Downloaded 13 times
More Related Content
Similar to Renal Physiology and Skin – Complete Overview
![Renal_Phsyiology_2021_INTRODUCTION[1].pptx](https://cdn.slidesharecdn.com/ss_thumbnails/renalphsyiology2021introduction1-240913164449-bc60bf41-thumbnail.jpg?width=640&height=640&fit=bounds)
More from BALAJI SOMA
Renal Physiology and Skin – Complete Overview
- 1. RENAL PHYSIOLOGY & SKIN BY DR. SOMABALAJI PT
- 2. Functional Anatomy andGeneral Functions KIDNEY
- 3. LOCATION AND EXTERNAL FEATURES •Pair of bean-shaped organs located in the posterior abdominal wall on either side of vertebral column • Dimensions: Length – 11 cm, Width – 6 cm, Thickness – 3 cm • Weight: 150 g (each) • Covered by fibrous capsule • Convex lateral and concave medial border (hilum) • At hilum: entry of renal artery, exit of renal vein and ureter
- 4. • Cortex: outerzone (granular appearance) • Medulla: inner zone – arranged in renal pyramids • Renal columns of Bertin separate pyramids • Apex of each pyramid = renal papilla • Papilla Minor calyces Major calyces Renal pelvis Ureter → → → → INTERNAL STRUCTURE OF KIDNEY
- 5. MICROSCOPIC ANATOMY • Structural& functional unit = Nephron • Each kidney has about 1 million nephrons • Two types: • Cortical nephrons (85%) – short loop of Henle • Juxtamedullary nephrons (15%) – long loop of Henle
- 6. • Excretion ofmetabolic waste products • Urea, uric acid, creatinine • Regulation of water and electrolyte balance • Acid-base balance • Secretion of H⁺ and reabsorption of HCO₃⁻ • Regulation of blood pressure • Via Renin-Angiotensin-Aldosterone System (RAAS) • Erythropoietin production • Stimulates RBC formation • Activation of Vitamin D • Converts to active form – calcitriol • Gluconeogenesis • In prolonged fasting GENERAL FUNCTIONS OF KIDNEY
- 7. APPLIED PHYSIOLOGY • Kidneyfailure accumulation of waste uremia → → • Inability to concentrate urine polyuria → • Renin secretion disorders hypertension or hypotension →
- 8.
- 9. INTRODUCTION • Nephron isthe structural and functional unit of the kidney • Each kidney contains about 1 million nephrons • Main function: Urine formation • Each nephron is a long tubular structure closed at one end and open at the other
- 10. • Renal corpuscle •Glomerulus (capillary tuft) • Bowman’s capsule (double-walled) • Renal tubule • Proximal Convoluted Tubule (PCT) • Loop of Henle ⚬ Descending limb ⚬ Thin ascending limb ⚬ Thick ascending limb • Distal Convoluted Tubule (DCT) • Collecting duct (from multiple nephrons) PARTS OF NEPHRON
- 11. CORTICAL VS JUXTAMEDULLARY NEPHRON FeatureCortical Nephron Juxtamedullary Nephron Location Cortex Near cortex-medulla junction Loop of Henle Short Long (extends into medulla) Vasa recta Poorly developed Well developed Number 85% 15% Urine concentration Less role Major role
- 12. • Present nearthe vascular pole of glomerulus Composed of: • Macula densa (of DCT) • Juxtaglomerular cells (of afferent arteriole) • Lacis cells (mesangial cells) Function: Regulates renal blood flow, GFR, and renin secretion JUXTAGLOMERULAR APPARATUS (BRIEF MENTION)
- 13. • PCT: Reabsorptionof glucose, amino acids, Na⁺, Cl⁻, water • Loop of Henle: Establishes medullary concentration gradient • DCT: Sodium and water reabsorption (aldosterone-sensitive) • Collecting duct: Final urine concentration (ADH-sensitive) FUNCTIONS OF DIFFERENT PARTS OF NEPHRON
- 14. Structure and Functionsin Renal Physiology JUXTAGLOMERULAR APPARATUS
- 15. • JGA isa specialized structure at the vascular pole of renal corpuscle • Located where DCT touches the afferent arteriole of its own nephron • Plays a key role in regulating blood pressure, GFR, and renin secretion INTRODUCTION
- 16. Macula densa • Specializedepithelial cells of DCT • Sensitive to Na⁺ and Cl⁻ concentration in tubular fluid Juxtaglomerular (JG) cells • Modified smooth muscle cells in the wall of afferent arteriole • Secrete renin Lacis cells (Extraglomerular mesangial cells) • Between afferent and efferent arterioles and DCT • Supportive role; may help in signaling and contraction COMPONENTS OF JGA
- 17. Regulation of GlomerularFiltration Rate (GFR) • Through tubuloglomerular feedback mechanism • ↓ NaCl at macula densa dilates afferent arteriole GFR → → ↑ Regulation of Blood Pressure • Via Renin-Angiotensin-Aldosterone System (RAAS) • ↓ BP JG cells release renin Angiotensin II vasoconstriction and aldosterone → → → release BP → ↑ Autoregulation of Renal Blood Flow • Maintains consistent GFR despite fluctuations in systemic BP FUNCTIONS OF JUXTAGLOMERULAR APPARATUS
- 18. • Macula densadetects Na⁺ in DCT fluid ↓ • Signals afferent arteriole to dilate • Increases renal plasma flow and GFR • Also stimulates renin release from JG cells TUBULOGLOMERULAR FEEDBACK
- 19. • Overactivity ofJGA excess renin → → secondary hypertension • Drugs targeting RAAS (e.g., ACE inhibitors, ARBs) help control high BP • Dysfunction may contribute to acute kidney injury or CKD APPLIED PHYSIOLOGY
- 20. Anatomy, Physiology, andRegulation of Renal Blood Flow RENAL CIRCULATION
- 21. • Kidneys receive~1,300 mL/min of blood (~26% of cardiac output) • High blood flow ensures efficient filtration and homeostasis INTRODUCTION
- 22. 1.Renal artery (fromabdominal aorta) 2.Segmental arteries 3.Interlobar arteries (between renal pyramids) 4.Arcuate arteries (arch over pyramids) 5.Interlobular arteries (into cortex) 6.Afferent arterioles Glomerular capillaries → 7.Efferent arterioles → • Peritubular capillaries (cortical nephrons) • Vasa recta (juxtamedullary nephrons) RENAL BLOOD VESSELS
- 23. Peritubular/vasa recta Interlobularveins Arcuate veins Interlobar veins Renal vein → → → → → IVC VENOUS DRAINAGE
- 24. • Two capillarybeds: glomerular & peritubular (portal system) • High pressure in glomerular capillaries (60–70 mmHg) favors filtration • Low pressure in peritubular capillaries (8–10 mmHg) favors reabsorption • Afferent arteriole diameter > efferent maintains high → glomerular pressure SPECIAL FEATURES OF RENAL CIRCULATION
- 25. • Done viaPAH (Para-aminohippuric acid) clearance • Indicates renal plasma flow, which helps calculate renal blood flow • Normal RBF 1,200 mL/min ≈ MEASUREMENT OF RENAL BLOOD FLOW
- 26. • Maintains GFRover MAP range of 60–180 mmHg • Mechanisms: 1.Myogenic Response – smooth muscle contraction of afferent arteriole 2.Tubuloglomerular Feedback – macula densa senses NaCl, adjusts arteriole tone AUTOREGULATION OF RENAL BLOOD FLOW
- 27. • Impaired autoregulationhypotension-induced acute kidney injury → • NSAIDs can reduce renal perfusion by inhibiting prostaglandins • Renal artery stenosis reduced renal perfusion renin activation hypertension → → → APPLIED PHYSIOLOGY
- 28. Glomerular Filtration, TubularReabsorption, and Secretion URINE FORMATION
- 29. • Urine formationoccurs in three stages: 1.Glomerular filtration 2.Tubular reabsorption 3.Tubular secretion INTRODUCTION
- 30. • Blood plasmafiltered from glomerular capillaries into Bowman’s capsule • Filtrate = water + small solutes (Na⁺, glucose, urea, amino acids) • Not filtered = plasma proteins, blood cells Filtration barrier includes: • Endothelium • Basement membrane • Podocytes of Bowman’s capsule STEP 1 – GLOMERULAR FILTRATION
- 31. • Filtration pressure: •Net filtration pressure 10 mmHg ≈ • → GFR (Glomerular Filtration Rate) = 125 mL/min
- 32. • Renal bloodflow • Hydrostatic pressure in glomerular capillaries • Oncotic pressure in capillaries • Tubuloglomerular feedback • Constriction of afferent/efferent arterioles FACTORS AFFECTING GFR
- 33. • 99% offiltrate is reabsorbed • Most occurs in proximal convoluted tubule (PCT) STEP 2 – TUBULAR REABSORPTION Substance Site & Mode of Reabsorption Glucose, amino acids PCT – active transport Na⁺ PCT, Loop, DCT, CD – active Water PCT, Loop (descending), CD – osmosis HCO₃⁻ PCT – active Urea Passive diffusion (later parts)
- 34. • Maximum rateof reabsorption via active transport • Tm for glucose 375 mg/min ≈ • Above this glucose appears in urine = → glucosuria TRANSPORT MAXIMUM (TM)
- 35. • Substances addedto filtrate from blood • Mainly in distal tubule and collecting duct • Examples: H⁺, K⁺, NH₄⁺, creatinine, drugs (penicillin) STEP 3 – TUBULAR SECRETION
- 36. • Glomerular Filtration •→ Tubular Reabsorption (selective) • → Tubular Secretion (fine-tuning) → Final urine = 1–1.5 L/day SUMMARY OF URINE FORMATION
- 37. • Renal failureGFR urea/creatinine → ↓ → ↑ • Diabetes mellitus Glucosuria → • Diuretics Alter tubular transport mechanisms → APPLIED PHYSIOLOGY
- 38. Countercurrent Mechanism andRole of ADH CONCENTRATION OF URINE
- 39. • Normal urineoutput: 1–1.5 L/day • Kidneys can excrete either dilute or concentrated urine • Concentration of urine is essential to conserve water, especially during dehydration INTRODUCTION
- 40. • Two components: 1.CountercurrentMultiplier – Loop of Henle 2.Countercurrent Exchanger – Vasa Recta • Both work to maintain a medullary osmotic gradient (300–1200 mOsm/L) KEY MECHANISM – COUNTERCURRENT SYSTEM
- 41. • Descending limb:permeable to water, not solutes • Ascending limb: impermeable to water, actively transports Na⁺, K⁺, Cl⁻ • Creates hyperosmolar medulla • Enables water reabsorption in collecting duct when ADH is present COUNTERCURRENT MULTIPLIER (LOOP OF HENLE)
- 42. • Vasa rectapreserves medullary gradient • Freely permeable to water and solutes • Solutes enter descending limb, water exits reversed in ascending → limb • Prevents washout of gradient COUNTERCURRENT EXCHANGER (VASA RECTA)
- 43. • Secreted byposterior pituitary • Acts on collecting duct increases → water permeability • Water reabsorbed due to high medullary osmolarity • Leads to concentrated urine ROLE OF ANTIDIURETIC HORMONE (ADH)
- 44. • Urea contributesto medullary hyperosmolarity • Reabsorbed in medullary collecting duct • Secreted into loop of Henle recycled → • Enhances water reabsorption via osmotic gradient UREA RECYCLING
- 45. • In absenceof ADH collecting duct remains impermeable to water → • Tubular fluid remains dilute → dilute urine formed DILUTION OF URINE
- 46. • Diabetes insipidusADH deficiency dilute urine (polyuria, polydipsia) → → • SIADH excessive ADH water retention, concentrated urine → → • Loop diuretics (e.g., furosemide) block Na⁺ reabsorption in thick ascending limb → ↓ concentration ability APPLIED PHYSIOLOGY
- 47. Mechanisms of H⁺Secretion and Buffer Systems ACIDIFICATION OF URINE AND ROLE OF KIDNEY IN ACID-BASE BALANCE
- 48. • Normal urinepH: 4.5 to 8 • Kidneys help maintain systemic pH (~7.4) • Achieved by acid excretion, base reabsorption, and buffer systems INTRODUCTION
- 49. • Endogenous acidproduction (CO₂, lactic acid, ketones) • Dietary proteins (sulfuric, phosphoric acids) • Acid load must be excreted to maintain pH SOURCES OF ACID LOAD
- 50. Occurs in: • ProximalConvoluted Tubule (PCT) • Distal Convoluted Tubule (DCT) • Collecting Duct (CD) H⁺ secretion mechanisms: • Na⁺-H⁺ antiport (PCT) • H⁺ ATPase (DCT and CD) • H⁺-K⁺ ATPase (intercalated cells of CD) MECHANISMS OF H⁺ SECRETION
- 51. • Most HCO₃⁻reabsorbed in PCT • H⁺ secreted combines with filtered HCO₃⁻ H₂CO₃ H₂O + CO₂ → → • CO₂ diffuses into cell reformation of HCO₃⁻ reabsorbed → → REABSORPTION OF HCO₃⁻
- 52. • H⁺ isexcreted in urine using three buffer systems: 1.Bicarbonate buffer (HCO₃⁻) 2.Phosphate buffer (HPO₄²⁻ H₂PO₄⁻) ↔ 3.Ammonia buffer (NH₃ NH₄⁺) – major role in ↔ acid load • Titratable acidity = H⁺ excreted with phosphate • Ammonium excretion = via NH₄⁺ trapping URINARY BUFFERS
- 53. • H⁺ Secretion– direct acid removal • HCO₃⁻ Reabsorption – prevents base loss • Ammoniagenesis – enhances acid excretion • Regulation of blood pH ROLE OF KIDNEY IN ACID-BASE BALANCE
- 54. • Renal tubularacidosis (RTA) – impaired H⁺ secretion or HCO₃⁻ reabsorption • Chronic kidney disease metabolic acidosis → • Urine pH as a diagnostic tool in acid-base disorders APPLIED PHYSIOLOGY
- 55. Assessment of Glomerular,Tubular, Concentrating, and Excretory Functions RENAL FUNCTION TESTS
- 56. Renal function tests(RFTs) assess kidney’s ability to: • Filter blood • Reabsorb and secrete substances • Concentrate/dilute urine • Maintain acid-base and fluid balance INTRODUCTION
- 57. 1.Glomerular function tests 2.Tubularfunction tests 3.Concentration and dilution tests 4.Miscellaneous (e.g., imaging, urine analysis) CATEGORIES OF RENAL FUNCTION TESTS
- 58. 1. Plasma ClearanceTests • Inulin clearance – gold standard (GFR = ~125 mL/min) • Creatinine clearance – commonly used • Urea clearance – less accurate • Formula: • C = (U × V) / P • Where C = clearance, U = urine conc., V = urine volume/min, P = plasma conc. GLOMERULAR FUNCTION TESTS
- 59. • Serum Creatinine:increases in renal failure • Blood Urea Nitrogen (BUN): also increases • BUN: Creatinine ratio: helps differentiate pre-renal vs renal causes SERUM MARKERS FOR GFR
- 60. 1. Concentration Tests: •Water deprivation test – assess ADH response • Urine osmolality measurement 2. Dilution Tests: • Water loading test – assess maximal urine dilution TUBULAR FUNCTION TESTS
- 61. • Phenolsulfonphthalein (PSP)test • Glucose tolerance test (renal threshold) • Specific gravity of urine (normal: 1.010–1.030) • Fractional excretion of Na⁺ (FENa) TESTS FOR TUBULAR REABSORPTION
- 62. PAH (Para-aminohippuric acid)clearance • Measures renal plasma flow • Secreted by PCT Acidification tests – ability to secrete H⁺ and ammonium TESTS FOR TUBULAR SECRETION
- 63. Urinalysis: • Color, clarity,pH, specific gravity • Protein, glucose, ketones, RBCs/WBCs Imaging: • USG, CT, MRI for anatomical/functional study MISCELLANEOUS TESTS
- 64. 1.Detect early kidneydysfunction 2.Guide diagnosis in conditions like: • AKI / CKD • Glomerulonephritis • Nephrotic syndrome • Tubular defects CLINICAL IMPORTANCE
- 65. Physiology of UrineStorage and Voiding Reflex MICTURITION
- 66. • Micturition =process of urine expulsion from bladder • Involves storage phase and voiding phase • Coordinated by nervous system reflexes INTRODUCTION
- 67. • Detrusor muscle:smooth muscle wall • Internal sphincter: involuntary (smooth muscle) • External sphincter: voluntary (skeletal muscle) Innervation: • Parasympathetic (S2–S4) → bladder contraction • Sympathetic (T11–L2) → bladder relaxation, internal sphincter contraction • Somatic (pudendal nerve) → external sphincter control ANATOMY OF URINARY BLADDER
- 68. • Low-pressure storageof urine • Detrusor relaxed, sphincters contracted • Bladder stretches → afferent signals to spinal cord • Bladder capacity: 400–600 mL • Urge to void felt at ~150–250 mL FILLING PHASE
- 69. • Bladder fillsstretch receptors stimulated → • Afferents via pelvic nerve spinal cord (S2– → S4) • Parasympathetic efferents detrusor → contraction • Internal sphincter relaxes • Voluntary relaxation of external sphincter voiding → MICTURITION REFLEX – STEPS
- 70. • Cerebral cortex:voluntary control over external sphincter • Pontine micturition center (PMC): coordinates contraction and relaxation • Hypothalamus: emotional influence (e.g., fear incontinence) HIGHER CENTERS IN MICTURITION
- 71. • Inhibition: cortexcan delay urination • Facilitation: descending input to allow voiding • In children: reflex is automatic • Toilet training cortical control develops ~2–3 years → INHIBITION AND FACILITATION OF MICTURITION
- 72. • Atonic bladder– spinal injury overflow incontinence → • Automatic bladder – spinal transection above sacral reflex emptying → • Neurogenic bladder – uncontrolled contractions • Stress/urge incontinence ABNORMALITIES OF MICTURITION
- 73. Life-Saving Renal ReplacementTherapies DIALYSIS AND KIDNEY TRANSPLANTATION
- 74. • When kidneyfails waste products accumulate → uremia → • Two major Renal Replacement Therapies (RRT): 1.Dialysis – artificial removal of waste 2.Kidney transplantation – replacement of failed kidney INTRODUCTION
- 75. • Dialysis =process of artificially removing metabolic waste, electrolytes, excess fluid • Based on diffusion, osmosis, and ultrafiltration across a semipermeable membrane DIALYSIS – DEFINITION
- 76. 1.Hemodialysis • Blood isfiltered through a dialysis machine • Commonly done 3 times/week, 4–5 hrs/session 2. Peritoneal dialysis • Dialysis fluid introduced into peritoneal cavity • Peritoneum acts as natural membrane • Done at home, e.g., CAPD (Continuous Ambulatory PD) TYPES OF DIALYSIS
- 77. • Requires vascularaccess: arteriovenous fistula or catheter • Blood pumped through dialyzer • Waste diffuses into dialysis fluid • Clean blood returned to body • Electrolyte balance and fluid control maintained HEMODIALYSIS – PROCEDURE
- 78. • Dialysate fluidinfused via catheter into peritoneal cavity • Wastes diffuse from blood fluid → → drained after hours • Used in chronic renal failure, especially in children and home patients PERITONEAL DIALYSIS – PROCEDURE
- 79. • Acute orchronic renal failure • Uremic symptoms: confusion, nausea, fatigue • Hyperkalemia, fluid overload, acidosis • GFR < 10 mL/min INDICATIONS FOR DIALYSIS
- 80. Hemodialysis: • Hypotension, infection,anemia, clotting Peritoneal Dialysis: • Peritonitis, weight gain, protein loss • Access site infections COMPLICATIONS OF DIALYSIS
- 81. • Preferred treatmentin end-stage renal disease (ESRD) • Donor: living or cadaver • Graft placed in iliac fossa • Immunosuppressive therapy mandatory E.g., corticosteroids, cyclosporine, tacrolimus KIDNEY TRANSPLANTATION
- 82. Graft rejection: • Hyperacute,acute, or chronic - Infections due to immunosuppression • Drug toxicity • Recurrence of original kidney disease COMPLICATIONS OF TRANSPLANT
- 83. • Better qualityof life • Less long-term complications • Improved survival rates • Fewer dietary restrictions ADVANTAGES OF KIDNEY TRANSPLANT OVER DIALYSIS
- 84. The Largest Organof the Human Body SKIN – INTRODUCTION AND FUNCTIONS
- 85. • Skin =largest organ, ~16% of body weight • Total area: ~1.5–2 m² • Acts as a protective barrier and interface between body and environment • Part of the integumentary system INTRODUCTION
- 86. 1.Epidermis • Outer, avascular •Made of stratified squamous epithelium 2. Dermis • Thick, connective tissue • Contains blood vessels, nerves, glands 3. Hypodermis (subcutaneous tissue) • Fat-rich layer connecting skin to muscles LAYERS OF THE SKIN
- 87. 1.Stratum basale –cell division 2.Stratum spinosum – keratinocytes 3.Stratum granulosum – keratohyalin granules 4.Stratum lucidum – thick skin only (palms, soles) 5.Stratum corneum – dead cells, keratin-rich EPIDERMAL LAYERS (FROM INSIDE TO OUTSIDE)
- 88. • Keratinocytes –main cells • Melanocytes – produce melanin • Langerhans cells – immune defense • Merkel cells – touch sensation CELLS OF EPIDERMIS
- 89. 1.Protection – barrierto mechanical, chemical, UV damage 2.Sensation – touch, pain, temperature 3.Thermoregulation – via sweating, blood flow 4.Metabolism – synthesis of vitamin D 5.Excretion – water, salts, urea 6.Immunity – Langerhans cells 7.Storage – fat, blood reservoir FUNCTIONS OF SKIN
- 90. 1.Hair follicles 2.Sebaceous glands– sebum secretion 3.Sweat glands Eccrine – all over body, watery sweat Apocrine – axilla, groin, protein-rich sweat 4. Nails APPENDAGES OF THE SKIN
- 91. 1.Melanin: determines skincolor 2.Produced by melanocytes in stratum basale 3.Influenced by genetics, UV exposure, hormones 4.Protects against UV radiation PIGMENTATION
- 92. 1.Meissner’s corpuscles –light touch 2.Pacinian corpuscles – pressure and vibration 3.Merkel discs – touch 4.Free nerve endings – pain, temperature SKIN RECEPTORS
- 93. Specialized Blood Flowfor Temperature Regulation CUTANEOUS CIRCULATION
- 94. • Cutaneous circulation= blood flow through the skin Major role in: • Thermoregulation • Nutrient delivery to skin tissues • Immunological defense • Wound healing INTRODUCTION
- 95. • Arterial supplyfrom subdermal plexus • Forms deep, middle, and superficial plexuses Arteriovenous anastomoses (AVAs): • Direct connection between arterioles and venules • Bypass capillaries • Important for temperature regulation BLOOD SUPPLY TO THE SKIN
- 96. • High arteriovenousanastomoses – abundant in palms, soles, ears, nose • Under autonomic nervous control – mainly sympathetic • Highly responsive to environmental temperature SPECIAL FEATURES OF CUTANEOUS CIRCULATION
- 97. 1.Neural control • Sympatheticvasoconstrictor fibers (norepinephrine) • Sudomotor sympathetic cholinergic fibers sweating → 1.Local control • Temperature-sensitive reflexes • Histamine, prostaglandins (e.g., during inflammation) REGULATION OF CUTANEOUS BLOOD FLOW
- 98. • Heat exposurevasodilation blood flow heat loss → → ↑ → • Cold exposure vasoconstriction blood flow conserve heat → → ↓ → • Mediated by hypothalamic thermoregulatory center EFFECT OF TEMPERATURE
- 99. • Red Reaction– local capillary dilation • Flare – arteriolar dilation via axon reflex • Wheal – localized edema due to increased permeability TRIPLE RESPONSE (LEWIS)
- 100. • Thermoregulation: primaryfunction • Defense: via immune cell transport • Healing: wound vascularization • Diagnostic utility: e.g., skin turgor, cyanosis FUNCTIONAL IMPORTANCE
- 101. 1.Raynaud’s phenomenon –exaggerated vasoconstriction 2.Burns – vascular damage, fluid loss 3.Pressure ulcers – ischemia due to prolonged pressure PATHOPHYSIOLOGY
- 102. Homeostasis Through HeatBalance BODY TEMPERATURE REGULATION
- 103. • Normal corebody temperature: ~37°C (98.6°F) • Maintained within ± 0.5°C by thermoregulatory mechanisms • Controlled by hypothalamus • Critical for enzyme function, cell metabolism, organ function INTRODUCTION
- 104. 1.Core temperature • Internalorgans (brain, thorax, abdomen) • Constant 1.Shell temperature • Skin & extremities • Varies with ambient temperature TYPES OF BODY TEMPERATURE
- 105. • Oral • Rectal •Axillary • Tympanic membrane • Esophageal & rectal (for core temp in clinical settings) SITES FOR MEASURING BODY TEMPERATURE
- 106. • Basal metabolicrate (BMR) – main contributor • Muscle activity – shivering, exercise • Hormonal thermogenesis – thyroxine, epinephrine • Thermogenic effect of food • Brown fat (in neonates) HEAT PRODUCTION (THERMOGENESIS)
- 107. 1.Radiation (~60%) 2.Conduction (~3%) 3.Convection(~15%) 4.Evaporation (~22%) – sweating, respiration • Enhanced by vasodilation & sweating HEAT LOSS (THERMOLYSIS)
- 108. 1.Anterior hypothalamus (preopticarea) – heat loss center 2.Posterior hypothalamus – heat gain center 3.Thermoreceptors: -Peripheral (skin) -Central (hypothalamus, spinal cord, viscera) REGULATION BY HYPOTHALAMUS
- 109. 1.Vasoconstriction 2.Shivering thermogenesis 3.Non-shivering thermogenesis(hormonal) 4.Piloerection 5.Behavioral response (e.g., wearing clothes) RESPONSE TO COLD EXPOSURE
- 110. • Vasodilation • Sweating(sympathetic cholinergic) • Behavioral adjustments (e.g., seeking shade) RESPONSE TO HEAT EXPOSURE
- 111. 1.Fever (pyrexia) • Causedby pyrogens hypothalamic set point → ↑ 1.Hyperthermia • ↑ temperature without change in set point (e.g., heat stroke) 1.Hypothermia • Core temp < 35°C bradycardia, metabolic depression → ABNORMALITIES OF BODY TEMPERATURE
- 112. 1.Exogenous pyrogens stimulatemacrophages release IL-1 → → 2.IL-1 acts on hypothalamus prostaglandin E2 resets set → → ↑ → point 3.Body reacts as if cold shivering, vasoconstriction temp → → ↑ FEVER MECHANISM
- 113. 1.To heat: ↑sweat efficiency, salt loss ↓ 2.To cold: metabolic rate, improved vasoconstriction ↑ 3.Gradual physiological adaptation over days/weeks ACCLIMATIZATION
- 114. Body's Adaptation andDefense Mechanisms in Cold Exposure APPLIED PHYSIOLOGY OF COLD
- 115. 1.Cold environment =challenge to core temperature homeostasis 2.Primary aim: Prevent hypothermia 3.Thermoregulatory responses are activated to conserve and generate heat INTRODUCTION
- 116. 1.Cutaneous vasoconstriction –reduces blood flow to skin 2.Shivering thermogenesis – involuntary muscle activity 3.Non-shivering thermogenesis – via thyroid & adrenal hormones 4.Piloerection – traps air (minimal in humans) 5.Behavioral responses – clothing, shelter-seeking PHYSIOLOGICAL RESPONSES TO COLD
- 117. • Increased thyroxine→ BMR ↑ • Increased adrenaline & noradrenaline → metabolism ↑ • Cortisol may also contribute in prolonged cold exposure HORMONAL CHANGES IN COLD
- 118. • Takes 2–3weeks • Increased BMR • Enhanced vasoconstrictor response • Improved thermal insulation via subcutaneous fat & clothing behavior ACCLIMATIZATION TO COLD
- 119. 1.Occasional vasodilation inextremities after prolonged vasoconstriction 2.Prevents cold injury (e.g., frostbite) 3."Hunting response" – cyclical opening and closing of blood vessels COLD-INDUCED VASODILATION (CIVD)
- 120. • Core temp< 35°C • Mild: Shivering, confusion • Moderate: Apathy, decreased consciousness • Severe: Arrhythmias, loss of consciousness, death • Treatment: gradual rewarming, supportive care HYPOTHERMIA
- 121. 1.Frostbite – freezingof skin and tissues 2.Trench foot – prolonged exposure to wet cold 3.Chilblains – inflammatory reaction to cold Caused by inadequate circulation and prolonged vasoconstriction COLD INJURIES
- 122. • Cryotherapy: localizedcold for pain and inflammation control • Therapeutic hypothermia: used post-cardiac arrest to reduce brain injury • Cold stress testing: for Raynaud’s disease evaluation APPLICATIONS IN MEDICINE
- 123. • Adequate insulationand clothing • Avoid prolonged exposure • Gradual rewarming • Proper hydration and nutrition PREVENTION OF COLD INJURY
- 124. Body’s Heat Defenseand Adaptation Mechanisms APPLIED PHYSIOLOGY OF HOT ENVIRONMENT
- 125. • Hot environmentsthreaten thermal homeostasis • Primary danger: Hyperthermia • The body activates cooling mechanisms to maintain core temperature INTRODUCTION
- 126. • Cutaneous vasodilation– increases heat loss • Sweating – evaporative cooling • Decreased muscle tone – reduces heat generation • Behavioral responses – removing clothes, seeking shade PHYSIOLOGICAL RESPONSES TO HEAT
- 127. • Anterior hypothalamus(preoptic area): Heat loss center • Receives signals from: - Peripheral thermoreceptors (skin) - Central thermoreceptors (hypothalamus, spinal cord) ROLE OF HYPOTHALAMUS
- 128. • Sympathetic cholinergicstimulation • Sweat glands: Eccrine glands • Composition: Initially isotonic becomes hypotonic → • Regulated by aldosterone (sodium conservation during prolonged heat) SWEATING MECHANISM
- 129. • Occurs over7–10 days • Increased sweat production • Earlier onset of sweating • Reduced electrolyte loss • Enhanced cardiovascular stability ACCLIMATIZATION TO HEAT
- 130. 1.Increased heart rateand cardiac output 2.Dehydration due to fluid loss 3.Electrolyte imbalance 4.Reduced performance & concentration EFFECTS OF HEAT ON BODY
- 131. 1.Heat cramps –muscle cramps due to sodium loss 2.Heat exhaustion – dehydration & circulatory collapse • Symptoms: fatigue, nausea, dizziness, hypotension 1.Heat stroke – medical emergency • Temp > 40°C, absence of sweating, CNS symptoms (confusion, coma) HEAT-RELATED ILLNESSES
- 132. • Immediate cooling:ice packs, cold IV fluids, evaporation techniques • Airway and circulatory support • Monitor for complications: kidney failure, DIC, seizures MANAGEMENT OF HEAT STROKE
- 133. • Hydration withelectrolytes • Avoid outdoor exposure during peak heat • Wear light, breathable clothing • Gradual acclimatization before heat exposure PREVENTIVE MEASURES
- 134. The Body’s LargestOrgan and its Vital Roles SKIN – STRUCTURE AND FUNCTIONS
- 135. • Skin isthe largest organ of the human body • Area: ~1.5–2.0 m²; Weight: ~15% of body weight • Performs vital protective, regulatory, and sensory functions INTRODUCTION
- 136. 1.Epidermis • Stratified squamousepithelium • Layers: Basale, Spinosum, Granulosum, Lucidum (palms/soles), Corneum • Contains keratinocytes, melanocytes, Langerhans & Merkel cells 1.Dermis • Dense connective tissue • Layers: Papillary & Reticular • Contains blood vessels, nerves, glands, hair follicles 1.Hypodermis (subcutaneous tissue) • Fat and connective tissue • Provides insulation and cushioning LAYERS OF SKIN
- 137. FUNCTIONS OF THESKIN – OVERVIEW
- 138. PROTECTIVE FUNCTION • Physicalbarrier: Prevents mechanical, chemical, microbial damage • Melanin: protects against UV radiation • Acidic pH and sebum: inhibit microbial growth • Keratin: resists dehydration and penetration
- 139. THERMOREGULATORY FUNCTION • Sweatingand cutaneous vasodilation for heat loss • Vasoconstriction and piloerection in cold • Controlled by hypothalamic thermoregulatory center
- 140. SENSORY FUNCTION Rich insensory receptors: • Meissner’s corpuscles – touch • Pacinian corpuscles – pressure • Merkel cells – tactile discrimination • Free nerve endings – pain and temperature
- 141. EXCRETORY AND METABOLIC FUNCTIONS •Sweat glands: excrete water, salts, urea • Vitamin D3 synthesis from 7-dehydrocholesterol under UV light • Helps in calcium and phosphorus homeostasis
- 142. IMMUNE AND EMOTIONAL ROLE •Langerhans cells: antigen-presenting • Plays a role in cutaneous immune responses • Changes in skin reflect emotional states (blushing, pallor)
- 143. SKIN APPENDAGES 1.Hair –sensory and protective 2.Nails – protection and support 3.Sebaceous glands – secrete sebum (lubricates and waterproofs skin) 4.Sweat glands: • Eccrine – thermoregulation • Apocrine – emotional sweating (axilla, genital area)
- 144.