Results for "epinephrine"

Endocrine System - Epinephrine Pathway

Pharmacological Actions of Epinephrine and Norepinephrine

Melatonin and Epinephrine

Endocrine System 1. What are hormones and what is their function in the body? Hormones are chemical messengers transported in the bloodstream that stimulate physiological responses in target cells or organs. 2. Types of hormones Endocrine System 1. What are hormones and what is their function in the body? Hormones are chemical messengers transported in the bloodstream that stimulate physiological responses in target cells or organs. 2. Types of hormones based on chemical composition and how they enter target cells: • Steroid hormones: Lipid-soluble, diffuse through cell membrane (e.g., cortisol). • Protein/Peptide hormones: Water-soluble, bind to surface receptors (e.g., insulin). • Biogenic/Monoamines: Derived from amino acids (e.g., T3/T4), may need carriers or membrane receptors. 3. Know all 6 hormones secreted by the anterior pituitary gland and their functions: • TSH: Stimulates thyroid to release T3 and T4. • ACTH: Stimulates adrenal cortex to release cortisol. • GH: Stimulates tissue growth and protein synthesis. • PRL: Stimulates milk production. • FSH: Stimulates egg maturation/sperm production. • LH: Triggers ovulation and testosterone production. 4. What is thymosin? Which gland secretes it? What is its function? Thymosin is secreted by the thymus and helps in the development and maturation of T-cells. 5. Know thyroid gland hormones, the cells that secrete them, and their functions: • T3 & T4 (follicular cells): Increase metabolism and regulate appetite. • Calcitonin (C cells): Lowers blood calcium levels. 6. Know the hormones secreted by the adrenal gland and their specific functions: • Cortex: • Aldosterone: Retains Na⁺, excretes K⁺, raises blood pressure. • Cortisol: Increases glucose, metabolism of fat/protein. • Androgens: Precursor to sex hormones. • Medulla: • Epinephrine/Norepinephrine: Increase heart rate, blood flow, and alertness. 7. Function of glucagon and insulin in maintaining homeostasis: • Insulin (beta cells): Lowers blood glucose. • Glucagon (alpha cells): Raises blood glucose. • Antagonistic: They have opposing effects to balance blood sugar levels. 8. Which cells are involved in spermatogenesis? Where does sperm production occur? • Sertoli (Sustentacular) cells support spermatogenesis. • Leydig (Interstitial) cells produce testosterone. • Occurs in the seminiferous tubules of the testes. 9. Know the hormones secreted by the testes and their functions: • Testosterone: Stimulates male development and sperm production. • Inhibin: Inhibits FSH to regulate sperm production. 10. What causes diabetes insipidus? How is it different from diabetes mellitus? • Diabetes insipidus: ADH deficiency → excessive urination. • Diabetes mellitus: Insulin issues → high blood glucose. 11. Know the 3 “P’s” of diabetes: • Polyuria: Excessive urination. • Polydipsia: Excessive thirst. • Polyphagia: Excessive hunger. 12. How are oxytocin and prolactin different? • Oxytocin: Stimulates uterine contractions and milk letdown. • Prolactin: Stimulates milk production. 13. Name the ovarian hormones and their functions: • Estrogen/Progesterone: Regulate cycle, pregnancy, and secondary sex characteristics. • Inhibin: Inhibits FSH secretion. ⸻ Muscle Physiology 14. Know 3 muscle types, their locations, and function: • Skeletal: Attached to bones; movement; voluntary. • Cardiac: Heart; pumps blood; involuntary. • Smooth: Organs/vessels; propels substances; involuntary. 15. Know the layers surrounding muscle: • Epimysium: Surrounds entire muscle. • Perimysium: Surrounds fascicle (bundle). • Endomysium: Surrounds individual fiber. 16. What is a fascicle? A bundle of muscle fibers. 17. What is a sarcomere? Name its regions: Smallest contractile unit (Z-disc to Z-disc). • Z-band, A-band (dark), I-band (light), H-zone. 18. What are actin and myosin? • Actin: Thin filament. • Myosin: Thick filament that pulls actin during contraction. 19. What is troponin and tropomyosin? • Tropomyosin blocks binding sites on actin. • Troponin binds Ca²⁺ to move tropomyosin and expose sites. 20. What is a motor unit? A motor neuron and all muscle fibers it controls. 21. Role of T-Tubule, SR, Terminal Cisternae: • T-Tubule: Conducts AP into cell. • SR: Stores calcium. • Terminal cisternae: Release calcium. 22. Which neurotransmitter is released at the neuromuscular junction? Acetylcholine (ACh). 23. What role does Ca²⁺ play in muscle physiology? Binds troponin, moves tropomyosin, exposes actin sites. 24. What happens to Ca²⁺ after action potential ends? Reabsorbed into SR by Ca²⁺ ATPase pump. 25. What is the function of ATP in muscle physiology? Powers myosin movement, detachment, and Ca²⁺ reuptake. 26. What is sliding filament theory? Myosin pulls actin filaments → sarcomere shortens → contraction. 27. What are DHP and Ryanodine receptors and their roles? • DHP: Voltage sensor in T-tubule. • Ryanodine: Releases Ca²⁺ from SR. 28. What is the function of AChE? Breaks down ACh to stop stimulation and contraction. 29. Difference between isotonic and isometric contractions: • Isotonic: Muscle changes length (shortens/lengthens). • Isometric: Muscle length stays same; tension builds. ⸻ Respiratory Physiology 30. Difference between conductive and respiratory divisions: • Conductive: Air passageways (nose to bronchioles). • Respiratory: Gas exchange (alveoli). 31. Type I & II alveolar cells and functions: • Type I: Gas exchange. • Type II: Secretes surfactant, repairs alveoli. 32. Dust cells and their functions: Alveolar macrophages that clean up particles/debris. 33. Muscles in relaxed vs. forced respiration: • Relaxed inhale: Diaphragm, external intercostals. • Forced inhale: Accessory neck muscles. • Forced exhale: Internal intercostals, abdominals. 34. What happens to pressure and volume when inhaling/exhaling? • Inhale: Volume ↑, pressure ↓. • Exhale: Volume ↓, pressure ↑. 35. Difference between systemic and pulmonary exchange: • Systemic: Gas exchange at tissues. • Pulmonary: Gas exchange in lungs. 36. What cells are involved in carrying gases? Red blood cells (RBCs). 37. Which enzyme converts CO₂ + H₂O → H₂CO₃? Carbonic anhydrase. 38. What does carbonic acid break into? H⁺ + HCO₃⁻ (bicarbonate ion). 39. What happens in hypoxia (low oxygen)? • ↓O₂, ↑CO₂, ↓pH (acidosis). 40. What happens in hypercapnia (high CO₂)? • ↑CO₂, ↓O₂, ↓pH (acidosis). 41. Receptors for blood pH and their locations: • Central (CSF pH): Medulla oblongata. • Peripheral (O₂, CO₂, pH): Carotid & aortic bodies. 42. CO₂ loading & O₂ unloading at tissues: • CO₂ enters blood → forms HCO₃⁻. • O₂ released to tissues. 43. CO₂ unloading & O₂ loading at alveoli: • CO₂ released from blood to lungs. • O₂ binds to hemoglobin. 44. Brain part for unconscious breathing: Medulla oblongata. 45. Obstructive vs. restrictive disorders + example: • Obstructive: Narrowed airways (asthma). • Restrictive: Reduced lung expansion (fibrosis). 46. Know spirometry volumes (not numbers): • Tidal volume, • Inspiratory/Expiratory reserve volume, • Residual volume, • Vital capacity, • Total lung capacity, • Inspiratory capacity, • Functional residual capacity. 47. Define eupnea, dyspnea, tachypnea, apnea, Kussmaul respiration: • Eupnea: Normal breathing. • Dyspnea: Labored breathing. • Tachypnea: Rapid, shallow breathing. • Apnea: No breathing. • Kussmaul: Deep, rapid (from acidosis Endocrine System 1. What are hormones and what is their function in the body? Hormones are chemical messengers transported in the bloodstream that stimulate physiological responses in target cells or organs. 2. Types of hormones based on chemical composition and how they enter target cells: • Steroid hormones: Lipid-soluble, diffuse through cell membrane (e.g., cortisol). • Protein/Peptide hormones: Water-soluble, bind to surface receptors (e.g., insulin). • Biogenic/Monoamines: Derived from amino acids (e.g., T3/T4), may need carriers or membrane receptors. 3. Know all 6 hormones secreted by the anterior pituitary gland and their functions: • TSH: Stimulates thyroid to release T3 and T4. • ACTH: Stimulates adrenal cortex to release cortisol. • GH: Stimulates tissue growth and protein synthesis. • PRL: Stimulates milk production. • FSH: Stimulates egg maturation/sperm production. • LH: Triggers ovulation and testosterone production. 4. What is thymosin? Which gland secretes it? What is its function? Thymosin is secreted by the thymus and helps in the development and maturation of T-cells. 5. Know thyroid gland hormones, the cells that secrete them, and their functions: • T3 & T4 (follicular cells): Increase metabolism and regulate appetite. • Calcitonin (C cells): Lowers blood calcium levels. 6. Know the hormones secreted by the adrenal gland and their specific functions: • Cortex: • Aldosterone: Retains Na⁺, excretes K⁺, raises blood pressure. • Cortisol: Increases glucose, metabolism of fat/protein. • Androgens: Precursor to sex hormones. • Medulla: • Epinephrine/Norepinephrine: Increase heart rate, blood flow, and alertness. 7. Function of glucagon and insulin in maintaining homeostasis: • Insulin (beta cells): Lowers blood glucose. • Glucagon (alpha cells): Raises blood glucose. • Antagonistic: They have opposing effects to balance blood sugar levels. 8. Which cells are involved in spermatogenesis? Where does sperm production occur? • Sertoli (Sustentacular) cells support spermatogenesis. • Leydig (Interstitial) cells produce testosterone. • Occurs in the seminiferous tubules of the testes. 9. Know the hormones secreted by the testes and their functions: • Testosterone: Stimulates male development and sperm production. • Inhibin: Inhibits FSH to regulate sperm production. 10. What causes diabetes insipidus? How is it different from diabetes mellitus? • Diabetes insipidus: ADH deficiency → excessive urination. • Diabetes mellitus: Insulin issues → high blood glucose. 11. Know the 3 “P’s” of diabetes: • Polyuria: Excessive urination. • Polydipsia: Excessive thirst. • Polyphagia: Excessive hunger. 12. How are oxytocin and prolactin different? • Oxytocin: Stimulates uterine contractions and milk letdown. • Prolactin: Stimulates milk production. 13. Name the ovarian hormones and their functions: • Estrogen/Progesterone: Regulate cycle, pregnancy, and secondary sex characteristics. • Inhibin: Inhibits FSH secretion. ⸻ Muscle Physiology 14. Know 3 muscle types, their locations, and function: • Skeletal: Attached to bones; movement; voluntary. • Cardiac: Heart; pumps blood; involuntary. • Smooth: Organs/vessels; propels substances; involuntary. 15. Know the layers surrounding muscle: • Epimysium: Surrounds entire muscle. • Perimysium: Surrounds fascicle (bundle). • Endomysium: Surrounds individual fiber. 16. What is a fascicle? A bundle of muscle fibers. 17. What is a sarcomere? Name its regions: Smallest contractile unit (Z-disc to Z-disc). • Z-band, A-band (dark), I-band (light), H-zone. 18. What are actin and myosin? • Actin: Thin filament. • Myosin: Thick filament that pulls actin during contraction. 19. What is troponin and tropomyosin? • Tropomyosin blocks binding sites on actin. • Troponin binds Ca²⁺ to move tropomyosin and expose sites. 20. What is a motor unit? A motor neuron and all muscle fibers it controls. 21. Role of T-Tubule, SR, Terminal Cisternae: • T-Tubule: Conducts AP into cell. • SR: Stores calcium. • Terminal cisternae: Release calcium. 22. Which neurotransmitter is released at the neuromuscular junction? Acetylcholine (ACh). 23. What role does Ca²⁺ play in muscle physiology? Binds troponin, moves tropomyosin, exposes actin sites. 24. What happens to Ca²⁺ after action potential ends? Reabsorbed into SR by Ca²⁺ ATPase pump. 25. What is the function of ATP in muscle physiology? Powers myosin movement, detachment, and Ca²⁺ reuptake. 26. What is sliding filament theory? Myosin pulls actin filaments → sarcomere shortens → contraction. 27. What are DHP and Ryanodine receptors and their roles? • DHP: Voltage sensor in T-tubule. • Ryanodine: Releases Ca²⁺ from SR. 28. What is the function of AChE? Breaks down ACh to stop stimulation and contraction. 29. Difference between isotonic and isometric contractions: • Isotonic: Muscle changes length (shortens/lengthens). • Isometric: Muscle length stays same; tension builds. ⸻ Respiratory Physiology 30. Difference between conductive and respiratory divisions: • Conductive: Air passageways (nose to bronchioles). • Respiratory: Gas exchange (alveoli). 31. Type I & II alveolar cells and functions: • Type I: Gas exchange. • Type II: Secretes surfactant, repairs alveoli. 32. Dust cells and their functions: Alveolar macrophages that clean up particles/debris. 33. Muscles in relaxed vs. forced respiration: • Relaxed inhale: Diaphragm, external intercostals. • Forced inhale: Accessory neck muscles. • Forced exhale: Internal intercostals, abdominals. 34. What happens to pressure and volume when inhaling/exhaling? • Inhale: Volume ↑, pressure ↓. • Exhale: Volume ↓, pressure ↑. 35. Difference between systemic and pulmonary exchange: • Systemic: Gas exchange at tissues. • Pulmonary: Gas exchange in lungs. 36. What cells are involved in carrying gases? Red blood cells (RBCs). 37. Which enzyme converts CO₂ + H₂O → H₂CO₃? Carbonic anhydrase. 38. What does carbonic acid break into? H⁺ + HCO₃⁻ (bicarbonate ion). 39. What happens in hypoxia (low oxygen)? • ↓O₂, ↑CO₂, ↓pH (acidosis). 40. What happens in hypercapnia (high CO₂)? • ↑CO₂, ↓O₂, ↓pH (acidosis). 41. Receptors for blood pH and their locations: • Central (CSF pH): Medulla oblongata. • Peripheral (O₂, CO₂, pH): Carotid & aortic bodies. 42. CO₂ loading & O₂ unloading at tissues: • CO₂ enters blood → forms HCO₃⁻. • O₂ released to tissues. 43. CO₂ unloading & O₂ loading at alveoli: • CO₂ released from blood to lungs. • O₂ binds to hemoglobin. 44. Brain part for unconscious breathing: Medulla oblongata. 45. Obstructive vs. restrictive disorders + example: • Obstructive: Narrowed airways (asthma). • Restrictive: Reduced lung expansion (fibrosis). 46. Know spirometry volumes (not numbers): • Tidal volume, • Inspiratory/Expiratory reserve volume, • Residual volume, • Vital capacity, • Total lung capacity, • Inspiratory capacity, • Functional residual capacity. 47. Define eupnea, dyspnea, tachypnea, apnea, Kussmaul respiration: • Eupnea: Normal breathing. • Dyspnea: Labored breathing. • Tachypnea: Rapid, shallow breathing. • Apnea: No breathing. • Kussmaul: Deep, rapid (from acidosis Endocrine System 1. What are hormones and what is their function in the body? Hormones are chemical messengers transported in the bloodstream that stimulate physiological responses in target cells or organs. 2. Types of hormones based on chemical composition and how they enter target cells: • Steroid hormones: Lipid-soluble, diffuse through cell membrane (e.g., cortisol). • Protein/Peptide hormones: Water-soluble, bind to surface receptors (e.g., insulin). • Biogenic/Monoamines: Derived from amino acids (e.g., T3/T4), may need carriers or membrane receptors. 3. Know all 6 hormones secreted by the anterior pituitary gland and their functions: • TSH: Stimulates thyroid to release T3 and T4. • ACTH: Stimulates adrenal cortex to release cortisol. • GH: Stimulates tissue growth and protein synthesis. • PRL: Stimulates milk production. • FSH: Stimulates egg maturation/sperm production. • LH: Triggers ovulation and testosterone production. 4. What is thymosin? Which gland secretes it? What is its function? Thymosin is secreted by the thymus and helps in the development and maturation of T-cells. 5. Know thyroid gland hormones, the cells that secrete them, and their functions: • T3 & T4 (follicular cells): Increase metabolism and regulate appetite. • Calcitonin (C cells): Lowers blood calcium levels. 6. Know the hormones secreted by the adrenal gland and their specific functions: • Cortex: • Aldosterone: Retains Na⁺, excretes K⁺, raises blood pressure. • Cortisol: Increases glucose, metabolism of fat/protein. • Androgens: Precursor to sex hormones. • Medulla: • Epinephrine/Norepinephrine: Increase heart rate, blood flow, and alertness. 7. Function of glucagon and insulin in maintaining homeostasis: • Insulin (beta cells): Lowers blood glucose. • Glucagon (alpha cells): Raises blood glucose. • Antagonistic: They have opposing effects to balance blood sugar levels. 8. Which cells are involved in spermatogenesis? Where does sperm production occur? • Sertoli (Sustentacular) cells support spermatogenesis. • Leydig (Interstitial) cells produce testosterone. • Occurs in the seminiferous tubules of the testes. 9. Know the hormones secreted by the testes and their functions: • Testosterone: Stimulates male development and sperm production. • Inhibin: Inhibits FSH to regulate sperm production. 10. What causes diabetes insipidus? How is it different from diabetes mellitus? • Diabetes insipidus: ADH deficiency → excessive urination. • Diabetes mellitus: Insulin issues → high blood glucose. 11. Know the 3 “P’s” of diabetes: • Polyuria: Excessive urination. • Polydipsia: Excessive thirst. • Polyphagia: Excessive hunger. 12. How are oxytocin and prolactin different? • Oxytocin: Stimulates uterine contractions and milk letdown. • Prolactin: Stimulates milk production. 13. Name the ovarian hormones and their functions: • Estrogen/Progesterone: Regulate cycle, pregnancy, and secondary sex characteristics. • Inhibin: Inhibits FSH secretion. ⸻ Muscle Physiology 14. Know 3 muscle types, their locations, and function: • Skeletal: Attached to bones; movement; voluntary. • Cardiac: Heart; pumps blood; involuntary. • Smooth: Organs/vessels; propels substances; involuntary. 15. Know the layers surrounding muscle: • Epimysium: Surrounds entire muscle. • Perimysium: Surrounds fascicle (bundle). • Endomysium: Surrounds individual fiber. 16. What is a fascicle? A bundle of muscle fibers. 17. What is a sarcomere? Name its regions: Smallest contractile unit (Z-disc to Z-disc). • Z-band, A-band (dark), I-band (light), H-zone. 18. What are actin and myosin? • Actin: Thin filament. • Myosin: Thick filament that pulls actin during contraction. 19. What is troponin and tropomyosin? • Tropomyosin blocks binding sites on actin. • Troponin binds Ca²⁺ to move tropomyosin and expose sites. 20. What is a motor unit? A motor neuron and all muscle fibers it controls. 21. Role of T-Tubule, SR, Terminal Cisternae: • T-Tubule: Conducts AP into cell. • SR: Stores calcium. • Terminal cisternae: Release calcium. 22. Which neurotransmitter is released at the neuromuscular junction? Acetylcholine (ACh). 23. What role does Ca²⁺ play in muscle physiology? Binds troponin, moves tropomyosin, exposes actin sites. 24. What happens to Ca²⁺ after action potential ends? Reabsorbed into SR by Ca²⁺ ATPase pump. 25. What is the function of ATP in muscle physiology? Powers myosin movement, detachment, and Ca²⁺ reuptake. 26. What is sliding filament theory? Myosin pulls actin filaments → sarcomere shortens → contraction. 27. What are DHP and Ryanodine receptors and their roles? • DHP: Voltage sensor in T-tubule. • Ryanodine: Releases Ca²⁺ from SR. 28. What is the function of AChE? Breaks down ACh to stop stimulation and contraction. 29. Difference between isotonic and isometric contractions: • Isotonic: Muscle changes length (shortens/lengthens). • Isometric: Muscle length stays same; tension builds. ⸻ Respiratory Physiology 30. Difference between conductive and respiratory divisions: • Conductive: Air passageways (nose to bronchioles). • Respiratory: Gas exchange (alveoli). 31. Type I & II alveolar cells and functions: • Type I: Gas exchange. • Type II: Secretes surfactant, repairs alveoli. 32. Dust cells and their functions: Alveolar macrophages that clean up particles/debris. 33. Muscles in relaxed vs. forced respiration: • Relaxed inhale: Diaphragm, external intercostals. • Forced inhale: Accessory neck muscles. • Forced exhale: Internal intercostals, abdominals. 34. What happens to pressure and volume when inhaling/exhaling? • Inhale: Volume ↑, pressure ↓. • Exhale: Volume ↓, pressure ↑. 35. Difference between systemic and pulmonary exchange: • Systemic: Gas exchange at tissues. • Pulmonary: Gas exchange in lungs. 36. What cells are involved in carrying gases? Red blood cells (RBCs). 37. Which enzyme converts CO₂ + H₂O → H₂CO₃? Carbonic anhydrase. 38. What does carbonic acid break into? H⁺ + HCO₃⁻ (bicarbonate ion). 39. What happens in hypoxia (low oxygen)? • ↓O₂, ↑CO₂, ↓pH (acidosis). 40. What happens in hypercapnia (high CO₂)? • ↑CO₂, ↓O₂, ↓pH (acidosis). 41. Receptors for blood pH and their locations: • Central (CSF pH): Medulla oblongata. • Peripheral (O₂, CO₂, pH): Carotid & aortic bodies. 42. CO₂ loading & O₂ unloading at tissues: • CO₂ enters blood → forms HCO₃⁻. • O₂ released to tissues. 43. CO₂ unloading & O₂ loading at alveoli: • CO₂ released from blood to lungs. • O₂ binds to hemoglobin. 44. Brain part for unconscious breathing: Medulla oblongata. 45. Obstructive vs. restrictive disorders + example: • Obstructive: Narrowed airways (asthma). • Restrictive: Reduced lung expansion (fibrosis). 46. Know spirometry volumes (not numbers): • Tidal volume, • Inspiratory/Expiratory reserve volume, • Residual volume, • Vital capacity, • Total lung capacity, • Inspiratory capacity, • Functional residual capacity. 47. Define eupnea, dyspnea, tachypnea, apnea, Kussmaul respiration: • Eupnea: Normal breathing. • Dyspnea: Labored breathing. • Tachypnea: Rapid, shallow breathing. • Apnea: No breathing. • Kussmaul: Deep, rapid (from acidosis based on chemical composition and how they enter target cells: • Steroid hormones: Lipid-soluble, diffuse through cell membrane (e.g., cortisol). • Protein/Peptide hormones: Water-soluble, bind to surface receptors (e.g., insulin). • Biogenic/Monoamines: Derived from amino acids (e.g., T3/T4), may need carriers or membrane receptors. 3. Know all 6 hormones secreted by the anterior pituitary gland and their functions: • TSH: Stimulates thyroid to release T3 and T4. • ACTH: Stimulates adrenal cortex to release cortisol. • GH: Stimulates tissue growth and protein synthesis. • PRL: Stimulates milk production. • FSH: Stimulates egg maturation/sperm production. • LH: Triggers ovulation and testosterone production. 4. What is thymosin? Which gland secretes it? What is its function? Thymosin is secreted by the thymus and helps in the development and maturation of T-cells. 5. Know thyroid gland hormones, the cells that secrete them, and their functions: • T3 & T4 (follicular cells): Increase metabolism and regulate appetite. • Calcitonin (C cells): Lowers blood calcium levels. 6. Know the hormones secreted by the adrenal gland and their specific functions: • Cortex: • Aldosterone: Retains Na⁺, excretes K⁺, raises blood pressure. • Cortisol: Increases glucose, metabolism of fat/protein. • Androgens: Precursor to sex hormones. • Medulla: • Epinephrine/Norepinephrine: Increase heart rate, blood flow, and alertness. 7. Function of glucagon and insulin in maintaining homeostasis: • Insulin (beta cells): Lowers blood glucose. • Glucagon (alpha cells): Raises blood glucose. • Antagonistic: They have opposing effects to balance blood sugar levels. 8. Which cells are involved in spermatogenesis? Where does sperm production occur? • Sertoli (Sustentacular) cells support spermatogenesis. • Leydig (Interstitial) cells produce testosterone. • Occurs in the seminiferous tubules of the testes. 9. Know the hormones secreted by the testes and their functions: • Testosterone: Stimulates male development and sperm production. • Inhibin: Inhibits FSH to regulate sperm production. 10. What causes diabetes insipidus? How is it different from diabetes mellitus? • Diabetes insipidus: ADH deficiency → excessive urination. • Diabetes mellitus: Insulin issues → high blood glucose. 11. Know the 3 “P’s” of diabetes: • Polyuria: Excessive urination. • Polydipsia: Excessive thirst. • Polyphagia: Excessive hunger. 12. How are oxytocin and prolactin different? • Oxytocin: Stimulates uterine contractions and milk letdown. • Prolactin: Stimulates milk production. 13. Name the ovarian hormones and their functions: • Estrogen/Progesterone: Regulate cycle, pregnancy, and secondary sex characteristics. • Inhibin: Inhibits FSH secretion. ⸻ Muscle Physiology 14. Know 3 muscle types, their locations, and function: • Skeletal: Attached to bones; movement; voluntary. • Cardiac: Heart; pumps blood; involuntary. • Smooth: Organs/vessels; propels substances; involuntary. 15. Know the layers surrounding muscle: • Epimysium: Surrounds entire muscle. • Perimysium: Surrounds fascicle (bundle). • Endomysium: Surrounds individual fiber. 16. What is a fascicle? A bundle of muscle fibers. 17. What is a sarcomere? Name its regions: Smallest contractile unit (Z-disc to Z-disc). • Z-band, A-band (dark), I-band (light), H-zone. 18. What are actin and myosin? • Actin: Thin filament. • Myosin: Thick filament that pulls actin during contraction. 19. What is troponin and tropomyosin? • Tropomyosin blocks binding sites on actin. • Troponin binds Ca²⁺ to move tropomyosin and expose sites. 20. What is a motor unit? A motor neuron and all muscle fibers it controls. 21. Role of T-Tubule, SR, Terminal Cisternae: • T-Tubule: Conducts AP into cell. • SR: Stores calcium. • Terminal cisternae: Release calcium. 22. Which neurotransmitter is released at the neuromuscular junction? Acetylcholine (ACh). 23. What role does Ca²⁺ play in muscle physiology? Binds troponin, moves tropomyosin, exposes actin sites. 24. What happens to Ca²⁺ after action potential ends? Reabsorbed into SR by Ca²⁺ ATPase pump. 25. What is the function of ATP in muscle physiology? Powers myosin movement, detachment, and Ca²⁺ reuptake. 26. What is sliding filament theory? Myosin pulls actin filaments → sarcomere shortens → contraction. 27. What are DHP and Ryanodine receptors and their roles? • DHP: Voltage sensor in T-tubule. • Ryanodine: Releases Ca²⁺ from SR. 28. What is the function of AChE? Breaks down ACh to stop stimulation and contraction. 29. Difference between isotonic and isometric contractions: • Isotonic: Muscle changes length (shortens/lengthens). • Isometric: Muscle length stays same; tension builds. ⸻ Respiratory Physiology 30. Difference between conductive and respiratory divisions: • Conductive: Air passageways (nose to bronchioles). • Respiratory: Gas exchange (alveoli). 31. Type I & II alveolar cells and functions: • Type I: Gas exchange. • Type II: Secretes surfactant, repairs alveoli. 32. Dust cells and their functions: Alveolar macrophages that clean up particles/debris. 33. Muscles in relaxed vs. forced respiration: • Relaxed inhale: Diaphragm, external intercostals. • Forced inhale: Accessory neck muscles. • Forced exhale: Internal intercostals, abdominals. 34. What happens to pressure and volume when inhaling/exhaling? • Inhale: Volume ↑, pressure ↓. • Exhale: Volume ↓, pressure ↑. 35. Difference between systemic and pulmonary exchange: • Systemic: Gas exchange at tissues. • Pulmonary: Gas exchange in lungs. 36. What cells are involved in carrying gases? Red blood cells (RBCs). 37. Which enzyme converts CO₂ + H₂O → H₂CO₃? Carbonic anhydrase. 38. What does carbonic acid break into? H⁺ + HCO₃⁻ (bicarbonate ion). 39. What happens in hypoxia (low oxygen)? • ↓O₂, ↑CO₂, ↓pH (acidosis). 40. What happens in hypercapnia (high CO₂)? • ↑CO₂, ↓O₂, ↓pH (acidosis). 41. Receptors for blood pH and their locations: • Central (CSF pH): Medulla oblongata. • Peripheral (O₂, CO₂, pH): Carotid & aortic bodies. 42. CO₂ loading & O₂ unloading at tissues: • CO₂ enters blood → forms HCO₃⁻. • O₂ released to tissues. 43. CO₂ unloading & O₂ loading at alveoli: • CO₂ released from blood to lungs. • O₂ binds to hemoglobin. 44. Brain part for unconscious breathing: Medulla oblongata. 45. Obstructive vs. restrictive disorders + example: • Obstructive: Narrowed airways (asthma). • Restrictive: Reduced lung expansion (fibrosis). 46. Know spirometry volumes (not numbers): • Tidal volume, • Inspiratory/Expiratory reserve volume, • Residual volume, • Vital capacity, • Total lung capacity, • Inspiratory capacity, • Functional residual capacity. 47. Define eupnea, dyspnea, tachypnea, apnea, Kussmaul respiration: • Eupnea: Normal breathing. • Dyspnea: Labored breathing. • Tachypnea: Rapid, shallow breathing. • Apnea: No breathing

8 Break down of norepinephrine epinephrine

Cardiovascular System - Detailed Summary 1. Functions of the Cardiovascular System • The cardiovascular system is a closed system consisting of the heart and blood vessels. • Main functions: • Transport oxygen, nutrients, hormones, and waste. • Maintain blood pressure and circulation. • Aid in immune function (through WBCs in blood). 2. Anatomy of the Heart • Location: Thoracic cavity, between the lungs, within the mediastinum. • Size: About the size of a fist. • Orientation: • Apex: Points toward the left hip (bottom). • Base: Directed toward the right shoulder (top, where large blood vessels attach). Heart Layers (Inside to Outside) 1. Endocardium – Inner lining of the heart, smooth to prevent clotting. 2. Myocardium – Thick muscular layer responsible for contraction. 3. Epicardium (Visceral Pericardium) – Outer covering of the heart. • Pericardium: A double-walled sac surrounding the heart. • Parietal Pericardium: Outer layer. • Visceral Pericardium: Inner layer (epicardium). • Pericardial Fluid: Lubricates and reduces friction during heartbeats. 3. Chambers of the Heart The heart has four chambers: • Atria (Right & Left): Upper receiving chambers. • Ventricles (Right & Left): Lower pumping chambers. • Right Side of the Heart: Pumps deoxygenated blood to the lungs (Pulmonary Circulation). • Left Side of the Heart: Pumps oxygenated blood to the body (Systemic Circulation). 4. Heart Valves Valves prevent backflow of blood: 1. Atrioventricular (AV) Valves – Between atria and ventricles: • Right AV Valve: Tricuspid Valve • Left AV Valve: Bicuspid (Mitral) Valve 2. Semilunar Valves – Between ventricles and arteries: • Pulmonary Semilunar Valve: Right ventricle → Pulmonary artery • Aortic Semilunar Valve: Left ventricle → Aorta • Chordae Tendineae (“Heart Strings”) anchor AV valves to prevent them from inverting. 5. Blood Flow Through the Heart 1. Deoxygenated Blood Pathway (Blue): • Superior/Inferior Vena Cava → Right Atrium → Tricuspid Valve → Right Ventricle → Pulmonary Semilunar Valve → Pulmonary Artery → Lungs 2. Oxygenated Blood Pathway (Red): • Lungs → Pulmonary Veins → Left Atrium → Bicuspid Valve → Left Ventricle → Aortic Semilunar Valve → Aorta → Body 6. Electrical Conduction System (Intrinsic Conduction System) The heart has automaticity (can contract on its own). • Sinoatrial (SA) Node (“Pacemaker”) – Sets the heart’s rhythm (~75 bpm). • Atrioventricular (AV) Node – Delays impulse so atria can contract first. • AV Bundle (Bundle of His) – Carries signal to ventricles. • Purkinje Fibers – Cause ventricles to contract. Disruptions in this system can cause arrhythmias (irregular heartbeats). 7. Cardiac Cycle (Heartbeat) Each cycle consists of: 1. Atrial Systole – Atria contract, pushing blood into ventricles. 2. Ventricular Systole – Ventricles contract, pumping blood to the lungs/body. 3. Diastole – Heart relaxes and fills with blood. • Heart Sounds: • “Lub” – Closing of AV valves during ventricular contraction. • “Dub” – Closing of semilunar valves during ventricular relaxation. 8. Cardiac Output (CO) • Definition: The amount of blood pumped by each ventricle per minute. • Formula: • CO = Heart Rate (HR) × Stroke Volume (SV) • Average CO = 5.25 L/min Factors affecting CO: • Sympathetic nervous system → Increases HR (exercise, stress) • Parasympathetic nervous system → Decreases HR (rest, sleep) • Hormones (epinephrine, thyroxine) → Increase HR 9. Blood Vessels & Circulation • Arteries: Carry oxygenated blood away from the heart (except pulmonary artery). • Veins: Carry deoxygenated blood to the heart (except pulmonary vein). • Capillaries: Tiny vessels for gas/nutrient exchange. Blood Vessel Structure 1. Tunica Intima – Inner layer, smooth to reduce friction. 2. Tunica Media – Middle layer, made of smooth muscle (controls blood pressure). 3. Tunica Externa – Outer layer for support. 10. Major Circulatory Routes • Pulmonary Circulation: Right ventricle → Lungs → Left atrium. • Systemic Circulation: Left ventricle → Body → Right atrium. Special Circulations: • Hepatic Portal Circulation: Blood from digestive organs goes through the liver before reaching the heart. • Fetal Circulation: Blood bypasses the lungs using special shunts (foramen ovale, ductus arteriosus). 11. Blood Pressure & Disorders • Blood Pressure (BP): The force of blood against vessel walls. • Normal BP: ~ 120/80 mmHg • Hypertension (High BP): >140/90 mmHg – Can damage arteries. • Hypotension (Low BP): <90/60 mmHg – Can cause dizziness or shock. Factors affecting BP: • Cardiac Output (CO) • Blood Volume • Vessel Resistance (narrower arteries = higher BP) 12. Common Cardiovascular Disorders • Hypertension (High Blood Pressure): Can lead to stroke, heart attack. • Atherosclerosis: Hardening of arteries due to plaque buildup. • Myocardial Infarction (Heart Attack): Blockage in coronary artery cuts off oxygen. • Arrhythmia: Irregular heartbeats due to conduction system issues no

Epinephrine (adrenaline)

Primary adrenal insufficiency = problem at level of adrenal glands Causes? Addison’s disease Pathophys? Autoimmune destruction of the adrenal glands Associated with hyperpigmentation POMC is precursor to both ACTH and MSH PAI → lack of negative feedback → high ACTH Lab findings? ACTH high Aldosterone low Destruction of zona glomerulosa Renin high Hypotension → RAAS activation Electrolytes Na+ low, K+ high CBC Eosinophils high Pathophys? Glucocorticoids → eosinophil apoptosis. Lack of glucocorticoids cause eosinophilia. Dx? Cosyntropin testing → no rise in cortisol Adrenal glands aren’t working, so no response to ACTH. Tx? prednisone/hydrocortisone/dexamethasone + fludrocortisone (mineralocorticoid) Stress-dose steroids for surgery, serious illness, etc. Secondary adrenal insufficiency = problem at level of pituitary, reduced ACTH release Causes? MC is prolonged steroid use → ACTH suppression Sheehan’s syndrome (infarction of pituitary) pregnancy Pituitary tumors (ACTH-producing tumor) Lab findings? ACTH low Anterior pituitary is being inhibited Aldosterone normal Zona glomerulosa under control of RAAS system Renin normal Electrolytes Na+ & K+ unaffected (Aldosterone levels are normal) CBC Neutrophilia due to demargination (if pt was recently taking steroids) Dx? Cosyntropin testing → rise in cortisol Adrenal gland is functional Tx? Glucocorticoids Do not need to replace mineralocorticoids since adrenals are functional and aldosterone is under RAAS control Stress-dose steroids for surgery, serious illness, etc. AI with a history of nuchal rigidity and purpuric skin lesions → Waterhouse-Friedrichson syndrome Pathophys? AI 2/2 hemorrhagic infarction of the adrenal glands in the context of Neisseria meningitidis infection Adrenal synthesis enzymes If the enzyme starts with 1 → HTN (high mineralocorticoids) and hypokalemia If the second # is 1 → virilization (high androgens) E.g. 11-beta hydroxylase deficiency → HTN & virilization E.g. 21 hydroxylase deficiency → virilization only E.g. 17-alpha hydroxylase deficiency → HTN only B12 deficiency Where does B12 come from? Animal products VS folic from plants Physiology R factor in saliva binds to B12 and protects it from acidity in the stomach. R factor protector -B12 travels to the duodenum. Parietal cells produce intrinsic factor, which travels to the duodenum. Pancreatic enzymes cleave B12 from R factor and B12 then binds IF. B12-IF complex is reabsorbed in the terminal ileum Reabsorption where? Terminal ileum Causes of B12 deficiency Extreme vegan Pernicious anemia Pancreatic enzyme deficiency Cystic Fibrosis Can’t cleave B12 from R factor Crohn’s Affects terminal ileum Lab markers Homocysteine HIGH MethlyManoicAcid HIGH Presentation? Megaloblastic anemia Subacute combined degeneration (of dorsal columns + lateral corticospinal tract) Peripheral neuropathy Dx of pernicious anemia? anti-IF Ab Folate deficiency Where does folate come from? Leafy things Causes of folate deficiency Poor diet (e.g. alcoholics, elderly) Phenytoin Lab markers Homocysteine HIGH MMA normal Presentation? Megaloblastic anemia Prophylaxis in HIV+ patients CD4 < 200 → PCP TMP-SMX, inhaled pentamidine, dapsone, atovaquone CD4 < 100 → Toxoplasm Treat: TMP-SMX CD4 < 50 → MAC Treat: Azithromycin If live in endemic area, CD4 < 250 → Coccidioides Immitis E.g. Arizona, Nevada, Texas, California Treat: Itraconazole If live in endemic area, CD4 < 150 → Histoplasma Capsulatum E.g. Kentucky, Ohio, Missouri Treat: Itraconazole Diabetes insipidus Dx? Water deprivation test Measure serum osmolality & urine osmolality Deprive pt of water Remeasure serum osmolality & urine osmolality If urine osmolality doesn’t go up → suspect DI Central DI → deficiency of ADH Pathophys? Supraoptic nucleus not making enough ADH Dx? Give desmopressin → urine osmolality increases significantly Nephrogenic DI → kidneys are not responding to ADH Dx? Give desmopressin → urine osmolality doesn’t change much Tx? Hydrochlorothiazide Unless 2/2 lithium, use amiloride or triametere Causes? Lithium SSRIs Carbamazepine Demeclocycline Tx of normovolemic hypernatremia? D5W to correct free water deficit Divine says NS, but most other resources I found said correct free water deficit Tx of hypovolemic hypernatremia? Give NS first until normal volume, then give D5W Consequence of correcting hypernatremia too rapidly? Cerebral edema Osteoarthritis Presentation? Old person with joint pain that gets worse throughout the day Risk Factr? Obesity vs decreases osteoporosis Imaging findings? Joint space narrowing Subchondral sclerosis Subchondral cysts Osteophytes Arthrocentesis findings? <2000 cells Tx? 1st line acetaminophen 2nd line NSAID (e.g. naproxen) 3rd line joint replacement surgery Returned from a business conference 1 week ago + Fever + Nonproductive cough + Abdominal pain + Hyponatremia → Legionella Dx? Urine antigen Tx? FQ or macrolide MaCroLide mnemonic = Mycoplasma, Chlamydia, Legionella What are the common causes of atypical PNA? Mycoplasma, Legionella, Chlamydia MC cause? Mycoplasma CXR findings? Interstitial infiltrates HY associations C. Psittaci → birds C. Burnetii → cows, goats, sheet Mycoplasma → college student w/ walking pneumonia Midsystolic click heard best at the apex. → mitral valve prolapse “Stenosnap & Proclick” Risk Factor? Connective tissue disease Marfarn Ehlers-Danlos ADPKD bilateral renal masses Classic demographic? Young woman psychiatric Pathophys? Myxomatous degeneration MVP vs aortic dissection: cystic medial necrosis Exam maneuvers Anything that increase amount of blood in LV → murmur softer Increase preload Increase afterload Anything that decreases amount of blood in LV → murmur louder Dx? Echo Scaly, itchy skin with yellowish crusting in the winter. → seborrheic dermatitis Tx? Topical antifungals e.g. ketoconazole or selenium sulfide shampoo Classic disease distribution? Hair → e.g. cradle cap Eyebrows Episodic/intermittent HTN + HA → pheochromocytoma Genetic disease associations MEN2A MEN2B VHL in brain (hemangioma) NF-1 growth in skin Pathophys? Catecholamine-secreting tumor Location? Adrenal medulla Posterior mediastinum Organ of Zuckerkandl (chromaffin cells along the aorta) Dx? 1st step: urine metanephrines If elevated → CT abdomen If nothing found on CT → MIBG scan Tx? Alpha blocker (e.g. phenoxybenzamine, phenotaline) THEN beta blocker Most common cause of a Lower GI Bleed in the elderly → diverticulosis Dx? Colonoscopy or barium enema Recall that you acutely do a CT scan for diverticulitis, then 6 weeks later colonoscopy to r/o cancer Ppx? Eat fiber Megaloblastic anemias Blood smear findings? Hypersegmented neutrophils MCV > 100 Classic patient demographic with folate deficiency? Alcoholics Elderly person with poor nutrition Folate synthesis inhibitors Pt with molar pregnancy → methotrexate Pulmonary issue? Pulmonary fibrosis HIV+ pt with ring-enhancing lesions → pyrimethamine-sulfadiazine Pyrimethamine inhibits DHFR AIDS pt on ppx for toxo → TMP-SMX TMP inhibits DHFR Use of leucovorin? Rescue bone marrow in setting of methotrexate toxicity Mechanism? Folinic acid analog CMV presentations Esophagitis → linear ulcers Colitis → post-transplant pt Retinitis → HIV pt with CD4 < 50 Congenital CMV → periventricular calcifications + hearing loss calcifications elsewhere → toxo Histology? Owl’s eye intranuclear inclusions Tx? Gancicyclovir Resistance? UL97 kinase mutation Tx for resistance? foscarnet CD4 < 200 + severe peripheral edema + frothy urine. → FSGS in HIV pt Variant classic in HIV+ pts? Collapsing variant Tx? Steroids + cyclophosphamide + ACE-I Indinavir AE? Kidney stones triad of fever, rash, and eosinophiluria → acute interstitial nephritis Drugs cause? Penicillins Tx? Stop the drug! Can add steroids if severe Vitamin D metabolism Liver converts Vit D to calcidiol (25OH-Vit D). Calcidiol goes to kidney. Alpha-1 hydroxylase converts calcidiol to calcitriol (1,25-OH Vit D). Common causes of Vitamin D deficiency CKD → 1-alpha hydroxyalse deficiency Liver disease → can’t make calcidiol CF → malabsorption Crohn’s → malabsorption Osteomalacia vs Rickets Osteomalacia in adults Rickets in kids Tx? Calcium + vit D Lab findings? Ca++ low Phos low Low in liver disease High in kidney disease (kidneys can’t get rid of phos) PTH high (2ary hyperpara) vs liver dx PTH low Alk phos Aspiration pneumonia Risk Factor? Alcoholism Dementia Neuromuscular problems (e.g. MG, ALS) Bugs? Anaerobes foul smelling Bacteroides FUsobacterium Peptostreptococcus Klebsiella → currant jelly sputum alcoholic Tx? Clindamycin CURB-65 criteria Purpose? Who to admit Cutoff? 2+ → hospitalize C = confusion U = uremia (BUN > 20) R = RR > 30 B = BP < 90/60 Age > 65 Drugs commonly used in PNA treatment Ceftriaxone Levofloxacin fluoroquinolone Macrolides - great for atypical PNA Pharmacological management of pulmonary arterial HTN Endothelin antagonists Bosentan ambrisentan PDE-5 inhibitors Sildenafil Tadalafil Prostacyclin analogs Iloprost Epoprostenol Treprostinil Causes? Young female → idiopathic PAH Mutation? BMPR2 55 yo F presents with a 5 week history of a rash on her forehead. PE reveals scaly macules with a sandpaper texture. → actinic keratosis Risk Factor? Sun exposure Tx? Topical 5-FU Possible dangerous sequelae? Squamous cell carcinoma Most likely disease sequelae? Resolution 1ary hyperparathyroidism 2ary hyperparathyroidism 3ary hyperparathyroidism Autonomous PTH production Causes? Adenoma Parathyroid hyperplasia PTH high Ca++ high Phos low Low Ca++ → PTH production Causes? CKD PTH high Ca++ low Phos high PTH production despite normalized of Ca++ levels Causes? CKD s/p transplant PTH high Ca++ high Phos low Tx? Parathyroidectomy (remove 3.5 glands) Cinacalcet (CSR modulator) Hypercalcemia Presentation? bones, stones, groans, psychic overtones Tx? 1st step: Normal Saline Hypercalcemia of malignancy → bisphosphonates EKG finding? Shortened QT Periumbilical pain that migrates to the right lower quadrant. → appendicitis PE findings? McBurney’s point tenderness Psoas sign (flex hip pain) Obturator sign (pain with internal rotation of hip) Rovsing’s sign (palpation of LLQ → pain in RLQ) Dx? CT scan Pregnant → US Kid → US Tx? Surgery Classic drug and viral causes of aplastic anemia. Drugs? Carbamazepine Chloramphenicol Viral? Parvovirus B19 (single stranded DNA virus) Fanconi anemia Pathophys? Problems with DNA repair Fanconi anemia vs Fanconi syndrome Fanconi anemia → cytopenias + thumb anomalies + short stature + cafe-au-lait spots Fanconi syndrome → type 2 RTA (proximal) CD4 count of 94 + MRI revealing ring enhancing lesions in the cortex → toxoplasmosis Tx? Pyrimethamine-sulfadiazine Rescue agent for pt who becomes leukopenic with treatment? leucovorin Who should get steroids? Increased ICP For PCP pneumonia: O2 sat < 92 PaO2 < 70 A-a gradient > 35 Ppx? TMP-SMX for CD4 < 100 Congenital toxo Hydrocephalus Chorioretinitis Intracranial calcifications Classic methods of transmission? handling cat litter Lupus nephritis Associated autoantibody? anti-dsDNA Classic “immunologic” description? “Full house” pattern Tx? Steroids + cyclophosphamide Osteoporosis Screening population? women > 65 Screening modality? DEXA scan Dx? T-score < -2.5 Risk Factor? Postmenopauseal Low BMI Smoking Alcohol Preventive strategies? Weight bearing exercise Smoking cessation Reduce alcohol consumption Tx? 1st line: bisphosphonates + Ca/Vit D supplementation Raloxifene (SERM) Agonist in bone Blocker Antagonist in breast Classic locations of osteoporotic fractures Vertebral compression fracture Hip fracture Name the PNA Red currant jelly sputum. → Klebsiella Rust colored sputum. → Strep pneumo PNA in an alcoholic. → Klebsiella Post viral PNA with a cavitary CXR lesion. → Staph aureus PNA in a patient that has chronically been on a ventilator. → Pseudomonas MC cause of Community Acquired Pneumonia. → Strep pneumo Pharmacological management of MRSA. Vancomycin Clindamycin Linezolid Ceftaroline (5th gen cephalosporin) Tigecycline, tertracycline Pharmacological management of Pseudomonas. Ceftazidime (only 3rd gen cephalosporin) Cefepime (4th gen cephalosporin) Pip-tazo Fluoroquinolones Carbapenems Aztreonam Aminoglycosides JVD and exercise intolerance in a patient with a recent history of an URI. → dilated cardiomyopathy 2/2 viral myocarditis MC cause? Coxsackie B VS Coxsackie A: Hand foot mouth dx Drug causes myocarditis Clozapine Anthracyclines Prevention? Dexrazoxane (iron chelator) Trastuzumab reversible tx for breast cancer Classic cause in a patient with recent history of travel to S. America? Chagas T. Cruzi Potential sequelae? Achalasia Dilated cardiomyopathy Megacolon (2/2 degeneration of myenteric plexus) Massive skin sloughing (45% BSA) in a patient that was recently started on a gout medication? TEN Dx? <10% BSA → SJS >30% BSA → TEN Tx? STOP the drug IVF Topical abx to prevention infection Tetany and a prolonged QT interval in a patient with recent surgical treatment of follicular thyroid carcinoma. → hypocalcemia due to removal of parathyroids Recurrent viral infections + QT prolongation + tetany → DiGeorge syndrome Pathophys? Failure of development of 3rd/4th pharyngeal pouches Trousseau and Chvostek signs. Trousseau → inflation of BP cuff causes carpopedal spasm Chvostek → taping on cheek causes facial muscle spasm Hypocalcemia that is refractory to repletion → consider hypomagnesemia Electrolyte/drug causes of prolonged QT intervals Electrolytes? Hypocalcemia Hypomagnesemia Hypokalemia Drugs? Macrolides FloroQunlones Haloperidol Ondensatron Methadone Hypoalbuminemia and Ca balance Hypoalbumenia → decrease in total body Ca++, no change in ionized Ca++ Drop of 1 in albumin → add 0.8 to Ca++ Abdominal pain radiating to the back → acute pancreatitis Causes? #1 = Gallstones #2 = Alcohol Hypertriglyceridemia Hypercalcemia Scorpion sting Handlebar injuries Lab markers? Lipase - most sensitive Amylase Physical exam signs in pancreatitis. Cullen’s sign = periumbilical ecchymosis Grey Turner sign = flank ecchymosis Tx? NPO + IVF + pain control Meperidine is a good agent because it doesn’t cause sphincter of Oddi spasms Management of gallstone pancreatitis Dx? US then ERCP Tx? DELAYED cholecystectomy What if the patient becomes severely hypoxic with a CXR revealing a “white out” lung? ARDS noncardiogenic pulm edema PCWP? <18 mmHg NORMAL 20 yo M with red urine in the morning + hepatic vein thrombosis + CBC findings of hemolytic anemia. → paroxysmal nocturnal hemoglobinuria Pathophys? Defect in GPI anchors, which attach CD55 and CD59 to cell (they prevent complement from destroying RBC) Sleep → hypoventilation → mild respiratory acidosis → activation of complement cascade Gene mutation? PIGA Dx? Flow cytometry Tx? Eculizumab (terminal complement inhibitor) Vaccine required? pnemococal Neisseria meningitidis Chronic diarrhea and malabsorption in a HIV+ patient + detection of acid fast oocysts in stool. → cryptosporidium parvum Acid-fast organisms Cryptosporidium TB MAC Nocardia Dx? Stool O&P Tx? Nitazoxanide Route of transmission? Contaminated water Muddy brown casts on urinalysis in a patient with recent CT contrast administration (or Gentamicin administration for a life threatening gram -ve infection) → Acute Tubular Necrosis Woman with morning joint stiffness > 1 hr → Rhematoid Arthritis. Antibodies? Rheum Factor (IgM against IgG) anti-CCP - more specific HLA? DR4 Pathophys? IgM constant region activates complement → inflammation → formation of pannus (hypertrophied synovium) → damage to cartilage and bone Caplan syndrome = RA + pneumoconiosis Felty syndrome = RA + neutropenia + splenomegaly (“RANS”) Classic hand/finger findings/distribution? MCP & PIP joints of hands (DIP joints spared) Imaging findings? Symmetric joint space narrowing Tx? Methotrexate (DMARDs) If no response → TNF alpha inhibitor (e.g. infliximab) Required testing prior to starting methotrexate? PFTs Required testing prior to starting infliximab? TB Hep B/Hep C Differentiating Strep pharyngitis from Infectious Mononucleosis LND distribution Anterior cervical → Strep Posterior cervical → Mono Disease onset Acute → Strep Over weeks → Mono Organ involvement Splenomegaly → Mono Pt with sore throat takes amoxicillin and gets rash → mono NOT allergic rxn! CENTOR criteria C = absence of Cough E = tonsillar Exudates N = nodes/anterior cervical lymphadenopathy T = temp (fever) OR <15 → +1 >=45 → -1 Using CENTOR score 0/1 → don’t test, don’t treat 2/3 → rapid antigen test Positive → treat Negative → throat culture 4/5 → treat empirically Tx of Strep pharyngitis? Amoxillcin If PCN allergic → azithromycin Potential sequelae of Strep pharyngitis RF - preventable with abx PSGN Endocarditis MC cause of endocarditis? IVDU Bug? Staph aureus Valve? tricuspid Prosthetic valve endocarditis Bug? Staph epidermidis Endocarditis after dental procedure? Viridans group streptococci Strep viridans, Strep mitis, Strep mutans, Strep sanguineous Patient with malar rash and echo showing vegetations on both sides of the mitral valve → Libman-Sacks endocarditis Presentation? Fever + night sweats + new murmur Splinter hemorrhages Roth spots (retinal hemorrhages) Painless Janeway lesions + painful Osler nodes (immune phenomenon) Dx? 1st step: blood cultures TEE Tx? Abx that include Staph aureus coverage (e.g. vancomycin) for WEEKS Bugs implicated in culture negative endocarditis HACEK H = haemophilus A = actinobacillus C = cardiobacterium E = eikenella K = kingella Coxiella burnetii Blood cultures in a patient with endocarditis reveal S. Bovis (or S. Gallolyticus bacteremia). NBS? Colonoscopy Who needs antibiotic prophylaxis? Hx endocarditis Prosthetic valve Unrepaired cyanotic congenital dz Heart transplant with valve dysfunction Erythematous salmon colored patch with silvery scale on the elbows and knees. → psoriasis Tx? Topical steroids If this patient presents with joint pain (especially in the fingers)? Psoriatic arthritis Imaging? Pencil-and-cup deformity Tx? NSAIDs T of 104 + tachycardia + new onset Afib in a patient with a history of Graves disease. → thyroid storm Lab findings? TSH low T3/T4 high Tx? 1st step: propranolol 2nd step: PTU Then: Prednisone Potassium iodide (Lugul’s solution) Wolff-Chaikoff effect → large amounts of iodine inhibit thyroid hormone synthesis Biopsy revealing tennis racket shaped structures in cells of immune origin. → Langerhans cell histiocytosis Electron microscopy? Birbeck granules (tennis rackets) Marker? S100 Small bowel obstruction in a HIV patient with purple macules on the face, arms, and lower extremities. → Kaposi’s sarcoma Bug? HHV8 Tx? HAART Pathophys of vascular lesions? Overexpression of VEGF Fever + rash + eosinophiluria 10 days after a patient started an antistaphylococcal penicillin. → acute interstitial nephritis Tx? STOP drug + steroids SLE SOAP BRAIN MD S = serositis O = oral ulcers A = arthritis P = photosensitivity B = blood disorders (cytopenias) R = renal A = ANA/anti-dsDNA I = immunologic N = neurologic findings M = malar rash D = discoid rash Type 2 vs 3 HSRs in lupus Type 2 → cytopenias Type 3 → all other manifestations Lupus Ab? ANA anti-dsDNA anti-Smith Lupus nephritis → full house pattern on IF Antiphospholipid antibody syndrome → recurrent pregnancy losses Pathophys? Thrombosis of the uteroplacental arteries. MC cause of death in lupus patients? What I’ve read recently: CV disease Per Divine: Treated → infection Untreated → renal dz Also 40x risk MI Endocarditis in lupus pt? Libman-Sacks endocarditis Neonatal 3rd degree heart block → neonatal lupus Maternal autoimmune dz? Sjogren’s SLE Ab? anti-SSA/anti-Ro anti-SSB/anti-La Tx? Steroids Cyclophosphamide Hydroxychloroquine → good for skin lesions Pulmonary abscesses Bugs? Staph Anaerobes Klebsiella RF? Alcoholism Elderly Post-viral pneumonia MC location of aspiration pneumonia? Superior segment of RLL Chest pain worsened by deep inspiration and relieved by sitting up in a patient with a recent MI or elevated creatinine or URI or RA/SLE. → pericarditis EKG findings? Diffuse ST elevations + PR depression PE finding? Friction rub (“scratchy sound on auscultation”) A few days after MI → fibrinous pericarditis Weeks after MI → Dressler’s Tx? NSAIDS Consider adding on colchicine Cardiac tamponade Beck’s triad = hypotension + JVD + muffled heart sounds EKG findings? Electrical alternans Type of shock? Obstructive cardiogenic (Amboss) CO low SVR high PCWP high Tx? Pericardiocentesis or pericardial Pearly lesion with telangiectasias on the ear in a farmer. → Basal Cell Carcinoma MC type skin cancer Location? Upper lip Dx? Biopsy Tx? Mohs surgery Cold intolerance in a 35 yo white F → hypothyroidism MC cause? Hashimoto’s Histology? lymphoid follicles w/ active germinal centers Lab findings? TSH high T3/T4 low Ab? anti-TPO Anti-thyroglobulin HLA? DR3/DR5 Tx? Levothyroxine Future complication? thyroid lymphoma Massive hematemesis in a patient with a history of chronic liver disease. → ruptured varices Pathophys? L gastric vein has anastomosis with azygos veins. Increased portal pressure → backward flow from L gastric veins to azygous vein (which empties into SVC). Acute tx? IVF + octreotide + ceftriaxone/cipro + EGD w/ ligation/banding Do NOT give a beta blocker for acute tx Prophalaxsis? Beta blocker + spironolactone Other manifestations of elevated portal pressures Caput medusa Internal hemorrhoids Tx for cirrhotic coagulopathies? FFP If uremia → give desmopressin Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH Hemophilia A Pathophys? deficiency of factor 8 Inheritance? XLR Coag labs? Bleeding time normal PTT HIGH b/c clotting problem PT normal Hemophilia B Pathophys? deficiency of factor 9 Inheritance? XLR Coag labs? Bleeding time normal PTT HIGH PT normal Hemophilia C Pathophys? deficiency of factor 11 Inheritance? AR Coag labs? Bleeding time normal PTT HIGH PT normal Bernard Soulier Syndrome Pathophys? Deficiency of GpIb Coag labs? Bleeding time HIGH PTT normal PT normal Glanzmann Thrombasthenia Pathophys? Deficiency of GpIIbIIIa Coag labs? Bleeding time HIGH PTT normal PT normal Von Willebrand’s disease Pathophys? Deficiency of vWF Inheritance? AD Coag labs? Bleeding time HIGH PTT HIGH vWF is a protecting group for factor 8 PT normal ITP Pathophys? Ab against GpIIbIIIa Classic pt? Pt with SLE Tx? Observation Steroids IVIG Splenectomy TTP Pathophys? Deficiency in ADAMTS13 enzyme → cannot cleave vWF multimers → activation of platelets → thrombosis → thrombocytopenia Presentation? microangiopathic hemolytic anemia + thrombocytopenia + renal failure + fever + neurologic problems Tx? Plasma exchange transfusion****** HUS Bugs? Shigella or E. coli O157:H7 Presentation? Fever+ microangiopathic hemolytic anemia + thrombocytopenia + renal failure + neurologic Platelet deficiency vs coagulation factor bleeds Platelet deficiency → mucosal bleeds, petechiae, heavy menses Coag factor deficiency bleeds → hemarthrosis Why do patients with CKD develop coagulopathy? Uremia → platelet dysfunction Tx? Desmopressin Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH Exercising caution with transfusion in patients with Bernard Soulier syndrome Do NOT give transfusion that includes platelets They can have an anaphylactic rxn to GpIb (since they don’t have GpIb) Oropharyngeal candidiasis. RF? HIV Chronic ICS use TNF inhibitor Micro finding? Germ tubes at 37 C Tx oral candidiasis? Nystatin swish-and-swallow Tx invasive candidiasis? Amphotericin B Prevention of Amphotericin B toxicity? Liposomal formulation Pleural effusions Light’s criteria (must meet all 3 to be considered transudative!) LDH < 2/3 ULN LOW Pleural LDH/serum LDH < 0.6 LOW Pleural protein/serum protein < 0.5 LOW Causes of transudative effusion CHF Cirrhosis Nephrotic syndrome Note: Per UW 2021: Mechanism of transudate effusion? Decreased pulmonary artery oncotic pressure, e.g. hypoalbuminemia in nephrotic syndrome Increased pulmonary capillary hydrostatic pressure, e.g. volume overload in heart failure Causes of exudative effusion Malignancy Cancer Parapneumonic effusion Tb Note: Per UW 2021: Mechanism of exudate effusion? Inflammatory increased in vascular permeability of membrane (increased flow of interstitial edema into pleural space) Unique cause of both transudative & exudative effusions? PE Classic Pleural Effusion findings? Decreased breath sounds Dullness to percussion Decreased tactile fremitus Tx? Chest tube Chylothorax = lymph in the pleural space Pathophys? Obstruction of thoracic duct or injury to the thoracic duct Pleural fluid findings? High Triglycerides Holosystolic murmur heard best at the apex with radiation to the axilla in a patient with a recent MI. → mitral regurg 2/2 papillary muscle rupture Dx? Echo Why widely split S2? Aortic valve is closing earlier (LV is emptying into both aorta & LA) Maneuvers that increase intensity Increase preload (putting more blood in that can be regurgitated) Increase afterload Decubitus ulcers RF? Elderly Paraplegic Fecal/urinary incontinence Poor nutrition Staging Stage 1 = non-blanchable erythema Tx? Repositioning q2hrs Stage 2 = loss of epidermis + partial loss of dermis Tx? Occlusive dressing superficial Stage 3 = involves entire dermis, extending to subQ fat Does NOT extend past fascia Tx? Surgical debridement Stage 4 = muscle/tendon/bose exposed Tx? Surgical debridement General tx strategies? Repositioning + good nutritional support Marjolin’s ulcer = non-healing wound that is actually squamous cell carcinoma T1DM Pathophys? Autoimmune destruction of pancreas Ab? anti-GAD 65 (glutamic acid decarboxylase) anti-IA2 (islet tyrosine phosphatase 2) Islet cell autoantibodies Insulin autoantibodies Dx? A1c > 6.5% (twice) Fasting BG >= 126 (twice) Oral glucose tolerance test >= 200 (twice) Sxs of DM + random glucose > 200 Tx? Long-acting insulin + mealtime insulin Long-acting Glargine Detemir Rapid-acting Lispro Aspart Glulisine 3 HY complications Nephropathy Retinopathy & cataracts Neuropathy Chronic DM care A1c q3 months Foot exam annually Eye exam annually Microalbumin:Cr ratio annually Nephroprotection in DM? ACE-I GI bleed algorithm 1st step: ABCs + 2 large-bore IVs + IVFs 2nd step: NG lavage Clear fluid → go deeper Blood → UGIB → upper endoscopy Bilious fluid → have ruled out UGIB → proceed to colonoscopy See source → intervene as needed See nothing → CT angiography for large bleed Tagged RBC scan for smaller bleed Antiplatelet Pharmacology Aspirin Mechanism? Irreversibly inhibits COX-1 and COX-2 Clopidogrel/ticlopidine = P2Y12 (ADP receptor) blockers Mechanism? Inhibit platelet activation Abciximab/eptifibatide/tirofiban = GpIIbIIIa receptor blockers Mechanism? Inhibit platelet aggregation Ristocetin cofactor assay Issues with adhesion step → abnormal result Abnormal ristocetin cofactor assays: Von Willebrand disease Bernard Soulier disease Normal ristocetin cofactor assay: Glanzmann Thrombasthenia Von Willebrand disease effects on PTT? Increased Pathophys? vWF is a protecting group for Factor 8. Treatment of VWD? Desmopressin Mechanism? Increases release of vWF from Weibel-Palade bodies of endothelial cells Note: Desmopressin = ADH analog → so, it can cause AE of hyponatremia 2/2 SIADH HSV1 vs HSV2. Oral herpes → HSV1 Genital herpes → HSV2 Dx? PCR (most up-to-date) Tzanck smear (outdated, not very sensitive, nonspecific) → intranuclear inclusions Brain area affected by HSV encephalitis? Temporal lobes CSF findings in HSV encephalitis? RBCs******* Tx herpes encephalitis? Acyclovir AE? Crystal nephropathy Can’t see, can’t pee, can’t climb a tree. → reactive arthritis HLA? B27 Classic bug? Chlamydia Tx? steroids Need abx? Only if ongoing infection Can’t see, can’t pee, can’t hear a bee → Alport syndrome Inheritance? X-linked dominant Tx of NG & CT NG → treat empirically for both → ceftriaxone + azithro/doxy CT → azithro/doxy Hypovolemic Septic Neurogenic Cardiogenic CO low PCWP low SVR high*** CO high PCWP normal SVR low Tx? norepi CO low SVR low CO low PCWP high*** SVR high*** Tx anaphylactic shock? epinephrine Melanomas ABCDE A = asymmetry B = irregular borders C = color variation D = diameter > 6 mm E = evolving Dx? Full-thickness biopsy Excisional for small lesions Punch for larger lesions Most important prognostic factor → Breslow depth DM pharmacology Lactic acidosis → metformin Decreases hepatic gluconeogenesis → metformin Hold before CT w/ contrast → metformin Weight gain → sulfonylureas & TZDs (-glitizones) Diarrhea → acarbose & migliton Inhibits disaccharidases (can’t reabsorb disaccharides) Recurrent UTIs → SGLT-2 inhibitors Weight loss → GLP-1 agonists (e.g. liraglutide, exenatide) & DPP4 inhibitors (-gliptins) Contraindicated in pt with HF → TZDs PPAR-gamma receptor found in kidney → water retention Contraindication in pt with MTC → GLP-1 agonists Biggest risk of hypoglycemia? Sulfonylureas RF esophageal adenocarcinoma Barrett’s esophagus RF esophageal squamous cell carcinoma Smoking Drinking Achalasia Location esophageal adenocarcinoma? Lower 1/3 Location esophageal squamous cell carcinoma? Upper 2/3 MC US? Adenocarcinoma MC worldwide? Squamous cell carcinoma Presentation? Dysphagia to solids → dysphagia to liquids Dx? EGD Staging? CT scan or esophageal US Factor V Leiden Pathophys? Resistance to protein C Dx? Activated Protein C resistance assay Patient needs super large doses of heparin to record any changes in PTT → AT-III deficiency Recall that heparin is a AT-III activator 35 yo with a hypercoagulable disorder that does not correct with mixing studies. → antiphospholipid antibody disorder Anaphylaxis in a patient with a long history of Hemophilia A → Ab against factor 8 that cause type 1 HSR with transfusion Hx of hemophilia, diagnosed 5 years ago. Before you would give them factor 8 concentrate and PTT would normalize. Now they’re requirizing larger doses of factor 8 to normalize PTT. → inhibitor formation (antibodies against clotting factors) Skin necrosis with Warfarin → protein C/S deficiency Prothrombin G20210 mutation → overproduction of factor II Rash in dermatomal distribution → VZV infection Contraindications to VZV vaccination? Pregnant woman Kid < 1 year Severe immunosuppression (e.g. HIV with CD4 < 200) Tx? Acyclovir If resistant, foscarnet Tzanck smear findings? Intranuclear inclusions Shingles vaccination guidelines? Adults over 60 #1 cause of ESRD in the US → DM nephropathy Histology? Kimmelsteil-Wilson nodules #2 cause of ESRD in the US → hypertensive nephropathy Pt with BP 240/150. How fast should you lower BP? 25% in first 24 hrs Drugs for hypertensive emergencies? Nicardipine Clevidipine Nitroprusside AE? Cyanide poisoning Tx? Amyl nitrate + thiosulfate OR hydroxocobalamin Labelol Renal protective medications in patients with DKD or hypertensive nephropathy? ACE-I Anemia + Cranial Nerve deficits + Thick bones + Carbonic Anhydrase 2 deficiency + Increased TRAP + Increased Alkaline Phosphatase. → osteopetrosis Pathophys? Carbonic anhydrase is defective → osteoclasts cannot produce acid to resorb bone Tx? IFN-gamma Osteoclasts are a specialized macrophage IFN-gamma is an activator of macrophages Clinical diagnostic criteria for Chronic Bronchitis Diagnostic criteria? 2 years 3 months/year of chronic cough PFT findings FEV1 low FEV1/FVC ratio low RV high TLC high Which PFT market can differentiate CB from emphysema? DLCO DLCO normal → CB DLCO low → emphysema ****** Tx acute exacerbation? Abx + bronchodilators + corticosteroids (“ABCs”) Prevention? Stop smoking! Afib #1 RF? Mitral stenosis #1 RF MS? Rheumatic fever #1 RF CAD and AAA: smoking #1 RF stroke and aortic dissection: HTN MC arrhythmia in hyperthyroidism → Afib MC site of ectopic foci in Afib → pulmonary veins EKG findings? “Irregularly irregular” + no P waves Location of emboli formation? LA appendage Who should be cardioverted back to sinus rhythm? New onset (<48 hrs) Afib Anticoagulated for 3 weeks + TEE negative for clot Afib that’s refractory to medical therapy Afib & HDUS Q on T phenomenon? Depolarization during T wave (repolarization) can cause QT prolongation → Torsades → death Prevention? SYNCHRONIZED cardioversion Tx? Rate control Beta blockers ND-CCB (e.g. verapamil, diltiazem) Rhythmic control Amiodarone Reducing stroke risk in Afib? Anticoagulation for CHA2DS2VASc score >= 2 Anticoagulation options Valvular cause (e.g. MS) → warfarin Any other cause → warfarin or NOAC (apixiban) Reversal of AC Warfarin → Vit K, four-factor PCC Heparin → protamine sulfate Dabigatran → idarucizumab Crusty, scaly, ulcerating lesion with heaped up borders → squamous cell carcinoma Classic location? Below Lower lip Precursor lesion? Actinic keratosis What if it arises in a scar or chronic wound? Marjolin ulcer Hypothermia + hypercapnia + non pitting edema + hyponatremia + HR of 35 + hypotension in a patient with a history of papillary thyroid cancer → myxedema coma Tx? Levothyroxine + steroids Lab findings? TSH high T3/T4 low LDL high Acute onset “dermatologic” breakout in a patient with a recent history of weight loss and epigastric pain. → Leser–Trélat sign associated with visceral malignancy pancreatic cancer Lymph node associations Supraclavicular → Virchow’s node Periumbilical → Sister Mary Joseph What are mets to the ovaries called? Kruckenberg tumor Classic bug associated with gastric cancer? H. pylori (MALToma) Classic histological finding in the diffuse type of gastric cancer? Signet ring cells RBCs without central pallor + elevated MCHC + anemia. → hereditary spherocytosis Inheritance? AD Pathophys? Deficiency of spectrin, ankyrin, or band 3.2 Intravascular or extravascular hemolysis? Extravascular (RBCs bound by IgG, attacked by splenic macrophages) Dx? Osmotic fragility test Eosin-5-maleimide Acidified glycerol lysis test Tx? Splenectomy Post-splenectomy preventative care? Strep pneumo Hinflue vaccine Neisseria Septic shock Hemodynamic parameters CO high SVR low PCWP normal MvO2 high Tx? IVF + norepi + broad-spectrum abx (cover MRSA + Pseudomonas) E.g. vanc + pip-tazo E.g

Chapter 15: Epinephrine & Atenolol (copy)

Chapter 15: Epinephrine & Atenolol

Ch 35 Endocrine Key Points • The principal endocrine glands include the pituitary, thyroid, parathyroid, adrenal, pineal, thymus. • The endocrine system alters chemical reactions and controls the rate at which chemical activities take place within cells. • Any type of dysfunction of the pituitary gland will affect one or more of the hormones and their target organs. • The thyroid gland secretes the hormones thyroxine (T4), triiodothyronine (T3), and thyrocalcitonin. • Parathormone is a hormone produced and secreted by the parathyroid glands that acts on the renal tubules to increase the excretion of phosphorus in the urine and to stimulate the reabsorption of calcium; it also stimulates the production of the active form of vitamin D, which enhances calcium absorption in the small intestine and acts on bone, causing the release of calcium from the bone into the bloodstream. • The adrenal medulla (middle portion) secretes two hormones—epinephrine and norepinephrine (called catecholamines)—in response to stimulation from the sympathetic nervous system. • T he two major types of hormones secreted by the adrenal cortex are the mineralocorticoids (aldosterone) and the glucocorticoids (cortisol). • The beta cells are responsible for producing and secreting insulin, while the alpha cells release glucagon. • Age-related changes in the endocrine system include the pituitary gland becoming smaller, the thyroid becoming more lumpy or nodular, increases and decreases in different hormones, and increases in blood glucose levels. • The endocrine system regulates metabolism, growth and development, sexual function, reproductive processes. • The secretion of a particular hormone normally depends on the need. • Endocrine disorders are caused by an imbalance in the production of hormone or by an alteration in the body’s ability to use the hormones produced. • Goiter, an overgrowth of the thyroid, may be prevented by sufficient intake of iodine. • Tests of the endocrine system are performed on blood samples; on urine samples; or by scans, ultrasounds, radiographs, or magnetic resonance imaging (MRI). • According to the 2020 American Diabetes Association guidelines, diagnosis of diabetes mellitus is based on one of four abnormalities: (1) Symptoms of diabetes mellitus plus a random glucose level greater than or equal to 200 mg/dL; (2) a fasting glucose level greater than or equal to 126 mg/dL; (3) a hemoglobin A1c level greater than 6.5%; and (4) a glucose tolerance test revealing a postprandial glucose greater than or equal to 200 mg/dL, 2 hours after 75 g of glucose is administered. • A full physical assessment and history are needed to evaluate a patient who is possibly experiencing an endocrine disorder. • An example of a problem statement for someone with an endocrine disorder is as follows: Altered fluid volume caused by increased urine output (DI, Hyperthyroidism, AD). An example of an expected outcome would be as follows: Patient will display a balance between intake and output. • Planning care for a patient with an endocrine disorder will depend on the type of disorder the patient has. Stress has a direct effect on endocrine function. Therefore, measures to help the patient decrease stress should be planned. • Evaluation is accomplished by determining whether symptoms are resolving and by laboratory testing to determine whether treatment of the endocrine problem is effective

Norepinephrine, Epinephrine, Serotonin, Histamine

Epinephrine and Insulin Biosignaling Pathways

20% of the mass of adrenal gland. It is made up of interlacing cords of cells known as chromaffin cells. Chromaffin cells are also called pheochrome cells or chromophil cells. These cells contain fine granules which are stained brown by potassium dichromate. Types of chromaffin cells Adrenal medulla is formed by two types of chromaffin cells: 1. Adrenaline-secreting cells (90%) 2. Noradrenaline-secreting cells (10%). „ HORMONES OF ADRENAL MEDULLA Adrenal medullary hormones are the amines derived from catechol and so these hormones are called catecholamines. Catecholamines secreted by adrenal medulla 1. Adrenaline or epinephrine 2. Noradrenaline or norepinephrine 3. Dopamine. „ PLASMA LEVEL OF CATECHOLAMINES 1. Adrenaline : 3 μg/dL 2. Noradrenaline : 30 μg/dL 3. Dopamine : 3.5 μg/dL „ HALF-LIFE OF CATECHOLAMINES Half-life of catecholamines is about 2 minutes. „ SYNTHESIS OF CATECHOLAMINES Catecholamines are synthesized from the amino acid tyrosine in the chromaffin cells of adrenal medulla (Fig. 71.1). These hormones are formed from phenylalanine also. But phenylalanine has to be converted into tyrosine. Stages of Synthesis of Catecholamines 1. Formation of tyrosine from phenylalanine in the presence of enzyme phenylalanine hydroxylase 2. Uptake of tyrosine from blood into the chromaffin cells of adrenal medulla by active transport 3. Conversion of tyrosine into dihydroxyphenylalanine (DOPA) by hydroxylation in the presence of tyrosine hydroxylase 440 Section 6tEndocrinology FIGURE 71.1: Synthesis of catecholamines. DOPA = Di- hydroxyphenylalanine, PNMT = Phenylethanolamine-N- methyltransferase. 4. Decarboxylation of DOPA into dopamine by DOPA decarboxylase 5. Entry of dopamine into granules of chromaffin cells 6. Hydroxylation of dopamine into noradrenaline by the enzyme dopamine beta-hydroxylase 7. Release of noradrenaline from granules into the cytoplasm 8. Methylation of noradrenaline into adrenaline by the most important enzyme called phenylethanolamine- N-methyltransferase (PNMT). PNMT is present in chromaffin cells. „ METABOLISM OF CATECHOLAMINES Eighty five percent of noradrenaline is taken up by the sympathetic adrenergic neurons. Remaining 15% of noradrenaline and adrenaline are degraded (Fig. 71.2). FIGURE 71.2: Metabolism of catecholamines. COMT = Catechol-O-methyltransferase, MAO = Monoamine oxidase. Stages of Metabolism of Catecholamines 1. Methoxylation of adrenaline into meta-adrenaline and noradrenaline into metanoradrenaline in the presence of ‘catechol-O-methyltransferase’ (COMT). Meta-adrenaline and meta-noradrenaline are together called metanephrines 2. Oxidation of metanephrines into vanillylmandelic acid (VMA) by monoamine oxidase (MAO) Removal of Catecholamines Catecholamines are removed from body through urine in three forms: i. 15% as free adrenaline and free noradrenaline ii. 50% as free or conjugated meta-adrenaline and meta-noradrenaline iii. 35% as vanillylmandelic acid (VMA). „ ACTIONS OF ADRENALINE AND NORADRENALINE Adrenaline and noradrenaline stimulate the nervous system. Adrenaline has significant effects on metabolic functions and both adrenaline and noradrenaline have significant effects on cardiovascular system. „ MODE OF ACTION OF ADRENALINE AND NORADRENALINE – ADRENERGIC RECEPTORS Actions of adrenaline and noradrenaline are executed by binding with receptors called adrenergic receptors, which are present in the target organs. Chapter 71tAdrenal Medulla 441 Adrenergic receptors are of two types: 1. Alpha-adrenergic receptors, which are subdivided into alpha-1 and alpha-2 receptors 2. Beta-adrenergic receptors, which are subdivided into beta-1 and beta-2 receptors. Refer Table 71.1 for the mode of action of these receptors. „ ACTIONS Circulating adrenaline and noradrenaline have similar effect of sympathetic stimulation. But, the effect of adrenal hormones is prolonged 10 times more than that of sympathetic stimulation. It is because of the slow inactivation, slow degradation and slow removal of these hormones. Effects of adrenaline and noradrenaline on various target organs depend upon the type of receptors present in the cells of the organs. Adrenaline acts through both alpha and beta receptors equally. Noradrenaline acts mainly through alpha receptors and occasionally through beta receptors. 1. On Metabolism (via Alpha and Beta Receptors) Adrenaline influences the metabolic functions more than noradrenaline. i. General metabolism: Adrenaline increases oxygen consumption and carbon dioxide removal. It increases basal metabolic rate. So, it is said to be a calorigenic hormone ii. Carbohydrate metabolism: Adrenaline increases the blood glucose level by increasing the glycogenolysis in liver and muscle. So, a large quantity of glucose enters the circulation iii. Fat metabolism: Adrenaline causes mobilization of free fatty acids from adipose tissues. Catecholamines need the presence of glucocorticoids for this action. 2. On Blood (via Beta Receptors) Adrenaline decreases blood coagulation time. It increases RBC count in blood by contracting smooth muscless

„ INTRODUCTION Medulla is the inner part of adrenal gland and it forms 20% of the mass of adrenal gland. It is made up of interlacing cords of cells known as chromaffin cells. Chromaffin cells are also called pheochrome cells or chromophil cells. These cells contain fine granules which are stained brown by potassium dichromate. Types of chromaffin cells Adrenal medulla is formed by two types of chromaffin cells: 1. Adrenaline-secreting cells (90%) 2. Noradrenaline-secreting cells (10%). „ HORMONES OF ADRENAL MEDULLA Adrenal medullary hormones are the amines derived from catechol and so these hormones are called catecholamines. Catecholamines secreted by adrenal medulla 1. Adrenaline or epinephrine 2. Noradrenaline or norepinephrine 3. Dopamine. „ PLASMA LEVEL OF CATECHOLAMINES 1. Adrenaline : 3 μg/dL 2. Noradrenaline : 30 μg/dL 3. Dopamine : 3.5 μg/dL „ HALF-LIFE OF CATECHOLAMINES Half-life of catecholamines is about 2 minutes. „ SYNTHESIS OF CATECHOLAMINES Catecholamines are synthesized from the amino acid tyrosine in the chromaffin cells of adrenal medulla (Fig. 71.1). These hormones are formed from phenylalanine also. But phenylalanine has to be converted into tyrosine. Stages of Synthesis of Catecholamines 1. Formation of tyrosine from phenylalanine in the presence of enzyme phenylalanine hydroxylase 2. Uptake of tyrosine from blood into the chromaffin cells of adrenal medulla by active transport 3. Conversion of tyrosine into dihydroxyphenylalanine (DOPA) by hydroxylation in the presence of tyrosine hydroxylase 440 Section 6tEndocrinology FIGURE 71.1: Synthesis of catecholamines. DOPA = Di- hydroxyphenylalanine, PNMT = Phenylethanolamine-N- methyltransferase. 4. Decarboxylation of DOPA into dopamine by DOPA decarboxylase 5. Entry of dopamine into granules of chromaffin cells 6. Hydroxylation of dopamine into noradrenaline by the enzyme dopamine beta-hydroxylase 7. Release of noradrenaline from granules into the cytoplasm 8. Methylation of noradrenaline into adrenaline by the most important enzyme called phenylethanolamine- N-methyltransferase (PNMT). PNMT is present in chromaffin cells. „ METABOLISM OF CATECHOLAMINES Eighty five percent of noradrenaline is taken up by the sympathetic adrenergic neurons. Remaining 15% of noradrenaline and adrenaline are degraded (Fig. 71.2). FIGURE 71.2: Metabolism of catecholamines. COMT = Catechol-O-methyltransferase, MAO = Monoamine oxidase. Stages of Metabolism of Catecholamines 1. Methoxylation of adrenaline into meta-adrenaline and noradrenaline into metanoradrenaline in the presence of ‘catechol-O-methyltransferase’ (COMT). Meta-adrenaline and meta-noradrenaline are together called metanephrines 2. Oxidation of metanephrines into vanillylmandelic acid (VMA) by monoamine oxidase (MAO) Removal of Catecholamines Catecholamines are removed from body through urine in three forms: i. 15% as free adrenaline and free noradrenaline ii. 50% as free or conjugated meta-adrenaline and meta-noradrenaline iii. 35% as vanillylmandelic acid (VMA). „ ACTIONS OF ADRENALINE AND NORADRENALINE Adrenaline and noradrenaline stimulate the nervous system. Adrenaline has significant effects on metabolic functions and both adrenaline and noradrenaline have significant effects on cardiovascular system. „ MODE OF ACTION OF ADRENALINE AND NORADRENALINE – ADRENERGIC RECEPTORS Actions of adrenaline and noradrenaline are executed by binding with receptors called adrenergic receptors, which are present in the target organs. Chapter 71tAdrenal Medulla 441 Adrenergic receptors are of two types: 1. Alpha-adrenergic receptors, which are subdivided into alpha-1 and alpha-2 receptors 2. Beta-adrenergic receptors, which are subdivided into beta-1 and beta-2 receptors. Refer Table 71.1 for the mode of action of these receptors. „ ACTIONS Circulating adrenaline and noradrenaline have similar effect of sympathetic stimulation. But, the effect of adrenal hormones is prolonged 10 times more than that of sympathetic stimulation. It is because of the slow inactivation, slow degradation and slow removal of these hormones. Effects of adrenaline and noradrenaline on various target organs depend upon the type of receptors present in the cells of the organs. Adrenaline acts through both alpha and beta receptors equally. Noradrenaline acts mainly through alpha receptors and occasionally through beta receptors. 1. On Metabolism (via Alpha and Beta Receptors) Adrenaline influences the metabolic functions more than noradrenaline. i. General metabolism: Adrenaline increases oxygen consumption and carbon dioxide removal. It increases basal metabolic rate. So, it is said to be a calorigenic hormone ii. Carbohydrate metabolism: Adrenaline increases the blood glucose level by increasing the glycogenolysis in liver and muscle. So, a large quantity of glucose enters the circulation iii. Fat metabolism: Adrenaline causes mobilization of free fatty acids from adipose tissues. Catecholamines need the presence of glucocorticoids for this action. 2. On Blood (via Beta Receptors) Adrenaline decreases blood coagulation time. It increases RBC count in blood by contracting smooth muscles of splenic capsule and releasing RBCs from spleen into circulation. 3. On Heart (via Beta Receptors) Adrenaline has stronger effects on heart than nor- adrenaline. It increases overall activity of the heart, i.e. i. Heart rate (chronotropic effect) ii. Force of contraction (inotropic effect) iii. Excitability of heart muscle (bathmotropic effect) iv. Conductivity in heart muscle (dromotropic effect). 4. On Blood Vessels (via Alpha and Beta-2 Receptors) Noradrenaline has strong effects on blood vessels. It causes constriction of blood vessels throughout the body via alpha receptors. So it is called ‘general vasoconstrictor’. Vasoconstrictor effect of noradrena- line increases total peripheral resistance. Adrenaline also causes constriction of blood vessels. However, it causes dilatation of blood vessels in skeletal muscle, liver and heart through beta-2 receptors. So, the total peripheral resistance is decreased by adrenaline. Catecholamines need the presence of glucocor- ticoids, for these vascular effects. 5. On Blood Pressure (via Alpha and Beta Receptors) Adrenaline increases systolic blood pressure by increasing the force of contraction of the heart and cardiac output. But, it decreases diastolic blood pressure by reducing the total peripheral resistance. Noradrenaline increases diastolic pressure due to general vasoconstrictor effect by increasing the total peripheral resistance. It also increases the systolic blood pressure to a slight extent by its actions on heart. The action of catecholamines on blood pressure needs the presence of glucocorticoids. TABLE 71.1: Adrenergic receptors Receptor Mode of action Response Alpha-1 receptor Activates IP3 through phospholipase C Mediates more of noradrenaline actions than adrenaline actions Alpha-2 receptor Inhibits adenyl cyclase and cAMP Beta-1 receptor Activates adenyl cyclase and cAMP Mediates actions of adrenaline and noradrenaline equally Beta-2 receptor Activates adenyl cyclase and cAMP Mediates more of adrenaline actions than noradrenaline actions IP3 = Inositol triphosphate 442 Section 6tEndocrinology Thus, hypersecretion of catecholamines leads to hypertension. 6. On Respiration (via Beta-2 Receptors) Adrenaline increases rate and force of respiration. Adrenaline injection produces apnea, which is known as adrenaline apnea. It also causes bronchodilation. 7. On Skin (via Alpha and Beta-2 Receptors) Adrenaline causes contraction of arrector pili. It also increases the secretion of sweat. 8. On Skeletal Muscle (via Alpha and Beta-2 Receptors) Adrenaline causes severe contraction and quick fatigue of skeletal muscle. It increases glycogenolysis and release of glucose from muscle into blood. It also causes vasodilatation in skeletal muscles. 9. On Smooth Muscle (via Alpha and Beta Receptors) Catecholamines cause contraction of smooth muscles in the following organs: i. Splenic capsule ii. Sphincters of gastrointestinal (GI) tract iii. Arrector pili of skin iv. Gallbladder v. Uterus vi. Dilator pupillae of iris vii. Nictitating membrane of cat. Catecholamines cause relaxation of smooth muscles in the following organs: i. Non-sphincteric part of GI tract (esophagus, stomach and intestine) ii. Bronchioles iii. Urinary bladder. 10. On Central Nervous System (via Beta Receptors) Adrenaline increases the activity of brain. Adrenaline secretion increases during ‘fight or flight reactions’ after exposure to stress. It enhances the cortical arousal and other facilitatory functions of central nervous system. 11. Other Effects of Catecholamines i. On salivary glands (via alpha and beta-2 receptors): Cause vasoconstriction in salivary gland, leading to mild increase in salivary secretion ii. On sweat glands (via beta-2 receptors): Increase the secretion of apocrine sweat glands iii. On lacrimal glands (via alpha receptors): Increase the secretion of tears iv. On ACTH secretion (via alpha receptors): Adrenaline increases ACTH secretion v. On nerve fibers (via alpha receptors): Adrenaline decreases the latency of action potential in the nerve fibers, i.e. electrical activity is accelerated vi. On renin secretion (via beta receptors): Increase the rennin secretion from juxtaglomerular apparatus of the kidney. „ REGULATION OF SECRETION OF ADRENALINE AND NORADRENALINE Adrenaline and noradrenaline are secreted from adrenal medulla in small quantities even during rest. During stress conditions, due to sympathoadrenal discharge, a large quantity of catecholamines is secreted. These hormones prepare the body for fight or flight reactions. Catecholamine secretion increases during exposure to cold and hypoglycemia also. „ DOPAMINE Dopamine is secreted by adrenal medulla. Type of cells secreting this hormone is not known. Dopamine is also secreted by dopaminergic neurons in some areas of brain, particularly basal ganglia. In brain, this hormone acts as a neurotransmitter. Injected dopamine produces the following effects: 1. Vasoconstriction by releasing norepinephrine 2. Vasodilatation in mesentery 3. Increase in heart rate via beta receptors 4. Increase in systolic blood pressure. Dopamine does not affect diastolic blood pressure. Deficiency of dopamine in basal ganglia produces nervous disorder called parkinsonism (Chapter 151). „ APPLIED PHYSIOLOGY – PHEOCHROMOCYTOMA Pheochromocytoma is a condition characterized by hypersecretion of catecholamines. Cause Pheochromocytoma is caused by tumor of chromophil cells in adrenal medulla. It is also caused rarely by tumor of sympathetic ganglia (extra-adrenal pheochromocytoma). Chapter 71tAdrenal Medulla 443 Signs and Symptoms Characteristic feature of pheochromocytoma is hyper- tension. This type of hypertension is known as endocrine or secondary hypertension. Other features: 1. Anxiety 2. Chest pain 3. Fever 4. Headache 5. Hyperglycemia 6. Metabolic disorders 7. Nausea and vomiting 8. Palpitation 9. Polyuria and glucosuria 10. Sweating and flushing 11. Tachycardia 12. Weight loss. Tests for Pheochromocytoma Pheochromocytoma is detected by measuring meta- nephrines and vanillylmandelic acid in urine and Cathecolamines in olasma

Epinephrine 1:1000

[4] Epinephrine 1:1,000

CHAPTER 12 PART 1 BIOCHEM SIGNALING GENERAL AND EPINEPHRINE PATHWAY

Negative and Positive Feedback Loops Control hormone levelsNegative feedback loopHormone release stops in response to decrease in stimulus- Stimulus (eating) raises blood glucose levels- Pancreas releases insulin in response to elevated blood   glucose- Blood glucose decreases as it is used by the body or  stored in the liver - Insulin release stops as blood glucose levels normalize Positive feedback loop As long as stimulus is present, action of hormone continues- Infant nursing at mother’s breast→stimulates  hypothalamus→stimulates posterior pituitary- Oxytocin released→stimulates milk production  and ejection from mammary glands- Milk release continues as long as infant  continues to nurse The Major Endocrine OrgansThe major endocrine organs of the body include: the pituitary, pineal, thyroid, parathyroid, thymus, and adrenal glands, pancreas, and gonads (ovaries and testes)Endocrine glands - Ductless - Release hormones - Directly into target tissues - Into bloodstream to be carried to target tissuesHormones(Greek word hormone – to set into motion)     Pituitary Gland and Hypothalamus o The pituitary gland is approximately the size of a pea. o It hangs by a stalk from the inferior surface of the hypothalamus of the brain, where it is snugly surrounded by the sella turcica of the sphenoid bone. o It has two functional lobes – the anterior pituitary (glandular tissue) and the posterior pituitary (nervous tissue). o The anterior pituitary gland controls the activity of so many other endocrine glands (“master endocrine gland”) o The release of each of its hormones is controlled by releasing hormones and inhibiting hormones produced by the hypothalamus. o The hypothalamus also makes two additional hormones, oxytocinand antidiuretic hormone, which are transported along the axons of the hypothalamic nuerosecretory cells to the posterior pituitary for storage. They are later released into the blood in response to nerve impulses from the hypothalamus. Oxytocin o Is released in significant amounts only during childbirth and nursing. o It stimulates powerful contractions of the uterine muscle during sexual relations, during labor, and during breastfeeding. o It also causes milk ejection (let-down reflex) in a nursing woman. Antidiuretic Hormone (ADH) o ADH is a chemical that inhibits or prevents urine production. o ADH causes the kidneys to reabsorb more water from the forming urine; as a result, urine volume decreases, and blood volume increases. o In larger amounts, ADH also increases blood pressure by causing constriction of the arterioles (small arteries). For this reason, it is sometimes referred to as vasopressin. Anterior Pituitary HormonesThe anterior pituitary produces several hormones that affect many body organs. Growth Hormone (GH) o Its major effects are directed to the growth of skeletal muscles and long bones of the body o At the same time, it causes fats to be broken down and used for energy while it spares glucose, helping to maintain blood sugar homeostasis. ProlactinIts only known target in humans is the breast.After childbirth, it stimulates and maintains milk production by the mother’s breasts.Gonadotropic Hormones (FSH and LH) o Regulate the hormonal activity of the gonads (ovaries and testes) o In women, the FSH stimulates follicle development in the ovaries. o In men, FSH stimulates sperm production by the testes. o LH triggers ovulation of an egg from the ovary and causes the ruptured follicle to produce progesterone and some estrogen. o LH stimulates testosterone production by the interstitial cells of the testes. Pineal Gland The pineal gland is a small, cone-shaped gland that hangs from the roof of the third ventricle of the brain. Melatonin o The only hormone secreted from pineal gland in substantial amounts o Believed to be a “sleep trigger” that plays an important role in establishing the body’s sleep-wake cycle. o The level of melatonin rises and falls during the course of the day and night. o The peak level occurs at night and makes us drowsy o The lowest level occurs during daylight around noon. Thyroid Gland • The thyroid gland is located at the base of the throat, just inferior to the Adam’s apple. • It is a fairly large gland consisting of two lobes joined by a central mass, or isthmus. • The thyroid gland makes two hormones, one called thyroid hormone, the other called calcitonin. Thyroid Hormone o Referred to as body’s major metabolic hormone o Contains two active iodine-containing hormones, thyroxine (T4)and thriiodothyronine (T3) o Most triiodothyronine is formed at the target tissues by conversion of thyronine to triiodothyronine o Thyroid hormone controls the rate at which glucose is “burned”, or oxidized, and converted to body heat and chemical energy (ATP). o Thyroid hormone is also important for normal tissue growth and development, especially in the reproductive and nervous systems. Homeostatic Imbalance ➢ Without iodine, functional thyroid hormones cannot be made. ➢ The source of iodine is our diet (seafoods) ➢ Goiter is an enlargement of the thyroid gland that results when the diet is deficient in iodine. Hyposecretion of thyroxine may indicate problems other than iodine deficiency. If it occurs in early childhood, the result is cretinism. ▪ Results in dwarfism and mental retardation (if discovered early, hormone replacement will prevent mental impairment) Hypothyroidism occurring in adults results in myxedema ▪ Characterized by both physical and mental sluggishness (no mental impairment) ▪ Other signs are puffiness of the face, fatigue, poor muscle tone, low body temperature, obesity, and dry skin (Oral thyroxine is prescribed to treat this condition)   ➢ Hyperthyroidism generally results from a tumor of the thyroid gland. ➢ Extreme overproduction of thyroxine results in a high basal metabolic rate, intolerance of heat, rapid heartbeat, weight loss, nervous and agitated behavior, and a general inability to relax. Graves’ disease o A form of hyperthyroidism o The thyroid gland enlarges, the eyes bulge (exophthalmos) Calcitonin ➢ Second important hormone product of the thyroid gland ➢ Decreases the blood calcium ion level by causing calcium to be deposited in the bones Parathyroid Glands ➢ The parathyroid glands are tiny masses of glandular tissue most often on the posterior surface of the thyroid gland. ➢ Parathyroid hormone (PTH) is the most important regulator of calcium ion homeostasis of the blood. ➢ Although the skeleton is the major PTH target, PTH also stimulates the kidneys and intestine to absorb more calcium ions. Homeostatic Imbalance o If blood calcium ion level falls too low, neurons become extremely irritable and overactive. They deliver impulses to the muscles so rapidly that the muscles go into uncontrollable spasms (tetany), which may be fatal. o Severe hyperparathyroidism causes massive bone destruction. The bones become very fragile, and spontaneous fractures begin to occur. Thymus o Is located in the upper thorax, posterior to the sternum. o Large in infants and children, it decreases in size throughout adulthood. o By old age, it is composed mostly of fibrous connective tissue and fat. o The thymus produces a hormone called thymosin and others that appear to be essential for normal development of a special group of white blood cells (T lymphocytes) and the immune response. Adrenal Glands o The two adrenal glands curve over the top of the kidneys like triangular hats. o It is structurally and functionally two endocrine organs in one.   • it has parts made of glandular (cortex) and neural tissue (medulla) • The central medulla region is enclosed by the adrenal cortex, which contains three separate layers of cells. Hormones of the Adrenal CortexThe adrenal cortex produces three major groups of steroid hormones, collectively called corticosteroids: 1. Mineralocorticoids (aldosterone) ➢ Are produced by the outermost adrenal cortex cell layer. ➢ Are important in regulating the mineral (salt) content of the blood, particularly the concentrations of sodium and potassium ions. ➢ These hormones target the kidney tubules(Distal Convulating Kidney Tubles) that selectively reabsorb the minerals or allow them to be flushed out of the body in urine. ➢ When the blood level of aldosterone rises, the kidney tubule cell reabsorb increasing amounts of sodium ions and secrete more potassium ions into the urine. ➢ When sodium is reabsorbed, water follows. Thus, the mineralocorticoids help regulate both water and electrolyte balance in body fluids. 2. Glucocorticoids (Cortisone and Cortisol)  ➢ Glucocorticoids promote normal cell metabolism and help the body to resist long-term stressors, primarily by increasing the blood glucose level. ➢ When blood levels of glucocorticoids are high, fats and even proteins are broken down by body cells and converted to glucose, which is released to the blood. ➢ For this reason, glucocorticoids are said to be hyperglycemic hormones. ➢ Glucocorticoids also seem to control the more unpleasant effects of inflammation by decreasing edema, and they reduce pain by inhibiting the pain-causing prostaglandins. ➢ Because of their anti-inflammatory properties, glucocorticoids are often prescribed as drugs to suppress inflammation for patients with rheumatoid arthritis. ➢ Glucocorticoids are released from the adrenal cortex in response to a rising blood level of ACTH (Adrenocorticotropic hormone). 3. Sex Hormones ➢ In both men and women, the adrenal cortex produces both male and female sex hormones throughout life in relatively small amounts. ➢ The bulk of the sex hormones produced by the innermost cortex layer are androgens (male sex hormones), but some estrogens (female sex hormones) are also formed. Homeostatic Imbalance1. Addisson’s disease (hyposecretion of all the adrenal cortex hormones) ✓ Bronze tone of the skin (suntan) ✓ Na (sodium) and water are lost from the body ✓ Muscles become weak and shock is a possibility ✓ Hypoglycemia (↓ glucocorticoids) ✓ Suppression of the immune system 2. Hyperaldosteronism (hyperactivity of the outermost cortical area) ✓ Excessive water and sodium ions retention ✓ High blood pressure ✓ Edema ✓ Low potassium ions level (hypokalemia) 3. Cushing’s Syndrome (Excessive glucocorticoids) ✓ Swollen “moon face” and “Buffalo hump” ✓ High blood pressure and hyperglycemia (steroid diabetes) ✓ Weakening of the bones (as protein is withdrawn to be converted to glucose) ✓ Severe depression of the immune system 4. Hypersecretion of the sex hormones leads to masculinization, regardless of sex. Hormones of the Adrenal Medulla ➢ When the medulla is stimulated by sympathetic nervous system neurons, its cells release two similar hormones, epinephrine(adrenaline) and norepinephrine (noradrenaline), into the bloodstream. ➢ Collectively, these hormones are called catecholamines. ➢ The catecholamines of the adrenal medulla prepare the body to cope with short-term stressful situations and cause the so-called alarm stage of the stress response. ➢ Glucocorticoids, by contrast, are produced by the adrenal cortex and are important when coping with prolonged or continuing stressors, such as dealing with the death of a family member or having a major operation (resistance stage). Pancreatic Islets ➢ The pancreas, located close to the stomach in the abdominal cavity, is a mixed gland. ➢ The pancreatic islets, also called the islets of Langerhans, are little masses of endocrine (hormone-producing) tissue of the pancreas. ➢ The exocrine, or acinar, part of the pancreas acts as part of the digestive system. ➢ Two important hormones produced by the islet cells are insulin and glucagon. Insulin ➢ Hormone released by the beta cells of the islets in response to a high level of blood glucose. ➢ Acts on all body cells, increasing their ability to import glucose across their plasma membranes. ➢ Insulin also speeds up these “use it” or “store it” activities. ➢ Because insulin sweeps the glucose out of the blood, its effect is said to be hypoglycemic. ➢ Without it, essentially no glucose can get into the cells to be used. Glucagon ➢ Acts as an antagonist of insulin ➢ Released by the alpha cells of the islets in response to a low blood glucose levels. ➢ Its action is basically hyperglycemic. ➢ Its primary target is the liver, which it stimulates to break down stored glycogen to glucose and to release the glucose into the blood. Gonads ➢ The female and male gonads produce sex cells. ➢ They also produce sex hormones that are identical to those produced by adrenal cortex cells. ➢ The major differences from the adrenal sex hormone production are the source and relative amounts of hormones produced. Hormones of the OvariesBesides producing female sex cells (ova, or eggs), ovaries produce two groups of steroid hormones, estrogens and progesterone. 1. Estrogen (Steroid Hormone) ➢ Responsible for the development of sex characteristics in women (primarily growth and maturation of the reproductive organs) and the appearance of secondary sex characteristics at puberty. ➢ Acting with progesterone, estrogens promote breast development and cyclic changes in the uterine lining (the menstrual cycle) 2. Progesterone (Steroid Hormone) ➢ Acts with estrogen to bring about the menstrual cycle. ➢ During pregnancy, it quiets the muscles of the uterus so that an implanted embryo will not be aborted and helps prepare breast tissue for lactation. Hormones of the TestesIn addition to male sex cells, or sperm, the testes also produce male sex hormones, or androgens, of which testosterone is the most important. 3. Testosterone ➢ Promotes the growth and maturation of the reproductive system organs to prepare the young man for reproduction. ➢ It also causes the male’s secondary sex characteristics to appear and stimulates the male sex drive. ➢ It is necessary for continuous production of sperm. ➢ Testosterone production is specifically stimulated by LH. Other Hormone-Producing Tissues and OrgansPlacenta ➢ During very early pregnancy, a hormone called human chorionic gonadotropin (hCG) is produced by the developing embryo and then by the fetal parts of the placenta. ➢ hCG stimulates the ovaries to continue producing estrogen and progesterone so that the lining of the uterus is not sloughed off in menses. ➢ In the third month, the placenta assumes the job of the ovaries of producing estrogen and progesterone, and the ovaries become inactive for the rest of the pregnancy. ➢ The high estrogen and progesterone blood levels maintain the lining of the uterus and prepare the breasts for producing milk. ➢ Human placental lactogen (hPL) works cooperatively with estrogen and progesterone in preparing the breasts for lactation. ➢ Relaxin, another placental hormone, causes the mother’s pelvic ligaments and the pubic symphysis to relax and become more flexible, which eases birth passage. Developmental Aspects of the Endocrine System ➢ In late middle age, the efficiency of the ovaries begins to decline, causing menopause. o Reproductive organs begin to atrophy o Ability to bear children ends o Problems associated with estrogen deficiency begin to occur (arteriosclerosis, osteoporosis, decreased skin elasticity, “hot flashes”) ➢ No such dramatic changes seem to happen in men. ➢ Elderly persons are less able to resist stress and infection. ➢ Exposure to pesticides, industrial chemicals, dioxin, and pother soil and water pollutants diminishes endocrine function, which may explain the higher cancer rates among older adults in certain areas of the country. ➢ All older people have some decline in insulin production, and type 2 diabetes mellitus is most common in this age group. BLOOD ➢ It is the only fluid tissue in the body. ➢ A homogenous liquid that has both solid and liquid components. ➢ Taste, Odor, 5x thicker than water ➢ Classified as a connective tissue ❖Living cells = formed elements ❖Non-living matrix = plasma (90% water) Components •Formed elements (blood cells)are suspended in plasma •The collagen and elastin fibers typical of other connective tissues are absent from blood; instead, dissolved proteins become visible as fibrin strands during blood clotting •If a sample of blood is separated, the plasma rises to the top, and the formed elements, being heavier, fall to the bottom. •Most of the erythrocytes (RBCs) settle at the bottom of the tube •There is a thin, whitish layer called the buffy coat at the junction between the erythrocytes and the plasma containing leukocytes (WBCs) and platelets   Physical Characteristics and Volume • Color range ➢ Oxygen-rich blood is scarlet red ➢ Oxygen-poor blood is dull red • pH must remain between 7.35–7.45 • Slightly alkaline • Blood temperature is slightly higher than body temperature • 5-6 Liters or about 6 quarts /body   Functions and Composition of Blood 1. Transport of gases, nutrients and waste products 2. Transport of processed molecules 3. Transport of regulatory molecules 4. Regulation of pH and osmosis 5. Maintenance of body temp 6. Protection against foreign substances 7. Clot formation   Plasma • The liquid part of the blood; 90 percent water • Over 100 different substances are dissolved in this straw-colored fluid: ➢ nutrients ➢ electrolytes ➢ respiratory gases ➢ hormones ➢ plasma proteins; and ➢ various wastes and products of cell metabolism   • Plasma proteins are the most abundant solutes in plasma (albumin and clotting proteins) • Plasma helps to distribute body heat, a by-product of cellular metabolism, evenly throughout the body. Formed Elements Erythrocytes (RBCs) • Function primarily to ferry oxygen to all cells of the body. • RBCs differ from other blood cells because they are anucleate (no nucleus) • Contain very few organelles (RBCs circulating in the blood are literally “bags” of hemoglobin molecules ) •Very efficient oxygen transporters (they lack mitochondria and make ATP by anaerobic mechanisms) • Their small size and peculiar shape provide a large surface area relative to their volume, making them suited for gas exchange • RBCs outnumber WBCs by about 1,000 to 1 and are the major factor contributing to blood viscosity. • There are normally about 5 million cells per cubic millimeter of blood. • The more hemoglobin molecules the RBCs contain, the more oxygen they will be able to carry. • A single RBC contains about 250 million hemoglobin molecules, each capable of binding 4 molecules of oxygen. • Normal hemoglobin count is 12-18 grams of hemoglobin per 100 ml of blood • Men: 13-18g/ml Women: 12-16 g/ml   Homeostatic Imbalance Anemia • a decrease in the oxygen-carrying ability of the blood, whatever the reason is. • May be the result of (1) a lower-than-normal number of RBCs or (2) abnormal or deficient hemoglobin content in the RBCs.   Polycythemia Vera • An excessive or abnormal increase in the number of erythrocytes; may result from bone marrow cancer or a normal physiologic response to living at high altitudes, where the air is thinner and less oxygen is available (secondary polycythemia)     Formed Elements Leukocytes (WBCs) • Are far less numerous than RBCs • They are crucial to body defense • On average, there are 4,800 to 10,800 WBCs/mm3 of blood • WBCs contain nuclei and the usual organelles, which makes them the only complete cells in the blood. • WBCs are able to slip into and out of the blood vessels – a process called diapedesis • WBCs can locate areas of tissue damage and infection in the body by responding to certain chemicals that diffuse from the damaged cells (positive chemostaxis) • Whenever WBCs mobilize for action, the body speeds up their production, and as many as twice the normal number of WBCs may appear in the blood within a few hours. • A total WBC count above 11,000 cells/mm3 is referred to as leukocytosis. • The opposite condition, leukopenia, is an abnormally low WBC count (commonly caused by certain drugs, such as corticosteroids and anti-cancer agents) • WBCs are classified into two major groups – granulocytes and agranulocytes – depending on whether or not they contain visible granules in their cytoplasm.   Granulocytes Neutrophils ➢ Are the most numerous WBCs. ➢ Neutrophils are avid phagocytes at sites of acute infection. Eosinophils ➢ Their number increases rapidly during infections by parasitic worms ingected in food such as raw fish or entering through the skin. Basophils ➢ The rarest of the WBCs, have large histamine-containing granules. Histamine ➢ is an inflammatory chemical that makes blood vessels leaky and attracts other WBCs to the inflamed site   Agranulocytes Lymphocytes ➢ Have a large, dark purple nucleus that occupies most of the cell volume. ➢ Lymphocytes tend to take up residence in lymphatic tissues, such as the tonsils, where they play an important role in the immune response. ➢ They are the second most numerous leukocytes in the blood Monocytes ➢ Are the largest of the WBCs. ➢ When they migrate into the tissues, they change into macrophages. ➢ Macrophages are important in fighting chronic infections, such as tuberculosis, and in activating lymphocytes Platelets   ➢ They are fragments of bizarre multinucleate cells called megakaryocytes, which pinch off thousands of anucleate platelet “pieces” that quickly seal themselves off from the surrounding fluids. ➢ Normal adult has 150,000 to 450,000 per cubic millimeter of blood ➢ Platelets are needed for the clotting process that stops blood loss from broken blood vessels. ➢ Average lifespan is 9 to 12 days   Hematopoiesis • Occurs in red bone marrow, or myeloid tissue. • In adults, this tissue is found chiefly in the axial skeleton, pectoral andpelvic girdles, and proximal epiphyses of the humerus and femur. • On average, the red marrow turns out an ounce of new bloodcontaining 100 billion new cells every day. • All the formed elements arise from a common stem cell, thehemocytoblast, which resides in red bone marrow. • Once a cell is committed to a specific blood pathway, it cannotchange. • The hemocytoblast forms two types of descendants – the lymphoidstem cell, which produces lymphocytes, and the myeloid stem cell,which can produce other classes of formed elements.   Formation of RBCs • Because they are anucleate, RBCs are unable to synthesizeproteins, grow, or divide. • As they age, RBCs become rigid and begin to fall apart in 100 to 120 days. • Their remains are eliminated by phagocytes in the spleen, liver, and other body tissues. • RBC components are salvaged. Iron is bound to protein as ferritin, and the balance of the heme group is degraded to bilirubin, which is then secreted into the intestine by liver cells where it becomes a brown pigment called stercobilin that leaves the body in feces. • Globin is broken down to amino acids which are released into the circulation.The rate of erythrocyte production is controlled by a hormone called erythropoietin (from the kidneys) • Erythropoietin targets the bone marrow prodding it into “high gear” to turn out more RBCs. • An overabundance of erythrocytes, or an excessive amount of oxygen in the bloodstream, depresses erythropoietin release and RBC production. • However, RBC production is controlled not by the relative number of RBCs in the blood, but by the ability of the available RBCs to transport enough oxygen to meet the body’s demands   Formation of WBCs and Platelets   • The formation of leukocytes and platelets is stimulated by hormones • These colony stimulating factors (CSFs) and interleukins not only prompt red bone marrow to turn out leukocytes, but also enhance the ability of mature leukocytes to protect the body. • The hormone thrombopoietin accelerates the production of platelets from megakaryocytes, but little is know about how process is regulated. • When bone marrow problems or disease condition is suspected, bone marrow biopsy is done.   Hemostasis If a blood vessel wall breaks, a series of reactions starts the process of hemostasis (stopping the bleeding). Phases of Hemostasis 1. Vascular spasms occur. 2. Platelet plug forms. 3. Coagulation events occur.       Human Blood Groups • An antigen is a substance that the body recognizes as foreign; it stimulates the immune system to mount a defense against it. • The “recognizers” are antibodies present in plasma that attach to RBCs bearing surface antigens different from those on the patient’s RBCs.   ABO and Rh Blood Types The blood group system recognizes four blood types: • Type A, B, AB, and O • They are distinguished from each other in part by their antigens and antibodies. • Specific antibodies are found in the serum based on the type of antigen on the surface of the RBC   ABO and Rh Blood Types BLOOD TYPE Can Accept From Can Donate To A A, O A, AB B B, O B, AB AB A, B, AB, O AB O O O, A, B, AB   The Rh Factor Rh-Positive Rh-Negative Contains the Rh antigen -No Rh antigen   -Will make antibodies if given Rh-positive blood   -Agglutination can occur if given Rh-positive blood     Summary • Blood is responsible for transporting oxygen, fluids, hormones, and antibodies and for eliminating waste materials. • The major components of blood include the formed elements and plasma. • RBCs transport oxygen and carbon dioxide; WBCs destroy foreign invaders. • WBCs include granulocytes and agranulocytes. • Plasma is the liquid portion of unclotted blood. Serum is the liquid portion of clotted blood • Hemostasis includes four stages: blood vessel spasm, platelet plug formation, blood clotting, and fibrinolysis. • ABO and Rh types are determined by the antigen found on the RBCs

compare the physical and psychological function of acetylcholine, epinephrine, norepinephrine, dopamine and serotonin