Summary

This document provides a review of the endocrine system, focusing on hypothyroidism and hyperthyroidism. It details causes, symptoms, diagnosis, and treatment for these conditions.

Full Transcript

Patho Exam 2 review: ENDOCRINE SYSTEM: 1. Know what HGA1C reflects: Normal levels are 6.5%) Glucose is attached to hemoglobin molecules for approx. 120 days (2-3 months) Reflects your average BS levels, diabetes dx & monitoring, risk of comp...

Patho Exam 2 review: ENDOCRINE SYSTEM: 1. Know what HGA1C reflects: Normal levels are 6.5%) Glucose is attached to hemoglobin molecules for approx. 120 days (2-3 months) Reflects your average BS levels, diabetes dx & monitoring, risk of complications and individual treatment goals Hypothyroidism Hyperthyroidism Thyroid gland itself produces low amounts Excessive production of thyroid hormones of T4 & T3, & increased TSH by the thyroid gland; low TSH and high T3 & T4 Causes: Causes: Hashimoto’s disease Grave’s disease Iodine definecy Thyroid nodules Thyroid surgery or radioactive iodine Thyroiditis tx Excessive iodine intake Medications Medications S/S: S/S: Fatigue & weakness Weight loss (increased metabolism) Weight gain High HR Cold intolerance Heat intolerance and excessive Depression sweating Dry skin, hair loss, brittle hair Anxiety Goiter Tremors Constipation Diarhea Slow HR Sleep disturbances myxedema Hair thinning Exopthalmous “buldging eyes” diplopia Dx: Dx: Measuring the TSH AND T3 &T4 Measuring the TSH AND T3 &T4 Levels; Levels; note: High TSH and low T3 note: High T3 & T4 and low TSH = & T4= “hypothyroidism” “hyperthyroidism” Tx- life-long Synthroid (levothyroxine) Tx- Methimazole or PTU (give PTU 1st trimester of pregnancy) Radioactive iodine therapy Thyroidectomy Pathophysiology of primary hypothyroidism Primary hypothyroidism - The thyroid gland “itself” is unable to produce sufficient amounts of T3 & T4; which leads to increasing levels of TSH as the pituitary gland attempts to compensate for low hormone levels Can be caused from: - Hashimoto’s thyroiditis- autoimmune disease - Iodine defienency- not enough iodine, which is essential for the production of thyroid hormones - Surgical removal- WILL NEED LIFE-LONG THERAPY (levothyroxine (Synthroid)) - Radioactive iodine therapy - Medications S/S: Cold intolerance Decreased sweating Depression/irritability Slow HR Weight gain Constipation Irregular & heavy periods Brittle nails, puffy face, goiter Muscle or joint pain Myxedema 2. Somatopause Age related decline of the GH levels & it effects on the body esp in adults Typically begins in middle age & continues to progress as individuals grow older GH decline- affects the body’s composition, physical capabilities, and metabolism Increase in body fat & decrease in lean muscle mass More challenging to lose weight d/t decrease in metabolism; may end up being a type 2 dm d/t insulin resistance Decrease in bone health, increase risk of osteoporosis & fx Reduced energy levels and increased fatigue 3. Effects of aging on pancreas: Impaired glucose intolerance and diabetes Pancreatic cells replaced with fat Decreased insulin secretion of the beta cells and insulin receptors (increases insulin resistance) 4. Function of amylin Co-secreted with insulin from the beta cells of the islets of Langerhans in the pancreas Helps to regulate BS by delaying gastric emptying and suppressing glucagon after meals; has a satiety effect 5. Beta cells (Insulin & Amylin) Secreted from the beta cells of the islets of Langerhans in the pancreas Amylin- Helps to regulate BS by delaying gastric emptying and suppressing glucagon after meals; has a satiety effect Insulin- secreted to help promote increased BS levels; has sensitivity of the insulin receptor; facilitates the transport of K+ 6. Glp1 and glucose dependent polypeptide The incretin hormones are GLP-1 & GIP that plays an important role postprandial insulin secretion and glucose homeostasis Control the postprandial glucose levels by: ** promoting the glucose-dependent insulin secretion- enhance insulin secretion from the pancreas when BS levels are elevated Inhibiting glucagon synthesis Promoting hepatic glucose secretion Delaying gastric emptying – promote fullness and helps prevent rapid spikes in BS after eating 7. Oxytocin function Causes uterine contractions and milk ejection in lactating women; acts on the uterus to stimulate contractions 8. Function of hypothalamus, especially what hormones are produced here Hypothalamus: Important role in homeostasis and bridges the nervous & endocrine system Primary functions are regulating the body’s temp, hunger, thirst, sleep-wake cycles, and circadian rhythms. Hormones are: Thytropin- releasing hormone (TRH)- stimulates the releases of TSH Gonadotropin-releasing hormone (GnRH)- promotes the release of LH and FSH; reproductive hormones Corticotropin-releasing hormone (CRH)- stimulates the ACTH which influences the body’s stress response and adrenal function Growth hormone-releasing hormone (GHRH)- encourage the GH, impacts growth and metabolism Somatostatin- inhibits release of growth hormone, helps to regulate growth and metabolic functions Oxytocin- key role in childbirth and lactation, social bonding Antidiuretic hormone (ADH)- vasopressin; regulates the water balance in the body by controlling the amount of water excreted by the kidneys 9. Parathyroid hormone regulates serum what? Regulates serum calcium & calcium concentration; decreases the phosphate level Serves as a co-factor with Vitamin D to increase calcium absorption 10. What are the effects of renin-angiotensin system on the body RAAS (renin-angiotensin-aldosterone system) RAAS Activated when the BP drops, low blood flow to the kidneys and low NA+ concentrations - Renin is releases- renin acts on angiotensin>changes into angiotensin I>angiotensin I turns into angiotensin II by an ACE enzyme>angiotensin II increases BP, releases aldosterone (reabsorbs Na+, excrete K+ and increases blood volume), and releases ADH (reabsorb water & increases blood volume & BP) Effects the body by: BP regulation Release aldosterone Potassium excretion Stimulate thirst Impacts kidneys If dysfunction happens: TN, HF, and chronic kidney disease Overactivity of the RAAS system causes fluid overload, high BP, while underactivity may lead to low BP and fluid retention 11. Facts about Insulin; function; where does it come from? Plays a key role in metabolism and BS levels Produced in the pancreas in the islets of Langerhans – beta cells ALONG WITH AMYLIN Function- lower BS levels After eating, BS levels are normally rise, and pancreas release insulin to prevent excessively high BS levels Aids in the storage of nutrients by converting excessive glucose into glycogen in the liver and muscles Stores fatty acids in adipose tissue Encourages the metabolism of fats & proteins Type 1 diabetics: body doesn’t produce enough insulin due to autoimmune destruction of the beta cells; THEY WILL NEED LIFELONG INSULIN Type 2 diabetics- insulin receptors become resistant, which leads to elevated BS levels; encourage to control diet, exercise; may need oral hyperglycemics and/or insulin 12. Glucagon; function; etc Insulin antagonist Secreted from the alpha cells in the pancreas compared to insulin and amylin being secreted from the beta cells It is secreted when BS levels are low It stimulates lipolysis (breakdown stored fat), glycogenolysis (breakdown of glycogen into glucose, so glucose can be released into the bloodstream), gluconeogenesis (synthesis of glucose from amino acids) PULMONLOGY SYSTEM 13. Clinical manifestation of asthma Asthma: bronchial hyperresponsiveness, constriction of airways, & variable airflow obstruction that is reversible Episodic attacks of bronchospasms, bronchial inflammation, mucosal edema, and increased mucous production Early response: Vasodilation Increased cap. Permeability Mucosal edema Bronchospasm Mucous secretion Late response: Begins 4-8 hours after early response Causes airway scarring, increased bronchial hyperresponsiveness, impaired mucociliary function w/ clogged airways Difficulty moving air in & out s/s: Chest constriction Expiratory wheezing Sob Nonproductive coughing Prolonged expiration Tachycardia Tachypnea Pulsus pradoxus (a drop in BP when inhaling) 14. Order of oxygenation to the cells (4 steps); ventilation, perfusion, diffusion Ventilation- movement of air into and out of the lungs; not the same as respirations Diffusion- Movement of gases between air spaces in the lungs & blood stream; ventilation and perfusion are both pulmonary processes Perfusion- movement of blood into & out of the capillary beds of the lungs into the body organs and tissues; cardiovascular process 15. Clinical manifestation on copd; risk factors, exacerbation, what will you typically see; what is the result of copd COPD- progressive resp condition characterized by airflow limitation and breathing difficulties; chronic bronchitis and emphysema Can lead to acute exacerbations s/s: Increased sob Increased cough (chronic bronchitis) Purulent sputum changes Wheezing Chest tightness Fatigue Tachycardia Risk factors: Smoking Air pollution Resp infections Physical inactivity Allergies Comorbidities Copd patients will appear: Cyanotic Barrell chest – hyperinflation of the lungs Pursed-lip breathing Increased accessory muscle use Thing appearance Results of copd: Chronic resp symptoms; chronic cough and sputum production Progressive decline in lung function Frequent exacerbations Potential for resp failure 16. Know what anatomy the gas exchange airway includes Gas Exchange Airway: Nasal cavity- air enters thru the nostrils into the nasal cavity; where it is warmed, humified, and filtered Larynx- voice box- serves as a pathway for air to enter the trachea while preventing food & liquids from entering the airway Trachea- breaks into right and left main bronchi; breaks into small bronchi Terminal bronchioles Resp bronchioles- first site of gas exchange Alveoli- small sacs where gas exchange happens; each are line with surfactant- producing cells, which reduces surface tension; this is where oxygen enters the blood and carbon dioxide is removed 17. Function of the goblet and cilia Goblet cells: produce mucus Cilia: are hairlike structures Both propel foreign material upward to be able to be coughed up and out the body 18. Familiar what lung compliance (all the following are true except) Lung compliance measures the lung and chest wall distensibility; how well it can expand; it represents the relative ease with structures that can be stretched Low compliance: increased work of inspiration (inhaling) Reduced ability of the lungs to expand and stretch during inhalation Stiff lungs; ie. Pneumonia; any increased work of breathing; pulmonary fibrosis; acute resp syndrome High compliance: increased work of expiration (exhaling) Easy to inflate/lungs expand easily, but has lost some elastic recoil; ex. Experiencing constant sob, copd, d/t aging What objective finding will you find in severe dyspnea If someone is having severe dyspnea, they will have: Flaring of the nostrils Using of accessory muscles of respiration Retraction of the intercostal spaces 19. Early asthma response vs a late response; know early response 20. Function of surfactant Surfactant works to keep the alveoli open & free of fluid and pathogens (collectins); prevents the alveoli from collapsing during exhalation by lowering the surface tension 21. Familiar with alveoli; anatomy & physiology; know what it does so you know what it doesn't do Alveoli are tiny-sac structures that are in the lungs where gas exchange occurs - The process is where oxygen and carbon dioxide are exchanged between the air in the lungs & the blood in the surrounding capillaries Gas exchange occurs thru diffusion: Oxygen from the air within the alveoli diffuses across the alveolar wall into the capillary blood, while carbon dioxide from the blood diffuses into the alveoli to be exhaled 22. Know definition of orthopnea: Dyspnea when lying down; sob while lying on your back, esp when sleeping CARDIOLOGY: 23. Chambers of heart regarding pressure systems; high vs low pressure Right-sided heart chamber: Pumps blood through the lungs & out the body via the pulmonary circulation Delivers blood to the lungs for oxygenation LOW PRESSURE SYSTEM Left-sided heart chamber: Pumps oxygenated blood through the systemic circulation Delivers metabolic waste products to the lungs, kidneys, and liver HIGH PRESSURE SYSTEM, to ensure adequate blood flow throughout the body 24. Heart failure typically a complication of: Heart failure occurs when the heart is unable to pump sufficient blood to meet the body’s needs or when it fails to fill adequately Caused by: CAD HTN MI Cardiomyopathy Heart valve disease Arrythmias Diabetes Obesity Chronic lung disease Thyroid disorders LEFT SIDED HEART FAILURE RIGHT SIDED HEART FAILURE Left ventricle is unable to pump Right ventricle fails to effectively pump blood into the body; leads up to a blood into the lungs; buildup of pressure in buildup in the left atrium and lungs the systemic venous system Causes: Causes: CAD Left-sided heart failure MI Chronic lung failure HTN Tricuspid valve disease or Heart valve disease pulmonary valve disorders Cardiomyopathy Pulmonary HTN s/s: S/S: Sob; esp. Orthopnea Peripheral edema Coughing or wheezing with frothy Ascites sputum Increased jugular vein distention Tachypnea Fatigue Fatigue Nausea Decreased activity tolerance Pulmonary edema Again- primarily affects the lung d/t Again- primary leads to systemic pulmonary congestion and resp congestion, causing fluid buildup in the symptoms & ineffective pumping of body, in the legs and abdomen blood into the systemic circulation 25. What happens in overactivity of sympathetic nervous system and the RAAS system results in this Sympathetic nervous system is activated when the cardiac output is reduced & BP, aiming to maintain blood flow to vital organs & preserve bp Overactivity of the sympathetic nervous system can lead to: Increased hr & contractility - can lead to myocardial ischemia Vasoconstriction- increases systemic vascular resistance, which adds a strain on the heart Arrythmias- chronic releases of norepinephrine which leads to arrhythmias Myocardial remodeling- hypertrophy and fibrosis Overactivity of the sympathetic nervous system and the RAAS can significantly worsen heart failure thru increased cardiac workload, fluid retention, vasoconstriction, and myocardial remodeling. 26. Pathophysiology of Heart Failure Hf is a complex heart disease that arises when the heart is unable to pump suffiecently to maintain an adequate blood supply to meet the body’s need. Systolic dysfunction- involves impaired contractility of the heart muscles, often d/t ischemic heart disease, which leads to reduced ejection fraction Diastolic dysfunction- inability for the heart to fill during diastole which leads to stiffness or hypertrophy of the heart (thickening of the heart muscle); preserved ejection fraction 27. Common tests of the heart; what are we looking at for ekg, mri, echo, stress test Ekg- electrical activity of the heart that can provide insight on: HR (afib, sb) Conduction abnormalities (right bundle branch block) Hypertrophy Ischemic changes (ST-segments changes, T-wave inversions) Chamber enlargement MRI- details the heart structures and functions Heart structure (size, shape, and thickness of the heart’s chambers) Scar and ischemia- previous infractions Echo- non-invasive ultrasound test that evaluates the cardaic structure and function EF measurement Valvular function Chamber size & function Diastolic function Pericardial effusion Stress test- examines how the heart responds to increased workload, performed thru exercise and medications Exercise tolerance; checking your HR, BP, ischemic changes, and echo responses Catherization with angiography- heart cath; invasive procedure of fluoroscopy that visualizes the coronary arteries 28. Be familiar with the baroreceptor reflex, frank staring law, Bainbridge reflex (define) Baroreceptor reflex- when the BP falls, the HR increases and arterioles constrict; ie. When you have dysfunctional baroreceptor reflex, you deal with orthostatic hypotension Bainbridge reflex- changes in HR from IV infusions; response that regulates HR in response to changes in blood volume returning to the heart; ie. Exercise, fluid infusions and changes in posture; hr increases in response to increased venous return Frank staring law: the greater the stretch of the cardiac muscle fibers (preload), the greater the force of contraction during systole; regulates cardaic output, ensuring it matches the venous return 29. Flow of blood thru (oxygenated, deoxygenated) Flow of deoxygenated blood: Body>SVC & IVC>Right atrium>tricuspid valve>right ventricle>pulmonary valve>pulmonary arteries>out thru the lungs Right side of the heart is low pressure system bc it goes out thru the lungs Flow of oxygenated blood: Lungs>pulmonary veins>left atrium>mitral valve>left ventricle>aortic valve>aorta>body tissue to deliver oxygen Left side of the heart, high pressure system bc it is going into the body tissues 30. Arteries and veins Arteries- carry oxygenated blood away from the heart; moves oxygen-rich blood under the high pressure from the heart to the tissues; A= away Veins- return deoxygenated blood to the heart; returns oxygen-poor blood at lower pressure back to the heart; V=” vroom vroom to the heart” 31. Right heart function Right heart function- manages deoxygenated blood from the body to the lungs Flow of deoxygenated blood: Body>SVC & IVC>Right atrium>tricuspid valve>right ventricle>pulmonary valve>pulmonary arteries>out thru the lungs Right side of the heart is low pressure system bc it goes out thru the lungs Ejection fraction- is the amount of blood being ejected per beat Indicator of the ventricular function Normal EF for women 66% and 58% for men Normal ef is 55-70% 32. Beta 1 and beta 2 cells; Stimulation of beta 1 & beta 2 does what (positive and negative terms) Stimulation of both B1 AND B2 cells: increases the HR (cHRonotropy) and force of heart contractility (iONtropy); heart pumps more blood; B2 stimulation increasing the coronary blood flow IF THE HR IS AFFCTED, IT IS CALLED CHRONTROPHY - NEGATIVE CHRONTROPHY- decrease HR - POSITIVE CHRONTROPHY- increased HR IF THE HEART CONTRACTION IS AFFECTED, IT IS CALLED IONTROPHY - NEGATIVE IONTROPHY- decrease force of contraction - POSITIVE CHRONTROPHY- increase force of contraction 33. Purkinje fibers Conducting fibers with excitability cells that directly delivers action potential from the AV node thru the bundle branches to the ventricular myocardium 34. Function of epi & norepinephrine Both give off the fight & flight response which prepares our body to respond; they both have positive inotropy (increase force of contraction) Epinephrine- ^ HR, bronchodilation, boosts BS and enhance alertness Norepinephrine- vasoconstriction, ^BP, ^HR 35. Alteration of aging in the cardiovascular system HF Valve changes Fibrosis ^ risk of arrythmias Slowed conduction Arterial stiffness atherosclerosis Impaired baroreceptor reflexes – leads to orthostatic hypotension GI SYSTEM 1. Cholelithiasis: Due to gallstone formation; cholesterol stone formation in the bile that is subsaturated by cholesterol Decreased secretion of bile acids, decreased resorption of bile salts, hypomotility of gallbladder smooth muscle, genetics s/s: Epigastric and right hypochondrium pain Intolerance to fatty foods Biliary colic, which can cause jaundice if a stone gets lodged in the common bile duct 2. Function of hydrochloric acid Same as gastric acid; essential for food breakdown/digestion, activates the enzyme pepsinogen into pepsin which is responsible for protein digestion 3. Function of pepsin The enzyme pepsinogen turns into pepsin based on the acidic environment & pepsin works to breakdown proteins into smaller pieces in the stomach; it is inactivated in an alkaline environment in the duodenum; strongest stimulation is acetylcholine 36. What do stomach secretions include? Hydrochloric acid ~ gastric acid Pepsinogen Hormones- gastrin; released in the presence of food, stimulates the secretion of gastric acid to help with the digestion of food Mucus – protective barrier; helps to prevent acid and enzymes form damaging the stomach lining Intrinsic factor- helps the intestine absorb vitamin b12 Gastroferrin- helps Facilite small intestine absorption of iron Electrolytes: Na+, K+, and chloride 37. Define peristalsis: Wave-like muscle contraction that occurs in the digestive tract, esophagus, stomach, and intestines; it helps to propel food and liquids down the gastrointestinal tract; essential for moving food from the mouth to the digestive system to the rectum 38. Define Peptic ulcer disease and its contributing factors; what is the pathology? Formation of ulcers in the lining of the stomach (gastric ulcers) or in the first part of the small intestine (duodenal ulcers) Contributing factors can be: - Increased acid production- stress, NSAIDS, smoking, alcohol, food such as high caffeinated drinks and spicy foods - Mucosal injury- protective mucosal lining can be compromised; ie. NSAIDs can lead to mucosal damage and increase chances of ulcers - H. Pylori infection- risk factor for peptic ulcers; it can lead to chronic inflammation (chronic gastritis) - Impaired mucosal defense- prolonged NSAIDs usage, excessive alcohol consumption, and smoking - Chronic stress - High Gastrin levels - Rapid gastric emptying - Genetic factors- family of PUD can make a genetic predisposition to developing ulcers Duodenal ulcers- most common; Chronic pain in the epigastric area pain lasting 30 minutes-2 hours after eating pain relieved by food and antacids Gastric Ulcers: Pain increased by meal not common vomiting occurs Caused by H.Pylori Happens 30 minutes-1hour after a meal 39. Function of the small intestine; what happens in the small intestine Responsible for the majority of nutrient absorption Digestion begins in the duodenum where chyme mixes with bile from the liver and the mixture aids in the breakdown of fats, proteins and carbs 40. What are the 3 phases of gastric secretions; what happens in each phase and an example of each gastric phase: Cephalic: 1st phase; sight, smell, taste or the thought of food; before food is consumed; stimulate the vagus nerve which leads to secretion of gastric juices before food enters the stomach; ie. Example is when you smell your favorite food Gastric- when the food enters the stomach; the presence of food stimulates the stretch receptors leading to the release of gastric secretions (hydrochloric acid and pepsinogen); ie. Secretion of gastric acid in response to distention of food in the stomach Intestinal: when chyme enters the small intestine; inhibiting gastric secretion and motility allowing for proper digestion and absorption in the intestine; hormones such as secretin and CCK are released in response to the presence of chyme; ie. Release of cck in response to fatty acids in the small intestine, which helps regulates gastric emptying 41. Alteration of aging on the GI System Decrease in the production of digestive enzymes- lead to slower digestion and may cause bloating, gas, and discomfort Constipation d/t decrease peristalsis IBS Decreased stomach acid, which affects vitamin B12, calcium, and iron Changes in gut motility, GERD, Diverticulosis

Use Quizgecko on...
Browser
Browser