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Renal > SM 200-201: Acid-Base > Flashcards

SM 200-201: Acid-Base Flashcards

1
Q

Definition of CKD

A

Persistent Loss of Function, unlikely to return to normal

Compensatory mechanisms invoked to improve physiological homeostasis, but may eventually fail

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2
Q

How do cells regulate pH? (What channels, what drugs block them)

A
  1. Na/H Antiport Exchange - MAIN one, most protective, blocked by amiloride
  2. Na dependent Cl/HCO3 exchanger - good for basic load
  3. Na independent Cl/HCO3 exchanger - both blocked by DIDS
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3
Q

How do kidneys reabsorb bicarb in the PT?

A
  1. CA produces H/HCO3 in cell
  2. Na/H antiporter (NHE3) and H-ATPase secrete H to lumen
  3. H binds filtered bicarb to H2CO3, converted to H2O/CO2 via CA
  4. CO2/H2O reabsorbed into cell, converted to HCO3/H by CA
  5. NBCe1A: key bicarb reabsorption across basal side, cotransporter with Na
    * bicarb reabsorption directly proportional to H secretion*
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4
Q

How do kidneys reabsorb bicarb in TAL?

A
  1. Cl/HCO3 exchanger on basolateral side
    CA inside cell generates H/bicarb; H secreted via Na/H exchanger (not ATPase) & H ATPase - CA outside cell not as necessary
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5
Q

How do kidneys reabsorb bicarb in CD?

A

NO Na/H EXCHANGER HERE
alpha-Intercalated Cell: H+ Secretion on apical side via H/K antiport ATPase and H ATPase - drives DE NOVO bicarb formation via CA in cell; HCO3 reabsorbed via basal HCO3/Cl Exchanger
beta-Intercalated Cell: Acid Reabsorption (Basal H ATPase), Base secretion (PENDRIN: HCO3/Cl exchanger apical) - activity increases in metabolic alkalosis

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6
Q

Factors influencing per-nephron load

A
  1. low birth weight = low # nephrons
  2. Obesity = more metabolism = higher GFR
  3. HTN = higher GFR
  4. Hx of AKI, higher risk of CKD
  5. Anemia = poor O2 delivery
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7
Q

How is ammonium formed/excreted in urine?

A

PT: glutamine metabolism produces NH3
NH3 diffuses to lumen, binds H+ from H/Na antiport and H ATPase to make NH4+
NH4+ trapped, drives HCO3 reabsorption through removing H+ from CA equation

TAL: NH4 can be reabsorbed like K in NKCC2 (helps with bicarb shuffling)

CD: more trapping through NH3 diffusion

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8
Q

How does bicarb reabsorption change with changes in volume? Aldosterone? Hypokalemia? Ang II?

A 
Volume Contraction (depletion) = stimulates bicarb reabsorption and H secretion (more Na/H exchanger activity)
Aldosterone/AngII/Hypokalemia: Stimulates bicarb reabsorption and H secretion (more Na/H exchanger activity due to wanting to reabsorb more Na) Aldo also causes more insertion of H+ ATPases into apical membrane - Na reabsorption balanced by H secretion
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9
Q

What is the henderson hasselbach equation?

A

pH = 6.1 + log(bicarb/(0.03*PCO2))

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10
Q

What are the three main mechanisms for metabolic acidosis?

A
  1. External Bicarb Loss: diarrhea, proximal RTA - loss of fx mutation in Na/solute cotransporter (includes bicarb, FANCONI - high wasting of glucose, P, uric acid, AA)
  2. Failure to Excrete Acid: CKD, distal RTA - loss of fx mutation in DT/CD alpha-intercalated cells - low H secretion/bicarb reabsorption - causes hypokalemia and hyperchloremia
  3. H+ buildup due to organic acid: lactic acidosis, diabetic ketoacidosis
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11
Q

What are the two types of Lactic Acidosis?

A

Type A: Increased Generation due to tissue hypoxia

Type B: Decreased Utilization due to liver failure, metformin medication, malignancy

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12
Q

Causes of high AG Metabolic Acidosis

A 
AG = (Na) - [bicarb + Cl]
MUDPILES
methanol
uremia (kidney failure)
diabetic ketoacidosis
propylene glycol
isoniazid
lactic acidosis
ethylene glycol
salicyclates
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13
Q

Causes of non-AG Metabolic Acidosis

A 
Adding Cl containing acid - NH4Cl, HCl
Bicarb wasting state - GI loss, proximal RTA, ureterostomy
Impaired renal secretion - distal RTA, renal insufficiency, hyperkalemia, aldosterone deficiency
USEDCARS
Uretero-enterostomy
Saline
Endocrine deficiency
Diarrhea
CA inhibitor
Ammonium Chloride
Renal Tubule Acidosis
Spironolactone
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14
Q

Urine Anion Gap: What is it? What does it tell you?

A

UAG: Na + K + NH4 = Cl
Use to determine if ammonium is being secreted, measure of kidneys’ response to metabolic acidosis
If NH4 abundant = diarrhea/extra-renal cause
If NH4 low = distal RTA

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15
Q

Causes of Metabolic Alkalosis

A

Loss of H+: GI Loss (vomiting, NG suction)
Kidney Loss: diuretics, aldosterone excess, barterr/gitelman’s - all cause hypokalemia/more Na/H exchange activity

Retention of bicarb: administration of NaHCO3 (antacids)

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16
Q

How to use urine electrolytes to differentiate types of metabolic acidosis?

A

Vomiting: Urine has low Cl, high K

Bartter’s and Diuretics: High Cl

17
Q

How does vomiting lead to metabolic alkalosis?

A

Vomit = lose H+ = stomach cells produce more H+ to secrete, producing more bicarb as byproduct - sent to blood = kidneys can’t excrete all the bicarb = alkalosis

18
Q

How to use urine chloride to differentiate metabolic alkalosis?

A

Low Urine Cl < 15: Saline Responsive - due to GI loss (vomiting, suction), adenoma

High Urine Cl > 20: Saline Resistant - due to alkali ingestion, bartter’s/gitelman’s, diuretics current use

19
Q

Why is the nephron especially vulnerable to injury?

A
  1. Concentrates toxins/metabolites
  2. Strong metabolic demands for transport
  3. Highly vascular
  4. High Throughput Filter
  5. Susceptible to Inflammation
20
Q

Progression of CKD pathogenesis

A

GFR drops = causes P to rise and Ca to fall = causes rise in PTH and FGF23 to lower P and increase Ca, eventually GFR falls too far

21
Q

Steps in Progressive Nephron Loss

A
  1. Remnant Nephron Hypertrophy (high SNGFR)
  2. Increased Filtered Load
  3. Increased Tubular Transport Work
  4. Increased Oxygen Utilization
  5. Tissue Hypoxia + Endothelial Dysfunction (further damage)
  6. Acidosis, ROS/HIF, Cell Stress, Inflammation
  7. Fibrosis and More Nephron Loss
22
Q

How do Acidosis, ROS/HIF, Cell Stress lead to fibrosis/nephron loss?

A

Acidosis: worsened by ischemia (anaerobic metabolism) - adaptive response is to increase acid secreting channels; maladaptive response is proinflammatory/profibrotic - more nephron loss - more ischemia - more acidotic

ROS - generated in response to hypoxia, causes off target oxidation/free radicals bad
HIF - increases fibrosis

Cell stress - inflammation, abnormal protein folding, protein catabolism, apoptosis

23
Q

Factors influencing per-nephron load

A
  1. low birth weight = low # nephrons
  2. Obesity = more metabolism = higher GFR
  3. HTN = higher GFR
    4.

Renal (23 decks)

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