23BMT21 - Biosciences for Medical Engineering CIA II Questions & Answer Key

Q1 Define Necrosis.

2 Marks CO3 K1 PO2 2.2.1

Definition: Necrosis is the unprogrammed, accidental, and irreversible form of cell death resulting from severe cell injury (such as ischemia, hypoxia, trauma, or toxic exposure).
Key Characteristics: It is characterized by cellular swelling, denaturation of proteins, organelle breakdown, plasma membrane rupture, and leakage of cellular contents, triggering a prominent local inflammatory response.

Q2 State the term Biopsy.

2 Marks CO3 K1 PO2 2.2.1

Definition: A biopsy is a diagnostic medical procedure involving the surgical extraction of a small tissue sample or cell collection from a living body.
Clinical Purpose: The removed tissue sample is subjected to microscopic, histological, or molecular examination to identify disease states, confirm malignancies (cancer), or evaluate inflammatory conditions.

Q3 What will be the reason for Diabetes Mellitus?

2 Marks CO4 K2 PO1 1.2.1

Primary Cause: Diabetes Mellitus is a metabolic disorder caused by impairment in insulin production, insulin action, or both, leading to persistent hyperglycemia.
Type 1 Diabetes Causes: Autoimmune destruction of pancreatic beta cells in the Islets of Langerhans leading to absolute insulin deficiency.
Type 2 Diabetes Causes: Peripheral insulin resistance combined with progressive compensatory secretion failure of beta cells, often exacerbated by obesity and sedentary lifestyle.

Q4 What is Blood Pressure and mention the normal value of Blood Pressure?

2 Marks CO4 K2 PO2 2.2.1

Definition: Blood Pressure (BP) is the lateral force exerted by circulating blood against the internal walls of systemic blood vessels (arteries) during cardiac cycles.
Normal Value: Standard resting arterial blood pressure in a healthy adult is approximately 120/80 mmHg.
Systolic / Diastolic: 120 mmHg represents Systolic Pressure (maximum pressure during ventricular contraction), and 80 mmHg represents Diastolic Pressure (minimum pressure during ventricular relaxation).

Q5 Define obesity.

2 Marks CO4 K1 PO2 2.2.1

Definition: Obesity is a complex medical lifestyle disease characterized by excessive and abnormal accumulation of body fat (adipose tissue) that presents a risk to health.
Clinical Criterion: It is clinically diagnosed when an individual's Body Mass Index (BMI) is equal to or exceeds 30 kg/m², increasing the risk for cardiovascular conditions, diabetes, and osteoarthritis.

Q6 State the term hyperemia.

2 Marks CO4 K1 PO1 1.2.1

Definition: Hyperemia refers to an active vascular process in which there is an increased volume of blood flow into a specific tissue or organ due to arteriolar dilation.
Mechanism & Example: It occurs in response to elevated metabolic demand (e.g., exercise in skeletal muscle) or neurogenic/humoral stimuli during acute inflammation, causing the affected tissue to appear red and warm (erythema).

Q7 Differ Gram positive and Gram negative bacteria.

2 Marks CO5 K2 PO2 2.2.1

Cell Wall Structure: Gram-positive bacteria have a thick peptidoglycan layer without an outer membrane; Gram-negative bacteria have a thin peptidoglycan layer surrounded by an outer lipopolysaccharide (LPS) membrane.
Gram Stain Reaction: Gram-positive retain Crystal Violet stain and appear purple/blue; Gram-negative lose primary stain during decolorization, retain Safranin, and appear pink/red.

Q8 Compare the key features between SEM and TEM.

2 Marks CO5 K2 PO2 2.1.1

Scanning Electron Microscope (SEM): Scans an electron beam across the surface to produce detailed 3D surface topography images with moderate magnification and resolution.
Transmission Electron Microscope (TEM): Passes an electron beam through an ultra-thin specimen slice to capture internal 2D ultrastructure with extremely high resolution and magnification.

Q9 Define microscope.

2 Marks CO5 K1 PO1 1.2.1

Definition: A microscope is an optical or electronic laboratory instrument designed to magnify small, microscopic structures (such as cells, tissue sections, or microorganisms) that are invisible to the unaided human eye.
Primary Functions: It resolves fine structural details by leveraging light photons or focused electron beams through a series of optical lenses or magnetic coils.

Q10 List the common bacterial diseases of human being.

2 Marks CO5 K1 PO2 2.2.1

Tuberculosis: Caused by Mycobacterium tuberculosis, primarily affecting lung parenchyma.
Typhoid Fever: Caused by Salmonella typhi, affecting gastrointestinal system.
Cholera: Caused by Vibrio cholerae, leading to severe intestinal fluid loss.
Pneumonia & Tetanus: Caused by Streptococcus pneumoniae and Clostridium tetani respectively.

Q11 (a) Apply your knowledge of cell injury to decide whether liver cell swelling and fat buildup from alcohol use is a reversible or irreversible cell injury.

16 Marks CO3 K3 PO2 2.1.1

1. Assessment Verdict and Decision

Liver cell swelling (hydropic change) and lipid accumulation (steatosis / fatty liver) caused by alcohol ingestion constitute reversible cell injury, provided that toxic exposure stops before permanent membrane breakdown or nuclear pyknosis occurs.

2. Pathophysiological Mechanism of Liver Cell Swelling (Hydropic Change)

Metabolism of alcohol (ethanol) into acetaldehyde via alcohol dehydrogenase consumes intracellular NAD⁺, impairing oxidative phosphorylation in hepatic mitochondria:

ATP Depletion: Failure of mitochondrial ATP production inactivates energy-dependent membrane transport pumps, notably the plasma membrane Na⁺/K⁺-ATPase pump.
Ionic Imbalance: Intracellular accumulation of sodium (Na⁺) draws water osmotically into hepatocytes, leading to cellular swelling, dilation of endoplasmic reticulum, and blebbing.

3. Pathophysiological Mechanism of Fat Buildup (Hepatic Steatosis)

Elevated NADH/NAD⁺ ratio suppresses mitochondrial beta-oxidation of fatty acids in hepatocytes:

Triglyceride Accumulation: Free fatty acids are re-esterified into triglycerides and stored within cytoplasm as lipid vacuoles.
Impaired Lipoprotein Export: Alcohol disrupts apolipoprotein synthesis required for VLDL secretion, trapping lipids inside the liver parenchyma.

4. Features Indicating Reversibility vs Irreversibility

Reversible State: Intact plasma membranes, intact nuclear chromatin structure, and functional recovery upon cessation of alcohol intake.
Transition to Irreversible State: Persistent exposure leads to irreversible damage marked by severe membrane breakdown, massive influx of calcium (Ca²⁺), nuclear degradation (pyknosis, karyorrhexis, karyolysis), and hepatic necrosis/cirrhosis.

Q11 (b) Plan the sequence of events that occur during the inflammatory response and explain these in the tissue repair.

16 Marks CO3 K3 PO2 2.2.1

1. Sequential Phases of the Inflammatory Response

Acute vascular and cellular events initiated to eliminate tissue injury sources:

Vascular Changes: Transient vasoconstriction followed by vasodilation mediated by histamine, increasing microvascular blood flow (rubor and calor). Increased vascular permeability causes protein-rich fluid exudation (tumor).
Leukocyte Cellular Events: Neutrophil recruitment via margination, rolling (selectins), firm adhesion (integrins), transmigration across endothelium (diapedesis), and chemotactic migration to tissue site.
Phagocytosis & Clearance: Opsonization, engulfment, and enzymatic degradation of debris by neutrophils and tissue macrophages.

2. Transition from Inflammation to Repair

Switching from pro-inflammatory (M1) to anti-inflammatory/reconstructive (M2) macrophages releasing growth factors (TGF-β, PDGF, VEGF) to stimulate wound healing mechanisms.

3. Tissue Repair Events (Granulation, Angiogenesis, Fibrosis)

Angiogenesis: VEGF-stimulated growth of new capillary blood vessels to supply oxygen and nutrients to repairing tissue.
Granulation Tissue Formation: Proliferation of fibroblasts depositing extracellular matrix (ECM), collagen type III, and proteoglycans.
Re-Epithelialization: Migration and proliferation of epithelial cells across the damaged surface to restore protective barrier.

4. Tissue Remodeling & Scar Maturation

Matrix metalloproteinases (MMPs) degrade fragile type III collagen and replace it with strong type I collagen, increasing tissue tensile strength over weeks to months.

Q12 (a) Explain the normal hemostasis and thrombosis with a neat sketch.

16 Marks CO4 K2 PO2 2.2.1

1. Stages of Normal Hemostasis

Physiological mechanism designed to arrest bleeding following vascular injury:

Arteriolar Vasoconstriction: Reflex neurogenic mechanisms and endothelin release temporarily reduce local blood flow.
Primary Hemostasis (Platelet Plug Formation): Platelet adhesion to subendothelial collagen via von Willebrand Factor (vWF), platelet activation, shape change, ADP/TXA2 release, and aggregation into a primary plug.
Secondary Hemostasis (Fibrin Clot Formation): Activation of the coagulation cascade (tissue factor activation of extrinsic pathway), converting prothrombin to thrombin, which cleaves fibrinogen to insoluble cross-linked fibrin networks.

2. Pathologic Thrombosis & Virchow's Triad

Thrombosis is inappropriate intravascular blood clot formation inside intact vessels. Governed by Virchow's Triad:

Endothelial Injury: Direct vascular trauma, hypertension, or atherosclerosis exposing collagen.
Abnormal Blood Flow (Stasis or Turbulence): Disruption of laminar flow seen in aneurysms or atrial fibrillation.
Hypercoagulability: Alterations in coagulation proteins leading to pro-thrombotic states.

3. Structural Schematic / Diagrammatic Representation

+-------------------------------------------------------------------------+ | NORMAL HEMOSTASIS | | Vascular Injury -> Collagen Exposure -> vWF Binding -> Platelet Plug | | | | | v | | Coagulation Cascade -> Thrombin Conversion -> Fibrin Mesh (Stable Clot)| +-------------------------------------------------------------------------+ | PATHOLOGIC THROMBOSIS | | +---------------------------------------------+ | | | VIRCHOW'S TRIAD | | | | Endothelial Damage + Stasis + Hypercoag. | | | +---------------------------------------------+ | | | | | v | | Intravascular Thrombus Formation -> Embolism | +-------------------------------------------------------------------------+

Q12 (b) Explain in detail the various hematological disorders with merits and demerits.

16 Marks CO4 K2 PO1 1.2.1

1. Classification of Major Hematological Disorders

Anemias: Deficiency in circulating RBC count or hemoglobin concentration (e.g., Iron Deficiency Anemia, Sickle Cell Anemia, Thalassemia).
Leukocyte Disorders / Leukemias: Uncontrolled neoplastic proliferation of white blood cells (AML, CML, ALL, CLL).
Hemostatic Disorders: Bleeding diatheses such as Hemophilia A/B (factor VIII/IX deficiency) and Thrombocytopenia.

2. Detailed Pathophysiology & Features

Sickle Cell Disease: Point mutation in β-globin gene forming HbS, causing RBC sickling under deoxygenation, leading to vaso-occlusion.
Thalassemia: Quantitative deficiency in alpha or beta globin chain synthesis resulting in microcytic hypochromic anemia.

3. Comparative Analytical Overview (Clinical Considerations / Merits & Demerits)

Evaluation of biological adaptations and diagnostic/therapeutic considerations across conditions:

Sickle Cell Heterozygote Advantage ("Merit"): Sickle cell trait (HbAS) offers evolutionary resistance against severe Plasmodium falciparum malaria infection.
Pathological Burden ("Demerit"): Homozygous states result in painful vaso-occlusive crises, organ infarction, hemolytic anemia, and reduced life expectancy.
Thalassemia Trait Advantage ("Merit"): Mild heterozygous carrier states confer malaria protection and balanced RBC production.
Severe Thalassemia Burden ("Demerit"): Transfusion dependency leading to secondary iron overload (hemochromatosis), requiring continuous chelation therapy.

Q13 (a) Make use of Balanced diet in the treatment of lifestyle diseases.

16 Marks CO4 K3 PO1 1.2.1

1. Fundamentals of a Balanced Diet in Health Management

A balanced diet supplies macro-nutrients (carbohydrates, proteins, fats) and micro-nutrients (vitamins, minerals) in optimal proportions to maintain metabolic homeostasis without caloric excess.

2. Role of Balanced Diet in Diabetes Mellitus

Low Glycemic Index (GI) Foods: Complex carbohydrates and fiber-rich dietary intake slow intestinal glucose absorption, preventing postprandial glucose spikes.
Improved Insulin Sensitivity: Fiber and lean proteins reduce metabolic strain on pancreatic beta cells.

3. Application in Cardiovascular Diseases & Hypertension

DASH Diet Principles: Reduced dietary sodium (Na⁺) intake paired with elevated potassium (K⁺) and magnesium controls systemic blood pressure.
Lipid Profile Management: Unsaturated fatty acids (omega-3, PUFAs) lower LDL cholesterol levels, preventing coronary atherosclerotic plaque buildup.

4. Application in Obesity & Metabolic Syndrome

Negative energy balance strategies using nutrient-dense foods regulate leptin/ghrelin appetite hormones, promoting sustainable adipose tissue loss and inflammation reduction.

Q13 (b) Demonstrate the mechanism of blood glucose regulation.

16 Marks CO4 K3 PO2 2.2.1

1. Physiological Range and Endocrine Control Nodes

Normal fasting plasma glucose concentration is maintained between 70-100 mg/dL through negative feedback mechanisms governed by endocrine hormones from the Islets of Langerhans in the pancreas.

2. Mechanism During Hyperglycemia (Postprandial State)

Insulin Secretion: Elevated blood glucose stimulates pancreatic beta cells to release insulin into circulation.
Glucose Uptake: Insulin binds to tyrosine kinase receptors, promoting GLUT4 translocation to skeletal muscle and adipose cell membranes.
Anabolic Pathways: Promotes glycogenesis (glycogen synthesis in liver/muscle), lipogenesis, and inhibits gluconeogenesis.

3. Mechanism During Hypoglycemia (Fasting State)

Glucagon Secretion: Decreased glucose levels trigger alpha cells of pancreas to secrete glucagon.
Catabolic Pathways: Glucagon stimulates hepatic glycogenolysis (glycogen breakdown) and gluconeogenesis (synthesis of glucose from non-carbohydrate precursors like amino acids and glycerol).

4. Secondary Hormonal & Autonomic Control

Epinephrine, cortisol, and growth hormone act as counter-regulatory hormones during severe stress or prolonged fasting to restore glucose balance.

Q14 (a) Discuss the morphological feature and structural organisation of bacteria and virus with neat sketch.

16 Marks CO5 K2 PO2 2.1.1

1. Structural Organization & Morphology of Bacteria

Prokaryotic cell organization lacking membrane-bound nuclei:

Morphologies: Cocci (spherical), Bacilli (rod-shaped), Spirilla (spiral), and Vibrio (comma-shaped).
Structural Components: Cell wall (peptidoglycan), plasma membrane, cytoplasm, nucleoid (circular DNA), ribosomes (70S), flagella (motility), pili/fimbriae (attachment), and capsule.

2. Structural Organization & Morphology of Viruses

Acellular infectious entities dependent on host cellular machinery for replication:

Genetic Core: DNA or RNA genome (single-stranded or double-stranded).
Capsid & Envelope: Protein coat (capsid) composed of capsomeres, arranged in helical, icosahedral, or complex structures. Enveloped viruses feature host-derived lipid membranes with viral glycoprotein spikes.

3. Structural Diagrammatic Schematics

Q14 (b) Discuss the working of TEM with neat sketch.

16 Marks CO5 K2 PO1 1.2.2

1. Principle of Transmission Electron Microscopy (TEM)

TEM operates by passing an accelerated beam of electrons through an ultra-thin specimen section (less than 100 nm). Image contrast is generated by differential electron scattering depending on sample density and atomic number.

2. Key Optical and Construction Components

Electron Gun: Emits high-energy electron beam (accelerated through 80-300 kV).
Electromagnetic Lenses: Condenser lenses focus electron beam onto sample; Objective lens forms primary magnified image; Projector lenses expand image onto viewing screen.
High Vacuum Column: Prevents electron beam scattering caused by air molecules.
Detection System: Phosphor fluorescent screen or high-resolution digital CCD/CMOS camera.

3. Sample Preparation & Working Step-by-Step

Fixation (glutaraldehyde), osmium tetroxide staining, dehydration, resin embedding, ultramicrotome sectioning, and placing onto copper grids for electron transmission.

4. Instrument Optical Ray Schematic

Q15 (a) Make use of SEM to study structural changes in medical tissue samples at the cellular level.

16 Marks CO5 K3 PO2 2.1.2

1. Operating Principle of SEM in Biomedical Analysis

Scanning Electron Microscopy (SEM) focuses a fine beam of electrons across a metallic-coated tissue surface. Detectors collect emitted secondary electrons (topography) and backscattered electrons (compositional contrast) to render high-resolution 3D surface images.

2. Tissue Sample Preparation Protocol for SEM

Fixation: Glutaraldehyde chemical fixation preserves delicate cellular architecture.
Dehydration & Critical Point Drying (CPD): Gradual ethanol dehydration followed by carbon dioxide CPD removes moisture without surface tension deformation.
Sputter Coating: Depositing thin conductive gold/platinum layer to prevent surface charge buildup during electron bombardment.

3. Cellular Application Scenarios in Pathology

Cellular Swelling & Necrosis Assessment: Observing membrane blebbing, pore formation, and cell lysis in ischemia models.
Biomaterial & Tissue Engineering Integration: Evaluating cell adhesion, spreading, and extracellular matrix deposition on synthetic scaffolds.
Blood Cell & Endothelial Pathology: Analyzing erythrocyte sickling or endothelial wall degradation during vascular injury.

Q15 (b) Apply the process of ELISA for the diagnosis of HIV in the blood sample.

16 Marks CO5 K3 PO1 1.2.1

1. Principle of Indirect ELISA for HIV Screening

Enzyme-Linked Immunosorbent Assay (ELISA) detects specific circulating anti-HIV antibodies (anti-gp120/gp41/p24) present in patient blood serum using antigen-antibody affinity binding coupled with an enzymatic colorimetric reaction.

2. Step-by-Step Diagnostic Execution Procedure

1. Antigen Coating: Recombinant HIV antigens (e.g., gp120, p24) are pre-immobilized onto microtiter plate wells.
2. Addition of Patient Serum: Diluted patient serum is added. If anti-HIV antibodies are present, they bind specifically to immobilized HIV antigens.
3. Washing Phase: Unbound serum proteins and non-specific antibodies are washed away with buffer.
4. Addition of Secondary Enzyme-Conjugated Antibody: Enzyme-linked anti-human IgG (e.g., Horseradish Peroxidase, HRP) is introduced, binding to primary patient anti-HIV antibodies.
5. Washing & Substrate Addition: Plate is washed to remove unbound enzyme conjugate, and chromogenic substrate (e.g., TMB) is added.

3. Signal Measurement and Clinical Interpretation

HRP enzyme hydrolyzes TMB substrate to produce a color change (blue turning yellow upon adding stop solution/acid). Optical density (OD) is measured at 450 nm using a spectrophotometric ELISA microplate reader. Absorbance values above the cutoff threshold confirm a positive reaction for HIV antibodies.