NURS611 EXAM 3 ACTUAL TEST BANK QUESTIONS AND CORRECT ANSWERS ALREADY GRADED A+

Pass your NURS611 Advanced Pathophysiology Exam 3 with confidence using the most current and comprehensive test bank available for the 2026 academic year. This resource features actual exam questions with verified correct answers—already graded A+ by successful graduate nursing students. Covering over 400 high-yield questions, this guide mirrors the exact content domains tested on NURS611 Exam 3: Cardiovascular Pathophysiology: Aneurysm formation (weakening of vessel wall, three layers involved, fusiform/circumferential types; atherosclerosis and hypertension found in 50% of patients), three causes of blood clots (stasis of blood, increased clotting ability, injury to blood vessel endothelium), heart failure with reduced ejection fraction (HFrEF – difficulty emptying, EF 40%), left ventricular hypertrophy from hypertension (increased oxygen demand → heart attack risk), acute coronary syndrome (may or may not be heart attack vs. temporary vessel squeezing), atrial fibrillation (not emergency; V-fib is emergency), stable angina (predictable with exertion, relieved by rest/nitroglycerin), coronary artery disease risk factors (family history, hyperlipidemia, hypertension, diabetes, smoking, sedentary lifestyle, diet), intermittent claudication (ischemic pain in lower extremities with walking, resolves with rest), thromboangiitis obliterans (inflammatory peripheral artery disease associated with smoking), Raynaud disease (vasospastic peripheral artery disease), chronic venous insufficiency (sustained inadequate venous return from valvular damage), varicose veins (distended superficial veins from damaged valves), postthrombotic syndrome (chronic pain/edema/ulceration after DVT), DVT danger (pulmonary embolism), arterial thrombus danger (systemic embolism), superior vena cava syndrome (tumor compression causing venous distention in upper extremities/head), dissecting aneurysm (blood runs between arterial wall layers), myocardial infarction risk (low HDL, high LDL), cardiac valve damage in rheumatic fever (abnormal immune response), infective endocarditis (streptococci or other organisms), constrictive pericarditis (chronic condition compressing heart), cardiac tamponade (compression of heart by pericardial fluid – pulsus paradoxus, Beck's triad), dilated cardiomyopathy (enlarged chambers, decreased contractility), hypertrophic cardiomyopathy (most common inherited heart defect, thickened septum, autosomal dominant, increased risk for sudden death), restrictive cardiomyopathy (rigid, non-compliant myocardium, reduced diastolic volume), mitral stenosis (impedes flow from LA to LV, most commonly caused by acute rheumatic fever, leads to pulmonary hypertension and right ventricular failure), mitral regurgitation (backflow from LV to LA during systole), aortic stenosis (narrow valve limits blood ejection → fatigue and fainting with exercise), peripheral arterial disease (atherosclerosis in limb arteries), cardiac cycle phases, Frank-Starling law (increased preload increases force of contraction), preload (LV end-diastolic pressure/volume), afterload (resistance to ejection), contractility (ability to shorten/generate force), SNS increases HR, PNS decreases HR, B-type natriuretic peptide (BNP – produced in response to pressure/volume overload; used to diagnose HF, monitor treatment, predict outcomes; BNP-guided treatment reduces cardiovascular events and readmissions). Endocrine Pathophysiology: Myxedema (nonpitting boggy edema from mucopolysaccharide infiltration in hypothyroidism; myxedema coma is life-threatening), hirsutism (excessive facial/body hair), Somogyi effect (low blood sugar at night → morning rebound hyperglycemia from counter-regulatory hormones; less common with long-acting insulin), dawn phenomenon (early morning rise in blood glucose from nocturnal GH elevation; managed by increased evening insulin), gestational diabetes (increased risk for type 2 DM later in life), metabolic syndrome (increased risk for type 2 DM), cretinism (untreated congenital hypothyroidism → mental retardation), type 1A diabetes (autoimmune destruction of pancreatic beta cells by cytotoxic T lymphocytes), type 1 diabetes deficit (insulin deficiency, relative excess of amylin and glucagon), microvascular disease (accelerated atherosclerosis leading to blindness, ESRD, neuropathy; proportional to disease duration 10 years and glycemic control), macrovascular disease (lesions in large/medium arteries → accelerated atherosclerosis, MI, stroke, PVD; higher mortality during acute MI due to asymptomatic presentation from autonomic neuropathy), diabetic retinopathy (progressive vision loss from microvascular disease: capillary basement membrane thickening, vein dilation, microaneurysm formation, hemorrhage, retinal ischemia, infarcts, scarring, new blood vessel formation), diabetic gastroparesis (autonomic neuropathy causing delayed gastric emptying), diabetic hypoglycemia unawareness (loss of sympathetic nervous system symptoms with longstanding diabetes), diabetic nephropathy (microalbuminuria first manifestation; annual urine screening needed), diabetic ketoacidosis (dehydration from profound insulin deficiency; precipitated by infection, nonadherence, new diagnosis; Kussmaul respirations, ketonuria, hyperglycemia, decreased pH), hyperosmolar hyperglycemic nonketotic syndrome (HHNKS/HHS – more common in type 2 diabetes, characterized by lack of ketosis, severe fluid deficiency), hypoglycemia (blood glucose 45-60 mg/dL; tachycardia, diaphoresis, tremors, pallor, confusion, seizures, coma), primary endocrine disorder (problem in gland that secretes hormone directed toward other tissues), secondary endocrine disorder (problem with gland that secretes hormone targeting another gland), thyrotoxicosis crisis (excess thyroid hormone effects), thyrotoxic crisis/thyroid storm (dangerously high thyroid hormone with high fever, extreme tachycardia, potential death), neurogenic diabetes insipidus (problem in hypothalamus/posterior pituitary → decreased ADH release), nephrogenic diabetes insipidus (problem in kidney → insensitivity to ADH), acromegaly (hypersecretion of GH in adults – enlarged jaw, forehead, tongue, hands, feet; long bones already closed so no height increase), gigantism (hypersecretion of GH in children/adolescents before epiphyseal plates close → tall stature), SIADH (high ADH levels without normal stimuli → lethargy, hyponatremia, seizures, decreased plasma osmolarity, concentrated urine, hypervolemia, weight gain), hypothyroidism (decreased energy metabolism; lethargy, cold intolerance, hoarseness, myxedema, coarse hair, bradycardia, constipation, weight gain, anemia; causes: Hashimoto's autoimmune thyroiditis, iatrogenic loss from surgical/radioactive treatment, head/neck radiation, medications, iodine deficiency; primary hypothyroidism – loss of functional thyroid tissue decreases TH production), hyperthyroidism/Graves' disease (autoantibodies against TSH receptor – thyroid-stimulating immunoglobulins override normal regulation; causes goiter and increased TH synthesis; weight loss with increased appetite, increased appetite, increased body temperature, tachycardia, heat intolerance, warm flushed skin, excessive sweating, fine hair, lid lag, staring quality, fine tremor, restlessness, emotional lability), pheochromocytoma (chromaffin cell tumor of adrenal medulla → hypertension, tachycardia, palpitations, severe headache, diaphoresis, heat intolerance, weight loss, constipation), primary hyperaldosteronism (adrenal adenoma or bilateral nodular hyperplasia → hypertension, hypokalemia, increased blood pH, increased urine potassium), Addison's disease (inadequate corticosteroid and mineralocorticoid synthesis, elevated ACTH; weakness, fatigue, hypotension, hyperkalemia, hypoglycemia, hyperpigmentation, vitiligo; hypocortisolism and hypoaldosteronism cause lightheadedness upon standing from low blood volume; addisonian crisis – severe hypotension and vascular collapse), Cushing disease (hypersecretion of ACTH from anterior pituitary → cortisol excess; truncated central obesity, moon face, buffalo hump, glucose intolerance, protein wasting, muscle weakness, loss of collagen → thin weakened skin, purple striae, easy bruising; cushing syndrome – chronic exposure to excessive cortisol from any cause), primary hyperparathyroidism (parathyroid adenoma → chronic hypercalcemia, increased bone resorption, kidney stones), secondary hyperparathyroidism (compensatory response to hypocalcemia from chronic renal failure or vitamin D deficiency), tertiary hyperparathyroidism (excessive PTH secretion after long-standing hypocalcemia), hyperprolactinemia/pituitary adenoma (prolactin-secreting tumors – prolactinomas; amenorrhea, infertility, galactorrhea in women; erectile dysfunction, infertility, osteopenia in men), parathyroid hormone (primary regulator of serum calcium and phosphate; decreased calcium increases PTH release which increases osteoclast activity; increased calcium suppresses PTH), aldosterone secretion controlled by renin-angiotensin-aldosterone system (RAAS; causes sodium reabsorption and potassium/hydrogen excretion in kidney). Hematologic Pathophysiology: Anemia (decreased erythrocytes or hemoglobin quantity/quality from impaired production, blood loss, increased destruction, or combination), sideroblastic anemia (iron-utilization anemia; hereditary X-linked recessive or acquired from ethanol abuse, isoniazid, lead; abnormal iron-saturated red cells; mild to moderate splenomegaly, hepatomegaly, bronze-colored skin, cardiac arrhythmias), aplastic anemia (autoimmune disease against hematopoiesis by activated cytotoxic T cells → pancytopenia – reduction of all three blood cell types from bone marrow failure), pernicious anemia (vitamin B12 deficiency from absence of intrinsic factor; gastric parietal cells destroyed by antibodies; develops slowly over 20-30 years, median diagnosis age 60; neurologic manifestations: numbness, tingling, paresthesias, difficulty walking; hematologic: macrocytic-normochromic anemia; glossitis – smooth beefy red tongue), iron deficiency anemia (microcytic-hypochromic; from inadequate dietary intake or chronic blood loss 2-4 mL/day; most common cause in developing countries: pregnancy and chronic blood loss; in females: menorrhagia; in males: ulcers, hiatal hernias, esophageal varices, cirrhosis, cancer, ulcerative colitis, hemorrhoids; early symptoms: fatigue, palpitations, SOB, pale earlobes/palms/conjunctivae), folate deficiency anemia (macrocytic-normochromic; associated with chronic malnourishment and chronic alcohol abuse), anemia of chronic disease (common in hospitalized patients; from decreased erythrocyte life span, suppressed erythropoietin production, ineffective bone marrow response, altered iron metabolism with iron sequestration in macrophages), posthemorrhagic anemia (acute blood loss → reduced tissue oxygenation stimulates erythropoietin → increased reticulocytes 10-15% after 7 days), hereditary spherocytosis (membrane defect, increased erythrocyte destruction in spleen by macrophages), G6PD deficiency (enzyme pathway defect, increased erythrocyte destruction), thalassemia (hemoglobin synthesis defect), paroxysmal nocturnal hemoglobinuria (membrane defect), sickle cell anemia (hemoglobin synthesis defect – pain crisis, increased erythrocyte destruction), polycythemia (increased erythrocytes; relative from dehydration; absolute from chronic hypoxia e.g., COPD), hemolysis from mismatched blood transfusion (immune-mediated, intravascular hemolytic anemia), drug-induced hemolytic anemia (antibiotic acts as hapten binding to erythrocyte proteins), erythropoietin (EPO – released by kidneys, acts on bone marrow to stimulate erythropoiesis; tissue hypoxia increases release; deficiency in chronic kidney disease causes anemia), thrombopoietin (regulates platelet formation), hepcidin (regulates iron homeostasis), ferritin (iron storage protein), transferrin (iron transport protein), hemosiderin (intracellular iron complex), D-dimer (fibrin degradation product indicating clot presence; elevated suggests thrombosis), platelets (thrombocytes – cytoplasmic fragments of megakaryocytes in bone marrow; actin/myosin filaments enable contraction, expelling serum from clot; activated platelets have jagged spiky edges), hemostasis (platelet adhesion and aggregation triggered by exposure to subendothelial collagen; nitric oxide and prostacyclin inhibit; thromboxane A2, epinephrine, thrombin, collagen trigger; stabilized by fibrin strands), plasmin (enzyme that dissolves fibrin clots; precursor plasminogen produced by liver), tissue thromboplastin (tissue factor – triggers extrinsic clotting pathway), intrinsic factor (secreted by gastric parietal cells; binds dietary vitamin B12 for absorption in ileum; absence causes pernicious anemia), transferrin saturation, total iron-binding capacity (TIBC), heparin-induced thrombocytopenia (HIT – immune-mediated adverse drug reaction from IgG antibodies against heparin-platelet factor 4 complex; hallmark is 50% decrease in platelet count; venous thrombosis most common → DVT/PE; arterial thrombosis affects large arteries of lower extremities → acute limb ischemia, CVA, MI; occurs in ~4% of patients receiving unfractionated heparin), disseminated intravascular coagulation (DIC – acquired syndrome with widespread activation of coagulation; fibrin clots in medium/small vessels throughout body; most common associated condition: sepsis; paradoxical risk for hemorrhage from excessive consumption of clotting factors and platelets; tissue factor exposure and increased expression from proinflammatory cytokines activates clotting through extrinsic pathway; insufficient activated protein C activity contributes – activated protein C is endogenous anticoagulant; widespread clotting causes inadequate tissue perfusion/ischemia → multi-organ dysfunction/failure of kidneys, liver, lungs). Hematopoiesis & Blood Cell Biology: Hematopoiesis (production of blood cells in bone marrow after birth; vascular niche has active HSCs, osteoblast niche has dormant HSCs), erythrocyte unique properties (biconcave shape for optimal gas diffusion; capacity for reversible deformity to squeeze through microcirculation), hemoglobin synthesis (dependent on nutritional intake – vitamin B6/pyridoxine and iron), iron cycle (tissue macrophages in spleen break down ingested erythrocytes and return iron to bloodstream directly or after storing as ferritin/hemosiderin; transferrin is plasma carrier), hemoglobin A molecule (four globin chains, four hemes; iron portion must be ferrous/Fe2+ to bind oxygen), bilirubin (produced from hemoglobin breakdown when RBCs die; liver conjugates and excretes; excess hemolysis causes jaundice when heme destruction exceeds liver's ability to excrete bilirubin), spleen removal (liver Kupffer cells – type of macrophage – take over old RBC removal), leukocytes (5,000-10,000/mm3; defend against microorganisms and remove debris; primarily act in tissues, transported in circulation), neutrophils (most numerous granulocyte; phagocytosis in early inflammation, kills bacteria; mature = segmented, immature = bands/stabs; "shift to left" when marrow releases immature neutrophils prematurely due to demand exceeding supply, often with fever – indicates acute infection), eosinophils (defend against parasites), basophils, monocytes (precursor cells for macrophages), macrophages (active phagocytosis in mononuclear phagocyte system; process and present antigens; participate in wound healing), dendritic cells (process antigens and present to lymphocytes), natural killer cells (kill tumor cells and virus-infected cells), B lymphocytes/plasma cells (produce antibodies against specific antigens), T lymphocytes, erythrocytes (no nucleus), neutrophils (multilobed nucleus), agranulocytes (macrophages, NK cells, lymphocytes, monocytes), granulocytes (neutrophils, basophils, eosinophils), myeloid lineage (erythrocytes, neutrophils, eosinophils, basophils, monocytes, platelets), lymphoid lineage (NK cells, T cells, B cells/plasma cells), endomitosis (cell division by megakaryocyte progenitors where DNA replication occurs but anaphase and cytokinesis are blocked → large polyploid nucleus that fragments into platelets), albumin (most abundant plasma protein), plasma (liquid portion of blood with dissolved substances), serum (plasma minus clotting factors), reticulocyte (immature erythrocyte with nucleus, mitochondria, ribosomes), anisocytosis (erythrocytes of different sizes), poikilocytosis (erythrocytes of different shapes), reticulocytosis (increased blood level of immature erythrocytes), eryptosis (premature death of damaged erythrocytes), hematocrit, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), red cell distribution width (RDW). Oncology/Hematologic Malignancies: Leukemias (uncontrolled production of WBCs in bone marrow, decreasing erythrocytes and platelets), lymphomas (cancers of lymphatic tissue), Reed-Sternberg cells (classic abnormal cells in Hodgkin lymphoma), Hodgkin lymphoma (progression from one lymph node group to another, systemic symptoms, presence of RS cells; first sign = enlarged painless lymph nodes in neck), non-Hodgkin lymphoma, multiple myeloma (malignant plasma cells in bone marrow; M protein – abnormal antibody released by malignant plasma cells; Bence Jones proteins – antibody pieces excreted in urine, help establish diagnosis, can damage kidneys; hypercalcemia and bone lesions characteristic because malignant cells reside in bone marrow, not circulating blood), acute myelogenous leukemia (AML), chronic lymphocytic leukemia (CLL), acute lymphoblastic leukemia (ALL – leukemia cells crowd out normal RBC production in bone marrow → fatigue from lack of oxygen-carrying RBCs), chronic myelogenous leukemia (CML – Philadelphia chromosome translocation between chromosomes 9 and 22 creates BCR-ABL1 variant oncoprotein, mutant tyrosine kinase driving cell proliferation), Burkitt lymphoma (rapidly growing B lymphocyte tumor in jaw and facial bones of children in Africa associated with Epstein-Barr virus), infectious mononucleosis (acute infection of B lymphocytes caused by Epstein-Barr virus; pharyngitis, fever, cervical lymphadenopathy), leukocytosis (higher than normal WBC count), leukopenia (lower than normal WBC count), neutropenia (lower than normal neutrophil count), granulocytosis (higher than normal neutrophils, eosinophils, basophils), granulocytopenia (lower than normal counts), agranulocytosis (complete absence of neutrophils, eosinophils, basophils), eosinophilia (most common causes: parasites, hypersensitivity reactions, toxic foreign particles), monocytosis (occurs during late phases of inflammation), neutrophilia (occurs during early phases of inflammation), localized lymphadenopathy (drainage from areas of inflammation), generalized lymphadenopathy (usually indicates malignant or nonmalignant disease), lymphadenopathy (enlarged lymph nodes), pancytopenia (decreased RBCs, WBCs, platelets – seen in aplastic anemia), clonal disorder (leukemias considered product of mutated progenitor cell that replicates uncontrollably), Philadelphia chromosome, BCR-ABL1, tyrosine kinase inhibitors (imatinib). Obesity & Metabolic Pathophysiology: Obesity defined as BMI 30 (5th leading cause of death in US; associated with CVD, type 2 DM, cancer, HTN, stroke, HL, gallstones, NASH, GERD, osteoarthritis, infections, asthma, OSA), overweight defined as BMI 25, visceral white adipose tissue (undergoes adipocyte hypertrophy with positive energy balance; visceral deposits produce proinflammatory cytokines and adipokines; visceral obesity greatest risk for accelerated lipolysis, chronic inflammation, insulin resistance), subcutaneous white adipose tissue (undergoes adipogenesis with positive energy balance; estrogen preferentially increases subcutaneous over visceral deposition – explains pear shape in young women vs. apple shape in men), brown adipose tissue (BAT – major source of nonshivering thermogenesis; multiple lipid droplets, numerous mitochondria; iron in mitochondria gives brown color; produces minimal leptin and adiponectin; UCP1 plays important role in nonshivering thermogenesis), beige adipose tissue (bAT – located within white adipose tissue; increases with exercise and chronic cold exposure), marrow adipose tissue (MAT – located in bone marrow), adipogenesis (formation of new fat cells), adipocyte hypertrophy (enlargement of preexisting fat cells), adipokines (cytokines and hormones secreted by adipose tissue), leptin (high levels normally decrease food intake and increase energy expenditure; obesity involves leptin resistance), ghrelin (stimulates food intake), adiponectin (antiatherogenic adipokine – decreased in obesity), tumor necrosis factor-alpha (TNF-α – secreted by fat tissue in obesity; causes inflammation, contributes to type 2 DM, heart disease, cancer), myokines (biologically active substances secreted by muscles in response to contractile activity), orexigenic neurons (hypothalamic neurons that promote appetite and decrease metabolism), anorexigenic neurons (hypothalamic neurons that suppress appetite and increase metabolism), arcuate nucleus of hypothalamus (regulates appetite and metabolism), obesogen (environmental chemical that helps obesity develop by stimulating fat cell formation, influencing appetite and fat burning rate), positive energy balance, negative energy balance, refeeding syndrome (rapid provision of nutrients after starvation causes severe hypophosphatemia and electrolyte imbalances – may be fatal), anorexia of aging (decreased appetite or food intake in older adults), cachexia (inability to adjust to starvation by decreasing metabolism – in contrast to healthy individuals), adipocyte (cells that store fat as triglycerides), WAT (white adipose tissue – located viscerally and subcutaneously; single lipid droplet), BAT (brown adipose tissue – multiple lipid droplets, numerous mitochondria), leptin resistance, insulin resistance, portal vein (visceral venous blood rich in free fatty acids drains into portal vein – increases risk for nonalcoholic steatohepatitis). Fluid & Electrolyte Pathophysiology: Hypokalemia (thready irregular pulse, orthostatic hypotension, confusion, prominent U wave on EKG), hyperkalemia (peaked T waves, cardiac arrest), hyponatremia (serum sodium 135 mEq/L), hypernatremia, dehydration (furrowed tongue, decreased intake/output, mental confusion, inelastic skin turgor, orthostatic hypotension), fluid overload (increased HR, BP, RR; edema, crackles, JVD), hypovolemia, hypervolemia, third-spacing. Nutrition & Starvation Pathophysiology: Short-term starvation (glycogenolysis and gluconeogenesis; small amount of protein catabolism; protects protein mass), long-term starvation (initial decreased dependence on gluconeogenesis, increased use of ketone bodies for cellular energy, followed by lipolysis in adipose tissue, then proteolysis; death from severe electrolyte alterations and loss of renal, pulmonary, and cardiac function). Hormone Biology: Water-soluble hormones (short half-life, circulate in free form, act as first messengers binding to plasma membrane receptors, activate second messengers like cAMP), lipid-soluble hormones (steroids and thyroid hormones; cross plasma membrane by diffusion, bind to cytoplasmic proteins or diffuse into nucleus and bind to nuclear receptors, alter gene expression when hormone-receptor complex binds to specific DNA sites), upregulation (increased number or affinity of hormone receptors, often in response to low hormone concentration), downregulation (decreased number or affinity of receptors, often in response to high hormone concentration), permissive effect (hormone-induced changes that facilitate maximal response of a cell), first messenger (water-soluble hormone or chemical that binds to receptors in plasma membrane), second messenger (chemical signal generated within cell that mediates action of water-soluble hormone), negative feedback (end result of hormone action on target cells suppresses secretion of that hormone), positive feedback (end result of hormone action increases secretion of that hormone), hypothalamic-pituitary axis (hypothalamus connected to posterior pituitary by nerve tract, to anterior pituitary by portal blood vessels), hypothalamic hormones (dopamine – inhibits prolactin secretion; TRH – affects thyroid hormone release; CRH – facilitates release of ACTH and endorphins; GHRH, somatostatin, GnRH, PRF), anterior pituitary hormones (ACTH, MSH, TSH, GH, LH, FSH, prolactin), posterior pituitary hormones (ADH/vasopressin, oxytocin), thyroid hormones (T4, T3, calcitonin), adrenal cortex hormones (aldosterone, cortisol, adrenal androgens), adrenal medulla hormones (epinephrine, norepinephrine), pancreatic islet hormones (insulin, glucagon, amylin, somatostatin), parathyroid hormone (PTH), melatonin (pineal gland), direct effect of hormone (changes in cell function from stimulation by a particular hormone), autocrine action (hormone acts on cells that produced it), paracrine action (hormone acts on nearby cell through interstitial fluid), endocrine communication (within cells – autocrine; between cells – paracrine; between remote cells – endocrine). Perfect for graduate-level pathophysiology courses (NURS611, NURS612), nurse practitioner students, medical students, and NCLEX-RN preparation. Each answer includes the verified correct response to ensure exam readiness.