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NUR 315 Pathophysiology Final Exam Study Guide 2 / NUR315 Pathophysiology Final Exam Study Guide 2: University of Miami (Latest, Best Preparation Document)

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NUR 315 Pathophysiology Final Exam Study Guide 2 / NUR315 Pathophysiology Final Exam Study Guide 2: University of Miami (Latest, Best Preparation Document)

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NUR 315 Study Guide Final Exam
Italics were written from class review

● Altered Cell Biology (1 question)
○ Hypertrophy: increase in cellular SIZE
■ Caused by an increase in cellular demands, such as working out
■ Cardiac and skeletal muscles that are not capable of mitotic division
■ Ex. Enlargement of kidney after removal of other one, myocardial enlargement from HTN
○ Hyperplasia: increase in the NUMBER of cells
■ In cells capable of mitotic division, such as the epidermis, intestinal epithelium, and glandular
tissue
■ Ex. Increase in uterine and breast size during pregnancy, connective tissue wound healing
○ Metaplasia: REPLACEMENT of one mature cell by another cell, change in cell TYPE
■ Occurs in response to chronic irritation and inflammation and allows for substitution of cells that
are better able to survive under circumstances in which a more fragile cell type might succumb
■ Ex. Replacement of tracheal epithelial cells in chronic smokers
○ Atrophy: normal decrease in cellular SIZE
■ Decrease in use or work load causes cells to revert to a smaller size and more efficient level of
functioning
■ Normal process of aging, ex. Heart and brain size decrease
○ Dysplasia: change in size, shape, or organization (added onto study guide)
■ Precursor of cancer
■ Ex. Pap smear

● Genetics (2 questions)
○ Autosomal dominant disorders
■ Male and female offspring are affected equally
■ One parent is heterozygous affected = 50% chance of child being affected
■ Both parents heterozygous affected = 75% chance of child being affected
● Know how to make a Punnett square
○ Marfan Syndrome
■ Etiology: autosomal dominant disorder of the connective tissue
● Linked to chromosome 15 and FBN1 gene
● Can affect one or all three systems: cardiovascular, skeletal, eyes
● Average lifespan is between 30-40 years
■ Sign and symptoms
● Arachnodactyly – long, tapering fingers, joint hypermobility
● Chest deformities, deeply depressed sternum, pigeon chest
● Myopia, bilateral dislocation of the lens
● Mitral valve prolapse, dissection and rupture of the aorta
○ Tay-Sachs Disease
■ Etiology: autosomal recessive disorder
● Accumulation of glycolipids in neurons of the CNS and retina because of a failure of
lysosomal degradation
● Deficiency of hexosaminidase A enzyme
■ Sign and symptoms
● Rapid deterioration of mental and motor function, general seizures, blindness
● Death before 5 years of age
○ Turner Syndrome
■ Etiology: chromosomal disorder
● Partial or total inactivation of X chromosomes
● Have 45 chromosomes  22 pairs of autosomes and 1 sex chromosome (X)
■ Sign and symptoms
● Range from severe to moderate depending on degree of inactivation of X
● Short stature
● Webbing of neck
● Absent ovaries, amenorrhea, lack of secondary sex characteristics

, 2

● Associated with congenital heart defects, may have learning disabilities

● Fluid and Electrolytes / acid base balance (6 questions)
○ Interpret ABGs – Two questions on this, know how to determine
■ NORMAL ABG VALUES:
● pH: 7.35-7.45
○ Acidosis <7.35 -- alkalosis >7.45
● PaCO2: 35-45
○ Acidosis >35 – alkalosis <35
● HCO3: 22-26
○ Acidosis <22 – alkalosis >26
● PaO2: 80-10
○ Hypoxemia <80 – normal >80
● O2 saturation: 95% or greater
■ Compensation of Disorders
● Metabolic Acidosis: decrease in bicarbonate, decreased pH
○ Respiratory: hyperventilation to decrease PCO2
○ Renal: increased H+ excretion, increased HCO3 reabsorption
○ Causes: diarrhea, renal failure, DKA
○ Side effects: hyperkalemia, abdominal pain, nausea, vomiting, decreased heart
rate, coma
○ Treatment: Lactate-containing solution (Ringer’s lactate)
● Metabolic Alkalosis: increase in bicarbonate, increase in pH
○ Respiratory: hypoventilation to increase PCO2
○ Renal: decreased H+ excretion, decreased HCO3 reabsorption
■ Retain H+ ions, excrete HCO3 ions
○ Causes: Antacids, gastric suctioning, vomiting, thiazide/loop diuretics
○ Side effects: hyperactive reflexes, nervous system (tetany, confusion, seizures),
hypotension
○ Treatment chloride-containing solutions
● Respiratory Acidosis: decrease pH, increase in PCO2
○ Respiratory: none
○ Renal: increased H+ excretion, increased HCO3 reabsorption
○ Causes: chest injury, airway obstruction, COPD, fever, burns, sepsis
○ Side effects: headache, behavioral changes, confusion, depression, weakness,
tremors, paralysis, coma
○ Treatment: increase oxygen, if serious ventilate
● Respiratory Alkalosis: increase in pH, decrease in PCO2
○ Respiratory: none
○ Renal: decreased H+ excretion, decreased HCO3 reabsorption
■ Retain H+ ions, excrete HCO3 ions
○ Causes: anxiety, pain, pregnancy, sepsis, encephalitis, hypoxia
○ Side effects: dizziness, panic, light headedness, tetany, numbness or tingling in
the fingers or toes, severe seizures
● Acidosis  excreting H+ ions -- Alkalosis  excrete bicarbonate, retain H+ ions



○ Antidiuretic Hormone (ADH, vasopressin)
■ ADH: regulates water metabolism by retaining water
● Does not control any electrolytes - will indirectly affect sodium, but DOES NOT affect
potassium
■ Normal Water Regulation
● ADH stored in pituitary  osmoreceptors sense increased osmolality (high solute, low
water)  pituitary releases ADH  kidneys increased water reabsorption  decreased urine
output  osmolality returns to normal
● ADH will get secreted in: low blood pressure, hyperosmolar patient (to dilute the sodium)

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