1
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)
, 3
■ Increase in ADH (SIADH) increase water retention, sodium becomes diluted decreased urine
output (high osmolality) hypoosmolar patient hyponatremia
■ Decrease ADH (Diabetes Insipidus) increase water excretion (large urine outputs) decreased
circulating volume hyperosmolar patient hypernatremia and dehydration
○ Renin Angiotensin Aldosterone System
■ Blood pressure falls or decreased renal perfusion renin is secreted renin activates
angiotensinogen to angiotensin 1 angiotensin 1 is converted to angiotensin 2 in the lungs
angiotensin 2 is a potent vasoconstrictor (causing BP to rise) angiotensin 2 causes aldosterone
secretion from the adrenal glands aldosterone increases sodium reabsorption blood pressure
rises
○ Electrolyte Imbalances
■ NORMAL ELECTROLYTE VALUES
● Sodium: 135-145 mEq/L
○ Major ECF
● Potassium: 3.5-5.0 mEq/L
○ Major ICF
● Calcium: 8.5-10.5 mg/dl
○ Bones
● Magnesium: 1.8-3.0 mg/dl
○ ICF, follows potassium
● Chloride: 98-106 mEq/L
○ ECF, follows sodium
● Phosphorous: 2.5-4.5
● Serum Osmolality: 275-290
■ Hyponatremia
● Values: <135
○ Serum osmolality: <275
○ Specific gravity: <1.010
● Clinical manifestations:
○ Muscle cramps, weakness, fatigue
○ Nausea, vomiting, abdominal cramps, diarrhea
○ Headache, confusion, lethargy, convulsions, coma most important
● Causes:
○ Excessive sweating and loss of sodium
○ GI suction
○ Adrenal insufficiency
○ Head injury, diuretic therapy
■ Hypernatremia
● Values: >145
○ Specific gravity = 1.030
● Clinical manifestations:
○ Thirst, dry mucous membranes, decreased skin turgor
○ Rapid, thready pulse, decreased blood pressure
○ Oliguria (increased ADH)
○ Muscle weakness, twitching, convulsions
● Causes:
○ Thirst deficit
○ Watery diarrhea
○ Fever
■ Hypokalemia
● Values: <3.5, metabolic alkalosis
○ Increased pH
○ Increased HCO3
● Clinical manifestations:
○ Muscle weakness, leg cramps, fatigue
, 4
○ Cardiac arrhythmias: prolonged PR interval, flattened T wave, ST segment
depression, postural hypotension
○ Anorexia, nausea, vomiting, distention, decreased bowel sounds
● Causes:
○ Vomiting, diarrhea, GI suction
○ Heavy sweating, increased urine production
○ Prolonged use of K+ wasting diuretics, poor intake of K+ in diet
■ Hyperkalemia
● Values: >5.0
● Clinical manifestations:
○ Parasthesias (early symptom)
○ Gastrointestinal hyperactivity – cramping, diarrhea, nausea, vomiting
○ Muscle weakness and cramps, extremity numbness
○ Cardiac arrhythmias, EKG irregularity – narrow T wave, widening of QRS
● Causes:
○ Crush injury, infection
○ Kidney disease, adrenal insufficiency
○ Potassium sparing diuretics, increased intake of potassium
■ Hypocalcemia
● Values: <8.5
○ Hypoparathyroidism
○ Hyperphosphatemia
● Clinical manifestations
○ Increased excitability of neural and muscle effects
■ Parasthesias, numbness, tingling
■ Skeletal muscle cramps
○ Abdominal cramps
○ Trosseau’s sign – blood pressure cuffed is inflated to a pressure greater than
systolic BP and held in place for three minutes
■ Positive: carpal spasm occurs
○ Chvostek’s sign – tap on facial nerve
■ Positive: contraction of face
○ Laryngeal stridor or spasm
○ Hypotension, cardiac insufficiency
● Causes:
○ Poor absorption – GI, vitamin D, pancreatitis
○ Renal failure
■ Hypercalcemia
● Values: >10.5
○ Hypophosphatemia
○ Hyperparathyroidism
● Clinical manifestations
○ Inability of kidneys to concentrate urine renal calculi
■ Polyuria, increased thirst, flank pain
○ Decreased excitability of neural and muscle effects
■ Muscle weakness, ataxia, lethargy
■ Decreased level of consciousness, coma
○ Hypertension, shortening of QT interval, AV blocks
○ Bone pain, fractures, calcifications
● Causes:
○ Increased GI absorption
○ Malignancies
Neuro System (7 questions)
○ Risk factors for CVA (stroke)
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)
, 3
■ Increase in ADH (SIADH) increase water retention, sodium becomes diluted decreased urine
output (high osmolality) hypoosmolar patient hyponatremia
■ Decrease ADH (Diabetes Insipidus) increase water excretion (large urine outputs) decreased
circulating volume hyperosmolar patient hypernatremia and dehydration
○ Renin Angiotensin Aldosterone System
■ Blood pressure falls or decreased renal perfusion renin is secreted renin activates
angiotensinogen to angiotensin 1 angiotensin 1 is converted to angiotensin 2 in the lungs
angiotensin 2 is a potent vasoconstrictor (causing BP to rise) angiotensin 2 causes aldosterone
secretion from the adrenal glands aldosterone increases sodium reabsorption blood pressure
rises
○ Electrolyte Imbalances
■ NORMAL ELECTROLYTE VALUES
● Sodium: 135-145 mEq/L
○ Major ECF
● Potassium: 3.5-5.0 mEq/L
○ Major ICF
● Calcium: 8.5-10.5 mg/dl
○ Bones
● Magnesium: 1.8-3.0 mg/dl
○ ICF, follows potassium
● Chloride: 98-106 mEq/L
○ ECF, follows sodium
● Phosphorous: 2.5-4.5
● Serum Osmolality: 275-290
■ Hyponatremia
● Values: <135
○ Serum osmolality: <275
○ Specific gravity: <1.010
● Clinical manifestations:
○ Muscle cramps, weakness, fatigue
○ Nausea, vomiting, abdominal cramps, diarrhea
○ Headache, confusion, lethargy, convulsions, coma most important
● Causes:
○ Excessive sweating and loss of sodium
○ GI suction
○ Adrenal insufficiency
○ Head injury, diuretic therapy
■ Hypernatremia
● Values: >145
○ Specific gravity = 1.030
● Clinical manifestations:
○ Thirst, dry mucous membranes, decreased skin turgor
○ Rapid, thready pulse, decreased blood pressure
○ Oliguria (increased ADH)
○ Muscle weakness, twitching, convulsions
● Causes:
○ Thirst deficit
○ Watery diarrhea
○ Fever
■ Hypokalemia
● Values: <3.5, metabolic alkalosis
○ Increased pH
○ Increased HCO3
● Clinical manifestations:
○ Muscle weakness, leg cramps, fatigue
, 4
○ Cardiac arrhythmias: prolonged PR interval, flattened T wave, ST segment
depression, postural hypotension
○ Anorexia, nausea, vomiting, distention, decreased bowel sounds
● Causes:
○ Vomiting, diarrhea, GI suction
○ Heavy sweating, increased urine production
○ Prolonged use of K+ wasting diuretics, poor intake of K+ in diet
■ Hyperkalemia
● Values: >5.0
● Clinical manifestations:
○ Parasthesias (early symptom)
○ Gastrointestinal hyperactivity – cramping, diarrhea, nausea, vomiting
○ Muscle weakness and cramps, extremity numbness
○ Cardiac arrhythmias, EKG irregularity – narrow T wave, widening of QRS
● Causes:
○ Crush injury, infection
○ Kidney disease, adrenal insufficiency
○ Potassium sparing diuretics, increased intake of potassium
■ Hypocalcemia
● Values: <8.5
○ Hypoparathyroidism
○ Hyperphosphatemia
● Clinical manifestations
○ Increased excitability of neural and muscle effects
■ Parasthesias, numbness, tingling
■ Skeletal muscle cramps
○ Abdominal cramps
○ Trosseau’s sign – blood pressure cuffed is inflated to a pressure greater than
systolic BP and held in place for three minutes
■ Positive: carpal spasm occurs
○ Chvostek’s sign – tap on facial nerve
■ Positive: contraction of face
○ Laryngeal stridor or spasm
○ Hypotension, cardiac insufficiency
● Causes:
○ Poor absorption – GI, vitamin D, pancreatitis
○ Renal failure
■ Hypercalcemia
● Values: >10.5
○ Hypophosphatemia
○ Hyperparathyroidism
● Clinical manifestations
○ Inability of kidneys to concentrate urine renal calculi
■ Polyuria, increased thirst, flank pain
○ Decreased excitability of neural and muscle effects
■ Muscle weakness, ataxia, lethargy
■ Decreased level of consciousness, coma
○ Hypertension, shortening of QT interval, AV blocks
○ Bone pain, fractures, calcifications
● Causes:
○ Increased GI absorption
○ Malignancies
Neuro System (7 questions)
○ Risk factors for CVA (stroke)
