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NR 507: Advanced Pathophysiology Midterm, Exams of Pathophysiology

NR 507: Advanced Pathophysiology Midterm

Typology: Exams

2024/2025

Available from 09/30/2024

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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
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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)

  • respiratory acidosis

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.