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Pathophysiology > Partial 6 - Acid-Base Disorders > Flashcards

Partial 6 - Acid-Base Disorders Flashcards

1
Q

Hydrogen concentration in acidemia and alkalemia

A

Acidemia: H+ more than 45
Alkalemia: H+ less than 35

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2
Q

If pCO2 doubles while HCO3 remains constant

A

pH will drop by 0.3 units

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3
Q

If you reduce pCO2 by half

A

pH will rise by 0.3 units

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4
Q

If HCO3 doubles while pCO2 remains constant

A

pH will rise by 0.3 units

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5
Q

If you reduce HCO3 by half

A

pH will drop 0.3 units

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6
Q

Henderson hasselback equation states that

A

pH is equal to pK plus the log of the ratio of the concentration of a base to its related acid.

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7
Q

Normal concentration of bicarbonate

A

22-26 mmol/L

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8
Q

Normal concentration of CO2

A

35-45 mmHg

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9
Q

Normal concentration of hydrogen

A

40 nmol/L

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10
Q

What happens to the potassium concentration in acidemia and alkalemia and why?

A

Acidemia produces hyperkalemia, and alkalemia produces hypokalemia due to potassium being exchanged for hydrogen between the cell and extracellular fluid

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11
Q

Why can severe acidosis lead to osteodystrophy?

A

In severe acidosis the bones accept hydrogen and releases calcium

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12
Q

Anion gap

A

The measured ions are sodium (Na+), chloride (Cl-) and bicarbonate.

The formula goes like this: Na + UC = Cl + HCO3 + UA.

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13
Q

Unmeasured cations include

A

Potassium, calcium, and magnesium, and together these are 11 mEq/L.

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14
Q

Unmeasured anions include

A

Sulfates, phosphates, Albumin, Lactic acid, and organic acids which together are 23 mEq/L

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15
Q

Normal anion gap value

A

8-15

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16
Q

Causes of increased anion gap

A

Accumulation of organic acids (ketones, lactate)

Toxic ingestions (methanol, ethylene glycol, salicylates)

Reduced inorganic acid excretion (phosphates, sulfates)

Decrease in unmeasured cations (decreased in unmeasured cations leads to increased measured cation because the blood is electroneutral).

17
Q

Increased anion gap value

A

more than 18

18
Q

Decreased/Negative anion gap causes

A

Decreased proteins (mainly albumin); There is 2-2.5 mEq/liter drop in AG for every 1 g drop in albumin.

Other etiologies; High potassium, magnesium, calcium, increased globulins
Lithium, bromide or iodine intoxication

19
Q

Increased globulins happens in which disease

A

Multiple myeloma

Increased lithium and bromide is also seen in multiple myeloma

20
Q

Compensation in acid-base disorders are rarely complete. In which cases are they complete?

A

High altitude and pregnancy (chronic respiratory alkalosis)

21
Q

Respiratory compensation to metabolic acidosis

A

Compensated by hyperventilation, called “kussmaul respiration” which is more deep than rapid, which means that it has high tidal volume

22
Q

Respiratory compensation to metabolic alkalosis

A

Hypoventilation, and is this is restricted by hypoxemia

23
Q

Metabolic compensation in acute hypercapnia

A

bicarbonate increases 1 mmol/L for each 10 mmHg increase in pCO2 more than 40

24
Q

Metabolic compensation in chronic hypercapnia

A

Bicarbonate increases 3.5 mmol/L for each 10 mmHg increase in pCO2 more than 40

25
Q

Metabolic compensation in acute hypocapnia

A

Bicarbonate decreases 2 mmol/L for every 10 mmHg decrease in pCO2 less than 40

26
Q

Metabolic compensation in chronic hypocapnia

A

Bicarbonate decreases 5 mmol/L for every 10 mmHg decrease in pCO2 less than 40

27
Q

Effects of metabolic acidosis

A 
Vascular collapse
Impaired cardiac contractility
Increased pulmonary vascular resistance
Inability to respond to catecholamines
Decreased threshold for ventricular fibrillation
Decreased hepatic and renal perfusion.
28
Q

Effects of alkalemia

A

Generalized and cerebral vasoconstriction
Shift of oxyhemoglobin dissociation to left
Hypokalemia
Increased systemic vascular resistance
Decreased contractility
Cardiac arrhythmias refractory
Seizures.

29
Q

Types of lactic acidosis

A 
Type A (tissue hypoxia)
Type B (normal oxygen, Paucity in NAD+, or excess NADH)
30
Q

Causes of Type A lactic acidosis

A

(1) Toxins such as iron, isoniazid, CN, methgb, CO, HS, and toluene
(2) Shock states
(3) Profound anemia
(4) Massive catecholamines
(5) Hypoxia
(6) Anaerobic exertion, seizures, sprinting
(7) Beriberi, total parenteral nutrition, and alcoholics

31
Q

Causes of Type B lactic acidosis

A

(1) Diabetes mellitus
(2) Liver failure
(3) renal failure
(4) Carcinoma
(5) Hypoglycemia
(6) EtOH ingestion and many others

Increased NADH leads to increased reduction of pyruvate to lactate.

32
Q

Causes of ketoacidosis

A

It can be due to increase in FFA load to liver, or increased conversion of FFA to ketoacids. Increased conversion of FFA to ketoacids may occur in diabetic ketoacidosis, in alcoholism, and to a lesser degree in prolonged starvation or a high-fat diet

33
Q

Causes of normal aniongap metabolic acidosis

A

(1) Loss of bicarbonate such as in chronic diarrhea, pancreatic fistulas, post-hypocapnia, uretroileostomy, acetazolamide
(2) Failure to excrete hydrogen such as in renal tubular acidosis and adrenal insufficiency
(3) Administration of hydrogen such as ammonium chloride, arginine hydrochloride, or aminoacidhydrochlorides

34
Q

Types of renal tubular acidosis

A

RTA1 involves failure of distal tubules to excrete hydrogen properly, while RTA2 involves bicarbonate wasting in proximal tubules, and both lead to normal AG metabolic acidosis, with hypokalemia.

RTA4 is caused by lack of aldosterone and leads to hyperkalemia and acidemia.

35
Q

Causes of metabolic alkalosis

A

Hypochloremia
Alkali ingestion
Massive transfusion

36
Q

Causes of respiratory acidosis

A

Inadequate ventilation; (1) Head, chest, spinal cord trauma, (2) Sedative, hypnotics, (3) Neuropathy/myopathy, (4) Pulmonary disorder, (5) Airway obstruction, (6) Sleep apnea.

Increased dead space ventilation; (1) COPD.

Increased carbohydrate metabolism; (1) Total parenteral nutrition.

37
Q

Causes of respiratory alkalosis

A

1) Salicylates (stimulate medullary chemoreceptor)
(2) increased intracranial pressure
(3) Liver failure (due to NH3)
(4) hypoxia, CHF, pericardial effusion, pulmonary embolus
(5) hyperthyroidism (due to increased metabolism and CO2)
(6) pregnancy (progesterone increases ventilation and lowers arterial pCO2 by as much as 5-10mmHG)
(7) Sympathomimetics (amphetamines, cocaine, and phencyclidine)
(8) Hyperventilation, in shock, sepsis, trauma/pain, psychogenic/anxiety
(9) CNS disease.

Pathophysiology (20 decks)

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