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PATHOLOGY QUESTION BANK - ALL ANSWERS

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📚 10 MARKS QUESTIONS

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Q1. Define Inflammation. Explain the mechanism of Acute Inflammation.

Definition:

1. Redness (Rubor)
2. Heat (Calor)
3. Swelling (Tumor)
4. Pain (Dolor)
5. Loss of function (Functio laesa)

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Types of Inflammation:

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Mechanism of Acute Inflammation (5 Steps - "5 R's"):

1. Recognition - Body recognizes the harmful agent (bacteria, virus, injury)
2. Recruitment - White blood cells (WBCs) are called to the site
3. Removal - WBCs destroy and remove the agent
4. Regulation - The inflammation is controlled so it doesn't go too far
5. Resolution - Damaged tissue is repaired

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Step-by-Step Mechanism:

• Blood vessels at the injury site become wider (vasodilation) - this causes redness and heat
• Blood flow increases
• Small blood vessels become more permeable (leaky) - fluid leaks out causing swelling

• WBCs (mainly neutrophils) move to the site in 4 steps:
  • Margination - WBCs move to edges of blood vessels
  • Rolling - WBCs roll along vessel walls
  • Adhesion - WBCs stick to vessel walls (using molecules like selectins and integrins)
  • Emigration - WBCs squeeze out of vessels and enter tissue

• WBCs recognize, engulf, and destroy bacteria or dead cells
• They use enzymes from lysosomes to digest the harmful agents
• Reactive oxygen species (ROS) also kill bacteria

• Chemical messengers (histamine, prostaglandins, cytokines) are released
• These help amplify and regulate the response

• Complete resolution - healing
• Abscess formation - pus collects
• Chronic inflammation - if the cause cannot be removed

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Q2. Explain the Etiology and Pathogenesis of Asthma.

Definition:

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Etiology (Causes):

• Dust, pollen, animal fur, mold
• Occurs in people with allergic tendency (atopy)

• Exercise, cold air, stress
• Respiratory infections (viral)
• Air pollution, smoke, chemicals

• Family history of asthma or allergies
• Genes that control immune response (IgE production)

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Pathogenesis (How it Develops):

• Patient is first exposed to an allergen (like pollen)
• The immune system makes antibodies called IgE
• IgE attaches to mast cells in the airway lining

• On second exposure to allergen, it binds to IgE on mast cells
• Mast cells degranulate (burst open) and release:
  • Histamine - causes bronchospasm (airway narrowing)
  • Leukotrienes - cause prolonged bronchospasm
  • Prostaglandins - increase mucus production
• Airways narrow, patient wheezes and feels breathless

• Eosinophils and T-lymphocytes flood into the airway
• More inflammation and tissue damage
• Airways become hyper-responsive (react to even mild triggers)

• Airway wall thickens
• Smooth muscle enlarges
• Mucus glands increase in size
• Airway remodeling occurs - permanent structural changes

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Symptoms:

• Wheezing (whistling sound while breathing)
• Shortness of breath (especially at night or early morning)
• Chest tightness
• Chronic cough

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Q3. Define Hypertension. Write in detail the pathogenesis of Hypertension.

Definition:

• Systolic: 140 mmHg or above
• Diastolic: 90 mmHg or above

• Primary (Essential) Hypertension - no known cause, 90-95% of cases
• Secondary Hypertension - due to kidney disease, hormonal disorders, etc.

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Pathogenesis of Primary Hypertension:

• Family history plays a major role
• Genes controlling sodium handling in kidneys, renin system, or sympathetic nervous system are involved

• Kidneys release Renin when blood pressure drops or sodium is low
• Renin converts Angiotensinogen → Angiotensin I
• Angiotensin I → Angiotensin II (by ACE enzyme)
• Angiotensin II:
  • Causes blood vessel constriction (raises BP)
  • Stimulates aldosterone release
  • Aldosterone causes kidneys to retain sodium and water (raises BP)

• Stress and anxiety activate the "fight or flight" system
• Releases adrenaline (epinephrine) and noradrenaline
• These increase heart rate, cardiac output, and cause vasoconstriction
• Result: Blood pressure rises

• Excess salt in diet → kidneys retain water
• More blood volume → higher blood pressure

• Blood vessel inner lining (endothelium) becomes damaged
• Less nitric oxide (NO) is produced (NO normally relaxes vessels)
• More endothelin (a vasoconstrictor) is produced
• Vessels stay narrowed → high BP

• Fat tissue produces hormones that raise BP
• Insulin resistance activates the sympathetic system
• Obstructive sleep apnea (in obese patients) further raises BP

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Consequences of Hypertension:

• Heart failure (enlarged heart)
• Stroke (brain bleed or clot)
• Kidney damage (nephrosclerosis)
• Vision problems (retinal damage)
• Atherosclerosis

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Q4. What are Cellular Adaptations? Give Examples.

Definition:

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Types of Cellular Adaptations:

• The cell enlarges (not divides)
• Cause: Increased workload or hormonal stimulation
• Example:
  • Heart enlarges in hypertension (cardiac hypertrophy)
  • Muscles enlarge in bodybuilders
  • Uterus enlarges during pregnancy

• The number of cells increases
• Cause: Hormonal stimulation or increased demand
• Example:
  • Breast tissue grows during pregnancy
  • Bone marrow produces more RBCs at high altitude
  • Thyroid gland grows when iodine is low (goiter)

• Cell shrinks due to decreased workload or lack of blood supply
• Example:
  • Muscles of a bed-ridden patient shrink
  • Limb muscles shrink after a cast (disuse atrophy)
  • Brain shrinks in old age (senile atrophy)

• One mature cell type is replaced by another type
• Usually in response to chronic irritation
• Example:
  • Smoker's airway: ciliated columnar cells change to squamous cells
  • Chronic acid reflux: stomach-type cells appear in esophagus (Barrett's esophagus)

• Cells become abnormal in size, shape, and organization
• Not yet cancer, but a warning sign
• Example: Cervical dysplasia (from HPV infection)

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Q5. Explain Etiology, Pathogenesis and Morphology of Reversible Cell Injury.

Definition:

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Etiology (Causes) of Cell Injury:

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Pathogenesis of Reversible Cell Injury (What happens inside the cell):

• Oxygen is cut off → Mitochondria cannot make ATP (cell's energy)

• Without ATP, Na+/K+ ATPase pump fails
• Sodium and water enter the cell
• Cell swells up (cellular swelling)

• Calcium floods into the cell
• Activates destructive enzymes (proteases, lipases, endonucleases)

• Cell switches to anaerobic metabolism (without oxygen)
• Lactic acid builds up → pH drops (acidosis)
• Enzymes inside the cell start to malfunction

• Protein synthesis stops
• Fatty acids accumulate → fatty change in liver/heart

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Morphology (What you see):

• Organ appears pale and swollen

• Cellular swelling - Cell appears larger, pale, puffy
• Fatty change - Fat droplets appear inside cells (especially liver)
• Vacuolation - Small clear spaces (vacuoles) inside the cell
• ER swells up
• Mitochondria swell

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Q6. Explain the Causes, Pathogenesis and Morphology of Irreversible Cell Injury.

Definition:

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Causes:

• Severe or prolonged hypoxia (heart attack, stroke)
• Strong poisons or toxins
• Severe infections
• Massive trauma
• Radiation damage

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Pathogenesis - What makes it irreversible?

• Severe injury damages the mitochondria permanently
• Large vacuoles (cavities) form in mitochondria
• ATP production cannot restart
• Without energy, all cell functions collapse

• Cell membrane is torn or severely damaged
• This is the point of no return
• Lysosomal enzymes leak out and digest the cell from inside
• Calcium floods in and activates destructive enzymes

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Two Types of Cell Death:

• Cell contents spill out into surrounding tissue
• Triggers inflammation
• Seen in: Heart attacks, infections, gangrene

• Cell destroys itself in an orderly way
• Cell shrinks, DNA fragments
• No inflammation
• Normal (embryo development) or pathological

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Morphology of Irreversible Injury/Necrosis:

• Pyknosis - Nucleus shrinks and becomes dark (condensed chromatin)
• Karyorrhexis - Nucleus breaks into fragments
• Karyolysis - Nucleus dissolves and disappears

1. Coagulative necrosis - Tissue hardens, structure preserved (e.g., heart attack)
2. Liquefactive necrosis - Tissue melts into liquid pus (e.g., brain infarct, abscess)
3. Caseous necrosis - Cheesy white appearance (TB - tuberculosis)
4. Fat necrosis - Chalky white spots (pancreatitis)
5. Gangrenous necrosis - Limb/tissue dies (diabetes, vascular disease)

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Q7. What is Atherosclerosis? Explain the Pathogenesis of Atherosclerosis.

Definition:

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Risk Factors:

• Major modifiable: High cholesterol, smoking, hypertension, diabetes
• Non-modifiable: Age, male gender, family history
• Emerging: Obesity, physical inactivity, high homocysteine

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Pathogenesis - Step by Step ("Response to Injury" Theory):

• The inner lining (endothelium) of artery is damaged by:
  • High blood pressure (mechanical stress)
  • Smoking (chemicals)
  • High cholesterol (lipid toxicity)
  • Diabetes (glucose damage)

• LDL cholesterol (bad cholesterol) enters through the damaged endothelium
• It gets trapped in the artery wall (intima layer)
• LDL gets oxidized (oxidized LDL is very dangerous)

• Blood monocytes are attracted to the area
• They enter the artery wall and become macrophages
• Macrophages eat up the oxidized LDL
• They become bloated with fat and become Foam cells
• Foam cells form the Fatty streak (earliest visible lesion)

• Smooth muscle cells from the middle artery layer (media) migrate to the intima
• They produce collagen and form a fibrous cap over the fatty core
• This forms the Atherosclerotic Plaque (Atheroma)

• Plaque grows and narrows the artery
• Stable plaque - thick fibrous cap, causes angina
• Unstable plaque - thin cap ruptures → blood clot forms → Heart attack or stroke

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Consequences:

• Heart - Coronary artery disease, heart attack
• Brain - Stroke
• Legs - Peripheral vascular disease, gangrene
• Kidneys - Renal artery stenosis

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Q8. Explain Etiology, Pathogenesis, Signs and Symptoms of Ischemic Heart Disease (IHD).

Definition:

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Forms of IHD:

1. Angina Pectoris (chest pain without cell death)
2. Myocardial Infarction - MI (heart attack - cells die)
3. Sudden Cardiac Death
4. Chronic Ischemic Heart Disease (heart failure)

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Etiology (Causes):

• Coronary artery spasm
• Blood clots (thrombosis)
• Embolism
• Coronary artery inflammation (vasculitis)

• Hypertension
• High LDL cholesterol
• Smoking
• Diabetes
• Obesity
• Physical inactivity
• Family history

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Pathogenesis:

1. Atherosclerotic plaques build up in coronary arteries
2. Arteries gradually narrow (stenosis)
3. When demand for oxygen increases (exercise, stress), narrowed arteries cannot supply enough blood
4. Ischemia (lack of blood/oxygen) occurs in heart muscle
5. If temporary → Angina (chest pain)
6. If complete blockage occurs (plaque rupture + clot) → Heart cells die → Myocardial Infarction

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Signs and Symptoms:

• Chest pain, pressure, or tightness - typically behind the sternum
• Pain may radiate to left arm, jaw, neck, back
• Triggered by exertion or stress
• Relieved by rest or nitroglycerine

• Severe, crushing chest pain lasting >20-30 minutes
• Not relieved by rest
• Sweating, nausea, vomiting
• Shortness of breath
• Sense of impending doom
• Dizziness or fainting

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📚 5 MARKS QUESTIONS

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Q1. Explain the Pathogenesis and Clinical Symptoms of COPD.

Definition:

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Pathogenesis:

• Cigarette smoke and air pollutants inhale into the airways
• Activate macrophages and neutrophils in the lungs

• Macrophages release enzymes (proteases) that destroy the lung tissue
• Normally, anti-protease enzymes (like alpha-1 antitrypsin) balance this
• In smokers, this balance is broken - proteases dominate

• Air sacs (alveoli) are permanently destroyed
• Lungs lose elasticity - air gets trapped inside
• Lungs over-inflate (barrel chest)

• Mucus glands in the airway enlarge
• Excessive mucus is produced
• Airways narrow and get blocked
• Frequent infections occur

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Clinical Symptoms:

• Chronic cough (productive - with mucus)
• Breathlessness (dyspnea) - especially on exertion
• Wheezing
• Barrel chest (chest becomes round due to trapped air)
• Reduced exercise tolerance
• Cyanosis (bluish lips/fingernails) - in severe cases
• Cor pulmonale - right-sided heart failure in late stage

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Q2. Define Chemical Mediators. Explain in detail the Cell-Derived Chemical Mediators.

Definition:

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Cell-Derived Chemical Mediators (Made by cells):

• Source: Mast cells, basophils, platelets
• Action: Dilates blood vessels, increases vascular permeability (leakage)
• Effect: Redness, heat, swelling
• Released immediately when injury occurs

• Source: From arachidonic acid in most cells
• Action: Cause vasodilation, pain, fever
• Key ones: PGE2 (pain and fever), PGI2 (vasodilation)
• Blocked by: Aspirin and NSAIDs

• Source: From arachidonic acid in mast cells and leukocytes
• Action: Cause bronchoconstriction (important in asthma), increase vascular permeability
• LTC4, LTD4, LTE4 - cause prolonged bronchospasm
• LTB4 - attracts neutrophils

• Source: Macrophages, lymphocytes
• Action: Regulate inflammation, fever, and immune response
• Key ones:
  • TNF (Tumor Necrosis Factor) - causes fever, activates endothelium
  • IL-1 (Interleukin-1) - causes fever, promotes leukocyte adhesion
  • IL-8 - attracts neutrophils (chemotaxis)

• Source: Mast cells, basophils, platelets
• Action: Activates platelets, increases vascular permeability, causes bronchoconstriction

• Source: Neutrophils, macrophages
• Action: Kill bacteria by oxidation
• Can also damage normal tissue if released in excess

• Source: Endothelial cells, macrophages
• Action: Dilates blood vessels, kills microbes
• Short-lived gas

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Q3. Explain the Role of Vitamin B12 and Folic Acid in Megaloblastic Anemia.

What is Megaloblastic Anemia?

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How Normal RBCs are Made:

• RBCs need DNA to divide and mature in bone marrow
• Vitamin B12 and Folic acid are essential for DNA synthesis
• Without them, DNA cannot be made → cells cannot divide → cells grow large but don't divide → Megaloblasts

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Role of Folic Acid:

• Folic acid is converted to Tetrahydrofolate (THF)
• THF helps carry carbon units needed for making thymidine (part of DNA)
• Without folic acid → DNA synthesis fails → megaloblastic changes
• RBCs cannot mature properly
• Sources: Green leafy vegetables, fruits, liver
• Deficiency causes: Poor diet, pregnancy (increased need), malabsorption, alcohol

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Role of Vitamin B12:

• B12 is needed to convert folate into its active form (that can be used for DNA synthesis)
• Without B12, folate gets "trapped" and cannot be used - called the "methyl trap" hypothesis
• B12 is also needed for myelin production (nerve sheaths)
• Sources: Meat, dairy, eggs (only animal products)
• Deficiency causes: Strict vegetarianism, pernicious anemia (lack of intrinsic factor), gastrectomy, malabsorption

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Features of Megaloblastic Anemia:

• Large, oval RBCs (macro-ovalocytes)
• Hypersegmented neutrophils (>5 lobes in nucleus)
• Weakness, fatigue, pallor
• Vitamin B12 deficiency additionally causes: Subacute combined degeneration of spinal cord (numbness, tingling in hands/feet)

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Q4. Define Cell Injury. Explain the Etiology of Cell Injury.

Definition:

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Etiology (Causes) of Cell Injury:

• Hypoxia = low oxygen supply
• Ischemia = reduced blood supply (lack of oxygen AND nutrients)
• Causes: Heart attack, stroke, anemia, respiratory failure
• Effect: Stops ATP production → cell swells and dies

• Mechanical trauma (cuts, crush injuries)
• Extreme heat (burns) or cold (frostbite)
• Radiation (X-rays, UV light) - damages DNA
• Electric shock

• Poisons: CCl4 (carbon tetrachloride), lead, mercury
• Drugs: Alcohol (liver damage), chemotherapy, antibiotics in excess
• Even salt and glucose in high concentrations can damage cells

• Viruses, bacteria, fungi, parasites
• They may directly destroy cells or release toxins

• Autoimmune diseases (body attacks its own cells)
• Allergic reactions
• Graft rejection after transplant

• Vitamin deficiencies (A, C, D, B12)
• Protein-calorie malnutrition
• Excess nutrition (fat buildup, obesity-related damage)

• Missing enzymes (inborn errors of metabolism)
• Abnormal proteins (sickle cell anemia)
• DNA repair defects

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Q5. What is Myocardial Infarction? Write the Etiology, Signs and Symptoms.

Definition:

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Etiology (Causes):

1. Atherosclerotic plaque builds up in coronary artery
2. Plaque ruptures (especially unstable plaques)
3. Blood clot (thrombus) forms on the ruptured plaque
4. Artery is completely blocked
5. Area of heart muscle dies within 20-40 minutes

• Coronary artery spasm (Prinzmetal angina)
• Embolism
• Coronary vasculitis
• Cocaine use (severe vasospasm)

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Signs and Symptoms:

• Sudden, severe chest pain - crushing, squeezing, or burning ("elephant sitting on chest")
• Pain radiates to left arm, jaw, neck, shoulder, or back
• Pain lasts more than 20-30 minutes
• Not relieved by rest or nitroglycerine

• Profuse sweating (diaphoresis)
• Nausea and vomiting
• Shortness of breath (dyspnea)
• Palpitations (irregular heartbeat)
• Dizziness or fainting
• Anxiety - sense of impending doom ("angor animi")
• Pale, cold, clammy skin

• ECG: ST elevation (STEMI) or ST depression (NSTEMI)
• Cardiac enzymes: Troponin I and T elevated (peak in 12-24 hours)
• CK-MB elevated

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Q6. Explain the Process of Wound Healing.

Definition:

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Types of Wound Healing:

1. Primary intention - clean wound, edges close together (e.g., surgical incision)
2. Secondary intention - large wound with gap, heals with more scarring (e.g., skin ulcer)
3. Tertiary intention - wound left open then closed later (infected wounds)

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Steps of Wound Healing:

• Bleeding stops first
• Blood vessels constrict
• Platelets form a clot (platelet plug)
• Fibrin forms a scab to seal the wound

• Neutrophils arrive first and clean the wound (eat bacteria and debris)
• Macrophages arrive (day 2-3) and continue cleaning
• Macrophages also release growth factors to stimulate healing

• Angiogenesis - New blood vessels grow into the wound
• Fibroblasts arrive and produce collagen (gives strength)
• A pink, granular tissue forms called granulation tissue
• Epithelial cells from edges grow over the wound surface (re-epithelialization)

• Collagen is reorganized and cross-linked (becomes stronger)
• Scar tissue forms - pale, flat
• Wound gradually gains tensile strength
• Maximum strength = ~80% of original tissue strength

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Factors Affecting Wound Healing (Impair healing):

• Infection
• Poor blood supply
• Diabetes
• Malnutrition (especially Vitamin C and protein deficiency)
• Steroids (anti-inflammatory drugs)
• Old age
• Large wound size

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Q7. Write the Mechanism of Free Radical-Induced Cell Injury.

What are Free Radicals?

• Superoxide (O2•-) - most common
• Hydroxyl radical (OH•) - most dangerous
• Hydrogen peroxide (H2O2)

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How Free Radicals are Generated:

• Normal cell metabolism (oxidative phosphorylation)
• Reperfusion injury (after blood flow restored to ischemic tissue)
• Radiation (X-rays, UV)
• Chemical toxins (CCl4, cigarette smoke)
• Inflammatory cells (neutrophils and macrophages produce ROS to kill bacteria)

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Mechanism of Cell Injury by Free Radicals:

• Free radicals attack the fatty acids (lipids) in cell membranes
• Chain reaction destroys the cell membrane
• Cell becomes leaky → ions flood in → cell swells and dies

• Free radicals denature (destroy) enzymes and structural proteins
• Cell loses its ability to function

• Free radicals attack DNA strands, causing breaks
• Mutations can lead to cancer or cell death
• Mitochondrial DNA is especially vulnerable

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Body's Defense Against Free Radicals (Antioxidants):

• Superoxide dismutase (SOD) - converts O2•- to H2O2
• Catalase - breaks down H2O2 to water
• Glutathione peroxidase - neutralizes free radicals
• Vitamin E - protects cell membranes
• Vitamin C - scavenges free radicals
• Vitamin A (beta carotene) - antioxidant

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Q8. Explain the Role of Chemical Mediators in the Process of Inflammation.

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Q9. Describe the Etiology and Pathogenesis of Asthma.

1. Allergen enters → IgE formed → attaches to mast cells
2. Re-exposure → mast cells release histamine, leukotrienes
3. Airways narrow (bronchospasm), mucus produced
4. Late response (4-8 hours) - eosinophil infiltration, more inflammation
5. Chronic disease - airway remodeling, smooth muscle thickening

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📚 2 MARKS QUESTIONS

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Q1 & Q8. Differentiate between Necrosis and Apoptosis.

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Q2. Mention the Factors Affecting Wound Healing.

1. Local factors: Infection, poor blood supply, wound size, foreign body in wound
2. Systemic factors:
   • Diabetes (poor circulation + immune function)
   • Malnutrition (low Vitamin C, protein deficiency)
   • Steroids (suppress inflammation)
   • Old age
   • Anemia
   • Immunosuppression

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Q3. Define Acidosis and Alkalosis.

• Types: Respiratory acidosis (CO2 retention) and Metabolic acidosis (DKA, lactic acidosis)
• Symptoms: Confusion, rapid breathing (compensating), weakness

• Types: Respiratory alkalosis (hyperventilation) and Metabolic alkalosis (vomiting, excess antacids)
• Symptoms: Muscle cramps, tingling, dizziness

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Q4. Define and Classify Angina Pectoris.

Definition:

Classification:

• Predictable, occurs with exertion/stress
• Relieved by rest or nitroglycerine
• Due to fixed atherosclerotic plaque

• Occurs at rest or with minimal activity
• More severe, prolonged
• Due to plaque rupture with partial clot
• Warning sign of possible heart attack

• Occurs at rest (often at night)
• Due to coronary artery spasm
• ST elevation on ECG during attack
• Responds to calcium channel blockers

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Q5. What are Ischemic Heart Diseases? Give Examples.

1. Angina Pectoris - chest pain, no cell death
2. Myocardial Infarction - heart attack, cell death
3. Sudden Cardiac Death - unexpected death from cardiac arrhythmia
4. Chronic Ischemic Heart Disease - gradual heart failure from repeated ischemia

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Q6. Mention the Different Mediators of Inflammation.

• Histamine
• Prostaglandins
• Leukotrienes
• Cytokines (TNF, IL-1, IL-8)
• Platelet activating factor (PAF)
• Reactive oxygen species (ROS)
• Nitric oxide (NO)

• Complement system (C3a, C5a, C3b)
• Bradykinin (kinin system)
• Clotting factors (fibrin)

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Q7. Define Atrophy with Example.

Definition:

Causes:

• Reduced workload (disuse atrophy)
• Loss of nerve supply (denervation atrophy)
• Reduced blood supply (ischemia)
• Inadequate nutrition
• Loss of hormonal stimulation (menopause → uterus atrophy)

Examples:

• Muscle atrophy in a limb after casting or prolonged bed rest
• Brain atrophy in Alzheimer's disease or old age
• Uterus atrophy after menopause
• Thyroid atrophy when iodine deficiency is corrected
• Bone atrophy (osteoporosis) in old age or immobilization

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Q9. Differentiate between Metaplasia and Dysplasia.

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Q10. Define Pyknosis, Karyorrhexis and Karyolysis.

• The nucleus shrinks and becomes very dark and dense
• Chromatin condenses (clumps together)
• Cell is dying but nucleus is still present

• The shrunken nucleus breaks into fragments
• Multiple small dark pieces are seen
• Advanced stage of nuclear death

• The nucleus completely dissolves and disappears
• No nuclear material is visible
• Final stage - ghost cell

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Q11. Define Atherosclerosis - Give Two Major Acquired Risk Factors.

1. Hypertension (High blood pressure) - damages the artery wall endothelium, allowing LDL to enter
2. Hyperlipidemia (High LDL Cholesterol) - excess LDL enters artery walls, gets oxidized, and triggers plaque formation

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Q12. What is COPD and CCF?

• A lung disease with permanent blockage of airflow
• Caused mainly by smoking
• Includes emphysema (destruction of air sacs) and chronic bronchitis (inflamed airways with excess mucus)
• Main symptoms: Chronic cough, breathlessness, wheezing

• The heart becomes too weak to pump blood efficiently
• Blood backs up ("congests") in lungs and body
• Causes: Hypertension, IHD, valve disease
• Symptoms: Breathlessness, leg swelling (edema), fatigue, orthopnoea (can't lie flat)

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Q13. Define Haemophilia and Megaloblastic Anaemia.

• A genetic bleeding disorder where the blood cannot clot properly
• Due to deficiency of clotting factor VIII (Haemophilia A) or factor IX (Haemophilia B)
• X-linked recessive - mainly affects males
• Symptoms: Excessive bleeding from minor cuts, joint bleeds (hemarthrosis), internal bleeding

• Anaemia caused by deficiency of Vitamin B12 or Folic acid
• Red blood cells are abnormally large (megaloblasts) because DNA synthesis is impaired
• Cells cannot divide properly
• Symptoms: Fatigue, pallor, weakness, sore tongue
• B12 deficiency also causes nerve damage (numbness, tingling)

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Q14. Write the Etiology and Symptoms of Chronic Renal Failure.

Definition:

Etiology (Causes):

1. Diabetes Mellitus - Number 1 cause worldwide (diabetic nephropathy)
2. Hypertension - Second most common (causes nephrosclerosis)
3. Glomerulonephritis - Immune-mediated kidney inflammation
4. Polycystic kidney disease - Genetic condition
5. Repeated kidney infections (pyelonephritis)
6. Obstruction - Kidney stones, enlarged prostate
7. SLE (Lupus nephritis)

Symptoms:

• Early: No symptoms (silent disease)
• Later:
  • Fatigue and weakness (anemia due to low EPO)
  • Swelling of legs (edema)
  • High blood pressure
  • Reduced urine output
  • Nausea, vomiting, loss of appetite
  • Itchy skin (uremia - waste buildup)
  • Bone pain (renal osteodystrophy)
  • Confusion (in severe cases - uremic encephalopathy)

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Q15. Define Angina Pectoris and Atherosclerosis.

• Chest pain or discomfort caused by temporary reduced blood flow to the heart
• Due to narrowed coronary arteries (usually from atherosclerosis)
• Pain is crushing or tight, behind the sternum, may radiate to left arm
• Triggered by exercise or stress, relieved by rest or nitroglycerine
• No permanent heart muscle damage (unlike MI)

• A chronic disease where fatty plaques (atheromas) build up inside artery walls
• Arteries harden and narrow over time
• Caused by damage to artery lining + LDL cholesterol deposits + inflammation
• Leads to IHD, stroke, and peripheral vascular disease
• Major risk factors: Hypertension, high cholesterol, smoking, diabetes

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Note: All answers are based on Robbins & Kumar Basic Pathology and standard pharmacology/physiology references. For exam writing, use these answers as your base and expand with diagrams where possible!