Human Physiology – 10 – Most important Long Questions

1. Digestion and Absorption

Question: Describe the complete process of protein digestion, absorption, and assimilation in the human body. Discuss the roles of various enzymes and organs involved.

Answer: Protein digestion begins in the stomach, where pepsin, secreted as inactive pepsinogen by gastric glands and activated by HCl, breaks down proteins into proteoses and peptones. The acidic environment of the stomach denatures proteins, making them more accessible to enzymes. From the stomach, the partially digested food (chyme) enters the small intestine. Here, pancreatic juice, containing trypsinogen and chymotrypsinogen, is released. These are activated by enteropeptidase (secreted by intestinal mucosa) and active trypsin, respectively, into trypsin and chymotrypsin. Trypsin and chymotrypsin further hydrolyze proteoses and peptones into smaller peptides. The small intestine also secretes intestinal juice (succus entericus) which contains peptidases (e.g., dipeptidases). These enzymes act on the smaller peptides to break them down into amino acids, which are the final products of protein digestion.

Amino acid absorption primarily occurs in the jejunum and ileum of the small intestine. Amino acids are absorbed into the enterocytes (intestinal cells) mainly by active transport, often co-transported with sodium ions. From the enterocytes, they are transported into the capillaries of the villi. These capillaries then drain into the hepatic portal vein, which carries the amino acids to the liver.

Assimilation is the process by which absorbed nutrients are utilized by the body's cells for various functions. In the liver, amino acids can be used for the synthesis of plasma proteins (e.g., albumin, globulins), clotting factors, and other essential compounds. Some amino acids are released into the general circulation and transported to various cells throughout the body. Cells then use these amino acids for protein synthesis (e.g., enzymes, structural proteins, hormones), tissue repair, and growth. Excess amino acids, if not needed for protein synthesis, can be deaminated in the liver (removal of amino group) and converted into glucose or fat for energy storage or immediate energy production.

2. Breathing and Respiration

Question: Explain the mechanism of breathing (inspiration and expiration) in humans, highlighting the roles of the diaphragm, intercostal muscles, and pressure changes. What is meant by "respiratory volumes" and name any three.

Answer: Breathing, or pulmonary ventilation, involves two phases: inspiration (inhalation) and expiration (exhalation), driven by pressure differences between the atmosphere and the lungs.

Inspiration: This is an active process. The diaphragm, a dome-shaped muscle separating the thoracic and abdominal cavities, contracts and flattens, moving downwards. Simultaneously, the external intercostal muscles contract, pulling the ribs and sternum upwards and outwards. These actions increase the volume of the thoracic cavity in both the antero-posterior and dorso-ventral axes. As the thoracic volume increases, the intra-pulmonary pressure (pressure within the lungs) decreases to below atmospheric pressure. This pressure gradient causes air from the atmosphere to rush into the lungs, filling them until the intra-pulmonary pressure equals the atmospheric pressure.

Expiration: This is typically a passive process during quiet breathing. The diaphragm relaxes and returns to its original dome shape. The external intercostal muscles also relax, allowing the ribs and sternum to return to their original position. These actions decrease the volume of the thoracic cavity. Consequently, the intra-pulmonary pressure increases to above atmospheric pressure. This pressure gradient forces air out of the lungs until the intra-pulmonary pressure again equals the atmospheric pressure. During forced expiration (e.g., exercise), the internal intercostal muscles and abdominal muscles actively contract to further decrease thoracic volume and expel more air.

Respiratory Volumes: Respiratory volumes refer to the amount of air that can be inspired or expired with each breath, or held within the lungs. They are important for assessing lung function.

Tidal Volume (TV):

The volume of air inspired or expired during a normal, quiet respiration. (Approximately 500 mL).

Inspiratory Reserve Volume (IRV):

The additional volume of air that can be inspired by a forceful inspiration after a normal tidal inspiration. (Approximately 2500-3000 mL).

Expiratory Reserve Volume (ERV):

The additional volume of air that can be expired by a forceful expiration after a normal tidal expiration. (Approximately 1000-1100 mL).

3. Body Fluids and Circulation

Question: Describe the structure and working of the human heart, outlining the path of blood flow through its chambers and major blood vessels. Briefly explain what is meant by "double circulation."

Answer: The human heart is a muscular, four-chambered organ located in the mediastinum between the lungs. It is roughly the size of a clenched fist and acts as a pump to circulate blood throughout the body. Structure:

Chambers: It has two upper, thinner-walled receiving chambers called atria (right atrium and left atrium) and two lower, thicker-walled pumping chambers called ventricles (right ventricle and left ventricle).

Septa: An interatrial septum separates the atria, and an interventricular septum separates the ventricles.

Valves:

Tricuspid valve: Between the right atrium and right ventricle.

Bicuspid (Mitral) valve: Between the left atrium and left ventricle.

Pulmonary semilunar valve: At the opening of the right ventricle into the pulmonary artery.

Aortic semilunar valve: At the opening of the left ventricle into the aorta.

Working and Path of Blood Flow (Cardiac Cycle):

Deoxygenated blood from the body tissues (via the superior and inferior vena cava) enters the right atrium.

From the right atrium, blood passes through the tricuspid valve into the right ventricle.

The right ventricle contracts, pushing deoxygenated blood through the pulmonary semilunar valve into the pulmonary artery, which carries it to the lungs for oxygenation.

Oxygenated blood from the lungs (via the pulmonary veins) enters the left atrium.

From the left atrium, blood passes through the bicuspid (mitral) valve into the left ventricle.

The left ventricle, being the strongest chamber, contracts forcefully, pushing oxygenated blood through the aortic semilunar valve into the aorta, which then distributes it to all parts of the body.

Double Circulation: Double circulation is a circulatory system in which blood passes through the heart twice during one complete cycle. In humans, it consists of two distinct pathways:

Pulmonary Circulation:

Deoxygenated blood is pumped from the right ventricle to the lungs, where it gets oxygenated, and then returns to the left atrium. This circuit is responsible for gas exchange.

Systemic Circulation:

Oxygenated blood is pumped from the left ventricle to all parts of the body (except the lungs), supplies oxygen and nutrients, collects waste products, and then returns as deoxygenated blood to the right atrium. This circuit distributes blood to the body tissues. This separation ensures efficient delivery of oxygenated blood to the tissues and removal of carbon dioxide.

4. Excretory Products and Their Elimination

Question: Explain the process of urine formation in the human kidney, detailing the three main steps involved. Discuss the role of the counter-current mechanism in concentrating the urine.

Answer: Urine formation is a complex process occurring in the nephrons of the kidneys, involving three main steps: glomerular filtration, tubular reabsorption, and tubular secretion.

Glomerular Filtration (Ultrafiltration):

This is the first step, occurring in the renal corpuscle (Bowman's capsule and glomerulus). Blood enters the glomerulus under high pressure. The glomerular capillaries are highly permeable, allowing water and small solutes (like glucose, amino acids, urea, salts) to filter out from the blood into the Bowman's capsule. Large molecules like proteins and blood cells are typically retained in the blood due to their size. The fluid collected in Bowman's capsule is called the glomerular filtrate, and its formation is a non-selective process.

Tubular Reabsorption:

As the glomerular filtrate flows through the renal tubule (proximal convoluted tubule - PCT, Loop of Henle, distal convoluted tubule - DCT, and collecting duct), many essential substances that were filtered out are reabsorbed back into the blood. This reabsorption can be active (requiring ATP, e.g., glucose, amino acids, Na+) or passive (e.g., water by osmosis, urea).

PCT: Most of the essential nutrients, 70-80% of electrolytes, and water are reabsorbed here.

Loop of Henle: Plays a crucial role in maintaining high osmolarity of the medullary interstitial fluid.

DCT and Collecting Duct: Conditional reabsorption of Na+ and water occurs here, regulated by hormones like ADH and aldosterone.

Tubular Secretion:

During this step, certain waste products (e.g., potassium, hydrogen ions, creatinine, drugs) that were not filtered out by the glomerulus are actively secreted from the blood in the peritubular capillaries into the renal tubule (primarily in the PCT and DCT). This process helps in maintaining acid-base balance and efficiently removing wastes. The fluid remaining in the collecting duct at this point is urine.

Counter-current Mechanism: This mechanism, involving the Loop of Henle and vasa recta (capillary network around the loop), is vital for concentrating urine.

The descending limb of the Loop of Henle is permeable to water but impermeable to electrolytes. As filtrate moves down, water exits due to the increasing osmolarity of the medullary interstitium, concentrating the filtrate.

The ascending limb is permeable to electrolytes (Na+, Cl-, K+) but impermeable to water. Electrolytes are actively transported out in the thick segment, and passively in the thin segment, making the filtrate dilute as it ascends and contributing to the high osmolarity of the medullary interstitium.

The vasa recta maintain this medullary osmotic gradient. Blood flows in the opposite direction (counter-current) to the filtrate in the Loop of Henle, allowing for efficient exchange of water and solutes, ensuring that the solutes reabsorbed from the Loop of Henle are not washed away, thereby preserving the gradient. This counter-current exchange and multiplier system allows the human kidney to produce urine that is up to four times more concentrated than the initial filtrate, conserving water.

5. Locomotion and Movement

Question: Describe the sliding filament theory of muscle contraction, explaining the roles of actin, myosin, troponin, tropomyosin, ATP, and calcium ions.

Answer: The sliding filament theory explains how skeletal muscles contract. It proposes that muscle contraction occurs when the thin actin filaments slide past the thick myosin filaments, resulting in the shortening of the sarcomere (the basic contractile unit of muscle). The lengths of the filaments themselves do not change.

Key Components and Their Roles:

Actin (Thin Filaments): Composed of two intertwined strands of G-actin (globular actin) monomers, forming F-actin (filamentous actin). Each G-actin has a binding site for myosin.

Myosin (Thick Filaments): Made up of many myosin molecules, each with a long tail and two globular heads. The myosin heads have ATPase activity (can bind and hydrolyze ATP) and actin-binding sites.

Tropomyosin: A filamentous protein that wraps around the actin filament, covering the myosin-binding sites on actin in a relaxed muscle.

Troponin: A complex of three proteins attached to tropomyosin. It has a binding site for calcium ions.

ATP (Adenosine Triphosphate): Provides the energy for muscle contraction. Myosin heads bind and hydrolyze ATP.

Calcium Ions (Ca2+): The critical trigger for muscle contraction.

Mechanism of Contraction:

Neural Stimulation and Ca2+ Release: A nerve impulse (action potential) arrives at the neuromuscular junction, releasing acetylcholine. This causes an action potential to propagate along the muscle fiber membrane and into the T-tubules. This signal triggers the release of Ca2+ ions from the sarcoplasmic reticulum (SR) into the sarcoplasm.

Ca2+ Binding to Troponin: The released Ca2+ ions bind to troponin.

Conformational Change and Exposure of Binding Sites: The binding of Ca2+ to troponin causes a conformational change in the troponin-tropomyosin complex. This shift moves tropomyosin away from the myosin-binding sites on the actin filament, exposing these sites.

Cross-Bridge Formation (Myosin-Actin Binding): With the binding sites exposed, the energized myosin heads (which have already hydrolyzed ATP into ADP and Pi, storing energy) bind to the actin filaments, forming cross-bridges.

Power Stroke: The release of ADP and Pi from the myosin head causes it to pivot or "power stroke," pulling the actin filament towards the center of the sarcomere (M-line). This shortens the sarcomere.

ATP Binding and Cross-Bridge Detachment: A new ATP molecule binds to the myosin head. This binding causes the myosin head to detach from the actin filament, breaking the cross-bridge.

ATP Hydrolysis and Re-cocking: The newly bound ATP is hydrolyzed by the myosin ATPase into ADP and Pi, re-energizing the myosin head and "re-cocking" it to its high-energy position, ready to bind to another actin site if Ca2+ is still present. This cycle of cross-bridge formation, power stroke, detachment, and re-cocking continues as long as Ca2+ ions are present and ATP is available, leading to progressive shortening of the muscle fiber and muscle contraction. When the nerve stimulation ceases, Ca2+ is actively pumped back into the SR, troponin and tropomyosin return to their original positions, blocking the binding sites, and the muscle relaxes.

6. Neural Control and Coordination

Question: Describe the structure of a neuron and explain how a nerve impulse (action potential) is generated and conducted along its axon.

Answer: Structure of a Neuron: A neuron (nerve cell) is the fundamental structural and functional unit of the nervous system, specialized for transmitting electrical signals. It typically consists of three main parts:

Cell Body (Soma/Perikaryon):

The main part of the neuron, containing the nucleus and most of the organelles (Nissl's granules, mitochondria, Golgi apparatus). It is involved in synthesizing proteins and maintaining the neuron's metabolic functions.

Dendrites:

Short, highly branched, tree-like extensions that project from the cell body. They are the primary receptive regions of the neuron, receiving incoming signals from other neurons and transmitting them towards the cell body.

Axon:

A single, long, slender projection extending from the cell body (at the axon hillock). It transmits nerve impulses away from the cell body to other neurons, muscles, or glands. Axons can be myelinated (covered by a myelin sheath formed by Schwann cells in PNS or oligodendrocytes in CNS, which provides insulation and increases conduction speed) or unmyelinated. The axon ends in terminal branches, each terminating in a synaptic knob (axon terminal), which contains neurotransmitters.

Generation and Conduction of a Nerve Impulse (Action Potential): A nerve impulse, or action potential, is a rapid, transient change in the membrane potential of a neuron, propagating along the axon without decrement. It's an "all-or-none" phenomenon.

Resting Membrane Potential (Polarized State):

In its resting state, the neuron's membrane is polarized, with the inside of the cell being negative relative to the outside (typically around -70 mV). This is maintained by the differential permeability of the membrane to ions (more K+ leak channels than Na+ channels)

and the action of the sodium-potassium pump (Na+/K+ pump), which actively pumps 3 Na+ ions out for every 2 K+ ions pumped in.

Depolarization (Generation of Action Potential):

When a sufficiently strong stimulus (reaching threshold potential, typically -55 mV) is applied to a neuron, it causes voltage-gated sodium (Na+) channels to open rapidly. This allows a massive influx of Na+ ions into the cell, making the inside of the membrane positive relative to the outside. This rapid change in polarity is depolarization.

Repolarization:

Shortly after depolarization, the voltage-gated Na+ channels inactivate and close, while voltage-gated potassium (K+) channels open. This allows K+ ions to flow out of the cell, making the inside of the membrane negative again. This process is repolarization.

Hyperpolarization (Undershoot):

In some cases, the K+ channels remain open slightly longer than necessary, leading to a brief period where the membrane potential becomes even more negative than the resting potential. This is hyperpolarization, making it harder for another action potential to be generated immediately (refractory period).

Restoration of Resting Potential:

The Na+/K+ pump continuously works to restore the ion concentrations across the membrane to their resting state.

Conduction along the Axon:

Unmyelinated Axon (Continuous Conduction):

In unmyelinated axons, the action potential propagates continuously along the entire length of the axon. The depolarization at one point generates a local current that depolarizes the adjacent region to threshold, opening new voltage-gated Na+ channels, and so on. This is a slower form of conduction.

Myelinated Axon (Saltatory Conduction):

In myelinated axons, the myelin sheath acts as an insulator, preventing ion flow across the membrane except at periodic gaps called Nodes of Ranvier. The action potential "jumps" from one Node of Ranvier to the next. This "skipping" of the impulse greatly increases the

speed of conduction (saltatory conduction), as depolarization only needs to occur at the nodes.

7. Chemical Coordination and Regulation

Question: Discuss the role of the hypothalamus and pituitary gland in regulating the human endocrine system. Provide examples of hormones produced by each and their target glands/functions.

Answer: The hypothalamus and pituitary gland form a crucial neuroendocrine complex that acts as the "master control center" of the endocrine system, regulating the function of many other endocrine glands.

Hypothalamus: The hypothalamus is a region of the brain located below the thalamus. It directly connects the nervous system to the endocrine system. Its primary role is to produce and release various "releasing hormones" and "inhibiting hormones" that control the secretion of hormones from the anterior pituitary gland. It also produces two hormones, ADH (Vasopressin) and Oxytocin, which are stored and released by the posterior pituitary.

Hormones produced by Hypothalamus:

Releasing Hormones:

Gonadotropin-Releasing Hormone (GnRH):

Stimulates the anterior pituitary to release FSH and LH.

Thyrotropin-Releasing Hormone (TRH):

Stimulates the anterior pituitary to release TSH.

Corticotropin-Releasing Hormone (CRH):

Stimulates the anterior pituitary to release ACTH.

Growth Hormone-Releasing Hormone (GHRH):

Stimulates the anterior pituitary to release GH.

Inhibiting Hormones:

Growth Hormone-Inhibiting Hormone (GHIH/Somatostatin):

Inhibits the release of GH from the anterior pituitary.

Prolactin-Inhibiting Hormone (PIH/Dopamine):

Inhibits the release of prolactin from the anterior pituitary.

Hormones for Posterior Pituitary (produced by hypothalamus, stored/released by posterior pituitary):

Antidiuretic Hormone (ADH/Vasopressin):

Targets kidney tubules; promotes water reabsorption, reducing urine output.

Oxytocin:

Targets uterus (causes contractions during childbirth) and mammary glands (milk ejection).

Pituitary Gland: The pituitary gland is a small, pea-sized gland located at the base of the brain, directly beneath the hypothalamus. It is often called the "master gland" because its hormones control the function of many other endocrine glands. It has two main parts:

Anterior Pituitary (Adenohypophysis): Develops from Rathke's pouch (oral ectoderm). Its hormone secretion is largely controlled by hypothalamic releasing and inhibiting hormones transported via the hypophyseal portal system.

Hormones produced by Anterior Pituitary:

Growth Hormone (GH):

Targets most body cells; promotes growth and metabolism.

Thyroid-Stimulating Hormone (TSH):

Targets the thyroid gland; stimulates thyroid hormone synthesis and release.

Adrenocorticotropic Hormone (ACTH):

Targets the adrenal cortex; stimulates the release of corticosteroids.

Follicle-Stimulating Hormone (FSH):

Targets gonads; promotes gamete production (sperm in males, ovarian follicle development in females).

Luteinizing Hormone (LH):

Targets gonads; stimulates sex hormone production (testosterone in males, ovulation and corpus luteum formation in females).

Prolactin (PRL):

Targets mammary glands; stimulates milk production.

Posterior Pituitary (Neurohypophysis):

Develops as an outgrowth of the hypothalamus. It does not synthesize hormones but stores and releases ADH and Oxytocin, which are produced by neurosecretory cells in the hypothalamus and transported down their axons to the posterior pituitary.

The hypothalamus and pituitary gland work together in a tightly regulated feedback loop to maintain homeostasis. For example, the hypothalamus releases TRH, which stimulates the anterior pituitary to release TSH, which in turn stimulates the thyroid gland to release thyroid hormones. High levels of thyroid hormones then inhibit the release of TRH and TSH, demonstrating negative feedback.

8. Digestion and Absorption

Question: Briefly explain the calorific value of proteins, carbohydrates, and fats. Describe any three nutritional or digestive disorders from the given syllabus, detailing their causes and symptoms.

Answer: Calorific Value: Calorific value (or energy content) refers to the amount of energy released when a certain mass of a substance is completely combusted. In the context of nutrition, it's the amount of energy provided by food components when metabolized in the body.

Carbohydrates:

Provide approximately 4 kcal/g (17 kJ/g). They are the body's primary and most readily available source of energy.

Proteins:

Provide approximately 4 kcal/g (17 kJ/g). While primarily for building and repairing tissues, they can also be used for energy.

Fats:

Provide approximately 9 kcal/g (37 kJ/g). They are the most energy-dense macronutrients and serve as a concentrated energy store.

Nutritional and Digestive Disorders:

Protein Energy Malnutrition (PEM):

Cause:

A range of conditions caused by a deficiency of protein and/or calories in the diet, particularly prevalent in developing countries affecting young children. It includes Kwashiorkor (primarily protein deficiency with adequate calories) and Marasmus (deficiency of both protein and calories).

Symptoms:

Kwashiorkor:

 

Edema

(swelling, particularly in the abdomen and legs due to fluid retention), stunted growth, changes in skin and hair pigmentation, apathy, fatty liver, impaired immune function.

Marasmus:

Severe wasting of muscles and subcutaneous fat ("skin and bones" appearance), stunted growth, extreme weight loss, dry and wrinkled skin, often alert but withdrawn.

Jaundice:

Cause:

A condition characterized by yellowing of the skin, eyes (sclera), and mucous membranes. It is caused by an excessive accumulation of bilirubin (a yellow pigment formed from the breakdown of red blood cells) in the blood. This can be due to:

Pre-hepatic: Increased breakdown of red blood cells (e.g., hemolytic anemia).

Hepatic: Liver disease preventing proper bilirubin processing (e.g., hepatitis, cirrhosis).

Post-hepatic: Obstruction of bile ducts, preventing bilirubin excretion (e.g., gallstones, tumors).

Symptoms: Yellow discoloration of skin and eyes, dark urine (due to bilirubin excretion), pale stools (due to lack of bilirubin in feces), itching, fatigue, nausea, and abdominal pain (depending on the underlying cause).

Constipation:

Cause: A condition where bowel movements are infrequent or difficult to pass. Common causes include:

Lack of dietary fiber.

Insufficient fluid intake.

Lack of physical activity.

Ignoring the urge to defecate.

Certain medications (e.g., opioids, antacids).

Underlying medical conditions (e.g., irritable bowel syndrome, hypothyroidism).

Symptoms: Infrequent bowel movements (less than three per week), straining during bowel movements, hard or lumpy stools, feeling of incomplete evacuation, abdominal discomfort or bloating.

9. Body Fluids and Circulation

Question: Describe the process of blood coagulation (clotting) in detail, mentioning the key factors involved. Explain why coagulation is a vital process for the human body.

Answer: Blood coagulation, or clotting, is a complex process that forms a blood clot at the site of vascular injury, preventing excessive blood loss. It involves a cascade of enzyme activations leading to the formation of a fibrin mesh.

Process of Blood Coagulation: Blood clotting can be initiated by two main pathways: the extrinsic pathway (triggered by tissue injury) and the intrinsic pathway (triggered by internal damage to blood vessels or contact with foreign surfaces). Both pathways converge into a common pathway.

1. Extrinsic Pathway (Tissue Factor Pathway):

Initiated when blood comes into contact with tissue factor (Factor III), a protein released from damaged extravascular tissues.

Tissue factor binds with Factor VII (present in plasma) to form an activated complex (Factor VIIa-Tissue Factor).

This complex then activates Factor X to Factor Xa.

2. Intrinsic Pathway (Contact Activation Pathway):

Initiated when blood comes into contact with negatively charged surfaces, such as exposed collagen in a damaged blood vessel wall or glass in a test tube.

Factor XII is activated to XIIa.

Factor XIIa then activates Factor XI to XIa.

Factor

XIa

activates Factor IX to

IXa

.

Factor IXa, in the presence of Factor VIIIa (activated by thrombin) and phospholipids and Ca2+, activates Factor X to Factor Xa.

3. Common Pathway:

Formation of Prothrombin Activator: Both extrinsic and intrinsic pathways lead to the activation of Factor X to Factor Xa. Factor Xa, along with Factor Va (activated by thrombin), phospholipids (from platelets), and Ca2+, forms the "prothrombin activator" complex.

Conversion of Prothrombin to Thrombin: The prothrombin activator converts inactive prothrombin (Factor II, a plasma protein) into active thrombin (Factor IIa). This is a crucial amplification step.

Conversion of Fibrinogen to Fibrin: Thrombin acts as an enzyme, converting soluble fibrinogen (Factor I, a plasma protein) into insoluble fibrin monomers.

Fibrin Polymerization and Clot Formation: Fibrin monomers spontaneously polymerize to form long, insoluble fibrin strands, which create a mesh-like network.

Fibrin Stabilization: Factor XIIIa (activated by thrombin) cross-links the fibrin strands, strengthening and stabilizing the fibrin mesh, trapping blood cells (especially platelets and red blood cells) to form a solid blood clot.

Key Factors Involved:

Platelets: Provide phospholipids essential for the activation of several clotting factors and form a temporary plug at the injury site.

Calcium Ions (Ca2+): Essential co-factor for many steps in the clotting cascade.

Clotting Factors: A series of plasma proteins (most synthesized in the liver, many are proenzymes), designated by Roman numerals (I to XIII, except for VI). Vitamin K is essential for the synthesis of Factors II, VII, IX, and X.

Why Coagulation is Vital: Blood coagulation is a vital process for the human body primarily for:

Hemostasis (Prevention of Blood Loss): It is the primary mechanism to stop bleeding from injured blood vessels. Without effective clotting, even minor cuts or internal injuries could lead to life-threatening hemorrhage.

Maintaining Blood Volume and Pressure: By preventing significant blood loss, clotting helps maintain adequate blood volume and, consequently, stable blood pressure necessary for proper organ perfusion.

Wound Healing: The fibrin clot not only stops bleeding but also provides a scaffold for the migration of fibroblasts and other cells involved in tissue repair, thus initiating the wound healing process.

10. Disorders of Circulatory System & Excretory System

Question: Compare and contrast Hypertension and Coronary Artery Disease (CAD) as circulatory disorders, explaining their causes and potential consequences. Briefly describe Uraemia and Renal Calculi as disorders of the excretory system.

Answer:

Comparison and Contrast of Hypertension and Coronary Artery Disease (CAD):

Feature	Hypertension (High Blood Pressure)	Coronary Artery Disease (CAD)
Definition	Persistently elevated arterial blood pressure (systolic ≥ 140 mmHg or diastolic ≥ 90 mmHg).	Narrowing or blockage of the coronary arteries (which supply blood to the heart muscle).
Primary Cause	Often idiopathic (essential hypertension, 90-95% of cases), but influenced by genetics, diet (high sodium), obesity, stress, lack of exercise, smoking, alcohol. Secondary hypertension can be due to kidney disease, endocrine disorders.	Primarily atherosclerosis: accumulation of fatty plaques (atheroma) within the arterial walls, leading to hardening and narrowing.
Mechanism	Increased peripheral resistance and/or increased cardiac output. Can be due to constricted arterioles, increased blood volume, or increased heart pumping force.	Plaque buildup reduces lumen size, restricts blood flow, and can rupture, leading to clot formation and acute blockage.
Symptoms	Often "silent killer" with no obvious symptoms until severe. Can include headaches, dizziness, nosebleeds, blurred vision in severe cases.	Angina pectoris (chest pain, often radiating to arm, neck, jaw), shortness of breath, fatigue, nausea, sweating. Can lead to heart attack (myocardial infarction).
Consequences	Increased risk of heart attack, stroke, kidney failure, heart failure, vision loss, peripheral artery disease. It is a major risk factor for CAD.	Angina, myocardial infarction (heart attack), heart failure, arrhythmias, sudden cardiac death.
Relationship	Hypertension is a significant risk factor for developing CAD. High blood pressure puts increased stress on arterial walls, accelerating atherosclerotic plaque formation and rupture.	CAD is a specific disease affecting the coronary arteries. While often caused by hypertension, it has its own distinct pathophysiology of plaque formation.

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Disorders of the Excretory System:

Uraemia:

Definition: A severe and life-threatening condition that occurs when the kidneys fail to adequately filter waste products from the blood, leading to a build-up of urea and other nitrogenous waste products (like creatinine, uric acid) in the blood. It is a clinical syndrome that can arise from chronic kidney disease or acute kidney injury.

Causes: Advanced renal failure from any cause (e.g., chronic glomerulonephritis, uncontrolled diabetes, hypertension, polycystic kidney disease).

Symptoms: Fatigue, nausea, vomiting, loss of appetite, metallic taste in mouth, uremic frost (urea crystals on skin), muscle cramps, itching, confusion, seizures, coma. It often necessitates dialysis or kidney transplantation.

Renal Calculi (Kidney Stones):

Definition: Hard, crystalline mineral deposits that form inside the kidneys. They can vary in size and composition (most commonly calcium oxalate, but also uric acid, struvite, or cystine stones).

Causes: Dehydration (insufficient fluid intake), high dietary intake of certain substances (e.g., oxalate, sodium, animal protein), genetic predisposition, certain medical conditions (e.g., hyperparathyroidism, gout, recurrent urinary tract infections), obesity.

Symptoms: Severe, sharp pain in the side and back, below the ribs (renal colic), pain that radiates to the lower abdomen and groin, painful urination, blood in urine (hematuria), cloudy or foul-smelling urine, nausea, vomiting, fever and chills (if infection is present). Smaller stones may pass spontaneously, while larger ones may require medical intervention (e.g., lithotripsy, surgery).