1. What symptom may occur with acute enlargement of cysts before menses?

Sudden-onset, severe localized breast pain.

2. Does fibrocystic disease increase breast cancer risk?

No, unless atypia (ADH) is present, which does increase risk.

3. What are the ultrasound features of a simple cyst?

Well-circumscribed, anechoic, posterior acoustic enhancement, no solid components.

4. How do complicated cysts appear on ultrasound?

May have internal echoes, debris, imperceptible wall, may lack posterior acoustic enhancement.

5. Are complicated cysts usually malignant?

Very rarely malignant. Often aspirated or followed with repeat imaging.

6. What makes a cyst "complex"?

Mixed solid and cystic components, thick wall, and/or internal septa.

7. How are complex cysts evaluated?

Core biopsy to rule out malignancy.

8. What are fibroadenomas?

Benign, movable, firm, round tumors made of glandular and stromal tissue.

9. What is the "triple test" for fibroadenoma diagnosis?

Clinical exam + imaging + biopsy.

10. When might fibroadenomas be excised?

If larger than 2 cm, painful, or causing significant anxiety.

11. What is Atypical Ductal Hyperplasia (ADH)

Abnormal cell growth within the ducts

12. What is lobular carcinoma in situ (LCIS)?

Abnormal proliferation of cells within breast lobules, usually found incidentally

13. Is LCIS considered cancer?

No, it is a risk marker, not true carcinoma.

14. What are management options for LCIS?

Increased surveillance, chemoprevention, possible prophylactic mastectomy, or enrollment in prevention trials.

15. What are the three categories of benign epithelial breast lesions?

Nonproliferative, proliferative without atypia, and atypical hyperplasia.

16. What is atypical hyperplasia?

Abnormal proliferative breast lesions not severe enough for carcinoma in situ but with increased breast cancer risk.

17. What dietary changes may help breast pain?

Reduce methylxanthines (caffeine, theophylline, theobromine found in coffee, tea, chocolate, cola) and lower dietary fat.

collapse of alveoli leading to loss of lung volume

19. What is absorptive atelectasis?

Collapse of alveoli due to surfactant inactivation or nitrogen washout.

20. What condition most commonly causes surfactant inactivation?

Acute respiratory distress syndrome (ARDS)

21. What is compressive atelectasis?

Collapse due to external pressure on lung tissue (pleural effusion, tumor, pneumothorax, hemothorax, abdominal distention).

22. What is obstructive atelectasis?

Obstructive atelectasis (most common)

23. What is the most common cause of atelectasis overall?

Airway obstruction by secretions, mucus, foreign bodies, tumors, or oxygen toxicity

24. Why are postoperative patients at high risk for atelectasis?

Hypoventilation from anesthesia/narcotics, incisional pain, abdominal distention, immobility.

25. List additional risk factors for atelectasis.

Chronic lung disease, obesity, opioids, blood transfusions, tobacco use, anesthesia >4 hours, prior CVA, lung cancer, pleural effusion, NG tube placement.

26. Common symptoms of atelectasis?

Dyspnea, cough, sputum production, leukocytosis.

29. positive end-expiratory pressure (PEEP)

Mechanical maintenance of pressure in the airway at the end of expiration to increase the volume of gas remaining in the lungs.

30. What are the classifications of pneumonia

Community-acquired (CAP), health care-associated (HCAP), hospital-acquired (HAP), and ventilator-associated (VAP).

Pneumonia that occurs outside of healthcare facilities or within 48 hours of hospital admission.

33. Other organisms that can cause CAP?

Haemophilus influenzae, Staphylococcus aureus, Moraxella catarrhalis, Legionella, viruses.

(excessive) urea and nitrogenous substances in the blood

Pneumonia that occurs in a patient hospitalized for at least 48 hrs

Pneumonia that occurs <48 hours after mechanical ventilation.

38. What are key prevention strategies for VAP?

Elevate HOB 30-45°, drain secretions, maintain cuff pressures, daily oral care (teeth brushing), early enteral feeding, safe suctioning, ventilator circuit changes only if soiled.

- hospitalized within 90 days of developing pneumonia- patients attending hemodialysis- patients receiving wound care,IV therapy at home- residents in long term care facilities or nursing homes

40. Who is considered immunocompromised?

Patients on steroids, chemotherapy, broad-spectrum antibiotics, with AIDS, genetic immune disorders, malnutrition, or long-term life-support.

deficient amount of oxygen in the blood

deficiency in the amount of oxygen reaching the tissues

43. Major risk factors for CAP?

Smoking, alcohol use, COPD, HF, diabetes, liver/kidney disease, poor dental hygiene, age >65, immunosuppressive therapy, poor nutrition, large households, environmental exposures.

44. Major risk factors for HAP/VAP?

Malnutrition, debilitation, altered mental status, prior antibiotics, hospitalization >5 days, intubation >48 hours, tracheostomy, surgeries, supine position, immunosuppressive therapy.

45. Classic symptoms of pneumonia?

Fever, cough (productive or dry), dyspnea, leukocytosis.

46. Other symptoms of pneumonia?

Rigors, pleuritic chest pain, tachypnea, tachycardia, fatigue, anorexia, muscle aches, headache, sore throat, rash.

47. What does chest x-ray show in pneumonia?

New infiltrates or consolidation, segmental or lobar, often within 48 hours of symptoms.

48. What bacteria causes TB?

Mycobacterium tuberculosis (acid-fast, aerobic bacillus).

49. What happens when TB bacteria reach the alveoli?

Macrophages ingest bacilli ’ if not destroyed, infection begins.

50. What is primary TB?

The first infection, usually silent (no obvious symptoms).

51. What is miliary TB?

Spread of TB through blood and lymph to other organs.

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Nur195 ~ Exam 1

Respiratory, Renal, & Reproductive Medsurg

Question	Answer
1. What symptom may occur with acute enlargement of cysts before menses?	Sudden-onset, severe localized breast pain.
2. Does fibrocystic disease increase breast cancer risk?	No, unless atypia (ADH) is present, which does increase risk.
3. What are the ultrasound features of a simple cyst?	Well-circumscribed, anechoic, posterior acoustic enhancement, no solid components.
4. How do complicated cysts appear on ultrasound?	May have internal echoes, debris, imperceptible wall, may lack posterior acoustic enhancement.
5. Are complicated cysts usually malignant?	Very rarely malignant. Often aspirated or followed with repeat imaging.
6. What makes a cyst "complex"?	Mixed solid and cystic components, thick wall, and/or internal septa.
7. How are complex cysts evaluated?	Core biopsy to rule out malignancy.
8. What are fibroadenomas?	Benign, movable, firm, round tumors made of glandular and stromal tissue.
9. What is the "triple test" for fibroadenoma diagnosis?	Clinical exam + imaging + biopsy.
10. When might fibroadenomas be excised?	If larger than 2 cm, painful, or causing significant anxiety.
11. What is Atypical Ductal Hyperplasia (ADH)	Abnormal cell growth within the ducts
12. What is lobular carcinoma in situ (LCIS)?	Abnormal proliferation of cells within breast lobules, usually found incidentally
13. Is LCIS considered cancer?	No, it is a risk marker, not true carcinoma.
14. What are management options for LCIS?	Increased surveillance, chemoprevention, possible prophylactic mastectomy, or enrollment in prevention trials.
15. What are the three categories of benign epithelial breast lesions?	Nonproliferative, proliferative without atypia, and atypical hyperplasia.
16. What is atypical hyperplasia?	Abnormal proliferative breast lesions not severe enough for carcinoma in situ but with increased breast cancer risk.
17. What dietary changes may help breast pain?	Reduce methylxanthines (caffeine, theophylline, theobromine found in coffee, tea, chocolate, cola) and lower dietary fat.
18. Atelectasis	collapse of alveoli leading to loss of lung volume
19. What is absorptive atelectasis?	Collapse of alveoli due to surfactant inactivation or nitrogen washout.
20. What condition most commonly causes surfactant inactivation?	Acute respiratory distress syndrome (ARDS)
21. What is compressive atelectasis?	Collapse due to external pressure on lung tissue (pleural effusion, tumor, pneumothorax, hemothorax, abdominal distention).
22. What is obstructive atelectasis?	Obstructive atelectasis (most common)
23. What is the most common cause of atelectasis overall?	Airway obstruction by secretions, mucus, foreign bodies, tumors, or oxygen toxicity
24. Why are postoperative patients at high risk for atelectasis?	Hypoventilation from anesthesia/narcotics, incisional pain, abdominal distention, immobility.
25. List additional risk factors for atelectasis.	Chronic lung disease, obesity, opioids, blood transfusions, tobacco use, anesthesia >4 hours, prior CVA, lung cancer, pleural effusion, NG tube placement.
26. Common symptoms of atelectasis?	Dyspnea, cough, sputum production, leukocytosis.
27. What is a classic postoperative sign of atelectasis?	Low-grade fever.
28. What complication can chronic atelectasis lead to?	Postobstructive pneumonia
29. positive end-expiratory pressure (PEEP)	Mechanical maintenance of pressure in the airway at the end of expiration to increase the volume of gas remaining in the lungs.
30. What are the classifications of pneumonia	Community-acquired (CAP), health care-associated (HCAP), hospital-acquired (HAP), and ventilator-associated (VAP).
31. What is CAP?	Pneumonia that occurs outside of healthcare facilities or within 48 hours of hospital admission.
32. What is the most common cause of CAP?	Streptococcus pneumoniae.
33. Other organisms that can cause CAP?	Haemophilus influenzae, Staphylococcus aureus, Moraxella catarrhalis, Legionella, viruses.
34. Azotemia	(excessive) urea and nitrogenous substances in the blood
35. What is HAP?	Pneumonia that occurs in a patient hospitalized for at least 48 hrs
36. What is VAP?	Pneumonia that occurs <48 hours after mechanical ventilation.
37. Common organisms causing HAP/VAP?	Gram-negative
38. What are key prevention strategies for VAP?	Elevate HOB 30-45°, drain secretions, maintain cuff pressures, daily oral care (teeth brushing), early enteral feeding, safe suctioning, ventilator circuit changes only if soiled.
39. What is HCAP	- hospitalized within 90 days of developing pneumonia- patients attending hemodialysis- patients receiving wound care,IV therapy at home- residents in long term care facilities or nursing homes
40. Who is considered immunocompromised?	Patients on steroids, chemotherapy, broad-spectrum antibiotics, with AIDS, genetic immune disorders, malnutrition, or long-term life-support.
41. Hypoxemia	deficient amount of oxygen in the blood
42. Hypoxia	deficiency in the amount of oxygen reaching the tissues
43. Major risk factors for CAP?	Smoking, alcohol use, COPD, HF, diabetes, liver/kidney disease, poor dental hygiene, age >65, immunosuppressive therapy, poor nutrition, large households, environmental exposures.
44. Major risk factors for HAP/VAP?	Malnutrition, debilitation, altered mental status, prior antibiotics, hospitalization >5 days, intubation >48 hours, tracheostomy, surgeries, supine position, immunosuppressive therapy.
45. Classic symptoms of pneumonia?	Fever, cough (productive or dry), dyspnea, leukocytosis.
46. Other symptoms of pneumonia?	Rigors, pleuritic chest pain, tachypnea, tachycardia, fatigue, anorexia, muscle aches, headache, sore throat, rash.
47. What does chest x-ray show in pneumonia?	New infiltrates or consolidation, segmental or lobar, often within 48 hours of symptoms.
48. What bacteria causes TB?	Mycobacterium tuberculosis (acid-fast, aerobic bacillus).
49. What happens when TB bacteria reach the alveoli?	Macrophages ingest bacilli ’ if not destroyed, infection begins.
50. What is primary TB?	The first infection, usually silent (no obvious symptoms).
51. What is miliary TB?	Spread of TB through blood and lymph to other organs.
52. What is a granuloma/Ghon tubercle?	A walled-off area of infection that may scar or calcify.
53. What is latent TB?	Infection is present but inactive, no symptoms, not contagious.
54. What is reactivation TB?	Latent TB becomes active again, often due to weak immunity.
55. What medical conditions increase TB risk?	Diabetes, kidney disease, malnutrition, silicosis.
56. Common symptoms of TB?	Low-grade fever, night sweats, weight loss, fatigue, cough.
57. What does the cough become as TB progresses?	Mucopurulent (mucus + pus), sometimes bloody (hemoptysis).
58. What is the Mantoux test (PPD)?	Skin test using purified protein derivative injected into the forearm.
59. What indicates a positive PPD reaction?	Induration (hard swelling), not redness.
60. What lab test identifies TB bacteria?	Acid-fast bacilli (AFB) smear and sputum culture.
61. Why is TB treated with multiple drugs?	To prevent resistance
62. What are the 4 first-line TB drugs?	Isoniazid (INH), Rifampin, Pyrazinamide, Ethambutol.
63. What is MDR-TB?	multi-drug resistant TB
64. Pleural effusion	A buildup of fluid in the pleural space.
65. What is pleural effusion a typical complication of?	Pneumonia
66. Pleurisy (pleuritis)	Inflammation of both layers of the pleura (parietal + visceral).
67. What causes pleurisy?	Pneumonia, TB, URI, trauma, PE, pulmonary infarction, cancer, thoracotomy, collagen diseases.
68. What cancers are most associated with pleural effusion?	Bronchogenic carcinoma and breast cancer.
69. What are the two main types of pleural effusion?	Transudate (clear, HF, hypoalbuminemia) and Exudate (inflammatory, infection, tumor).
70. What is an empyema?	A type of pleural effusion with pus (purulent fluid).
71. How does effusion affect breathing?	Large effusion ’ dyspnea. Small/moderate effusion ’ minimal symptoms.
72. What assessment findings suggest effusion?	“ or absent breath sounds, “ fremitus, dull percussion, dyspnea.(Severe
73. What imaging/tests diagnose pleural effusion?	CXR, CT, ultrasound, lateral decubitus x-ray, thoracentesis (fluid analysis).
74. What usually causes empyema?	Bacterial pneumonia, lung abscess, trauma, surgery, or TB.
75. What microbe most often causes empyema?	Streptococcus pneumoniae.
76. What symptoms are seen in empyema?	Fever, chills, cough, dyspnea, chest pain, tachycardia.
77. What procedure removes pleural fluid for relief or diagnosis?	Thoracentesis
78. Why should no more than 1,000-1,500 mL be removed in one thoracentesis?	To prevent reexpansion pulmonary edema and hypovolemia.
79. What is pleurodesis?	Instilling a chemical irritant (like talc) into pleural space to stick pleura together and prevent fluid reaccumulation.
80. What is decortication?	Surgical removal of fibrous tissue ("pleural peel") trapping the lung.
81. What is a tunneled pleural catheter (TPC)?	A long-term catheter that allows patients to drain fluid at home.
82. Why does the patient need frequent turning and movement during tPA/DNase therapy or pleurodesis?	To spread the medication evenly over the pleural surface.
83. Pulmonary edema	accumulation of fluid in the lungs
84. Ph range	7.35-7.45
85. Metabolic acidosis	low pH, low HCO3
86. Metabolic alkalosis	high pH, high HCO3
87. HCO3 range	22-26
88. PaCO2 range	35-45 mmHg
89. Respiratory Alkalosis	high pH, low CO2
90. Respiratory Acidosis	low pH, high CO2
91. A patient's ABG results are	pH = 7.30, PaCO₂ = 50 mmHg, HCO₃⁻ = 24 mEq/L Which condition is most likely?
92. Which finding is most consistent with metabolic alkalosis?	Persistent vomiting
93. A nurse is caring for a patient with diabetic ketoacidosis (DKA). Which ABG pattern is expected?	pH “, HCO₃⁻ “
94. A patient with pneumonia has ABGs	pH 7.28, PaCO₂ 55 mmHg, HCO₃⁻ 26 mEq/L. Which intervention is priority?
95. Which ABG result indicates respiratory alkalosis?	pH 7.50, PaCO₂ 28 mmHg
96. A patient is anxious and hyperventilating. What acid-base imbalance is most likely?	Respiratory alkalosis
97. Which condition can cause metabolic acidosis?	Diarrhea
98. ABG results	pH = 7.48, PaCO₂ = 40 mmHg, HCO₃⁻ = 30 mEq/L. Which disorder is this?
99. A patient with renal failure is at highest risk for which imbalance?	Metabolic acidosis
100. Which nursing intervention is appropriate for respiratory alkalosis due to anxiety?	Encourage slow breathing into cupped hands or paper bag
101. What is acute respiratory failure (ARF)?	A sudden, life-threatening inability of the lungs to exchange oxygen and carbon dioxide.
102. What PaO₂ and PaCO₂ values define ARF?	PaO₂ < 50 mmHg (hypoxemia) and/or PaCO₂ > 50 mmHg with pH < 7.35 (hypercapnia).
103. Hypercapnia	excessive carbon dioxide in the blood
104. Give an example of decreased respiratory drive leading to ARF.	Brain injury, sedative overdose, or severe hypothyroidism.
105. What chest wall disorders can lead to ARF?	Muscular dystrophy, Guillain-Barré, spinal cord injury, flail chest.
106. What lung conditions can lead to ARF?	Pneumonia, ARDS, pulmonary edema, atelectasis, COPD exacerbation, pulmonary embolism.
107. What are early signs of ARF?	Restlessness, headache, dyspnea, tachycardia, tachypnea, high BP.
108. What are late/worsening signs of ARF?	Confusion, cyanosis, diaphoresis, lethargy, respiratory arrest.
109. What treatments may be used for ARF?	Oxygen therapy, mechanical ventilation, bronchodilators, steroids, reversal agents (naloxone/flumazenil).
110. When positioning a patient with ARF, which lung should be placed down?	The least affected lung (to improve perfusion and oxygenation).
111. What acid-base disorder is commonly associated with ARF?	Respiratory acidosis
112. What does ARDS stand for?	acute respiratory distress syndrome
113. How does ARDS usually present on chest X-ray?	Bilateral infiltrates (patchy, white areas) similar to pulmonary edema.
114. What is the hallmark sign of ARDS?	Severe hypoxemia that does not improve with oxygen (refractory hypoxemia).
115. What causes ARDS?	An inflammatory trigger that damages the alveolar-capillary membrane, leading to fluid leakage into the alveoli.
116. What happens to alveoli in ARDS?	They collapse due to fluid, inflammatory cells, and loss of surfactant ’ causing stiff lungs and poor gas exchange.
117. What is the most common cause of death in ARDS?	Multisystem organ failure
118. Name 3 major risk factors for ARDS.	Sepsis, aspiration (gastric contents or drowning), and trauma.
119. What is the normal PaO2/FiO2 ratio?	Greater than 300 mm Hg.120. How is ARDS severity measured?
121. What is PEEP and why is it used in ARDS?	Positive End-Expiratory Pressure. It keeps alveoli open, improves oxygenation, and reduces shunting.
122. What position may improve oxygenation in ARDS?	Prone
123. Why are low tidal volumes used in ARDS ventilation?	To prevent further lung injury (barotrauma/volutrauma).
124. A.R.D.S Pneumonic	Atelectasis, Refractory hypoxemia, Decreased lung compliance, Surfactant is decreased
125. 3 phases of ARDS	1. Exudative 2. Proliferative 3. Fibrotic
126. What is the normal mean pulmonary artery pressure?	12-15 mm Hg.
127. How is pulmonary artery pressure measured?	Right-sided heart catheterization (gold standard) or estimated with echocardiogram
128. What are the two main types of PAH?	Idiopathic (unknown cause) and secondary (due to another disease)
129. What is a common cause of secondary PAH?	Pulmonary artery constriction from chronic hypoxemia and hypercapnia in COPD.
130. What structural change occurs in PAH?	Thickening of pulmonary vessels ’ stiff, narrowed, noncompliant arteries.
131. What happens to the right ventricle in PAH?	It works harder ’ hypertrophy and eventual failure (cor pulmonale).
132. What is the most common symptom of PAH?	dyspnea on exertion
133. Name 3 other symptoms of PAH besides dyspnea.	Chest pain, fatigue/weakness, syncope (fainting), hemoptysis, signs of right-sided heart failure (edema, ascites, JVD, hepatomegaly).
134. What is hemoptysis	coughing up blood
135. What diagnostic test confirms PAH?	Right heart catheterization
136. Why is supplemental oxygen important in PAH?	It reverses hypoxia-induced vasoconstriction in pulmonary vessels.
137. What common medications may be used in PAH treatment?	Diuretics, digoxin, anticoagulants, calcium channel blockers, vasodilators (prostacyclin, sildenafil, bosentan).
138. Which heart sound may be heard with PAH?	Right ventricular S3 gallop or a heart murmur.
139. What is pulmonary artery hypertension (PAH)	High blood pressure in the arteries of the lungs that is progressive and eventually fatal.
140. What does PAH cause	Right sided heart failure
141. What is the leading cause of preventable hospital death?	Pulmonary embolism (PE).
142. What is Virchow's triad (3 factors leading to venous thrombosis)?	1) Venous stasis (slowed blood flow), 2) Vessel wall injury, 3) Hypercoagulability.
143. Where do most thrombi that cause PE originate?	Deep veins of the legs (DVT).
144. Name 3 risk factors for PE.	Major surgery, immobility >2 days, cancer, trauma, obesity, age >40, pregnancy, central venous catheters, prior thromboembolism (any 3).
145. Besides blood clots, what other types of emboli can cause PE?	Air, fat, amniotic fluid, tumor cells, septic emboli, IV particulates.
146. What is the most common symptom of PE?	Sudden onset of dyspnea (shortness of breath).
147. Other symptoms of PE include...?	Pleuritic chest pain, cough, hemoptysis, palpitations.
148. Common signs of PE on assessment?	Common signs of PE on assessment?A
149. What happens if a massive PE occurs?	Shock, severe dyspnea, hypotension, weak rapid pulse, syncope, sudden death.
150. What hemodynamic effect does PE have on the heart?	Increases pulmonary vascular resistance ’ strain on right ventricle ’ right heart failure ’ shock.
151. What is the gold standard imaging for diagnosing PE today?	CT pulmonary angiography (CTPA).
152. What initial diagnostic test can rule out PE with high accuracy if negative?	D-dimer blood test.
153. What is the best prevention for PE?	Prevent DVT with early ambulation, leg exercises, compression devices, and prophylactic anticoagulants.
154. A nurse is caring for a patient who suddenly develops shortness of breath, chest pain, and tachycardia. Which condition should the nurse suspect first?	Pulmonary embolism
155. Which of the following is the most common symptom of a pulmonary embolism?	Dyspnea
156. A patient with a suspected PE has a negative D-dimer test. What does this indicate?	The diagnosis of PE is effectively ruled out
157. Which triad of factors (Virchow's triad) increases the risk for thrombus formation leading to PE?	Hypercoagulability, venous stasis, vessel wall injury
158. A patient with a massive pulmonary embolism is most at risk for which complication?	Shock and circulatory collapse
159. Which statement made by a patient with a history of PE indicates a need for further teaching?	"I can stop my prescribed anticoagulant when I feel better."
160. The nurse recognizes that alveolar dead space in a patient with PE means
161. What are the three major pathophysiologic states caused by chest trauma?	Hypoxemia (airway disruption, lung injury, collapsed lung, pulmonary contusion, pneumothorax) Hypovolemia (fluid/blood loss from great vessels, hemothorax, cardiac rupture)Cardiac failure (cardiac tamponade, contusion, ‘ intrathoracic pressure)
162. What is the primary assessment sequence in chest trauma according to ATLS?	CABCDE (Castrophic bleeding, Airway, Breathing, Circulation, Disability (neuro status), Exposure/Environmental control)
163. What are key diagnostics for chest trauma?	Chest x-ray, CT scan, ABGs, pulse oximetry, CBC, coagulation studies, type & crossmatch, ECG.
164. Why is the drainage system kept below chest level?	To prevent fluid from flowing back into the pleural space.
165. Main signs of rib fractures?	Severe pain, tenderness, bruising, shallow breathing, risk for atelectasis.
166. What are ribs 1-3 fractures associated with?	High mortality, subclavian vessel injury
167. What is flail chest?	When e3 adjacent ribs are fractured in e2 places, creating a free-floating rib segment.
168. How does the flail segment move?	Paradoxically - inward on inspiration, outward on expiration.
169. What is a pulmonary contusion?	Bruised lung tissue causing bleeding + edema inside alveoli and interstitium.
170. What is cardiac tamponade?	Compression of the heart from blood/fluid in pericardial sac.
171. What is a pneumothorax?	Air in the pleural space ’ lung collapse.
172. What are the different types of pneumothorax	-Closed-Open-Tension-Hemothorax-Chylothorax
173. What is the most life threatening pneumothorax	Tension pneumothorax
174. tension pneumothorax	A life-threatening collection of air within the pleural space; the volume and pressure have both collasped the involved lung and caused a shift of the mediastinal structures to the opposite side.
175. Signs of tension pneumothorax?	Severe distress, tracheal shift, absent breath sounds, hyperresonance, hypotension, tachycardia, cyanosis.
176. What is subcutaneous emphysema?	Air leaks into skin tissue (face, neck, chest, scrotum).
177. Hemothorax	blood in the pleural cavity
178. Chylothorax	a condition marked by lymphatic fluid in the pleural space caused by a leak in the thoracic duct.
179. Pruitus	severe itching
180. What are the 3 phases of acute kidney injury	Oliguric, diuretic, recovery
181. What is the urine output characteristic of the oliguric phase in acute kidney injury?	100-400 mL/24 hr
182. What happens to serum creatinine and BUN levels during the oliguric phase of acute kidney injury?	They increase.
183. What electrolyte imbalance is commonly seen in the oliguric phase of acute kidney injury?	Hyperkalemia
184. What metabolic condition is associated with the oliguric phase of acute kidney injury?	Bicarbonate deficit (metabolic acidosis)
185. What is a common sodium imbalance in the oliguric phase of acute kidney injury?	Hyponatremia
186. What is pyelonephritis	A bacterial infection of the kidneys
187. Acute pyelonephritis symptoms	Chills, fever, flank pain, and tenderness, tachycardia, pyuria, N/V, HA, malaise, dysuria
188. Chronic pyelonephritis symptoms	Fatigue, poor appetite, polyuria, weight loss, progressive scarring of the kidney
189. What is renal lithiasis?	Stone formation (calculi) in the kidney.
190. What is a common symptom of renal lithiasis?	Intense, colicky pain starting in your back or side, radiating to groin.
191. What urine changes may indicate renal lithiasis?	Bloody, cloudy or foul-smelling urine.
192. What are some gastrointestinal symptoms associated with renal lithiasis?	Nausea and vomiting.
193. What urinary symptom may occur with renal lithiasis?	Persistent urge to urinate.
194. What systemic symptoms may indicate an infection in renal lithiasis?	Fever and chills.
195. A male patient reports burning urination, perineal pain, and purulent discharge. Which condition is most likely?	Prostatitis
196. Which assessment finding best indicates pyelonephritis?	Fever with flank pain
197. A patient suddenly develops absent breath sounds on the right after intubation. What is most likely?	Pneumothorax or right mainstem intubation
198. What is the most effective priority nursing action to slow CKD progression?	Tight glucose control
199. What finding differentiates pyelonephritis from cystitis?	White blood cell casts in urine. This shows the infection has reached the kidneys.
200. What is the priority intervention for a suspected tension pneumothorax?	Immediate needle decompression (followed by chest tube).
201. What is the first priority intervention for severe hyperkalemia (K⁺ > 6.5)?	IV calcium gluconate ’ stabilizes myocardium and prevents lethal arrhythmias.
202. After a long flight, patient has sudden SOB, tachycardia, and pleuritic chest pain. What condition should be suspected?	Pulmonary embolism
203. Which ABG finding explains confusion and agitation in pneumonia?	Low PaO₂ (hypoxemia) ’ brain is very sensitive to low oxygen levels
204. A COPD patient with ABG	pH 7.28, PaCO₂ 55, HCO₃ 24 is drowsy. What's the nurse's priority?
205. Post-op patient has unilateral leg swelling, warmth, and pain. What should the nurse do first?	Notify the provider immediately, Classic DVT signs. Don't elevate or ambulate before confirming orders, since clot may dislodge ’ PE risk.
206. Patient on high-flow O₂ develops decreased breath sounds with O₂ >60%. What complication do you suspect?	Absorptive atelectasis, High O₂ washes out nitrogen ’ alveoli collapse ’ decreased breath sounds & hypoxemia.
207. A post-MVC patient has severe hypoxemia that doesn't improve with oxygen. What condition is most likely?	ARDS (Acute Respiratory Distress Syndrome) Hallmark of ARDS = refractory hypoxemia (doesn't improve even with oxygen).
208. Patient post-hip replacement suddenly has dyspnea, chest pain, and tachycardia. What's the first nursing action?	Elevate the head of bed and apply oxygen Likely pulmonary embolism ’ first priority = improve oxygenation while awaiting definitive treatment.
209. Symptoms of COPD	dyspnea, chronic cough, sputum production, barrel chest
210. What is emphysema	a condition in which the air sacs of the lungs are damaged and enlarged, causing breathlessness.
211. What do COPD patients store	Carbon dioxide
212. A patient with COPD has an oxygen level of 92%, how should the nurse respond	They should note this as a normal finding for a patient with COPD
213. What do patients with COPD have a higher risk for	Right sided heart failure, Pulmonary hypertension,
214. A patient with COPD is on 6mL of o2 via NC, what is the patient at risk for	Decreased respiratory drive
215. What is status asthmaticus	Life-threatening episode of airway obstruction that is unresponsive to common treatment
216. What will be elevated on the CBC of a patient having an asthma exacerbation	Eosinophils because it is an immune response
217. What is acute glomerulonephritis	inflammation of the glomerulus
218. Symptoms of glomerulonephritis	Hematuria, Edema, Azotemia, HTN, Proteinuria, Cloudy or coffee colored urine, Flank pain, Malaise
219. What are risk factors for acute glomerulonephritis?	strep throat, lupus, and skin infections
220. A patient with chronic glomerulonephritis (GN) is most at risk for developing which complication?	End-stage kidney disease (ESKD)
221. Which underlying conditions are the most common causes of chronic glomerulonephritis in the U.S.?	Diabetes mellitus and hypertension
222. Which symptom would the nurse expect in a patient with chronic GN?	Nighttime foot edema and fatigue
223. A patient with chronic GN reports nausea, vomiting, and decreased urine output. What is the nurse's priority action?	Notify the healthcare provider immediately (sign of worsening kidney failure)
224. In a patient with chronic GN, which electrolyte imbalance is linked to tetany and a positive Chvostek's sign?	Hypocalcemia
225. The nurse assesses an ECG of a patient with chronic GN and notes tall, tented T waves. What condition does this indicate?	Hyperkalemia
226. A patient with chronic GN shows anemia on labs. What is the most likely cause?	Decreased erythropoietin production
227. What is the gold standard diagnostic test for glomerular disease?	Kidney biopsy
228. A patient with chronic GN presents with acute weight gain of 6%, crackles in the lungs, and distended neck veins. Which imbalance does the nurse suspect?	Fluid volume excess
229. Which treatment helps lower serum potassium in hyperkalemia?	IV glucose and insulin (drives K⁺ into cells).
230. A patient has tingling around the mouth, hyperactive reflexes, and a positive Trousseau's sign. What imbalance is suspected?	Hypocalcemia
231. A patient with chronic GN presents with pallor, fatigue, and soft flabby muscles. Which imbalance is most likely?	Protein deficit
232. The nurse notes facial flushing, depressed reflexes, and respiratory depression in a renal patient. Which imbalance does this indicate?	Hypermagnesemia
233. Which finding is most associated with phosphorus excess (hyperphosphatemia)?	Tetany and muscle spasms
234. What is the hallmark clinical finding of nephrotic syndrome?	Proteinuria >3.5 g/day, usually with hypoalbuminemia and edema.
235. What is nephrotic syndrome	a clinical state of glomerular injury
236. A patient with nephrotic syndrome has serum albumin of 2.0 g/dL. Which complication should the nurse monitor for most closely?	Generalized edema (anasarca) due to decreased colloid osmotic pressure.
237. Why are patients with nephrotic syndrome at increased risk for infection?	Loss of immunoglobulins in the urine decreases immune protection.
238. Which lab finding is most consistent with nephrotic syndrome?	Cholesterol 350 mg/dL (hyperlipidemia is a key finding).
239. What is the most common cause of nephrotic injury	Diabetic nephropathy
240. What is the pathophysiologic reason nephrotic syndrome patients develop hyperlipidemia?	The liver increases lipid synthesis in response to hypoalbuminemia.
241. Which teaching point is essential for a patient on immunosuppressive therapy for nephrotic syndrome?	Report any sign of infection promptly
242. Which dietary recommendation is most appropriate for a patient with nephrotic syndrome?	Moderate protein, low-salt, reduced cholesterol diet.
243. What distinguishes acute kidney failure from chronic kidney failure?	Acute develops over hours to days; chronic develops over months to years.
244. Kidney failure leads to which electrolyte and acid-base imbalance?	Hyperkalemia and metabolic acidosis due to impaired excretion of potassium and hydrogen ions.
245. What is the definition of kidney failure?	The inability of the kidneys to remove metabolic wastes or regulate fluid, electrolytes, and acid-base balance.
246. Which lab values would the nurse expect in kidney failure?	‘ BUN, ‘ creatinine, ‘ potassium, “ GFR, metabolic acidosis.
247. A patient with CKD is at risk for bone disease. Why?	Impaired vitamin D activation and phosphate retention cause hypocalcemia, stimulating parathyroid hormone release and bone demineralization.
248. Which clinical finding is most concerning in AKI?	Hyperkalemia
249. What dietary restrictions are common in kidney failure?	Low sodium, low potassium, low phosphorus; protein restriction depending on disease stage; fluid restriction in advanced disease.
250. The nurse is caring for a patient with AKI who is oliguric. What complication should the nurse monitor for most closely?	Fluid overload leading to pulmonary edema.
251. Which intervention is priority before a patient with CKD undergoes a kidney biopsy?	Assess coagulation studies (PT, PTT, platelets) to prevent bleeding risk.
252. Which nursing diagnosis is most appropriate for a patient with CKD who has fatigue, pallor, and low hemoglobin?	Activity intolerance related to anemia (due to decreased erythropoietin production).
253. What are the three main classifications of AKI?	Prerenal
254. What is the most common cause of AKI in hospitalized patients?	Septic shock
255. What is the hallmark sign of prerenal AKI?	Oliguria (<30 mL/hr) with evidence of hypoperfusion (low MAP <65 mmHg).
256. What is the gold standard imaging test for suspected postrenal AKI?	Renal ultrasonography.
257. Which phase of AKI is associated with fluid overload, hyperkalemia, and rising BUN/creatinine?	Oliguric phase
258. During which AKI phase should the nurse monitor closely for dehydration and hypokalemia?	diuretic phase
259. A patient with AKI after IV contrast exposure is at risk for what condition?	Contrast-induced nephropathy (CIN).
260. Which medication should be held before contrast dye procedures in patients at risk for AKI?	Metformin (risk for lactic acidosis).
261. What is the typical timeline for recovery after AKI if renal function returns?	3-6 months, but full GFR recovery may take up to 1 year.
262. Why is chronic kidney disease (CKD) called the "silent killer"?	Because kidneys can maintain fluid and electrolyte balance until late disease, so symptoms appear only after significant nephron loss.
263. How is CKD defined?	Kidney damage or decreased renal function for 3 months with evidence of irreversible nephron loss and scarring.
264. What GFR cutoffs define CKD and ESKD?	CKD
265. What are the top 3 causes of CKD in the U.S.?	Diabetes mellitus (DM), hypertension (HTN), and glomerulonephritis (GN).
266. What are common neurologic manifestations of CKD/uremia?	Lethargy, confusion, muscle twitching, agitation, seizures, peripheral neuropathy, cramps.
267. What hematologic abnormality is common in CKD and why?	Anemia, due to decreased erythropoietin production by the kidneys.
268. What electrolyte disturbances occur in advanced CKD?	Hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis
269. What systemic signs of uremia may be seen in late CKD?	Yellow-gray skin pigmentation, periorbital or peripheral edema, pruritus, uremic frost, Kussmaul respirations.
270. What is the major complication of CKD?	ESRD requiring dialysis
271. How can nurses help reduce CKD progression?	Educate on BP and glucose control, proteinuria management, medication adherence, diet and fluid modifications, and reporting worsening symptoms.
272. What causes pericarditis in CKD?	Irritation of the pericardium by uremic toxins, sometimes leading to pericardial effusion or tamponade.
273. What GI manifestations are common in CKD?	Anorexia, nausea, vomiting, hiccups, uremic fetor (ammonia odor to breath), metallic taste, and mouth ulcers.
274. Why do CKD patients have increased bleeding risk despite normal platelet counts?	Platelet function is defective ’ prolonged bleeding time.
275. What reproductive issues can CKD cause?	Erectile dysfunction, decreased libido, amenorrhea, infertility, and testicular atrophy.
276. What electrolyte imbalance develops as GFR falls below 30 mL/min?	Hyperphosphatemia with hypocalcemia, leading to secondary hyperparathyroidism.
277. What lab test is the most sensitive indicator of kidney function?	Serum creatinine, since BUN is influenced by diet, meds, and catabolism.
278. Why are ACE inhibitors or ARBs prescribed in CKD?	They lower BP, reduce proteinuria, and slow progression of kidney disease.
279. Why are phosphate binders used in CKD?	To reduce serum phosphate levels, prevent hyperphosphatemia, and help control secondary hyperparathyroidism.
280. What parts of the urinary tract are affected by lower UTIs?	Bladder (cystitis), prostate (prostatitis), and urethra (urethritis).
281. What parts of the urinary tract are affected by upper UTIs?	Kidneys and renal pelvis (pyelonephritis), interstitial nephritis, renal abscesses.
282. What is the most common cause of UTIs?	Coliform bacteria, especially E. coli.
283. How are uncomplicated UTIs usually classified?	Community-acquired, common in young AFAB/female patients, and not usually recurrent.
284. How are complicated UTIs usually classified?	Often hospital-acquired, linked to catheterization, urologic abnormalities, diabetes, pregnancy, or immunosuppression; often recurrent.
285. What symptoms are most commonly associated with acute cystitis (bladder infection)?	Dysuria, frequency, urgency, suprapubic pain.
286. What protein provides a protective water barrier in the bladder against bacterial adherence?	Glycosaminoglycan (GAG).
287. What is urethrovesical reflux and how does it increase UTI risk?	It is backward flow of urine from the urethra into the bladder, carrying bacteria back into the bladder.
288. Which sexually transmitted infections can also cause prostatitis?	Chlamydia trachomatis, Neisseria gonorrhoeae, and Trichomonas vaginalis.
289. What is the most common causative organism of prostatitis?	Escherichia coli (E. coli).
290. Why should a digital rectal exam (DRE) be avoided in suspected acute prostatitis?	It can cause severe pain and increase the risk of bacteremia/septicemia.
291. What are hallmark symptoms of acute bacterial prostatitis?	Fever, chills, perineal or low back pain, dysuria, urgency, frequency, and nocturia.
292. What is the goal of antibiotic therapy in acute bacterial prostatitis?	Prevent abscess formation and septicemia.
293. What are common obstructive urinary symptoms of BPH?	Hesitancy, weak stream, intermittency, incomplete emptying, dribbling, and urinary retention.
294. Which pharmacologic therapy relaxes prostate smooth muscle and bladder neck to improve urine flow?	Alpha-adrenergic blockers.
295. What emergency intervention is required for acute urinary retention due to BPH?	Catheterization (preferably with a Coude catheter).
296. What surgical intervention is considered the "gold standard" for severe obstructive BPH?	Transurethral resection of the prostate (TURP).

Created by: luminousea555

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