Human Health and Disease — Class 12 Biology NCERT Solutions (Free)
Free step-by-step NCERT solutions for Class 12 Biology chapter "Human Health and Disease" — 5 important questions with detailed answers for CBSE board exam preparation.
TL;DR: Free step-by-step NCERT solutions for Class 12 Biology chapter "Human Health and Disease" — 5 important questions with detailed answers for CBSE board…
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NCERT Solutions for Class 12 Biology — Human Health and Disease. Step-by-step answers to all 5 textbook questions from this chapter, written for CBSE board preparation and free to use.
Human Health and Disease — All 5 Questions Solved
Q1. Define disease. Explain the difference between infectious and non-infectious diseases with examples.
Disease: Abnormal condition of body or part of body, characterized by symptoms and impaired function. Disruption of normal physiology.
Infectious diseases:
Definition: Diseases caused by pathogens (disease-causing organisms or toxins) transmissible from infected person to healthy person.
Causative agents:
- Bacteria: single-celled prokaryotes
- Viruses: obligate intracellular parasites (RNA or DNA)
- Fungi: eukaryotic organisms
- Protozoa: single-celled eukaryotes
- Parasitic worms: multicellular organisms
- Prions: infectious proteins
Transmission:
- Direct contact: touching, fluid exchange
- Airborne: droplets, aerosols
- Food/water: contaminated food/water
- Vectors: insects, animals
- Blood transfusion/needle sharing
Characteristics:
- Contagious (spreads to others)
- Incubation period (time before symptoms)
- Often seasonal or endemic
- Can be prevented by vaccines
- Can be treated with antibiotics/antivirals
Examples:
- Bacterial: tuberculosis (Mycobacterium tuberculosis), tetanus (Clostridium tetani), cholera (Vibrio cholerae)
- Viral: influenza, COVID-19, measles, HIV/AIDS, dengue
- Fungal: ringworm, candidiasis
- Protozoal: malaria (Plasmodium), sleeping sickness
- Parasitic: filariasis (worms)
Non-infectious diseases:
Definition: Diseases not caused by pathogens; not transmissible; related to genetics, lifestyle, environmental factors, or age.
Causes:
- Genetic: inherited mutations, hereditary conditions
- Lifestyle: diet, smoking, alcohol, sedentary lifestyle
- Environmental: pollution, radiation, toxic substances
- Age: degenerative conditions
- Stress: chronic stress effects
- Metabolic: diabetes, obesity
Characteristics:
- Non-contagious (not spread between people)
- Multifactorial (multiple causative factors)
- Often chronic (long-lasting)
- Often preventable through lifestyle changes
- Treated symptomatically or with lifestyle modifications
Examples:
- Cancer: abnormal cell growth; genetic mutations and environmental factors
- Cardiovascular disease: hypertension, atherosclerosis, heart attack, stroke
- Diabetes: Type 1 (autoimmune), Type 2 (lifestyle)
- Respiratory: asthma, COPD (smoking-related)
- Neurodegenerative: Alzheimer's, Parkinson's
- Autoimmune: rheumatoid arthritis, lupus
- Genetic: cystic fibrosis, hemophilia, sickle cell anemia
- Nutritional deficiencies: scurvy (vitamin C), rickets (vitamin D)
Key differences:
Infectious:
- Caused by pathogens
- Transmissible
- Incubation period
- Fever, inflammation common
- Diagnosed by pathogen detection
- Treated with antimicrobials
Non-infectious:
- Caused by internal/external factors
- Not transmissible
- Gradual onset usually
- Varied symptoms
- Diagnosed by clinical/laboratory tests
- Treated by addressing cause or managing symptoms
Overlap:
- Some infectious diseases have non-infectious consequences (HIV damage)
- Some non-infectious diseases have inflammatory component (autoimmune)
- Some pathogens predispose to non-infectious disease (HPV and cancer)
Q2. Explain the symptoms and transmission of AIDS. How is HIV different from AIDS?
HIV (Human Immunodeficiency Virus) and AIDS (Acquired Immune Deficiency Syndrome):
HIV vs AIDS:
HIV:
- Virus causing infection
- Attacks CD4+ T cells (helper T cells), macrophages, dendritic cells
- Can be present without symptoms
- Treatable with antiretroviral therapy (ART)
- Does not necessarily mean AIDS
AIDS:
- Clinical syndrome resulting from severe CD4+ T cell depletion
- CD4+ count below 200 cells/μL (or <14% of lymphocytes)
- Opportunistic infections and cancers develop
- Without treatment, fatal within months to few years
HIV infection progression:
1. Acute infection (2-4 weeks after exposure):
- Flu-like symptoms: fever, fatigue, sore throat, rash
- High viral load in blood
- Symptoms subside
- Person remains highly infectious
2. Asymptomatic phase (5-10 years, variable):
- No symptoms (may think cured)
- Virus replicates slowly in blood and lymphoid tissues
- CD4+ count gradually declines
- Person highly infectious
- Opportunistic infections may begin
3. Symptomatic phase (AIDS stage):
- CD4+ count below 200
- Symptoms reappear and worsen
- Opportunistic infections: pneumocystis pneumonia (PCP), tuberculosis
- Opportunistic cancers: Kaposi sarcoma, non-Hodgkin lymphoma
- Neurological symptoms: cognitive decline, peripheral neuropathy
- Wasting syndrome: severe weight loss
- Fungal infections: candidiasis, cryptococcosis
- Without treatment, death within 1-3 years
Transmission of HIV:
1. Sexual transmission:
- Vaginal, anal, or oral intercourse with infected person
- Risk higher with: untreated infection, ulcerative STIs, high viral load
- Condoms prevent transmission
2. Parenteral transmission:
- Sharing injection drug equipment (needles, syringes)
- Blood transfusion with infected blood
- Needle stick injury in healthcare settings
3. Mother-to-child transmission (Vertical):
- During pregnancy: virus crosses placenta
- During delivery: infant exposed to blood and vaginal secretions
- During breastfeeding: virus in breast milk
- Prevention: maternal treatment, planned C-section, infant ART
- Risk without treatment: 15-45% transmission rate
4. Organ transplantation:
- Rare with screening
NOT transmitted by:
- Saliva, sweat, tears (enzymes destroy virus)
- Touching, hugging, kissing
- Sharing food, utensils, water
- Coughing, sneezing
- Toilet seats, doorknobs
- Insects
- Casual contact
Symptoms of AIDS:
Infectious complications:
- Tuberculosis (bacterial)
- Pneumocystis pneumonia (fungal)
- Mycobacterium avium complex (bacterial)
- Cryptococcosis (fungal)
- Toxoplasmosis (parasitic)
- Cytomegalovirus (viral)
- Candidiasis (fungal, oral or esophageal)
Neoplasms (cancers):
- Kaposi sarcoma (HHV-8 related, skin tumors)
- Non-Hodgkin lymphoma (CNS or systemic)
- Cervical cancer (HPV related, women)
Neurological:
- HIV-associated dementia: cognitive decline, memory loss
- Peripheral neuropathy: pain, numbness in extremities
- Myelopathy: weakness, spasticity
Gastrointestinal:
- Chronic diarrhea
- Esophagitis
- Hepatitis
- Wasting syndrome: loss of 10% body weight
General symptoms:
- Fever (prolonged)
- Night sweats
- Fatigue
- Lymphadenopathy (enlarged lymph nodes)
- Skin conditions
- Anemia
- Thrombocytopenia
Prevention of HIV:
1. Safe sex:
- Condom use
- Monogamy with uninfected partner
- Testing before sexual activity
- PrEP (pre-exposure prophylaxis) for high-risk individuals
2. Injection drug use:
- Avoid sharing equipment
- Needle exchange programs
- Treatment programs
3. Occupational:
- Universal precautions in healthcare
- Post-exposure prophylaxis after needle stick
4. Blood transfusion:
- Screening of blood supply
- Testing for donors
5. Mother-to-child:
- Maternal treatment
- Safe delivery practices
- Infant prophylaxis
- Avoid breastfeeding (if formula available)
Treatment (Antiretroviral therapy):
- Combination of drugs targeting HIV enzymes
- Reverse transcriptase inhibitors (NRTIs, NNRTIs)
- Protease inhibitors
- Integrase inhibitors
- Entry inhibitors
- CD4+ count typically recovers to >500 with treatment
- Viral load becomes undetectable
- Life expectancy near normal with adherence
- Reduces transmission (undetectable = untransmittable)
Q3. Explain the concept of immunity. Distinguish between innate and adaptive immunity.
Immunity: Ability of body to resist infection and disease. Protection against pathogens and toxins through immune system.
Innate (Non-specific) Immunity:
Definition: Inborn, non-specific defense against all pathogens. First line of defense. Requires no prior exposure to pathogen. No memory of infection.
Characteristics:
- Present from birth
- Non-specific (responds to many pathogens)
- Rapid response (hours)
- No memory (same response to repeated exposure)
- Does not improve with repeated exposure
Components:
1. Physical barriers:
- Skin: intact barrier, sheds dead cells
- Mucous membranes: line respiratory, digestive, urinary, reproductive tracts
- Mucus: traps pathogens
- Cilia: sweep particles out
- Stomach acid: kills many pathogens
- Lysozyme in tears/saliva: breaks bacterial cell walls
2. Chemical barriers:
- Stomach acid: denatures proteins
- Pancreatic enzymes: digest pathogens
- Bile acids: antimicrobial
- Sebaceous gland secretions: skin protection
- Complement proteins: blood proteins that kill pathogens
3. Cellular immunity (innate):
- Phagocytes:
* Neutrophils: most abundant, engulf bacteria
* Macrophages: large phagocytes, present in tissues
* Dendritic cells: antigen-presenting cells
- NK (Natural Killer) cells: kill infected cells
- Complement system: proteins that lyse pathogens
4. Inflammatory response:
- Histamine release from mast cells: increases vascular permeability
- Cytokines (IL-1, TNF-α): recruit immune cells
- Increased blood flow and cell migration to injury site
- Fever: increases immune function
Adaptive (Specific) Immunity:
Definition: Specific immune response against particular pathogen. Second line of defense. Improves with repeated exposure (memory). Requires prior sensitization.
Characteristics:
- Acquired after exposure to antigen
- Highly specific (recognizes particular pathogen)
- Slower initial response (days to weeks)
- Memory of infection (faster second exposure)
- Improves with repeated exposure
- Basis of vaccination
Components:
1. Cellular (T cell-mediated) immunity:
- T lymphocytes develop in thymus
- Types:
* Cytotoxic T cells (CTLs, CD8+): kill infected cells
* Helper T cells (Th, CD4+): coordinate immune response
* Regulatory T cells: suppress immune response
- Recognize antigen on MHC molecules
- Effective against viral infections, intracellular bacteria, cancers
2. Humoral (B cell-mediated) immunity:
- B lymphocytes develop in bone marrow
- Produce antibodies (immunoglobulins)
- Recognize free antigens
- Types of antibodies:
* IgM: first antibody in response; good complement activator
* IgG: secondary response; opsonizes pathogens; crosses placenta
* IgA: secreted in mucous; protects mucosal surfaces
* IgE: mast cell binding; mediates allergies
* IgD: B cell receptor
- Effective against extracellular bacteria, toxins
3. Immune memory:
- Memory T cells: persist years, mount rapid response to reinfection
- Memory B cells: produce antibodies rapidly on reinfection
- Provides long-term immunity
- Basis of vaccines
Key differences:
Innate:
- Present from birth
- Non-specific
- No antibodies
- No lymphocytes involved
- Rapid
- No memory
- Same response to repeated exposure
Adaptive:
- Develops after exposure
- Specific
- Antibodies produced
- Lymphocytes involved
- Slower initial
- Memory develops
- Faster response to repeated exposure
Cooperation:
- Innate response provides signals to activate adaptive immunity
- Dendritic cells present antigen to T cells
- Macrophages activate T cells
- T cells help B cells produce antibodies
- Adaptive immunity enhances innate response (antibodies opsonize for phagocytosis)
Example: Response to new pathogen
1. First exposure:
- Innate: immediate response (hours)
- Adaptive: slower response (1-2 weeks)
- IgM antibodies first
- IgG antibodies develop later
- Memory forms
2. Second exposure:
- Innate: same as first
- Adaptive: rapid response (2-3 days)
- Rapid IgG production
- Often prevents disease
- Basis of vaccines
Vaccination exploits adaptive immunity:
- Vaccine contains antigen (weakened pathogen or component)
- Stimulates antibody and memory development
- No disease development
- Upon exposure, rapid immune response prevents infection
- Examples: DPT, polio, measles, hepatitis B, COVID-19
Q4. Explain allergies and hypersensitivity reactions. What are autoimmune diseases?
Allergies and hypersensitivity:
Allergy (Hypersensitivity): Exaggerated immune response to harmless antigen (allergen). Immune system overreacts causing tissue damage.
Types of hypersensitivity reactions:
1. Type I (Immediate hypersensitivity, IgE-mediated):
- Onset: within minutes
- Mechanism:
* Previous exposure sensitizes immune system
* IgE antibodies bind to mast cells and basophils
* Re-exposure to allergen cross-links IgE on mast cells
* Triggers degranulation
* Release of histamine, leukotrienes, prostaglandins
- Symptoms: itching, swelling, redness, hives, anaphylaxis
- Examples:
* Pollen allergies (hay fever): sneezing, rhinitis, conjunctivitis
* Food allergies: peanuts, shellfish, tree nuts (swelling, gastrointestinal symptoms)
* Drug allergies: penicillin (rash, anaphylaxis)
* Insect sting allergies: bee, wasp (localized or systemic reaction)
- Anaphylaxis: life-threatening systemic reaction
* Shock: low blood pressure
* Airway constriction: breathing difficulty
* Causes: severe food allergies, drug allergies, insect stings
* Treatment: epinephrine injection (EpiPen)
2. Type II (Cytotoxic hypersensitivity, IgG/IgM-mediated):
- Onset: hours to days
- Mechanism:
* IgG or IgM antibodies bind to antigen on cell surface
* Complement activation and complement-mediated lysis
* Antibody-dependent cell-mediated cytotoxicity (ADCC)
* Opsonization and phagocytosis
- Results in: cell destruction, tissue damage
- Examples:
* Hemolytic transfusion reaction: incompatible blood transfusion
* Hemolytic disease of newborn: Rh incompatibility
* Drug-induced hemolytic anemia: penicillin coating RBC
* Graves' disease: antibodies stimulate thyroid (autoimmune)
* Goodpasture syndrome: antibodies attack basement membrane
3. Type III (Immune complex-mediated):
- Onset: 3-8 hours
- Mechanism:
* Antigen-antibody complexes form
* Deposit in tissues (blood vessels, joints, kidneys)
* Complement activation
* Neutrophil infiltration
* Tissue damage from inflammation
- Results in: vasculitis, arthritis, nephritis
- Examples:
* Serum sickness: reaction to foreign serum (antiserum), drugs
* Systemic lupus erythematosus (SLE): autoimmune, immune complexes in joints, kidneys, skin
* Post-streptococcal glomerulonephritis: immune complexes in kidneys
* Arthus reaction: localized immune complex reaction
4. Type IV (Delayed-type hypersensitivity, T cell-mediated):
- Onset: 24-72 hours
- Mechanism:
* T cells (mainly CD8+) recognize antigen
* T cell activation and proliferation
* Cytokine release (IFN-γ, TNF-α, TNF-β)
* Macrophage activation
* Tissue inflammation and damage
- No antibodies involved
- Results in: contact dermatitis, delayed skin reactions
- Examples:
* Contact dermatitis: poison ivy, nickel, latex (localized)
* Tuberculin skin test: intradermal injection of antigen
- Induration appears 48-72 hours in sensitized individuals
- Indicates prior TB exposure or immunity
* Organ transplant rejection: T cell attack on foreign tissue
* Drug allergies: some drugs cause delayed reactions
Autoimmune diseases:
Definition: Diseases caused by immune system attacking body's own cells and tissues. Loss of self-tolerance. Immune system mistakes self-antigen for foreign antigen.
Mechanisms:
- Genetic predisposition: HLA gene association
- Environmental triggers: infections, UV exposure, chemicals
- Loss of immune tolerance:
* Defective regulatory T cells
* Defective negative selection in thymus (elimination of self-reactive T cells)
* Defective B cell tolerance
* Cross-reactivity: antibodies against pathogen cross-react with self-antigens
Examples:
1. Systemic autoimmune diseases:
- Systemic lupus erythematosus (SLE):
* Antibodies against nuclear antigens (ANAs)
* Immune complexes deposit in tissues
* Affects: joints, kidneys, heart, lungs, skin
* Symptoms: malar rash, arthritis, nephritis, photosensitivity
* More common in women
- Rheumatoid arthritis:
* Antibodies against IgG (rheumatoid factor) and citrullinated proteins
* T cell attack on joint synovium
* Affects: joint cartilage, bone erosion
* Symptoms: joint pain, swelling, stiffness
2. Organ-specific autoimmune diseases:
- Type 1 diabetes:
* T cells attack pancreatic beta cells
* Loss of insulin production
* High blood glucose
- Graves' disease:
* IgG antibodies stimulate thyroid TSH receptors
* Excess thyroid hormone production
* Symptoms: hyperthyroidism, eye symptoms (exophthalmos)
- Hashimoto's thyroiditis:
* Antibodies and T cells attack thyroid
* Thyroid destruction
* Hypothyroidism
- Multiple sclerosis:
* T cells attack myelin in CNS
* Demyelination; impaired nerve conduction
* Progressive disability
- Celiac disease:
* T cell response to gluten (wheat protein)
* Intestinal epithelium destruction
* Malabsorption of nutrients
- Myasthenia gravis:
* Antibodies block acetylcholine receptors at neuromuscular junction
* Muscle weakness
Treatment of allergies:
1. Avoidance: eliminate allergen exposure
2. Antihistamines: block histamine effects
3. Corticosteroids: reduce inflammation
4. Immunotherapy:
- Desensitization: gradual allergen exposure
- Monoclonal antibodies: anti-IgE (omalizumab)
5. Emergency: epinephrine for anaphylaxis
Treatment of autoimmune diseases:
1. Immunosuppression: corticosteroids, cytotoxic drugs
2. Targeted therapy: TNF-α inhibitors, IL-6 inhibitors
3. Biological agents: monoclonal antibodies against immune cells
4. Symptom management: specific to disease
Q5. Explain cancer at cellular and molecular level. What are oncogenes and tumor suppressors?
Cancer: Malignant disease characterized by uncontrolled cell growth, invasion of surrounding tissues, and metastasis (spreading to distant sites). Results from accumulation of mutations in genes controlling cell growth and death.
Characteristics of cancer cells:
1. Loss of growth control:
- Uncontrolled cell division
- Ignore growth-inhibitory signals
- Escape from contact inhibition
- Form multilayered growth
2. Immortality:
- Unlimited replicative potential
- Telomerase reactivation (maintains chromosome ends)
- Bypass of senescence (cell aging)
3. Dedifferentiation:
- Loss of specialized characteristics
- Revert to stem cell-like state
- Altered gene expression
4. Invasion and metastasis:
- Loss of cell-cell adhesion (E-cadherin downregulation)
- Epithelial-mesenchymal transition (EMT)
- Invasion through basement membrane
- Entry into blood vessels (intravasation)
- Survival in circulation
- Exit into new tissue (extravasation)
- Colonization and growth at new site
5. Evasion of immune system:
- Loss of immunogenic antigens
- Production of immunosuppressive factors
- Evasion of T cell recognition
6. Evasion of apoptosis:
- Resistance to programmed cell death
- Mutations in apoptotic pathways
- p53 mutations prevent death signals
7. Angiogenesis:
- Formation of new blood vessels
- Tumor growth requires nutrient supply
- VEGF (vascular endothelial growth factor) secretion
Oncogenes:
Definition: Genes that promote cell growth. Mutated or overexpressed oncogenes drive cancer development.
Normal function:
- Growth factors: signal for cell division
- Growth factor receptors: receive growth signals (tyrosine kinase receptors)
- Signal transduction proteins: relay growth signals (RAS, RAF)
- Transcription factors: activate genes for proliferation (MYC)
Mechanisms of oncogene activation:
1. Point mutation:
- Single nucleotide change
- Example: RAS mutation (90% of pancreatic cancers)
- Changes amino acid; alters protein function
- Results in constitutive (constant) activation
- Protein sends continuous growth signal
2. Gene amplification:
- Multiple copies of oncogene
- Overproduction of growth-promoting protein
- Example: HER2 amplification in breast cancer (25-30% of cases)
- High HER2 protein drives excessive cell division
3. Chromosomal translocation:
- Gene moved to new chromosome location
- Placed under different regulatory control
- Overexpressed or abnormal protein produced
- Example: BCR-ABL fusion in chronic myeloid leukemia (CML)
* Chromosome 9 and 22 break and rejoin
* Creates fusion gene with abnormal activity
* Constitutive tyrosine kinase activity
* Uncontrolled cell growth
4. Insertional activation:
- Viral insertion into oncogene
- Disrupts normal regulation
- Example: HPV insertion near oncogenes in cervical cancer
Common oncogenes:
- RAS: growth signaling (30% of human cancers)
- MYC: transcription factor (30% of cancers)
- HER2: growth factor receptor (breast, ovarian cancers)
- BCR-ABL: tyrosine kinase (CML)
- BRAF: MAP kinase (melanoma)
- ALK: tyrosine kinase (lymphoma, lung cancer)
Tumor suppressor genes:
Definition: Genes that inhibit cell growth and promote apoptosis. Loss of tumor suppressors contributes to cancer. "Brakes" on cell division.
Normal functions:
- Growth inhibition: respond to anti-growth signals
- DNA repair: detect and fix DNA damage
- Apoptosis: trigger programmed cell death in damaged cells
- Cell cycle checkpoints: prevent division with DNA damage
Mechanisms of inactivation:
1. Loss-of-function mutation:
- Point mutation disrupts protein
- Deletion removes gene
- Truncation produces non-functional protein
- Loss of growth inhibition
2. Epigenetic silencing:
- Promoter methylation: gene not transcribed
- Chromatin condensation: gene inaccessible
- Loss of gene expression without mutation
Two-hit hypothesis (Knudson):
- Both copies of tumor suppressor must be inactivated
- First hit: inherited or acquired mutation in one copy
- Second hit: acquired mutation in other copy
- Both mutations must occur for cancer development
- Example: RB gene in retinoblastoma
* One inherited mutation predisposes
* Second mutation in eye cell causes tumor
* Bilateral tumors often develop (both eyes affected)
Common tumor suppressors:
1. p53 (TP53 gene):
- "Guardian of genome"
- Most frequently mutated in cancers (50-70%)
- Functions:
* Detects DNA damage via ATM kinase
* Activates p21 (CDK inhibitor) → cell cycle arrest
* Allows DNA repair
* If damage irreparable: activates apoptotic genes (BAX, PUMA)
* Triggers programmed cell death
- Mutated in:
* Li-Fraumeni syndrome: inherited p53 mutation; high cancer risk
* Lung, breast, colon, ovarian cancers
2. RB (Retinoblastoma):
- Controls G1/S cell cycle checkpoint
- Binds E2F transcription factor (normally active)
- Prevents S phase entry
- Loss leads to uncontrolled S phase entry
- Mutated in: retinoblastoma, lung cancer, breast cancer
3. PTEN:
- Phosphatase antagonizing PI3K/AKT pathway
- Growth inhibition
- Loss leads to PI3K/AKT activation (excessive growth signaling)
- Mutated in: breast cancer, prostate cancer, ovarian cancer
4. APC:
- Controls Wnt signaling (growth pathway)
- Loss leads to constitutive Wnt signaling
- Mutated in: colorectal cancer (familial adenomatous polyposis)
5. BRCA1/BRCA2:
- DNA repair genes (homologous recombination)
- Loss leads to genomic instability
- Inherited mutations: high breast and ovarian cancer risk
- 5-10% of breast cancers associated with BRCA mutations
Multistep carcinogenesis:
Cancer develops through accumulation of multiple mutations:
1. Initiation: first mutation (oncogene activation or tumor suppressor loss)
- Single cell acquires growth advantage
2. Promotion: additional mutations select for advantageous variants
- Clonal expansion: mutant cells divide repeatedly
- Additional mutations in descendant cells
3. Progression: more mutations accumulate
- Invasion capability acquired
- Metastatic potential develops
- Multiple clones compete
- Most aggressive clones dominate
Typically 4-7 critical mutations required for fully malignant cancer
Molecular signatures of cancer:
- Karyotypic changes: extra/missing chromosomes, translocations
- Gene expression profiling: abnormal patterns identify cancer type
- Genomic instability: microsatellite instability, aneuploidy
- Mutational burden: number of mutations
- Microarray/RNA-seq: identifies gene expression changes
Treatment strategies:
1. Targeted therapy: block specific oncogenes or restore tumor suppressors
- Example: Gleevec for BCR-ABL in CML
- Example: Herceptin for HER2 breast cancers
- Example: EGFR inhibitors for EGFR-mutant lung cancers
2. Chemotherapy: damage DNA or prevent cell division
- Damages rapidly dividing cells (cancer and some normal cells)
3. Immunotherapy: enhance immune recognition of cancer
- Checkpoint inhibitors: remove immune suppression
- CAR-T cells: engineered T cells targeting cancer antigens
4. Surgery: remove primary tumor
5. Radiation: destroy cancer cells with ionizing radiation
6. Gene therapy (emerging): correct mutations causing cancer
Human Health and Disease — Practice MCQs with Answers
Attempt these 20 multiple-choice questions after working through the solutions above. Each carries the correct option and the reasoning behind it, so a wrong answer tells you which idea to revisit.
MCQ 1. Which of the following defines 'health' according to the World Health Organization (WHO)?
- A. Absence of disease
- B. Absence of physical disease only
- C. A state of complete physical, mental, and social well-being
- D. Being able to perform daily tasks without fatigue
Answer: C. A state of complete physical, mental, and social well-being — WHO defines health as a state of complete physical, mental, and social well-being, and not merely the absence of disease or infirmity.
MCQ 2. Typhoid fever in humans is caused by which pathogen?
- A. Plasmodium vivax
- B. Salmonella typhi
- C. Wuchereria bancrofti
- D. Rhino virus
Answer: B. Salmonella typhi — Typhoid fever is caused by the pathogenic bacterium Salmonella typhi, which commonly enters the small intestine through contaminated food and water.
MCQ 3. Which of the following is a diagnostic test for typhoid fever?
- A. ELISA test
- B. Widal test
- C. Mantoux test
- D. PCR test
Answer: B. Widal test — The Widal test is a serological test commonly used to diagnose typhoid fever by detecting antibodies against Salmonella typhi in the patient's blood serum.
MCQ 4. The common cold is caused by which type of pathogen?
- A. Bacteria
- B. Fungi
- C. Viruses
- D. Protozoa
Answer: C. Viruses — The common cold is a viral infection primarily caused by rhinoviruses, affecting the nose and respiratory passage.
MCQ 5. Which mosquito species acts as a vector for malaria?
- A. Aedes aegypti
- B. Anopheles
- C. Culex
- D. Mansonia
Answer: B. Anopheles — Female Anopheles mosquitoes are the vectors that transmit the Plasmodium parasite, which causes malaria, from an infected person to a healthy person.
MCQ 6. The infective stage of Plasmodium that enters the human body is:
- A. Gametocytes
- B. Sporozoites
- C. Merozoites
- D. Trophozoites
Answer: B. Sporozoites — When the infected female Anopheles mosquito bites a human, it injects sporozoites, which are the infective form of Plasmodium, into the bloodstream.
MCQ 7. Amoebiasis (amoebic dysentery) in humans is caused by:
- A. Plasmodium vivax
- B. Entamoeba histolytica
- C. Wuchereria bancrofti
- D. Giardia intestinalis
Answer: B. Entamoeba histolytica — Amoebiasis is an intestinal infection caused by the protozoan parasite Entamoeba histolytica, which lives in the large intestine.
MCQ 8. Filariasis, also known as elephantiasis, is caused by which organism?
- A. Ascaris lumbricoides
- B. Taenia solium
- C. Wuchereria bancrofti
- D. Ancylostoma duodenale
Answer: C. Wuchereria bancrofti — Filariasis is caused by filarial worms like Wuchereria bancrofti or Wuchereria malayi, which reside in the lymphatic vessels.
MCQ 9. Which of the following is a barrier under innate immunity?
- A. Antibodies
- B. Vaccination
- C. Skin
- D. Lymphocytes
Answer: C. Skin — Skin is a physical barrier, which is a component of innate immunity, preventing the entry of microorganisms into the body.
MCQ 10. Colostrum, the yellowish fluid secreted by the mother during the initial days of lactation, is rich in which antibody?
- A. IgG
- B. IgM
- C. IgA
- D. IgE
Answer: C. IgA — Colostrum provides passive immunity to the newborn due to its richness in IgA antibodies, protecting the infant's digestive and respiratory tracts.
MCQ 11. Which cells are primarily responsible for cell-mediated immunity (CMI)?
- A. B-lymphocytes
- B. T-lymphocytes
- C. Macrophages
- D. Neutrophils
Answer: B. T-lymphocytes — T-lymphocytes (T-cells) are responsible for cell-mediated immunity, directly attacking infected cells and regulating immune responses.
MCQ 12. The causative agent of Acquired ImmunoDeficiency Syndrome (AIDS) is a retrovirus called:
- A. Human Papillomavirus (HPV)
- B. Human Immunodeficiency Virus (HIV)
- C. Herpes Simplex Virus (HSV)
- D. Ebola Virus
Answer: B. Human Immunodeficiency Virus (HIV) — AIDS is caused by the Human Immunodeficiency Virus (HIV), which is a retrovirus that attacks the immune system.
MCQ 13. HIV primarily infects which type of cells in the human body?
- A. B-lymphocytes
- B. Cytotoxic T-lymphocytes
- C. Helper T-lymphocytes (CD4+ cells)
- D. Natural Killer cells
Answer: C. Helper T-lymphocytes (CD4+ cells) — HIV specifically targets and destroys helper T-lymphocytes (CD4+ T-cells), which are crucial for a healthy immune response, leading to immunodeficiency.
MCQ 14. Which of the following is NOT a mode of transmission for HIV?
- A. Sexual contact with an infected person
- B. Sharing infected needles
- C. Breastfeeding from an infected mother
- D. Casual contact like shaking hands
Answer: D. Casual contact like shaking hands — HIV is transmitted through specific body fluids (blood, semen, vaginal fluids, breast milk) and not through casual contact, air, or food.
MCQ 15. Cancer cells differ from normal cells in their property of:
- A. Contact inhibition
- B. Apoptosis
- C. Differentiation
- D. Metabolism
Answer: A. Contact inhibition — Cancer cells lose the property of contact inhibition, which normally regulates cell growth, leading to uncontrolled proliferation and tumor formation.
MCQ 16. Which of the following is a physical carcinogen?
- A. Mustard gas
- B. UV radiations
- C. Nicotine
- D. Aflatoxin
Answer: B. UV radiations — UV radiations are known physical carcinogens that can cause DNA damage and lead to skin cancer.
MCQ 17. MRI (Magnetic Resonance Imaging) is used for the detection of cancer in:
- A. Surface tissues only
- B. Internal organs and tissues
- C. Blood samples only
- D. Bone marrow only
Answer: B. Internal organs and tissues — MRI uses strong magnetic fields and non-ionizing radiations to detect pathological and physiological changes in living tissues, making it effective for internal organs and soft tissues.
MCQ 18. Which of the following drugs is obtained from the latex of the poppy plant (Papaver somniferum)?
- A. Cannabinoids
- B. Cocaine
- C. Opioids
- D. LSD
Answer: C. Opioids — Opioids like morphine, heroin (diacetylmorphine), and codeine are derived from the latex of the opium poppy plant.
MCQ 19. Receptors for cannabinoids are primarily found in which organ of the human body?
- A. Heart
- B. Brain
- C. Lungs
- D. Kidneys
Answer: B. Brain — Cannabinoid receptors are prominently present in the brain, especially in regions associated with pleasure, memory, concentration, and movement.
MCQ 20. What are the characteristics of withdrawal syndrome experienced by individuals dependent on drugs?
- A. Increased appetite and improved mood
- B. Mild headache and drowsiness
- C. Anxiety, shakiness, nausea, and sweating
- D. Enhanced cognitive function and alertness
Answer: C. Anxiety, shakiness, nausea, and sweating — Withdrawal symptoms are unpleasant and often severe, including anxiety, tremors, nausea, vomiting, and sweating, experienced when regular drug intake is abruptly stopped.
How to Use These Solutions
Attempt each question yourself first and only then compare with the worked answer. Marks in the CBSE board exam are awarded for the METHOD as much as the final result, so reproduce the steps rather than memorising the last line. Where a solution states a law, a formula or a definition, learn that wording — examiners look for it.
Related practice for this chapter: chapter MCQs, previous-year questions, revision notes and sample papers.