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3B

Andrew Susilo Part 1-3 None Inglés 66 fichas

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  1. 1Heart muscle layers: endocardium (thin layer similar to lining of blood vessels) // myocardium // pericardium (including visceral + space + parietal + fibrous, slightly thinner than myocardium) Intraventricular septum layers: membranous (closer to atria) // muscularPapillary muscles - projections @ inner surface of ventricles for anchor of chordae tendinae
    Fibrous skeleton - 4 dense connective tissue rings surrounding valves (fused), for insulation between atria // ventricles + anchoring of cardiac muscle
  2. 2Cardiac cycle: blood from atria to ventricles (both sides concurrent) -> AV valves open -> atrial systole -> ventricles fill with blood -> AV valves shut and semilunar valves open (lub, ventricular systole start) -> ejection -> semilunar valves close and AV valves open (dub, diastole start)Blood from coronary arteries drain via coronary veins to right atrium during relaxation (due to high aortic pressure)
    Conduction system: SA node propagates action potential -> atria contract -> (via internodal tract) to AV node -> bundle of His -> bundle branches -> Purkinje fibers (from apex to ventricular myocardium)
  3. 3Analysing ECG: P wave (atrial depolarisation) // P-Q (lengthened during scarring) // QRS (ventricular depolarisation, enlarged in AMI) // S-T (elevated in AMI, depressed in hypoxia) // Q-T (lengthened in AMI) // T wave (ventricular repolarisation, elevated in hyperkalemia, flattened in CAD).
  4. 4Cardiac reserve = maximum CO minus resting CO (usually 4-5x \ greater for athletes) Factors regulating SV: preload (degree of stretch before contracting, proportional to EDV) / contractility / afterload (pressure to exceed for ejection)Frank-Starling law = EDV can stretch cardiac muscle fibers to optimal sarcomere length for actin overlap
    Factors determining EDV: enough filling time / venous return
    +ve inotropic effect = increase contractility (eg digitalis, via G_s)
  5. 5SNS regulation of HR: NE from post-ganglionic cardiac accelerator nerves bind to b1-R @ SA node -> activate G_s -> cAMP binds to F-type Na+ -> pacemaker potential -> (via internodal tract) stimulate AV node; b1-R @ ventricular myocardium activates G_q -> increase Ca^2+ -> increase contractilityPSNS regulation of HR: vagus (X) nerve synapse with post-ganglionic @ heart wall -> ACh bind to muscarinic receptor @ SA node -> activate G_i -> open K+ channel + closure of F-type Na+ (due to decreased cAMP) -> decrease pacemaking and conduction
  6. 6Formed elements = cellular elements of blood Blood vessel layers: intima (endothelial cells + collagenous basement membrane) // media (smooth muscle, have elastin for arteries) // adventia (connective tissue mostly collagen, with vasa varosum + nerve endings)Blood composition @ body: 65% @ veins // 15% @ arteries // 10% @ lungs // 5% @ capillaries // 5% @ heart
    Poiseuille's law: R = 8 * L * eta (viscosity) ./. [pi * r^4]
    dP = beginning minus end = CO * PR
    MAP = DP + 0.33 * PP = CO * TPR
  7. 7Factors promoting venous return: pressure difference between venule and atrium (can be affected by leaky AV valve) / venous valves / skeletal muscle pump / respiratory pump / veno-constriction Vascular tone = basal state of partial contractionControl of arteriolar radii: intrinsic (myogenic response to stretch / local mediators released from metabolically active tissue) // extrinsic (eg E activates b2-R for arteriole vasodilation)
    Control of MAP: baroreceptor reflex (carotid sinus / aortic, input to CV center) / chemoreceptor (to respiratory center)
  8. 8Components of blood: plasma (least dense, 55%) / WBC and platelets (<1%) / Hb (most dense, normally 45%) Hematocrit = volume of RBC ./. total blood Hb releases O2 to muscle because p(O2) low \ p(CO2) high (-> CO2 and H+ compete for O2).
  9. 9Response to vessel damage: vascular spasm (wall smooth muscle contract immediately) + platelet plug formation (platelets adhere to exposed collagen with help of vWF from endothelial cells -> activation -> liberation of ADP + thromboxane A2 -> vasoconstriction -> platelet aggregation) + coagulationPlatelet activation: vWF / thrombin (protease) binds to PAR platelet receptor -> receptor cleavage -> tethering -> activate G_12 (-> Rho -> actin reorganisation -> extend projections -> contact other platelets) // G_q (PKC phosphorylates SNARE -> exocytosis of granules, PLA2 activates COX pathway)
  10. 10Blood clotting process: platelets coagulate by sticking with collagen -> fibrin strengthens plug to form mesh Coagulation cascade: XII activates XI -> activate IX -> (+VIII, intrinsic) // III activates VII -> (extrinsic) activate X (most important) -> (+ V) activate thrombin (II) -> activate fibrin (I)Factor XIIIa cross-links fibrins together to form mesh
    IIa activates XI / VIII / V / XIII
    Ca^2+ activates IX / X / II / XIIIa + Ia
    Negative feedback loops: IIa activates plasmin (-> breaks cross-links) / stimulates antithrombin (-> impedes X / II activation)
  11. 11RBC lasts ~4 days, platelets last 1-2 days RBC homeostasis: low oxygen -> stimulate EPO -> produce more RBC via bone marrow; old RBCs engulfed by spleen monocytes (sometimes @ liver) Platelet homeostasis: thrombopoietin stimulates more megakaryocytes -> platelets bud off as cytoplasm bitsEryhtropoiesis: pluripotent HSC -> myeloid stem cell -> progenitor cell -> pro-erythroblast -> RBC (synthesised Hb + enucleated) -> squeeze between endothelial cells -> get to capillaries
    Fe^3+ binds to transferrin @ plasma (later taken up by progenitor cells via RME) // ferritin @ liver / spleen / muscle
  12. 12Respiratory mucosa = epithelia (contains cilia + goblet cells surrounded by periciliary fluid) + underlying layer of connective tissue Mucociliary escalator = movement of mucus towards pharynx -> swallowed / expectoratedRespiratory membrane = alveolar epithelium (type I pneumocytes + type II septal cells secreting alveolar fluid) + epithelial BM + capillary BM (fused to epithelial BM) + capillary endothelium
  13. 13Conducting zone: terminal bronchioles -> respiratory bronchioles (< 0.5mm) -> alveolar duct; respiratory zone - direct site of gaseous exchange Inhalation: intercostal muscles contract, diaphragm contract (flatten), ~757 mmHg, elastin stretches open alveoli; exhalation driven by recoil of elastin*Residual volume can NOT be measured directly
    VC = ERV (~1.2L) + tidal volume (~0.5L) + IRV (~3.1L); inspiratory capacity = tidal volume + IRV; FRC = residual volume (~4.8L) + ERV
    High FEV1 ./. FVC ratio - uncompliant; low ratio - resistance (eg fibrosis)
  14. 14Flow-resistive work = work of alveoli / lung tissues, increased when increase RR; elastic work = work of intercostal muscle / diaphragm, increased when decrease RR Surfactant reduces surface tension (T) --> reduce tendency for alveolar collapse; p = 2 * T ./. r maintainedCauses of decreased gas exchange: resistance (obstruction @ airways, eg emphysema / asthma / pulmonary edema / bronchitis) // compliance (less elasticity --> alveoli collapse during exhalation --> trap some air @ lungs, eg RDS, possibly due to excessive surface tension)
  15. 15Respiratory quotient = ratio of O2 consumption ./. CO2 produced = alveolar P_O2 ./. [inspired P_O2 minus alveolar P_CO2]; usually 0.7-0.8 Alveolar P_O2 ~100 mmHg; pulmonary capillary (same as systemic tissue) P_O2 ~40 mmHg; alveolar P_CO2 ~40 mmHg; pulmonary capillary P_CO2 ~45 mmHgHenry's law: concentration dissolved = partial pressure into solvent ./. K_H (constant, indicates likelihood of solute leaving); CO2 @ blood ~22x more soluble than O2
    Fick's law of diffusion: J (flux) = rate ./. A = dP * D ./. T; D = K_H ./. sqrt (MW)
  16. 16V/Q mismatch: anatomical dead space (eg standing up -> pleural pressure gradient -> increased ventilation @ bottom -> broncho-constriction due to low CO2 // vasodilation due to high O2, or less energy to pump blood to bottom in prone position) / physiological dead space (eg infection / edema).
  17. 17Respiratory center: medullary (DRG stimulates phrenic nerves + external intercostal nerves + maybe VRG inspiratory neurons for forceful inspiration, VRG stimulates accessory muscles) // pontine (pneumotaxic area inhibits DRG to increase RR, apneustic area excites DRG to prolong respiration).
  18. 18Central chemoreceptors - adjacent to respiratory center, detect CO2 + pH; peripheral - stimulated by CO2 + pH + O2, aortic bodies -> nerve IX // carotid -> vagus Mechanoreceptors @ nose connect to respiratory center via nerve V (trigeminal); others via vagusOther sources of information to respiratory center: hypothalamus (eg fear sensation) / cerebrum (controls some voluntary actions)
    Motor nerves controlled by respiratory center: C1-3 (accessory muscles) // C3-5 (diaphragm) // T1-11 (intercostal) // T6-L1 (abdominal)
  19. 19Inhaled cool air equilibrates with blood temperature, exhaled air @ body temperature Factors affecting Hb saturation: temperature / p(CO2) / 2,3-BPG / acidity (all decrease O2 affinity) / diffusion / blood flow relative to ventilation (slower if alveolar pressure higher)Bohr effect: p(O2) increases O2 bound to Hb slowly until saturated, increased CO2 and H+ makes O2 delivery higher than just from low p(O2) (sigmoid graph shift right)
    Haldane effect: p(CO2) increases CO2 bound to Hb in a linear fashion, increased O2 shifts graph down
  20. 20Lymphatic system starts where fluid exit from capillaries -> some flow back shortly due to concentration gradient, different branches come together to deposit lymph back to circulation (mainly subclavian, non-closed loop); pathogens never recirculatedLymphatic ducts: thoracic (largest, for lower body / left upper body) // right lymphatic (for right upper body)
    One-way valves @ lymph vessels prevent fluid from moving opposite direction
    Maintaining flow of lymph: wall smooth muscle + skeletal muscle + respiratory pump (lower pressure @ thoracic)
  21. 21Chylomicrons package FA out of intestinal wall to diffuse into lymph; other peptides / waste products not absorbed @ small intestine also enter lymphatic system Smaller proteins exit into lymph easier --> more smaller ones than larger ones (overall more proteins than @ blood).
  22. 22Renal capillary beds: vasa recta (@ LoH, deliver O2) // peritubular (recollect nutrients from efferent arteriole to vein) Renal corpuscle = Bowman's capsule + glomerulus Calyx = nephron part @ medulla, first part where urine present; renal pelvis = central area of all calyces togetherFiltration process: ~20% blood fluid from glomerulus goes into Bowman's space -> PCT uses ATP to pump out Na+ (surrounded by peritubular capillaries) -> descending LoH for H2O to diffuse out (passive or active) -> ascending LoH pumps salts out using ATP -> collecting duct porousness dictated by ADH
  23. 23Glomerular capillary layers: endothelium (have large fenestrations, plasma proteins can pass \ RBC cannot) // basement membrane (fused to endothelium) // epithelial podocyte (tubular cells with filtration slits, attached to basement membrane via pedicels) // thin diaphragm (final barrier).
  24. 24Maintaining high GFR: constriction of efferent arterioles (can be boosted during exercise) as blood exits glomerulus provides resistance to flow (also prevents pressure drop), efferent arterioles smaller than afferent; counteracted by urinary hydrostatic + colloidal osmotic pressureRegulation of GFR: autoregulation (myogenic / tubulo-glomerular, adjust afferent arterioles to counteract BP via GFR) // neural (eg contraction of afferent arteriole during blood loss, may need RAAS in addition) // ANP (produced @ heart, secreted when plasma volume increases -> increase GFR)
  25. 25Nephron walls - single layer of cuboidal epithelium, microvilli @ brush border (luminal), densely packed with mitochondria PCT reabsorbs mostly NaCl + NaHCO3, + other essential substances (eg glucose / amino acids / phosphate / lactate / citrate) via secondary active transportNa+ reabsorption @ PCT: Na+/K+ ATPase (@ early PCT, opposite side of epithelium) / Na+/H+ exchanger (@ early PCT, enables reabsorption of HCO3^- to blood via trans-cellular CO2 diffusion) / Cl-/formate exchanger (@ late PCT) / symporter (eg with glucose) / paracellular via spaces between epithelial cells
  26. 26Na+ reabsorption @ thick ascending LoH (only in juxtamedullary): Na+/K+ ATPase (opposite side of epithelium) / three-ion cotransporter (1 Na+ + 2 Cl- in, 1 K+ out) Reabsorption of other ions: Ca^2+ (largely similar with Na+) / phosphate (primarily @ PCT) / Mg^2+ (mainly @ ascending LoH, mostly paracellular)ADH increases water permeability @ late DCT and collecting duct principal cells -> concentrate urine -> increase active transport of NaCl @ thick ascending; also increases urea permeability @ inner medullary collecting duct -> urea passively flow to interstitial fluid
  27. 27Counter-current multiplication largely by juxtamedullary (20-30% of nephrons) than cortical LoH characteristics for counter-current: descending permeable to water, thin ascending passively permeable to small solutes, thick ascending actively reabsorbsSteps of counter-current: single effect (active transport of NaCl from thick ascending limb into interstitial fluid -> water diffuses passively) -> fluid flow (new tubular fluid pushes concentrated fluid down -> osmotic gradient); vasa recta also helps by delaying blood flow (solutes can diffuse in)
  28. 28Ureter valves prevent backflow Bladder lined with transitional epithelium -- allow bladder to expand Micturition reflex: detrusor muscle contract, vs sphincter muscle relax Stasis: ureter valves malfunction -> urine @ ureter -> can cause infection; females more susceptible (shorter urethra)Internal urethra sphincter - involuntary, smooth muscle; external - membranous, skeletal muscle (voluntary)
    Male urethra system: internal sphincter -> prostatic urethra (pass through prostate) -> external sphincter -> spongy urethra @ penis
  29. 29Juxtaglomerular apparatus: macula densa (@ DCT, stimulates juxtaglomerular cells via paracrine prostaglandin signalling) + juxtaglomerular (granular) cells @ tunica media (mostly afferent arteriole) + sympathetic nerve @ tunica externa + mesangial cells (for structural support)RAAS system: juxtaglomerular cells sense low BP / sympathetic stimulation / low Na+ (@ DCT, indicates reabsorption due to low BP, sensed by macula densa) \ *NOT just low plasma electrolyte -> release renin -> cleaves angiotensinogen into angiotensin I -> further cleaved by endothileal ACE into angiotensin II
  30. 30Effects of angiotensin II: vasoconstriction (increase resistance -> increase arteriole blood pressure) / increase Na+ reabsorption @ kidneys (increase water reabsorption -> increase SV) / stimulate ADH and aldosterone releaseADH works @ region impermeable to water (vs aldosterone / angiotensin II - can retain water just by Na+ absorption)
    Triggers for ADH: high osmolarity / low blood volume (sensed by nerve endings of vena cava / right atrium) / low BP (sensed by arteriole baroreceptor @ aortic arch / carotid sinus)
  31. 31Triggers for aldosterone: low BP / angiotensin II / increase in K+ Aldosterone effects on principal cell @ late DCT / collecting duct: make Na+/K+ pump work harder / open K+ channel + Na+ channel @ apical --> blood lose K+ and gain Na+ -> osmolarity increased -> ADH secretedAlpha-intercalated cells @ collecting duct: secrete H3O+ + absorb HCO3-, HCO3- out to capillary @ basolateral + bring in Cl-, H+ out to urine via active transport / secondary transport with Na+ gradient (these two driven by aldosterone) / active with K+ antiport (apical) / Na+/K+ pump (basolateral)
  32. 32Tongue muscles: extrinsic (elevation vs depression / protrusion vs retraction) / intrinsic (run A-vs-P / L-vs -R) Teeth map: 4 central + 4 lateral incisor (for cutting) / 4 canine (gripping / pulling) / 8 premolar / 12 molar (3rd molar usually wisdom teeth coming up from gingiva holes; latter two for grinding)Serous content - with hydrolytic enzymes; mucin - wet food to make easier to form bolus
    Mouth glands: Von Ebner (@ tongue tip, for lipase, <5% saliva) / sublingual (mainly mucin, ~5%) / parotid (~25%) / submandibular (~70%, latter three release alpha amylase)
  33. 33GI tract layers: mucosa (epithelium + lamina propria connective tissue + muscularis smooth muscle) // submucosa (thick elastic connective tissue + exocrine glands + submucosal plexus of Meissner) // muscularis externa (peristaltic muscles + myenteric plexus of Auerbach) // serosaGI smooth muscle syncytium: autorhythmic fibers (ICC, alternating de/repolarisation sub-threshold for basic electrical rhythm) // contractile fibers (action potentials conveyed from ICC via gap junctions)
    Peristalsis vs segmentation: throughout GI tract vs only small intestine
  34. 34Upper esophageal sphincter - skeletal muscle only opens when voluntary; lower esophageal sphincter - diaphragm (encircles esophagus, smooth muscle) Esophageal hernia: esophagus moving up diaphragm causing acid refluxSteps of making chyme by stomach: receive bolus -> churn -> hydrolyse
    Gastric glands: parietal (HCl) / chief (pepsinogen + lipase) / mucosal (mucous to protect stomach from pepsin and HCl) / G cells (gastrin)
    Gastro-colic/ileal reflex: presence of food @ stomach signals push
  35. 35Digestion @ duodenum: pancreatic trypsinogen (converted later by enteropeptidase) / other proteolytic pro-enzymes, brush border (amino-)peptidase, pancreatic amylase, brush border lactidase (can be knocked off during inflammation), brush border nucleosidase, pancreatic lipaseAbsorption @ jejunum: amino acid into enterocyte with primary active transport, monosaccharides into and then out of enterocyte with secondary active transport, P-pentose / ntirogenous base enter and exit with primary active transport, fatty acids diffuse and organised into chylomicrons
  36. 36Storage @ liver: carbohydrates as glycogen, fats as lipoprotein and triglycerides, proteins turned into other molecules eg albumin Portal triad structure: portal vein branches into sinusoids, central vein @ center of lobule collects blood (-> becomes hepatic vein)Biliary tree: bile (pigments + salts) travels through common hepatic duct into cystic duct -> temporarily stored @ gallbladder; CCK triggers gallbladder contraction to squeeze back into cystic duct (also trigger pancreatic secretions + inhibit gastric motility) -> common bile duct -> released @ duodenum
  37. 37Pancreas found @ retroperitoneum, unencapsulated Exocrine pancreas secretions: HCO3- (neutralise gastric acid) / amylase / lipase / trypsinogen (converted by entero-peptidase) / chymotrypsinogen / pro-(carboxy-)peptidase / pro-elastase (last few converted by trypsin) / D/RNAse.
  38. 38Functions of large intestine: absorbing water and inorganic ions / digestion of carbohydrates (only) by micro-organisms (-> make CH4 + H2S + Vit K) Internal anal sphincter - smooth muscle (relax first when time to release stool, push against external sphincter); external sphincter - skeletal muscle.
  39. 39Endocrine control of GI tract: gastrin (food @ stomach -> G cells to release -> triggers gastric secretions + motility, stopped by somatostatin from D cells) // secretin (sensed chyme acid -> S cells to release -> oppose gastrin + trigger pancreatic secretions) // CCK (sensed chyme fat -> I cells to release)Neural responses to food: cephalic (sensation / thought of food -> salivation + secretion of gastric juices) // gastric (stimulated by distension / acidic pH / undigested material, builds on cephalic stimulation) // intestinal (controls rate of gastric emptying + coordinate other activities including accessory organs)
  40. 40Other digestive system hormones: incretin (GIP / GLP, secreted @ small intestine -> stimulate insulin in feedforward anticipation) / motility hormones (motilin / substance P / bombesin) / VIP (stimulates intestinal secretions \ inhibit gastric acid secretion) / GRP (stimulates gastrin) / somatostatin.
  41. 41Tendon - connective tissue, continuous with epimysium Layers of muscle cell: epimysium >>- perimysium >>- fasciculus (filled with endomysium between fibers) >>- myofiber (filled with sarcoplasm, contain nuclear bumps + SR + myoglobin + mitochondria + glycogen + myofibrils)SR = membranous structure surrounding each myofibril, transmit action potential by releasing stored Ca2+ via ryanodine receptors (once action potential gets far enough to T tubule and activate L-type DHP receptors)
    Triad = 2 terminal cisternae (from SR) + 1 T-tubule (folding of sarcolemma)
  42. 42Z-lines (= Z-disks, alpha-actinin) = striations for anchor of actin and titin Sarcomere = space between Z-lines; myosin anchored by titin @ M-line (myomesin) connecting to Z-disk A-band = length of myosin (include actomyosin + H-zone of myosin-only); I-band = actin-only (Z-line @ center)Myosin - 2 heads joining double-helix tail @ hinge (from 2 heavy chains) + 4 light chains, ATPase involved in motility
    G actin = individual actin (globular); F actin = double-helix long polymer from cross-linking of G actin
  43. 43Muscular contraction: ATP binds to myosin head of acto-myosin -> myosin release actin -> ATP hydrolysis -> myosin adopts high energy conformation (cocked) -> cross-bridge formation -> Pi release -> power stroke on actin -> ADP released -> cycle continuesTropomyosin coils around actin, attached by troponin -- blocks myosin from attaching to actin / keeps myosin from moving
    Ca^2+ binds to troponin to change conformation -> tropomyosin moves out -> contraction can happen
  44. 44Muscular twitch = brief contraction of group of muscles (20-200ms); consist of latent period /->/ contraction (graded) /->/ relaxation (Ca^2+ actively transported back, actin blocked by tropomyosin, myosin detach from actin)Factors affecting muscle tension: frequency of stimulation (refractory period right after contraction \ wave summation occurs after refractory period over -> fused / unfused) / length before contraction / thickness / motor unit size / motor unit recruitment
  45. 45Type 1 vs type 2 muscle fibers: red (more mitochondria) vs white, slow (rely on mitochondria) vs fast twitch, more lasting (eg back / thigh) vs shorter contraction (eg arms), fatigue-resistant vs fast fatigue, more overall energy vs more instantaneous force, storage mainly @ TG vs ATP and creatinine.
  46. 46Skeletal vs cardiac muscle: straight vs branched, nuclei @ periphery vs center, trigger of Ca^2+ release by depolarisation vs more intracellular Ca^2+ Skeletal vs smooth muscle: striated vs non-striated, straight vs spindle-shaped, multiple nuclei vs single nuclei.
  47. 47Cardiac muscles have intercalated discs containing desmosomes (connect ends of fibers) / gap junction (allow action potentials to spread across) --> interconnected as functional syncytium (auto-rhythmic non-contracting + contractile fibers)Excitation->contraction coupling in cardiac muscles: action potential @ sarcolemma reach L-type DHP receptors @ T tubule -> Ca^2+ enter -> bind to ryanodine receptors @ SR -- Ca^2+-induced Ca^2+ release
    Ca^2+ levels restored by Ca^2+ ATPase pump / Na+/Ca^2+ exchanger
  48. 48Smooth muscle - thick filaments have myosin heads projecting throughout, no regular pattern, no T tubules (\ have caveolae invaginations to contain Ca^2+), dense bodies for attachment of thin filaments ANS branches into varicosities to innervate smooth musclesSmooth muscle contraction: Ca^2+ bind to calmodulin -> activate MLCK -> phosphorylate light chains @ myosin heads (\ work slowly) -> bind to actin -> contraction (can remain in latch state for long periods without ATP consumption); dephosphorylation done by myosin phosphatase
  49. 49Pacemaker potential = spontaneous depolarisation always reaching threshold (more Ca^2+ in / less K+ out); slow-wave potential = fluctuations never reaching threshold (periodic changes in activity of Na+/K+ pumps?); plateau phase - prolonged opening of L-type DHP with partial opening of slow K+Excitation->contraction coupling in smooth muscle: depolarisation from action potential opens few L-type DHP receptors, weak CICR via ryanodine channels; other players eg GPCR / IP3 / store-operated channels (allow Ca^2+ from ECF) / mechanically-gated channels (sense stretch)
  50. 50Types of smooth muscle: single-unit (visceral, can be autorythmic, organised as syncytium connected via gap junctions) // multi-unit (independent fibers, graded contraction possible, richer supply of ANS nerve endings) New smooth muscle fibers can arise from pericytes.
  51. 51Hydrostatic vs exoskeleton vs endoskeleton: for invertebrates vs arthropods vs vertebrates Growth plate for long bones found @ metaphysis (between diaphysis /x/ epiphysis) Red vs yellow marrow: @ epiphysis vs diaphysis, hematopoiesis vs fat storageSpongey bone - filled with trabecula cavities; compact bone - organised into parallel osteon functional units (Haversian system, concentric lamella layers wrapped around, canaliculli branch out from Haversian central canal of lamella to lacuna)
    Volkmann's canal connects osteons
  52. 52Building blocks of bone matrix: osteoid (organic, consist of soft highly ordered structure of protein + type I collagen) + hydroxyapatite (inorganic) Osteoid proteins: osteocalcin / osteopontin Hydroxyapatite made with help of alkaline phosphataseBone cells @ bone: osteo-progenitor (differentiate into osteoblasts under some growth factors) / osteoblasts (synthesise collagen + proteins + alkaline phosphatase) / osteocytes (@ lacuna, have little branched projections to communicate with other bone cells via gap junctions) / osteoclasts
  53. 53Chondrocytes - derive from bone fibroblast precursor, avascular (\ receive immune protection + nutrition from surrounding fluid), secrete collagen (fibrous) / elastin (elastic) Bone growth stages: tissue forms collagen mesh -> held by polysaccharide -> calcium salts depositedTypes of cartilages: hyalin (articular, @ larynx / trachea / joints) / elastic (@ outer ear / epiglottis, provide shape / support) / fibrous (@ intervertebral discs / pubic symphysis)
    Types of joints: synarthroses (fused) // antiarthroses (slightly movable, eg vertebral) // diarthroses (synovial)
  54. 54Intramembranous ossification (from fibrous membrane): mesenchymal cells template -> differentiate into osetoblasts @ ossification center, osteoid forms spongy bone around blood vessels, matrix connective tissue differentiates into red marrow; for skull flat bones / mandible / clavicleEndochodral ossification (from hyaline cartilage): chondrocyte template -> calcification prevents diffusion of nutrients into matrix -> chondrocytes die -> open cavities @ diaphysis cartilage -> osteoblasts + osteoclasts modify into spongy bone, dense irregular connective tissue forms periosteum
  55. 55Lengthening of long bones: chondrocytes @ epiphyseal side divide, 1 remains undifferentiated \ 1 moves towards diaphysis (-> mature + destroyed via calcification) -> epiphyseal plate closure (chondrocytes stop dividing, cartilage replaced by bone) -> epiphysis fuse with diaphysisAppositional growth = increase in diameter of bones by addition of bony tissue to surface of bone; osteoblasts @ bone surface secrete matrix -> differentiate into osteocytes, osteoclasts @ inner surface break down bone
  56. 56Proper bone growth / maintenance requires Vit A + C + D / PTH / GH / calcitonin Bones @ head of femur replaced much faster than bone along shaft Remodeling allows thickening and strengthening when subjected to stressBone repair stages: blood vessels tear -> haemorrhage -> hematoma -> severed blood vessels sealed -> (after days) capillaries grow -> phagocytosis of dead cells -> fibroblasts (secrete collagen to connect bone ends) + osteoblasts come -> fibrocartilaginous callus formation -> convert to bony callus (like ossification)
  57. 57Epidermis strata: basale (most inferior, keratinocytes secrete cytokeratin for toughness, + melanocytes) // spinosum (desmosomes permit water loss, + Langerhans cells) // granluosum (keratohyalin granules @ cells, also release lamellar bodies to secrete lipids) // lucidum (clear) // corneumDermis layers: papillary (just below stratum basale, thin flexible connective tissue for movement of structures, contain nerve endings) // reticular (dense connective tissue for anchoring glands / follicle)
    Hypodermis = subcutaneous layer
  58. 58Nail root attached to epidermis, cells emerge from stratum basale (made up of keratin packed into dead cells) Hair follicle originates from reticular dermis, shaft emerges outwards to other layers (hair also made of keratin); receptor requires constantly changing stimulus (otherwise collagen fill in)Reticular dermis glands: holocrine (eg sebaceous gland, disintegrates entire cell) / apocrine (release proteins / lipids / steroids from apex straight into hair follicle after puberty, usually @ armpit / groin / around nipples) / merocrine (eg sudoriferous, release watery sweat via exocytosis, usually @ palms / soles)
  59. 59A-delta fibers - for pain and temperature; A-beta - for everything else (including mechanoreception) Meissner corpuscle - for light touch @ glaborious skin; Pacinian - deep rapid touch (both need changing stimulus); Merkel - sustained light touch; Ruffini - sustained deep touch / stretch / warmthTrpV1 senses both pain and temperature
    Thermoregulation: anterior hypothalamus respond to heat // posterior respond to cold -> arteriole smooth muscle relax (to dissipate heat) // contract, skeletal muscle shiver less // more (with ATP)
  60. 60Scrotum - regulates testes temperature -3degC below core; muscles contract // relax to tighten // loosen scrotum + move testes closer // further -> reduce // enhance heat loss Testes compartments contain seminiferous tubules (site of sperm production)Sertoli cells - embedded among spermatogenic cells @ seminiferous tubules, extend from BM to lumen, joined by tight junctions for blood//testis barrier
    Lyedig cells (interstitial) - clusters @ spaces between adjacent tubules
  61. 61Male accessory sex glands: seminal vesicles (secrete alkaline fluid with fructose + prostaglandin + fibrinogen) / prostate (secrete milky fluid with citric acid + clotting enzymes + proteases + seminal-plasmin antibiotic + phosphatase) / Cowper's (secrete mucus + alkaline fluid).
  62. 62Erection process: sexual stimulation -> PSNS release NO (+ also ACh -> bind to muscarinic receptor of endothelium -> produce more NO) -> vasodilation of penile arterioles (via cGMP pathway) \ penile veins compressed Erectile tissues: corpora cavernosa (upper) / corpus spongiosum (lower)Orgasm process: intense sexual stimulation -> SNS stimulate smooth muscles of epididymis / vas deferens / ejaculatory ducts -> sperm propelled to urethra // also stimulate accessory gland secretions -> movement of semen (emission) -> ejaculation; later coagulated @ vagina -> liquefied for mobility
  63. 63Ovarian follicular development: primoridal follicle -> (after puberty, stimulated monthly by FSH) primary follicle -> secondary follicle -> mature (graafian) follicle -> rupture (ovulation) -> remnants develop into corpus luteum (become scarred into corpus albicans if no fertilisation)Structure of ovarian follicle: primoridal follicle contains primary oocyte + single layer of follicular cells -> layers of follicular cell develop into granulosa cell in primary follicle, with zona pellucida between primary follicle and granulosa -> granulosa secrete follicular fluid into antrum in secondary follicle
  64. 64Ovarian hormones: estrogen (from secondary / graafian follicles) / inhibin (from granulosa) / progesterone (from corpus luteum) / relaxin ( from corpus luteum, produced every month, especially during pregnancy, increases flexibility of public symphysis + dilates uterine cervix during childbirth)Female sexual response: excitement (vasocongestion -> erection of clitoris + swelling of labia and vagina + secretion of fluid to lubricate vagina by mucosal / Bartholin's glands -> lubricating fluid exudates through epithelium) -> plateau (sex flush) -> orgasm (usually without refractory period) -> resolution
  65. 65Uterine wall layers: endometrium (many blood vessels + epithelial tissue + connective tissue + glands, stratum basalis gives rise to new stratum functionalis after each month) // myometrium // perimetrium (epithelium + connective tissue).
  66. 66Development of primitive bipotential gonad: female reproductive tract develops by default if no testicular androgens; SRY triggers differentiation into testes -> primitive Lyedig cells secrete testosterone -> develop Wolffian, Sertoli cells secrete MIH -> degenerate Mullerian.

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None Part 1-3 Fichas sobre 3B, creado por Andrew Susilo el 02/01/2023.
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