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Renal II, Exam 3 > acid/base disorders > Flashcards

acid/base disorders Flashcards

1
Q

acidemia vs. acidosis

A

Acidemia is a decreased blood pH (normal is 7.36-7.44)

Acidosis is a clinical process in the body that decreases blood pH

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2
Q

alkalemia vs. alkalosis

A
  • alkalemia = increased blood pH

- alkalosis = clinical process in body that increases blood pH

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3
Q

hyperkapnia

A

increased pCO2 in blood

hypokapnia = low pCO2

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4
Q

minute ventilation

A

rate by which air reaches alvoli

= RR x Tidal volume

hyperventilation = increased minute ventilation

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5
Q

hyperventilation

A

= hypokapnia

hypoventilation = hypercapnia

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6
Q

metabolic disorders

A

follow pH

decrease in pH = decrease in Hco3- = metabolic alkalosis

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7
Q

compensation

A

resp = w/in hours

metabolic = w/in 2-3 days

  • if resp. disorder if over 3 days old, then it it most likely metabolic compensation
  • chronic resp. disorders are fully compensated and pH is close to normal after 3 days
  • subacute resp. disorders = partially compensated, 2 days
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8
Q

anion gap

A

A.G.=Na+– HCO3- - Cl-

MUDPILES:
Methanol
Uremia (End Stage Renal Disease)
Diabetic ketoacidosis
Paraldehyde
Infection, Iron, Isoniazide
Lactic acidosis
Ethylene glycol (antifreeze), alcohol
Salicylates, starvation ketoacidosis
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9
Q

Uremic acidosis

A

Occurs when renal function is severely decreased (Creatinine clearance is less than 25ml/min)

Due to:
decreased excretion of acids
decreased excretion of H+
Decreased reabsorption/synthesis of HCO3

Accumulation of organic and inorganic anions:
Phosphates
Sulfates

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10
Q

Causes of Lactic Acidosis

A

caused due to anaerobic metabolism in tissues due to:

  • hypoxemia
  • hypotension/sepsis
  • peripheral vessel blockage
  • anemia
  • hypoperfusion of vital organs

Medications: METFORMIN!

  • Liver failure due to decreased clearance
  • Thiamine deficiency in alcoholics
  • Hypophosphatemia
  • Sepsis (decreased perfusion of tissues, impaired gluconeogensis and poor clearance)
  • seizures: due to release of lactate from mm.
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11
Q

diabetic ketoacidosis

A

insulin deficiency ==> increased lypolysis –> FA delivery to liver –> production of ketones –> acidosis

  • associated w/ hyperglycemia
  • more often assoc. with Type 1 DM
  • may be caused by patients non-compliance w/ insulin, infection and pancreatitis
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12
Q

alcoholic ketoacidosis

A

ethanol intake –> ketone production

  • main difference b/w DM ketoacidosis = NO hyperglycemia
  • high osmol gap (normal is less than 10)
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13
Q

osmol gap

A

(normal is less than 10)
= Difference between measured serum Osmolality and calculated serum osmolality

Calculated Osmolality = 2 (Na+) + (Glucose/18) + BUN/2.8

OG should be equal to Ethanol level/4.6 – if it is more than this, then need to look for other alcohols
If OG more than that, look for other alcohols (alcohols that are in cleaning supplies, etc.)

  • used to determine cause of alcoholic ketoacidosis
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14
Q

other alcohol poisoning?

A
  1. Ethylene glycol: antifreeze, increased OG, calcium oxalate crystals in urine, acute renal failure common
  2. Methanol: found in wood alcohol and windshield fluid, causes blindness and acute renal failure, increased OG
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15
Q

salicylate poisoning

A

usually due to accidental or intentional overdose

may cause metabolic acidosis or respiratory alkalosis

Sx: hemorrhage, fever, nausea, vomiting, diaphoresis, tinnitus, pulmonary edema

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16
Q

normal AG metabolic acidosis

A
  1. Diarrhea or illeal drainage with stomach bypasses (due to loss of HCO3)
  2. Decreased reabsorption of HCO3 by renal tubules (“renal loss”): due to diuretics, or renal tubular acidosis
  3. increase in anion intakes
  4. large amount of NaCl (expansion acidosis) - due to dilution of bicarb and decreased renal bicarb reabsorption as result of volume expansion
17
Q

RTA I

A

renal tubular acidosis type I (distal) = low pH, kidney stones, hypokalemia

  • Decreased hydrogen ions excretion in the collecting ducts leading to alkaline urine and acidic serum
  • Increased calcium excretion and decreased citric acid concentration leading to kidney stone formation
  • Increased potassium loss leading to hypokalemia
18
Q

RTA II

A

Proximal renal tubular acidosis

  • acidosis: acidic urine, no kidney stones, hypokalemia
  • defect in bicarb reabsorption in proximal tubule, so more bicarb is excreted –> increased bicarb in urine
  • increased Ca2+ in urine, doesn’t lead to kidney stones, due to normal citric acid concentration
  • distal tubules work OK, ability to acidify urine in response to acidemia is intact, so urine pH is low
  • high K+ loss also leads to hypokalemia
19
Q

RTA IV

A

distal hyperkalemic acidosis
* see hyperkalemia and metabolic acidosis

  • occurs in patients w/ moderate chronic renal failure
  • insufficient aldo production
20
Q

urinary anion gap

A

UAG = Na + K - Cl

  • used to differentiate b/w renal and extrarenal HCO3 loss (RTA vs diarrhea)
  • Negative = extra renal loss, diarrhea (bicarb not lost in urine, but kidney increases excretion of ammonia to compensate for acidosis caused by diarrhea)
  • due to high level of unmeasured NH4+, excretion of NH4+ by healthy kidneys is compensatory mechanism for acidosis
  • Positive = non-existant in renal loss
  • due to low level of NH4+ and increased level of HCO3
21
Q

what causes respiratory alkalosis?

A 
hyperventilation- usually acute
pain
anxiety
Salicylates overdose
Fever
Sepsis
Hypoxia from some pulmonary disorders:
CHF
Pneumonia
PE
Mild asthma
Mechanical ventilation
22
Q

what causes metabolic alkalosis?

A

Vomiting/NG suction
- Due to lose of hydrochloric acid

Contraction alkalosis due to increased HCO3- reabsorption

  • Dehydration
  • Diuresis (with diuretics other than CAI)

Hypokalemia
- Due to resulting increased mineralocorticoid secretion

Recent correction of chronic respiratory acidosis
- Due to recent metabolic compensation.

23
Q

Kussmaul breathing

A

a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also renal failure. It is a form of hyperventilation, which is any breathing pattern that reduces carbon dioxide in the blood due to increased rate or depth of respiration.

24
Q

what do you see clinically with metabolic acidosis?

A

Kussmaul breathing, vomiting, arrhtymias and hypotension, confusion, lethargy, coma

25
Q

what is seen clinically w/ respiratory acidosis?

A
  • ineffective respiration/respiratory distress

- arrhthmias/hypotension, confusion, lethargy, coma (hypercapnic), CO2 narcosis

26
Q

whats seen clinically w/ metabolic alkalosis?

A
  • decreased respiration (compensatory) may lead to hypoxia
  • parasthesia, tingling, carpopedal spasm due to secondary hypocalcemia, spasm in forearm
  • confusion
  • seizures
  • dizziness
  • coma
  • weakness
27
Q

clinically w/ respiratory alkalosis?

A
  • hyperventilation, parasthesia, dizziness
28
Q

step wise approach to ABG

A
  1. Look at pH: acidemia (7.4).
  2. Look at HCO3- to determine if primary process is metabolic or respiratory.
  3. Determine if process is compensated (chronic), uncompensated (acute), or partially compensated (somewhere in between)
  4. Calculate anion gap to classify the metabolic acidosis or to determine if there is a mixed disorder with other types of acid-base disturbances
  5. If anion gap is present, Calculate delta-delta gap to find mixed disorders
  6. If metabolic disorder, look at pCO2 to determine if additional respiratory process exist.
  7. Refer back to clinical picture and see if your calculations make any clinical sense

Renal II, Exam 3 (9 decks)

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