MARYVILLE PATHO 611 EXAM 1 QUESTIONS WITH COMPLETE SOLUTIONS 2022

MARYVILLE PATHO 611 EXAM 1 QUESTIONS WITH COMPLETE SOLUTIONS 2022Describe the characteristics of apoptosis. A programmed cell death that is regulated or programmed. Necrosis: characterized by rapid loss of the plasma membrane structure, organelle swelling, mitochondrial dysfunction. Hypoxia is the #1 major cause of cellular injury leading to necrosis especially to the kidneys and heart. (Myocardial infarction) Page 52: What's new: Current research supports that after muscle heart injury that stem cells exist in the heart and differentiate into various cardiac cell lineages and is profoundly changing the understanding of myocardial biology!! Cellular adaptation: Atrophy Physiologic: thymus gland atrophy (childhood) Cellular adaptation: Hypertrophy Increase in size of cell Another cellular adaptation that can actually be beneficial is hypertrophy of myocardial cells such as an endurance training-this is referred to as physiologic hypertrophy. Versus pathologic hypertrophy that occurs secondary to HTN. Cellular adaptation: Hyperplasia Increase in number of cells Compensatory: removal of 70% off liver-can regenerate in about 2 weeks. Pathologic: endometrial hyperplasia Cellular adaptation: Metaplasia Replacement of cells Normal columnar ciliated epithelial cells of the bronchial lining have been replaced by stratified squamous epithelial cells. Can be reversed if irritant is stopped. Cellular metabolism: During ischemia, what effect does the loss of the adenosine triphosphate (ATP) level have on cells? ATP = energy BUT needs oxygen - aerobic metabolism A reduction in ATP levels causes the plasma membrane's sodium-phosphate (Na+, K+) pump and sodium-calcium exchange to fail, which leads to an intracellular accumulation of sodium and calcium and diffusion of potassium out of the cell. (The Na+, K+ pump is discussed in chapter one). Sodium and water then can enter the cell freely, and cellular swelling results. Anaerobic metabolism (glycolysis) Results when oxygen reserves are depleted. Free radicals play a major role in the initiation and progression of which diseases? A free radical is an electrically uncharged atom or group of atoms having an unpaired electron. Having one unpaired electron makes the molecule unstable; thus to stabilize, it gives up an electron to another molecule or steals one. Therefore, it is capable of injurious chemical bond formation with proteins, lipids, carbohydrates—key molecules in membranes and nucleic acids. Cardiovascular, HTN, IHD. Emerging data indicate that reactive oxygen species play major roles in the initiation and progression of cardiovascular alterations associated with hyperlipidemia, diabetes mellitus, hypertension, ischemic heart disease, and chronic heart failure. Cellular injury: What is a consequence of leakage of lysosomes during chemical injury? Lysosomes: Enzymatic digestion of cellular organelles, including the nucleus and nucleolus, ensues, halting synthesis of DNA and ribonucleic acid (RNA). Fatty Liver Ethanol: Liver enzymes metabolize ethanol to acetaldehyde which causes hepatic cellular dysfunction. Peroxisomes helps detoxify ethanol - if not functioning properly the ethanol is turned to Fat in the liver Deoxyribonucleic acid (DNA) The cell component most vulnerable to the target of radiation. Aging and the cell/tissues: Every physiologic process can be shown to function less efficiently. Muscular atrophy (Sarcopenia) o "Stiffness" or "rigidity" of systems: Peripheral vascular resistance increases. Decreased production of HCL and delayed emptying of stomach. Decreased immune response F & E: Total body potassium concentration also decreases because of decreased cellular mass. An increased sodium/potassium ratio suggests that the decreased cellular mass is accompanied by an increased extracellular compartment. Indications of dehydration Marked water deficit is manifested by S & S of dehydration: headache, thirst, dry skin and mucous membranes, elevated temperature, weight loss, and decreased or concentrated urine. Skin turgor may be normal or decreased. Symptoms/signs of hypovolemia, including tachycardia, weak pulses, dizziness and postural hypotension, may be present. Thirst: Osmoreceptors are activated by an increase in osmotic pressure of the plasma Vulnerable populations to FVD: --Infants: 75-80% TBW --Obese: fat is water repelling --Older: thirst sensation is diminished At the arterial end of capillaries, fluid moves from the intravascular space into the interstitial space because the [fill in the blank]: ...capillary hydrostatic pressure (influenced by the Cardiac system) is higher than the capillary oncotic pressure. Oncotic pressure Heavily influenced by plasma proteins. Low plasma albumin ______ causes edema as a result of a reduction in plasma oncotic pressure. Natriuretic peptides They decrease blood pressure and increase sodium and water retention. Natriuretic peptides are hormones that include atrial natriuretic peptide (ANP) produced by the myocardial atria, brain natriuretic peptide (BNP) produced by the myocardial ventricles, and urodilatin within the kidney. Natriuretic peptides decrease blood pressure and increase sodium and water excretion. (ANTAGONIST OF THE RAAS) RAAS - Renin angiotensin-aldosterone system When circulating blood volume or blood pressure is reduced, renin, an enzyme secreted by the juxtaglomerular cells of the kidney, is released in response to sympathetic nerve stimulation and decreased perfusion of the renal vasculature. Increase in plasma osmolarity ADH: Secretion of antidiuretic hormone (ADH) and the perception of thirst are stimulated by an increase in __________ What does Na+ do? Regulator of fluids; maintenance of neuromuscular irritability for conduction of nerve impulses (134-145) Clinical manifestations of severe hypernatremia confusion, convulsions, cerebral hemorrhage, and comma Water is drawn from the intracellular space to the extravascular space in an effort to restore fluid balance. BRAIN: The high sodium in the blood vessels pulls water out of brain cells into the blood vessels, causing brain cells to shrink. Cerebral hemorrhage from stretching/contraction of veins. Manifestations and causes of hyponatremia (less than 135) Pure sodium deficits: diuretics, vomiting, diarrhea. Dilutional hyponatremias: hypotonic IV solutions (post-op) Diseases: Kidney failure, Heart failure; liver failure (ascites) S & S: headache, lethargy, confusion; seizures, coma Role of potassium (K+) Major determinant of the resting membrane potential necessary for transmission of nerve impulses. The ratio of K + in the ICF to K + in the ECF is the major determinant of the resting membrane potential, which is necessary for the transmission and conduction of nerve impulses, maintenance of normal cardiac rhythms, and skeletal and smooth muscle contraction. Causes of hyperkalemia Renal failure and Addison's disease (decreased production of aldosterone thus body holds onto K+). Hyperkalemia should be investigated when there is a history of renal disease, massive trauma, insulin deficiency, Addison disease, use of potassium salt substitutes, or metabolic acidosis. If extracellular potassium concentration increases without a significant change in intracellular potassium, the resting membrane potential becomes more positive (i.e., changes from -90 to -80 mV) and the cell membrane is hypopolarized (the inside of the cell becomes less negative or partially depolarized (increase excitability - demonstrated with Tall-peaked T waves). Page 118 Why do hyperkaliemia and acidosis often occur together? In states of acidosis, hydrogen ions shift into the cells in exchange for ICF potassium. How is insulin used to treat hyperkalemia? Insulin transports potassium from the blood to the cell along with glucose. Insulin contributes to the regulation of plasma potassium levels by stimulating the Na + , K + -ATPase pump, thereby promoting the movement of potassium into liver and muscle cells simultaneously with glucose transport after eating. The intracellular movement of potassium prevents an acute hyperkalemia related to food intake. Insulin also can be used to treat hyperkalemia. What are causes and manifestation of hypokalemia? Hyperaldosteronism causes which fluid and electrolyte imbalances: Hypokalemia, hypernatremia, and fluid volume excess Manifestations: Cardiac: flattened-T waves; AV block; bradycardia; paralytic ileus Hypocalcemia causes Inadequate intestinal absorption, massive blood administration, decreases in PTH and vitamin D levels; nutritional deficiencies -malnutrition; alkalosis, elevated calcitonin level; pancreatitis; hypoalbuminemia Hypocalcemia manifestations Increased neuromuscular excitability; tingling, muscle spasms (particularly in hands, feet, and facial muscles), intestinal cramping, hyperactive bowel sounds; osteoporosis and fractures; severe cases show convulsions and tetany; prolonged QT interval, cardiac arrest Hypercalcemia causes Hyperparathyroidism; bone metastases with calcium resorption from breast, prostate, renal, and cervical cancer; sarcoidosis; excess vitamin D; many tumors that produce PTH; calcium-containing antacids Normal calcium level 8.5-10mg/dL Hypercalcemia manifestations Many nonspecific; fatigue, weakness, lethargy, anorexia, nausea, constipation; impaired renal function, kidney stones; dysrhythmias, bradycardia, cardiac arrest; bone pain, osteoporosis, fractures Hypophosphatemia (<2.0) causes Intestinal malabsorption related to vitamin D deficiency, use of magnesium- and aluminum- containing antacids, long-term alcohol abuse, and malabsorption syndromes; respiratory alkalosis; increased renal excretion of phosphate associated with hyperparathyroidism Hypophosphatemia manifestations (<2.0) Conditions related to reduced capacity for oxygen transport by red blood cells and disturbed energy metabolism; leukocyte and platelet dysfunction; deranged nerve and muscle function; in severe cases, irritability, confusion, numbness, coma, convulsions; possibly respiratory failure (because of muscle weakness), cardiomyopathies, bone resorption (leading to rickets or osteomalacia) Normal phosphorus level 2.0-4.7 Hyperphosphatemia causes (>4.7) Acute or chronic renal failure with significant loss of glomerular filtration; treatment of metastatic tumors with chemotherapy that releases large amounts of phosphate into serum; long-term use of laxatives or enemas containing phosphates; hypoparathyroidism Hyperphosphatemia manifestations Symptoms primarily related to low serum calcium levels (caused by high phosphate levels) similar to symptoms of hypocalcemia; when prolonged, calcification of soft tissues in lungs, kidneys, joints Hypomagnesemia causes (<1.5) Malnutrition, malabsorption syndromes, alcoholism, urinary losses (renal tubular dysfunction, loop diuretics) Hypomagnesemia manifestations (<1.5) Behavioral changes, irritability, increased reflexes, muscle cramps, ataxia, nystagmus, tetany, convulsions, tachycardia, hypotension Normal magnesium level 1.5-3.0 Hypermagnesemia causes (>3.0) Usually renal insufficiency or failure; also excessive intake of magnesium-containing antacids, adrenal insufficiency Hypermagnesemia manifestations (>3.0) Lethargy, drowsiness; loss of deep tendon reflexes; nausea and vomiting; muscle weakness; hypotension; bradycardia; respiratory distress; heart block, cardiac arrest Which three substances influence the calcium and phosphate balance? Calcium and phosphate balance is regulated by three hormones: parathyroid hormone (PTH), vitamin D, and calcitonin. Respiratory acidosis - full compensation pH = 7.36 pCO 2 = 75.1 HCO 3 = 40.6 Metabolic alkalosis - partial compensation pH = 7.59 pCO 2 = 49 HCO 3 = 48.2 Respiratory acidosis - no compensation pH = 7.31 pCO 2 = 58.5