NIGHTINGALE PATHOPHYSIOLOGY MIDTERM ACTUAL VERIFIED EXAM | NIGHTINGALE COLLEGE
2026/2027 ACADEMIC YEAR | VERIFIED Q&A | UNIVERSITY-LEVEL NURSING STUDENTS
NIGHTINGALE
PATHOPHYSIOLOGY
MIDTERM 2026/2027
Nightingale Pathophysiology Midterm
Nightingale College - Actual Verified Exam
2026/2027 Academic Year | Verified Q&A for University-Level
Nursing Students | Pathophysiology Midterm
150Q VERIFIED NEWEST EXAM RATIONALES
MIDTERM EXAM 2026/2027 NURSING
INCLUDES:
• Cellular Injury, Inflammation, Immunity, Fluid Electrolytes, Acid-Base
• Cardiovascular, Respiratory, Renal, Neuro, Endocrine Pathophysiology
• 150 Verified Questions + Answers + Detailed Rationales | Midterm
• Professional Study Guide | Borders + Page Numbers | 2026/2027 Edition
Nightingale Pathophysiology Midterm | Nightingale College | Not affiliated
Confidential Study Guide - Educational Purposes Only | 2026/2027 Edition
,Cellular Injury Inflammation Immunity Fluid Electrolytes Acid-Base
Description: Cellular injury etiology hypoxia ischemia chemical toxins infectious microbial, mechanisms ATP depletion oxidative stress, reversible injury cell swelling
hydropic change organelle swelling membrane blebbing fatty change steatosis, irreversible injury membrane damage lysosomal enzyme release necrosis morphological
types coagulative protein denaturation most organs except brain, liquefactive brain, caseous TB cheese-like, fat saponification, gangrenous, apoptosis programmed cell
death caspases, inflammation acute inflammation rapid onset short duration cardinal signs redness heat swelling pain loss function, vascular response vasodilation
increased permeability, cellular response neutrophils first macrophages monocytes, chemical mediators histamine mast cells vasodilation, prostaglandins pain fever,
leukotrienes chemotaxis, cytokines IL-1 TNF IL-6, complement, chronic inflammation prolonged weeks months macrophages lymphocytes plasma cells granuloma,
systemic manifestations leukocytosis fever acute phase proteins, healing regeneration labile stable permanent cells repair fibrosis scar, immunity innate non-specific first
line physical chemical barriers skin acidic pH mucous lysozyme cilia, second line phagocytes neutrophils monocytes macrophages NK natural killer, inflammation
complement, adaptive specific third line humoral B lymphocytes plasma cells antibodies IgG IgM IgA IgE IgD, cell-mediated T lymphocytes CD4 helper CD8 cytotoxic
memory primary secondary response, fluid electrolytes body fluids ICF intracellular 2/3 ECF extracellular 1/3 interstitial plasma, sodium 135-145 mEq/L hypernatremia
water deficit dehydration causes confusion seizures treatment hypotonic fluids, hyponatremia water excess causes cerebral edema, potassium 3.5-5.0 hyperkalemia
cardiac arrest peaked T wide QRS causes renal failure, hypokalemia U waves arrhythmia causes diuretics, acid-base pH 7.35-7.45 regulation buffers lungs kidneys,
metabolic acidosis low pH low HCO3 causes DKA lactic acidosis, metabolic alkalosis high pH high HCO3 vomiting NG suction, respiratory acidosis high pH? low pH high
CO2 hypoventilation, respiratory alkalosis low CO2 hyperventilation compensation buffering.
Cardiovascular Respiratory Renal Pathophysiology Midterm
Description: Cardiovascular pathophysiology cardiac function cardiac output CO = HR x SV stroke volume preload afterload contractility, heart failure inability pump
sufficient blood left HF dyspnea orthopnea paroxysmal nocturnal dyspnea crackles, right HF peripheral edema JVD hepatomegaly, systolic HFrEF EF <40% impaired
contraction diastolic HFpEF impaired relaxation, pathophysiology remodeling RAAS SNS activation, coronary artery disease atherosclerosis plaque formation MI
myocardial infarction types STEMI NSTEMI coronary occlusion plaque rupture thrombus ischemia necrosis biomarkers troponin CK-MB ECG changes, hypertension
primary essential secondary renal endocrine complications, shock hypovolemic cardiogenic distributive septic neurogenic obstructive, valvular disease, respiratory
pathophysiology ventilation perfusion, asthma reversible airway obstruction bronchospasm inflammation hyperresponsiveness triggers allergic, pathophysiology IgE mast
cell histamine, status asthmaticus, COPD Chronic Obstructive Pulmonary Disease chronic bronchitis productive cough 3 months 2 years blue bloater, emphysema
destruction alveolar walls air trapping pink puffer, irreversible FEV1/FVC <0.7, pneumonia infection alveoli bacterial viral community vs hospital acquired, lobar
bronchopneumonia, ARDS Acute Respiratory Distress Syndrome acute hypoxemic respiratory failure PaO2/FiO2 <300 bilateral infiltrates, pulmonary edema cardiogenic
non-cardiogenic, renal pathophysiology AKI Acute Kidney Injury sudden decline GFR increased creatinine BUN classification prerenal decreased perfusion hypovolemia
intrinsic ATN Acute Tubular Necrosis nephrotoxic glomerulonephritis postrenal obstruction stones BPH, RIFLE criteria Risk Injury Failure Loss ESRD, CKD Chronic Kidney
Disease GFR <60 for 3 months stages 1-5 ESRD <15 uremic syndrome, glomerulonephritis inflammation glomeruli immune mediated nephritic nephrotic syndrome.
Neurologic Endocrine Pathophysiology Nursing Concepts Midterm
Description: Neurologic pathophysiology CNS central PNS peripheral, stroke cerebrovascular accident CVA ischemic 87% thrombotic embolic decreased perfusion
penumbra, hemorrhagic 13% intracerebral subarachnoid hypertension aneurysm, manifestations contralateral deficits aphasia hemiplegia, TIA transient ischemic attack
<24 hr warning, seizures abnormal excessive synchronous neuronal activity classification focal partial vs generalized tonic-clonic absence, epilepsy recurrent, status
epilepticus >5 min emergency, increased ICP intracranial pressure normal 5-15 mmHg Monroe-Kellie doctrine brain blood CSF compensatory, causes mass lesion edema
hydrocephalus, manifestations Cushing triad hypertension bradycardia irregular respirations headache vomiting papilledema, herniation, head injury concussion contusion,
endocrine pathophysiology hormone regulation feedback, diabetes mellitus hyperglycemia Type 1 autoimmune beta cell destruction absolute insulin deficiency juvenile
onset DKA Diabetic Ketoacidosis, Type 2 insulin resistance relative deficiency adult onset risk obesity, complications acute DKA HHS Hyperosmolar Hyperglycemic State
chronic microvascular retinopathy nephropathy neuropathy macrovascular CAD stroke, thyroid disorders hyperthyroidism excess thyroid hormone Graves disease
autoimmune TSH receptor antibodies heat intolerance weight loss tachycardia goiter exophthalmos treatment antithyroid radioactive iodine, hypothyroidism low thyroid
Hashimoto autoimmune cold intolerance weight gain bradycardia myxedema, nursing concepts pathophysiology midterm exam Nightingale College covers cellular
adaptation injury inflammation immunity fluid electrolytes acid-base genetics neoplasia.
Page 2 - Nightingale Patho Midterm 150Q 2026/2027
,Question 1: Q1: Cellular injury - reversible vs irreversible injury?
A. Cellular injury reversible cell swelling fatty change membrane blebbing, irreversible membrane damage lysosomal rupture necrosis types coagulative
liquefactive caseous fat
B. Reversible injury membrane rupture
C. Irreversible injury cell swelling only
D. No difference reversible irreversible
CORRECT ANSWER: A. Cellular injury reversible cell swelling fatty change membrane blebbing, irreversible membrane damage lysosomal
rupture necrosis types coagulative liquefactive caseous fat
RATIONALE:
Rationale: Cellular injury reversible cell swelling fatty change membrane blebbing, irreversible membrane damage lysosomal rupture necrosis types coagulative
liquefactive caseous fat. Per Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level
nursing students midterm 2026/2027.
Question 2: Q2: Inflammation - acute vs chronic inflammation mediators?
A. Chronic inflammation neutrophils only
B. Acute inflammation macrophages only
C. Inflammation acute rapid onset neutrophils mediators histamine prostaglandins leukotrienes cytokines, chronic prolonged macrophages lymphocytes
granuloma
D. No mediators inflammation
CORRECT ANSWER: C. Inflammation acute rapid onset neutrophils mediators histamine prostaglandins leukotrienes cytokines, chronic
prolonged macrophages lymphocytes granuloma
RATIONALE:
Rationale: Inflammation acute rapid onset neutrophils mediators histamine prostaglandins leukotrienes cytokines, chronic prolonged macrophages lymphocytes
granuloma. Per Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students
midterm 2026/2027.
Question 3: Q3: Immunity - innate vs adaptive immunity?
A. Only adaptive immunity
B. Only innate immunity
C. No immunity
D. Immunity innate nonspecific barriers skin mucous phagocytes NK complement, adaptive specific B cells antibodies humoral T cells cellular memory
CORRECT ANSWER: D. Immunity innate nonspecific barriers skin mucous phagocytes NK complement, adaptive specific B cells antibodies
humoral T cells cellular memory
RATIONALE:
Rationale: Immunity innate nonspecific barriers skin mucous phagocytes NK complement, adaptive specific B cells antibodies humoral T cells cellular memory. Per
Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm
2026/2027.
Question 4: Q4: Fluid electrolytes - sodium potassium imbalances?
A. No sodium imbalances fluid electrolytes
B. Fluid electrolytes sodium hypernatremia water deficit hyponatremia water excess, potassium hyperkalemia cardiac arrest hypokalemia arrhythmia,
causes symptoms
C. No potassium imbalances fluid electrolytes
D. Only sodium fluid electrolytes
CORRECT ANSWER: B. Fluid electrolytes sodium hypernatremia water deficit hyponatremia water excess, potassium hyperkalemia cardiac
arrest hypokalemia arrhythmia, causes symptoms
RATIONALE:
Rationale: Fluid electrolytes sodium hypernatremia water deficit hyponatremia water excess, potassium hyperkalemia cardiac arrest hypokalemia arrhythmia, causes
symptoms. Per Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students
midterm 2026/2027.
Question 5: Q5: Acid-base - metabolic respiratory acidosis alkalosis?
A. Acid-base pH 7.35-7.45 metabolic acidosis low HCO3 respiratory acidosis high CO2 metabolic alkalosis high HCO3 respiratory alkalosis low CO2
compensation
B. pH normal 7.0 acid-base
C. No metabolic acidosis acid-base
D. No respiratory acidosis acid-base
CORRECT ANSWER: A. Acid-base pH 7.35-7.45 metabolic acidosis low HCO3 respiratory acidosis high CO2 metabolic alkalosis high HCO3
respiratory alkalosis low CO2 compensation
RATIONALE:
Rationale: Acid-base pH 7.35-7.45 metabolic acidosis low HCO3 respiratory acidosis high CO2 metabolic alkalosis high HCO3 respiratory alkalosis low CO2
compensation. Per Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing
students midterm 2026/2027.
Question 6: Q6: Cardiovascular pathophysiology - heart failure and MI?
A. No MI cardiovascular patho
B. No heart failure cardiovascular patho
C. Cardiovascular heart failure left right systolic diastolic, MI myocardial infarction coronary occlusion atherosclerosis, hypertension, shock
D. Only hypertension cardiovascular patho
CORRECT ANSWER: C. Cardiovascular heart failure left right systolic diastolic, MI myocardial infarction coronary occlusion atherosclerosis,
hypertension, shock
Page 3 - Nightingale Patho Midterm 150Q 2026/2027
, RATIONALE:
Rationale: Cardiovascular heart failure left right systolic diastolic, MI myocardial infarction coronary occlusion atherosclerosis, hypertension, shock. Per Nightingale
College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm 2026/2027.
Question 7: Q7: Respiratory pathophysiology - asthma COPD and pneumonia?
A. Only COPD respiratory patho
B. Only asthma respiratory patho
C. No pneumonia respiratory patho
D. Respiratory asthma reversible bronchospasm COPD chronic bronchitis emphysema irreversible, pneumonia infection alveoli, ARDS, pulmonary
edema
CORRECT ANSWER: D. Respiratory asthma reversible bronchospasm COPD chronic bronchitis emphysema irreversible, pneumonia infection
alveoli, ARDS, pulmonary edema
RATIONALE:
Rationale: Respiratory asthma reversible bronchospasm COPD chronic bronchitis emphysema irreversible, pneumonia infection alveoli, ARDS, pulmonary edema. Per
Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm
2026/2027.
Question 8: Q8: Renal pathophysiology - AKI CKD and glomerulonephritis?
A. No AKI renal patho
B. Renal AKI Acute Kidney Injury prerenal intrinsic postrenal, CKD Chronic Kidney Disease GFR <60 stages, glomerulonephritis inflammation glomeruli
C. No CKD renal patho
D. Only glomerulonephritis renal patho
CORRECT ANSWER: B. Renal AKI Acute Kidney Injury prerenal intrinsic postrenal, CKD Chronic Kidney Disease GFR <60 stages,
glomerulonephritis inflammation glomeruli
RATIONALE:
Rationale: Renal AKI Acute Kidney Injury prerenal intrinsic postrenal, CKD Chronic Kidney Disease GFR <60 stages, glomerulonephritis inflammation glomeruli. Per
Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm
2026/2027.
Question 9: Q9: Neurologic pathophysiology - stroke seizures increased ICP?
A. Neurologic stroke ischemic hemorrhagic CVA, seizures abnormal electrical activity, increased ICP intracranial pressure causes Cushing triad
B. No stroke neurologic patho
C. No seizures neurologic patho
D. No ICP neurologic patho
CORRECT ANSWER: A. Neurologic stroke ischemic hemorrhagic CVA, seizures abnormal electrical activity, increased ICP intracranial
pressure causes Cushing triad
RATIONALE:
Rationale: Neurologic stroke ischemic hemorrhagic CVA, seizures abnormal electrical activity, increased ICP intracranial pressure causes Cushing triad. Per Nightingale
College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm 2026/2027.
Question 10: Q10: Endocrine pathophysiology - diabetes thyroid disorders?
A. Only hyperthyroidism endocrine patho
B. Only Type 1 diabetes endocrine patho
C. Endocrine diabetes Type 1 autoimmune Type 2 insulin resistance complications, thyroid hyperthyroidism Graves hypothyroidism Hashimoto
D. No diabetes endocrine patho
CORRECT ANSWER: C. Endocrine diabetes Type 1 autoimmune Type 2 insulin resistance complications, thyroid hyperthyroidism Graves
hypothyroidism Hashimoto
RATIONALE:
Rationale: Endocrine diabetes Type 1 autoimmune Type 2 insulin resistance complications, thyroid hyperthyroidism Graves hypothyroidism Hashimoto. Per Nightingale
College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm 2026/2027.
Page 4 - Nightingale Patho Midterm 150Q 2026/2027
2026/2027 ACADEMIC YEAR | VERIFIED Q&A | UNIVERSITY-LEVEL NURSING STUDENTS
NIGHTINGALE
PATHOPHYSIOLOGY
MIDTERM 2026/2027
Nightingale Pathophysiology Midterm
Nightingale College - Actual Verified Exam
2026/2027 Academic Year | Verified Q&A for University-Level
Nursing Students | Pathophysiology Midterm
150Q VERIFIED NEWEST EXAM RATIONALES
MIDTERM EXAM 2026/2027 NURSING
INCLUDES:
• Cellular Injury, Inflammation, Immunity, Fluid Electrolytes, Acid-Base
• Cardiovascular, Respiratory, Renal, Neuro, Endocrine Pathophysiology
• 150 Verified Questions + Answers + Detailed Rationales | Midterm
• Professional Study Guide | Borders + Page Numbers | 2026/2027 Edition
Nightingale Pathophysiology Midterm | Nightingale College | Not affiliated
Confidential Study Guide - Educational Purposes Only | 2026/2027 Edition
,Cellular Injury Inflammation Immunity Fluid Electrolytes Acid-Base
Description: Cellular injury etiology hypoxia ischemia chemical toxins infectious microbial, mechanisms ATP depletion oxidative stress, reversible injury cell swelling
hydropic change organelle swelling membrane blebbing fatty change steatosis, irreversible injury membrane damage lysosomal enzyme release necrosis morphological
types coagulative protein denaturation most organs except brain, liquefactive brain, caseous TB cheese-like, fat saponification, gangrenous, apoptosis programmed cell
death caspases, inflammation acute inflammation rapid onset short duration cardinal signs redness heat swelling pain loss function, vascular response vasodilation
increased permeability, cellular response neutrophils first macrophages monocytes, chemical mediators histamine mast cells vasodilation, prostaglandins pain fever,
leukotrienes chemotaxis, cytokines IL-1 TNF IL-6, complement, chronic inflammation prolonged weeks months macrophages lymphocytes plasma cells granuloma,
systemic manifestations leukocytosis fever acute phase proteins, healing regeneration labile stable permanent cells repair fibrosis scar, immunity innate non-specific first
line physical chemical barriers skin acidic pH mucous lysozyme cilia, second line phagocytes neutrophils monocytes macrophages NK natural killer, inflammation
complement, adaptive specific third line humoral B lymphocytes plasma cells antibodies IgG IgM IgA IgE IgD, cell-mediated T lymphocytes CD4 helper CD8 cytotoxic
memory primary secondary response, fluid electrolytes body fluids ICF intracellular 2/3 ECF extracellular 1/3 interstitial plasma, sodium 135-145 mEq/L hypernatremia
water deficit dehydration causes confusion seizures treatment hypotonic fluids, hyponatremia water excess causes cerebral edema, potassium 3.5-5.0 hyperkalemia
cardiac arrest peaked T wide QRS causes renal failure, hypokalemia U waves arrhythmia causes diuretics, acid-base pH 7.35-7.45 regulation buffers lungs kidneys,
metabolic acidosis low pH low HCO3 causes DKA lactic acidosis, metabolic alkalosis high pH high HCO3 vomiting NG suction, respiratory acidosis high pH? low pH high
CO2 hypoventilation, respiratory alkalosis low CO2 hyperventilation compensation buffering.
Cardiovascular Respiratory Renal Pathophysiology Midterm
Description: Cardiovascular pathophysiology cardiac function cardiac output CO = HR x SV stroke volume preload afterload contractility, heart failure inability pump
sufficient blood left HF dyspnea orthopnea paroxysmal nocturnal dyspnea crackles, right HF peripheral edema JVD hepatomegaly, systolic HFrEF EF <40% impaired
contraction diastolic HFpEF impaired relaxation, pathophysiology remodeling RAAS SNS activation, coronary artery disease atherosclerosis plaque formation MI
myocardial infarction types STEMI NSTEMI coronary occlusion plaque rupture thrombus ischemia necrosis biomarkers troponin CK-MB ECG changes, hypertension
primary essential secondary renal endocrine complications, shock hypovolemic cardiogenic distributive septic neurogenic obstructive, valvular disease, respiratory
pathophysiology ventilation perfusion, asthma reversible airway obstruction bronchospasm inflammation hyperresponsiveness triggers allergic, pathophysiology IgE mast
cell histamine, status asthmaticus, COPD Chronic Obstructive Pulmonary Disease chronic bronchitis productive cough 3 months 2 years blue bloater, emphysema
destruction alveolar walls air trapping pink puffer, irreversible FEV1/FVC <0.7, pneumonia infection alveoli bacterial viral community vs hospital acquired, lobar
bronchopneumonia, ARDS Acute Respiratory Distress Syndrome acute hypoxemic respiratory failure PaO2/FiO2 <300 bilateral infiltrates, pulmonary edema cardiogenic
non-cardiogenic, renal pathophysiology AKI Acute Kidney Injury sudden decline GFR increased creatinine BUN classification prerenal decreased perfusion hypovolemia
intrinsic ATN Acute Tubular Necrosis nephrotoxic glomerulonephritis postrenal obstruction stones BPH, RIFLE criteria Risk Injury Failure Loss ESRD, CKD Chronic Kidney
Disease GFR <60 for 3 months stages 1-5 ESRD <15 uremic syndrome, glomerulonephritis inflammation glomeruli immune mediated nephritic nephrotic syndrome.
Neurologic Endocrine Pathophysiology Nursing Concepts Midterm
Description: Neurologic pathophysiology CNS central PNS peripheral, stroke cerebrovascular accident CVA ischemic 87% thrombotic embolic decreased perfusion
penumbra, hemorrhagic 13% intracerebral subarachnoid hypertension aneurysm, manifestations contralateral deficits aphasia hemiplegia, TIA transient ischemic attack
<24 hr warning, seizures abnormal excessive synchronous neuronal activity classification focal partial vs generalized tonic-clonic absence, epilepsy recurrent, status
epilepticus >5 min emergency, increased ICP intracranial pressure normal 5-15 mmHg Monroe-Kellie doctrine brain blood CSF compensatory, causes mass lesion edema
hydrocephalus, manifestations Cushing triad hypertension bradycardia irregular respirations headache vomiting papilledema, herniation, head injury concussion contusion,
endocrine pathophysiology hormone regulation feedback, diabetes mellitus hyperglycemia Type 1 autoimmune beta cell destruction absolute insulin deficiency juvenile
onset DKA Diabetic Ketoacidosis, Type 2 insulin resistance relative deficiency adult onset risk obesity, complications acute DKA HHS Hyperosmolar Hyperglycemic State
chronic microvascular retinopathy nephropathy neuropathy macrovascular CAD stroke, thyroid disorders hyperthyroidism excess thyroid hormone Graves disease
autoimmune TSH receptor antibodies heat intolerance weight loss tachycardia goiter exophthalmos treatment antithyroid radioactive iodine, hypothyroidism low thyroid
Hashimoto autoimmune cold intolerance weight gain bradycardia myxedema, nursing concepts pathophysiology midterm exam Nightingale College covers cellular
adaptation injury inflammation immunity fluid electrolytes acid-base genetics neoplasia.
Page 2 - Nightingale Patho Midterm 150Q 2026/2027
,Question 1: Q1: Cellular injury - reversible vs irreversible injury?
A. Cellular injury reversible cell swelling fatty change membrane blebbing, irreversible membrane damage lysosomal rupture necrosis types coagulative
liquefactive caseous fat
B. Reversible injury membrane rupture
C. Irreversible injury cell swelling only
D. No difference reversible irreversible
CORRECT ANSWER: A. Cellular injury reversible cell swelling fatty change membrane blebbing, irreversible membrane damage lysosomal
rupture necrosis types coagulative liquefactive caseous fat
RATIONALE:
Rationale: Cellular injury reversible cell swelling fatty change membrane blebbing, irreversible membrane damage lysosomal rupture necrosis types coagulative
liquefactive caseous fat. Per Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level
nursing students midterm 2026/2027.
Question 2: Q2: Inflammation - acute vs chronic inflammation mediators?
A. Chronic inflammation neutrophils only
B. Acute inflammation macrophages only
C. Inflammation acute rapid onset neutrophils mediators histamine prostaglandins leukotrienes cytokines, chronic prolonged macrophages lymphocytes
granuloma
D. No mediators inflammation
CORRECT ANSWER: C. Inflammation acute rapid onset neutrophils mediators histamine prostaglandins leukotrienes cytokines, chronic
prolonged macrophages lymphocytes granuloma
RATIONALE:
Rationale: Inflammation acute rapid onset neutrophils mediators histamine prostaglandins leukotrienes cytokines, chronic prolonged macrophages lymphocytes
granuloma. Per Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students
midterm 2026/2027.
Question 3: Q3: Immunity - innate vs adaptive immunity?
A. Only adaptive immunity
B. Only innate immunity
C. No immunity
D. Immunity innate nonspecific barriers skin mucous phagocytes NK complement, adaptive specific B cells antibodies humoral T cells cellular memory
CORRECT ANSWER: D. Immunity innate nonspecific barriers skin mucous phagocytes NK complement, adaptive specific B cells antibodies
humoral T cells cellular memory
RATIONALE:
Rationale: Immunity innate nonspecific barriers skin mucous phagocytes NK complement, adaptive specific B cells antibodies humoral T cells cellular memory. Per
Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm
2026/2027.
Question 4: Q4: Fluid electrolytes - sodium potassium imbalances?
A. No sodium imbalances fluid electrolytes
B. Fluid electrolytes sodium hypernatremia water deficit hyponatremia water excess, potassium hyperkalemia cardiac arrest hypokalemia arrhythmia,
causes symptoms
C. No potassium imbalances fluid electrolytes
D. Only sodium fluid electrolytes
CORRECT ANSWER: B. Fluid electrolytes sodium hypernatremia water deficit hyponatremia water excess, potassium hyperkalemia cardiac
arrest hypokalemia arrhythmia, causes symptoms
RATIONALE:
Rationale: Fluid electrolytes sodium hypernatremia water deficit hyponatremia water excess, potassium hyperkalemia cardiac arrest hypokalemia arrhythmia, causes
symptoms. Per Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students
midterm 2026/2027.
Question 5: Q5: Acid-base - metabolic respiratory acidosis alkalosis?
A. Acid-base pH 7.35-7.45 metabolic acidosis low HCO3 respiratory acidosis high CO2 metabolic alkalosis high HCO3 respiratory alkalosis low CO2
compensation
B. pH normal 7.0 acid-base
C. No metabolic acidosis acid-base
D. No respiratory acidosis acid-base
CORRECT ANSWER: A. Acid-base pH 7.35-7.45 metabolic acidosis low HCO3 respiratory acidosis high CO2 metabolic alkalosis high HCO3
respiratory alkalosis low CO2 compensation
RATIONALE:
Rationale: Acid-base pH 7.35-7.45 metabolic acidosis low HCO3 respiratory acidosis high CO2 metabolic alkalosis high HCO3 respiratory alkalosis low CO2
compensation. Per Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing
students midterm 2026/2027.
Question 6: Q6: Cardiovascular pathophysiology - heart failure and MI?
A. No MI cardiovascular patho
B. No heart failure cardiovascular patho
C. Cardiovascular heart failure left right systolic diastolic, MI myocardial infarction coronary occlusion atherosclerosis, hypertension, shock
D. Only hypertension cardiovascular patho
CORRECT ANSWER: C. Cardiovascular heart failure left right systolic diastolic, MI myocardial infarction coronary occlusion atherosclerosis,
hypertension, shock
Page 3 - Nightingale Patho Midterm 150Q 2026/2027
, RATIONALE:
Rationale: Cardiovascular heart failure left right systolic diastolic, MI myocardial infarction coronary occlusion atherosclerosis, hypertension, shock. Per Nightingale
College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm 2026/2027.
Question 7: Q7: Respiratory pathophysiology - asthma COPD and pneumonia?
A. Only COPD respiratory patho
B. Only asthma respiratory patho
C. No pneumonia respiratory patho
D. Respiratory asthma reversible bronchospasm COPD chronic bronchitis emphysema irreversible, pneumonia infection alveoli, ARDS, pulmonary
edema
CORRECT ANSWER: D. Respiratory asthma reversible bronchospasm COPD chronic bronchitis emphysema irreversible, pneumonia infection
alveoli, ARDS, pulmonary edema
RATIONALE:
Rationale: Respiratory asthma reversible bronchospasm COPD chronic bronchitis emphysema irreversible, pneumonia infection alveoli, ARDS, pulmonary edema. Per
Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm
2026/2027.
Question 8: Q8: Renal pathophysiology - AKI CKD and glomerulonephritis?
A. No AKI renal patho
B. Renal AKI Acute Kidney Injury prerenal intrinsic postrenal, CKD Chronic Kidney Disease GFR <60 stages, glomerulonephritis inflammation glomeruli
C. No CKD renal patho
D. Only glomerulonephritis renal patho
CORRECT ANSWER: B. Renal AKI Acute Kidney Injury prerenal intrinsic postrenal, CKD Chronic Kidney Disease GFR <60 stages,
glomerulonephritis inflammation glomeruli
RATIONALE:
Rationale: Renal AKI Acute Kidney Injury prerenal intrinsic postrenal, CKD Chronic Kidney Disease GFR <60 stages, glomerulonephritis inflammation glomeruli. Per
Nightingale College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm
2026/2027.
Question 9: Q9: Neurologic pathophysiology - stroke seizures increased ICP?
A. Neurologic stroke ischemic hemorrhagic CVA, seizures abnormal electrical activity, increased ICP intracranial pressure causes Cushing triad
B. No stroke neurologic patho
C. No seizures neurologic patho
D. No ICP neurologic patho
CORRECT ANSWER: A. Neurologic stroke ischemic hemorrhagic CVA, seizures abnormal electrical activity, increased ICP intracranial
pressure causes Cushing triad
RATIONALE:
Rationale: Neurologic stroke ischemic hemorrhagic CVA, seizures abnormal electrical activity, increased ICP intracranial pressure causes Cushing triad. Per Nightingale
College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm 2026/2027.
Question 10: Q10: Endocrine pathophysiology - diabetes thyroid disorders?
A. Only hyperthyroidism endocrine patho
B. Only Type 1 diabetes endocrine patho
C. Endocrine diabetes Type 1 autoimmune Type 2 insulin resistance complications, thyroid hyperthyroidism Graves hypothyroidism Hashimoto
D. No diabetes endocrine patho
CORRECT ANSWER: C. Endocrine diabetes Type 1 autoimmune Type 2 insulin resistance complications, thyroid hyperthyroidism Graves
hypothyroidism Hashimoto
RATIONALE:
Rationale: Endocrine diabetes Type 1 autoimmune Type 2 insulin resistance complications, thyroid hyperthyroidism Graves hypothyroidism Hashimoto. Per Nightingale
College pathophysiology curriculum, McCance & Huether Pathophysiology and Porth's Pathophysiology for university-level nursing students midterm 2026/2027.
Page 4 - Nightingale Patho Midterm 150Q 2026/2027
