Metabolic & Acid-Base Balance

1- When lactic acid accumulates, body will respond by:

a) Decrease production of bicarbonate
b) Excrete C02 from the lungs
c) Excrete Chloride from the kidneys
d) Metabolize lactic acid in the liver

During power exercises such as sprinting, when the rate of demand for energy is high, lactate is
produced faster than the ability of the tissues to remove it and lactate concentration begins to rise.
This is a beneficial process since the regeneration of NAD+ ensures that energy production is
maintained and exercise can continue. The increased lactate produced can be removed in a number
of ways including
 oxidation to pyruvate by well-oxygenated muscle cells which is then directly used to fuel the
Krebs cycle,
 conversion to glucose via gluconeogenesis in the liver and release back into the circulation, see
the Cori cycle.

2- What is the initial management of acute hypercalcemia?

a) Correction of exter-cellular fluid (by adequate rehydration)

- The first step in the management of acute hypercalcemia should be:

A. Correction of deficit of Extra Cellular Fluid volume.
B. Hemodialysis.
C. Administration of furosemide.
D. Administration of mithramycin.
E. Parathyroidectomy.

 The initial step in the care of severely hypercalcemic patients is hydration with saline.
Hydration helps decrease the calcium level through dilution. The expansion of extracellular
volume also increases the renal calcium clearance. The rate of fluid therapy is based upon the
following:
1. Degree of hypercalcemia
2. Severity of dehydration
3. Ability of the patient to tolerate rehydration - Vigilance to prevent volume overload is
critical.
4. Hydration is ineffective in patients with kidney failure because diuresis is impossible.
Dialysis is necessary to correct hypercalcemia in patients with renal failure.
 Loop diuretics
1. A loop diuretic (eg, furosemide) may be used with hydration to increase calcium excretion. This
may also prevent volume overload during therapy.
2. In contrast to loop diuretics, avoid thiazide diuretics because they increase the reabsorption of
calcium.
 Bisphosphates - These agents will inhibit osteoclast activity for up to a month.

3- All of the following signs or symptoms are characteristics of an extracellular fluid volume
deficit except: means dehydration
A. Dry, sticky oral mucous membranes.
B. Decreased body temperature.
C. Decreased skin turgor.
D. Apathy.
E. Tachycardia.
Extracellular Fluid Volume Deficit
 ECFVD is loss of extracellular fluids: interstitial, intravascular, gastric etc.
 Sodium is a major extracellular electrolyte whose primary function is to regulate body fluid.
 Osmolarity is the osmotic pull exerted by all particles per unit of solution: Hyper-osmolar, Hypo-
osmolar, Iso-osmolar fluid volume deficits.
Cinical Manifestations Mild ECFVD for the average adult
 2% weight loss
 2 liter of water loss. Aging population at particular risk having little water reserve.
 Thirst
 Apprehension
Moderate ECFVD for the average adult
 5% weight loss
 3-5 liters of water loss
 Marked thirst with flushed skin.
 Restlessness
 Dry mucous membranes & poor turgor
 Inc. pulse, Inc. resps., decreased systolic B/P of 10-15 mm Hg when standing, & narrowing of pulse
pressure.
Severe ECFVD for the average adult
 8% weight loss
 5-10 liters of water loss
 Marked thirst & cold, clammy skin
 Lethargic, irritable, delirium, disorientation
 Dry mucous membranes & poor turgor
 Tachycardia, tachypnea, systolic B/P < 70, decreased CVP
 Labs- serum osmolality > 295, and serum sodium . BUN ᡖ, Hgb > 18, Hct > 55% &PWP < 6mm Hg.

Apathy (also called impassivity or perfunctoriness) is a state of indifference, or the suppression of emotions
such as concern, excitement, motivation and passion. An apathetic individual has an absence of interest or
concern to emotional, social, or physical life. They may also exhibit an insensibility or sluggishness. The
opposite of apathy is flow.[

4- Blood pH
a) high after diarrhea
b) low after vomiting
c) more in Rt atrium than Lt atrium
d) lower in Rt atrium than Lt ventricle
e) lower in renal vein than renal artery
Causes of Metabolic Acidosis
With increased anion gap, these causes include:
1. Lactic acidosis (from inadequate tissue oxygenation, hepatic failure, neoplasms)
2. Ketoacidosis (from diabetes, starvation, alcoholism)
3. Poisons/drugs (salicylates, methanol, ethylene glycol)
4. Renal failure (chronic, end-stage disease) With normal anion gap, these causes include:
5. Renal tubular disorders (renal tubular acidosis, potassium-sparing diuretics, hypoaldosteronism)
6. Loss of base (diarrhea, carbonic anhydrase inhibitors, ureterosigmoidoscopy, pancreatic fistula)
7. Excess acid intake (ammonium chloride, cationic amino acids)

Causes of Metabolic Alkalosis

Disorders include:
1. Volume loss with chloride depletion (vomiting, gastric drainage, diuretics, villous adenoma)
2. Hypermincralocorticoid states (exogenous steroid treatment, primary aldosteronism. Cushing's syndrome,
renovascular disease)
3. Severe potassium deficiency
4. Excess alkali intake (milk-alkali syndrome, bicarbonate administration)

Causes of Respiratory Acidosis

Disorders include:
1. Acute respiratory failure (drug intoxication, cardiopulmonary arrest)
2. Chronic respiratory failure (chronic obstructive pulmonary disease, neuromuscular disorders, obesity)

Causes of Respiratory Alkalosis

Disorders include:
1. Hypoxia stimulating hyperventilation (asthma, pulmonary edema, pulmonary fibrosis, high altitude, congenital
heart disease)
2. Increased respiratory drive (pulmonary disease, anxiety, salicylate intoxication, cerebral disease, fever)
3. Cirrhosis, pregnancy
4. Excessive mechanical ventilation

Transport of Hydrogen Ions between Tissues and Lungs

To repeat, as blood flows through the tissues, a fraction of oxyhemoglobin loses its oxygen to become deoxyhemoglobin,
while simultaneously a large quantity of carbon dioxide enters the blood and undergoes the reactions that generate bicarbonate and
hydrogen ions.

What happens to these hydrogen ions?

Deoxyhemoglobin has a much greater affinity for H_ than does oxyhemoglobin, and so it binds (buffers) most of the hydrogen ions
(Figure 15–28). Indeed, deoxyhemoglobin is often abbreviated HbH rather than Hb to denote its binding of H _. In effect, the reaction
is HbO2 _ H_ 34 HbH _ O2. In this manner, only a small number of the hydrogen ions generated in the blood remains free. This
explains why the acidity of venous blood (pH _ 7.36) is only slightly greater than that of arterial blood (pH _ 7.40).As the venous
blood passes through the lungs, all these reactions are reversed. Deoxyhemoglobin becomes converted to oxyhemoglobin and, in the
process, releases the hydrogen ions it had picked up in the tissues. The hydrogen ions react with bicarbonate to give carbonic acid,
which dissociates to form carbon
dioxide and water, and the carbon dioxide diffuses into the alveoli to be expired. Normally all the hydrogen ions that are generated in
the tissue capillaries from the reaction of carbon dioxide and water recombine with bicarbonate to form carbon dioxide and water in
the pulmonary capillaries. Therefore, none of these hydrogen ions appear in the arterial blood. But what if the person is
hypoventilating or has a lung disease that prevents normal elimination of carbon dioxide? Not only would arterial PCO2 rise as a result
but so would arterial H_ concentration. Increased arterial H_ concentration due to carbon dioxide retention is termed respiratory
acidosis. Conversely, hyperventilation would lower the arterial values of both PCO2 and H_ concentration, producing respiratory
alkalosis. In the course of describing the transport of oxygen,
carbon dioxide, and H_ in blood, we have presented multiple factors that influence the binding of these substances by hemoglobin.
They are all summarized in Table 15–8. One more aspect of the remarkable hemoglobin molecule should at least be mentioned—its
ability to bind and transport nitric oxide. As described in Chapters 8, 14, and 20 respectively, nitric oxide is an important
neurotransmitter and is also released by endothelial cells and macrophages. A present hypothesis is that as blood passes through the
lungs, hemoglobin picks up and binds not only oxygen but nitric oxide
synthesized there, carries it to the peripheral tissues, and releases it along with oxygen. Simultaneously, via a different binding site
hemoglobin picks up and catabolizes nitric oxide produced in the peripheral tissues. Theoretically this cycle could play an important
role in determining the peripheral concentration of nitric oxide and, thereby, the overall effect of this vasodilator agent. For example,
by supplying net nitric oxide to the periphery, the process could cause additional
vasodilation by systemic blood vessels; this would have effects on both local blood flow and systemic arterial blood pressure.
6- All cause recent loss of weight, except:
• AIDS
• Cancer
• Nephritic syndrome
• Kwashiorkor

5 -In a patient with weight loss, all can be a cause except:

a) Thyrotoxicosis.
b) Nephrotic syndrome.
c) TB.
d) AS.
Causes of unintentional weight loss

Cancer, a very common and sometimes fatal cause of unexplained (idiopathic) weight loss.
About one-third of unintentional weight loss cases are secondary to malignancy. Cancers to
suspect in patients with unexplained weight loss include gastrointestinal, prostate,
hepatobillary (hepatocellular carcinoma, pancreatic cancer), ovarian, hematologic or lung
malignancies should be considered in any patient presenting with unexplained weight loss.

AIDS can cause weight loss and should be suspected in high-risk individuals presenting
with weight loss.

Gastrointestinal disorders are another common cause of unexplained weight loss - in fact
they are the most common non-cancerous cause of idiopathic weight loss. Possible
gastrointestinal etiologies of unexplained weight loss are celiac disease, a fairly common
and well-known disease caused by intolerance of gluten, peptic ulcer, inflammatory bowel
disease (crohns disease and ulcerative colitis), pancreatitis, gastritis, diarrhea and many
other GI conditions can cause weight loss.

Infection. Some infectious diseases can cause weight loss. These include fungal illness,
endocarditis, many parasitic diseases, AIDS, and some other sub-acute or occult infections
may cause weight loss.

Renal disease. Patients who have uremia often have poor or absent appetite, emesis and
nausea. This can cause weight loss.

Cardiac disease. Cardiovascular disease, especially congestive heart failure, may cause
unexplained weight loss.

Pulmonary disease.

Connective tissue disease

Neurologic disease, including dementia[4]

6- The most common cause of hypercalcaemia in a hospitalized patient is:

a. Dietary, such as milk-alkali syndrome.
b. Drug related, such as the use of thiazide diuretics.
c. Granulomatous disease.
d. Cancer.
e. Dehydration
7- Hyperkalemia is characterized by all of the following except:
a) nausea and vomiting.
b) Peaked T-waves.
c) Widened QRS complex.
d) Positive Chvostek sign.
e) Cardiac arrest in diastole.
Hyperkalemia
Causes are outlined in Table 2-4; in most cases, hyperkalemia is due to
1. decreased renal K+ excretion.
2. However, increases in dietary K+ intake can have a major effect in susceptible pts, e.g., diabetics with hyporeninemic
hypoaldosteronism and chronic kidney disease.
3. Drugs that impact on the renin-angiotensinaldosterone axis are also a major cause of hyperkalemia, particularly given recent trends
to coadminister these agents, e.g., spironolactone or angiotensin receptor blockers with an ACE inhibitor in cardiac and/or renal
disease.

The first priority in the management of hyperkalemia is to

1. assess the need for emergency treatment (ECG changes and/or K + ≥6.0 mM).
2. This should be followed by a comprehensive workup to determine the cause (Fig. 2-3).
3. History and physical examination should focus on medications (e.g., ACE inhibitors, NSAIDs, trimethoprim /sulfa-methoxazole),
diet and dietary supplements (e.g., salt substitute), risk factors for acute kidney failure, reduction in urine output, blood pressure,
and volume status.
4. Initial laboratory tests should include electrolytes, BUN, creatinine, serum osmolality, Mg 2+, and Ca2+, a complete bloodcount,
and urinary pH, osmolality, creatinine, and electrolytes. A urine [Na +] <20 meq/L suggests that distal Na + delivery is a limiting
factor in K+ excretion; volume repletion with 0.9% saline or treatment with furosemide may then be effective in reducing serum
[K+] by increasing distal Na+ delivery. Serum and urine osmolality are required for calculation of the TTKG. The expected values
of the TTKG are largely based on historic data: <3 in the presence of hypokalemia and >7–8 in the presence of hyperkalemia.
8- Normal daily caloric intake is:
a) 0.3 kcal/kg
b) 1.3kcal/kg
c) 2.Okcal/kg
d) 3.Skcal/kg
e) 35kcallkg

Recommended daily calorie intake varies from person to person, but there are guidelines for calorie
requirements you can use as a starting point.

UK Department of Health Estimated Average Requirements (EAR) are a daily calorie intake of
1940 calories per day for women and 2550 for men.

Reference Daily Intake - Wikipedia, the free encyclopedia - Reference Daily Intake (or
Recommended Daily Intake) (RDI ... For people 4 years or older, eating 2,000 calories per ...
agencies to direct citizens' nutritional intake also took food .....

9-Hypokalemia occurs with all except:

a) Metabolic alkalosis.
b) Acute tubular acidosis.
c) Chronic diarrhea.
d) Hyperaldosteronism.
e) Furosemide.