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FA17 Nephrology > Acid Base Disorders > Flashcards

Acid Base Disorders Flashcards

1
Q

acids produced by the body (+source) (4)

A
  1. sulfuric, phosphoric and uric acids - metabolism
  2. ketone bodies - fat oxidation
  3. lactic acid - anaerobic glucose metabolism
  4. carbonic acid - dissolved CO2
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2
Q

normal pH of body

A

7.38-7.42

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3
Q

mechanisms body uses to maintain alkaline pH

A
  1. buffer system of blood
  2. lungs regulate carbonic acid concentration
  3. kidneys regulate bicarb concentration
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4
Q

normal ratio bicarb/carbonic acid

A

20 parts bicarb to 1 part carbonic acid

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5
Q

carbonic acid

A

H2CO3

CO2 + H2O conversion by carbonic anhydrase in kidney

dissociates into H+ and bicarbonate ions

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6
Q

renal control of pH (H+)

A

H+ ions enter renal tubule in exchange for sodium ions

sodium enters plasma with HCO3

maintains concentration of sodium w/in body and removes acid

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7
Q

metabolic acidosis lab valvues

A

low pH

low bicarbonate

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8
Q

metabolic alkalosis

A

high pH

high bicarbonate

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9
Q

respiratory acidosis

A

low pH

high pCO2

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10
Q

respiratory alkalosis

A

high pH

low CO2

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11
Q

acidosis symptoms (CNS)

A

DEPRESSION of CNS

cardiac arrhythmia (hyperK)

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12
Q

alkalosis symptoms (CNS)

A

EXCITED CNS

altered mental status, spasm, contraction, seizures

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13
Q

acidosis symptoms (cardiac, vascular, pulmonary)

A

decreased CO, arrhythmias, increased risk of VFib

vasodilation/HoTN

vasoconstriction in lungs, hyperventilation (move blood thru faster and unload CO2)

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14
Q

alkalosis symptoms (cardiac, vascular, pulmonary)

A

increased contractility (then decrease) refractory ventricular arrhythmia

coronary vasospasm/constriction

vasodilation of pulmonary vasculature, hypoventilation (move blood thru slower)

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15
Q

acidosis symptoms (Neuro, endocrine)

A

confusion, coma

insulin resistance, inhibitor of ATP synthesis

hyperkalemia

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16
Q

alkalosis symptoms (Neuro, endocrine)

A

cerebral vasoconstriction – HA, lethargy, tetany, seizures

hypokalemia (all low electrolytes)

stimulation of anaerobic glycolysis/lactic acid production

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17
Q

acid base disturbance with normal ABG

A

compensatory acid base disorders often develop to counteract

however, the body NEVER overcorrects

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18
Q

2 things req. for diagnosing acid base problems

A

arterial blood gas
basic metabolic panel

clinical presentation often clues you in

management is focused on correcting UNDERLYING cause

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19
Q

pH values

normal, panic

A

normal: 7.35-7.45
panic: <7.3, >7.6

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20
Q

pCO2 values

normal, panic

A

norm: 35-45 mmHg

Panic: <20 or >70

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21
Q

HCO3 values

normal, panic

A

normal: 22-26
panic: <10, >40

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22
Q

venous blood gas

A

convert venous sample measurements to arterial if this is what is given

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23
Q

steps in approaching an acid base problem

A
  1. academia or alkemia?
  2. respiratory or metabolic?
  3. acute or chronic (if respiratory)?
  4. anion gap? (metabolic acidosis)
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24
Q

respiratory acidosis patho

A

increased pCO2

lungs fail to excrete carbon dioxide –> retention leads to rise in pCO2 in plasma

increased formation of carbonic acid and lowered pH

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25
Q

compensatory mechanisms of respiratory acidosis

A

stimulate kidney to make more bicarb

hold onto bicarb and excrete acid

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26
Q

respiratory acidosis lab values (clinical)

A

pH: low
pCO2: high
HCO3: elevated

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27
Q

causes of respiratory acidosis

A

sleep apnea

stroke

choking

pneumonia

CNS depressive meds (opioids)

rib fracture/chest wall trauma

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28
Q

respiratory alkalosis

A

hyperventilation which lowers plasma carbonic acid

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29
Q

respiratory alkalosis compensatory

A

increasing renal excretion of bicarbonate

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30
Q

respiratory alkalosis labs

A

pH high
pCO2 low
HCO3 normal to low

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31
Q

causes of respiratory alkalosis

A

hypoxia (hyperventilation, high altitude)

CNS problems (pregnancy, gram - sepsis)

Pulmonary (PE)

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32
Q

increased amount of plasma bicarb

A

metabolic alkalosis

often has concomitant K+ depletion and volume contraction

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33
Q

metabolic alkalosis compensatory mechanisms

A

decreased RR

inefficient bc can’t decrease RR enough to cure the issue

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34
Q

what induces metabolic alkalosis

A

diuretic therapy

loss of gastric secretions (vomiting or nasogastric suction)

large amounts of exogenous alkali

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35
Q

elevation in plasma bicarbonate concentration can result from

A

hydrogen loss

hydrogen movement into cells

alkali administration

volume contraction

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36
Q

increased net bicarbonate reabsorption by kidney

A

volume and potassium depletion

prevents excess bicarbonate from being excreted, worsening alkalosis

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37
Q

why does volume depletion cause increased renal bicarbonate?

A

kidney tries to hold onto Na+ to increase free water

therefore, kidney reabsorbs sodium bicarbonate from tubule and water follows

38
Q

potassium depletion increases metabolic alkalosis by:

A
  1. hydrogen loss

2. H+ movement into cells

39
Q

hydrogen loss in metabolic alkalosis

A

potassium depletion causes distal pumps in kidney secrete H+ in exchange for K+

40
Q

movement of hydrogen into cells worsens metabolic alkalosis by

A

H+ is moved into cells to move K+ out

intracellular environment is acidotic, so H+ secretion by kidneys increases

also raises plasma bicarb concentration, H+ is no longer in serum suffer

41
Q

kidney compensation for K+ loss is ba bc

A

tries to correct volume contraction by absorbing sodium bicarbonate and excreting hydrogen

worsens alkalosis

req. simultaneous correction of K+ def.

42
Q

etiologies of metabolic alkalosis (6)

A
  1. GI acid loss
  2. renal acid H+ loss
  3. post-hypercapnia alkalosis
  4. milk-alkali syndrome
  5. administration of exogenous alkali
  6. metabolic contraction alkalosis
43
Q

metabolic alkalosis from GI acid loss

A

H+ in stomach is removed (vomiting or suctioning off) but no stimulation to stop producing bicarbonate

therefore:

net hydrogen loss and bicarbonate is still being produced/reabsorbed from kidney (decreased H w/o decreased HCO3)

44
Q

metabolic alkalosis renal acid loss is caused by which hormone?

A

aldosterone

45
Q

high levels of aldosterone cause

A
  1. stimulation of H+ secretion in renal tubule
  2. tubule lumen is more electronegative so Na+ reabsorption is not = to H+ loss

distal K+ secretion is enhanced, resulting in concurrent hypokalemia

46
Q

renal acid loss metabolic alkalosis

A

typically presents in pts on loop diuretic or TZD

increase in H+ secretion and volume contraction = metabolic alkalosis

47
Q

post hypercapnic metabolic alkalosis

A

COPD/acidosis pts hold onto bicarbonate to control mild respiratory acidosis

the acidosis is rapidly fixed but kidney doesn’t get stimulation to decrease Bicarb causing metabolic alkalosis

48
Q

metabolic alkalosis due to milk alkali syndrome results when

A
  1. increased alkaline load (oral calcium)
  2. hypercalcemia-mediated constriction of afferent arteriole, induces renal AKI

too much bicarb + increased base going in + kidney can’t get rid of excess

49
Q

metabolic alkalosis due to administration of exogenous alkali

A

giving large amounts of sodium bicarbonate or citrate

  1. blood infusion (>8 units)
  2. citrate rather than heparin to anticoagulant
  3. extensive use of crack cocaine
  4. FFP administration during plasmapheresis
  5. correction alkalosis
50
Q

metabolic contraction alkalosis

A

loos of relatively large volume of bicarbonate free fluid

contraction of extracellular volume around constant quantity of extracellular bicarbonate

51
Q

what causes metabolic contraction alkalosis

A

use of IV loop diuretics

underlying electrolyte disorder coupled with high chloride loss

52
Q

saline responsive metabolic alkalosis patients vitals

A

normotensive, volume contracted and hypokalemic

53
Q

saline unresponsive patient vitals

A

normo or hypotensive

fluid overloaded

54
Q

causes of saline responsive metabolic alkalosis

A

renal causes (diuretic use, post-hypercapnia alkalosis)

GI causes (vomiting/suctioning/diarrhea, exogenous alkali)

55
Q

diuretic use and saline responsive metabolic alkalosis

A

high NaCl and H2O loss from meds cause contraction of vascular volume and relative concentration of HCO3 increases

56
Q

treatment of saline responsive metabolic alkalosis

A
  1. correction of volume depletion with normal saline

2. correction of potassium depletion

57
Q

correction of volume depletion in saline metabolic alkalosis

A

less bicarb and sodium reabsorbed, no longer volume contracted

more bicarbonate secreted by kidney

58
Q

correction of potassium depletion in saline metabolic alkalosis

A

K+ moves into cells, H+ moves out

increased extracellular H+ buffers

H+ leaving the cell causes pH to return to normal (stop kidney secretion of H+ and reabsorption of bicarb)

59
Q

causes of in saline non responsive metabolic alkalosis

A

hyperaldosteroneism (kidney retains sodium and H+ is excreted)

milk alkali syndrome

60
Q

treatment of in saline unresponsive metabolic alkalosis

A
  1. if pt is hypokalemic, KCl will correct both hypokalemia dn alkalosis
  2. Acetazolamide (diamox) = inhibits renal sodium bicarb reabsorption and causes diuresis
61
Q

mechanisms of metabolic acidosis

A
  1. increased acid generation (ketoacidosis and lactic acidosis)
  2. loss of bicarbonate (diarrhea) or bicarbonate precursors (ketoacidosis)
  3. diminished renal excretion
62
Q

amount of acid produced exceeds body’s buffering capacity

A

metabolic acidosis

fall in concentration of bicarbonate bc it is consumed in neutralization of excess acid

63
Q

etiologies of metabolic acidosis

A
  1. intestinal loss of bicarb
  2. renal tubular acidosis
  3. excessive acid production/diminshed excretion
  4. lactic acidosis
  5. poisons
64
Q

metabolic acidosis due to intestinal loss of bicarb

A

too much acid precursor without bicarbonate excretion

65
Q

metabolic acidosis due to RTA

A

genetic defect: kidney can’t excrete adequate H+ or reabsorb adequate HCO3

three types (I, II, IV)

hyperchloremic, metabolic acidosis w/o anion gap

normal GFR, no diarrhea

66
Q

uremia and metabolic acidosis

A

AKI or late stage CKD

failing kidneys can’t excretion acids from normal metabolism

67
Q

ketosis and metabolic acidosis

A

metabolism of fat produces excess ketone bodies and decreases bicarbonate precursors

found in DM, starvation, alcohol

68
Q

lactic acid is normally produced?

A

by RBCs, skeletal muscles, skin, and brain

metabolized by liver and kidney

69
Q

when does accumulation of lactic acid occur?

A 
tissue hypoxia (over production) 
hepatic failure (deficient removal) 
circulatory collapse

esp. seen in sepsis, bowel or extremity infarction, respiratory failure, seizures

70
Q

main clinical feature of lactic acidosis?

A

hyperventilation

this is due to the compensatory mechanisms

this level exceeds 4-5 meq/L

71
Q

poisons that can cause metabolic acidosis

A 
carbon monoxide 
cyanide
ethylene glycol 
methanol 
meds
72
Q

meds that cause metabolic acidosis (5)

A

iron

isoniazid

metformin

ibuprofen

salicylates

73
Q

carbon monoxide

A

odorless, colorless gas from exhaust, fire

comes from improperly ventilated heater/appliances

CO has a large affinity for HgB 250x that of oxygen – therefore CO never unloads

74
Q

10-20% carboxyhemoglobin

A

HA, dizziness, abd pain or nausea

75
Q

30-40% carboxyhemoglobin

A

confusion, dyspnea, syncope

76
Q

50-60% carboxyhemoglobin

A

HoTN, coma, seizures

survivors may have permanent neurological deficits

77
Q

treatment of CO poisoning

A

high flow oxygen

HBO

78
Q

Cyanide poisoning (patho, symptoms, tx)

A

cells fail to take up arterial oxygen

HA, nausea, abdominal pain, dizziness, confusion, shock, seizures, death

tx: cyanide antidote package

79
Q

where is cyanide found?

A 
industry 
labs 
apricot pits 
nitroprusside 
fires of burning plastics (firefighters)
80
Q

methanol poising

A

wood alcohol

organic solvent found in paint remover, industrial cleaners, and perfumes

81
Q

when does methanol become harmful

A

metabolized to formaldehyde and then formic acid which accumulates metabolic acidosis and several adverse effects

82
Q

methanol intoxication occurs byL

A

children ingesting poisons accidentally

alcoholics substituting methanol for ethanol

bootleg alcohol

inhalation of methanol fumes by factory workers

83
Q

effects of methanol

A

rapid retinal edema and permanent vision loss

development of parkinsonism like movement disorder due to accumulation of formic acid in the putamen

84
Q

methanol toxicity workup

A

anion gap metabolic acidosis
osmolar gap

methanol levels are detected, but not accurate

if severe symptoms (vision loss) hemodialysis is indicated

85
Q

ethylene glycol toxicity

A

found in antifreeze and radiator fluid, taste sweets

occurs due to accidental ingestion, suicide attempts

its appear drunk and develop severe anion gap acidosis, tachypnea, confusion, seizures and coma

86
Q

ethylene glycol toxicity workup

A

serum calcium level and UA looking for calcium oxalate crystals

profound anion gap acidosis and hypocalcemia

87
Q

tx for methanol/ethylene glycol

A

ethanol - actual booze
fomepizole (antizol or 4MP) - preferred

slow conversion of methanol or ethylene glycol to toxic metabolites, therefore allowing them to be excreted

hemodialysis is also one

88
Q

anion gap

A

sorry out cause of metabolic acidosis

represents unmeasured anions in serum sample

Na - (HCO3 + Cl), normal value is 8-16

89
Q

why is the anion gap useful?

A

bc irregardless of pH or HCO3 levels

presence of increased anion gap always means there is underlying anion gap metabolic acidosis

90
Q

decreased anion gap

A

low level of negative ion charge
BAM

Bromisim
Albumin
Multiple Myeloma

91
Q

normal anion gap

DURHAM

A 
DURHAM 
Diarrhea 
Ureteral diversion 
Renal Tubular acidosis 
Hyperalimentation 
Addison's disease/Acetazolemide 
Miscellanous
92
Q

increased anion gap

A 
MUD PILES 
Methanol 
Uremia 
DKA/Drugs (metformin) 
Phosphate/paraldehyde 
Ischemia/Iron
Lactate 
Ethylene Glycol 
Starvation

FA17 Nephrology (13 decks)

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