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Modules 4-5 Activity 5 Explanations

This document contains a module activity checking understanding of biochemistry concepts with multiple choice questions and rationales. It addresses topics like enzymes, cofactors, vitamins, and their roles in biochemical processes and effects of deficiencies. For example, it explains that thiamine pyrophosphate is the active form of thiamine and a coenzyme involved in carbohydrate metabolism, and thiamine deficiency can cause Wernicke-Korsakoff syndrome in alcoholics. It also notes that cyanocobalamin injections treat vitamin B12 deficiency from various causes like pernicious anemia.

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0% found this document useful (0 votes)
425 views7 pages

Modules 4-5 Activity 5 Explanations

This document contains a module activity checking understanding of biochemistry concepts with multiple choice questions and rationales. It addresses topics like enzymes, cofactors, vitamins, and their roles in biochemical processes and effects of deficiencies. For example, it explains that thiamine pyrophosphate is the active form of thiamine and a coenzyme involved in carbohydrate metabolism, and thiamine deficiency can cause Wernicke-Korsakoff syndrome in alcoholics. It also notes that cyanocobalamin injections treat vitamin B12 deficiency from various causes like pernicious anemia.

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You are on page 1/ 7

Course Code: BIO 024 (Biochemistry/Biomolecules)

Module #4

Name: ____________________________________________________________ Class number: _______


Section: ____________ Schedule: ____________________________________ Date: _______________

Module 4 - Activity 5: CHECK FOR UNDERSTANDING RATIONALE

1. B, Rationale: Formula of enzyme reaction: E + S <- -> ESC -> E + P


2. A, E, Rationale: As the reaction proceeds, it is available for substrate binding and that enzyme is
increasingly interacting with the substrate until such saturation level is achieved.
3. B, E Rationale: Since the enzyme saturation curve is achieved, all of the enzyme’s active site are
occupied.
4. B, Rationale: Increasing the enzyme concentration beyond point C causes the reaction to proceed
in an increasing or higher level.
5. B, E, Rationale: At high temperatures, the rate of enzyme action decreases because the increased
heat would alter the active site of the enzyme or if not denatures the protein part of the enzyme
causing the reaction to slow down or stop eventually if no more enzyme is actively available for
catalysis.
6. D, Rationale: Proenyzme- a biologically inactive substance which is metabolized into an
enzyme.
7. C, Rationale: AST, or aspartate aminotransferase, is one of the two liver enzymes. It is also
known as serum glutamic-oxaloacetic transaminase, or SGOT. AST is a protein made by liver
cells. Both aminotransferases are highly concentrated in the liver. AST is also diffusely
represented in the heart, skeletal muscle, kidneys, brain and red blood cells, and ALT has low
concentrations in skeletal muscle and kidney; an increase in ALT serum levels is, therefore, more
specific for liver damage. ALT aka SGPT. but since ALT is Alalanine aminoTRANSFERASE, and the
question as for TRANSAMINASE, then the best answer is SGPT - serum glutamic pyruvic
TRANSAMINASE.
8. D, Rationale: CKM isoenzyme that is an important marker in the diagnosis of AMI. Since CK-MB
form of an enzyme found primarily in heart muscle cellsCK-MB is one of three forms (isoenzymes) of
the enzyme creatine kinase (CK). These isoenzymes include: CK-MM (found in skeletal muscles and
the heart) CK-BB (found in the brain). Cardiac troponins are: Troponin I and T are sensitive markers
of cardiac injury. Troponin I is found solely in the cardiac muscle, and Troponin T is found in both
cardiac and skeletal muscle.
9. D, Rationale: Enzymes are chemically, proteins and rarely ribonucleic acids.
10. B, F Rationale: The apoenzyme is the protein part of the conjugated enzyme activated by a cofactor
to form holoenzyme. Simple enzyme: are made up of only protein (polypeptide). They contain no
chemical groups other than amino acid residues. Such enzymes are known as simple enzymes, e.g.,
pepsin, trypsin, steapsin.
Coenzyme (Ex. Prosthetic group): the organic cofactor of a conjugated enzyme
Metal-ions: the inorganic cofactor of the unconjugated enzyme
Holoenzyme: the biologically active enzyme
11. B, Rationale: competitive inhibitor can be reversed by increasing substrate concentration. If the
substrate predominates in the mixture, it will tend to displace the inhibitor bound to the enzyme.
12. A, Rationale: enzyme speeds up a chemical reaction by 103-108 times by lowering the energy of
activation. In general, the lower the free energy of activation, the more molecules have sufficient
energy to pass through the transition state, and, thus, the faster the rate of the reaction. Coversely,
with high (ΔG) free energy of activation, the rates of uncatalyzed chemical reactions are often slow.
13. C, Rationale: Absolute specificity is the property of some enzymes only to convert a single substrate
into one or more substances. Catalase, an absolute specific enzyme, acts as the catalyzing enzyme
in the decomposition of the harmful substance in the liver hydrogen peroxide.

This document is the property of PHINMA EDUCATION


Course Code: BIO 024 (Biochemistry/Biomolecules)
Module #4

Name: ____________________________________________________________ Class number: _______


Section: ____________ Schedule: ____________________________________ Date: _______________

14. A, E Rationale: Line B shows competitive and reversible inhibitor. That when a substrates are
increased Vmax can still be achieved. The effect of a competitive inhibitor is reversed by increasing [S].
At a sufficiently high substrate concentration, the reaction velocity reaches the Vmax observed in the
absence of inhibitor.
15. B, Rationale: Allosteric enzymes also are enzymes with two or more protein chains and two kinds
of binding sites
16. A,B,E, Rationale: The relationship between an enzyme and a reactant molecule can best be
described as complementary temporary association or transient in reaction most of the time
17. A, Rationale: oxidoreductase enzyme (oxidases, oxygenases, peroxidases) are enzymes that
catalyze the transfer of electrons from one molecule (the oxidant, the hydrogen or the electron
donor) to another molecule (the reductant, the hydrogen or electron acceptor).
18. C, Rationale: Isomerases are enzymes that catalyze the formation of a substrate's isomer. In other
words, they facilitate the transfer of specific functional groups intramolecularly without adding or
removing atoms from the substrate. This conversion can be simply represented in the form A → B,
where A and B are isomers.
19. B,E Rationale: Vitamin C as a supplement here act as a coenzyme or an organic cofactor which
may enhance the action of Homogenistic acid oxidase enzyme to reverse alkaptonuria.
20. E, F, Rationale: Cellulase are for cellulose and sucrase are for sucrose. Decarboxylase,
Hexokinase, Peptidase and Ligase are example of non-substrate specific.
21. D, E, Rationale: Hexokinase and Oxidoreductase are non-substrate specific.
22. B, Rationale: Because it shows normal substrate and enzyme reactions.
23. D, E, F, Rationale: Graph D shows that the enzyme concentration is a limiting factor.
Meaning, as the substrate concentration increases with a steady concentration of the enzyme, the
enzymes will be saturated. Hence, with an increasing enzyme concentration, saturation level will be not
permitted.
24. B,C,D, Rationale: The rate of reaction of salivary amylase would be affected once either of factors
like substrate concentration, enzyme concentration, pH and temperature are changed.
25. A, D, Rationale: Lock and Key model shows enzyme specificity. While induced-fit model shows
enzyme flexibility.

This document is the property of PHINMA EDUCATION


Course Code: BIO 024 (Biochemistry/Biomolecules)
Module #5

Name: ____________________________________________________________ Class number: _______


Section: ____________ Schedule: ____________________________________ Date: _______________

Module 5 - Activity 5: Check your Understanding Rationale

1. B: Sideroblastic anemia causes include excessive alcohol use (the most common cause of
sideroblastic anemia), pyridoxine deficiency (vitamin B6 is the cofactor in the first step of heme
synthesis), lead poisoning and copper deficiency.\
2. B: Thiamin: It is well known that chronic alcoholics are at high risk for being deficient in vitamin B1
(thiamine), which is known to put the patient at an increased risk for Wernicke-Korsakoff Syndrome,
cerebellar degeneration, and cardiovascular dysfunction.
3. B: Thiamine pyrophosphate (TPP), the active form of thiamine, functions as a coenzyme for a
number of enzymes involved in carbohydrate metabolism, thus making metabolites from this
metabolism and keto analogues from amino and fatty acid metabolism available for the production of
energy. Thiamine deficiency is the established cause of an alcohol–linked neurological disorder
known as Wernicke–Korsakoff syndrome (WKS), but it also contributes significantly to other forms of
alcohol–induced brain injury, such as various degrees of cognitive impairment, including the most
severe, alcohol–induced persisting dementia (i.e., “alcoholic dementia”).
4. B: Vitamin C. One of the best-established functions of vitamin C is in the regulation of
neurotransmitter biosynthesis, including that of catecholamines dopamine, norepinephrine, and
epinephrine. Vitamin C acts as a cofactor for the enzyme dopamine β-hydroxylase, which converts
dopamine to norepinephrine.
5. D: Cyanocobalamin injection is used to treat and prevent a lack of vitamin B12 that may be caused
by any of the following: pernicious anemia (lack of a natural substance needed to absorb vitamin
B12 from the intestine); certain diseases, infections, or medications that decrease the amount of
vitamin B12 absorbed from food or a vegan diet (strict vegetarian diet that does not allow any animal
products, including dairy products and eggs). Lack of vitamin B12 may cause anemia (condition in
which the red blood cells do not bring enough oxygen to the organs) and permanent damage to the
nerves. Cyanocobalamin injection also may be given as a test to see how well the body can absorb
vitamin B12. Cyanocobalamin injection is in a class of medications called vitamins. Because it is
injected straight into the bloodstream, it can be used to supply vitamin B12 to people who cannot
absorb this vitamin through the intestine. Pernicious anemia usually is easy to treat with vitamin B12
shots or pills. If you have severe pernicious anemia, your doctor may recommend shots first. Shots
usually are given in a muscle every day or every week until the level of vitamin B12 in your blood
increases.
6. D: Pellagra is caused by cellular deficiency of niacin or its precursor amino acid, tryptophan.
Isoniazid preventive therapy (IPT) is the administration of isoniazid (INH) to latent tuberculosis (TB)
infection affected people preventing advancement to active TB disease. Although potentially life-
saving for human immunodeficiency virus (HIV)-infected people with no active TB, IPT is arguably a
possible player in pellagra in addition to well-known malnourishment determinants particularly in
developing nations where diagnosis is often overlooked or delayed.

This document is the property of PHINMA EDUCATION


Course Code: BIO 024 (Biochemistry/Biomolecules)
Module #5

Name: ____________________________________________________________ Class number: _______


Section: ____________ Schedule: ____________________________________ Date: _______________

A case study examines clinical presentation and possible causes of pellagra, in HIV + patient
on isoniazid prophylaxis. The 30 year old female on routine antiretroviral therapy presented
with diarrhea, abdominal discomfort, painful swallowing, and epigastric pain, facial rash spread
on the forehead, nose, cheeks and the chin, upper and lower limbs. Withdrawal of isoniazid,
administration of nicotinamide and niacin supplements showed clinical improvement in four
weeks. Decreased serum tryptophan in persons living with HIV (PLHIV) under IPT and lack of
minimum dietary proteins threshold would be pointers to isoniazid induced pellagra risk.
Appropriate dietary intake and counseling ought to be emphasized among PLHIV. Tryptophan
and nicotinamide serum levels should be part of baseline investigations in PLHIV starting
IPT and where feasible clinically, niacin/nicotinamide supplementation be adopted.
7. C: Vitamin B6 supplementation is recommended, especially in people with poor nutritional status, to
prevent development of isoniazid-induced peripheral neuritis (inflamed nerves). INH inhibits the
enzyme pyridoxine phosphokinase; this enzyme is necessary to activate pyridoxine to pyridoxal 5'
phosphate, the cofactor in many "pyridoxine-dependent" reactions. Functional pyridoxine deficiency
is the likely mechanism of INH-induced peripheral neuropathy.
8. C: The March of Dimes recommends that women of childbearing age take 400 mcg of vitamin B-9
daily before and after pregnancy. Your folic acid needs will increase when you become pregnant.
Vitamin B-9 can help to reduce your baby's risk for developing birth defects, including spina bifida
and other neural tube defects.
9. B: Vitamin D is actually a hormone rather than a vitamin; it is required to absorb calcium from the gut
into the bloodstream. Vitamin D is mostly produced in the skin in response to sunlight and is also
absorbed from food eaten (about 10% of vitamin D is absorbed this way) as part of a healthy
balanced diet. The liver and kidneys convert vitamin D (produced in the skin and taken up in the
diet), into the active hormone, which is called calcitriol. Active vitamin D helps to increase the
amount of calcium the gut can absorb from eaten food into the bloodstream and also prevents
calcium loss from the kidneys. Vitamin D modifies the activity of bone cells and is important for the
formation of new bone in children and adults.
10. B: Vitamin D is actually a hormone rather than a vitamin; it is required to absorb calcium from the gut
into the bloodstream. Vitamin D is mostly produced in the skin in response to sunlight and is also
absorbed from food eaten (about 10% of vitamin D is absorbed this way) as part of a healthy
balanced diet. The liver and kidneys convert vitamin D (produced in the skin and taken up in the
diet), into the active hormone, which is called calcitriol. Active vitamin D helps to increase the
amount of calcium the gut can absorb from eaten food into the bloodstream and also prevents
calcium loss from the kidneys. Vitamin D modifies the activity of bone cells and is important for the
formation of new bone in children and adults.
11. D: Vitamin D deficiency is known to cause hypertrophic costochondral junctions in children (“rachitic
rosaries”) and sternal pain with adults diagnosed with osteomalacia. We propose that vitamin D
deficiency may be related to the chest pain associated with costochondritis. Vitamin D is integral for
bone health, and severe deficiency can cause rickets in children and osteomalacia in adults.
Although osteomalacia can cause severe generalized bone pain, there are only a few case reports of
chest pain associated with vitamin D deficiency. We describe 2 patients with chest pain that were
initially worked up for cardiac etiologies but were eventually diagnosed with costochondritis and
vitamin D deficiency. Vitamin D deficiency is known to cause hypertrophic costochondral junctions in

This document is the property of PHINMA EDUCATION


Course Code: BIO 024 (Biochemistry/Biomolecules)
Module #5

Name: ____________________________________________________________ Class number: _______


Section: ____________ Schedule: ____________________________________ Date: _______________

children (“rachitic rosaries”) and sternal pain with adults diagnosed with osteomalacia. We propose
that vitamin D deficiency may be related to the chest pain associated with costochondritis. In patients
diagnosed with costochondritis, physicians should consider testing and treating for vitamin D
deficiency.
https://www.hindawi.com/journals/crim/2012/375730/

12. A: Prior to World War II, there was great interest and debate surrounding the use of vitamin A as
“anti-infective” therapy. An idea was conceived that vitamin A could strengthen the immune system
and would help fight infections. For a while, serum treatment upstaged vitamin A as a possible
weapon against infectious diseases. In the 1930s, serum treatment was widely used against
infections, because it was thought to help neutralize the infection, shorten the course of illness, and
minimize complications. Vitamin A prevents drying of the skin. This may protect the body from
infectious diseases. It also helps maintain the immune system.
13. A: Vitamin A supplementation helps to prevent blindness and child mortality in many developing
nations with underserved populations. According to the World Health Organization, vitamin A
deficiency is a leading cause of preventable blindness and death in children and pregnant women.
14. E: Niacin (nicotinic acid) favorably affects all lipids and lipoproteins, making it an alternative to
fibrates for treating patients with mixed hyperlipidemia, and may be used either alone or in
combination with other agents. Niacin is known to suppress the release of free fatty acids from the
adipocyte, resulting in a transient reduction in circulating NEFAs. When taken at prescription-level
doses, niacin has been shown to improve “good” HDL cholesterol levels and lower triglyceride levels.
It works by blocking the enzyme responsible for making cholesterol in the liver. In the doses needed
to improve cholesterol, niacin is a drug "" and a potent drug at that. On average, it can lower LDL
("bad") cholesterol levels by 10%""25%.
15. D: Wernicke-korsakoff syndrome is a Vitamin B1 deficiency related condition. The signs and
symptoms of biotin deficiency typically appear gradually and can include thinning hair with
progression to loss of all hair on the body; scaly, red rash around body openings (eyes, nose, mouth,
and perineum); conjunctivitis; ketolactic acidosis (which occurs when lactate production exceeds
lactate clearance) and aciduria (abnormal amounts of acid in urine); seizures; skin infection; brittle
nails; neurological findings (e.g., depression, lethargy, hallucinations, and paresthesias of the
extremities) in adults; and hypotonia, lethargy, and developmental delay in infants [2,3,13]. The rash
and unusual distribution of facial fat in people with biotin deficiency is known as “biotin deficiency
facies”. Other causes of biotin deficiency include prolonged treatment with anticonvulsants such as
phenytoin, primidone, carbamazipine, phenobarbital, and valproic acid, as well as ingestion of high
doses of lipoic acid, long-term use of antibiotics, excessive alcohol consumption, and habitual or
regular consumption of raw egg. Biotinidase deficiency is another rare cause of intractable epilepsy
in neonates caused by mutations of the biotinidase BTD gene.129 It is associated with optic atrophy
with visual loss, sensorineural hearing loss, conjunctivitis, cheilosis, and alopecia.
16. D: Vitamin K-dependent (VKD) carboxylation is a post-translational modification that converts
specific glutamate residues (Glu) to gamma-carboxyglutamate residues (Gla) in VKD proteins. It is
essential for the biological function of proteins that control blood coagulation, vascular calcification,
bone metabolism, and other important physiological processes.Carboxylation has mostly been
associated with coagulation, since it was originally observed in the clotting factor, prothrombin (PT).
Defects of VKD carboxylation have long been known to cause bleeding disorders.There are two

This document is the property of PHINMA EDUCATION


Course Code: BIO 024 (Biochemistry/Biomolecules)
Module #5

Name: ____________________________________________________________ Class number: _______


Section: ____________ Schedule: ____________________________________ Date: _______________

types of coagulation factors, one is procoagulant proteins which include PT, FVII, FIX, and FX. The
other is anticoagulant proteins which include PC, PS, and PZ. The biological functions of these
clotting factors require 9-13 Glu residues at the N-terminus of the mature protein (referred to as the
Gla domain) to be properly modified by VKD carboxylation.

Prothrombin, or factor II, is one of the clotting factors made by the liver. Vitamin K is needed to make
prothrombin and other clotting factors. Prothrombin time is an important test because it checks to
see if five different blood clotting factors (factors I, II, V, VII, and X) are present.
17. C: The signs and symptoms of riboflavin deficiency (also known as ariboflavinosis) include skin
disorders, hyperemia (excess blood) and edema of the mouth and throat, angular stomatitis (lesions
at the corners of the mouth), cheilosis (swollen, cracked lips), hair loss, reproductive problems, sore
throat, itchy and red eyes, and degeneration of the liver and nervous system. People with riboflavin
deficiency typically have deficiencies of other nutrients, so some of these signs and symptoms might
reflect these other deficiencies. Severe riboflavin deficiency can impair the metabolism of other
nutrients, especially other B vitamins, through diminished levels of flavin coenzymes. Anemia and
cataracts can develop if riboflavin deficiency is severe and prolonged.
Groups at Risk of Riboflavin Inadequacy at vegetarian athletes, pregnant and lactating women and
their infants, People who are vegan and/or consume little milk and People with riboflavin transporter
deficiency (formerly known as Brown-Vialetto-Van Laere or Fazio-Londe syndrome).

18. C: Your body needs pantothenic acid to synthesize cholesterol. A derivative of pantothenic acid
called pantethine is being studied to see if it may help lower cholesterol levels in the body. Vitamin
B5 deficiency is rare, but may include symptoms such as fatigue, insomnia, depression, irritability,
vomiting, stomach pains, burning feet, and upper respiratory infections.

19. A, C and D: Vitamin E (fat soluble vitamin) in normal doses maintains collagen. Topical vitamin E
has emerged as a popular treatment for a number of skin disorders owing to its antioxidant
properties. It has been seen that reactive oxygen species have the ability to alter the biosynthesis of
collagen and glycosaminoglycans in skin. Various studies have evaluated the antioxidant effects of
vitamin E in the prevention or treatment of coronary artery disease (CAD). In vitro data suggest that
vitamin E protects against oxidation of low-density lipoprotein and decreases the deposition of
atherogenic oxidized low-density lipoprotein in arterial walls. Various observational and
epidemiological studies also suggest a relationship between vitamin E serum concentrations or
intake and CAD. One prospective, randomized trial suggested that low-dosage vitamin E
supplementation (50 IU/d) decreases the risk of angina in patients without previously diagnosed
CAD. Another study, using high-dosage vitamin E supplementation (400 or 800 IU/d), demonstrated
a decrease in the combined end point of nonfatal myocardial infarction and cardiovascular death in
patients with established CAD. Discordant data, however, have been published that imply no

This document is the property of PHINMA EDUCATION


Course Code: BIO 024 (Biochemistry/Biomolecules)
Module #5

Name: ____________________________________________________________ Class number: _______


Section: ____________ Schedule: ____________________________________ Date: _______________

cardiovascular benefit of low-dosage vitamin E supplementation (50 IU/d) and detrimental effects if
vitamin E is combined with beta carotene. At this point, clinicians should emphasize a low-fat diet
with high intake of fruits and vegetable sources containing vitamin E. Supplemental vitamin E may
be considered in patients at high risk for CAD or with documented CAD, but the potential beneficial
effects should be weighed against possible long-term adverse effects. If vitamin E supplementation
is initiated, the literature suggests dosages of 100 to 400 IU/d, with the higher dosage considered in
patients with documented CAD. Additional investigation is warranted to further define the role of
vitamin E supplementation in CAD and to critically evaluate the optimal dosage, duration of use, and
method of consumption (dietary vs supplemental).

Taking vitamin E supplements increased the risk of hemorrhagic stroke by 22% but reduced the risk
of ischemic stroke by 10%.

20. D: Thiamine deficiency, or beriberi, refers to the lack of thiamine pyrophosphate, the active form of
the vitamin known as thiamine (also spelled thiamin), or vitamin B-1. There are two main types in
adults: wet beriberi, and dry beriberi. Wet beriberi affects the cardiovascular system resulting in a
fast heart rate, shortness of breath, and leg swelling. Dry beriberi affects the nervous system
resulting in numbness of the hands and feet, confusion, trouble moving the legs, and pain.[1] A form
with loss of appetite and constipation may also occur. Another type, acute beriberi, is found mostly in
babies and presents with loss of appetite, vomiting, lactic acidosis, changes in heart rate, and
enlargement of the heart. Wernicke encephalopathy and Korsakoff syndrome are forms of dry
beriberi.

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