SUBJECT: BIOCHEMISTRY

TOPIC: EVALS 12 SET M

LECTURER: DR.BALLESTEROS

DATE: MARCH 2011

Micronutrients (5 pts.) are the only ones included in this evaluation. (nos. 56-69)
item
answer explanation
number

56 a HYPOKALEMIC: The med student is Hypokalemic because she has a serum potassium level of 2.1 mmol/L
which is below normal. (Refer to next number.)
57 b The normal range for plasma K is 3.5-5mmol/L.
DIARRHEA and VOMITING could cause hypokalemia.
Potassium is the major intracellular cation in the body that is found widely in vegetables which means that we
can take in K by eating high-K foods (RDA=2000mg). This also means that we can lose K through the GIT (by
58 b excessive vomiting, severe diarrhea, using laxatives, and having callous adenoma)!
Also, excretion of K could also be by urination (diuretics, Conn’s tumor, licorice, Cushing’s syndrome –
adrenocortical hyperfunction).
Remember that potassium excretion increases when there is excessive dietary intake of sodium.
59 d ALL OF THE ABOVE  Sweet potato, banana, orange juice are good sources of Potassium.
IODINE is the mineral most essential in synthesis of thyroxine, a thyroid hormone.
Here’s the table for other microminerals:
Elements Metabolic Function Deficiency
Chromium Potentiate the effect of Impaired glucose
insulin metabolism
Cobalt Constituent of B12 Macrocytic anemia
Copper Constituent of oxidase Microcytic
enzymes hypochromic
anemia
Iron Absorption and
metabolism Depigmentation of
skin and hair
Fluoride Constituent of bone and Dental Carries
teeth
Iodine Constituent of thyroid Cretinism, goiter
hormone
Iron Constituent of heme Microcytic anemia
60 d and non-heme
compounds
Manganese Cofactor for number of Not well defined
enzymes eg. Arginase
and carboxylase
Molybdenum Constituent of xanthine Xanthinuria
oxidase, sulfite oxidase
and aldehyde oxidase
Selenium Antioxidant, cofactor for Cardiomyopathy
glutathione peroxidase,
protects against cell
membrane, lipid
peroxidation
Zinc Cofactor for enzymes in Growth failure,
DNA, RNA and protein impaired wound
synthesis, constituent of healing and loss of
insulin, carbonic appetite
anhydrase,
carboxypeptidase,
alcohol dehydrogenase
CALCIFEROL stimulates the absorption of calcium.
Calcium absorption is dependent on Vitamin D (Calciferol is the active form), because with its presence,
Calcium binding proteins in the intestinal epithelial cells are formed. The body responds to low blood calcium
by producing Parathyroid Hormone (PTH). PTH’s primary action is to increase blood calcium by bone
61 a resorption, secondarily by converting Vit D to 1,25-dihydroxycalciferol in the small intestine (duodenum –
increase dietary Ca absorption).
Calcium absorption is high during growth, pregnancy and lactation.
On the other hand, high blood Calcium stimulates the thyroid gland to produce Calcitonin. As a result, there is
decreased osteoclastic activity in the bones, increase renal calcium excretion by the kidneys, and decreased

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 Ca absorption by the intestines.
LYSYL OXIDASE’s activity is reduced when there is the deficiency in copper.
62 d
Copper is a constituent of oxidase enzymes (Refer to table in no. 60).
CALCIUM DEFIENCY PRODUCES BRITTLE BONES CALLED SCURVY. (FALSE!)
SCURVY is brought about by the deficiency in Vitamin C not by Calcium.
According to Wikipedia, Ascorbic acid is needed for a variety of biosynthetic pathways, by accelerating
hydroxylation and amidation reactions. In the synthesis of collagen, ascorbic acid is required as a cofactor for
63 c prolyl hydroxylase and lysyl hydroxylase. These two enzymes are responsible for the hydroxylation of the
proline and lysine amino acids in collagen. Hydroxyproline and hydroxylysine are important for stabilizing
collagen by cross-linking the propeptides in collagen. Defective collagen fibrillogenesis impairs wound healing.
Collagen is also an important part of bone, so bone formation is also affected. Defective connective tissue
also leads to fragile capillaries, resulting in abnormal bleeding. (Thanks wiki!! )
SELENIUM has a sparing action on Vitamin E. It forms the active site of glutathione peroxidase. This enzyme in
64 d
the presence of selenium converts Vit C and Vit E radicals in their unharmful form.
65 d ALL OF THE ABOVE.  Iron, Copper and Cobalt are minerals that can cause anemia. (Refer to table.)
CHROMIUM potentiates the effect of Insulin, that is why it is known to be the Glucose Tolerance Factor. (Refer
66 a
to table.)
ALL OF THE ABOVE.
Calcitriol’s action to increase plasma calcium is by:
1. Absorption of Calcium from INTESTINE
 (+) Differentiation of absorptive mucosal cells
 (+) Transcription of genes encoding proteins involved in Ca absorption and transport
2. Reabsorption of Calcium from KIDNEY
67 d Increases Ca retention via:
 (+) Transcription of genes encoding proteins involved in Ca++ uptake and transport
3. Mobilization of Calcium from the BONE (bone resorption)
Increases Ca release from matrix via:
 (+) osteoclast differentiation and proliferation
 (+) osteoclast activity (synthesis/secretion of matrix degrading enzyme)
*Calcitriol is the active form of Vitamin D.
ALL OF THE ABOVE.  Tobacco smoking, malnutrition, and estrogen deficiency are risk factors for
osteoporosis.
Osteoporosis Prevention:
 A balanced diet rich in
o Calcium (1000mg <50, 1200mg >50)
68 d
o Vitamin D (400 – 800 mg)
 Weight-bearing exercise – promotes bone density
 A healthy lifestyle with no smoking or excessive alcohol intake and
 Bone density testing and medication when appropriate
 Hormonal replacement therapy (HRT) in menopausic women: estrogens, calcitonin
The answer should’ve OSTEOPETROSIS because, unlike osteoporosis, osteomalacia, osteogenesis imperfecta,
and rickets, it is characterized by an increase in bone mass.
Total mukha naming puro calcium tinatanong, ito na oh…
Hypercalcemia Hypocalcemia
o Serum calcium level exceed 11.0 mg/dL o Serum calcium level less than 8.5 mg/dl
 Normal serum calcium level is 9-11 o Causes:
mg/dl  Reduction in serum albumin
o Causes:  Hypoparathyroidism
 Primary hyperparathyroidism: most  Renal diseases and renal failure
common for OPD  Psuedohypothyrodism
-May be due to  Hypoparathyrodism? lolz
o Familial  Osteomalacia and rickets
o Hyperplasia – increase in the  Magnesium deficiency
69 number of chief cells in  Drug induced (foscarnate:
BONUS parathyroid gland cytomegalovirus retinitis (AIDS)
(hmmm)
o Tumors (multiple adenomas,  Osteoporosis
parathyroid carcinoma, solitary o Adult Bone loss
adenoma) o Condition where the bones
o Ectopic Hyperthyroidism become fragile and porous
 Malignancy o Characterized by low bone mass
-Due to: and structural deterioration of
o Humoral Factors (HHM – Humoral bone tissue, leading to bone
Hypercalcemia of malignancy) fragility and increase susceptibility
o Direct skeletal involvement by the to fractures of the hip, spine &
tumors wrist
o Haematological malignancies o “Silent disease”: no symptoms
 Drug Induced until a fracture occurs
 Other endocrine causes o Higher rate of bone resorption
 Overdosage compared to bone deposition

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