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2024/2025 Nursing 611 study guide with questions and
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Test 1 Patho Apoptosis - A programmed death Example: Inflammatory process Necrosis -Irreversible injury Examples: Mr. Bax r/t arteriosclerosis *Hypoxia #1 cellular injury (MI) and the most common cause of cellular injury is hypoxic injury Atrophy : Physiologic: thymus gland atrophy (childhood) Hypertroph y: (increase in size of cell) Another cellular adaptation that can actually be beneficial is hypertrophy of myocardial cells such as in endurance training – this is referred to as physiologic hypertrophy. Versus Pathologic hypertrophy that occurs secondary to HTN. Hyperplasia : (increase in # of cells) Compensatory: removal of 70% of liver – can regenerate in about 2 weeks. Pathological: endometrial hyperplasia Hyperplasia is cellular adaptation would take place after a portion of the liver has been dissected. Metaplasia : (replacement of cells) normal columnar ciliated epithelial cells of the bronchial lining have been replaced by stratified squamous epithelial cells.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 stopped. Dysplasia – not adaptive ATP =energy BUT needs Oxygen – aerobic metabolism A reduction in ATP levels causes the plasma membrane’s sodium-potassium (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.
Sodium and water then can enter the cell freely, and cellular swelling results. What happens when oxygen reserves are depleted? Anaerobic metabolism (glycolysis) 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. Injurious chemical bond formation with proteins, lipids, carbohydrates—key molecules in membranes and nucleic acids. Cardiovascular, HTN, IHD, HF, DM *The consequence of leakage of lysosomal enzymes during chemical injury enzymatic digestion of the nucleus and nucleolus occurs halting DNA synthesis. Lysosomes : Enzymatic digestion of cellular organelles, including the nucleus and nucleolus, ensues, halting synthesis of DNA and ribonucleic acid (RNA). 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 (Thus the term Fatty Liver) Radiation : Which cell component is the most vulnerable target of radiation? Deoxyribonucleic acid (DNA) Muscular atrophy (Sarcopenia)- “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. Fluid Deficits and Dehydration Marked water deficit is manifested by S & S of dehydration (decreased perfusion): headache, Thirst (Osmoreceptors are activated by an increase in osmotic
Inadequate free water intake, Inappropriate administration of hypertonic saline solution, Over secretion of aldosterone Clinical manifestations: confusion, convulsions, cerebral hemorrhage, and coma 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 Hyponatremia Manifestations and causes of hyponatremia? (less than 135 meq/L) 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 (brain – cerebral edema) POTASSIUM 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. If extracellular potassium concentration increases without a significant change in intracellular potassium, the resting membrane potential becomes more positive 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
Causes and manifestations 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. **Remember, in hyperkalemia, cardiac rhythm changes are a direct result of cardiac cell hypopolarization. In states of acidosis, hydrogen ions shift into the cells in exchange for ICF potassium; hyperkalemia and acidosis therefore often occur together. 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. Causes and manifestations 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 *Remember calcium and phosphate balance is influenced by three substances parathyroid hormone, calcitonin, and vitamin D. CALCIUM- HYPOCALCEMIA AND HYPERCALEMIA- SIGNS AND SYMPTOMS Remember the major cause of hypocalcemia is repeated blood administration or pancreatitis. PHOSPHATE- HYPO AND HYPER- SIGNS AND SYMPTOMS MAGNESIUM- HYPO AND HYPER-SIGNS AND SYMPTOMS ACID-BASE BALANCE KNOW WELL! RESPIRATORY ACIDOSIS, RESPIRATORY ALKALOSIS, METABOLIC ACIDOSIS, AND
Because an individual must be homozygous for a recessive allele to express the disease, the carriers are phenotypically normal. Because most recessive alleles are maintained in normal carriers, they are able to survive in the population from one generation to the next. Which genes are responsible for an autosomal dominant form of breast cancer? 17 (BRCA1) and 13 (BRCA2). Women who inherit a mutation in BRCA1 or BRCA experience a 50% to 80% lifetime risk of developing breast cancer. Breast cancer aggregates strongly in families. If a woman has one affected first-degree relative, her risk of developing breast cancer doubles. The incidence rate is the number of new cases of a disease reported during a specific period (typically 1 year) divided by the number of individuals in the population. Relative risk is a common measure of the effect of a specific risk factor. It is expressed as a ratio of the incidence rate of the disease among individuals exposed to a risk factor divided by the incidence of the disease among individuals not exposed to a risk factor. A MAJOR CHARACTERISTIC OF TYPE I DIABETES MELLITUS Type 1 diabetes, which is characterized by T-cell infiltration of the pancreas and destruction of the insulin-producing beta cells. In addition to T-cell infiltration of the pancreas, autoantibodies are formed against pancreatic cells; the latter can be observed long before clinical symptoms occur. These findings, indicate that this is an autoimmune disease.
ACID BASE IMBALANCES
**pH = 7. pCO2 =
HCO3 = 40.**
**pH = 7. pCO2 = 49 HCO3 = 48. Resp acidosis – full compMet alkalosis – partial comp
pH = 7. pCO2 =
HCO3 = 24**
**pH = 7. pCO2 = 30 HCO3 = 15 Resp acidosis – no comp Met acidosis – full comp
pH =
pCO2 = 34 HCO3 = 26**
pH = 7. pCO2 = 33. HCO3 = 18. Resp alkalosis – no compMet acidosis – partial comp
Atelectasis Respiratory muscle weakness Mechanical hypoventilatio n pH 7. PaCO2 54 mm Hg HCO3− 25 mEq/L Pulmonary edema Respiratory Alkalosis Hyperventilati on (e.g., hypoxia, anxiety, fear, pain, exercise, fever) Stimulated respiratory center (e.g., septicemia, stroke, meningitis, encephalitis, brain injury, salicylate poisoning) Liver failure Mechanical hyperventila tion Metabolic Acidosis
↑ CO
excretion from hyperventila tion Compensato ry response is ↑ HCO3− excretion by kidney ↑ Plasma pH ↓ PaCO HCO3− normal (uncompensated) ↓ HCO3− (compensated) Sample ABG Uncompensated: pH 7. PaCO2 27 mm Hg HCO3− 24 mEq/L Gain of fixed acid, inability to ↓ Plasma pH
INCREASED NON–CARBONIC ACIDS
(ELEVATED ANION
GAP)BICARBONATE LOSS (NORMAL ANION
GAP)
Increased H+ loadDiarrhea Ketoacidosis (diabetes mellitus)Ureterosigmoidoscopy Renal failure Lactic acidosis (shock)Proximal renal tubule acidosis Ingestions (ethylene glycol, salicylates) excrete acid or loss of base Compensat ory response is ↑ CO excretion by lungs (Kussmaul respiration s) PaCO2 normal (uncompensated) ↓ PaCO2(compens ated) ↓ HCO3− Sample ABG Uncompensa ted: pH 7. PaCO2 38 mm Hg Metabolic Alkalosis Vomiting Loss of strong acid or gain of ↑ Plasma pH HCO3− 18 mEq/L
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 >10-12mg/dl 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 Many nonspecific; fatigue, weakness, lethargy, anorexia, nausea, constipation; impaired renal function, kidney stones; dysrhythmias, bradycardia, cardiac arrest; bone pain, osteoporosis, fractures Hypophosphatemia <2.0mg/dl
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 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) Hyperphosphatemia >4.7mg/dl 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 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 <1.5mEq/L Malnutrition, malabsorption syndromes, alcoholism, urinary losses (renal tubular dysfunction, loop diuretics) Behavioral changes, irritability, increased reflexes, muscle cramps, ataxia, nystagmus, tetany, convulsions, tachycardia, hypotension Hypermagnesemia >3.0mEq/L Usually renal insufficiency or failure; also excessive intake of magnesium- containing antacids, adrenal insufficiency Lethargy, drowsiness; loss of deep tendon reflexes; nausea and vomiting; muscle weakness; hypotension; bradycardia; respiratory distress; heart block, cardiac arrest Other things to please remember -myocytes will increase in size with subsequent enlargement of the heart when a person has long standing HTN -that the action of natriuretic peptides is to decrease blood pressure and increase sodium and water excretion
