Essay Questions Final A&P II

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Discuss the following disease, disorders, or life treating injuries. Be sure to include hallmark signs, landmarks and symptoms that patients may exhibit: 1. Chronic Obstruction Pulmonary Diseases (COPD) (emphysema, chronic bronchitis, and asthma) 2. Pneumothorax 3. Tension Pneumothroax 4. Congestive Heart Failure (CHF) 5. Right and Left ARDS 6. Hypoxia drive/hypoxia drive with COPD
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1. Chronic Obstruction Pulmonary Disease (COPD)- gas exchange obstruction Emphysema- Irreversible, destruction of alveoli in lungs, permanent damage, difficulty exhaling. Indication: \”pink puffer\” face red difficulty catching breath. gasping. smokers. Chronic Bronchitis- infection, inflammation leaves scarring of bronchi. Heavy mucus, bacterial infection, deeper breaths. Indication: Blue bloaters, bark sound when coughing. Asthma- Bronchial walls inflammed. Smooth muscles constricted. Excess mucus, wheezing (stridor) getting air out is problem. Massive mucus can turn to CF (cystic fibrosis. Trtment: vest to break up mucus)sitting in tripod position (leaning forward in chair). Nurse has to zip through posterior of lungs- dead space (may have fluid). With all the above smooth muscle is constricted. 2. Pneumothorax- Bullet wound 760mm/Hg Atmospheric pressure = intrapleural pressure. Increasing intrapleural pressure usually at 758mm/Hg. This results in increased lung capacity, increased volume of lungs collapsing ONE of the lungs (atelectasis).Pressure comes inside separating the visceral and parietal pleura. Treatment: (1) Impermeable bandage taped on 3 sides (2) Chest tube (3) Applying suction. 3.Tension Pneumothorax is fatal and occurs when pneumothorax is untreated. The equalization of pressure between interpleural and atmospheric pressure starts to affect the uninjured lung collapsing it. No escape of the pressure causing both (TWO) lungs to collapse. Treatment: needle decompresssion Symptoms: JVD (jugular vein distention), tracheal displacement (agitation, shock, sinosus, blue lip/palms no oxygen) cold, clamey and sweaty \”sense of doom\”. 4. Congested Heart Failure (CHF) – L sided: Pink frothy sputum, crackles/wheezes, confusion/restlessness R sided: JVD (jugular vein distention) , dependent edema, swollen hands and fingers 5. ARDS- Acute respiratory distress syndrome • special form of atelectasis, alveoli collapse • inflammation in lungs • can be triggered by respiratory infection (pneumonia) • more often due to sepsis or physical trauma. Treatment: mechanical ventilation 6. Hypoxia drive/hypoxia drive with COPD- • Hypoxia a form of respiratory drive oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle. • Hypoxic drive is REVERSED in COPD patient • COPD patients have increase levels of CO2 (compensated over yrs.) • 3-7L of O2 vs. the normal 12-15L of O2.
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Diabetes (pancreas) Essay
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Mechanism No insulin = no key = no sugar in cell WHERE IT FAILS: IDDM (Insulin Dependent Diabetes Mellitus) •Type 1, Juvenile, diabetic •Autoimmune disease, beta cells destroyed, •artenosclerosis (kidney disease). Treatment: Insulin NIDDM (Non-insulin Dependent Diabetes Mellitus) •Type 2, non diabetic, No insulin •90-95% of all diabetic patients •age 30-40’s • normally obese; gradually occurs no symptoms at first Treatment: Glucose fasting test, diet, exercise DKA (Diabetic Ketone Acidosis) • Diabetic Type 1 • Use fat route to make ATP • Ketones are by-product (dehydrated hypertonic cells) • Blood sugar very high > Carbonic acid produced Co2 + H2O > patient’s blood 650 usually around 1000 mg/dL Treatment: Massive IV solution to hydrate. insulin administration may be needed. Meatabolic Syndrome (risk for heart attack, stroke) Female •Waist size >35 in • Fail glucose fasting test • high blood pressure • high cholesterol PANCREAS MECHANISM Too High • Ate French Fries • Stimulus: Increase Blood Glucose • Receptors: Beta cells detect increase in blood glucose •Control Center: From pancreas, Beta cells release insulin (hormone) to put sugar into cell [ATP] •Effectors: Insulin (a) promotes movement of glucose into certain cells (b) produces glycogen (fat) from glucose. excess sugar goes to Liver and glycogen (fat). •Response: Desired SETPOINT, decrease in blood glucose, inhibit of insulin secretion 71-120mg/dL Too Low •Hungry (altered mental status) •Stimulus: Decrease in blood glucose •Receptor: Alpha cells detect decrease in blood glucose •Control Center: From pancreas alpha cells release glucagon (hormone) •Effectors: Glucagon (a) breaksdown glycogen to glucose (b) converts noncarbs to glucogen (protein) •Response: Desired SETPOINT, increase in blood glucose, inhibit of glucagon secretion, sugar enters the cell (ATP) WORKS The body continues to find homostasis (balance). Negative feedback is caused by the hypothalamus to keep body in balance.
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Describe how Cardiac stretch reflexes, brain functions. Membrane potential, cardiac conduction, EKG’s, and muscle contraction work collectively. Once you have completed this discussion explain how ION(S) IMBALANCES may alter the normal contractions and impulses of the heart.
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1. Baroreceptors- sense changes in BP/BV • \”stretch receptors\” • VASOconstrict / VASOdialate 2. Baroreceptors send impulses to Medulla Oblingata • Cardiac accelerator (speeds up) • Vagus Nerve (slows down) 3. Membrane potential occurs • Depolarization : (-70mv to 0mv) site for stimulus; Na+ and K+ ions exchange around membrane • Repolarizating: Ions return to normal position around membrane. Measured by decrease 4. Contraction: Fibrin composed of troponin, tropomyosin, myosin, and actin. Calcium makes stronger heartbeat. • Troponin and Tropomyosin move change shape > expose binding • crossbridge forms- ATP > ADP (loses phosphate) this moves to next site. • regenerate ATP by: Cellular respiration, creatine phosphate 5. EKG/ECG • SA node (70-80 BPM) • AV node (40-60 BPM) • AV Bundle ] 15-40 BPM • Purkinje fibers ] 15-40 BPM 6. Cardiac conduction system: • P-wave: depolarization of atria, site for stimulus • QRS:depolarization of ventricles • T-wave: repolarization of ventricles 7. Ions alter stimulate changes in cardiac conduction system ↑ K+ = Cardiac Arrest (Hyperkalcemia) ↓K+ = Abnormal rhythm (Hypokalcemia) ↑Ca+ = extended contraction (Hypercalcemia) ↓Ca+ = depression heart action (Hypocalcemia)
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Renin Angiotensin Aldosteron System Steps (RAA) Low BP
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• ↓BP ↓BV • Kidney (stimulus) • (RAAS) Liver produces angiotensinogen converts to angiotensin I which occurs through action of renin enzyme released from kidney due to ↓ fluid volume • Angiotensin I converts to Angiotensin II by ACE enzyme which comes from the lungs • Angiotensin II acts on the adrenal cortex causing a release of aldosterone (steroid hormone) which causes nephron to retain water and sodium •results in ↑BV ↑BP Drugs: •Ace Inhibitors •Beta Blockers •Calcium Channel Blockers •Diuretic Risk Factors: •Alcohol/ smoking •High Cholesterol •Obesity •Genetics

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