Metabolic Alkalosis

METABOLIC ALKALOSIS

Q. 1

A  55-yrs-old  male  presents  with prolonged epigastric pain and, severe vomiting.   Lab   evaluation   finds    that   his blood  pH  is  7.46,  while  his  serum  HCO3  is
30. PaC02 is 60. Most likely  diagnosis?
 A Metabolic    alkalosis    with     respiratory compensation
 B Mixed metabolic acidosis and metabolic alkalosis
 C Respiratory acidosis with renal compensation
 D Respiratory alkalosis with no compensation
Q. 1

A  55-yrs-old  male  presents  with prolonged epigastric pain and, severe vomiting.   Lab   evaluation   finds    that   his blood  pH  is  7.46,  while  his  serum  HCO3  is
30. PaC02 is 60. Most likely  diagnosis?
 A Metabolic    alkalosis    with     respiratory compensation
 B Mixed metabolic acidosis and metabolic alkalosis
 C Respiratory acidosis with renal compensation
 D Respiratory alkalosis with no compensation
Ans. A

Explanation:

•   The uncomplicated  acid-base disorders, which may be of metabolic or respiratory origin, are classified as being metabolic acidosis, metabolic alkalosis, respiratory acidosis, or respiratory alkalosis.The  pH (normal 7.38 to 7.44) determines whether the primary process is an acidemia (pH < 7.38) or an alkalemia (PH > 7.44). (Note that compensation  for an alkalosis is always acidosis, while compensation  for acidosis is always alkalosis, but in either case, compensation  does not bring the pH into the normal range.)

 

•     Bicarbonate  levels in metabolic acidosis are <21 mM, while those in metabolic alkalosis are >28 mM. Similarly, with respiratory disorders, examine the Pac02 (normal PC02 is 35 to 40 mmHg arterial, 40 to

45 mmHg venous). in patient with respiratory alkalosis the Pac02  is <35, while with respiratory acidosis the Pac02 is >40.

•   Patients with metabolic alkalosis lose acid, and this causes an increase in the blood pH the body compensates  for – this increased pH by decreasing the respiratory rate, which increases blood CO2  levels (hypercapnia)  and increases the renal excretion of bicarbonate.  Causes of metabolic alkalosis include vomiting

(losing gastric acid), increased aldosterone secretion (which causes increased [H· ] excretion by the kidneys), and certain diuretics.

•     In contrast, metabolic acidosis increases serum acid (increased hydrogen ion concentration),  which decreases serum pH and decreases serum bicarbonate concentration.  The causes of metabolic acidosis are broken down clinically into two groups: those with a normal anion gap and those with an increased anion gap. (The serum anion gap is found by taking the serum sodium concentration  and subtracting the concentration  of two anions, namely chloride and bicarbonate.

•     Normally, the anion gap is between 10 and 16 meq/L.) Increased anion gaps result from increased unmeasured anions, such as may occur in the following clinical situations: ketoacidosis  (increased beta- hydroxybutyric  acid and acetoacetic acid, seen with diabetic ketoacidosis);  lactic acidosis (hypoxic conditions); chronic renal failure (uremia); and ingestion of certain substances such as salicylates, ethylene glycol, methanol, and formaldehyde.

•   A normal anion gap metabolic acidosis may result from either loss of bicarbonate (diarrhea) or loss of renal regeneration  of bicarbonate,  seen with renal tubular acidosis type 1 (decreased excretion of titratable acid, i.e., NH and renal tubular acidosis type 4.

•   In a patient with metabolic acidosis, the body tries to combat the decreased pH by increasing the respiratory rate (tachypnea),  which helps to raise the pH by blowing off CO2  and decreasing the serum CO2 (hypocapnia).  The body also compensates  through renal mechanisms  that increase H excretion and increase bicarbonate reabsorption.


Q. 2

In severe metabolic alkalosis all are seen EXCEPT:

 A Pulmonary edema
 B

Hypoxia

 C Hypocalcaemia
 D

Tetany

Q. 2

In severe metabolic alkalosis all are seen EXCEPT:

 A Pulmonary edema
 B

Hypoxia

 C Hypocalcaemia
 D

Tetany

Ans. A

Explanation:

Pulmonary edema REF: Harrison 17th edition, chapter 48

With metabolic alkalosis, changes in central and peripheral nervous system function are similar to those of hypocalcaemia; symptoms include mental confusion, obtundation, and a predisposition to seizures, paresthesia, muscular cramping, tetany, aggravation of arrhythmias, and hypoxemia in chronic obstructive pulmonary disease. Related electrolyte abnormalities include hypokalemia and hypophosphatemia.


Q. 3

Which of the following metabolic abnormality is seen with long term use of loop diuretics?

 A

Metabolic acidosis

 B

Metabolic alkalosis

 C

Hyperkalemia

 D

None of the above

Q. 3

Which of the following metabolic abnormality is seen with long term use of loop diuretics?

 A

Metabolic acidosis

 B

Metabolic alkalosis

 C

Hyperkalemia

 D

None of the above

Ans. B

Explanation:

By inhibiting salt reabsorption in the TAL, loop diuretics increase delivery to the collecting duct.

Increased delivery leads to increased secretion of K+ and H+ by the duct, causing hypokalemic metabolic alkalosis.

This toxicity is a function of the magnitude of the diuresis and can be reversed by K+ replacement and correction of hypovolemia.

Ref: Katzung, 11th edition, Chapter 15.

Q. 4

Which is the MOST common biochemical abnormality seen in congenital pyloric stenosis?

 A

Hyperkalemic metabolic acidosis

 B

Hypokalemic metabolic acidosis

 C

Hyperkalemic metabolic alkalosis

 D

Hypokalemic metabolic alkalosis

Q. 4

Which is the MOST common biochemical abnormality seen in congenital pyloric stenosis?

 A

Hyperkalemic metabolic acidosis

 B

Hypokalemic metabolic acidosis

 C

Hyperkalemic metabolic alkalosis

 D

Hypokalemic metabolic alkalosis

Ans. D

Explanation:

Neonates with congenital pyloric stenosis develop projectile postprandial vomiting between 2 and 4 weeks of age but may start as late as 12 weeks.

Due to this vomiting they develop hypokalemic hypochloremic metabolic alkalosis. 

 
Congenital pyloric stenosis is more commonly found in males.

Projectile vomiting occurring in neonate is nonbilious.

On examination, the upper abdomen gets distended after feeding, and prominent gastric peristaltic waves can be seen from left to right.

An oval mass in the shape of an olive can be palpated in the right upper abdomen, especially after vomiting.

USG done in them shows a hypoechoic muscle ring greater than 4 mm thick with a hyperdense center and a pyloric channel length greater than 15 mm. 
 
Ref: CURRENT Diagnosis & Treatment: Pediatrics, 21e chapter 21.

Q. 5

The following are statements regarding Cushing Syndrome

 
1. Medullary carcinoma thyroid is a cause
2. Metabolic alkalosis and hypokalemia is seen
3. Mitotane is used to treat metastatic adrenal carcinoma
4. Late night salivary cortisol is effective in screening
5. Acne, amenorrhea and diabetes are some common manifestations
 A

1, 2, 3 – True & 4, 5 – False

 B

1, 5 – True & 2, 3, 4 – False

 C

4, 5 – True & 1, 2, 3 – False

 D

All are true

Q. 5

The following are statements regarding Cushing Syndrome

 
1. Medullary carcinoma thyroid is a cause
2. Metabolic alkalosis and hypokalemia is seen
3. Mitotane is used to treat metastatic adrenal carcinoma
4. Late night salivary cortisol is effective in screening
5. Acne, amenorrhea and diabetes are some common manifestations
 A

1, 2, 3 – True & 4, 5 – False

 B

1, 5 – True & 2, 3, 4 – False

 C

4, 5 – True & 1, 2, 3 – False

 D

All are true

Ans. D

Explanation:

Tumors responsible for ectopic secretion of ACTH are small cell carcinoma, bronchial carcinoid, medullary thyroid carcinoma, pancreatic carcinoma and pheochromocytoma. It can lead to Cushing’s syndrome.

Common clinical features of Cushing’s syndrome are central obesity with moon face, buffalo hump, thin extremities, muscle weakness, diabetes, hypertension, amenorrhea, osteoporosis, poor wound healing and psychosis.

Hypokalemia and metabolic alkalosis is seen particularly in patients with ectopic ACTH secretion. Earliest screening test for diagnosing Cushing’s syndrome is dexamethasone supression test. If its abnormal a high 24 hour urine free cortisol helps in confirming diagnosis. Late night salivary cortisol test have high sensitivity and specificity for Cushing’s syndrome.


Q. 6

In Metabolic alkalosis, which is true about excretion in urine?

 A

More of NH3

 B

Less of aceto acetic acid

 C

Betahydroxy butyric acid

 D

Less ammonia

Q. 6

In Metabolic alkalosis, which is true about excretion in urine?

 A

More of NH3

 B

Less of aceto acetic acid

 C

Betahydroxy butyric acid

 D

Less ammonia

Ans. D

Explanation:

Q. 7

Metabolic alkalosis is seen in all except –

 A

Thiazide diuretics

 B

Uretersigmoid_ostomy

 C

Prolonged vomiting

 D

Systemic antacid therapy

Q. 7

Metabolic alkalosis is seen in all except –

 A

Thiazide diuretics

 B

Uretersigmoid_ostomy

 C

Prolonged vomiting

 D

Systemic antacid therapy

Ans. B

Explanation:

B i.e. Uretersigmoidostomy


Q. 8

A child had repeated vomiting and developed metabolic alkalosis. The treatment given is ‑

 A

Ringer lactate

 B

I.V. normal saline and potassium

 C

ORS

 D

I.V. Normal saline

Q. 8

A child had repeated vomiting and developed metabolic alkalosis. The treatment given is ‑

 A

Ringer lactate

 B

I.V. normal saline and potassium

 C

ORS

 D

I.V. Normal saline

Ans. B

Explanation:

Ans. is ‘b i.e., I.V. Normal saline and potassium

Treatment of metabolic alkalosis due to vomiting or nasogastric suction.

o Most children with metabolic alkalosis have one of the chloride responsive etiology (e.g., vomiting).

o In these situations, administration of sufficeint sodium chloride and potassium chloride to correct volume deficit is necessary to correct metabolic alkalosis.

o Adequate replacement of gastric losses of sodium and potassium in a child with vomiting can minimize or prevent the development of metabolic alkalosis.

o With adequate intravascular volume and a normal serum potassium concentration, the kidney is able to excrete the excess bicarbonate within a couple of days.


Q. 9

In a case of hypertrophic pyloric stenosis, the metabolic disturbance is

 A

Respiratory alkalosis

 B

Metabolic acidosis

 C

Metabolic alkalosis with paradoxical aciduria

 D

Metabolic alkalosis with alkaline urine

Q. 9

In a case of hypertrophic pyloric stenosis, the metabolic disturbance is

 A

Respiratory alkalosis

 B

Metabolic acidosis

 C

Metabolic alkalosis with paradoxical aciduria

 D

Metabolic alkalosis with alkaline urine

Ans. C

Explanation:

Ans. is ‘c’ i.e., Metabolic alkalosis with paradoxical aciduria 

  • Repetitive vomiting leads to hypochloremic, hypokalemic metabolic alkalosis. The urine is alkaline initially but eventually it becomes acidic (paradoxical aciduria)
  • Cause of paradoxical aciduria

– Initially the kidney compensate for metabolic alkalosis by reabsorbing hydrogen and chloride ions in exchange for sodium, potassium and bicarbonate. But gradually as the body stores of sodium and especially potassium become depleted, kidney starts retaining these ions in exchange of hydrogen ions. thus the urine becomes acidic and metabolic alkaline state is further aggravated.


Q. 10

Persistent vomiting in G.O.O. causes –

 A

Hyponatremic hyperchloremia occur

 B

Hypernatremia without led Cl- alkalosis

 C

Hypokalemic metabolic alkalosis

 D

All

Q. 10

Persistent vomiting in G.O.O. causes –

 A

Hyponatremic hyperchloremia occur

 B

Hypernatremia without led Cl- alkalosis

 C

Hypokalemic metabolic alkalosis

 D

All

Ans. C

Explanation:

Answer is ‘c’ i.e. Hypokalemic metabolic alkalosis

  • Repetitive vomiting leads to hypochloremic, hypokalemic metabolic alkalosis. The urine is alkaline initially but eventually it becomes acidic (paradoxical aciduria)
  • Cause of paradoxical aciduria
  • Initially the kidney compensate for metabolic alkalosis by reabsorbing hydrogen and chloride ions in exchange for sodium, potassium and bicarbonate. But gradually as the body stores of sodium and especially potassium become depleted, kidney starts retaining these ions in exchange of hydrogen ions, thus the urine becomes acidic and metabolic alkaline state is further aggravated.



Q. 11

20 mEq (mmol) of potassium chloride in 500 ml of 5% dextrose solution is given intravenously to treat‑

 A

Metabolic alkalosis

 B

Respiratory alkalosis

 C

Metabolic acidosis

 D

Respiratory acidosis

Q. 11

20 mEq (mmol) of potassium chloride in 500 ml of 5% dextrose solution is given intravenously to treat‑

 A

Metabolic alkalosis

 B

Respiratory alkalosis

 C

Metabolic acidosis

 D

Respiratory acidosis

Ans. A

Explanation:

Ans. is ‘a’ i.e., Metabolic alkalosis 


Q. 12

The commonest cause of metabolic alkalosis is ‑

 A

Cancer stomach

 B

Pyloric stenosis

 C

Small-bowel obstruction

 D

Diuretics

Q. 12

The commonest cause of metabolic alkalosis is ‑

 A

Cancer stomach

 B

Pyloric stenosis

 C

Small-bowel obstruction

 D

Diuretics

Ans. B

Explanation:

Ans. is ‘b’ i.e., Pyloric stenosis 


Q. 13

In Accelerated HTN what is metabolic defect:

 A

Normal non-ionic metabolic acidosis

 B

Ionic gap met acidosis

 C

Hypomagnesemia

 D

Metabolic alkalosis

Q. 13

In Accelerated HTN what is metabolic defect:

 A

Normal non-ionic metabolic acidosis

 B

Ionic gap met acidosis

 C

Hypomagnesemia

 D

Metabolic alkalosis

Ans. D

Explanation:

Answer is D (Metabolic Alkalosis)

Accelerated Hypertension is associated with metabolic alkalosis.

Accelerated Hypertension is a state in which there is renal underperfusion, high renin and increased aldosterone. This may result in hypokalemia and metabolic alkalosis.


Q. 14

An adolescent male presents with Hypokalemia, Metabolic Alkalosis, Hypercalciuria and Nephrocalcinosis. His Blood Pressure is normal. The likely diagnosis is:

 A

Bartter Syndrome

 B

Gitelman’s Syndrome

 C

Liddle’s Syndrome

 D

Renal Tubular Acidosis

Q. 14

An adolescent male presents with Hypokalemia, Metabolic Alkalosis, Hypercalciuria and Nephrocalcinosis. His Blood Pressure is normal. The likely diagnosis is:

 A

Bartter Syndrome

 B

Gitelman’s Syndrome

 C

Liddle’s Syndrome

 D

Renal Tubular Acidosis

Ans. A

Explanation:

Answer is A (Bartter Syndrome):

Hypokalemic Metabolic Alkalosis with Hypercalciuria in a patient with normal blood pressure suggests a diagnosis of Bartter Syndrome.

Hypokalemic metabolic alkalosis with normal blood pressure may be seen in both Banter Syndrome and Gitelman’s Syndrome. Presence of Nephrocalcinosis from Increased Urinary excretion of Calcium is typically seen in Bartter’s

Syndrome and distinguishes Bartter’s Syndrome from Gitelman’s Syndrome (Decreased Urinary Calcium Excretion). Liddle’s Syndrome also causes Hypokalemic metabolic alkalosis but this disorder is typically associated with Hypertension (Blood Pressure is elevated)

Presentation

Diagnosis

Hypokalemic Metabolic alkalosis with Hypertension

Liddle’s Syndrome

Hypokalemic Metabolic Alkalosis without Hypertension

Banner Syndrome (Increased Urinary Ca Excretion)

Gitelman Is Syndrome (Decreased Urinary Ca Excretion)

 

Important Mfferences Between Bartter Syndrome and Gitelman’s Syndrome

Feature

Bartter Syndrome

Gitelman     Syndrome

Location of kidney defect

Ascending loop of Henle

(Mimics effects of loop diuretics)

Distal tubule

(Mimics effects of thiazides)

Urinary Calcium excretion

Normal or increased, commonly with nephrocalcinosis

Decreased

Serum Mg level

Normal Magnesium levels (May be decreased)

Decreased, sometimes greatly

Renal prostaglandin E2

production

Increased

Normal

Usual age at presentation

Before birth to early childhood, often with intellectual

disability and growth disturbance

Late childhood to adulthood

Neuromuscular symptoms

(e.g., muscle spasms, weakness)

Uncommon or mild

Common


Q. 15

Causes of metabolic alkalosis include all the following except :

 A

Mineralocorticoid deficiency

Recurrent vomiting

 B

Bartter’s syndrome

 C

Thiazide diuretic therapy

 D

Recurrent vomiting

Q. 15

Causes of metabolic alkalosis include all the following except :

 A

Mineralocorticoid deficiency

Recurrent vomiting

 B

Bartter’s syndrome

 C

Thiazide diuretic therapy

 D

Recurrent vomiting

Ans. A

Explanation:

Ans. is A Mineralocorticoid deficiency


Q. 16

Metabolic alkalosis is seen in all except :

 A

Thaizide diuretic therapy

 B

Prolonged vomiting

 C

Uretero-sigmoidostomy

 D

Cushing’s disease

Q. 16

Metabolic alkalosis is seen in all except :

 A

Thaizide diuretic therapy

 B

Prolonged vomiting

 C

Uretero-sigmoidostomy

 D

Cushing’s disease

Ans. C

Explanation:

Answer is C (Uretero-sigmoidostomy):

Ureterosigmoidostomy is a cause for normal anion gap type M eta bolic acidosis produced due to loss of bicarbonate in feces. All other options mentioned in the question are causes of metabolic alkalosis.


Q. 17

In a case of hypertrophic pyloric stenosis, the meta­bolic disturbance is:  

March 2004

 A

Respiratory alkalosis

 B

Metabolic acidosis

 C

Metabolic alkalosis with paradoxical aciduria

 D

Metabolic alkalosis with alkaline urine

Q. 17

In a case of hypertrophic pyloric stenosis, the meta­bolic disturbance is:  

March 2004

 A

Respiratory alkalosis

 B

Metabolic acidosis

 C

Metabolic alkalosis with paradoxical aciduria

 D

Metabolic alkalosis with alkaline urine

Ans. C

Explanation:

Ans. C i.e. Metabolic alkalosis with paradoxical aciduria


Q. 18

Symptoms of disease shown in Photograph is NOT characterized by

 A

 Hyponatremia 

 B

Hyperkalemia

 C

 Hypotension 

 D

Metabolic alkalosis

Q. 18

Symptoms of disease shown in Photograph is NOT characterized by

 A

 Hyponatremia 

 B

Hyperkalemia

 C

 Hypotension 

 D

Metabolic alkalosis

Ans. D

Explanation:

Ans is D  Metabolic alkalosis

These are the symptoms of addition’s Disease

Addison’s disease, also known as primary adrenal insufficiency and hypocortisolism, is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones.[1] Symptoms generally come on slowly and may include abdominal pain, weakness, and weight loss. Darkening of the skin in certain areas may also occur. Under certain circumstances, an adrenal crisis may occur with low blood pressure, vomiting, lower back pain, and loss of consciousness. An adrenal crisis can be triggered by stress, such as from an injury, surgery, or infection



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