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NURS 617 2025 Advanced Pathophysiology
Exam 1 (Retake) Test Questions and Correct
Answers (Score A)
Chronic infection of the cervix by the human papillomavirus results in cervical: A. metaplasia B. hormonal hyperplasia C. Atrophy D. Dysplasia In compensatory hyperplasia, growth factors stimulate cell division in response to: A. Ischemia B. Tissue loss C. Decreased hormonal stimulation D. Puberty In response to an increased workload, such as that caused by high blood pressure (hypertension), myocardial cells in the left ventricle will adapt through the process of: A. Dysplasia B. Hypertrophy
C. Hyperplasia D. Atrophy Which of the following molecules is likely to accumulate in any dead or dying tissues? A. Calcium B. Melanin C. Protein D. Uric acid The process of muscle hypertrophy involves an increase in: A. cell division. B. water accumulation. C. plasma membrane thickness. D. protein synthesis. Metaplasia involves the replacement of normal cells by: A. cancer cells. B. abnormal cells of the same tissue type.
Manifestations of hypokalemia Decrease in neuromuscular excitability, skeletal muscle weakness, smooth muscle atony causing constipation, intestinal distention, anorexia, nausea, and vomiting, cardiac dysrhythmias, glucose intolerance, impaired concentration ability, severe loss can cause paralysis and respiratory arrest Interventions for hypokalemia Replacement of lost potassium via IV therapy or diet Pathophysiology of hypocalcemia Occurs when concentrations of calcium are less than 9.0. Inadequate intestinal absorption, deposition of ionized calcium into bone or soft tissue, blood administration, or decreases in PTH and vitamin D levels; nutritional deficiencies occur with inadequate sources of dairy products or green, leafy vegetables; alkalosis, elevated calcitonin levels Manifestations of hypocalcemia Increased neuromuscular excitability, chvostek sign (clinical sign refers to a twitch of the facial muscles that occurs when gently tapping an individual's cheek, in front of the ear), tingling, muscle spasms (particularly in the hands, feet, and facial muscles), intestinal cramping, hyperactive bowel sounds, osteoporosis and fractures, severe cases show seizures and tetany; prolonged QT interval, and cardiac arrest Interventions for hypercalcemia
Treatment with IV calcium gluconate, volume repletion and ECG monitoring. Oral calcium replacement should be initiated, and serum calcium levels should be monitored. Pathophysiology of hypercalcemia Total serum calcium exceeding 10.5. Caused by hyperparathyroidism (associated with thyrotoxicosis), bone metastases with bone reabsorption from breast, prostate, or cervical cancer, hematologic malignance, sarcoidosis (growth of inflammatory cells in different parts of the body), or excessive vitamin D. Prolonged immobilization from enhanced bone reabsorption and decreased calcium deposition. Acidosis decreases calcium binding to serum albumin increasing ionized calcium levels. Manifestations of hypercalcemia Nonspecific symptoms. Fatigue, weakness, lethargy, anorexia, nausea, constipation, change in mental status, confusion, impaired renal function, kidney stones form as precipatates Interventions for hypercalcemia Administration of large amounts of NS to enhance renal excretion, administration of bisphosphonates in the absence of renal failure (absorption), administration of calcitonin (absorption), denoaumab given due to malignancies, ultimately the underlying condition needs to be treated Pathophysiology of hypernatremia
Interventions for hyponatremia Depends on the contributing disorder. Restrict water intake, hypertonic saline solutions. Hyperplasia Increase in the number of cells in an organ or tissue resulting from an increased rate of cellular division. Occurs in response to an injury with a production of growth factors or stem cells. Compensatory Hyperplasia An adaptive mechanism that allow certain organ cells to regenerate (liver, epidermal and intestinal epithelia, bone marrow, and fibroblasts). One example of this is a callus. Hormonal hyperplasia Mainly in estrogen-dependent organs (uterus/breast) Pathologic hyperplasia abnormal proliferation of normal cells and can occur as a response to excessive hormonal stimulation or effects of growth factors on target cells. One example of this is endometriosis (excessive menstrual bleeding due to a failure in growth inhibition controls with excess estrogen)
Hypertrophy Increase in size of cells that increases size of the affected organ Physiologic hypertrophy Caused by increased demand, stimulation of hormones and growth factors. Skeletal muscles when working out and uterine enlargement during pregnancy. Pathologic hypertrophy Results from chronic hemodynamic overload. An example of this is heart valve dysfunction or hypertension, mechanical signals such as stretch and trophic signals such as growth factors and vasoactive agents make the heart stretch then synthesize new proteins to remodel the heart size Atrophy Decrease or shrinkage in cellular size. Skeletal, heart, secondary sex organds, and the brain are most common. Aging causes brain cells to do this and endocrine-dependent organs, such as gonads, to shrink as hormonal stimulation decreases. Physiologic atrophy Type of atrophy that occurs with early development-ex: the thymus gland undergoes this during childhood
C. Skin D. Brain Pathophysiology of hypermagnesemia Magnesium level greater than 3.0. Usually oliguric renal disease; also excessive intake of magnesium-containing antacids, adrenal insufficiency manifestations of hypermagnesemia Lethargy, drowsiness, loss of deep tendon reflexes, nausea and vomiting, muscle weakness, hypotension, bradycardia, respiratory depression or arrest, heart block, cardiac arrest Interventions for hypermagnesemia Avoidance of magnesium containing substances and removal of magnesium by dialysis Pathophysiology of hypomagnesemia Serum magnesium concentration of less than 1.5. Malnutrition, malabsorption syndromes, alcoholism, urinary losses (renal tubular dysfunction, loop diuretics), metabolic acidosis, prolonged use of proton pump inhibitors.
manifestations of hypomagnesemia Behavioral changes, irritability, increased reflexes, muscle cramps, ataxia, nystagmus, tetany, seizures, tachycardia, hypotension Interventions for hypomagnesemia Intramuscular administration of magnesium sulfate. Magnesium supplementation may be beneficial preeclampsia, migraine, depression, cardiovascular disease, metabolic syndrome, and asthma Pathophysiology of hyperphosphatemia Acute or chronic oliguric renal disease 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 Manifestations of hyperphosphatemia Symptoms primarily related to low serum calcium levels (caused by high phosphate levels) like symptoms of hypocalcemia; when prolonged, calcification of soft tissues in lungs, kidneys, joints Interventions for hyperphosphatemia The underlying pathologic condition must be identified and treated.
Pathophysiology of hypochloremia a low level of serum chloride (less than 97 mEq/L). is rare and usually occurs with hyponatremia or an elevated bicarbonate concentration, as in metabolic alkalosis. Cystic fibrosis is a genetic disease characterized by this. Manifestations of hypochloremia Sodium deficit associated with restricted intake, use of diuretics, and vomiting is accompanied by chloride deficiency Interventions for hypochloremia In all cases, treatment of the underlying cause is required. Pathophysiology of hyperchloremia Elevation of serum chloride concentration greater than 105 mEq/L) often accompanies hypernatremia. Plasma bicarbonate deficits, as occur in hyperchloremic metabolic acidosis. Manifestations of hyperchloremia There are no specific symptoms for chloride excess.
Interventions for hyperchloremia Treatment is related to management of the underlying disorder. Autosomal Dominant One copy causes the phenotype to be presented. Diseases caused by these genes are rare, with the most common occurring in 1 in 500 individuals. Therefore, it is uncommon for two individuals who are both affected by the same disease of this type of gene to produce offspring together. Best known disease of this type is Huntington Disease. Huntington Disease Autosomal dominant neurologic disorder whose main features are progressive dementia and increasingly uncontrollable limb movements. A key feature of this disease is its delayed age of onset; symptoms usually are not seen until 40 years of age or later. Autosomal Recessive Two copies are needed to cause the presentation of the phenotype. Diseases caused by these genes are rare, but there could be numerous asymptomatic carriers. The most common lethal kind of this gene is cystic fibrosis, which occurs about 1 in 2500 births. Some diseases of this type are characterized by delayed age of onset, incomplete penetrance, and variable expressivity. Cystic Fibrosis
Klinefelter Syndrome Presence of 2 or more x chromosomes with one Y chromosome. 2/3 cases are caused by nondisjunction of the X chromosomes in the mother and the frequency of the disorder rises with maternal age. Has a male appearance but usually sterile. Possible development of female like breasts, small testes, sparse body hair, high pitched voice, long limbs, moderate degree of mental impairment possible. Cri Du Chat Syndrome Caused by deletion of part of the short arm of chromosome 5. Characteristic cry (sounds like a cat), low birth weight, severe mental retardation, microcephaly, heart defects, facial appearance (wide set eyes, small mouth) Trisomy 18 (Edwards syndrome) Extra chromosome that can come from either the mothers egg cell or fathers sperm cell. Likelihood increases with maternal age. Short life expectancy due to severe life- threating complications. Overlapping fingers, low set ears, heart/lung abnormalities, decreased muscle tone, club feet, small physical size, low birth weight, respiratory failure, kidney disease, GI tract issues, hernias, scoliosis. Trisomy 21 - Downs Syndrome Distinctive facial appearance with low nasal bridge, epicanthal folds, protruding tongue, and flat, low set ears. poor muscle tone and short stature, increased susceptibility to leukemia, reduced ability to fight respiratory tract infections and higher risk for congenital heart disease.
Trisomy 13 (Patau Syndrome) Severe intellectual disability, heart defects, spinal cord defects, very small or poorly developed eyes, extra fingers or toes, cleft lip, weak muscle tone Prader-willis syndrome Genetic multisystem disorder inherited from the father - caused by imprinting of a gene where 4 million base pairs of the long arm of chromosome 5 are deleted. Manifests as lethargy, diminished muscle tone, truncal obesity, small hands and feet, inverted v shaped upper lip, short stature, mild to moderate mental retardation, and hypogonadism. B. Inherited from the father Prader-Willi syndrome causes a chromosomal defect that is what? A. Initiated by postnatal exposure to a virus B. Inherited from the father C. Related to maternal alcohol abuse D. Transferred from mother to child B. These conditions are passed from affected father to all of his female children. Which statement is true regarding X-linked recessive conditions? A. 25% of an affected individual’s grandsons will be affected.
D. Fragile X A. Maternal nondisjunction What is the most common cause of Down syndrome? A. Maternal nondisjunction B. Paternal translocation C. Maternal translocations D. Paternal nondisjunction B. An IQ of 25 to 70, low nasal bridge, protruding tongue, and flat, low-set ears A healthcare professional is assessing a child who has complete trisomy of the twenty-first chromosome. What findings does the professional relate to this condition? A. High-pitched voice, tall stature, gynecomastia, and an IQ of 60 to 90 B. An IQ of 25 to 70, low nasal bridge, protruding tongue, and flat, low-set ears C. Widely spaced nipples, reduced carrying angle at the elbow, and sparse body hair D. Circumoral cyanosis, edema of the feet, short stature, and mental slowness
Adaptive Immunity Also known as acquired or specific immunity. Develops over a lifetime of the individual and provides long-term protection against specific invaders. This is the body's third line of defense. Innate immunity Defense mechanisms that are present at birth and provide the initial nonspecific response to invasion and injury. This defense consists of natural barriers and the inflammatory response. Natural Barriers First line of defense of the Innate Immune system. These are broadly specific, constant, and no memory is involved. Examples of these defenses include epithelial cells of the respiratory tract that trap microorganisms through mucus which is then expunged through coughing or sneezing. Other examples include mucus, perspiration, tears, and earwax. Inflammatory response. Second line of defense of the innate immune system. This occurs after tissue injury or infection surpassed the first line of defense barriers. Leukocytes such as macrophages or phagocytes are summoned to try and eat/destroy the invader, regardless of what kind of invader it is. If the inflammatory response is unable to destroy the invader, then the third line of defense comes in for a specific response.
