N212 Pathophysiology Exam 2 2026 Actual Test Bank | Eastwick College | 200+ Questions with Correct Answers & Detailed Rationales | Latest Update

Pass your N212 Pathophysiology Exam 2 at Eastwick College on the first attempt. This comprehensive practice test bank contains 200+ original, high-yield questions covering all N212 Exam 2 domains, including fluid and electrolyte imbalances, acid-base disorders, endocrine disorders (diabetes, thyroid, adrenal, pituitary), cardiovascular disorders (heart failure, hypertension, CAD, valvular disease), respiratory disorders (COPD, asthma, pneumonia, ARDS), renal disorders (AKI, CKD, glomerulonephritis), gastrointestinal disorders (liver, pancreas, GI bleed), neurological disorders (stroke, seizures, increased ICP), hematologic disorders (anemia, coagulopathies), and immune system disorders (autoimmunity, HIV). Complete with detailed rationales explaining correct answers and why distractors are wrong. Updated for the 2026 testing cycle. What's included in this exam bank: Section 1: Fluid and Electrolyte Imbalances (Questions 1-20) SIADH hyponatremia cerebral edema – extracellular hypotonicity → water shifts into neurons via aquaporins Spironolactone hyperkalemia exacerbated by – metabolic acidosis (H+ shifts into cells, K+ out) Vomiting hypokalemia mechanism – aldosterone secretion (volume contraction) increases K+ secretion DKA hyperkalemia despite total body depletion – insulin deficiency reduces cellular K+ uptake Hypercalcemia nephrogenic diabetes insipidus – inhibits aquaporin-2 insertion in collecting duct Hypophosphatemia respiratory muscle weakness – reduced ATP synthesis in skeletal muscle Hypermagnesemia ECG finding – prolonged PR interval and widened QRS complex Hyperparathyroidism hypophosphatemia – PTH increases renal phosphate excretion Cirrhosis hyponatremia – impaired renal water excretion due to non-osmotic ADH release TPN refeeding hypokalemia/hypophosphatemia – insulin-mediated cellular uptake SIADH exacerbation with – 5% dextrose in water (hypotonic) Metabolic alkalosis hypokalemia – intracellular shift of K+ in exchange for H+ Loop diuretics effect on calcium – inhibit calcium reabsorption → hypocalcemia Tumor lysis syndrome electrolytes – hyperkalemia, hyperphosphatemia, hypocalcemia CKD hypermagnesemia – decreased renal excretion (reduced GFR) Vomiting metabolic alkalosis urine finding – low urine chloride (10 mEq/L) Acid-base disorder with hyperkalemia – metabolic acidosis Hyperaldosteronism pattern – hypernatremia, hypokalemia, metabolic alkalosis DKA corrected sodium calculation – add 1.6 mEq/L per 100 mg/dL glucose above 100 → 140 mEq/L Hypernatremia pure water loss initial fluid – 0.45% sodium chloride (hypotonic) Section 2: Acid-Base Disorders (Questions 21-40) ABG: pH 7.25, PaCO2 60, HCO3- 26 – partially compensated respiratory acidosis COPD chronic ABG: pH 7.36, PaCO2 65, HCO3- 36 – chronic respiratory acidosis with renal compensation Diarrhea metabolic acidosis ABG – pH 7.30, PaCO2 35, HCO3- 18 ABG: pH 7.50, PaCO2 30, HCO3- 24 – acute respiratory alkalosis CKD anion gap – 25 mEq/L (high anion gap metabolic acidosis) Salicylate overdose ABG – mixed respiratory alkalosis and metabolic acidosis Normal ABG – pH 7.40, PaCO2 40, HCO3- 24 Metabolic acidosis compensation – hyperventilation to decrease PaCO2 (Winter's formula) Severe vomiting ABG interpretation – metabolic alkalosis with respiratory compensation Normal anion gap metabolic acidosis – hyperchloremic metabolic acidosis from diarrhea Metabolic acidosis with appropriate compensation – pH 7.25, PaCO2 30, HCO3- 12 Respiratory alkalosis renal compensation – increased excretion of bicarbonate Acute respiratory acidosis ABG – pH 7.30, PaCO2 55, HCO3- 24 Sepsis respiratory alkalosis – pH 7.48, PaCO2 28, HCO3- 22 Section 3: Endocrine Disorders (Questions 41-60) Metformin mechanism – AMPK activation (increases glucose uptake, reduces hepatic gluconeogenesis) Radioactive iodine for Graves' hypothyroidism – destroys thyroid follicular cells (persistent stimulating antibodies) Primary aldosteronism – high aldosterone, low renin, hypertension, hypokalemia, metabolic alkalosis DKA glucagon role – inhibits acetyl-CoA carboxylase → reduces malonyl-CoA → disinhibits CPT-1 (ketogenesis) Primary adrenal insufficiency – low cortisol, low aldosterone, high ACTH, high renin SIADH vs. hypothyroidism/adrenal insufficiency – low Na, high urine osmolality, low uric acid, normal thyroid/adrenal Diabetic nephropathy microalbuminuria – thickening of GBM and loss of negatively charged heparan sulfate Primary hyperparathyroidism stone mechanism – increased 1,25-dihydroxyvitamin D → increased intestinal calcium absorption Prolactinoma differentiation – elevated prolactin that does not increase after TRH SGLT2 inhibitor mechanism – inhibit glucose reabsorption in proximal tubule → glucosuria Sulfonylurea secondary failure – progressive beta-cell dysfunction PTU therapeutic effect – decreased free T4, increased TSH Primary adrenal insufficiency profile – low cortisol, low aldosterone, high ACTH, high renin DKA insulin therapy potassium change – decrease (insulin drives K+ into cells) Hashimoto's goiter – lymphocytic infiltration → compensatory hypertrophy in response to elevated TSH Adrenal adenoma Cushing's – low ACTH, high cortisol Hypoglycemia unawareness – blunted counterregulatory hormone responses due to prior hypoglycemic episodes Graves' vs. toxic multinodular goiter – exophthalmos and pretibial myxedema (Graves'-specific) Adrenal insufficiency stress-dose steroids – mimics normal cortisol surge for vascular tone and immune function Type 2 diabetes oral agent failure – progressive decline in beta-cell function and insulin secretion Section 4: Cardiovascular Disorders (Heart Failure, Hypertension, CAD) (Questions 61-80) HFrEF symptoms mechanism – increased LVEDP → pulmonary venous congestion SERCA2a inhibition effect – impaired relaxation (increased diastolic filling pressures) Diabetes hypertension evidence-based combo – ACE inhibitor + thiazide diuretic Heart failure hyponatremia – non-osmotic ADH release (reduced effective circulating volume) STEMI acute occlusion mechanism – rupture of thin-cap fibroatheroma (tissue factor exposure, platelet activation) Exertional angina hemodynamics – increased LVEDP (ischemia-induced diastolic dysfunction) mTOR inhibition in cardiac hypertrophy – reduces pathological hypertrophy and fibrosis SGLT2 inhibitor HF benefit – natriuresis and diuresis (reduced preload) Exercise stress test BP drop – left ventricular systolic dysfunction (reduced cardiac output) Primary aldosteronism pathophysiology – autonomous aldosterone secretion (sodium retention, volume expansion) Persistent HFrEF symptoms on GDMT – add sacubitril/valsartan (ARNI) Resistant hypertension mechanism – enhanced renal sodium reabsorption (volume expansion) Coronary flow reserve with 90% stenosis – decreased (fixed resistance limits maximal flow) Acute cardiogenic pulmonary edema initial intervention – NIPPV Chronic hypertension LVH mechanism – pressure overload induces parallel sarcomere addition (concentric hypertrophy) Exercise ischemia ST depression – increased lactate production (anaerobic glycolysis) HFpEF treatment to reduce hospitalizations – ARNI (angiotensin receptor-neprilysin inhibitor) Thiazide diuretic compensatory mechanism – RAAS activation Drug-eluting stent mechanism – inhibits smooth muscle cell proliferation and migration ACE inhibitor worsening renal function in HF – efferent arteriolar vasodilation (decreases GFR) Section 5: Respiratory Disorders (COPD, Asthma, Pneumonia) (Questions 81-100) COPD airflow limitation primary mechanism – loss of elastic recoil (emphysema) Asthma airway remodeling distinguishing feature – subepithelial fibrosis with basement membrane thickening COPD persistent inflammation despite ICS – increased expression of glucocorticoid receptor beta (GR-β) COPD pneumonia predisposition – impaired mucociliary clearance and alveolar macrophage dysfunction Lobar pneumonia sequence – neutrophil infiltration → alveolar edema → red hepatization → gray hepatization Beta-2 agonist bronchodilation – activation of adenylyl cyclase → increased cAMP in airway smooth muscle Methacholine challenge assesses – airway hyperresponsiveness (AHR) COPD hypercapnia mechanism – increased dead space ventilation and reduced alveolar ventilation COPD exacerbation airway neutrophilia – IL-8 (CXCL8) Aspirin-exacerbated respiratory disease (AERD) – COX-1 inhibition → shunting to 5-lipoxygenase pathway COPD polycythemia worsening pulmonary hypertension – increased blood viscosity (elevates PVR) GINA step-up for uncontrolled asthma – add LABA and use as-needed low-dose ICS-formoterol Parapneumonic effusion mechanism (S. pneumoniae) – pneumolysin disrupts alveolar-capillary membrane COPD dyspnea despite bronchodilators – dynamic hyperinflation (loss of elastic recoil) Eosinophil MBP in airway remodeling – activates fibroblasts (collagen deposition, subepithelial fibrosis) Cor pulmonale hemodynamic finding – elevated RVEDP, normal LV function CF Pseudomonas susceptibility – defective CFTR → dehydrated airway surface liquid (impaired mucociliary clearance) Acute asthma exacerbation bronchoconstriction – mast cell degranulation (histamine, leukotrienes) Legionella pneumonia characteristic lab finding – hyponatremia (SIADH) COPD exacerbation purulent sputum pathogen – Moraxella catarrhalis Section 6: Renal Disorders (AKI, CKD, Glomerulonephritis) (Questions 101-120) Sepsis AKI with muddy brown granular casts, FENa 3.2% – acute tubular necrosis (ATN) CKD anemia mechanism – decreased erythropoietin production Lupus nephritis (class IV) injury mechanism – deposition of circulating immune complexes (nuclear antigens + antibodies) Diabetic nephropathy hyperkalemia – hyperoninemie hypoaldosteronism (type 4 RTA) Rhabdomyolysis AKI lab finding – elevated CK, dipstick + for blood but no RBCs CKD hypocalcemia – phosphate retention → precipitation of calcium phosphate (decreased ionized Ca) Minimal change disease proteinuria – loss of negative charge on GBM (podocyte foot process effacement) Anti-GBM disease (Goodpasture) biopsy finding – linear IgG along GBM ACE inhibitor in CKD creatinine rise – hemodynamically mediated (efferent arteriolar dilation) Post-cardiac surgery AKI – prerenal azotemia (low urine Na, low FENa) Prerenal AKI lab pattern – low urine Na (20), low FENa (1%) CKD secondary hyperparathyroidism – decreased renal 1-alpha-hydroxylase → low calcitriol → hypocalcemia Granular IgG along GBM – post-streptococcal glomerulonephritis Nephrotic syndrome lab finding – serum albumin 2.1 g/dL, urine protein 5.8 g/24h AKI oliguric phase – highest risk of hyperkalemia and metabolic acidosis ATN vs. prerenal azotemia – ATN has parenchymal damage; prerenal has intact structure Hepatitis C associated glomerular disease – membranoproliferative glomerulonephritis (MPGN) type I CKD hyperphosphatemia complication – vascular calcification (increased cardiovascular mortality) RPGN defining finding – crescents on renal biopsy CKD anemia primary mechanism – decreased erythropoietin production Section 7: Gastrointestinal Disorders (Liver, Pancreas, GI Bleed) (Questions 121-140) Hepatorenal syndrome mechanism – renal vasoconstriction secondary to splanchnic vasodilation (reduced effective arterial blood volume) Severe acute pancreatitis with Grey Turner/Cullen sign – retroperitoneal hemorrhage (erosion of pseudoaneurysm) Primary biliary cholangitis (PBC) – molecular mimicry between mitochondrial pyruvate dehydrogenase complex and bacterial antigens Acute variceal hemorrhage hemostatic failure – increased fibrinolysis (elevated t-PA) Chronic pancreatitis steatorrhea – decreased fecal elastase, low serum trypsinogen NASH hepatocellular carcinoma mechanism – chronic inflammation and oxidative stress → p53 mutations Diverticular bleeding mechanism – vasa recta rupture at diverticulum (arterial) Acute liver failure cerebral edema – increased ammonia → glutamine in astrocytes → osmotic swelling Hereditary hemochromatosis HCC – iron-induced oxidative stress (direct mutagenesis) Vitamin K deficiency vs. hepatic dysfunction differentiation – factor V activity (low in liver disease, normal in vitamin K deficiency) Acute pancreatitis poor prognosis marker – CRP 150 mg/L at 48 hours Cirrhosis with tense ascites acute pancreatitis – pancreatic duct hypertension (increased intra-abdominal pressure) MELD score interpretation – predicts 3-month mortality (prioritizes liver transplantation) Duodenal ulcer high rebleeding risk – non-bleeding visible vessel (pigmented protuberance) Hepatorenal syndrome pathophysiology – splanchnic vasodilation → decreased effective arterial blood volume → renal vasoconstriction Exocrine pancreatic insufficiency test – fecal elastase-1 (sensitive, specific) Large-volume paracentesis complication prevention – albumin infusion (6-8 g per liter ascites removed) Octreotide mechanism in variceal bleed – inhibits glucagon → splanchnic vasoconstriction (reduces portal pressure) Post-ERCP pancreatitis – cannulation-induced papillary trauma NASH vs. simple steatosis histological distinction – lobular inflammation and hepatocyte ballooning Section 8: Neurological Disorders (Stroke, Seizures, Increased ICP) (Questions 141-160) Acute stroke with normal CT – cardioembolic occlusion (left MCA) Hyperdense MCA sign – clot within vessel lumen (fibrin and erythrocytes) Large hemispheric stroke deterioration – malignant cerebral edema (uncal herniation) Left neglect and anosognosia – inferior division of right MCA (parietal lobe) Jacksonian march – focal aware motor seizure (spreads somatotopically) Carbamazepine adverse effect – Stevens-Johnson syndrome (HLA-B*1502) Low CPP (50 mmHg) intervention – vasopressor to increase MAP to 90 mmHg Subarachnoid hemorrhage day 7 deterioration – cerebral vasospasm (delayed cerebral ischemia) Thalamic hemorrhage vertical gaze palsy – compression of superior colliculus (dorsal midbrain) Right cerebellar stroke – posterior inferior cerebellar artery (PICA) Post-thrombectomy petechial hemorrhage – reperfusion injury (increased MMP activity, BBB disruption) Levetiracetam mechanism – binds SV2A (modulates neurotransmitter release) Increased ICP despite increased MAP – jugular venous compression (reduces venous outflow) Left MCA stem occlusion – global aphasia, right hemiplegia, right neglect Barbiturate coma mechanism in status epilepticus – prolongs GABA-A chloride channel opening time Malignant MCA infarction intervention – decompressive hemicraniectomy Temporal lobe epilepsy first-line monotherapy – lamotrigine Delayed cerebral ischemia after SAH – microthrombi formation (platelet activation, endothelial dysfunction) Propofol advantage in increased ICP – decreases CMR02 and CBF in parallel (reduces cerebral blood volume) Right parietal lobe stroke – left neglect, anosognosia, constructional apraxia Section 9: Hematologic Disorders (Anemia, Coagulopathies) (Questions 161-180) CKD anemia pathophysiology – impaired EPO production with functional iron deficiency (elevated hepcidin) Prolonged aPTT not correcting with mixing – lupus anticoagulant Hemophilia A lab findings – normal PT, prolonged aPTT, low factor VIII, normal vWF Lupus anticoagulant – prolonged aPTT corrects with excess phospholipid Pernicious anemia Schilling test – abnormal stage I, corrects with intrinsic factor DIC primary driver – excessive activation of coagulation (consumption of clotting factors) Sickle cell anemia – hemolytic anemia with compensatory erythropoiesis (elevated reticulocytes) Factor V Leiden with pregnancy loss – consider coexisting thrombophilia (hyperhomocysteinemia, antithrombin III deficiency, lupus anticoagulant) Myelodysplastic syndrome anemia – dyserythropoiesis with ineffective erythropoiesis Mucocutaneous bleeding, normal platelet count, prolonged bleeding time – von Willebrand disease Sickle cell vaso-occlusive crisis exacerbation by acidosis – low pH stabilizes T state (reduces solubility of deoxygenated HbS) CKD anemia pathogenesis – decreased EPO + hepcidin-mediated iron restriction Antiphospholipid syndrome (APS) confirmatory test – positive lupus anticoagulant with hexagonal phase phospholipid neutralization Hereditary spherocytosis characteristic test – increased osmotic fragility DIC in metastatic adenocarcinoma – tumor-derived procoagulants (tissue factor) Hemophilia A with inhibitor acute bleeding – rFVIIa (bypass intrinsic pathway) CML anemia mechanism – hypersplenism (sequestration and destruction) Polycythemia vera bleeding tendency – acquired von Willebrand disease (high shear stress → proteolysis of vWF multimers) Antiphospholipid syndrome lab finding – positive anti-beta-2 glycoprotein I antibodies Oral iron therapy earliest response – increased reticulocyte count Section 10: Immune System Disorders (Inflammation, Autoimmunity, HIV) (Questions 181-200) SIRS cytokine profile – elevated TNF-α, IL-1β, IL-6; decreased IL-10, IL-4 Goodpasture syndrome autoantibody – anti-alpha-3 chain of type IV collagen (type II hypersensitivity) HIV chronic infection mechanism – integration of proviral DNA into host genome (latency with minimal viral protein expression) Abatacept mechanism – blocks CD80/CD86-CD28 co-stimulation (T cell anergy) Gouty arthritis inflammasome – NLRP3 activation by MSU crystals → caspase-1 → IL-1β release IRIS after ART – rising CD4 count with new fever (exaggerated inflammation against subclinical OIs) APS-1 autoimmunity – defective central tolerance (AIRE mutation impairs negative selection) EAE induction – adoptive transfer of CD4+ Th17 cells specific for myelin protein HIV Nef immune evasion – downregulates CD4 and MHC class I (reduces CTL recognition) Chronic granulomatous disease (CGD) – recurrent staphylococcal abscesses, granuloma formation (NADPH oxidase defect) HIV patient with immune recovery, fever, weight loss, lymph node caseous necrosis – IRIS unmasking tuberculosis Rheumatoid arthritis transition to chronic synovitis – presentation of citrullinated peptides by HLA-DR4 to autoreactive CD4+ T cells (Th17 differentiation) 5-lipoxygenase inhibitor effect – impaired chemotaxis (decreased leukotriene production) SLE diffuse proliferative GN – positive anti-dsDNA, low complement Classical complement deficiency (C1q, C4) and SLE – impaired clearance of apoptotic debris (self-antigen accumulation) HIV esophageal candidiasis (CD4 80) – empiric fluconazole Sarcoidosis immunologic abnormality – oligoclonal expansion of CD4+ T cells (Th1/Th17) Tenofovir-induced Fanconi syndrome – proximal tubular injury (glycosuria, proteinuria, hypophosphatemia) HIV elite controllers – robust CTL response targeting multiple conserved epitopes CD28-CD80/86 blockade – T cell anergy (reduced adaptive immune responses) Key features: 200+ questions covering all N212 Pathophysiology Exam 2 domains Detailed rationales with cellular mechanisms, molecular pathways, and clinical correlations Quantitative problems – corrected sodium calculation, anion gap, Winter's formula, MELD, Schilling test interpretation Real-world scenarios – case-based questions integrating multiple pathophysiological concepts Updated for 2026 – reflects current Eastwick College N212 curriculum Perfect for – N212 Pathophysiology Exam 2, nursing pathophysiology, pre-nursing, pre-med, health sciences Last updated: [Insert current month/year] – reflects the latest N212 course objectives and pathophysiology standards.