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NURS 611 AP Review Notes Exam 1 Summer 2020 Patho

NURS 611 AP Review Notes Exam 1 Summer 2020 Patho Summer 2020 Review Exam 1 CONCEPTS TO FOCUS ON FOR EXAM 1 Week 1 & 2 Cellular Biology &... [Show More] Genetics 1. Main components of the cell: The nucleus contains the nucleolus, a small, dense structure composed largely of RNA; most of the cellular DNA; and the DNA- binding proteins, the histones, that regulate its activity. The DNA chain in eukaryotic cells is so extensive that the risk of breakage is high. Therefore, the histones binding to DNA cause DNA to fold into chromosomes (see Fig. 1.2, C). The wrapping of DNA into tight packages of chromosomes is essential for cell division in eukaryotes. Ribosomes are RNA-protein complexes (nucleoproteins) that are synthesized in the nucleolus and secreted into the cytoplasm through pores in the nuclear envelope called nuclear pore complexes (NPCs). These tiny ribosomes may float free in the cytoplasm or attach themselves to the outer membranes of the endoplasmic reticulum (see Fig. 1.1, A). Their chief function is to provide sites for cellular protein synthesis. The Golgi complex (or Golgi apparatus) is a network of flattened, smooth membranes and vesicles frequently located near the nucleus of the cell (Fig. 1.4). Proteins from the endoplasmic reticulum are processed and packaged into small membrane- bound sacs or vesicles called secretory vesicles, The Golgi complex is a refining plant and directs traffic (e.g., protein, polynucleotide, polysaccharide molecules) in the cell. Lysosomes maintain cellular health: • efficient removal of toxic cellular components • removal of useless organelles, • termination of signal transduction, • signals cellular adaptation They are signaling hubs of a sophisticated network for cellular adaptation and maintenance of metabolic homeostasis. Aging can lead to progressive loss of lysosomal efficiency and decline of the regenerative capacity of organs and tissues. Lysosomes are key. Altogether these components integrate functions, such as nutrient abundance, energy levels, and cell stressors, and translate them into instructions that regulate cellular metabolism toward either proliferation or inactivity. The signaling functions have far-reaching implications for metabolic regulation in health and in disease. Mitochondria are organelles found in large numbers in most cells, are responsible for cellular respiration and energy production. The inner membrane contains the enzymes of the respiratory chain—the name given to the electron-transport chain. These enzymes are essential to the process of oxidative phosphorylation that generates most of the cell's ATP. Metabolic pathways involved in the metabolism of carbohydrates, lipids, and amino acids and special pathways involving urea and heme synthesis are located in the mitochondrial matrix. 2. Apoptosis versus Necrosis. Cellular injuries from various causes have different clinical and pathophysiologic manifestations. Stresses from metabolic derangements may be associated with intracellular accumulations and include carbohydrates, proteins, and lipids. The most important changes are nuclear; clearly, without a healthy nucleus, the cell cannot survive. The two main types of cell death are necrosis and apoptosis. Apoptosis: A programmed cell death that is regulated or programmed. Cellular self-destruction for elimination of unwanted cell populations. 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) 3. CELLULAR ADAPTATION: Atrophy: Physiologic atrophy occurs with early development. For example, the thymus gland undergoes physiologic atrophy during childhood. Pathologic atrophy occurs as a result of decreases in workload, use, pressure, blood supply, nutrition, & hormonal stimulation (FOR EXAMPLE: Pathological atrophy would be the shrinking of gonads in an adolescent patient in response to decreased hormonal stimulation). Another example: Individuals immobilized in bed for a prolonged time exhibit a type of skeletal muscle atrophy called disuse atrophy. Hypertrophy: (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 (AMAZING!!!). Pathological: endometrial hyperplasia 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. 4. Cellular metabolism: ATP functions as the energy-transferring molecule (very important). 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-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. (The Na+, K+ pump is discussed in Chapter 1.) Sodium and water then can enter the cell freely, and cellular swelling results. 5. Free radicals play a major role in the initiation and progression of 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. 6. 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). 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: Ionizing radiation (IR) is any form of radiation capable of removing orbital electrons from atoms, resulting in the production of negatively charged free electrons and positively charged ionized atoms. Ionizing radiation is emitted by x-rays, γ-rays, and alpha and beta particles (which are emitted from atomic nuclei in the process of radioactive decay) and from subatomic particles such as neutrons, deuterons, protons, and pions. A main mechanism of damage to DNA (VERY BAD!) by ionizing radiation is from generation of reactive oxygen species from reactions with free radicals by radiolysis of water. 7. Aging and the cell/tissues. • Every physiologic processes can be shown to function less efficiently. o 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 to T-dependent antigens ▪ 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. GENETICS 1. Chromosomal aberrations and associate diseases: Aneuploid cells are defined as those that do not contain a multiple of 23 chromosomes. Monosomy, the presence of only one copy of a given chromosome in a diploid cell, is the other common form of aneuploidy. Among the autosomes, monosomy of any chromosome is lethal. However, newborns with trisomy of chromosomes 13, 18, or 21 can survive. This difference illustrates an important principle: loss of chromosome material has more serious consequences than duplication of chromosome material. An aneuploid cell containing three copies of one chromosome is said to be trisomic (a condition termed trisomy). The most well-known example of aneuploidy in an autosome is trisomy of the twenty-first Chromosome: Down syndrome was formerly called mongolism, but this inappropriate term is no longer used. Individuals with this disease typically have intelligence quotients (IQs) between 25 and 70. The facial appearance is distinctive, with a low nasal bridge, protruding tongue, and flat, low-set ears. 2. Some genetic principles: Penetrance versus Expressivity The penetrance of a trait is the percentage of individuals with a specific genotype who also exhibit the expected phenotype. Incomplete penetrance means that individuals who have a disease- causing allele may not exhibit the disease phenotype at all, even though the allele and the associated disease may be transmitted to the next generation. Huntington disease is a well-known autosomal dominant condition and its main features are progressive dementia and increasingly uncontrollable movements of the limbs. One of the key features is that symptoms/signs are not usually seen until age 40 or later, thus known as age-dependent penetrance. Most genetic diseases exhibit variable expressivity. Expressivity is the extent of variation in phenotype associated with a particular genotype. If the expressivity of a disease is variable, the penetrance may be complete but the severity of the disease can vary greatly. A well-known example of variable expressivity in an autosomal dominant disease is type 1 neurofibromatosis, or von Recklinghausen disease. The expression of this gene can vary from a few harmless café-au-lait spots (“coffee with milk,” describing the light brown color) on the skin to malignant tumors, scoliosis, seizures, gliomas, hypertension, learning disabilities, and neuromas. 3. Cystic fibrosis is caused by what type of gene? The most common lethal autosomal recessive disease in white children, cystic fibrosis. 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. An autosomal dominant form of breast cancer accounts for approximately 5% of breast cancer cases in the United States. Genes responsible for this form of breast cancer have been mapped to chromosomes 17 (BRCA1) and 13 (BRCA2). Women who inherit a mutation in BRCA1 or BRCA2 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. 4. How common is a given disease in a population? Well- established measures are used to answer this question. (DO NOT NEED TO CALCULATE THESE FOR THE EXAM, BUT DO KNOW THE DEFINITIONS) 1. 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. 2. 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. EXAMPLE: The incidence of death from lung cancer was 1.66 (per 1000 person-years) in heavy smokers (more than 25 cigarettes daily), but it was only 0.07 in the nonsmokers. The ratio of these two incidence rates is 1.66/0.07, which yields a relative risk of 23.7 deaths. Thus, it is concluded that the risk of dying from lung cancer increased by about 24-fold in heavy smokers compared with nonsmokers. 5. A major characteristic of type 1 diabetes mellitus is: 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. 6. Genetic processes demystified. • Epigenetics bridges DNA information and function by modifying gene expression without any alteration in DNA sequence. • Epigenetic modification can cause individuals with the same DNA (IDENTICAL TWINS) to have different disease profiles – For example the occurrence of asthma in only one of a pair of identical twins. • As twins age, they demonstrate increasing differences in methylation patterns of their DNA sequences, causing increasing numbers of phenotypic differences. • Environmental factors, such as diet and exposure to certain chemicals, may cause epigenetic modification. • Unlike DNA sequence mutations, which cannot be directly altered, epigenetic modifications can be reversed. 7. When Messenger RNA (mRNA) is over-expressed it results in metastasis of an already existing cancer. Hypermethylation is seen in miRNA genes that bind to the ends of mRNAs, degrading them and preventing their translation. When miRNA genes are methylated, their mRNA targets are over-expressed, and this over-expression has been associated with metastasis. Week 3 Fluids & Electrolytes, Acid and Bases 1. 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 2. At the arterial end of capillaries, fluid moves from the intravascular space into the interstitial space because capillary hydrostatic pressure (influenced by the Cardiac system) is higher than the capillary oncotic pressure. Oncotic pressure is heavily influenced by plasma proteins (albumin). Low plasma albumin causes edema as a result of a reduction in plasma oncotic pressure 3. Natriuretic peptides 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. ADH: Secretion of antidiuretic hormone (ADH) and the perception of thirst are stimulated by an Increase in plasma osmolality. ELECTROLYTES Sodium 4. What does Na+ do? Regulator of fluids; maintenance of neuromuscular irritability for conduction of nerve impulses. (135-145 meq/L) 5. Clinical manifestations of severe hypernatremia: 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. 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 Potassium 6. K+ is the 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. 7. 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). In states of acidosis, hydrogen ions shift into the cells in exchange for ICF potassium; hyperkalemia and acidosis therefore often occur together. 8. 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. 9. What are 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 Calcium, phosphate, magnesium TABLE: ALTERATIONS IN CALCIUM, PHOSPHATE, AND MAGNESIUM LEVELS CAUSES MANIFESTATIONS Hypocalcemia (<8.5 mg/dl) Inadequate intestinal absorption, massive blood administration, decreases in PTH and vitamin D levels; nutritional deficiencies – malnutrition; alkalosis, elevated calcitonin level; pancreatitis; hypoalbuminemia 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 (>10-12 mg/dl) Hyperparathyroidism; bone metastases with calcium resorption from breast, prostate, renal, and cervical Many nonspecific; fatigue, weakness, lethargy, anorexia, nausea, constipation; impaired renal function, kidney stones; CAUSES MANIFESTATIONS cancer; sarcoidosis; excess vitamin D; many tumors that produce PTH; calcium-containing antacids dysrhythmias, bradycardia, cardiac arrest; bone pain, osteoporosis, fractures Calcium and phosphorous balance is a reciprocal relationship and influenced by PTH, calcitonin, and vitamin D Hypophosphatemia (<2.0 mg/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 (>4.7 mg/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 (<1.5 mEq/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 (>3.0 mEq/L) Usually renal insufficiency or failure; also excessive intake of magnesium-containing antacids, Lethargy, drowsiness; loss of deep tendon reflexes; nausea and vomiting; muscle weakness; CAUSES MANIFESTATIONS adrenal insufficiency hypotension; bradycardia; respiratory distress; heart block, cardiac arrest Causes Pathophysiology Laboratory Findings Respiratory Acidosis • Chronic respiratory disease (e.g., COPD) • Barbiturate or sedative overdose • Chest wall abnormality • Severe pneumonia • Atelectasis • Respiratory muscle weakness Mechanical hypoventilation • Pulmonary edema • ↑ CO2 retention from hypoventilation • Compensatory response is ↑ HCO − 3 retention by kidney ↓ Plasma pH ↑ PaCO2 HCO − normal 3 (uncompensate d) ↑ HCO3− (compensated) Sample ABG Uncompensate d: pH 7.31 PaCO2 54 mm Hg HCO − 25 mEq/L 3 Respiratory Alkalosis • Hyperventilation (e.g., hypoxia, anxiety, fear, pain, exercise, fever) • Stimulated respiratory center (e.g., septicemia, stroke, meningitis, encephalitis, brain injury, salicylate poisoning) • Liver failure • Mechanical hyperventilation • ↑ CO2 excretion from hyperventilation • Compensatory − response is ↑ HCO3 excretion by kidney ↑ Plasma pH ↓ PaCO2 HCO − normal 3 (uncompensa ted) ↓ HCO3− (compensate d) Sample ABG Uncompensate d: pH 7.52 PaCO2 27 mm Hg Causes Pathophysiology Laboratory Findings HCO − 24 mEq/L 3 Metabolic Acidosis • Gain of fixed acid, ↓ Plasma pH PaCO2 normal (uncompensa ted) ↓ PaCO2 (compensate d) ↓ HCO3− Sample ABG Uncompensate d: pH 7.29 PaCO2 38 mm Hg HCO − 18 mEq/L 3 inability to excrete INCREASE D NON– CARBONI C ACIDS (ELEVATE D ANION GAP) BICARBONATE LOSS (NORMAL ANION GAP) acid or loss of base • Compensatory response is ↑ CO2 excretion by lungs (Kussmaul respirations) Increased H+ load Diarrhea Ketoacido sis (diabetes mellitus) Ureterosigmoid oscopy Renal failure Lactic acidosis (shock) Proximal renal tubule acidosis Ingestion s (ethylene glycol, salicylate s) Metabolic Alkalosis • Vomiting • Loss of strong acid or gain of base • Compensatory response is ↑ CO2 retention by lungs ↑ Plasma pH PaCO2 normal (uncompensa ted) ↑ PaCO2 (compensate d) ↑ HCO3− Sample ABG • Nasogastric suctioning • Diuretic therapy • Hypokalemia • Excess NaHCO3 intake • Mineralocorticoid use Causes Pathophysiology Laboratory Findings Uncompensate d: pH 7.50 PaCO2 40 mm Hg − HCO3 34 mEq/L ACID-BASE IMBALANCE: Practice for ABG interpretation ABG’s #1 #4 pH = 7.36 pH = 7.59 pCO2 = 75.1 pCO2 = 49 HCO3 = 40.6 HCO3 = 48.2 Resp acidosis – full comp Met alkalosis – partial comp #2 #5 pH = 7.31 pH = 7.36 pCO2 = 58.5 pCO2 = 30 HCO3 = 24 HCO3 = 15 Resp acidosis – no comp Met acidosis – full comp #3 #6 pH = 7.49 pH = 7.30 pCO2 = 34 pCO2 = 33.9 HCO3 = 26 HCO3 = 18.2 Resp alkalosis – no comp Met acidosis – partial comp [Show Less]

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