Pathophysiology Final Exam Study
Guide 1
Pathophysiology Final Exam Study Guide
Fall 2011
i. Altered Cell Biology (1 question)
a. Atrophy – decrease in cellular size
b. Hypertrophy – increase in cell size
c. Hyperplasia – increase in the number of cells
d. Metaplasia – replacement of one mature cell by another
e. Dysplasia – abnormal changes in the size, shape and organization of mature cell
f. Cellular Adaptation
i. Allows the stressed tissue to survive or maintain function
ii. Genetics (2 questions)
a. Autosomal dominant disorders
i. Male/female offspring affected equally
ii. One of the parents is usually affected
iii. If one of the parents is heterozygous
affected, the children have a 50% chance of
being affected
iv. If both parents are heterozygous affected, the
children have a 75 % chance of being affected
b. Marfan Syndrome
i. Etiology – disease of the connective tissue
1. Ocular, skeletal, and CV anomalies
2. It is an autosomal dominant disease – linked to chromosome 15
3. Affects men and women equally
ii. Signs and symptoms
1. Joint hypermobility
2. Spinal deformity
3. Mitral valve prolapse
4. Aortic valve disease
c. Tay Sachs Disease
, Pathophysiology Final Exam Study
Guide 2
i. Etiology – accumulation of glycolipids in the brain neurons &
retina b/c of deficiency in Hexosaminidase A enzyme
ii. Signs and symptoms
1. Mental retardation and motor problems
2. Blindness and seizures
3. Death in 2-5 years
4. Cherry red spot in retina will occur
d. Turner Syndrome
i. Etiology – partial or full inactivation of X chromosomes
1. 45 chromosomes instead of 46, b/c only one X
2. Diagnosed through genetic testing
3. Associated with Coronary Heart Disease
ii. Signs and symptoms
1. Affects girls, typically are shorter, no breasts/ovaries, sterile
2. Webbing of neck
3. Amenorrhea
4. May have signs of mental retardation
iii. Fluid and Electrolytes / Acid-Base Balance (6 questions)
a. Interpret ABGs
i. Compensation of disorders
Acid/Base
Ph Range 7.35-7.45
C02 35-45 mm Hg
HC03 22-26 mEq/L
PaO2 80-100mm Hg
02 Stat 95% or greater
b. Acidosis
i. H+ diffuses into cells and drives out K+, elevating K+ concentration in ECF
ii. Compensate by excreting hydrogen ions
c. Alkalosis
i. H+ diffuses out of cells and K+ diffuses in
ii. Excrete bicarbonate and hold hydrogen ions
d. Compensation
i. Acute vs. Chronic
1. Acute compensation of acid base balance is done by the
respiratory system
2. Chronic compensation is done by the kidneys to slowly
but completely balance the disorder
ii. The body’s attempt to return the ratio of acid to base back toward
1:20(1 acid for every 20 bases) to maintain the pH between 7.35-
7.45
iii. The patient is not considered to be compensated unless pH
is within normal range
iv. If changes in that direction are noted either in PaCo2 or HCO3
with minimal changes in pH, the patient is considered to be
partially compensated
v. Respiratory compensation
1. Eliminating or retaining CO2 by the lungs also regulates
acid-base balance
, Pathophysiology Final Exam Study
Guide 3
2. The response is rapid, occurs within minutes by altering the
rate and depth of respiration
3. Carbon Dioxide is a powerful stimulator of the respiratory system
vi. Metabolic compensation
1. For acute metabolic acidosis – body will compensate with
respiratory alkalosis
2. They are the ultimate long-term regulator of acid-base balance
3. They are slower to respond, but their response is more
permanent and selective
4. Maintain acid-base balance by excreting or conserving
bicarbonate and hydrogen ions
a. When pH decreases, H+ ions are excreted, and
bicarbonate acid ions are formed and retained
b. When pH increases, H+ are retained, and
bicarbonate acids are excreted
e. Respiratory alkalosis
i. Decrease PCO2 with increased pH
ii. Caused by:
1. Hyperventilation
2. Central stimulation of respiratory center
3. Stimulation of peripheral pathways to respiratory center
iii. Very common in anxiety attacks
f. Respiratory acidosis
i. Increase in CO2 with decreased pH
ii. Caused by:
1. Acute disorders of ventilation
2. Chronic disorders of ventilation
3. Increased Carbon dioxide production
iii. **Emphysema, COPD, pulmonary fibrosis and chronic bronchitis
can cause respiratory acidosis
iv. Increased PCO2 Production
1. Exercise
2. Fever
3. Sepsis
4. Burns
5. Carbohydrate rich diet
g. Metabolic alkalosis
i. Increased bicarbonate with elevated pH
ii. Caused by:
1. Increased bicarbonate administration
2. Excess loss of acid via kidneys/GI
3. Increased bicarb levels by contraction of ECF via
hypokalemia & hypochloremia
iii. Alkalosis always related to hypocalcemia
h. Metabolic acidosis
i. Caused by:
1. Increased chloride
2. Chronic renal failure and DKA
ii. They will try to compensate by going into respiratory alkalosis
which would increase RR they will be hyperventilating
, Pathophysiology Final Exam Study
Guide 4
iii. When you increase respiratory rate you exhale more CO2 and
become more alkalotic
iv. If you decrease respiratory rate you hold CO2 and become acidotic.
v. When patient is acidic- potassium is going out of the cell and
patient comes hypercalcemic
i. ADH – function of ADH is water metabolism
i. If you increase ADH you have increased water retention and your
sodium will be diluted and patient will be hypoosmolar and
hyponatremic,
ii. If you decrease ADH you increase water excretion and you decrease
circulating volume and then the patient will be hyperosmolar and
hypernatremic
iii. ADH only affects sodium and not potassium
iv. ADH would be excreted when a patient has a high osmolarity
because its going to try and dilute the sodium
v. Released from the pituitary gland
j. Renin Angiotensin System
i. Renin gets secreted when you have decreased kidney perfusion
ii. Renin activates angiotensinogen to angiotensin 1 which
converts to angiotensin 2 in the lungs
iii. Renin is a potent vasoconstrictor which will go to the adrenal
cortex to secrete aldosterone which increases sodium
reabsorption
iv. ADH will be secreted from angiotensin 2 so both increases
circulating volume which will increase the blood pressure
k. Hypokalemia
i. Clinical manifestations: muscle weakness and leg cramps, fatigue,
anorexia and N+V, decreased bowel sounds, cardiac arrhythmias
(prolonged PR interval, flattened T wave)
l. Hyperkalemia
i. Clinical manifestations: Gastrointestinal Hyperactivity, Cardiac Arrhythmia,
Muscle weakness, Paresthesias
m. Hyponatremia
i. Clinical manifestations: Malaise, muscle cramps, Apprehension,
Abdominal cramps, Nausea and Vomiting, Diarrhea, Headache,
Confusion and Lethargy, Convulsions and Coma
Guide 1
Pathophysiology Final Exam Study Guide
Fall 2011
i. Altered Cell Biology (1 question)
a. Atrophy – decrease in cellular size
b. Hypertrophy – increase in cell size
c. Hyperplasia – increase in the number of cells
d. Metaplasia – replacement of one mature cell by another
e. Dysplasia – abnormal changes in the size, shape and organization of mature cell
f. Cellular Adaptation
i. Allows the stressed tissue to survive or maintain function
ii. Genetics (2 questions)
a. Autosomal dominant disorders
i. Male/female offspring affected equally
ii. One of the parents is usually affected
iii. If one of the parents is heterozygous
affected, the children have a 50% chance of
being affected
iv. If both parents are heterozygous affected, the
children have a 75 % chance of being affected
b. Marfan Syndrome
i. Etiology – disease of the connective tissue
1. Ocular, skeletal, and CV anomalies
2. It is an autosomal dominant disease – linked to chromosome 15
3. Affects men and women equally
ii. Signs and symptoms
1. Joint hypermobility
2. Spinal deformity
3. Mitral valve prolapse
4. Aortic valve disease
c. Tay Sachs Disease
, Pathophysiology Final Exam Study
Guide 2
i. Etiology – accumulation of glycolipids in the brain neurons &
retina b/c of deficiency in Hexosaminidase A enzyme
ii. Signs and symptoms
1. Mental retardation and motor problems
2. Blindness and seizures
3. Death in 2-5 years
4. Cherry red spot in retina will occur
d. Turner Syndrome
i. Etiology – partial or full inactivation of X chromosomes
1. 45 chromosomes instead of 46, b/c only one X
2. Diagnosed through genetic testing
3. Associated with Coronary Heart Disease
ii. Signs and symptoms
1. Affects girls, typically are shorter, no breasts/ovaries, sterile
2. Webbing of neck
3. Amenorrhea
4. May have signs of mental retardation
iii. Fluid and Electrolytes / Acid-Base Balance (6 questions)
a. Interpret ABGs
i. Compensation of disorders
Acid/Base
Ph Range 7.35-7.45
C02 35-45 mm Hg
HC03 22-26 mEq/L
PaO2 80-100mm Hg
02 Stat 95% or greater
b. Acidosis
i. H+ diffuses into cells and drives out K+, elevating K+ concentration in ECF
ii. Compensate by excreting hydrogen ions
c. Alkalosis
i. H+ diffuses out of cells and K+ diffuses in
ii. Excrete bicarbonate and hold hydrogen ions
d. Compensation
i. Acute vs. Chronic
1. Acute compensation of acid base balance is done by the
respiratory system
2. Chronic compensation is done by the kidneys to slowly
but completely balance the disorder
ii. The body’s attempt to return the ratio of acid to base back toward
1:20(1 acid for every 20 bases) to maintain the pH between 7.35-
7.45
iii. The patient is not considered to be compensated unless pH
is within normal range
iv. If changes in that direction are noted either in PaCo2 or HCO3
with minimal changes in pH, the patient is considered to be
partially compensated
v. Respiratory compensation
1. Eliminating or retaining CO2 by the lungs also regulates
acid-base balance
, Pathophysiology Final Exam Study
Guide 3
2. The response is rapid, occurs within minutes by altering the
rate and depth of respiration
3. Carbon Dioxide is a powerful stimulator of the respiratory system
vi. Metabolic compensation
1. For acute metabolic acidosis – body will compensate with
respiratory alkalosis
2. They are the ultimate long-term regulator of acid-base balance
3. They are slower to respond, but their response is more
permanent and selective
4. Maintain acid-base balance by excreting or conserving
bicarbonate and hydrogen ions
a. When pH decreases, H+ ions are excreted, and
bicarbonate acid ions are formed and retained
b. When pH increases, H+ are retained, and
bicarbonate acids are excreted
e. Respiratory alkalosis
i. Decrease PCO2 with increased pH
ii. Caused by:
1. Hyperventilation
2. Central stimulation of respiratory center
3. Stimulation of peripheral pathways to respiratory center
iii. Very common in anxiety attacks
f. Respiratory acidosis
i. Increase in CO2 with decreased pH
ii. Caused by:
1. Acute disorders of ventilation
2. Chronic disorders of ventilation
3. Increased Carbon dioxide production
iii. **Emphysema, COPD, pulmonary fibrosis and chronic bronchitis
can cause respiratory acidosis
iv. Increased PCO2 Production
1. Exercise
2. Fever
3. Sepsis
4. Burns
5. Carbohydrate rich diet
g. Metabolic alkalosis
i. Increased bicarbonate with elevated pH
ii. Caused by:
1. Increased bicarbonate administration
2. Excess loss of acid via kidneys/GI
3. Increased bicarb levels by contraction of ECF via
hypokalemia & hypochloremia
iii. Alkalosis always related to hypocalcemia
h. Metabolic acidosis
i. Caused by:
1. Increased chloride
2. Chronic renal failure and DKA
ii. They will try to compensate by going into respiratory alkalosis
which would increase RR they will be hyperventilating
, Pathophysiology Final Exam Study
Guide 4
iii. When you increase respiratory rate you exhale more CO2 and
become more alkalotic
iv. If you decrease respiratory rate you hold CO2 and become acidotic.
v. When patient is acidic- potassium is going out of the cell and
patient comes hypercalcemic
i. ADH – function of ADH is water metabolism
i. If you increase ADH you have increased water retention and your
sodium will be diluted and patient will be hypoosmolar and
hyponatremic,
ii. If you decrease ADH you increase water excretion and you decrease
circulating volume and then the patient will be hyperosmolar and
hypernatremic
iii. ADH only affects sodium and not potassium
iv. ADH would be excreted when a patient has a high osmolarity
because its going to try and dilute the sodium
v. Released from the pituitary gland
j. Renin Angiotensin System
i. Renin gets secreted when you have decreased kidney perfusion
ii. Renin activates angiotensinogen to angiotensin 1 which
converts to angiotensin 2 in the lungs
iii. Renin is a potent vasoconstrictor which will go to the adrenal
cortex to secrete aldosterone which increases sodium
reabsorption
iv. ADH will be secreted from angiotensin 2 so both increases
circulating volume which will increase the blood pressure
k. Hypokalemia
i. Clinical manifestations: muscle weakness and leg cramps, fatigue,
anorexia and N+V, decreased bowel sounds, cardiac arrhythmias
(prolonged PR interval, flattened T wave)
l. Hyperkalemia
i. Clinical manifestations: Gastrointestinal Hyperactivity, Cardiac Arrhythmia,
Muscle weakness, Paresthesias
m. Hyponatremia
i. Clinical manifestations: Malaise, muscle cramps, Apprehension,
Abdominal cramps, Nausea and Vomiting, Diarrhea, Headache,
Confusion and Lethargy, Convulsions and Coma
