nur 315 pathophysiology final exam study guide 1 ortega
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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
, Pathophysiology Final Exam Study Guide 2
4. Aortic valve disease
c. Tay Sachs Disease
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
, Pathophysiology Final Exam Study Guide 3
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
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
, Pathophysiology Final Exam Study Guide 4
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
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
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