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NR 507: Advanced Pathophysiology Midterm
1. Asthma: Chronic disease due to bronchoconstriction and an excessive inflam-
matory response in the bronchioles
2. What are 5 s/s of asthma: coughing
wheezing shortness of breath rapid breathing chest tightness
3. Pathophysiology of asthma (5): -airway inflammation, bronchial hyper-reactivity
and smooth muscle spasm -excess mucus production and accumulation -hypertrophy of bronchial smooth muscle -airflow obstruction -decreased alveolar ventilation
4. Bronchioles: smaller passageways that originate from the bronchi that become
the alveoli
5. 3 layers of the bronchioles: innermost layer
middle layer - lamina propria outermost layer
6. lamina propria: the middle layer of the bronchioles
7. structure of the lamina propria: embedded with connective tissue cells and
immune cells
8. purpose of the lamina propria: white blood cells are present to help protect the
airways
9. How does the lamina propria effect the lungs in regards to asthma: the WBCs
protective feature goes into overdrive causing an inflammatory response that
damages host tissue
10. What does the innermost layer of the bronchioles contain: columnar epithe- lial
ells and mucus producing goblet cells
11. What does the outermost layer of the bronchioles contain: smooth muscle cells
12. what does the outermost layer of the bronchioles do: control the airways ability
to constrict and dilate
13. alveolar hyperinflation: When air is unable to move out of the alveolar like it
should due to bronchial walls collapsing around possible mucus plug thus trapping air inside
14. how does hyperinflation occur?: the ongoing inflammatory process of asthma
produces mucus and pus plug that the bronchial walls collapse around
15. Effect of hyperinflation of the alveolar: -expanded thorax and hypercapnia
(retention of CO2)
16. What are two anticholinergic drugs used for asthma: tiotropium and iprat-
ropium
17. What do anticholinergics do in the lungs?: These drugs block the effects of the
parasympathetic nervous system
- increasing bronchodilation
18. MOA of anticholinergic drugs for asthma: the parasympathetic system is
stimulated by the vagal nerve to release acetylcholine which binds to the cholinergic receptors of the respiratory tract to cause bronchial constriction = decreased airflow
- blocking the cholinergic receptors prevents acetylcholine binding preventing the bronchial constriction
- thickening and rigidity of bronchial basement membrane
29. What does smooth muscle hypertrophy do in lungs?: causes increased
bronchoconstriction
30. Hypertrophy and hyperplasia of goblet cells do what in the bronchials: pro- motes
hypersecretion of mucus
31. What are characteristics of epithelial cell metaplasia?: squamous cells be- come
nonciliated and are less protective; allow passage of toxins and WBCs
32. What does the migration of WBCs to the bronchials do?: increases inflam- mation
of the cite and causes fibrosis in the bronchial wall
33. How does the thickening and rigidity of bronchial basement membranes effect the
lungs?: leads to further narrowing of the bronchial passageways
34. What acid-base disorder is seen in chronic bronchitis?: respiratory acidosis
35. how does chronic bronchitis lead to respiratory acidosis?: hyperinflation of the
alveoli causes CO2 retention
36. Where does air enter the body?: naso and oropharynx (mouth and nose)
37. Where does air go after it passes through the nose and mouth?: it passes through
the trachea
38. After air passes through the trachea where does it go?: goes into the left or right
bronchi
39. Where does air flow after the bronchi?: into the smaller bronchioles
40. Where does air flow after the bronchioles?: into the alveoli
41. Describe how blood flows to become oxygenated: - deoxygenated systemic blood
flows from the vena cava to R atrium
- Tricuspid valve opens to flow to R ventricle -Pulmonary semilunar valve opens and blood flows to the alveolar capillaries for gas exchange from the pulmonary trunk and L & R pulmonary arteries
- blood goes from alveolar capillaries to pulmonary veins to return oxygenated
blood to the left atrium
- bicuspid valve opens to allow blood to go to left ventricle
- aortic semilunar valve opens and blood goes to the aorta
- aorta pushes oxygenated blood out to the body
42. What is the formula for cardiac output: CO = HR x SV
43. cardiac reserve: difference between resting and maximal CO; should be about
4-5x as high but does decrease 1% per year after age 30
44. What type of relationship does heart rate and stroke volume have?: inverse low HR
= longer fill time = increase stroke volume high HR = lower fill time = lower stroke volume
58. What increases cardiac muscle contraction: sympathetic stimulation; fear
anxiety and increased thyroxine
59. what decreases cardiac muscle contraction: low ATP levels; ischemia hypox- ia or
acidosis
60. Stimulation of what set a resting HR (chronotropic state): parasympathetic
system
61. what stimulates the parasympathetic system: the vagus nerve
62. What does the parasympathetic system do?: It releases acetycholine which
decreases heart rate and causes vasodilation
63. What can extreme vagal response result in?: life threatening bradycardia
64. What mediates the sympathetic system: epinephrine and norepinephrine
65. What does the sympathetic system promote in the cardiac system: vaso-
constriction and increased HR
66. What can uncontrolled tachycardia lead to?: reduced stroke volume and
fatigue
67. What are the two parts of the cardiac cycle?: diastole and systole
68. What causes blood to move from the atria to the ventricles: gravity and atriole
systole
69. What causes the S1 heart sound?: Bicuspid/Mitral and Tricuspid valves clos- ing
70. What are the atrioventricular valves?: tricuspid and bicuspid (mitral) valves
71. What are the semilunar valves?: pulmonary and aortic valves
72. What causes the semilunar valves to open?: As ventricles contract and
intraventricular pressure rises, blood is pushed up against the SL valves, forcing them to open
73. ejection fraction: measurement of the volume percentage of left ventricular
contents ejected with each contraction
74. What causes the semilunar valves to close?: ventricles relax and intraven-
tricular pressure falls, blood flows back from the arteries, and fill the cusps of the semilunar valves
75. What causes the S2 heart sound?: closing of semilunar (aortic and pul-
monary) valves
76. What prevents the backflow into the ventricles: semilunar valves
77. Stenosis of heart valve: A narrowing of the valve opening, causing turbulent
flow and enlargement of the emptying chamber
78. Stenosis of a heart valve, may result in what?: Narrowing of the heart valves
means that blood moves with difficulty out of the heart. Results may include chest pain, edema in the feet or ankles, and irregular heartbeat. and hypertrophy
79. heart failure: cardiac dysfunction caused by the inability of the heart to provide
adequate CO resulting in inadequate tissue perfusion
80. Left sided heart failure characteristic: inability of the left ventricle to provide
adequate blood flow into systemic circulation
81. Causes of left sided heart failure: systemic hypertension left
ventricle MI LV hypertrophy Aortic SL valve or bicuspid valve damage Secondary to right heart failure
82. How does LV hypertrophy lead to left sided heart failure: The hypertrophy is
secondary to cardiac damage resulting in an enlarged by weaker structure that holds more blood
83. How does Aortic SL valve or bicuspid valve damage lead to heart failure-
: damage leads to back flow into the left atrium or ventricle after ejection
- RV Hypertrophy
- pulmonary SLV or tricuspid valve damage
- secondary to left heart failure
90. What is the most common cause of right sided heart failure: pulmonary
hypertension
91. Progression of right sided heart failure: - damage causes the right ventricle to
increase contraction force to eject/unload the blood
- over time EF is reduced and right ventricle us unable to eject the normal amount of blood
- the blood remaining in the RV increases and RA preload increases until the RA is unable to eject the normal amount of blood into the RA
- the amount of blood remaining in the right atrium increases causing an increase in RA preload
- blood volum enad pressure then backs up into the vena cava and systemic veins
92. signs and symptoms of right sided heart failure: jugular vein distension
hepatosplenomegaly peripheral edema
93. Why does hepatosplenomegaly develop in right sided heart failure: the large
volume of blood flow through the liver and spleen causes these areas to be engorged
94. why does peripheral edema occur in right sided heart failure: Increased
pressure forces fluid from the systemic capillaries into the peripheral tissues and flood those areas
95. High output failure: inability of the heart to pump sufficient amounts of blood to
meet the circulatory needs of the body despite normal blood volume and cardiac contractility
96. causes of high output failure: Severe anemia
Nutritional deficiencies Hyperthyroidis m Sepsis Extreme febrile state
97. Process of high output failure: - impaired oxygen delivery of excessive tissue
oxygen demands cause tissue hypoxia
- catecholamines initiation increase HR and stroke volume
104. Erythropietin: Produce: Kidney (small amount in
liver) Released: Kidney Target: Bone Marrow Functions: Stimulates bone marrow to produce more red blood cells
105. hematopoietic stem cells: The stem cells that give rise to RBC WBC
and platelets through the process of haematopoiesis.
106. How does a hematopoietic stem cell produce a red blood cell: hematopoi-
etic stem cells produces an unndifferentiated hemocytoblast
- erythropoietin binds to it and createsa a proerythroblast
- cell develops into an erythrocyte 7 days later
107. Erythrocyte function: transport oxygen and carbon dioxide
108. Erythrocyte life span: 120 days
109. anemia risk factors: acute or chronic blood loss, increased hemolysis,
inade- quate dietary intake or malabsorption, bone marrow suppression, age
110. function of hemoglobin: In red blood cells, carries oxygen from the
lungs to body's tissues and returns carbon dioxide from tissues back to lungs. It also maintains the shape of red blood cells.
111. causes of anemia: - impaired RBC production
- excessive blood loss
- increased RBC destruction
112. hemolytic anemia: premature destruction of RBCs
113. causes of hemolytic anemia:
infection transfusion reaction
hemolytic disease of the newborn (Rh incompatibility) autoimmune reaction drug induced
114. development of anemia due to gastrectomy: loss of intrinsic factor from
surgery results in the loss of protein necessary for vitamin B12 absorption an can lead to anemia
115. what kind of anemia can result from incorrect blood transfusion: hemolytic
anemia
116. normocytic normochromic anemia: Characterized by red cells that are
rela- tively normal in size and hemoglobin content but insufficient in number
117. hemolytic anemia is what kind of anemia: normocytic normochromic anemia
118. polycythemia vera: condition characterized by too many erythrocytes;
blood becomes too thick to flow easily through blood vessels
nitrogen waste is a product of protein metabolism (ammonia) liver converts ammonia to urea and the kidneys secreted urea into the tubule for secretion also possible to eliminate products that are in excess in the blood -- potassium, hydrogen, metabolites or medications can secrete things that were too larger to fit through the glomerulus's pore
127. filtration (kidney): movement of solutes from blood to filtrate at
bowman's capsule 20% of the blood that goes through the glomerulus is passed as filtrate into the bowman's capsule
depends on the hydrostatic and oncotic pressures/ starling forces between the glomerulus and bowman's capsule hydrostatic pressure: a lot higher in the glomerulus (move into the nephron/bow- man's capsule) oncotic pressure: higher in the blood/glomerulus than in the bowman's capsule (move into the blood/glomerulus) hydrostatic pressure is greater so there will be movement into bowman's capsule usually favors the filtrate to go into the bowman's capsule each persons full body is filtered about every 40 minutes
128. Conditions associated with renal failure: - congenital abnormalities in the
urethral tract development
- kidney and bladder cancer
- infections
- glomerulonephritis
- acute/ tubular necrosis
- AKI
129. vesicoureteral reflux: Abnormal ureter-bladder connection allowing
retro- grade flow of urine from bladder to ureters and/or kidneys
130. renal agenesis: unilatral or bilateral failure of the kidneys to develop in
utero
131. Potter syndrome: Syndrome characterized by bilateral renal agenesis
and incompatibility of live birth
132. Wilms tumor: - Embryonal kidney tumor associated with defective tumor
136. Ascending infection: - urethra to bladder, and then to kidney
- due to: bacteria from residual fecal contamination
137. glomerulonephritis: inflammation of the glomeruli of the kidney
138. tubular necrosis: the renal tubules cells are highly sensitive to low
oxygen levels or presence of toxins and leads to tubular necrosis
139. Causes of tubular necrosis: - being post operative
- severe sepsis
- burns
- trauma
- contrast chemical use in medical imaging procedures
140. Pathophysiology of tubular necrosis: - ischemia or nephrotoxin exposure
occurs to the renal tubules
- inflammation and tubular injury occur
- cast formation and tubular obstruction occurs
- tubular injury, leakage, increased glomerular pressure causes decreased capillary perfusion further decrease in GFR occurs
- oliguria results
141. Acute Kidney Injury: Sudden decline in kidney function with a decrease
in GFR and an increase in plasma creatinine and BUN levels -results in oliguria
142. Prerenal disease: decreased blood flow to and through the kidney
143. prerenal disease causes: - hypotension
- decreased cardia output
- decreased blood volume
144. What are most cases of AKI caused by?: prerenal issues
145. Intrarenal disease: disease or damage within the kidney
146. Causes of intrarenal disease:
ATN Acute glomerulonephritis
147. postrenal disease: obstruction in the lower urinary tract that prevents
urine flow from the kidneys
148. Causes of postrenal disease:
BPH Calculi Inflammatio n Tumors
149. Chronic kidney disease: progressive, irreversible deterioration in renal
func- tion Labs: elevated BUN, Cr Phosphorus. Rx: meds for hypertension, statins, epoetin, diuretics, calcium, LOW protein, low salt, restrict K, phosphorus (no chicken, milk, legumes, carbonated drinks), dialysis.
