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[Mine] core curric - 2016 > Ch 7.2: Acid-Base Disorders > Flashcards

Ch 7.2: Acid-Base Disorders Flashcards

1
Q

Acid

A

Substance that donates hydrogen ions (H+)

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2
Q

Base

A

Substance that accepts or combines with hydrogen ions

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3
Q

pH

A

Free H+ concentration that determines the acidity of body fluids

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4
Q

An increase in hydrogen ions → _ _ _ in pH
A decrease in hydrogen ions → _ _ _ in pH

A

An increase in hydrogen ions → decrease in pH
A decrease in hydrogen ions → increase in pH

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5
Q

Arterial blood pH range

A

7.35 to 7.45

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6
Q

“-emia”

Acidemia, Alkalemia

A

Refers to the measurement of pH in the blood
* Acidemia: pH below 7.35
* Alkalemia: pH above 7.45

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7
Q

“-osis”

Acidosis, Alkalosis

A

Refers to the clinical condition associated with the blood pH
* Acidosis: processes that raise H+ concentration
* Alkalosis: processes that lower H+ concentration

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8
Q

Mixed Acid-Base Disorders

A

disorders where acidotic and alkalotic processes may coexist

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9
Q

Body’s regulation of acid-base via 3 mechanisms

A
  1. Chemical buffering by extracellular (ECF) and intracellular (ICF) mechanisms
  2. Control of the partial pressure of CO2 (PCO2) in the blood by alterations in the rate and depth of ventilation
  3. Control of the serum bicarbonate (HCO3-) concentration by changes in renal H+ excretion and HCO3- reabsorption
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10
Q

Buffers

A

Prevent large changes in H+ concentration in the body

Buffers reversibly consume or release [H+] to maintain normal pH

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11
Q

Most abundant ECF buffer
& other buffer systems:

A

Carbonic acid/bicarbonate system

Others: plasma proteins, hemoglobin, phosphates

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12
Q

Lungs

A
  • Regulate the pressure excreted by CO2 gas in the blood (PCO2)
  • Begins to compensate for acid-base disturbances from diet/metabolism within minutes
  • Conditions that impair respiratory system function (opiate overdose can cause acid-base imbalances
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13
Q

Respiratory Acidosis/Alkalosis

pH and PCO2 levels

A

Respiratory Acidosis: ↓ pH ↑ PCO2
Respiratory Alkalosis: ↑ pH ↓ PCO2

Opposites

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14
Q

Metabolic Acidosis/Alkalosis

pH and PCO2 levels

A

Metabolic Acidosis: ↓ pH ↓ PCO2
Metabolic Alkalosis: ↑ pH ↑ PCO2

The same

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15
Q

Kidneys

A
  • Alterations in renal H+ excretion
  • Slowest mechanism to maintain acid-base balance

Two processes involved to achieve this:
1) Reabsorption of filtered HCO3 (bicarbonate)
2) Excretion of H+ produced daily as a result of protein metabolism

Only the kidneys can regulate alkaline substances in the blood and eliminate metabolic acids

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16
Q

Arterial blood gas (ABG)

A

reflect the ability of lungs to oxygenate blood

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17
Q

Venous blood gas (VBG)

A

reflect tissue oxygenation

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18
Q

PCO2

A

The acid component

Lung’s ability to excrete CO2
* Increases in PCO2 = acidosis
* Decreases in PCO2 = alkalosis

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19
Q

PO2

A

Ability of Hgb to carry oxygen
* Higher PO2 = more saturated Hgb is with oxygen

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20
Q

HCO3: bicarbonate

A

the base component

Changes are associated with metabolic processes that can lead to acid-base disorders
* Increases in HCO3 = alkalosis
* Decreases in HCO3 = acidosis

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21
Q

Steps to evaluate acid-base disorders

A

1) Assess the pH of blood
* Acidemic: pH <7.4
* Alkalemic: pH >7.4
* pH 7.4 = possible mixed acid-base disorder

2) Assess PCO2 to determine whether respiratory process is contributing to acid-base disorder
* High PCO2 = respiratory acidosis
* Low PCO2 = respiratory alkalosis

3) Assess serum HCO3 to determine whether a metabolic process may be contributing to an acid-base disorder
* High HCO3 = metabolic alkalosis
* Low HCO3 = metabolic acidosis

4) Calculate the anion gap to determine whether metabolic acidosis is present
* Critical in determining the etiology and treatment of the acid-base disorder

5) Determine whether the acid-base disorder is acute or chronic
* If compensation is not appropriate, the patient has a mixed acid-base disorder

22
Q

Compensatory Response
For respiratory disorders

A
  • Kidneys regulate HCO3- via alterations in renal HCO3- excretion
  • Compensation fully activated in 2 – 3 days
23
Q

Compensatory Response
For metabolic disorders

A
  • Lungs regulate PCO2 by altering the rate and depth of ventilation to allow for excretion of CO2 generated by diet and cellular metabolism
  • Compensation starts within minutes
24
Q

Respiratory Acidosis

A

Almost always results from decreased effective alveolar ventilation, NOT an increase in CO2 production

Hypoventilation

25
Q

Respiratory Acidosis
Acute Causes

A

Acute airway disorders
* Airway obstruction
* Asthma/COPD exacerbation

Acute central nervous system depression
* Drug overdose
* Head trauma
* Stroke
* Infections

Acute neuromuscular disorders
* Guillain-Barre
* Spinal cord injury
* Neuromuscular blocking agents

Acute respiratory disorder
* Pneumonia
* Pulmonary edema
* Pulmonary embolus
* Hemothorax
* Pneumothorax

Parenteral or enteral nutrition overfeeding
* Excess CHO calories in PN solutions can lead to increased CO2 production and potential difficulty in weaning from respirators

In setting of hypoventilation = retaining CO2 (acid)

26
Q

Respiratory Acidosis
Chronic Causes

acute & chronic

A
  • Asthma
  • COPD, emphysema
  • Obstructive sleep apnea
  • Hypoventilation syndromes
  • Diaphragmatic paralysis
  • Myasthenia gravis
  • Amyotrophic lateral sclerosis (ALS)
  • Spinal cord injury
  • Multiple sclerosis
  • Muscular dystrophy
  • Poliomyelitis
  • Kyphoscoliosis
  • Hypothyroidism

In setting of hypoventilation = retaining CO2 (acid)

27
Q

Respiratory Alkalosis

A

Occurs when effective alveolar ventilation is increased beyond the level necessary to eliminate metabolically produced CO2

Hyperventilation

Disease in which, due to reduced oxygen in blood (hypoxemia), the respiratory center is stimulated can result in respiratory alkalosis.

28
Q

Respiratory Alkalosis - Causes

A
  • Central nervous system disorders (anxiety, pain, infections, head trauma, malignancy, cerebrovascular disease)
  • Hypoxia, high altitudes
  • Lung disorder (Pneumonia, pulmonary edema, pulmonary embolism, asthma, hyperventilation, interstitial fibrosis)
  • Mechanical ventilation
  • Pregnancy
  • Sepsis
  • Medications (Xanthine derivatives, nicotine, catecholamines, salicylates)
  • Hepatic encephalopathy / cirrhosis

In setting of hyperventilation = blowing off CO2 (acid)

29
Q

Anion gap formula

A

= Na – (Cl + HCO3)

Decreased AG = decreased unmeasured anions (e.g., Albumin)

30
Q

_ _ _ can falsely decrease the anion gap

What is the formula to correct AG?

A
  • Hypoalbuminemia
  • = AG + 2.5 x (4.5 – measured albumin)

For 1g/dL decrease of Alb, 2.5 mEq/L must be added to the anion gap

31
Q

Anion gap

A

Used to differentiate the 2 main types of metabolic acidosis

  • Normal anion gap acidosis (hyperchloremic acidosis)
  • Elevated anion gap acidosis
32
Q

Normal anion gap acidosis (hyperchloremic acidosis)

A
  • mEq for mEq replacement of extracellular HCO3 by Cl
  • the anion gap doesn’t change because the sum of major anions remains constant
33
Q

Causes of normal anion gap acidosis (hyperchloremic acidosis)

USEDCAR

A
  • GI bicarb losses – diarrhea, pancreatic or SB fistula
  • Renal bicarb losses – type 2 renal tubular acidosis, hyperparathyroidism, hypoaldosteronism
  • Ingestion of ammonium chloride or PN containing chloride salts

USEDCAR
* Ureteroenterostomy (urinary diversion)
* Small bowel (pancreatic / biliary) fistula
* Excessive chloride salts (IVF / parenteral nutrition)
* Diarrhea
* Carbonic anhydrase inhibitors (acetazolamide) / chronic kidney disease
* Adrenal insufficiency / aldosterone deficiency / ammonium chloride
* Renal tubular acidosis

34
Q

Elevated anion gap acidosis

A

Accumulation of unmeasured anions → elevation in the anion gap

35
Q

Causes of elevated anion gap acidosis

GOLDMARK

A
  • Increased production of endogenous acids (lactic acidosis; ketoacidosis - diabetic, starvation, ETOH; inborn errors of metabolism)
  • Failure to excrete acids (renal failure)
  • Ingestion of exogenous acid (salicylates, methanol, ethanol)

GOLDMARK
* Glycols – ethylene and propylene
* Oxoproline (acetaminophen)
* Lactic acidosis
* D-lactate acidosis (small bowel bacterial overgrowth)
* Methanol
* Aspirin
* Renal failure
* Ketoacidosis – diabetic and starvation

36
Q

What should a PN formulation for a high-output ileostomy contain?

A
  • Maximum amounts of acetate salts to prevent or correct a hyperchloremic metabolic acidosis
  • The sodium concentration should be ~normal saline to approximate sodium concentration of the ileostomy fluid
37
Q

Metabolic Acidosis

A
  • Characterized by reduced pH, reduced HCO3
  • Compensatory hyperventilation → decreased PCO2 (acid)
38
Q

Metabolic Acidosis can be induced by 2 mechanisms:

A
  1. Inability of kidneys to excrete dietary H+ load
  2. Increase in the generation of H+ – either by addition of H+ or loss of HCO3
39
Q

Causes/examples in Metabolic Acidosis

A

Lactic acidosis (all cells produce lactic acid if deficient of oxygen; increased lactic acid production and resulting metabolic acidosis occur in any condition in which oxygen delivery to the tissues is severely compromised
* Cardiac arrest
* Any condition associated with hypovolemic shock (e.g. massive fluid loss)
* Liver failure – the liver plays a major role in removing the small amount of lactic acid that is produced during normal cell metabolism, so that lactic acidosis can be a feature of liver failure

Diabetic ketoacidosis (abnormally high blood concentrations of keto-acids)

Diarrhea – abnormal loss of bicarbonate from the body

Renal failure – failure to regenerate bicarbonate and excrete hydrogen ions

40
Q

Metabolic Alkalosis

A

Characterized by elevated pH, increased HCO3
* Compensatory hypoventilation → rise in PCO2

41
Q

Causes/examples in Metabolic Alkalosis

A
  • Loss of gastric acid (vomiting, NG suction)
  • Loss of intravascular volume and chloride 2/2 diuretic use
  • In hospital setting: overzealous treatment of metabolic acidosis with bicarb or an excess of acetate in the PN
  • Transcellular shift of H+ that occurs with severe hypokalemia
42
Q

How can severe potassium depletion cause metabolic alkalosis?

A

Due to the reciprocal relationship between hydrogen and potassium ions

43
Q

In normal circumstances, the kidneys can correct by …

A

excreting the excess HCO3 in the urine

44
Q

Urine chloride concentration:

A

is useful in differential diagnosis of metabolic alkalosis and predicts those who will respond to volume repletion

45
Q

Mechanisms to sustain metabolic alkalosis:

Volume-mediated processes (saline responsive)

  • Urine chloride level
  • Treatment
  • Causes
A

Urine chloride <20 mEq/L

Treatment: administration of half-isotonic or isotonic (0.9%) saline
* Will not reverse metabolic alkalosis r/t moderate to severe hypokalemia – only KCl administration will correct this disorder

Causes: GI loss, vomiting, NG suction, renal loss, diuretics, excessive bicarb administration, rapid correction of hypocapnia

46
Q

Mechanisms to sustain metabolic alkalosis:

Volume-independent processes (saline unresponsive)

  • Urine chloride level
  • Treatment
  • Causes
A

Urine chloride >20 mEq/L

High urinary chloride concentration

Typically associated with hyperaldosteronism

Treatment: management of underlying cause of mineralocorticoid (a class of steroid hormones that regulate salt and water balances) excess
* Aggressive potassium repletion with hypokalemia in setting of primary aldosteronism

Causes: excess mineralocorticoids, cushing’s syndrome, hyperaldosteronism, profound hypokalemia (<2mEq/L), excessive licorice ingestion (ex: from chewing tobacco)

47
Q

Mixed

A
48
Q

Examples of Mixed Acid-Base Disorders

A
  • High output fistula presenting with respiratory failure
  • Diabetic ketoacidosis (DKA) presenting with pneumonia
49
Q

A patient presents with a metabolic acidosis. Which ABG pattern fits this disorder?
A. Decreased pH, decreased HCO3-
B. Decreased pH, increased PCO2
C. Increased pH, increased HCO3-
D. Increased pH, decreased PCO2

Nutr Fundamentals - Acid Base ppt

A
50
Q

For a patient with metabolic acidosis, what is the appropriate method of compensation seen on an ABG?
A. Hyperventilation leading to an increase in pCO2
B. Hyperventilation leading to a decrease in pCO2
C. Hypoventilation leading to an increase in pCO2
D. Hypoventilation leading to an increase in pCO2

Nutr Fundamentals - Acid Base ppt

A
51
Q

Which of the following can lead to metabolic alkalosis?
A. Pulmonary embolism
B. Septic shock
C. High nasogastric output
D. Morphine overdose

Nutr Fundamentals - Acid Base ppt

A

[Mine] core curric - 2016 (22 decks)

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