N212 Pathophysiology Exam 1 2026 Actual Test Bank | Eastwick College | 200+ Questions with Correct Answers & Detailed Rationales | Latest Update

Pass your N212 Pathophysiology Exam 1 at Eastwick College on the first attempt. This comprehensive practice test bank contains 200+ original, high-yield questions covering all N212 exam domains, including cellular adaptation and injury, inflammation and repair, fluid and electrolyte balance, acid-base disorders, immune system disorders, infection and sepsis, neoplasia and cancer biology, genetic and developmental disorders, hemodynamic disorders (edema, shock, thrombosis), and pain/temperature regulation. 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: Cellular Adaptation and Injury (Questions 1-20) Hepatocytes exposed to mitochondrial toxin – hypertrophy (increase in SER for detoxification) Myocardial ischemia-reperfusion contraction band necrosis – intracellular calcium at time of reperfusion Gastric reflux esophageal metaplasia – activation of transcription factors altering cell-type-specific gene expression High glucose in renal tubular cells – hypertrophy (increased matrix production, diabetic nephropathy) MPTP inhibitor prevents cytochrome c release – apoptosis via intrinsic pathway Obstructive jaundice hepatocyte bile pigment accumulation – pigment accumulation due to impaired excretion Mild sustained calcium elevation in neurons – apoptosis via intrinsic pathway (calpain cleaves Bid) Chronic anemia bone marrow erythroid precursors – hyperplasia (increased cell number) Proteasome inhibitor – increased autophagy to clear protein aggregates Partial hepatectomy increased S phase – hyperplasia Sublethal stressor increased organelles – hypertrophy Inhibited ubiquitin-proteasome pathway – increased accumulation of misfolded proteins and reduced apoptosis Pressure overload cardiac hypertrophy transition to failure – upregulation of antioxidant enzymes (protective, not maladaptive) Chronic hypoxia adaptation – enhanced glycolysis with increased lactate production (HIF-1α) Autophagy in nutrient deprivation – recycles cytoplasmic components to generate amino acids and energy Irreversible protein cross-linking – necroptosis (cellular swelling, membrane rupture) Reversible vs. irreversible injury – reversible: cellular swelling and fatty change; irreversible: membrane damage and lysosomal enzyme leakage Cellular swelling in reversible ischemic injury – increased permeability to sodium due to ATP depletion Metaplasia – reprogramming of stem cells via altered transcription factor expression Neuronal adaptation to oxidative stress – upregulation of glutathione synthesis and heme oxygenase-1 Section 2: Inflammation and Repair (Questions 21-40) Chronic inflammation persistence – deficiency of lipoxins and resolvins (impaired resolution) TNF-α upregulates endothelial adhesion molecules – NF-κB pathway activation Inflammasome role – cleaves pro-IL-1β and pro-IL-18 into active forms Selectin blockade inhibits – leukocyte rolling Excessive scarring after burn – myofibroblasts (excessive collagen deposition) Resolution of inflammation marker – annexin A1 on leukocyte surfaces Myeloperoxidase deficiency – reduced production of hypochlorous acid (HOCl) Leukocyte recruitment sequence – rolling → adhesion → transmigration → chemotaxis Chronic inflammation simultaneous destruction and repair – macrophages release both pro-inflammatory cytokines and growth factors NSAID mechanism confirmation – decreased prostaglandin E2 (PGE2) levels Integrin blocking firm adhesion (not rolling) – LFA-1 (αLβ2) Chronic granulomatous disease – reduced neutrophil extracellular trap (NET) formation (NADPH oxidase defect) Resolution phase efferocytosis mediator – Resolvin E1 (RvE1) Granulation tissue predominant cell – fibroblasts (synthesis of ECM components) SIRS early lab finding – elevated C-reactive protein (CRP) and procalcitonin Chronic inflammation fibrosis – persistent activation of Th2 lymphocytes and macrophages producing TGF-β 5-lipoxygenase inhibitor – reduced LTB4 and impaired neutrophil chemotaxis Hereditary angioedema – C1 esterase inhibitor deficiency → bradykinin production Cystic fibrosis impaired airway defense – mucociliary clearance (abnormal ion transport, thick mucus) Chronic venous stasis ulcer non-healing – iron overload from extravasated RBCs generates free radicals Section 3: Fluid and Electrolyte Balance (Questions 41-60) SIADH oliguria – enhanced aquaporin-2 insertion in collecting duct principal cells Loop diuretics: orthostatic hypotension, K+ 3.1, pH 7.48, HCO3- 32, PaCO2 46 – metabolic alkalosis with appropriate respiratory compensation Acute hyponatremia (Na 115) cerebral edema – rapid loss of brain organic osmolytes (cell swelling) CKD hypocalcemia – decreased intestinal calcium absorption due to vitamin D deficiency Vomiting hypernatremia (Na 148) – loss of free water in vomitus exceeding electrolyte loss Primary hyperaldosteronism – Na 135, K 2.8, renin low, aldosterone high Diabetes insipidus: urine osmolality 150, serum osmolality 310, desmopressin increases to 450 – central diabetes insipidus Hyperkalemia cardiac arrest – depolarization of cardiac myocytes reduces sodium channel availability Acute pancreatitis tetany with Mg 1.0 – correct hypomagnesemia before calcium administration Severe hypothermia (30°C) electrolyte shift – hypokalemia due to intracellular shift SIADH Na 120, 3% hypertonic saline – slowly raises serum sodium by providing sodium without free water Hyperkalemia with ECG peaked T waves – intravenous calcium gluconate (stabilizes cardiac membrane) Cirrhosis hyponatremia (Na 125) fluid restriction – limits intake of hypotonic fluids, allowing serum sodium to increase Loop diuretics metabolic alkalosis – hypokalemia CKD stage 4 hypocalcemia – decreased renal production of 1,25-dihydroxyvitamin D DKA K+ 5.8 on admission, drops to 3.2 after insulin – insulin stimulates cellular uptake of K+ via Na-K-ATPase Furosemide hypomagnesemia – increased renal excretion of magnesium Malignancy hypercalcemia (Ca 14.2) ECG finding – shortened QT interval Vomiting metabolic alkalosis maintenance mechanism – increased renal reabsorption of bicarbonate due to hypokalemia Oliguric AKI with Na 124, K 6.8 – 0.9% sodium chloride (isotonic, no potassium) Section 4: Acid-Base Disorders (Questions 61-80) COPD exacerbation: pH 7.25, PaCO2 65, HCO3- 30 – acute respiratory acidosis superimposed on chronic respiratory acidosis Prolonged vomiting – primary metabolic alkalosis with compensatory respiratory acidosis ABG: pH 7.50, PaCO2 30, HCO3- 24 – acute respiratory alkalosis Chronic respiratory acidosis renal compensation – increased reabsorption of filtered bicarbonate Acute asthma exacerbation ABG – pH 7.48, PaCO2 28, HCO3- 22 (acute respiratory alkalosis) ABG: Na 140, Cl 100, HCO3- 16, pH 7.32, PaCO2 30 – high anion gap metabolic acidosis with appropriate compensation CKD: pH 7.31, PaCO2 35, HCO3- 17, Na 138, Cl 108 – high anion gap metabolic acidosis (uremic acidosis) Acid-base disorder with hypokalemia – metabolic alkalosis due to vomiting ABG: pH 7.55, PaCO2 48, HCO3- 40 – metabolic alkalosis with appropriate respiratory compensation Severe sepsis ARDS: pH 7.20, PaCO2 25, HCO3- 10 – metabolic acidosis with appropriate respiratory compensation COPD exacerbation: pH 7.28, PaCO2 55, HCO3- 24 – acute respiratory acidosis Severe diarrhea: pH 7.25, PaCO2 30, HCO3- 14 – appropriate compensation (Winter's formula: expected PaCO2 29) TPN metabolic alkalosis – acetate metabolism in TPN (bicarbonate precursor) DKA Kussmaul respirations, pH 7.20, PaCO2 25, HCO3- 10 – elevated beta-hydroxybutyrate (ketoacidosis) CKD stage 4: pH 7.33, PaCO2 32, HCO3- 16 – hyperventilation lowers PaCO2 (respiratory compensation) Severe vomiting: pH 7.55, PaCO2 48, HCO3- 40 – partially compensated metabolic alkalosis Serum anion gap 18, delta-delta 0.8 – high anion gap metabolic acidosis with concurrent metabolic alkalosis Salicylate overdose: pH 7.48, PaCO2 20, HCO3- 14 – mixed respiratory alkalosis and metabolic acidosis Loop diuretics: Na 140, Cl 90, HCO3- 32, K 3.0, pH 7.50, PaCO2 46 – concurrent respiratory acidosis (PaCO2 at upper limit of compensation) Sepsis with renal failure: pH 7.10, PaCO2 30, HCO3- 9, lactate 5, creatinine 4.2 – combined high anion gap metabolic acidosis (lactate + uremia) Section 5: Immune System Disorders (Questions 81-100) Anti-CD40L antibody effect – class switching and affinity maturation of B cells in germinal centers Recurrent infections, absent B cells, normal T cells – BTK mutation (X-linked agammaglobulinemia) Goodpasture syndrome – Type II hypersensitivity (linear IgG along GBM) Common variable immunodeficiency – low IgG and IgA with normal or low B cell numbers Regulatory T cells prevent autoimmunity – CTLA-4 outcompetes CD28 for B7 ligands on APCs Pre-sensitized mouse skin graft – hyperacute rejection (pre-existing antibodies) SLE anti-dsDNA antibodies – deposition of immune complexes in renal glomeruli (lupus nephritis) Chronic granulomatous disease – absent nitroblue tetrazolium (NBT) reduction by neutrophils Rheumatoid arthritis anti-CCP antibodies – formation of immune complexes in joint space (complement activation) HIV CD4 depletion – direct cytopathic effect + immune-mediated killing SCID HLA-matched sibling donor preferred – higher risk of GVHD with haploidentical grafts (MHC mismatch) Calcineurin inhibitor – reduced nuclear translocation of NFAT CVID with autoimmune hemolytic anemia – low serum IgG and IgA, normal IgM, absent vaccine responses C3 deficiency – impaired deposition of C3b on bacterial surfaces (opsonization) SLE anti-dsDNA tissue damage – immune complex deposition in glomeruli HIV ART early CD4 increase – redistribution of memory CD4+ T cells from lymphoid tissues into circulation Anti-Fc region monoclonal antibody – targets Fc gamma receptors (FcγR) on immune cells TLR3 mutation – impaired recognition of double-stranded RNA (dsRNA) X-linked agammaglobulinemia with live polio vaccine – vaccine strain replication (paralytic poliomyelitis) CGD with Aspergillus – mutation in NADPH oxidase subunit gp91phox Section 6: Infection and Sepsis (Questions 101-120) Septic shock vasoplegia – excessive nitric oxide synthesis via iNOS induction in vascular smooth muscle Compensated to decompensated shock in sepsis – depletion of mitochondrial ATP reserves despite adequate oxygen delivery TLR2 signaling adaptor – MyD88 Sepsis-induced coagulopathy (SIC) – platelets 60,000, INR 1.8, fibrinogen 150 mg/dL Early sepsis increased capillary permeability – glycocalyx shedding induced by TNF-α and MMPs Septic shock lactate 6.2 after fluids – increased glycolysis with pyruvate conversion to lactate (aerobic glycolysis) Inflammasome in sepsis – cleaves pro-IL-1β and pro-IL-18 into active forms Sepsis-associated AKI histology – minimal histologic changes despite severe functional impairment Anti-TNF-α failure in sepsis – impairs host defense against infection, increasing mortality Septic shock ScvO2 90% – cytopathic hypoxia with impaired oxygen utilization Refractory hypotension despite vasopressors – overproduction of nitric oxide LPS recognition – LBP binds LPS, transfers to CD14, presents to TLR4/MD-2 complex Sepsis AKI low urine sodium, FeNa 1% – prerenal azotemia (systemic vasodilation, reduced renal perfusion) DIC secondary to sepsis – low fibrinogen, thrombocytopenia, prolonged PT/aPTT, elevated D-dimer Antibiotic-induced endotoxin release – bactericidal antibiotics lyse bacteria, releasing LPS Septic shock post-fluid resuscitation hemodynamics – high cardiac output, low systemic vascular resistance, normal to high CVP Sepsis ARDS – increased alveolar-capillary permeability due to inflammatory mediators Early pro-inflammatory phase of sepsis – elevated TNF-α, IL-1β, and IL-6 Sepsis lactate 6 mmol/L – anaerobic glycolysis in hypoperfused tissues (microcirculatory dysfunction) Complement in sepsis – C5a generation promotes neutrophil chemotaxis and activation (contributes to organ damage) Section 7: Neoplasia and Cancer Biology (Questions 121-140) Constitutively active GPCR in colorectal cancer – RAS-MAPK pathway Promoter hypermethylation confirmation – bisulfite sequencing Warburg effect mechanism – upregulation of hexokinase II and LDH A via HIF-1α + increased pyruvate dehydrogenase kinase CTNNB1 mutation in HCC – nuclear accumulation of β-catenin, activation of TCF/LEF transcription IDO limits checkpoint blockade efficacy – depletes tryptophan (T cell anergy) + produces kynurenine (Treg differentiation) PTEN loss – increased PIP3 levels and sustained AKT phosphorylation BRAF inhibitor resistance in melanoma – mutation in MEK1 (downstream reactivation) Telomerase in cancer cells – maintains telomere length (unlimited replicative potential) CRISPR screen: knockout increases cisplatin sensitivity – nucleotide excision repair (NER) Malignant vs. benign histology – high nuclear-to-cytoplasmic ratio and pleomorphism Constitutively active RTK – RAS-RAF-MEK-ERK pathway Anaplasia – loss of differentiation (pleomorphism, high N/C ratio, increased mitoses) BRCA1 mutation – homologous recombination repair defect Most frequently mutated tumor suppressor – p53 (TP53) Angiogenesis inhibitor target – VEGF receptor (VEGFR) Microsatellite instability – frameshift mutations in repetitive DNA sequences Multistep colorectal carcinogenesis – APC loss → KRAS activation → SMAD4 loss → TP53 loss Anti-apoptotic protein binding BAX/BAK – Bcl-2, Bcl-XL, Mcl-1 (all of the above) BRAF V600E targeted therapy – vemurafenib Telomerase activation in cancer – prevents cellular senescence (unlimited replication) Section 8: Genetic and Developmental Disorders (Questions 141-160) Global hypomethylation in embryonic stem cells – loss of imprinting at IGF2/H19 (Beckwith-Wiedemann syndrome) Cystic fibrosis carriers (both Ff) – probability of at least one delta F508 allele = 75% (FF + Ff) Same FBN1 mutation, different phenotypes – variable expressivity Rare disorder: affected grandfather → unaffected daughter → affected grandson – X-linked recessive Supernumerary marker chromosome 15q11-q13 – duplication of maternal 15q11-q13 (Angelman-like) Huntington negative predictive testing critical factor – possibility of de novo mutation in affected parent Rare disorder increased frequency in isolated population – founder effect 22q11.2 deletion on aCGH – DiGeorge syndrome (22q11.2 deletion syndrome) NF1 tumor predisposition – loss of function of a Ras GTPase-activating protein (neurofibromin) Familial early-onset breast/ovarian cancer, no BRCA mutation, hypermethylation in tumor – inherited germline epimutation Autosomal dominant incomplete penetrance: unaffected individual with affected parent and child – inherited mutant allele but did not express (incomplete penetrance) Cystic fibrosis child, no family history – compound heterozygous (one mutation from each parent, both asymptomatic carriers) MEN2 RET mutation – autosomal dominant, gain-of-function (constitutive activation) Genomic imprinting: paternal deletion of ICR – deletion removes imprinting control region on maternal allele 22q11.2 deletion – DiGeorge syndrome (abnormal neural crest migration) Homozygous frameshift mutation – autosomal recessive with complete penetrance X-linked recessive: normal woman with affected son and affected brother – heterozygous carrier Factor V Leiden – gain-of-function (resistance to inactivation by activated protein C) Prader-Willi (paternal deletion) vs. Angelman (maternal deletion) – deleted region contains imprinted genes expressed only from paternal allele Preimplantation genetic diagnosis for autosomal dominant disorder – select embryo with wild-type allele from father Section 9: Hemodynamic Disorders (Edema, Shock, Thrombosis) (Questions 161-180) Severe hypoalbuminemia edema – decreased plasma oncotic pressure Massive pulmonary embolism obstructive shock – increased PCWP, decreased CO, increased SVR Atrial fibrillation embolic stroke – fibrin-rich red thrombus DIC secondary to septic shock – decreased fibrinogen, decreased platelets, elevated D-dimer Cirrhosis ascites – increased hepatic lymph production (sinusoidal hypertension) Glycocalyx prevents thrombosis – physical barrier repelling platelets and clotting factors Hypovolemic shock with normal BP but rising lactate – decompensated (progressive) shock Most common inherited thrombophilia – Factor V Leiden (G1691A) Septic shock refractory hypotension – overexpression of iNOS in vascular smooth muscle Thrombus vs. postmortem clot – all of the above: attached, lines of Zahn, granular surface Decompensated heart failure pitting edema – increased capillary hydrostatic pressure DIC simultaneous thrombosis and bleeding – excess thrombin generation consumes clotting factors and platelets Heparin monitoring – activated partial thromboplastin time (aPTT) Cardiogenic shock pulmonary edema mechanism – increased left atrial pressure elevates pulmonary capillary hydrostatic pressure Cirrhosis ascites pathophysiologic factors – portal hypertension and hypoalbuminemia Hypovolemic shock rapid saline infusion – release of atrial natriuretic peptide (ANP) Arterial vs. venous thrombus – arterial: platelet-rich (white); venous: red cell-rich (red) Neurogenic shock – hypotension with bradycardia (loss of sympathetic tone) Pulmonary embolism obstructive shock mechanism – increased RV afterload → decreased LV preload Symptomatic PE determinant – proximal vs. distal vein location Section 10: Pain and Temperature Regulation (Questions 181-200) Nav1.7 in nociception – upregulated in peripheral sensory neurons after nerve injury (hyperexcitability, chronic pain) PAG stimulation analgesia – serotonergic projections from raphe nuclei Spinal cord injury pain below level – loss of descending inhibitory controls (dorsal horn hyperexcitability) Malignant hyperthermia temperature rise – excessive muscle contraction (uncontrolled calcium release from SR) Sepsis fever chill phase – endogenous pyrogens reset hypothalamic set point upward; body initiates heat conservation/generation Stocking-glove burning pain – small fiber neuropathy (affects A-delta and C fibers) Acetaminophen analgesic mechanism – inhibition of cyclooxygenase activity in hypothalamus (COX-3) Brainstem lesion: right facial/left body pain loss – right spinal trigeminal nucleus and left spinothalamic tract Chronic opioid hyperalgesia – activation of NMDA receptors and central sensitization Hypothalamic preoptic lesion poikilothermia – impaired ability to regulate heat loss and conservation (core temperature drifts toward ambient) Noxious heat (43°C) transducer – TRPV1 CRPS temperature asymmetry – sympathetic nervous system dysfunction (vasomotor instability) Exercise-induced hyperthermia limiting mechanism – increased sweating and cutaneous vasodilation Fibromyalgia neuroimaging finding – enhanced connectivity between default mode network and insula Menthol cooling sensation – activates TRPM8 (cold-sensitive channel) Central post-stroke pain – loss of GABAergic inhibition in thalamic sensory nuclei Febrile response critical cytokine – Interleukin-1 beta (IL-1β) Insular cortex lesion asymbolia for pain – affective-motivational processing of pain unpleasantness impaired Neuropathic pain DRG ion channel changes – downregulation of Kv, upregulation of HCN, increased Nav1.8 (all of the above) Heat stroke transition from heat exhaustion – systemic inflammatory response syndrome (SIRS) and endothelial damage Key features: 200+ questions covering all N212 Pathophysiology Exam 1 domains Detailed rationales with cellular mechanisms, molecular pathways, and clinical correlations Quantitative problems – Winter's formula, anion gap, delta-delta, genetics probabilities (Mendelian ratios), dilutions Real-world scenarios – case-based questions integrating multiple pathophysiological concepts Updated for 2026 – reflects current Eastwick College N212 curriculum Perfect for – N212 Pathophysiology Exam 1, nursing pathophysiology, pre-nursing, pre-med, health sciences Last updated: [Insert current month/year] – reflects the latest N212 course objectives and pathophysiology standards