proteins
  • Hemoglobin
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13
Q
  • If acidemia occurs, ICF does what to H+?
A
  • Takes in H+
  • Cell will take in H+ and kick K+ out of the cell
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14
Q
  • If alkalemia occurs, ICF does what to H+?
A
  • ICF donates H+
  • H+ raised in ECF
  • Lower ECF K+ by bringing it into cells
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15
Q
  • How does an increase in alveolar ventilation change pH?
A
  • An increase in alveolar ventilation increases pH
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16
Q
  • Of the bicarbonate filtered by the kidney, _ % is reabsorbed
  • Where does reabsorption of HCO3- occur?
A

99.9%

  • Reabsorption occurs in
    • PCT (85%)
    • Thick Ascending Limb of LOH (10%)
    • Collecting Duct (>4.9%)
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17
Q
  • How is bicarb reabsorbed in the proximal tubule?
A
  • Na+/H+ exchanger on the APICAL membrane pumps H+ into tubular fluid
  • H+ will combine with the HCO3- that has been filtered into the glomerulus
  • Via Carbonic acid, H2CO3 will be converted to H2O and CO2
  • H2O and CO2 will diffuse into the cell
  • Will combine AGAIN via carbonic anhydrase INTRACELLULARLY
  • H+ will be recycled back into tubular fluid
  • HCO3- will be reabsorbed via:
    • Na+/3HCO3- cotransporter on basolateral membrane
    • HCO3-/Cl- antiporter on basolateral membrane
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18
Q
  • How does phosphate buffering of secreted H+ ions work?
  • What does this buffer system help regenerate?
A
  • NaHPO4- in the tubular lumen combines with H+ that is secreted into the tubular lumen via that Na+/H+ exchanger on the basolateral membrane
  • This buffers the H+ ion and then NaH2PO4 is eliminated in the urine
  • Buffering of secreted H+ regenerates that plasma HCO3- that has been consumed elsewhere when the NaH2PO4 lost an H+ to a less acidid body compartment and now carries the H+ into the urine
19
Q
  • What is the most abundant AA in the bloodstream?
20
Q
  • Production, Transport, and Excretion of Ammonia by the Nephron for Generation of New Bicarbonate
A
  • Ammonium is transported by the NKCC in the TAL of the LOH on the APICAL membrane
  • It replaces K+ and diffuses into the cell where it is “ion trapped”
21
Q
  • Alpha intercalated cells are present in the _
  • They are responsible for the _ of H+ and _ of HCO3-
A
  • Collecting Ducts
  • SECRETION
  • REABSORPTION
22
Q
  • Beta intercalated cells are present in the _
  • They are responsible for the _ of H+ and the _ of HCO3-
A
  • Collecting duct
  • Reabsorb H+
  • Secrete HCO3-
23
Q
  • “New bicarbonate” is generated during the process of _ when secreted H+ is buffered by NH3, NH4+, phosphate, etc for excretion
A
  • Urinary acidification
24
Q
  • _ must equal nonvolatile adid production to maintain acid-base balance
A
  • NAE (Net Acid Excretion)
25
Q

_ synthesis and secretion is responsible for ~2/3 of NAE

A
  • Ammonium (NH4+)
26
Q
  • How do you calculate NAE?
27
Q
  • What is an Acid-Base Nomogram
A
  • Superimposed on Davenport DIagram Depicting HCO3, pH and PCO2
28
Q
  • How do you calculate ANION GAP?
  • What is a normal range?
A
  • ANION GAP=[Na+]-[Cl-]-[HCO3-]
  • Can be anywhere from 3-11 or 8-16 (use lab values provided on exam)
29
Q
  • Causes of metabolic acidosis (high anion gap)
A
  • MUDPILERS
  • M=Methanol
  • U=Uremia
  • D=DKA/Alcoholic KA
  • P=Paraldehyde
  • I=Isoniazid (tb tx)
  • L=Lactic Acidosis
  • E=EtOH/Ethylene Glycol
  • R=Rhabdo/Renal Failure
  • S=Salicylates
30
Q
  • Causes of non-anion gap metabolic acidosis
A
  • HARDUPS
  • H=Hypealimentation
  • A=Acetazolamide
  • R=Renal Tubular Acidosis
  • D=Diarrhea
  • U=Uretero-Pelvic Shunt
  • P=Post-Hypocapnia
  • S=Spironolactone
31
Q
  • Renal tubular acidosis
A
  • Accumulation of acid in the body d/t a failure of the kidneys to properly acidify the urine
32
Q
  • Type I RTA
A
  • Distal tubules
  • Acidosis
  • Hypokalemia
  • Failure of alphaH+ secretion by the intercalated cells
33
Q
  • Type 2 RTA
A
  • Occurs in the proximal tubule as a failure of the HCO3- channel on the basolateral surface to function, impairing HCO3- reabsorption
  • Now there is no bicarb buffer
  • Acidosis
  • Hypokalemia
34
Q
  • Type 4 RTA
A
  • Adrenal gland is not synthesizing aldosterone
  • HIGH K+
  • Decreases NH3 synthesis by the PT
35
Q
  • Sx associated with Metabolic Acidosis
A
  • Mild-asymptomatic
  • With pH <7.10:
    • Nausea
    • Vomiting
    • Malaise
  • See long breaths at a normal rate with respiratory compensation
36
Q
  • Causes of metabolic alkalosis
A
  • CLEVER PD
  • C-Volume Contraction
  • L-Licorice
  • E-Endo (Conn, Cushing, [Bartter])
  • V-Vomiting
  • E-Excess Alkali
  • R-Refeeding Alkalosis
  • P-Post-hypercapnia
  • D-Diuretics
37
Q
  • Physiologic/Biochemical Causes of Metabolic Alkalosis
A
  • Loss of H+
    • EX: Vomiting, Hyperaldosteronism
  • Gain of HCO3-
    • EX: Ingestion of NaHCO3, Milk-alkali syndrome
  • Volume contraction alkalosis
    • EX: Loop or thiazide diuretics
38
Q
  • Metabolic alkalosis symptoms
A
  • Mild-shows signs and symptoms of underlying cause
  • More severe-increased binding of Ca2+ and hypocalcemia
    • ​Headache, Lethargy, Neuromuscular excitability, Delirium, Tetany, Seizures
    • Lower threshold for angina sx, arrythmias
    • Possible weakness if hypokalemia is also present
39
Q
  • Causes of respiratory acidosis
A
  • CANS
  • C-CNS depression
  • A-Airway Obstruction
  • N=Neuromuscular Disorders
  • S=Severe pneumonia,embolism, edema

Chronic

COPD

Any disease leading to imparied ventilation

40
Q
  • Respiratory acidosis sx?
A
  • Acute
    • Headache
    • Confusion
    • Anxiety
    • Drowsiness
    • Stupor
    • Tremors
    • Convulsions
    • Possible Coma (CO2 Narcosis)
  • Slowly Developing, Stable
    • May be well tolerated
    • Memory loss
    • Sleep disturbances
    • Excessive daytime sleepiness
    • Personality changes
    • Gait disturbance
    • Tremor
    • Blunted DTRs
    • Myoclonic Jerks
    • Asterixis (Flapping Wrist)
    • Papilledema
41
Q
  • Causes of respiratory alkalosis
A
  • CHAMPS
  • C=CNS Disease
  • H=Hypoxia
  • A=Anxiety
  • M=Mechanical Ventilators
  • P=Progesterone
  • S=Salicylates, Sepsis
42
Q
  • Respiratory alkalosis sx?
A
  • Acute
    • Light headedness
    • Syncope
    • Confusion
    • Peripheral and circumoral paresthesias
    • Cramps
    • All of these are thought to be d/t changes in cerebral blood flow and pH
    • Tachypnea or hyperpnea is often the only sign
    • Severe-carpopedal spasm d/t decreased levels of Ca2+ (since it is driven inside of the cell in exchange for H+ coming out of the cell and bringing the blood pH back towards normal)
  • Chronic-asymptomatic

Renal Exam 2 (8 decks)

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