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Human Physiology
| Question | Answer |
|---|---|
| What are the 3 phases of hemostasis, and their role in vascular integrity? | Vascular spasm—vasoconstriction to reduce blood flow. Primary hemostasis—platelet adhesion, activation, and aggregation to form a temporary plug. Secondary hemostasis—coagulation cascade produces fibrin to stabilize the clot. |
| How do platelet surface receptors contribute to clot formation in hemostasis? | Platelet receptors like GP Ia/IIa, GP IIb/IIIa, and P2Y12 bind to collagen and fibrinogen, activating platelets and facilitating aggregation to form a primary clot. |
| How are the intrinsic and extrinsic coagulation pathways initiated? | Intrinsic pathway—triggered by blood contact with negative surfaces. Extrinsic pathway—activated by tissue factor from damaged tissues. |
| What is thrombin’s role in coagulation? | Converts fibrinogen into fibrin, amplifies clotting by activating upstream factors, and activates Factor XIII to stabilize the clot. |
| How does the protein C pathway regulate clotting? | Thrombin-thrombomodulin activates protein C, which degrades Factors Va and VIIIa, creating a negative feedback loop to prevent excessive coagulation. |
| What is fibrinolysis, and why is it important? | Fibrinolysis is the enzymatic breakdown of fibrin clots, mainly via plasmin. It prevents persistent thrombi and ensures proper blood flow. |
| How do endothelial cells prevent thrombosis? | They secrete anticoagulants (NO, prostacyclin, heparan sulfate) to inhibit platelet aggregation and limit coagulation, maintaining blood flow. |
| What is disseminated intravascular coagulation (DIC), and why is it dangerous? | A pathological condition (triggered by infection/trauma) that consumes clotting factors causing thrombosis and uncontrolled bleeding. |
| How do aspirin and heparin affect hemostasis? | Aspirin inhibits COX-1 to reduce thromboxane A₂, limiting platelet aggregation. Heparin enhances antithrombin III to inhibit clot formation. |
| Which tests assess coagulation efficiency? | Prothrombin time (PT): measures extrinsic pathway, Activated partial thromboplastin time (aPTT): evaluates intrinsic pathway. Thrombin time (TT): measures fibrin formation, diagnosing bleeding disorders. |
| What are the phases of the cell cycle and their checkpoints? | TG1, S, G2, and M phases. Checkpoints: G1/S (checks conditions for DNA replication), G2/M (ensures DNA integrity), and spindle assembly (verifies chromosome alignment in mitosis). |
| How do cyclins and cyclin-dependent kinases (CDKs) regulate cell cycle? | Cyclins activate CDKs, which phosphorylate proteins to drive phase transitions; their regulation prevents uncontrolled cell growth. |
| What is contact inhibition, and why is it important? | Contact inhibition stops cell proliferation upon contact, maintaining tissue structure and preventing overgrowth. |
| How do growth factors and RTKs stimulate cell proliferation? | Growth factors bind RTKs, activating signaling pathways (MAPK, PI3K/Akt) that drive gene expression, cell division, and survival. |
| What is p53’s role in genomic stability? | The tumor suppressor protein detects DNA damage and triggers cell cycle arrest, DNA repair, or apoptosis to prevent mutation propagation and cancer. |
| What is the Hayflick limit and how is it significant? | Finite number of cell divisions before telomere shortening induces senescence, preventing unlimited proliferation. |
| How do apoptosis and necrosis differ? | Apoptosis—controlled, energy-dependent, and non-inflammatory. Necrosis—uncontrolled, injury-induced, and causes inflammation. |
| How do oncogenes and tumor suppressor genes influence cancer? | Oncogenes (e.g., Ras) drive cell proliferation when activated Tumor suppressors (e.g., p53) inhibit growth. Imbalances or mutations in these genes can lead to uncontrolled cell division and tumor formation. |
| What is the role of the PI3K/Akt pathway in cell survival? | It inhibits apoptosis and supports growth processes; its dysregulation is linked to cancer. |
| How does autophagy support cellular homeostasis? | It recycles damaged organelles and proteins, providing energy and clearing debris during stress or starvation. |
| How does protein phosphorylation influence enzyme activity in cells? | Phosphorylation of proteins, often by kinases, alters their conformation and activity, thereby regulating cellular processes like metabolism, signal transduction, and gene expression. |
| How does an enzyme’s structure enable its function? | Its active site binds substrates and lowers activation energy, ensuring precise and efficient metabolism. |
| How is enzyme activity regulated? | Via allosteric effects, covalent modifications (e.g., phosphorylation), and competitive or noncompetitive inhibition to control metabolism. |
| How do protein structure levels affect function? | Primary structure (amino acid sequence) directs folding into secondary (α-helices, β-sheets), forming the tertiary shape. Quaternary structure assembles subunits—all crucial for proper function. |
| How do saturated and unsaturated fatty acids differ, and why does it matter for membranes? | Saturated fatty acids (no double bonds) pack tightly, increasing rigidity. Unsaturated fatty acids (with double bonds) create kinks, enhancing membrane fluidity and function. |
| What roles do carbohydrates play beyond energy storage? | Aid in cell recognition, signaling (glycoproteins, glycolipids), and structural integrity (e.g., glycosaminoglycans in the extracellular matrix). |
| Describe the structure of a nucleotide and its role in genetics. | It has a phosphate group, pentose sugar, and nitrogenous base which polymerize to form nucleic acids (DNA/RNA) that store and transmit genetic information. |
| How do hydrogen bonds stabilize biomolecules? | They stabilize protein secondary structures (α-helices, β-sheets) and hold DNA base pairs together, ensuring structural integrity and function. |
| How do enzymes in human metabolic pathways maintain substrate specificity? | They have active sites that specifically bind substrates based on size, shape, and chemical interactions, ensuring that metabolic reactions proceed efficiently and selectively. |
| How does the Michaelis-Menten model explain enzyme kinetics? | It relates substrate concentration to reaction velocity (Vmax, Km). |
| What structural features of DNA are essential for its function? | Double helix, antiparallel strands, complementary base pairing, hydrogen bonds, and base stacking ensure accurate replication and information storage. |
| How is high-fidelity DNA replication achieved? | DNA polymerase proofreading removes mismatched bases, mismatch repair corrects errors, and coordinated replication ensures accuracy during cell division. |
| What do helicases, primases, and DNA ligases do in DNA replication? | Helicases unwind the double helix, primases synthesize RNA primers for initiation, and ligases seal Okazaki fragments to complete the lagging strand. |
| What are telomeres, and how does telomerase influence aging? | Telomeres protect chromosome ends from degradation. Telomerase lengthens telomeres, delaying cellular aging and enabling prolonged cell division. |
| How do epigenetic modifications regulate gene expression? | DNA methylation silences genes, while histone acetylation loosens chromatin, enhancing gene expression—both modify accessibility without altering DNA sequence. |
| How does chromatin organization affect gene expression? | Euchromatin is loose and active, allowing transcription. Heterochromatin is condensed and inactive, restricting access to transcription factors. |
| What are the major steps of transcription? | Initiation (RNA polymerase binds promoter), elongation (RNA synthesis), and termination (transcript release)— all regulated by transcription factors and epigenetic markers. |
| Why are DNA repair mechanisms critical in human physiology? | They correct genetic errors and environmental damage via processes like base excision repair, nucleotide excision repair, and homologous recombination—to maintain genomic stability and proper cell function. |
| How can mutations in DNA affect human physiology and contribute to disease? | Mutations can alter protein function or gene regulation, leading to cellular dysfunction and contributing to diseases such as cancer, metabolic disorders, and genetic syndromes in humans. |
| How does the fluid mosaic model explain the structure of the cell membrane? | It describes the membrane as a dynamic phospholipid bilayer with embedded proteins, cholesterol, and glycoproteins, allowing flexibility and molecular movement. |
| What function do integrins have in cell adhesion and signaling? | They mediate cell adhesion to the extracellular matrix, transmit mechanical forces, and activate intracellular signaling pathways involved in cell migration, proliferation, and survival. |
| How does cholesterol regulate cell membrane fluidity? | Cholesterol stabilizes membrane viscosity by reducing fluidity at high temperatures and preventing tight packing at low temperatures. |
| How do G-protein coupled receptors (GPCRs) mediate signal transduction in human cells? | GPCRs activate intracellular signaling pathways by binding ligands, triggering conformational changes that activate G proteins, which then influence downstream effectors like adenylate cyclase or phospholipase C. |
| What factors contribute to the selective permeability of the cell membrane? | The hydrophobic core of the lipid bilayer restricts the passage of polar molecules, while membrane proteins (channels, transporters) facilitate selective entry and exit of ions and nutrients. |
| How does endocytosis support nutrient uptake and receptor regulation? | Endocytosis (via receptor-mediated, pinocytosis, or phagocytosis) allows cells to absorb nutrients, regulate receptors, and clear extracellular debris. |
| What are lipid rafts, and why are they important in cell signaling? | Lipid rafts are cholesterol- and sphingolipid-rich microdomains that cluster signaling proteins, improving signal transduction efficiency and regulation. |
| How do interactions between the plasma membrane and the cytoskeleton regulate membrane fluidity and influence cellular dynamics, such as changes in shape and motility? | Cytoskeletal elements (e.g., actin filaments) attach to membrane proteins, creating subdomains that restrict or guide lipid movement. This interplay modulates local fluidity, enabling rapid shape changes and coordinated cell motility. |
| What is membrane asymmetry, and which enzymes maintain it? | Membrane asymmetry is the unequal lipid distribution between bilayer leaflets; flippases, floppases, and scramblases regulate this balance. |
| How do temperature and pH changes affect membrane fluidity? | DNA polymerase proofreading, mismatch repair, and coordinated replication minimize errors during cell division. |
| What roles do aquaporins and ion channels play in homeostasis? | Aquaporins facilitate water transport, while ion channels control ion flow, both essential for osmotic balance, nerve signaling, and muscle contraction. |
| How do the structural components of the skin contribute to its protective function? | The epidermis forms a waterproof barrier, the dermis provides strength and elasticity through collagen and elastin, and the hypodermis cushions and insulates the body. |
| How does the stratified structure of the epidermis enhance its barrier function? | The multilayered arrangement of keratinocytes, reinforced by tight junctions and desmosomes, creates a robust barrier that prevents pathogen entry, dehydration, and chemical damage. |
| What role do melanocytes play in protecting the skin from UV radiation? | Melanocytes produce melanin, which absorbs and disperses ultraviolet radiation, thereby protecting skin cells from DNA damage and reducing the risk of skin cancers. |
| Describe keratinization and its importance for human skin integrity. | The process by which basal keratinocytes differentiate and migrate to form the stratum corneum, a tough, protective layer that minimizes water loss and resists mechanical injury. |
| How do Langerhans cells function in the immune defense of the skin? | They act as antigen-presenting cells, capturing pathogens and initiating adaptive immune responses. |
| What is the significance of the extracellular matrix in the dermis? | The dermal extracellular matrix, made of collagen, elastin, and proteoglycans, provides strength and elasticity, maintaining skin integrity and resilience. |
| How do skin appendages enhance physiological functions? | Hair and nails provide protection, while sweat and sebaceous glands regulate temperature and sebum, and contribute to sensory and immune functions. |
| What are the phases of wound healing in human skin? | Inflammatory phase (immune response), proliferative phase (re-epithelialization, angiogenesis, granulation tissue), and remodeling phase (collagen reorganization, scar formation). |
| How does UV radiation lead to skin cancer at the molecular level in human cells? | UV radiation causes DNA damage, particularly the formation of pyrimidine dimers, which, if not repaired, can lead to mutations in tumor suppressor genes like p53, increasing skin cancer risk. |
| What cellular and molecular changes are associated with skin aging? | Decreased collagen/elastin, increased metalloproteinase activity, oxidative damage, and reduced regenerative capacity cause thinning, wrinkling, and loss of elasticity. |
| What are the primary cell types involved in bone remodeling? | Osteoblasts synthesize bone, osteoclasts resorb bone, and osteocytes maintain the matrix and coordinate remodeling. |
| What is endochondral ossification and its role in skeletal development? | It replaces cartilage with bone, involving chondrocyte growth, cartilage calcification, and osteoblast activity, essential for forming long bones. |
| How does intramembranous ossification differ from endochondral ossification? | Intramembranous ossification forms bone directly from mesenchymal cells, without cartilage, creating flat bones like the skull, while endochondral ossification replaces cartilage with bone, forming long bones. |
| What role does the periosteum play in bone growth and repair? | The periosteum is a dense connective tissue layer covering bones and contains osteoprogenitor cells, aiding in appositional growth and fracture repair. |
| What is the role of osteoprotegerin (OPG) in bone resorption regulation in human physiology? | OPG inhibits osteoclast differentiation and activity by binding to RANKL, preventing RANKL from interacting with RANK receptors on osteoclast precursors, thus reducing bone resorption. |
| How are hormones involved in bone metabolism regulation? | Parathyroid hormone increases osteoclast activity, calcitonin inhibits resorption, and vitamin D promotes calcium absorption, regulating bone turnover and mineral balance. |
| How does bone matrix mineralization occur? | Osteoblasts secrete collagen and non-collagenous proteins, forming a scaffold for hydroxyapatite crystal deposition, strengthening the bone matrix. |
| How do imbalances in osteoblast and osteoclast activity lead to osteoporosis? | Excessive osteoclast activity over osteoblast function reduces bone density, increasing fracture risk, leading to osteoporosis. |
| How do cytokines like TNF-α influence osteoclastogenesis and bone loss in humans? | TNF-α promotes osteoclastogenesis by stimulating the expression of RANKL on osteoblasts and stromal cells, enhancing osteoclast formation and activity, which can lead to bone loss in inflammatory diseases like rheumatoid arthritis. |
| How do defects in bone remodeling mechanisms contribute to osteoarthritis and other degenerative bone diseases? | Impaired osteoblast or osteoclast function disrupts bone remodeling, leading to cartilage breakdown and subchondral bone changes in osteoarthritis. |
Created by:
Khanyisile Maphosa
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