Results for "constriction"

NEUS 609 - Astrocytes

Postorbital Constriction

Cranial Nerves Overview Twelve pairs of nerves originating from the brain; numbered I–XII using Roman numerals. Origin of Cranial Nerves First two pairs (I–II) arise from forebrain; remaining pairs (III–XII) arise from brainstem. Function of Cranial Nerves Primarily serve head and neck structures; one exception (vagus nerve) extends into thoracic and abdominal cavities. Cranial Nerve Numbering Begin anteriorly and move posteriorly along the inferior surface of the brain. Cranial Nerve Naming Names reflect location, innervation, or function. Mnemonic for Cranial Nerve Names Olfactory, Optic, Oculomotor, Trochlear, Trigeminal, Abducens, Facial, Vestibulocochlear, Glossopharyngeal, Vagus, Accessory, Hypoglossal. Fun Mnemonic Phrase (Names) On Occasion Our Trusty Truck Acts Funny — Very Good Vehicle Any How. Mnemonic for Cranial Nerve Functions (Sensory/Motor/Both) Some Say Marry Money But My Brother Says Bad Business Marry Money. CN I: Olfactory Nerve Sensory; responsible for sense of smell; passes through cribriform plate of ethmoid bone. CN II: Optic Nerve Sensory; responsible for vision; exits through optic canal (optic foramen). CN III: Oculomotor Nerve Motor; controls most eye movements and pupil constriction; exits through superior orbital fissure. Oculomotor Somatic Function Controls superior rectus, inferior rectus, medial rectus, and inferior oblique eye muscles. Oculomotor Autonomic Function Controls sphincter pupillae muscle for pupil constriction. CN IV: Trochlear Nerve Motor; controls superior oblique muscle of the eye; exits through superior orbital fissure. Trochlear Function Allows eye to move inferolaterally (downward and outward). CN V: Trigeminal Nerve Both sensory and motor; major sensory nerve of the face with three divisions (V1, V2, V3). Trigeminal Divisions V1 Ophthalmic (superior orbital fissure), V2 Maxillary (foramen rotundum), V3 Mandibular (foramen ovale). Trigeminal Function Sensory input from face, scalp, teeth, and anterior tongue; motor control of muscles of mastication. CN VI: Abducens Nerve Motor; controls lateral rectus muscle of the eye for lateral movement; exits through superior orbital fissure. Eye Movement Coordination Controlled by oculomotor (III), trochlear (IV), and abducens (VI) nerves. Abducens Palsy Results in inability to move eye laterally (damage to lateral rectus muscle). Trochlear Palsy Causes weakness in downward eye movement; patient may tilt head to compensate. Oculomotor Palsy Causes drooping eyelid (ptosis), dilated pupil, and inability to move eye upward, downward, or inward. CN VII: Facial Nerve Both sensory and motor; innervates muscles of facial expression and taste from anterior two-thirds of tongue. Branches of Facial Nerve Five branches: Temporal, Zygomatic, Buccal, Mandibular, and Cervical. Facial Nerve Function Motor control of facial muscles, secretion from salivary and lacrimal glands, and taste sensation. CN VIII: Vestibulocochlear Nerve Sensory; responsible for equilibrium (vestibular branch) and hearing (cochlear branch). Vestibulocochlear Function Transmits sound and balance information from inner ear to brain. CN IX: Glossopharyngeal Nerve Both sensory and motor; innervates pharynx and posterior tongue. Glossopharyngeal Functions Controls swallowing, taste on posterior one-third of tongue, and salivary gland secretion. CN X: Vagus Nerve Both sensory and motor; only cranial nerve extending beyond head and neck into thorax and abdomen. Vagus Nerve Function Regulates heart rate, breathing, digestive activity, and contributes to swallowing and voice production. Vagus Sensory Component Provides visceral sensation and taste from epiglottis and pharynx. CN XI: Accessory Nerve Motor; controls muscles of the larynx, pharynx, and neck; assists in head and shoulder movement. Accessory Nerve Function Innervates sternocleidomastoid and trapezius muscles for head rotation and shoulder elevation. CN XII: Hypoglossal Nerve Motor; controls tongue movements for chewing, swallowing, and speech. Hypoglossal Function Allows food mixing, manipulation, and articulation during speech. Cranial Nerve Functional Summary Sensory: I, II, VIII. Motor: III, IV, VI, XI, XII. Both: V, VII, IX, X. Cranial Nerve Function Mnemonic I–Sensory, II–Sensory, III–Motor, IV–Motor, V–Both, VI–Motor, VII–Both, VIII–Sensory, IX–Both, X–Both, XI–Motor, XII–Motor. Cranial Nerve Testing Used clinically to identify brainstem lesions, neuropathies, or localized nerve damage. Clinical Importance of Cranial Nerves Critical for assessing neurological health and localizing brain or skull base disorders.

Chapter 7:6 Study Guide NERVOUS SYSTEM P179-187 Nervous System-complex, highly organized system that coordinates all the activities of the body. *The basic structural unit of the nervous system is the neuron, or nerve cell. It consists of a cell body containing:  Nucleus  Nerve fibers called dendrites (carry impulses toward the cell body)  Single nerve fiber called axon (carry impulses away from the cell body) Many axons have a lipid covering called a myelin sheath, which increases the rate of impulse transmission and insulates and maintains the axon. The axon of one neuron lies close to the dendrites of many other neurons. The spaces between them are known as synapses. Special chemicals, called neurotransmitters, located at the end of each axon allow the nerve impulses to pass from one neuron to another. Nerves are a combination of many nerve fibers located outside the brain and spinal cord. Meninges are membranes or protective lining that covers the brain and spinal cord. Afferent, or sensory, nerves carry messages from all parts of the body to the brain and spinal cord. Efferent, or motor, nerves carry messages from the brain and spinal cord to the muscles and glands. Associative, or internuncial, nerves carry both sensory and motor messages. There are two main divisions to the nervous system: 1. 2. Central nervous system: consists of the brain and spinal cord Peripheral nervous system: consists of the nerves. A separate division of the peripheral nervous system is the autonomic nervous system. This system controls involuntary body functions. *Brain-mass of nerve tissue well protected by membranes and the cranium, or skull. The main sections include:  Cerebrum-the largest and highest section of the brain. Responsible for: reasoning, thought, memory, speech, sensation, sight, smell, hearing, and voluntary body movement.  Cerebellum-section below the back of the cerebrum. Responsible for: muscle coordination, balance and posture, muscle tone.  Diencephalon-section between the cerebrum and midbrain. o Thalamus-acts as a relay center and directs sensory impulses to the cerebrum. o Hypothalamus-regulates and controls the autonomic nervous system, temperature, appetite, water balance sleep and blood vessel constriction and dilation. Also involved in emotions such as anger, fear, pleasure, pain and affection.  Midbrain-the section located below the cerebrum at the top of the brain stem. Responsible for conducting impulses between brain parts and for certain eye and auditory reflexes.  Pons-located below the midbrain and in the brain stem. Responsible for conducting messages to other parts of the brain; for certain reflex actions including chewing, tasting, and saliva production; and for assisting with respiration.  Medulla oblongata-the lowest part of the brain stem. Connects with the spinal cord and is responsible for regulating heartbeat, respiration, swallowing, coughing, and blood pressure. The spinal cord continues down from the medulla oblongata and ends at the first or second lumbar vertebrae. *The meninges are three membranes that cover and protect the brain and spinal cord. 1. 2. 3. Dura mater-thick, tough, outer layer Arachnoid membrane-delicate and web like Pia mater-closely attached to the brain and spinal cord and contains blood vessels that nourish the nerve tissue. The brain has four ventricles, hollow spaces that connect with each other and with the space under the arachnoid membrane. The ventricles are filled with a fluid called cerebrospinal fluid. This fluid circulates continually between the ventricles and through the subarachnoid space. It serves as a shock absorber to protect the brain and spinal cord. It also carries nutrients to some parts of the brain and spinal cord and helps remove metabolic products and wastes. After circulating, it is absorbed into the blood vessels of the dura mater and returned to the bloodstream through special structures called the arachnoid villi. The peripheral nervous system consists of the somatic and autonomic nervous systems. The somatic nervous system consists of 12 pairs of cranial nerves and their branches and 31 pairs of spinal nerves and their branches. Some of the cranial nerves are responsible for special senses such as sight, hearing, taste, and smell. The Autonomic nervous system is an important part of the peripheral nervous system. It helps maintain a balance in the involuntary functions of the body and allows the body to react in times of emergency. *There are two divisions to the autonomic nervous system: Sympathetic nervous system: prepares the body in times of emergencies. Prepares the body to act by increasing heart rate, respiration, and blood pressure and slowing activity in the digestive tract. This is known as the fight or flight response. Parasympathetic nervous system: After the emergency, this slows down the heart rate, decreases respirations, lowers blood pressure and increases activity in the digestive tract. Cerebral Palsy is a disturbance in voluntary muscle action and is caused by brain damage. Lack of oxygen to the brain, birth injuries, prenatal rubella, and infections can all cause cerebral palsy. Cerebrovascular Accident or CVA (stroke) occurs when the blood flow to the brain is impaired, resulting in a lack of oxygen and a destruction of brain tissue. CVA includes loss of consciousness; weakness or 1. 2. paralysis on one side of the body (hemiplegia); dizziness; dysphagia (difficulty swallowing); visual disturbances; mental confusion; aphasia (speech and language impairment); and incontinence. When a CVA occurs, immediate care within the first three hours can help prevent brain damage. Treatment with thrombolytic or “clot-busting” drugs such as TPA (tissue plasminogen activator) can dissolve the blood clot and restore blood flow to the brain. Aphasia is a speech or language impairment. There are different types. ALS is amyotrophic lateral sclerosis. Also called Lou Gehrig’s disease. This is a chronic degenerative neuromuscular disease. The cause is unknown. Carpal tunnel syndrome is a progressive, painful condition of the wrist and hand. It occurs when the median nurse is pinched or compressed. Concussions are traumatic brain injuries, usually from a blow to the head by an accident, injury or fall. The brain slides back/forward and forcefully hits against the skull. Think of it like a bruise on the brain. Encephalitis is an inflammation of the brain and is caused by a virus, bacterium, or chemical agent. Epilepsy or seizure syndrome is a brain disorder associated with abnormal electrical impulses in the neurons of the brain. Hydrocephalus is an excessive accumulation of cerebrospinal fluid in the ventricles and, in some cases, the subarachnoid space of the brain. It is usually cause by a congenital (at birth) defect, infection, or tumor that obstructs the flow of cerebrospinal fluid out of the brain. The condition is treated by the surgical implantation of a shunt (tube) between the ventricles and the veins, heart, or abdominal peritoneal cavity to provide for drainage of the excess fluid. Meningitis is an inflammation of the meninges of the brain and/or spinal cord and is caused by a bacterium, virus, fungus, or toxins such as lead and arsenic. Multiple Sclerosis (MS) is a chronic, progressive, disabling condition resulting from a degeneration of the myelin sheath in the central nervous system. Neuralgia is nerve pain. Inflammation, pressure, toxins, and other disease cause it. Paralysis usually results from a brain or spinal cord injury that destroys neurons and results in a loss of function and sensation below the level of injury. Hemiplegia is paralysis on side of the body and is caused by a tumor, injury, or CVA. Paraplegia is paralysis in the lower extremities or lower part of the body and is caused by a spinal cord injury. Quadriplegia is paralysis of t harems, legs, and body below the spinal cord injury. Parkinson’s disease is a chronic, progressive condition involving degeneration of brain cells, usually in persons over 50 years of age

Degrees of Constriction and Locations of Constriction

CNS Stimulants ADHD Medications Amphetamine (Adderall, Dexedrine) Mechanism of Action: Stimulates excitatory neurons, increases dopamine & norepinephrine. Indications: ADHD, narcolepsy. Adverse Effects: Increased HR/BP, anxiety, tremor, insomnia, headache, decreased appetite, GI distress, dry mouth. Contraindications: Cardiac abnormalities, hypertension, anxiety, agitation, glaucoma, MAOI use (within 14 days). Nursing Implications: Administer 4-6 hours before bedtime. Take on an empty stomach. Monitor BP, pulse, weight, growth patterns in children. Avoid abrupt withdrawal. Methylphenidate (Ritalin, Concerta) Mechanism of Action: CNS stimulant affecting dopamine reuptake. Indications: ADHD, narcolepsy. Adverse Effects: Same as amphetamines. Nursing Implications: Same as amphetamines. Lisdexamfetamine (Vyvanse) Mechanism of Action: Converted into dextroamphetamine. Indications: ADHD, binge-eating disorder. Nursing Implications: Similar to amphetamines. Atomoxetine (Strattera) Mechanism of Action: Selective norepinephrine reuptake inhibitor. Indications: ADHD (children >6 and adults). Adverse Effects: Lower abuse potential, less insomnia, but Black Box Warning for suicidal thoughts. Nursing Implications: Monitor mental health for suicidal ideation. Narcolepsy Medications Modafinil (Provigil) Mechanism of Action: Low abuse potential stimulant. Indications: Narcolepsy, shift work sleep disorder. Nursing Implications: Monitor BP & mental health. Antimigraine Medications Rizatriptan (Maxalt), Sumatriptan (Imitrex) Mechanism of Action: Serotonin receptor agonist, causing vasoconstriction. Indications: Acute migraine treatment. Adverse Effects: Tingling, flushing, chest tightness, rebound headaches if overused. Contraindications: Cardiovascular disease, hypertension, glaucoma. Nursing Implications: Administer at first sign of migraine. Avoid triggers. Monitor cardiac history. Endocrine Medications Pituitary Medications Somatropin (Humotrope) Mechanism of Action: Growth hormone replacement. Indications: Growth failure (hypopituitarism, HIV wasting). Adverse Effects: Hyperglycemia, hypothyroidism, injection site reactions. Nursing Implications: Monitor growth, motor skills, thyroid, and glucose levels. Rotate injection sites. Octreotide (Sandostatin) Mechanism of Action: GH antagonist. Indications: Acromegaly, GH-producing tumors. Adverse Effects: GI distress, glucose changes, cardiac conduction issues. Nursing Implications: Monitor glucose, EKG, growth. ADH Medications Vasopressin (Pitressin) & Desmopressin (DDAVP) Mechanism of Action: Mimics ADH. Indications: Vasopressin: Hypotension, hemorrhage. Desmopressin: Diabetes insipidus, bedwetting. Adverse Effects: Increased BP, headache, GI distress. Nursing Implications: Monitor VS, urine output, cardiac status. Thyroid Medications Levothyroxine (Synthroid) Mechanism of Action: Synthetic T4. Indications: Hypothyroidism. Adverse Effects: Hyperthyroid symptoms. Nursing Implications: Administer before breakfast on an empty stomach. Monitor thyroid labs (TSH, T3, T4). Avoid iodine-rich foods, iron/calcium supplements. Propylthiouracil (PTU) Mechanism of Action: Inhibits thyroid hormone production. Indications: Hyperthyroidism, thyroid storm. Adverse Effects: GI distress, bone marrow suppression. Nursing Implications: Monitor thyroid levels & CBC. Avoid iodine-rich foods. Radioactive Iodine (I-131) Mechanism of Action: Destroys thyroid tissue. Indications: Hyperthyroidism, thyroid cancer. Adverse Effects: Radiation sickness, Pregnancy Category X. Nursing Implications: Radiation precautions: Avoid close contact, use separate utensils, increase fluids. Adrenal Medications Glucocorticoids Hydrocortisone (Solu-Cortef), Prednisone (Deltasone), Dexamethasone (Decadron), Methylprednisolone (Solu-Medrol) Mechanism of Action: Anti-inflammatory, immunosuppressant. Indications: Adrenal insufficiency, inflammatory/autoimmune diseases. Adverse Effects: Metabolic: Hyperglycemia, weight gain, Cushing’s syndrome. Musculoskeletal: Osteoporosis, muscle wasting. CV: Hypertension, edema. Neuro: Mood swings, insomnia. Nursing Implications: Administer in the morning with food. Taper off slowly to prevent adrenal crisis. Monitor glucose levels with long-term use. Avoid sick contacts due to immune suppression. Mineralocorticoids Fludrocortisone (Florinef) Mechanism of Action: Mimics aldosterone (Na & water retention). Indications: Addison’s disease, adrenal insufficiency. Adverse Effects: Hypertension, hypokalemia, edema. Nursing Implications: Monitor BP, electrolytes (Na, K). Immunosuppressants Cyclosporine (Sandimmune), Tacrolimus (Prograf) Mechanism of Action: Suppresses immune response. Indications: Organ transplant, autoimmune diseases. Adverse Effects: Increased risk for infections, nephrotoxicity, diabetes. Nursing Implications: Strict dosing schedule (same time every day). Avoid grapefruit juice & styrofoam cups. No live vaccines (MMR, Varicella, Smallpox). Report any signs of infection immediately. Lifespan Considerations Pediatrics: Monitor growth in children using ADHD meds & growth hormones. Pregnancy: Avoid radioactive iodine (I-131) & immunosuppressants. Elderly: Caution with stimulants & corticosteroids (risk of cardiac issues, osteoporosis). Patient Teaching CNS Stimulants: Avoid abrupt withdrawal. Monitor growth (children). Thyroid Meds: Take levothyroxine on an empty stomach. Avoid iodine-rich foods if on PTU. Corticosteroids: Taper off gradually. Monitor glucose, avoid infections. Immunosuppressants: No live vaccines. Strict dosing schedule. Insulins Rapid-acting Insulins (Insulin lispro - Humalog, Insulin aspart - Novolog) Mechanism of Action: Fast-acting insulin that mimics natural insulin secretion in response to meals. Indications: Type 1 or Type 2 Diabetes. Adverse Effects: Hypoglycemia, weight gain, lipodystrophy at injection sites. Nursing Implications: Must eat a meal after injection. Administer subcutaneously (SQ) or via infusion pump. Clear, colorless solution. Short-acting Insulin (Regular insulin - Humulin R) Mechanism of Action: Provides short-term glucose control. Indications: Type 1 & Type 2 Diabetes. Adverse Effects: Hypoglycemia, weight gain. Nursing Implications: Onset: 30-60 min, Peak: 2.5 hr, Duration: 6-10 hr. Can be administered IV, IM, or SQ. Clear, colorless solution. Intermediate-acting Insulin (NPH - Isophane insulin suspension) Mechanism of Action: Delayed onset but prolonged glucose control. Indications: Often combined with regular insulin for Type 1 & Type 2 Diabetes. Adverse Effects: Hypoglycemia, weight gain. Nursing Implications: Onset: 1-2 hr, Peak: 4-8 hr, Duration: 10-18 hr. Cloudy suspension, administered SQ. Usually given twice daily before meals. Long-acting Insulins (Insulin glargine - Lantus, Insulin detemir - Levemir) Mechanism of Action: Provides basal insulin coverage with no peak effect. Indications: Type 1 & Type 2 Diabetes. Adverse Effects: Hypoglycemia (less risk), weight gain. Nursing Implications: Onset: 1-2 hr, No peak, Duration: 24 hr. DO NOT mix with other insulins. Clear, colorless solution. Oral Antidiabetics Biguanides (Metformin - Glucophage) Mechanism of Action: Decreases hepatic glucose production & increases insulin sensitivity. Indications: First-line treatment for Type 2 Diabetes. Adverse Effects: GI discomfort, diarrhea, metallic taste, reduced B12 levels. Black Box Warning: Risk of lactic acidosis (especially in renal failure). Nursing Implications: Administer 30 min before meals. Hold if contrast dye is used (renal failure risk). Sulfonylureas (Glipizide - Glucotrol) Mechanism of Action: Stimulates pancreatic insulin release. Indications: Type 2 Diabetes (early stages). Adverse Effects: Hypoglycemia, weight gain, nausea. Contraindications: Sulfa allergy. Nursing Implications: Give 30 min before meals. Monitor for hypoglycemia. Glinides (Repaglinide - Prandin) Mechanism of Action: Increases insulin secretion from beta cells. Indications: Type 2 Diabetes (postprandial glucose control). Adverse Effects: Hypoglycemia, weight gain. Black Box Warning: May exacerbate heart failure. Nursing Implications: Take with each meal, skip if meal is skipped. Glitazones (Pioglitazone - Actos) Mechanism of Action: Improves insulin sensitivity. Indications: Type 2 Diabetes (often combined with metformin or sulfonylureas). Adverse Effects: Fluid retention, weight gain, fractures. Black Box Warning: May exacerbate heart failure. Nursing Implications: Weigh daily. Monitor for heart failure signs. Alpha-glucosidase Inhibitors (Acarbose - Precose) Mechanism of Action: Delays carbohydrate absorption. Indications: Type 2 Diabetes (postprandial glucose control). Adverse Effects: GI issues (flatulence, diarrhea). Contraindications: GI disorders (IBD, malabsorption). Nursing Implications: Take with first bite of meal. DPP-4 Inhibitors (Gliptins) (Sitagliptin - Januvia) Mechanism of Action: Enhances incretin hormone function. Indications: Adjunct to diet/exercise in Type 2 Diabetes. Adverse Effects: URI, headache, diarrhea. Nursing Implications: Take once daily, with or without food. SGLT-2 Inhibitors (Canagliflozin - Invokana) Mechanism of Action: Inhibits glucose reabsorption in kidneys. Indications: Type 2 Diabetes (weight loss benefit). Adverse Effects: UTIs, yeast infections, dehydration, ketoacidosis. Nursing Implications: Take once daily before breakfast. Injectable Non-Insulin Medications Amylin Agonists (Pramlintide - Symlin) Mechanism of Action: Slows gastric emptying, suppresses glucagon. Indications: Type 1 & Type 2 Diabetes. Adverse Effects: Nausea, vomiting, anorexia. Contraindications: Gastroparesis. Nursing Implications: Inject before meals. Take at least 1 hr before oral meds. Incretin Mimetics (Exenatide - Byetta) Mechanism of Action: Enhances insulin secretion. Indications: Type 2 Diabetes (used when oral meds fail). Adverse Effects: GI symptoms, weight loss, thyroid tumors (Black Box Warning). Nursing Implications: Administer SQ 1 hr before meals. Glucose-Elevating Agents Glucagon Indications: Severe hypoglycemia. Adverse Effects: Vomiting (turn patient on side). Nursing Implications: Used when patient cannot take oral glucose. Dextrose 50% in Water (D50W) Indications: Emergency treatment of hypoglycemia. Nursing Implications: Administer IV. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) Salicylates (Aspirin - ASA) Mechanism of Action: COX-1 & COX-2 inhibitor, antiplatelet. Indications: Pain, fever, inflammation, CV prevention. Adverse Effects: GI bleeding, Reye’s syndrome in children. Nursing Implications: Do not give to children with viral infections. Acetic Acid Derivative (Ketorolac - Toradol) Indications: Short-term pain management (up to 5 days). Adverse Effects: Renal impairment, GI distress. COX-2 Inhibitor (Celecoxib - Celebrex) Indications: Osteoarthritis, rheumatoid arthritis. Adverse Effects: CV risk (Black Box Warning). Contraindications: Sulfa allergy. Propionic Acid Derivatives (Ibuprofen, Naproxen) Indications: Pain, inflammation, fever. Adverse Effects: GI distress, bleeding risk. Antigout Medications Allopurinol (Zyloprim) Mechanism of Action: Reduces uric acid production. Indications: Chronic gout prevention. Adverse Effects: Stevens-Johnson syndrome. Nursing Implications: Take with food. Colchicine (Colcrys) Mechanism of Action: Reduces inflammatory response. Indications: Acute gout attack. Adverse Effects: GI distress, bleeding risk. Nursing Implications: Hydration (3L/day). Immunizations Active Immunizing Drugs Mechanism of Action: Stimulate the immune system to produce antibodies against specific pathogens, offering long-term immunity. Indications: Prevention of infectious diseases. Adverse Effects: Common: Soreness, fever, mild rash. Severe: Fever >103°F, encephalitis, convulsions, anaphylaxis. Contraindications: Immunocompromised patients, pregnancy (some vaccines), active infections. Nursing Implications: Assess medical history, immune status, and pregnancy. Administer vaccines at appropriate sites: Infants: Mid-lateral thigh. Older children/adults: Deltoid muscle. Use warm compresses, Tylenol for mild reactions. Report severe reactions to VAERS (Vaccine Adverse Event Reporting System). Examples of Active Immunizations: Diphtheria, tetanus toxoids, acellular pertussis (DTaP, Td): Prevents diphtheria, tetanus, and pertussis. Haemophilus influenzae type B (Hib): Prevents bacterial infections, especially in children. Hepatitis B vaccine: Prevents Hep B infection. Influenza vaccine: Annual vaccine for flu prevention. Measles, mumps, rubella (MMR): Prevents viral infections. Pneumococcal vaccine: Protects against pneumococcal infections (pneumonia, meningitis). Poliovirus vaccine (IPV): Prevents poliomyelitis. Rabies vaccine: Given for rabies exposure or pre-exposure prophylaxis. Human papillomavirus (HPV - Gardasil): Prevents HPV-related cancers. Herpes zoster (Zostavax, Shingrix): Protects against shingles. Varicella vaccine: Prevents chickenpox. Passive Immunizing Drugs Mechanism of Action: Provides preformed antibodies for immediate protection; temporary immunity. Indications: Post-exposure prophylaxis in high-risk patients. Examples: Hepatitis B immunoglobulin: Post-exposure protection for Hepatitis B. Immunoglobulin: General immune support. Rabies immunoglobulin: Post-exposure prophylaxis after animal bites. Tetanus immunoglobulin: Used in unvaccinated individuals exposed to tetanus. Dermatologic Medications Antibacterials Bacitracin Mechanism of Action: Inhibits bacterial cell wall synthesis. Indications: Minor skin infections. Adverse Effects: Burning, itching. Neomycin & Polymyxin B (Neosporin) Mechanism of Action: Broad-spectrum antibacterial. Indications: Minor wounds. Adverse Effects: Local irritation. Mupirocin (Bactroban) Indications: Topical: Treats impetigo (Staphylococcus, Streptococcus infections). Intranasal: Used for MRSA colonization. Adverse Effects: Burning, itching. Silver Sulfadiazine (Silvadene) Mechanism of Action: Acts on bacterial cell wall. Indications: Burn treatment (prevention of infection). Adverse Effects: Pain, burning, contraindicated in sulfa allergy. Antiacne Medications Benzoyl Peroxide Mechanism of Action: Releases oxygen, killing acne bacteria. Indications: Mild to moderate acne. Adverse Effects: Red, peeling skin, warmth. Tretinoin (Retin-A) Mechanism of Action: Vitamin A derivative, stimulates cell turnover. Indications: Acne, UV damage. Adverse Effects: Skin peeling, severe sunburn risk (use sunscreen). Isotretinoin (Accutane) Mechanism of Action: Sebaceous gland suppression. Indications: Severe cystic acne. Adverse Effects: Teratogenic (Pregnancy Category X), liver toxicity, mood changes. Black Box Warning: IPLEDGE Program (2 contraceptive methods required). Antifungals Clotrimazole (Lotrimin) Mechanism of Action: Inhibits fungal growth. Indications: Athlete’s foot, ringworm, yeast infections. Adverse Effects: Local irritation. Miconazole (Monistat) Mechanism of Action: Antifungal, some Gram-positive action. Indications: Yeast infections, jock itch, athlete’s foot. Adverse Effects: Burning, itching, pelvic cramps. Antivirals Acyclovir (Zovirax) Mechanism of Action: Inhibits viral DNA replication. Indications: Herpes simplex (HSV-1 & HSV-2), shingles. Adverse Effects: Stinging, rash. Miscellaneous Dermatologics Permethrin (Elimite) Mechanism of Action: Neurotoxic to lice/scabies. Indications: Head lice, scabies. Adverse Effects: Itching, burning. Ophthalmic Medications Cholinergic Drugs (Miotics) Acetylcholine (Miochol-E) Indications: Induces miosis (pupil constriction) during surgery. Adverse Effects: Eye discomfort, blurred vision. Pilocarpine (Pilocar) Mechanism of Action: Stimulates cholinergic receptors, reduces intraocular pressure. Indications: Glaucoma, ocular surgery. Adverse Effects: Blurred vision, tearing, reduced night vision. Beta-Adrenergic Blockers Timolol (Timoptic) Mechanism of Action: Reduces aqueous humor production & increases outflow. Indications: Glaucoma, ocular hypertension. Adverse Effects: Eye irritation, systemic effects possible (bradycardia, hypotension). Otic Medications Ofloxacin (Floxin Otic) Mechanism of Action: Fluoroquinolone antibiotic (bacterial DNA disruption). Indications: Otitis externa & media. Adverse Effects: Mild itching/pain. Carbamide Peroxide (Debrox) Mechanism of Action: Softens & breaks down earwax. Indications: Earwax removal. Adverse Effects: Ear irritation. Nursing Considerations Lifespan Considerations Pediatrics: Infants: Thigh for vaccines, avoid aspirin (Reye’s syndrome risk). Monitor growth with long-term corticosteroids. Pregnancy: Avoid live vaccines (MMR, varicella, HPV, Zoster). Avoid isotretinoin (teratogenic). Elderly: Caution with ophthalmic beta-blockers (can cause systemic effects). Monitor renal function with fluoroquinolones (ototoxicity risk). Patient Teaching Vaccines: Keep records, report reactions. Use Tylenol, not aspirin for fever. Dermatologics: Apply with gloves, wash hands before & after. Sunscreen required with tretinoin & isotretinoin. Ophthalmic/Otic: Apply pressure to inner canthus after eye drops (reduce systemic absorption). Hold ear up & back (adults), down & back (children) for otic drops

„ 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

Day 2 Innervation and Bronchial Constriction

URETERIC CONSTRICTIONS (2)

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

Physiology Exam 3 Constriction vs. Dilation

chemical mediators that control constriction/dilation

infinitive constriction de/à/rien