CARBOHYDRATE METABOLISM

Essay Questions: 12 markers

1. Describe the pathway of glycolysis with reactions, enzymes, energy yield, and regulation.
Add a note on its significance.

2. Explain the reactions of the tricarboxylic acid (TCA) cycle, its regulation, and its
significance in energy prodcution.

[Link] the process of gluconeogenesis, highlighting key enzymes, regulation, and its
significance in maintaining blood glucose levels.

[Link] the synthesis and degradation of glycogen with regulatory mechanisms. Add a
note on glycogen storage disorders.

[Link] the hexose monophosphate shunt, its two phases, regulatory enzymes, and
significance in cellular metabolism.

6. Describe the Cori cycle and glucose-alanine cycle, explaining their role in metabolism
during fasting and exercise.

7. Discuss the metabolic alterations in diabetes mellitus, including insulin resistance,

ketoacidosis, and long-term complications.

8. Explain the changes in carbohydrate metabolism during prolonged fasting and starvation.

9. Outline the metabolism of fructose and galactose, and explain disorders associated with
their metabolism.

[Link] the role of insulin, glucagon, and other hormones in glucose homeostasis.

[Link] the causes, biochemical basis, and consequences of lactic acidosis.

[Link] key inborn errors of carbohydrate metabolism, such as galactosemia, glycogen

storage diseases, and hereditary fructose intolerance.

Short assays (Applied aspect): 5marker

1. Describe the biochemical pathway of glycogen synthesis. Discuss how defects in this
pathway can lead to glycogen storage diseases, providing specific examples.

[Link] the role of the pentose phosphate pathway in cellular metabolism. How does a
deficiency in

3. glucose-6-phosphate dehydrogenase affect red blood cells, and what clinical condition
does this lead to?

4. Discuss the process of gluconeogenesis and its significance during fasting. How can
impairments in gluconeogenesis contribute to hypoglycemia?
[Link] the Cori cycle and its importance in muscle metabolism during anaerobic
conditions. What are the potential consequences of a malfunctioning Cori cycle?

5. A 45-year-old male presents with frequent urination, excessive thirst, and unexplained
weight loss. His fasting blood glucose is 180 mg/dL. Explain the biochemical basis of his
condition, the role of insulin in glucose metabolism, and the importance of glycogenesis and
glycogenolysis in maintaining blood glucose levels.

6. A neonate develops jaundice within 48 hours of birth, and laboratory tests reveal a
deficiency of glucose-6-phosphate dehydrogenase (G6PD). Explain the biochemical basis of
hemolysis in G6PD deficiency and its relation to the pentose phosphate pathway.

7.A 25-year-old athlete experiences extreme fatigue and muscle cramps after prolonged
exercise. Laboratory tests show an accumulation of lactic acid. Explain the role of anaerobic
glycolysis in energy production, the Cori cycle, and the metabolic basis of lactic acidosis.

8. A 3-year-old child presents with hepatomegaly, fasting hypoglycemia, and increased

glycogen accumulation in the liver. Based on these findings, discuss the possible glycogen
storage disease (GSD), its enzymatic defect, and how it affects glucose homeostasis.

9. A patient with chronic alcoholism develops neurological symptoms such as confusion,

ataxia, and ophthalmoplegia. Discuss the role of thiamine in carbohydrate metabolism, the
biochemical basis of Wernicke-Korsakoff syndrome, and the importance of pyruvate
dehydrogenase in energy production.

Scenario-Based MCQs

1. A 50-year-old man presents with polyuria, polydipsia, and unexplained weight loss. His
fasting blood glucose is 190 mg/dL. His HbA1c is 8.2%. He is diagnosed with Type 2
Diabetes [Link] of the following best describes the biochemical basis of his
condition?

A. Increased insulin secretion and enhanced glucose uptake in peripheral tissues

B. Defective insulin receptor signaling leading to impaired glucose uptake and increased
hepatic

C. Increased glycogen storage in the liver leading to hyperglycemia

D. Inhibition of gluconeogenesis and enhanced glycogenesis

Answer: [Link] insulin receptor signaling leading to impaired glucose uptake and
increased hepatic gluconeogenesis gluconeogenesis.
2. A 2-day-old male neonate develops jaundice. His blood smear shows Heinz bodies, and
his parents mention a family history of glucose-6-phosphate dehydrogenase (G6PD)
[Link] is the primary cause of hemolysis in this condition?

A. Decreased ATP production leading to RBC lysis

B. Excessive glycogen breakdown causing oxidative stress

C. Reduced NADPH production leading to oxidative damage of RBCs

D. Increased pentose phosphate pathway activity causing red cell fragility

Answer: [Link] NADPH production leading to oxidative damage of RBCs

3. A 25-year-old athlete reports muscle cramps and fatigue after intense exercise. His blood
test shows an increase in lactic acid [Link] of the following pathways is responsible
for this condition?

A. Increased activity of the citric acid cycle

B. Increased anaerobic glycolysis due to oxygen deficiency

C. Increased gluconeogenesis leading to lactate accumulation

D. Defective pentose phosphate pathway

Answer: [Link] anaerobic glycolysis due to oxygen deficiency

4. A 3-year-old child presents with hepatomegaly, severe fasting hypoglycemia, and lactic
acidosis. Liver biopsy shows excessive glycogen [Link] enzyme is most likely
deficient in this patient?

A. Glycogen phosphorylase

B. Glucose-6-phosphatase

C. Pyruvate dehydrogenase

D. Phosphofructokinase

Answer: [Link]-6-phosphatase
5. A 45-year-old chronic alcoholic presents with confusion, ataxia, and ophthalmoplegia. His
condition improves with thiamine [Link] enzyme in carbohydrate
metabolism is most affected by thiamine deficiency?

A. Pyruvate dehydrogenase

B. Glucose-6-phosphatase

C. Hexokinase

D. Lactate dehydrogenase

Answer: [Link] dehydrogenase

6. A 30-year-old man has been fasting for 24 hours. His blood glucose levels are still within
the normal [Link] of the following metabolic pathways is the primary source of glucose
in this state?

A) Glycolysis

B) GlycogenolysisC) Gluconeogenesis

D) Lipogenesis

Answer: C) Gluconeogenesis

7. A 25-year-old athlete starts sprinting during a 100-meter race. His muscles require an
immediate and rapid supply of [Link] metabolic pathway provides the fastest source of
ATP in this situation?

A) Oxidative phosphorylation

B) Anaerobic glycolysis

C) Beta-oxidation

D) Gluconeogenesis

Answer: B) Anaerobic glycolysis

8. A 45-year-old man with Type 1 Diabetes Mellitus (T1DM) has not taken his insulin for the
past 24 hours. He presents with fatigue, dehydration, and rapid [Link] of the
following complications is most likely due to the unchecked metabolism of fatty acids in this
patient?

A) Hypoglycemia

B) Ketoacidosis

C) Hyperinsulinemia

D) Increased glycogen stores

Answer: B) Ketoacidosis

9. A newborn is diagnosed with von Gierke’s disease (Glycogen Storage Disease Type I)
due to a deficiency of [Link] symptom is most characteristic of this
disorder?

A) Hyperglycemia

B) Severe fasting hypoglycemia

C) Increased muscle glycogen breakdown

D) Decreased glycolysis

Answer: B) Severe fasting hypoglycemia

10 .A 50-year-old alcoholic is brought to the emergency room with confusion and low blood
sugar after binge [Link] does excessive alcohol consumption cause hypoglycemia,
especially in fasting individuals?

A) It promotes excessive insulin secretion

B) It inhibits gluconeogenesis by increasing NADH/NAD+ ratio

C) It enhances glycogenolysis

D) It increases glycolysis

Answer: B) It inhibits gluconeogenesis by increasing NADH/NAD+ ratio

 DETOXIFICATION

Short notes (4 Marks)

[Link] the mechanism of detoxification of the following compounds in the body

i. Ethanol; ii. Steroids; iii. Benzoic Acid; iv. Picric Acid; v. Aspirin

2. Explain the outcome and effects of biotransformation of

i. Methanol; ii. Acetaminophen (Paracetamol)

Short essays (5 marks)

1. Cytochrome P450

2. Phase I reactions of detoxification

3. Phase I detoxification – Hydrolysis reactions with examples

4. Phase II detoxification reaction with examples

5. Define biotransformation. Discuss the different phases of biotransformation with an

example

6. Explain the role of glutathione in detoxification.

Give Reasons

1. Case: Paracetamol Overdose and Liver Damage

A 25-year-old male overdosed on paracetamol and developed severe liver toxicity. His liver
enzyme levels (AST,ALT) were significantly elevated.

Give Reason: Why does paracetamol overdose cause liver damage?

Paracetamol is primarily metabolized by glucuronidation and sulfation (Phase II reactions).

However, in overdose conditions, excess drug is metabolized by CYP2E1, producing NAPQI
(N-acetyl-p-benzoquinoneimine), a highly reactive intermediate. If glutathione (GSH) is
depleted, NAPQI accumulates, leading to oxidative stress, hepatocyte damage, and
necrosis.
2. Case: Jaundice in a Newborn

A 3-day-old newborn develops yellowish discoloration of the skin and sclera. Laboratory
tests show elevated unconjugated [Link] Reason: Why does neonatal jaundice
occur?

Newborns have immature UDP-glucuronosyltransferase (UGT) enzyme activity, which leads

to impaired bilirubin conjugation in the liver. As a result, unconjugated bilirubin accumulates,
causing jaundice. If bilirubin levels rise excessively, there is a risk of kernicterus
(bilirubin-induced neurotoxicity).

3. Case: Dark Urine and Hemolysis

A 30-year-old male experiences fatigue, dark-colored urine, and jaundice after taking
antimalarial medication (primaquine). Laboratory tests show hemolyticanemia and low G6PD
[Link] Reason: Why does glucose-6-phosphate dehydrogenase (G6PD) deficiency lead
to hemolysis?

G6PD deficiency impairs the pentose phosphate pathway (PPP), reducing NADPH levels.
NADPH is essential for glutathione (GSH) regeneration, which protects red blood cells
(RBCs) from oxidative damage. Without adequate GSH, reactive oxygen species (ROS)
accumulate, leading to RBC membrane damage, hemolysis, and dark urine
(hemoglobinuria).

4. Case: Alcoholic Liver Disease

A 50-year-old chronic alcoholic presents with hepatomegaly, jaundice, and increased serum
AST & ALT. Liver biopsy shows fatty liver and [Link] Reason: Why does chronic
alcohol consumption cause liver damage?

Alcohol is metabolized by alcohol dehydrogenase (ADH) to acetaldehyde, which is further

detoxified by aldehyde dehydrogenase (ALDH). Chronic alcohol consumption: Increases
NADH/NAD+ ratio, leading to fatty liver (steatosis). Acetaldehyde induces oxidative stress,
causing hepatocellular damage and fibrosis. CYP2E1 activation produces reactive oxygen
species (ROS), further damaging liver cells.

5. Case: Bluish Skin After Nitrite Exposure

A 30-year-old farmer accidentally ingests nitrates from contaminated water and develops
cyanosis (bluish skin) despite normal oxygen levels in blood. Give Reason: Why does nitrite
poisoning cause cyanosis?

Nitrates are converted to nitrites, which oxidize ferrous iron (Fe²⁺) in hemoglobin to ferric iron
(Fe³⁺), forming methemoglobin (MetHb). MetHb cannot bind oxygen, leading to functional
hypoxia despite adequate oxygen availability in the blood.
6. Case: Chronic Fatigue and Lead PoisoningA 40-year-old battery factory worker presents
with fatigue, anemia, and peripheral neuropathy. Blood tests show elevated lead levels and
basophilic stippling of RBCs. Give Reason: Why does lead poisoning cause anemia?

Lead inhibits δ-aminolevulinic acid dehydratase (ALAD) and ferrochelatase, key enzymes in
heme [Link] results in impaired hemoglobin production, causing anemia. Lead also
disrupts mitochondrial function and increases oxidative stress, leading to neurotoxicity.

MCQs

1. Which organ is the primary site of detoxification in the human body?

A) Kidney

B) Liver

C) Lungs

D) Skin

Answer: B) Liver

Explanation: The liver is the major detoxification organ, metabolizing xenobiotics, drugs, and
toxins through Phase I, Phase II, and Phase III reactions.

2. Which enzyme family is primarily responsible for Phase I detoxification reactions?

A) Glutathione-S-transferase

B) UDP-glucuronosyltransferase

C) Cytochrome P450

D) N-acetyltransferase

Answer: C) Cytochrome P450 Explanation: The cytochrome P450 (CYP450) enzyme system
carries out oxidation, reduction, and hydrolysis reactions in Phase I detoxification, converting
lipophilic toxins into reactive intermediates.

3. Which of the following is a Phase II detoxification reaction?

A) Oxidation

B) Glucuronidation

C) Hydrolysis

D) Reduction

Answer: B) Glucuronidation
Explanation: Phase II detoxification involves conjugation reactions, including glucuronidation,
sulfation,methylation, and glutathione conjugation, which make metabolites more
water-soluble for excretion.

4. N-acetyltransferase (NAT) is involved in the detoxification of which compound?

A) Paracetamol

B) Sulfonamides

C) Ethanol

D) Benzene

Answer: B) Sulfonamides Explanation: N-acetyltransferase (NAT) mediates acetylation, a

Phase II detoxification process, important for drugs like sulfonamides and isoniazid.

5. Which of the following is a key enzyme in alcohol detoxification?

A) Glutathione-S-transferase

B) Alcohol dehydrogenase

C) UDP-glucuronosyltransferase

D) Cytochrome P450 2E1

Answer: B) Alcohol dehydrogenase Explanation: Alcohol dehydrogenase (ADH) converts

ethanol to acetaldehyde, which is further detoxified by aldehyde dehydrogenase (ALDH) into
acetate.

6. Paracetamol overdose leads to liver toxicity due to the accumulation of which toxic
metabolite?

A) Acetate

B) Bilirubin

C) NAPQI (N-acetyl-p-benzoquinone imine)

D) Ethanol

Answer: C) NAPQI (N-acetyl-p-benzoquinone imine)

Explanation: Excessive paracetamol metabolism by CYP2E1 generates NAPQI, a

hepatotoxic metabolite. If glutathione is depleted, NAPQI causes liver damage.
7. Glutathione-S-transferase is involved in the detoxification of:

A) Free radicals

B) Acetaminophen

C) Heavy metals

D) All of the above

Answer: D) All of the above

Explanation: Glutathione-S-transferase (GST) catalyzes the conjugation of toxins with

glutathione, detoxifying free radicals, drugs, and heavy metals.

8. The cytochrome P450 enzyme system is located in which part of the cell?

A) Mitochondria

B) Cytoplasm

C) Smooth endoplasmic reticulum

D) Golgi apparatus

Answer: C) Smooth endoplasmic reticulum

Explanation: CYP450 enzymes are embedded in the smooth endoplasmic reticulum (SER),
where they perform oxidation and hydroxylation reactions in detoxification.

9. Which of the following is NOT a Phase II detoxification reaction?

A) Methylation

B) Sulfation

C) Reduction

D) Glutathione conjugation

Answer: C) Reduction

Explanation: Reduction is a Phase I reaction, whereas methylation, sulfation, and glutathione

conjugation are Phase II reactions that enhance toxin excretion.
10. Which of the following is responsible for the excretion of conjugated bilirubin?

A) Liver

B) Kidney

C) Lungs

D) Pancreas

Answer: A) Liver

Explanation: Conjugated bilirubin is excreted via bile into the intestines and converted to
stercobilin (stool pigment) or urobilinogen (partly reabsorbed and excreted in urine).

11. In drug detoxification, which of the following best describes a Phase I reaction?

A) Hydrolysis

B) Acetylation

C) Glucuronidation

D) Sulfation

Answer: A) Hydrolysis

Explanation: Phase I reactions include oxidation, reduction, and hydrolysis, making drugs
more polar but sometimes generating reactive metabolites.

12. What is the primary excretion route of detoxified compounds?

A) Sweat

B) Bile and urine

C) Lungs

D) Saliva

Answer: B) Bile and urine

Explanation: Most detoxified compounds are excreted via the kidneys (urine) or liver (bile).
13. Which enzyme catalyzes the conversion of biliverdin to bilirubin?

A) Heme oxygenase

B) Biliverdin reductase

C) Glutathione-S-transferase

D) UDP-glucuronosyltransferase

Answer: B) Biliverdin reductase

Explanation: Biliverdin reductase converts biliverdin to bilirubin, which is then conjugated in

the liver for excretion.

14. The drug isoniazide used in the treatment of Tubeculosis is detoxified by

a) Methylation

b) Active sulphate

c) Acetylation

d) Glutathione
 MINERALS

MCQ:

1. Selenium deficiency leads to:

A. Liver necrosis

B. Diarrhoea

C. Multiple sclerosis

D. Crohn's disease

2. Which of the following vitamin is essential for the absorption of calcium from the intestinal
tract?

A. Vitamin D

B. Vitamin B

C. Vitamin A

D. Vitamin E

3. Zinc deficiency is most likely to lead to which of the following?

A. Decreased synthesis of thyroid hormones

B. Impaired wound healing

C. Decreased insulin secretion

D. Hyperkalemia

4. In which of the following conditions is copper deficiency most likely to occur?

A. Cystic fibrosis

B. Menkes disease

C. Hemochromatosis

D. Hyperthyroidism
5. A patient presents with a history of recurrent fractures, muscle cramps, and a slightly
prolonged QT interval on ECG. Which mineral deficiency is most likely to be responsible?

A) Calcium

B) Magnesium

C) Phosphorus

D) Potassium

6. Which mineral is critical for the synthesis of hemoglobin and is involved in the reduction of
methemoglobin to hemoglobin?

A) Copper

B) Iron

C) Calcium

D) Zinc

7. In which of the following conditions would you expect to see elevated serum levels of
zinc?

A) Acute infection

B) Chronic renal failure

C) Severe malnutrition

D) Alcoholism

8. A 28-year-old woman presents with frequent muscle cramps, tetany, and positive
Chvostek’s and Trousseau’s signs. Her serum calcium is low, and her PTH is elevated.
Which of the following is the most likely to be the cause of her hypocalcemia?

A) Hypoparathyroidism

B) Vitamin D deficiency

C) Hyperphosphatemia

D) Renal failure
9. A 30-year-old male presents with fatigue, pallor, and a smooth, red tongue. His serum
ferritin is normal, but his total iron-binding capacity (TIBC) is high. What is the most likely
diagnosis?

A) Iron deficiency anemia

B) Anemia of chronic disease

C) Thalassemia

D) Sideroblastic anemia

10. What is the effect of hypercalcemia on parathyroid hormone (PTH) secretion?

A) It stimulates PTH secretion.

B) It inhibits PTH secretion.

C) It has no effect on PTH secretion.

D) It increases PTH synthesis but decreases its release.

11. Which of the following is the main regulator of iron absorption in the body?

A. Erythropoietin

B. Hepcidin

C. Ferritin

D. Transferrin

12. Which mineral is required for the cross-linking of collagen and elastin, contributing to the
structural integrity of tissues?

A) Iron

B) Zinc

C) Copper

D) Manganese

13. Which of the following factors inhibits the absorption of magnesium from the
gastrointestinal tract?

A) High dietary calcium intake

B) High potassium intake

C) Alcohol consumption
D) Vitamin D deficiency

14. Which mineral plays a vital role in the immune responseand the sense of taste?

A) Zinc

B) Iron

C) Magnesium

D) Copper

LONG QUESTIONS:

1. Write dietary Sources, RDA, factors affecting absorption, functions and deficiency
manifestations of calcium. Explain the biochemical mechanisms regulating calcium
homeostasis.

2. Write Dietary Sources, RDA factors affecting absorption, function and deficiency
manifestations of Iron. Add a note on its regulation.

SHORT QUESTIONS:

1. Regulation of Calcium and Phosphorus.

2. Biochemical functions of Zn and Cu

3. Absorption of Iron.

4. Disorders related to copper metabolism

5. Iron Toxicity

6. Wilson’s disease

7. Explain the process of iron absorption and transport in the [Link] the regulation of
iron homeostasis by hepcidin and other related proteins.

8. Describe the role of iodine in thyroid function and elucidate the functions of magnesium in
cellular processes.

9. Discuss the impact of excess iron in the body, including the mechanisms and
consequences of iron overload disorders like hemochromatosis.
CBL

1. A 20-year old female presented to Medicine OPD with the chief complaints of excessive
tiredness, loss of appetite, generalized weakness and inability to concentrate. On
examination there was pallor and [Link] findings showed low serum iron
level, low serum ferritin level, decrease in hemoglobin and MCV. Total iron binding capacity
(TIBC), Transferin and RDW were increased.

a) Analyse the case and give probable diagnosis.

b) What are the common causes for such condition?

c) Mention the functions of ferritin & transferrin.

2. An 8-yearold boy is born of a second degree consanguineous marriage. Patient came with
complaints of distension of abdomen, edema in feet, melena. Family history revealed that his
sibling died of liver failure at age of 7 years, whose diagnosis was pending. On ophthalmic
examination, presence of Kayser- Fleisher ring was observed.

Laboratory findings:

a)Serum copper - 95.6 mcg/dl (30-150 mcg/dl)

b) Serum ceruloplasmin - 6.04 mg/dl (20-60 mg/dl)

c) 24 hours urine copper - 375.3 mcg/24hr (7-12 mcg/24hr)

1. Analyse the case and give probable diagnosis.

2. Explain the basic defect in this condition.

3. Mention the role of Ceruloplasmin and reason for its decreased level.

Ans: WILSON’S DISEASE

3. A 45-year-old man presents with fatigue, muscle weakness, and tremors. Blood tests
reveal low calcium levels and elevated parathyroid hormone (PTH) levels. The patient also
has a history of renal stones.

a)Explain the role of calcium in the body and the consequences of calcium imbalance.

B)Discuss the pathophysiology behind the elevated PTH and its relation to calcium
metabolism.

C)Based on the case, what could be the cause of the patient's symptoms, and what would
be the clinical management?
4. A 30-year-old woman presents with fatigue, muscle cramps, and tingling in her hands and
feet. She also reports difficulty swallowing and a history of recent neck surgery for thyroid
cancer. On physical examination,she has a positive Chvostek sign and a positive Trousseau
sign. Her laboratory results show low serum calcium and elevated parathyroid hormone
(PTH) levels.a) b) Based on the clinical presentation and laboratory findings, what is the
likely cause of this patient's hypocalcemia?

A) Explain the biochemical role of calcium and parathyroid hormone in calcium

homeostasis.
B) How does neck surgery for thyroid cancer relate to the development of
hypocalcemia in this case?
C) What would be your treatment approach for this patient?

Ans: Hypoparathyroidism due to Thyroid Surgery

 ORGAN FUNCTION TEST

Long Essays (12 Marks)

1. A 40 year old woman admitted with recurrent pain abdomen with vomiting and yellowish
discoloration of skin and sclera, passing yellow colored urine and clay colored stool.

Laboratory investigation reveals

a) b) Serum total bilirubin – 20 mg/dl

Serum direct bilirubin (conj.) – 16 mg/dl

c) Serum indirect bilirubin (unconj.) – 4mg/dl

d) AST – 85.0 IU/L

e) ALT – 98.0 IU/L

f) ALP – 1000 IU/L

1. What is your diagnosis?

2. What are the most likely causes?

3. What are the urinary changes to confirm your diagnosis?

4. Discuss bilirubin metabolism in detail.

5. Describe Vandenberg test interpretation. (1+1+2+6+2)

2. A 40 Old female was brought to hospital with on and off complaints of dull aching pain in
the right hypochondriac region following a fatty meal. On examination patient was icteric.
Biochemical investigation asfollows

PARAMETER RESULT

1. Blood Glucose: 252mg/dl

2. Serum Total bilirubin : 7.8mg/dl

3. Conjugated bilirubin: 7.1

[Link] bilirubin: 0.7

5. Aspartate aminotransferase: 54 IU/L

6. Alanine aminotransferase: 30 IU/L

7. Alkaline phosphatase: 1048 IU/L

8. Stool examination Clay coloured

9. Urobilinogen Positive

1. Analyze the above case and give your probable diagnosis

2. List any 4 causes for the above diagnosis

3. Explain van den berg reaction

4. Discuss bilirubin metabolism in detail (2+2+2+6)

3. A 21 old boy had 5 days history of fever, loss of appetite, nausea, vomiting with high
colored urine since 3 days. On examination icterus was present with tender hepatomegaly.

PARAMETER RESULT

1. Blood Glucose: 120mg/dl

2. Serum Total bilirubin: 9.8mg/dl

3. Conjugated bilirubin: 5.3

4. Unconjugated bilirubin: 4.5

5. Aspartate aminotransferase: 958 IU/L

6. Alanine aminotransferase: 1020 IU/L

7. Alkaline phosphatase

1. Analyze the above case and give your probable diagnosis

2. What are the urinary changes to confirm your diagnosis?

3. Discuss bilirubin metabolism in detail.

4. Discuss the role of liver enzymes in assessing the liver function (2+2+6+2)

Short Essays (6/ 5 marks)

1. A four year old boy was brought to the physician by his parents. He was having facial and
generalized oedema. Physican has asked for the following investigations.

Serum protein 3 gm/dl 6-8 gm/dl

Serum cholesterol 600 mg/dl 150-250 mg/dlBlood urea 80 mg/dl 15-40 mg/dl

Serum Creatinine 4.5 mg/dl 0.7-1.5 mg/dl

Urine proteins + + + Nil

a) What is the probable diagnosis?

b) What is the cause for the hypoproteinemia?

c) What is the cause for oedema and hyperlipidemia?

e) Discuss the blood urea & serum creatinine levels as markers of kidney diseases?

2. A 37 year old servant had complaints of weakness, constipation weight gain, easy fatigue,
indecisive, intolerant to cold and lethargy. On physical examination revealed wrinkled skin,
lusterless hair, mild hypertension (122/ 95mm/Hg) and pulse rate (66/ min).

Following are biochemical investigations:

Serum T3: 40 ng/dl (70-180 ng/dl)

Serum T4: 3.8 (5.5 - 12 microg/dl)

Serum TSH: 7 U/L (< 5.7 U/L)

[Link] is your probable diagnosis?

[Link] T3 & T4 levels are decreased in this case?

[Link] TSH level is increased?

[Link] the functions of thyroid hormones?

[Link] the following Liver Function Test

Total Bilirubinn : 7.7 mg/dl

Direct Bilirubin: 3.6 mg/dl

Alkaline Phosphatase: 265 IU/L

Ehrlich’s test : negative

Stool sample: Clay Color

[Link] is the probable diagnosis?

[Link] the possible causes for the above condition?

[Link] with reason for increase in conjugated fraction of bilirubin?

4. A known case of diabetes and hypertension on irregular treatment presented with swelling
of both lower limbs and puffiness of face. He was diagnosed with chronic kidney disease
(CKD)

1. Mention 2 biochemical parameters altered in CKD2. Explain the test to assess glomerular
function of the kidney

Reasoning questions (3 Marks)

[Link] Bilirubin increased in Neonates Justify.

[Link] increased in Hypothyroidism Justify.

[Link] decreased in Hyperthyroidism Justify.

[Link] as a marker for Glomerular permeability Justify.

[Link] Creatinine or Creatinine clearance which is better as a marker to assess kidney

function.

[Link] deficiency leads to thyroid disorders Justify.

[Link] is seen in liver disorders Justify.

[Link] jaundice as a sign for liver disease.

Short Notes (3 Marks)

[Link] Clearance and name two tests to assess Kidney functions.

[Link] thyroid hormones and its functions.

[Link] Vandenberg test and its interpretation.

[Link] elevated in Liver disorders.

MCQ’S

1. Conjugated hyperbilirubinemia with raised alkaline phosphatase levels are characteristic

of :

a) Obstructive jaundice

b) b.) Hemolytic jaundice

c) c.) Viral hepatitis

d) d.) Physiological jaundice

2. Creatinine is used in clearance test because:

a) Neither secreted nor absorbed.

b) Secreted

c) Absorbed

d) None of the above

3. A Patient with infective hepatitis is likely to have all of the following findings except:

a) Hyperbilirubinemia

b) Bilirubinuria

c) Absence of bile salts in urine

d) Elevated AST

4. A four year old boy was brought to the physician by his parents. He was having facial and
generalized oedema diagnosed as a case of nephrotic syndrome. Oedema is caused due to:

a) Increased urea

b) Decreased Albumin

c) Decreased Cholesterol

d) Increased Albumin

5. A 37 year old servant had complaints of weakness, constipation weight gain, easy fatigue,
indecisive, intolerant to cold and lethargy diagnosed as a case of Hypothyroidism . Hormone
elevated in the above case is

a) TSH

b) T4

c) T3

d) Both b and c
6. Enzyme more specific to Liver diseases is

a) AST

b) ALT

c) Both a and b

d) ALP

7. A 40 year old woman admitted with recurrent pain abdomen with vomiting and yellowish
discoloration of skin and sclera, passing yellow colored urine and clay colored stool.
Diagnosis of Obstructive jaundice was made and the reason for clay colored stool is:

a) Absence of urobilinogen

b) Absence of stercobilinogen

c) Both a and b

d) None of the above

8. Normal specific gravity of urine is:

a) – 1.014

b) – 1.025

c) 1.030 -1.040

d) 1.050-1.065

9. A 56 yr old male recently diagnosed with diabetes mellitus should undergo screening test
for complications of diabetic nephropathy, the best test is

a) Protein

b) Microalbumin

c) Serum Creatinine

d) Specific gravity of urine

10. Goitre is caused due to deficiency of

a) Iodine

b) Selenium

c) Iron

d) Magnesium
 LIPID METABOLISM

MCQs on cholesterol metabolism

1. All of the following organs contribute largely to body’s cholesterol pool EXCEPT

a) liver

b) testis

c) ovary

d) pancreas

Answer : d. pancreas.

The liver, testis, and ovary contribute significantly to the body's cholesterol pool, as they are
involved in the synthesis and regulation of cholesterol. However, the pancreas does not play
a major role in cholesterol synthesis. The pancreas is primarily involved in the production of
digestive enzymes and hormones such as insulin.

2. Starting molecule required for cholesterol synthesis is –

a) acetyl CoA

b) succinyl CoA

c) propionyl CoA

d) methylmalonyl CoA

Answer : a. acetyl CoA

Acetyl-CoA is the fundamental building block for the synthesis of cholesterol, through a
series of reactions that include the mevalonate pathway.

3. Cholesterol synthesis takes place in –

a) cytosol & lysosomes

b) mitochondria & cytosol

c) Golgi Complex & lysosomes

d) endoplasmic reticulum & cytosol

Answer : d. Endoplasmic reticulum & cytosolCholesterol synthesis primarily takes place in
the cytosol and endoplasmic reticulum (ER) of the cell. The processinvolves several stages,
with key enzymes located in these two compartments.

4. Rate limiting enzyme in cholesterol synthesis pathway is -

a) thiolase

b) squalene synthase

c) HMG CoA reductase

d) acetoacetyl CoA synthase

Answer : C. HMG CoA reductase

HMG CoA reductase plays a critical role in the conversion of HMG-CoA to mevalonate,
which is a key step in the cholesterol biosynthesis process.

5. Isoprenoid unit containing 15 carbon is –

a) acetyl pyrophosphate

b) geranyl pyrophosphate

c) farnesyl pyrophosphate

d) isopentanyl pyrophosphate

Answer : C. farnesyl pyrophosphate.

Farnesyl pyrophosphate (FPP) has 15 carbon atoms, and it is a key intermediate in the
biosynthesis of many important biological molecules, including sterols and certain terpenes.

6. ‘Feedback inhibition’ of cholesterol synthesis occurs by –

a) squalene

b) mevalonate

c) acetoacetyl CoA

d) isopentanyl pyrophosphate

Answer : B. mevalonate.

Feedback inhibition of cholesterol synthesis occurs when the intermediate mevalonate

inhibits the activity of HMG-CoA reductase, the rate-limiting enzyme in the pathway. This
helps regulate the synthesis of cholesterol in the body.
7. Hormone which favors the formation of active form of HMG CoA reductase is

a) insulin

b) glucagon

c) glucocorticoidsd) paratharmone

Answer :A. insulin.

Insulin favors the formation of the active form of HMG-CoA reductase. HMG-CoA reductase
is the key enzyme in the cholesterol biosynthesis pathway, and insulin stimulates its activity
by promoting its dephosphorylation, leading to the active form of the enzyme. In contrast,
glucagon and other factors like glucocorticoids typically inhibit its activity.

8. Vitamin involved in the formation of bile acids is –

a) vitamin A

b) vitamin C

c) vitamin D

d) vitamin K

Answer : C. vitamin D.

Vitamin D is involved in the formation of bile acids. Bile acids are crucial for the digestion
and absorption of fats, and vitamin D plays a role in regulating bile acid synthesis in the liver.

MCQs on lipid digestion and absorption

1. What is the role of bile salts in lipid digestion?

A) They break down triglycerides into fatty acids and glycerol.

B) They emulsify fats, increasing the surface area for lipase action.

C) They neutralize stomach acids in the small intestine.

D) They help in the absorption of amino acids.

Answer :B) They emulsify fats, increasing the surface area for lipase action.

Explanation : Bile salts, produced by the liver and stored in the gallbladder, emulsify fats into
smaller [Link] increases the surface area for pancreatic lipase to act upon, facilitating
more efficient fat digestion.
2. Where does the digestion of lipids primarily begin?

A) Mouth

B) Stomach

C) Small intestine

D) Large intestine

Answer: C) Small intestine

Explanation: Lipid digestion primarily starts in the small intestine, where bile from the liver
emulsifies fats, and pancreatic lipase breaks down triglycerides into fatty acids and glycerol.
Although some lipase activity occurs in the mouth and stomach, the majority of digestion
occurs in the small intestine.

3. Which enzyme is responsible for breaking down triglycerides in the small intestine?

A) Amylase

B) Lipase

C) Pepsin

D) Sucrase

Answer: B) Lipase

Explanation: Pancreatic lipase is the primary enzyme responsible for breaking down
triglycerides (the most common form of fat) into fatty acids and monoglycerides in the small
intestine.

4. Chylomicrons are responsible for transporting which of the following?

A) Exogenous lipids

B) Proteins

C) Endogenous lipids

D) Carbohydrates

Answer: A) Exogenous lipids

Explanation: Chylomicrons are lipoprotein particles transport the exogenous lipids from
intestine to the adipose tissues for storage.
5. Which of the following substances is essential for the formation of micelles in the small
intestine?

A) Amylase

B) Bile salts

C) Glucose

D) Proteins

Answer: B) Bile salts

Explanation: Bile salts are essential for forming micelles, which are small aggregates of bile
salts and lipid molecules. These micelles help in the solubilization of digested lipids, making
it easier for them to be absorbed by enterocytes in the small intestine.

6. What is the main function of the pancreatic lipase in lipid digestion?

A) To break down starches into glucose

B) To emulsify fats into smaller droplets

C) To break down triglycerides into fatty acids and monoglycerides

D) To neutralize acidic chyme entering the small intestineAnswer: C) To break down

triglycerides into fatty acids and monoglycerides

Explanation: Pancreatic lipase is the enzyme that breaks down triglycerides into fatty acids
and monoglycerides, which are small enough to be absorbed by enterocytes in the small
intestine.

8. What is the primary method of transport for absorbed lipids from the intestines to other
parts of the body?

A) Through blood plasma

B) Through chylomicrons

C) Through red blood cells

D) Through albumin

Answer: B) Through chylomicrons

Explanation: Once lipids are absorbed by the enterocytes in the small intestine, they are
re-esterified into triglycerides and packaged into chylomicrons. These chylomicrons enter the
lymphatic system and eventually the bloodstream, where they are transported to tissues
throughout the body.
9. Which of the following is NOT involved in the digestion of lipids?

A) Bile

B) Lipase

C) Pepsin

D) Pancreatic enzymes

Answer: C) Pepsin

Explanation: Pepsin is involved in protein digestion in the stomach, not lipid digestion. Bile,
lipase, and pancreatic enzymes (like pancreatic lipase) are all critical in the digestion and
absorption of lipids.

MCQs on Denovo synthesis of fatty acids

1. Which of the following is the primary source of acetyl-CoA for de novo fatty acid
synthesis?

A) Glucose

B) Pyruvate

C) Acetyl-CoA from the diet

D) Citrate

Answer: D) Citrate

Explanation: Acetyl-CoA is primarily produced in the mitochondria from pyruvate. For fatty
acid synthesis, acetyl-CoA is transported to the cytoplasm in the form of citrate. Once citrate
reaches the cytoplasm, it is broken down into acetyl-CoA and oxaloacetate by the enzyme
ATP-citrate lyase, providing the acetyl-CoA needed for fatty acid synthesis.

2. Which enzyme is responsible for the first committed step in the de novo synthesis of fatty
acids?A) Acetyl-CoA carboxylase

B) Fatty acid synthase

C) ATP-citrate lyase

D) Acyl-CoA desaturase

Answer: A) Acetyl-CoA carboxylase

Explanation: Acetyl-CoA carboxylase (ACC) catalyzes the carboxylation of acetyl-CoA to

form malonyl-CoA,which is the first committed step in fatty acid synthesis. This step is
essential because malonyl-CoA serves as thedonor of two-carbon units during the
elongation process.
3. Which of the following molecules is directly involved in the elongation of fatty acids during
de novo synthesis?

A) NADPH

B) FADH2

C) Coenzyme A

D) ATP

Answer: A) NADPH

Explanation: NADPH provides the reducing equivalents needed during the fatty acid
synthesis process, particularly for the reduction steps in the elongation cycle of fatty acids.
NADPH is required by the enzyme fatty acid synthase during the addition of two-carbon units
from malonyl-CoA to elongate the growing fatty acid chain.

4. What is the final product of the de novo synthesis of fatty acids in humans?

A) Palmitic acid (C16:0)

B) Stearic acid (C18:0)

C) Oleic acid (C18:1)

D) Arachidonic acid (C20:4)

Answer: A) Palmitic acid (C16:0)

Explanation: The de novo synthesis of fatty acids in humans primarily results in the
production of palmitic acid (C16:0), a saturated fatty acid. This is because the fatty acid
synthase enzyme typically synthesizes palmitic acid, although additional elongation and
desaturation reactions can modify this product into longer or unsaturated fatty acids.

5. Acetyl CoA fromed in the mitochondria is made available in the cytoplasm for de novo
synthesis of fatty acids

by the activity of the enzyme.

A)Carnitine acyltransferase

B)ATPcitrate lyase

C)Acetly CoA carboxylaseD) Pyruvate dehydrogenase

Answer: B) ATP-citrate lyase.

ATP-citrate lyase is the enzyme that helps transport acetyl-CoA from the mitochondria to the
cytoplasm for denovo fatty acid synthesis. It does this by converting citrate (which is
transported out of the mitochondria) backinto acetyl-CoA and oxaloacetate in the cytoplasm.
This acetyl-CoA is then used for fatty acid biosynthesis.

MCQs on Ketone body metabolism

1. What is the primary organ involved in ketogenesis?

A) Liver

B) Muscle

C) Brain

D) Kidney

Answer: A) Liver

Explanation: Ketogenesis occurs primarily in the liver, where fatty acids are converted into
ketone bodies(acetoacetate, β-hydroxybutyrate, and acetone) during periods of fasting,
prolonged exercise, or carbohydrate restriction.

2. Which enzyme is responsible for the first step in ketogenesis, converting acetyl-CoA to
acetoacetyl-CoA?

A) Acetyl-CoA carboxylase

B) HMG-CoA synthase

C) Acetyl-CoA acetyltransferase

D) 3-Hydroxy-3-methylglutaryl-CoA synthase

Answer: C) Acetyl-CoA acetyltransferase

Explanation: The first step in ketogenesis involves the enzyme acetyl-CoA acetyltransferase
(also known as thiolase), which converts two molecules of acetyl-CoA into acetoacetyl-CoA.

3. Which of the following ketone bodies is used by extrahepatic tissues (such as muscles) for
energy?

A) Acetone

B) Acetoacetate

C) β-Hydroxybutyrate

D) Both B and C
Answer: D) Both B and CExplanation: Acetoacetate and β-hydroxybutyrate are the primary
ketone bodies that are exported from the liver and used by extrahepatic tissues (e.g.,
muscles and brain) for energy. Acetone is generally exhaled and not usedfor energy.

4. During periods of fasting, which molecule acts as the main fuel source for the brain and
muscles?

A) Glucose

B) Ketone bodies

C) Free fatty acids

D) Lactate

Answer: B) Ketone bodies

Explanation: During fasting, the liver produces ketone bodies (acetoacetate and
β-hydroxybutyrate) from fatty acids. These ketone bodies serve as the main fuel source for
the brain and muscles, especially when glucose levels are low.

5. In the process of ketogenesis, what is the source of acetyl-CoA?

A) Glycolysis

B) Fatty acid oxidation

C) Amino acid catabolism

D) Pentose phosphate pathway

Answer: B) Fatty acid oxidation

Explanation: Acetyl-CoA is primarily derived from the breakdown of fatty acids via
beta-oxidation, which occurs in the mitochondria of liver cells during periods of low
carbohydrate availability.

6. Which condition is most likely to induce ketogenesis?

A) High carbohydrate diet

B) Starvation

C) Increased glucose availability

D) Excessive insulin secretion

Answer: B) Starvation
Explanation: Starvation or prolonged fasting leads to a decrease in glucose availability,
prompting the liver toincrease the production of ketone bodies for use by the brain and
muscles. High carbohydrate diets or excessive insulin secretion inhibit ketogenesis.

7. Which ketone body is primarily exhaled as a by-product of ketogenesis?

A) Acetone

B) AcetoacetateC) β-Hydroxybutyrate

D) Acetyl-CoA

Answer: A) Acetone

Explanation: Acetone is a volatile ketone body that is often exhaled through the lungs. It is
not used as a significant energy source and is considered a waste product of ketogenesis.

8. In ketolysis, what is the final product formed when β-hydroxybutyrate is oxidized?

A) Acetate

B) Acetyl-CoA

C) Glucose

D) Pyruvate

Answer: B) Acetyl-CoA

Explanation: In ketolysis, β-hydroxybutyrate is oxidized to acetoacetate, which is then

converted to [Link] acetyl-CoA enters the citric acid cycle to produce ATP.

MCQs on Lipoprotein metabolism

1. Which of the following lipoproteins is primarily responsible for the transport of cholesterol
from the peripheral

tissues to the liver?

a) Chylomicrons

b) Low-density lipoproteins (LDL)

c) High-density lipoproteins (HDL)

d) Very low-density lipoproteins (VLDL)

Answer: c) High-density lipoproteins (HDL)

Explanation: HDL is responsible for reverse cholesterol transport, where it picks up excess
cholesterol fromperipheral tissues and returns it to the liver for excretion or recycling. This is
why it is considered "good" cholesterol. LDL (Low-Density Lipoprotein) transports cholesterol
from the liver to peripheral tissues, which can contribute to atherosclerosis if levels are too
high.

2. What is the primary function of chylomicrons in lipoprotein metabolism?

a) To deliver triglycerides to adipose tissue and muscle

b) To transport cholesterol from liver to peripheral tissues

c) To reverse cholesterol transport

d) To carry phospholipids from the liver to the intestines

Answer: a) To deliver triglycerides to adipose tissue and muscleExplanation: Chylomicrons

are formed in the intestines after the digestion of dietary fats and primarily transport
triglycerides to peripheral tissues, including adipose tissue and muscle. They also carry
small amounts of cholesterol. Chylomicrons are crucial for the digestion and absorption of
dietary lipids.

3. Which enzyme is responsible for the hydrolysis of triglycerides in chylomicrons and

VLDL?

a) Lipoprotein lipase (LPL)

b) Hepatic lipase

c) Pancreatic lipase

d) Acetyl-CoA carboxylase

Answer: a) Lipoprotein lipase (LPL)

Explanation: Lipoprotein lipase (LPL) is the enzyme responsible for hydrolyzing triglycerides
into free fatty acids and glycerol in the capillaries of muscle and adipose tissue. This process
helps in the delivery of fatty acids for energy storage or use. LPL acts on both chylomicrons
and VLDL to release their triglyceride content.

4. What is the role of apolipoprotein B (ApoB) in lipoprotein metabolism?

a) To activate lipoprotein lipase

b) To serve as the structural component of lipoproteins

c) To facilitate cholesterol esterification

d) To mediate the uptake of lipoproteins by cells

Answer: b) To serve as the structural component of lipoproteins

Explanation: Apolipoprotein B (ApoB) is a major structural protein of various lipoproteins,
including VLDL,LDL, and chylomicrons. ApoB provides structural integrity to lipoproteins and
is involved in the recognition and binding to specific cell surface receptors, allowing the
uptake of lipoproteins into cells.

5. Which of the following lipoproteins is the major carrier of triglycerides in the bloodstream?

a) Chylomicrons

b) HDL

c) LDL

d) VLDL

Answer: a) Chylomicrons

Explanation: Chylomicrons are the major lipoproteins responsible for the transport of dietary
triglycerides. They are produced in the intestines and transport triglycerides to peripheral
tissues, including adipose and muscle tissues, where triglycerides can be stored or used for
energy.

6. What is the primary role of very low-density lipoproteins (VLDL)?a) To carry dietary
cholesterol to peripheral tissues

b) To transport triglycerides from the liver to peripheral tissues

c) To reverse cholesterol transport

d) To carry phospholipids to the intestines

Answer: b) To transport triglycerides from the liver to peripheral tissues

Explanation: VLDL is synthesized in the liver and primarily carries triglycerides to peripheral
tissues, including adipose tissue and muscle. After triglycerides are removed, VLDL
becomes LDL, which mainly transports cholesterol to peripheral tissues.

7. Which lipoprotein is typically considered "bad cholesterol"?

a) Chylomicrons

b) HDL

c) LDL

d) VLDL

Answer: c) LDL
Explanation: Low-Density Lipoprotein (LDL) is often referred to as "bad cholesterol" because
high levels of LDL cholesterol are associated with an increased risk of atherosclerosis, which
can lead to cardiovascular diseases. LDL carries cholesterol from the liver to peripheral
tissues, and excessive cholesterol can deposit in the walls of arteries, leading to plaque
formation.

[Link] of the following lipoproteins is responsible for reverse cholesterol transport?

a) Chylom icrons

b) VLDL

c) LDL

d) HDL

Answer: d) HDL

Explanation: HDL is responsible for reverse cholesterol transport, which involves the
movement of excess cholesterol from peripheral tissues back to the liver. This process helps
reduce the risk of cholesterol buildup in the arteries, making HDL beneficial for
cardiovascular health.

9. Which enzyme is responsible for converting cholesterol into cholesteryl ester in HDL?

a) Lecithin-cholesterol acyltransferase (LCAT)

b) Acyl-CoA:cholesterol acyltransferase (ACAT)

c) Phospholipase A2

d) Lipoprotein lipase

Answer: a) Lecithin-cholesterol acyltransferase (LCAT)Explanation: LCAT is an enzyme

found in the bloodstream that esterifies cholesterol, converting it into cholesteryl ester. This
process occurs primarily in HDL particles and allows the cholesterol to be carried more
efficiently for reverse cholesterol transport to the liver.

Questions on Lipid metabolism

Reasoning questions:( 3 marks)

1. Statins are used to reduce high cholesterol levels. Justify

2. Hypercholesterolemia is seen in Diabetes mellitus. Explain.

[Link] cholesterol lowers the risk of cardiovascular disease.

[Link] of Essential fatty acids causes dermatitis . Give reason

[Link] of lipotrophic factors causes fatty liver. Justify.

[Link] is involved in Reverse cholesterol transport pathway. Explain.

Short note question: (Applied aspect) (5 marks)

1. A 40 year old man is brought to hospital in a comatose state. On examination, he was

found to be dehydrated and toxic with a characteristic breathing pattern and a sweet smell
on his breath. The following are the blood investigations report.

Blood glucose (Random) – 380mg/dl

Urine benedicts test - brick red

Rothera’s test – positive

Serum bicarbonate – 15meq/l

Plasma pH – 7.2

1. What is your probable diagnosis? (1 mark)

2. Why there is sweet smell in his breath? (1 mark)

[Link] in detail the role of ketosis in diabetes mellitus. (3 marks)

Structured long essay : (12 marks)

1. Discuss the biochemical pathways involved in cholesterol metabolism, including its

synthesis,regulation, transport, and degradation. Name the rate limiting step of cholesterol
synthesis. Explain the role of

2. cholesterol in atherosclerosis. (8+1+3)

Explain the steps of beta oxidation of Palmitic acid. Add a note on its energetic. Give an
account on sources and fate of Acetyl CoA ( 6+3+3)3. Discuss the steps of Ketogenesis and
Ketolysis with its regulation. Add a note on its significance(4+4+2+2)

Short notes : (6/5 marks)

[Link] is Fatty liver? Explain in detail the causes of fatty liver.(1 + 4 marks)

[Link] the steps of denovo synthesis of fatty acids . How it is regulated(3+2)

[Link] the role of carnitine in beta oxidation of fatty acids.

 ACID BASE BALANCE

Long Essay(12 marks)

1. A 40 year old male patient brought to the causality with complaints of persistent vomiting
since one week and generalized muscle cramps, O/E dehydration, shallow respiration were
present. Laboratory report revealed: pH 7.8, bicarbonate 35 mEq/l and pCO2: 55 mm of Hg,

a) Identify the acid base disorder

b) Mention the causes for above condition.

c) Write the normal values for pH, bicarbonate and pCO2 in arterial blood.

d) Explain compensatory mechanism to correct the above condition.

e) Describe the renal mechanism of pH regulation. (1+1+3+1+5)

2. A 50 year old man, a heavy smoker with cough and sputum was admitted to the hospital
because of difficulty in breathing. He was drowsy and cyanosed.O/E BP was 100/60 mmHg,
tachycardia was present, respiration decreased. ABG analysis shows pH: 7.24, pCO2: 60
mm of Hg, Bicarbonate:35 mmol/L

[Link] is your probable diagnosis?

b. What are the causes for such condition?

c. Write the normal values for pH, bicarbonate and pCO2 in arterial blood

d. Discuss the compensatory mechanismto correct the above condition.

e. Describe the role of kidney in pH regulation. (1+1+3+1+5)

3. A 25-year-old type 1 diabetes mellitus patient presented with hypertension, dry mucous
membrane and poor skin turgor.O/E patient was tachypneic with fruity odourin breath. Blood
investigation showed; RBS: 550mg/dl, pH: 7.25 Bicarbonate:16 mEq/l, pCO2: 38 mm of Hg.

a. What is the acid base disorder present in this case?

b. What is the most probable cause?

c. Discuss the compensation in this condition.

d. Describe the role of respiratory system in pH regulation.

e. Explain anion gap and causes for increased anion gap. (1+1+2+4+4)4. Mention the
normal blood pH. Name the mechanisms that regulate blood pH. Classify acid base
disorders with the causes for each type. Add a note on metabolic acidosis. (1+2+4+5)

Short Essays (6/5 marks)

1. Explain the importance of acid base balance in the body. Explain how kidneys help in
maintaining acid base balance

[Link] are Blood buffers? Mention different buffer systems and their role in the regulation of
pH.

3. Define anion [Link] the normal anion gap and two examples of high anion gap
metabolic acidosis.

[Link] the serum reference range for the following; pH, pCO2, bicarbonate, sodium,
potassium and chloride

Short Essays – Applied aspects (5 marks)

1. Describe the basic defect, causes, features, compensation in case of metabolic acidosis.

2. Describe the basic defect, causes, features, compensation in case of metabolic alkalosis.

Reasoning questions

1. Why does hyperventilation cause respiratory alkalosis?

2. Why do the kidneys play a crucial role in long-term acid-base balance?

3. Why does vomiting lead to metabolic alkalosis?

4. Why does diarrhea lead to metabolic acidosis?

5. Why does an increase in CO₂ levels cause a decrease in blood pH?

MCQs

1. A patient presents with prolonged vomiting. How would this affect their acid-base
balance?

a) Metabolic acidosis

b) Metabolic alkalosis

c) Respiratory acidosis

d) Respiratory alkalosis

Answer:b) Metabolic alkalosis

Reasoning: Vomiting leads to the loss of gastric acid (HCl), which results in an increased pH
(alkalosis) and elevated bicarbonate levels.

2. A patient with chronic obstructive pulmonary disease (COPD) has an arterial blood pH of
7.28, PaCO₂ of 55 mmHg, and HCO₃⁻ of 30 mEq/L. What is the primary disorder?

a) Respiratory acidosis

b) Respiratory alkalosisc) Metabolic acidosis

d) Metabolic alkalosis

Answer:a) Respiratory acidosis

Reasoning: The high PaCO₂ indicates CO₂ retention due to impaired lung function, leading to
acidosis. The elevated HCO₃⁻ suggests partial renal compensation.

3. A patient is hyperventilating due to anxiety. What acid-base imbalance is most likely?

a) Metabolic acidosis

b) Metabolic alkalosis

c) Respiratory acidosis

d) Respiratory alkalosis

Answer:d) Respiratory alkalosis

Reasoning: Hyperventilation causes excessive CO₂ loss, which raises blood pH, leading to
alkalosis.

4. A person with severe diarrhea is likely to develop which acid-base disorder?

a) Metabolic acidosis

b) Metabolic alkalosis

c) Respiratory acidosis

d) Respiratory alkalosis

Answer:a) Metabolic acidosis

Reasoning:Diarrhea leads to the loss of bicarbonate (HCO₃⁻) from intestinal secretions,

causing acidosis.
5. Which organ system primarily compensates for metabolic acidosis?

a) Lungs

b) Liver

c) Kidneys

d) Pancreas

Answer:a) Lungs

Reasoning: The lungs compensate by increasing ventilation to "blow off" CO₂ and reduce
acidity.

6. A patient with diabetic ketoacidosis (DKA) presents with deep, rapid breathing (Kussmaul

respiration). What is the physiological reason behind this?

a) The body is trying to retain CO₂

b) The body is compensating for metabolic acidosis

c) The body is conserving bicarbonate

d) The body is reducing pH

Answer:b) The body is compensating for metabolic acidosisReasoning:Kussmaul breathing

helps eliminate CO₂, reducing acidity and compensating for ketoacid accumulation.

7. A patient has an arterial pH of 7.50, PaCO₂ of 48 mmHg, and HCO₃⁻ of 34 mEq/L. What is
the likely diagnosis?

a) Metabolic acidosis

b) Metabolic alkalosis

c) Respiratory acidosis

d) Mixed disorder

Answer:b) Metabolic alkalosis

Reasoning: The high pH and elevated HCO₃⁻ indicate alkalosis. The slightly high PaCO₂
suggests respiratory compensation.
8. In chronic renal failure, patients often develop metabolic acidosis. Why?

a) Excessive loss of CO₂

b) Reduced acid excretion and bicarbonate production

c) Increased hydrogen ion loss

d) Overproduction of bicarbonate

Answer:b) Reduced acid excretion and bicarbonate production

Reasoning: The kidneys fail to excrete H⁺ and regenerate bicarbonate, leading to acidosis.

9. A patient with aspirin overdose presents with hyperventilation. What is the initial acid-base

disorder?

a) Metabolic acidosis

b) Metabolic alkalosis

c) Respiratory acidosis

d) Respiratory alkalosis

Answer:d) Respiratory alkalosis

Reasoning: Aspirin (salicylate) toxicity initially stimulates the respiratory center, leading to
CO₂ loss and alkalosis.

10. A blood gas analysis shows pH 7.32, PaCO₂ 30 mmHg, and HCO₃⁻ 18 mEq/L. What is
the likely diagnosis?

a) Metabolic acidosis with respiratory compensation

b) Respiratory acidosis with metabolic compensation

c) Respiratory alkalosis with metabolic compensationd) Metabolic alkalosis with respiratory

compensation

Answer:a) Metabolic acidosis with respiratory compensation

Reasoning: The low HCO₃⁻ indicates metabolic acidosis. The low PaCO₂ suggests the lungs
are compensating by increasing ventilation.
11. A patient has metabolic acidosis with a high anion gap. What is the most likely cause?

a) Diarrhea

b) Vomiting

c) Ketoacidosis

d) Renal tubular acidosis

Answer:c) Ketoacidosis

Reasoning: High anion gap metabolic acidosis is caused by ketoacidosis, lactic acidosis, or
toxin ingestion.

12. In a patient with acute asthma exacerbation, what acid-base imbalance is expected
initially?

a) Metabolic acidosis

b) Metabolic alkalosis

c) Respiratory acidosis

d) Respiratory alkalosis

Answer:d) Respiratory alkalosis

Reasoning: Initially, hyperventilation decreases CO₂, raising pH (alkalosis). If prolonged,

respiratory fatigue can lead to acidosis.

13. A patient with advanced chronic kidney disease presents with metabolic acidosis and
normal anion gap. What is the mechanism?

a) Decreased bicarbonate reabsorption

b) Excess lactic acid production

c) Increased ketone production

d) Increased ammonia excretion

Answer:a) Decreased bicarbonate reabsorption

Reasoning: Normal anion gap metabolic acidosis (hyperchloremic acidosis) occurs due to
defective bicarbonate reabsorption.
14. A newborn has respiratory distress syndrome and develops respiratory acidosis. What is
the primary defect?

a) Excess CO₂ production

b) Decreased CO₂ excretion due to poor lung function

c) Increased bicarbonate loss

d) Increased acid excretion

Answer:b) Decreased CO₂ excretion due to poor lung function

Reasoning: Respiratory distress leads to CO₂ retention, causing respiratory acidosis.

15. A patient is hypokalemic and has metabolic alkalosis. Which condition is most likely
responsible?

a) Diabetic ketoacidosis

b) Chronic vomiting

c) Salicylate toxicity

d) Renal failure

Answer:b) Chronic vomiting

Reasoning: Vomiting leads to loss of H⁺ and Cl⁻, causing metabolic alkalosis and
hypokalemia.

16. What is the normal pH range of arterial blood?

a) 6.8 – 7.2

b) 7.35 – 7.45

c) 7.5 – 7.8

d) 8.0 – 8.5

Answer:b) 7.35 – 7.45

[Link] organ system primarily regulates CO₂ levels in the body?

a) Kidneys

b) Liver

c) Lungs

d) Intestines

Answer:c) Lungs

[Link] of the following acts as the primary buffer system in blood?

a) Sodium-potassium pump

b) Phosphate buffer system

c) Bicarbonate buffer system

d) Protein buffer system

Answer:c) Bicarbonate buffer system

19. Which equation describes the relationship between pH, bicarbonate (HCO₃⁻), and carbon
dioxide (CO₂)?

a) Michaelis-Menten equation

b) Henderson-Hasselbalch equation

c) Nernst equation

d) Hill equation

Answer:b) Henderson-Hasselbalch equation

20. Which of the following is the most common cause of respiratory acidosis?

a) Hyperventilation

b) Chronic obstructive pulmonary disease (COPD)

c) Severe vomiting

d) Diarrhea

Answer:b) Chronic obstructive pulmonary disease (COPD)

21. What happens to blood pH when CO₂ levels increase?

a) pH increases

b) pH decreases

c) pH remains unchanged

d) pH fluctuates randomly

Answer:b) pH decreases

22. Which organ system is responsible for long-term regulation of acid-base balance?

a) Respiratory system

b) Renal system

c) Digestive system

d) Nervous system

Answer:b) Renal system

23. Which of the following is a cause of metabolic acidosis?

a) Excessive CO₂ retention

b) Loss of bicarbonate through diarrhea

c) Hyperventilation

d) Excessive vomiting

Answer:b) Loss of bicarbonate through diarrhea

24. A decrease in blood bicarbonate (HCO₃⁻) levels leads to which condition?

a) Metabolic alkalosis

b) Metabolic acidosis

c) Respiratory alkalosis

d) No effect on acid-base balance

Answer:b) Metabolic acidosis

25. What is the primary mechanism of compensation for metabolic acidosis?

a) Retaining bicarbonate in the kidneys

b) Hyperventilation to remove CO₂

c) Decreasing hydrogen ion excretion

d) Increasing CO₂ retention

Answer:b) Hyperventilation to remove CO₂

26. A patient has an arterial pH of 7.30, PaCO₂ of 50 mmHg, and HCO₃⁻ of 24 mEq/L. What
is the primary acid-base disorder?

a) Respiratory acidosis

b) Respiratory alkalosis

c) Metabolic acidosis

d) Metabolic alkalosis

Answer:a) Respiratory acidosis

Reasoning: The low pH indicates acidosis. The high PaCO₂ suggests CO₂ retention due to
impaired ventilation, confirming respiratory acidosis.

27. A patient with renal failure develops metabolic acidosis. What is the primary cause?

a) Excess bicarbonate reabsorption

b) Reduced hydrogen ion excretion and bicarbonate regeneration

c) Increased pulmonary ventilation

d) Loss of gastric acid

Answer:b) Reduced hydrogen ion excretion and bicarbonate regeneration

Reasoning: The kidneys play a major role in excreting H⁺ and generating HCO₃⁻. In renal
failure, these functions are impaired, leading to acidosis.
28. A person with severe dehydration has an arterial pH of 7.50. What acid-base disorder is
most likely?

a) Respiratory acidosis

b) Respiratory alkalosis

c) Metabolic acidosis

d) Metabolic alkalosis

Answer:d) Metabolic alkalosis

Reasoning: Dehydration leads to fluid loss, causing hypovolemia. This often triggers
aldosterone release, leading to bicarbonate retention and metabolic alkalosis.

29. A patient with chronic diarrhea is at risk of developing metabolic acidosis. Why?

a) Excessive loss of hydrochloric acid

b) Loss of bicarbonate from intestinal secretions

c) Increased CO₂ retention

d) Increased hydrogen ion secretion in urineAnswer:b) Loss of bicarbonate from intestinal

secretions

Reasoning: The intestines contain bicarbonate-rich fluids. Chronic diarrhea leads to

bicarbonate loss, reducing blood pH and causing acidosis.

30. A person suffering from a panic attack starts hyperventilating. How does this affect blood
pH?

a) pH increases due to CO₂ loss

b) pH decreases due to CO₂ retention

c) pH remains unchanged

d) pH decreases due to HCO₃⁻ loss

Answer:a) pH increases due to CO₂ loss

Reasoning: Hyperventilation leads to excessive CO₂ elimination, reducing carbonic acid

concentration and increasing pH (respiratory alkalosis).
Moderate Reasoning Questions

1. A patient with diabetic ketoacidosis has Kussmaul breathing. What is the physiological
reason for this?

a) The body is trying to conserve CO₂

b) The body is compensating for metabolic acidosis

c) The body is trying to retain bicarbonate

d) The body is lowering pH

Answer:b) The body is compensating for metabolic acidosis

Reasoning:Kussmaul breathing (deep, rapid respiration) helps eliminate CO₂, which reduces
acidity and partially compensates for ketoacid accumulation.

2. A person ingests a large amount of aspirin. What is the initial acid-base disturbance?

a) Metabolic acidosis

b) Metabolic alkalosis

c) Respiratory acidosis

d) Respiratory alkalosis

Answer:d) Respiratory alkalosis

Reasoning: Aspirin (salicylates) initially stimulates the respiratory center, causing

hyperventilation and CO₂ loss, leading to respiratory alkalosis.

3. A patient presents with an arterial pH of 7.28 and a low HCO₃⁻ concentration. Which of the

following is the most likely compensation?

a) Increased bicarbonate reabsorption by the kidneys

b) Decreased breathing ratec) Increased CO₂ retention

d) Decreased hydrogen ion excretion

Answer:a) Increased bicarbonate reabsorption by the kidneys

Reasoning: The low HCO₃⁻ and acidic pH indicate metabolic acidosis. The kidneys
compensate by reabsorbing bicarbonate to buffer the blood.
4. A patient with chronic obstructive pulmonary disease (COPD) has an arterial pH of 7.36,
PaCO₂ of 55 mmHg, and HCO₃⁻ of 32 mEq/L. What does this indicate?

a) Acute respiratory acidosis

b) Chronic respiratory acidosis with renal compensation

c) Metabolic alkalosis with respiratory compensation

d) Uncompensated metabolic acidosis

Answer:b) Chronic respiratory acidosis with renal compensation

Reasoning: The high PaCO₂ indicates CO₂ retention (respiratory acidosis), but the normal
pH and elevated HCO₃⁻ suggest renal compensation.

5. A patient with vomiting and dehydration has an arterial blood pH of 7.48 and high
bicarbonate levels. What is the likely cause?

a) Excessive hydrogen ion loss

b) CO₂ retention

c) Bicarbonate loss through kidneys

d) Increased lactic acid production

Answer:a) Excessive hydrogen ion loss

Reasoning: Vomiting leads to gastric acid (HCl) loss, reducing H⁺ concentration and
increasing pH, resulting in metabolic alkalosis.

Advanced Reasoning Questions

1. A patient with a blood pH of 7.20 and normal PaCO₂ has metabolic acidosis. What test
would help

determine the cause?

a) Blood glucose level

b) Anion gap calculation

c) Serum sodium level

d) Arterial oxygen saturation

Answer:b) Anion gap calculationReasoning: The anion gap helps differentiate causes of
metabolic acidosis, such as ketoacidosis (high anion gap) or diarrhea (normal anion gap).
2. In a patient with acute asthma exacerbation, what acid-base disorder occurs initially?

a) Metabolic acidosis

b) Metabolic alkalosis

c) Respiratory acidosis

d) Respiratory alkalosis

Answer:d) Respiratory alkalosis

Reasoning: In the early stages of an asthma attack, hyperventilation reduces CO₂ levels,
causing an increase in pH (respiratory alkalosis). If the attack persists, respiratory acidosis
may develop due to CO₂ retention.

3. A patient in septic shock develops metabolic acidosis. What is the underlying cause?

a) Loss of bicarbonate through urine

b) Hypoxia leading to lactic acid accumulation

c) Increased bicarbonate production

d) Hyperventilation

Answer:b) Hypoxia leading to lactic acid accumulation

Reasoning: In septic shock, poor tissue perfusion leads to anaerobic metabolism, increasing
lactic acid production and causing metabolic acidosis.

4. A blood gas analysis shows pH 7.32, PaCO₂ 55 mmHg, and HCO₃⁻ 28 mEq/L. What is the
likely cause?

a) Acute metabolic acidosis

b) Uncompensated respiratory acidosis

c) Respiratory acidosis with renal compensation

d) Metabolic alkalosis with respiratory compensation

Answer:c) Respiratory acidosis with renal compensation

Reasoning: The high PaCO₂ suggests CO₂ retention (respiratory acidosis). The elevated
HCO₃⁻ indicates the kidneys are compensating by retaining bicarbonate
 BIOLOGICAL OXIDATION

Short essays (5 marks)

1. Describe the structure, components and organization of ETC (Electron Transport Chain)
with neat labeled diagram. List any three inhibitors of ETC.

2. What is Oxidative phosphorylation? Explain Chemiosmotic theory.

3. Classify enzymes involved in biological oxidation with examples.

4. Discuss the shuttle systems to transport extra mitochondrial reducing equivalents.

5. What are high energy compounds? Classify them and describe their biological
significance.

6. Describe the structure of ATP Synthase. Add a note on Boyer’s binding change model.

7. Discuss about the following with examples

a. Uncouplers b. Inhibitors of oxidative phosphorylation (2.5+2.5)

8. Discuss the metabolism in brown adipose tissue. Add a note on its significance.

Reasoning Qs (3 marks)

1. Oxidative phosphorylation is a very tightly coupled process. Justify

2. ATP is an example of high energy compound. Justify.

3. ATP synthase is probably the smallest motor on the earth. Why?

4. Uncouplers break the link between electron transport and ATP synthesis. Give reason.

MCQs

1. A scientist is studying a patient with a mutation that prevents Complex I from functioning.
Which of the following would be the most likely consequence?

a) Decreased ATP production and increased lactate levels

b) Increased ATP production due to compensation by Complex II

c) Increased NADH oxidation and ATP synthesis

d) No effect on oxidative phosphorylation

Answer: a) Decreased ATP production and increased lactate levels

Explanation: If Complex I is nonfunctional, NADH cannot donate electrons to the ETC,
reducing ATP production. Cells compensate via anaerobic glycolysis, leading to lactate
buildup.

2. A toxin is discovered that binds to ubiquinone (Coenzyme Q), preventing its ability to
transfer electrons to Complex III. What would be the expected outcome?

a) Oxygen consumption increases

b) ATP production continues as usualc) Electron flow through Complex I and II stops

d) NADH and FADH₂ oxidation remain unaffected

Answer: c) Electron flow through Complex I and II stops

Explanation: Coenzyme Q is necessary for transferring electrons from Complexes I and II to

III. Blocking it stops electron transport beyond this point.

3. A patient presents with cyanide poisoning. Which step in the electron transport chain is
most directly affected?

a) Electron transfer from NADH to Complex I

b) Reduction of oxygen by Complex IV

c) Proton pumping by Complex III

d) ATP synthesis by ATP synthase

Answer: b) Reduction of oxygen by Complex IV

Explanation: Cyanide binds to Complex IV, preventing oxygen from being reduced to water.
This stops electron flow, halting ATP production.

4. A researcher adds a compound that selectively inhibits Complex II of the ETC. How would
this affect ATP synthesis?

a) No effect, since Complex I is still functional

b) ATP synthesis stops completely

c) ATP production decreases but does not stop entirely

d) Oxygen consumption increases

Answer: c) ATP production decreases but does not stop entirely

Explanation: Complex II transfers electrons from FADH₂ to CoQ, bypassing Complex I.

Inhibition reduces FADH₂ oxidation but NADH electrons still flow, so ATP production
decreases but does not stop.
5. During an experiment, a student finds that oxygen consumption is occurring, but no ATP is
being synthesized. What is the most likely explanation?

a) A blockage in Complex I

b) ATP synthase is inhibited or uncoupling is occurring

c) The proton gradient is too strong

d) Cytochrome c is overactive

Answer: b) ATP synthase is inhibited or uncoupling is occurring

Explanation: If the ETC is active but ATP synthesis is not happening, an uncoupler might be
dissipating the proton gradient or ATP synthase is inhibited.

6. A scientist isolates mitochondria and treats them with oligomycin, an inhibitor of ATP
synthase. What will happen?

a) ATP synthesis will increase

b) Oxygen consumption will stop

c) The proton gradient will dissipate

d) NADH oxidation will speed up

Answer: b) Oxygen consumption will stop

Explanation: Oligomycin prevents protons from flowing through ATP synthase, leading to a
backlog of protons, stopping ETC function and oxygen consumption.

7. A mitochondrion is found to be actively oxidizing NADH, but ATP synthesis is severely

reduced. Which of the following best explains the observation?

a) Increased glycolysis

b) Presence of an uncoupler

c) Inhibition of Complex I

d) Decreased oxygen consumption

Answer: b) Presence of an uncoupler

Explanation: If NADH oxidation is occurring but ATP is not being generated efficiently, an
uncoupler is likely disrupting the proton gradient.
8. A new drug is found to inhibit Complex III in the ETC. What would be the expected
consequences?

a) Increased oxygen consumption

b) Accumulation of NADH and FADH₂

c) Increased ATP synthesis

d) Increased proton pumping

Answer: b) Accumulation of NADH and FADH₂

Explanation: If Complex III is blocked; electrons cannot pass through, leading to buildup of
NADH and FADH₂.

9. Which of the following is responsible for generation of heat in newborns?

a) Complex IV

b) ATP synthase

c) Thermogenin

d) 2, 4-Dinitrophenol

Answer: c)

10. The P:O ratio for the oxidation of NADH is______

a) 1 b) 1.5 c) 2 d) 2.5

Answer: d)
 NUCLEIC ACID CHEMISTRY

Short Essays (5/6 Marks)

1. Explain the Watson and crick model of DNA with neat labeled diagram. Mention the
functions of DNA

2. Mention different types of RNA with their functions. Draw a neat labeled diagram of t-RNA

3. Differentiate between DNA and [Link] a note on Chargaff’s rule.

4. Enumerate biologically important nucleotides with their significance.

5. What are synthetic nucleotides? Write four examples with their significance.

Reasoning Qs (3 marks)

1. Hydrogen bonds play a crucial role in DNA structure. Give reasons

2. Total purines in DNA is equal to total pyrimidines. Justify.

MCQs

1. A scientist is analyzing a nucleotide sequence and finds uracil instead of thymine. What
type of nucleic acid is she studying?

a) DNA

b) RNA

c) Protein

d) Lipid

Answer: b) RNA

2. A researcher heats a DNA sample to 95°C. What is most likely to happen?

a) The sugar-phosphate backbone breaks

b) The hydrogen bonds between base pairs break

c) The DNA sequence changes

d) The DNA remains unchanged

Answer: b) The hydrogen bonds between base pairs break

3. A biochemist finds that a DNA sample contains 30% adenine. What percentage of the
sample is guanine?

a) 20%

b) 30%

c) 40%

d) 60%

Answer: a) 20%

4. Which of the following is the basic structural unit of nucleic acids?

a) Amino acids

b) Nucleotides

c) Monosaccharides

d) Fatty acids

Answer: b) Nucleotides

5. Which sugar is present in DNA?

a) Ribose

b) Deoxyribose

c) Glucose

d) Fructose

Answer: b) Deoxyribose

6. Which of the following bases is NOT found in DNA?

a) Adenine

b) Cytosine

c) Uracil

d) Thymine

Answer: c) Uracil
7. What type of bond holds the two strands of DNA together?

a) Covalent bonds

b) Ionic bonds

c) Hydrogen bonds

d) Peptide bonds

Answer: c) Hydrogen bonds

8. Which of the following is a pyrimidine base?

a) Adenine

b) Guanine

c) Cytosine

d) None of the above

Answer: c) Cytosine

9. In RNA, adenine pairs with which nitrogenous base?

a) Thymine

b) Guanine

c) Cytosine

d) Uracil

Answer: d) Uracil

10. Which type of RNA carries amino acids to the ribosome during protein synthesis?

a) mRNA

b) tRNA

c) rRNA

d) snRNA

Answer: b) tRNA
11. Which statement is true about the DNA double helix?

a) It is left-handed

b) It consists of three strands

c) The strands run antiparallel to each other

d) It does not contain hydrogen bonds

Answer: c) The strands run antiparallel to each other