NSG533 / NSG 533 Exam 2 (Latest 2026 /2027) Advanced Pharmacology | Questions and Verified Answers with Rationales | 100% Correct | Grade A - Wilkes

NSG533 / NSG 533 Exam 2 (Latest 2026 /2027) Advanced Pharmacology | Questions and Verified Answers with Rationales | 100% Correct | Grade A - Wilkes Q: What would you be concerned with regarding the first patient's use of Vicodin in terms of the dose acetaminophen? Answer In elderly patients, it is recommended not to exceed 3,000mg per day of acetaminophen. Q: What medication could you recommend for a diabetic patient in pain that could also be used to help treat depression? Answer SNRIs; either duloxetine or venlafaxine have been successfully used in diabetic peripheral neuropathy. Q: In addition, be sure to understand which non-opiod medications you would use for a patient with neuropathic pain. Answer Gabapentin, pregabalin, transdermal lidocaine, TCAs. Q: If a patient has a true allergy to morphine, what opioid, if any, could you try instead? Answer True opioid allergies are rare. When a true allergy is present, an agent from another opiate classed should be used. For example, a patient with a true opiate allergy could receive fentanyl. Q: Know the common side effects which opioids can cause: Answer Excessive sedation (reduce dose by 25%), constipation (senna, dulcolax, N/V (hydroxyzine/ diphenhydramine), gastroparesis, vertigo, resp. depression, CNS irritability. Q: Know the WHO pain treatment algorithm: Answer Mild pain (1-3) non-opioid analgesic scheduled ATC Moderate pain (4-6) Add opioid to scheduled non-opioid ATC Severe pain (7-10) Switch to high dose opioid, ATC Q: Understand when you would use acetaminophen versus an NSAID or an NSAID instead of acetaminopehn Answer NSAIDs work best on inflammatory pain or pain mediated by prostaglandins (RA, menstrual and post-surgical pain) and bony metastasis. NSAIDS come with increased GIB risk and renal impairment. APAP is a good first line for mild to moderate pain and considered the first line in low back pain and osteoarthritic. APAP hepatotoxicity has occured in those w. liver injury or chronic drinkers. Q: What class of prophylaxis for migraines should be avoided in asthmatics? Answer Beta blockers would usually be a medication used in the prophylaxis of migraines but this would not be the best choice in an asthmatic. Q: What could you use for prophylaxis of migraines? Answer -beta-blockers if not contraindicated (or CCB) -low-dose TCAs (amitriptyline, venlafaxine) -antiepileptics (topiramate, valproic acid, divalproex sodium) Q: What could you use in the treatment of acute migraine symptoms? Answer mild to moderate: APAP, ASA or combination products w/ caffeine moderate to severe: triptans are 1st line Q: What absolute contraindications would prevent you from using triptans? Answer Hx of neurologic focality Stroke Poorly controlled HTN Unstable angina Q: What triggers would you want to tell a patient to avoid to help prevent migraines (non pharmacologic interventions): Answer -emotional stress -sleep excess or deficient -strong smells -alcohol -caffeine -fermented foods -nitrates -tobacco -MSG Q: Know what are the "red flag symptoms" of headaches which signify the need for urgent medical care: Answer -new onset sudden, severe pain -systemic signs (fever, weight loss, HTN) -focal neuro symptoms -papilledema (swelling of both optic discs in eyes d/t increased ICP -cough/ exertion triggered by HA -pregnancy or postpartum state -HIV -cancer patients -seizure activity Q: Know the stepwise treatment algorithm for the treatment of chronic headaches/ migraines: Answer 1. PMH, family hx, med hx 2. Assess info: triggers? Timing? 3. Develop POC: recommend pharmacotherapy that is financially feasible 4. Implement plan- log HA diary 5. Follow up- 4 weeks after starting new med Q: If you had a patient w/ a hx of GERD and required a calcium supplement, what would be the best supplement to recommend? Answer A patient w/ GERD is likely taking an antacid or something to decrease the acidity within the stomach. Calcium citrate does not require an acidic environment for absorption. Understand the use of bisphosphonates and counseling points when giving bisphosphonates (alendronate, risedronate and ibandronate): Answer Follow specific instructions to avoid GI side effects Remain upright after taking If you had a male patient w/ osteoporosis, what could you recommend as a 1st line treatment? Answer Bisphosphonates are considered 1st line therapy in male patients w/ osteoporosis. What medication would you recommend for a patient who has symptomatic hyperuricemia and is an over-producer and under excretor: Answer Allopurinol is the medication of choice for symptomatic hyperuricemia and for over-producers and under excretors. What doses of calcium and vitamin D would you recommend for a patient based on their age? Men: 51-70: 1,000 mg calcium Woemn 51+/ Men 71+: 1,200mg calcium Men/ Women 50+: 800-1000 iu vitamin D Know current treatment guidelines of The American College of Rheumatology for the tx of OA: -lifestyle modifications -PT -heat/ cold therapy -oral NSAIDs, topical NSAIDs on superficial joints -APAP -tramadol -duloxetine Know which herbal/ OTC product is commonly used in the tx of OA Glucosamine and chondroitin Know all about tramadol; how it works, daily dose limits, interactions and side effects: -centrally acting synthetic opioid -weak SSRI/ SNRI -can cause dizzinesss, vertigo, N/V, lethargy -seizures reported; dose related, more so with TCAs and other SSRIs -risk for SEROTONIN SYNDROME -Max 200mg/ day Understand when you would initiate prophylaxis therapy in a patient w. gout (you would not typically recommend prophylaxis for a patient experiencing symptoms for the first time): -patients with 2 or more flares/ year -radiographic evidence attributable to gout -or one subcutaneous tophi are candidates for prophylaxis treatment What meds could you recommend for prophylaxis? Allopurinol is generally well tolerated, effective and affordable and treats overproduction of uric acid and underexcretion of uric acid. Febuxostat was found to be less effective in people with CVD. Probenecid acid increases excretion of uric acid. What meds would you recommend in the tx of acute symptoms of gout? -NSAIDs -cholchicine -glucocorticoids Colchicine works well if given w/in the first 24 hours of attack. What if a patient has gout and chronic kidney disease (which gout treatment would you want to avoid in this case): -avoid NSAIDS in chronic kidney disease -those with peptic ulcers -those taking anticoagulants What non-pharmacological interventions could you recommend to help a patient avoid gout attacks (what triggers should they avoid)? -life style modifications: weight loss, smoking + alcohol cessation -lower BP by following DASH diet -increase non-sugary fluid intake If a physician said a patient's community acquired pneumonia was caused by a virulent pathogen, what is the physician saying about the pathogen? More virulent pathogens will cause more severe disease What are risk factors for aspiration pneumonia? -dysphagia -change in oropharyngeal bacterial colonization -GERD -lowered host defense -oropharyngeal colonization can be from poor oral care, dental disease, tube feedings and medications -GERD creates lowered mucosal and cilia production, altered cough reflex and promotion of gram-negative bacilli colonization What microorganisms would you expect to cause CAP? S. pneumoniae is the predominant microorganism associated w/ CAP -other common organisms: haemophilus influenzae, mycoplasma pneumoniae, mortadella catarrhalis If the patient w/ CAP has comorbidities, what would an appropriate treatment regimen include? Beta-lactam or cephalosporin in combination w/ either a macrolide or doxycycline If opting for monotherapy, current reccomendations are a fluoroquinolone such as levofloxacin 750 mg daily, moxifloxacin 400 mg daily or gemifloxacin 320 mg daily If you chose monotherapy w/ a fluoroquinolone, what counseling points would you want to give regarding the use of antacids in a patient also taking a fluoroquinolone? Antacids may cause decreased effects of antibiotics, separate meds by at least 2 hours. Know how a gram stain works and what it tells us about the organism Gram stain gives rapid information that can be applied immediately and determines bacterial morphologic characteristics Know which organisms are a part of your "normal GI flora" stomach: lactobacillus, streptococcus sp small intestine: lactobacillus, streptococcus enterococcus, enterococcus, enterobacteriaceae, diphtheroids ileum: enterobacteriaceaea, enterococcus, peptostreptococcus, bacteroides, clostridium If the first patient had acute pyelonephritis, how would you change your selection of antibiotic, if at all? For complicated UTIs (pyelonephritis), usually fluoroquinolone is prescribed for a 7-14 day course of treatment What could you give if the patient was pregnant (what should you avoid)? Avoid fluoroquinolones, B-lactams are generally considered 1st line treatments What lab test would you order and monitor to determine if treatment for a UTI was required? Urine culture Which of the medication options for the second patient carries the highest risk of causing c. diff? Clindamycin Also, fluoroquinolones, cephalosporins, carbapenems and penicillins are most associated w/ c. diff If the patient was diagnosed w/ methicillin-sensitive staphylococcus aureus (MSSA) and had a penicillin allergy, how would this change your recommendation, if at all? Cefezolin Know about acute bacterial rhinosinusitis (ABRS)- common causes (bacterial pathogens) and treatment. ABX should target S. pneumoniae and H. influenzae Standard dose amoxicillin or amoxicillin clavulanate Know about serious side effects associated w/ the use of tetracyclines -Avoid use in pregnancy and children (tooth discoloration) -N/V/D -Photosensitivity Know the treatment guidelines for otitis media Most cases of AOM do not require abx, except in children younger than 2 ABX should be reserved for those likely to benefit Our second patient, Jimmy Chipwood had a mild cause of CAP MRSA. What oral antibiotics could you recommend? Dicloxacillin or cephalexin w/ cover s. aureus But if CAP MRSA is suspected, oral abx include -clindamycin, doxycycline or trimethoprim- sulfamethazole (TMP/ SMX) What if the patient had a penicillin allergy (there is another class of antibiotics, other than penicillins, that you would want to avoid in a patient w/ a penicillin allergy)? doxycyline or trimethoprim-sulfamethazole for (ca) MRSA and SEVERE PCN allergy MILD non-immunologic pcn allergies may receive B-lactam abx. Non-IgE reactions like Stevens-Johnson syndrome, toxic epidermal necrolysis or interstitial nephritis should avoid offending agents. What common pathogens would you expect to cause Jimmy's infection (skin/ soft tissue infection)? Furuncles (boils) and larger furuncles (carbuncles) are commonly caused by staphylococci. Those furuncles and carbuncles w/ purulent drainage w/ s/s of infection (fever) should be treated w/ an agent that will cover s. aureus (dicloxacillin or cephalexin) What treatment could you recommend if Jimmy's infection was methicillin susceptible staphylococcus aureus? MSSA coverage- dicloxacillin Sex-linked traits Traits that are inherited with sex chromosomes Autosomal traits Traits that are inherited with non-sex chromosomes X-linked recessive disorders Genetic variants on the X chromosome; more common in males. Both copies of the gene must be altered in female, but only one copy must be altered in males. Ex: colorblindness. X-linked dominant disorders Genetic variants on the X chromosome. Only one altered copy of the gene is needed to cause the condition in both males and females. Very rare. Autosomal dominant disorders Caused by variants in genes found on non-sex chromosomes. Only one altered copy of the gene is needed to cause an effect. Ex: Huntington dx. Autosomal recessive disorders Caused by variants in genes found on non-sex chromosomes. Both copies of the gene must be altered to cause an effect. Ex: cystic fibrosis. Lack of variability in a species may lead to more ________ . autosomal recessive disorders Define heterozygote advantage An individual with one mutated copy of a gene and one normal copy may have advantages against certain pathogens without suffering from symptoms of the disease. Explains why certain diseases stay prevalent over history in geographical regions or cultures. Give two examples of the heterozygote advantage Tay-Sachs heterozygote advantage against tuberculosis, and Sickle Cell heterozygote advantage against malaria. Mutations in the tumor suppressor gene BRCA 1 and 2 may lead to _____ . breast and ovarian cancers Inactivation of tumor suppressor gene APC may result in ______ . colorectal cancers How do mutations in the retinoblastoma (Rb) gene lead to cancer? Rb monitors antigrowth cellular signals (like contact with other cells) and blocks activation of the growth/division phase in the cell cycle. Mutations lead to perisistant growth. Genotype The unique sequence of DNA Phenotype The detectable expression of the genotype, or clinical presentation Penetrance The proportion of individuals with a disorder-causing mutation who actually exhibit clinical symptoms. Ex: Huntington dx is autosomal dominant, and therefore has a 100% penetrance. Cosanguinity Genetic relatedness between individuals descended from at least one common ancestor. Cosanguineous relationships result in decreased variability of a population. Anticipation A tendency of certain genetic disorders to present earlier in life and more severely as they are passed down in generations. Ex: grandchild is severely affected in infancy while the grandparent was only mildly affected in adulthood. CRISPR-Cas-9 gene editing DNA "scissors" that can be used to delete and insert segments of DNA, potentially curing genetic disorders. Many ethical implications. Signs and symptoms of acute viral hepatitis Fever, fatigue, loss of appetite, nausea/vomiting, abdominal pain, dark urine, clay-colored stools, joint pain, jaundice, elevated AST/ALT Transmission of Hepatitis A Fecal-oral route, 28-day incubation period, soley an acute illness with supportive treatment. Transmission of Hepatitis B Via mucosal contact with infected blood or body fluid, typically sexual activity, IV drug use and hemodialysis Transmission of Hepatitis C Blood and body fluids, typically through IV drug use, hemodialysis, nasal cocaine, transfusions, perinatal, unregulated tattoos, and (uncommonly) sexual activity. Transmission of Hepatitis D Requires an associated HBV infection for transmission. Commonly IV drug use. To be diagnosed with chronic viral hepatitis, the virus must have been present for at least _____ . six months Signs and symptoms of chronic hepatitis B Hepatosplenomegaly, spidere telangiectasis (vascular abnormality), jaundice, ascites, and peripheral edema. What are the established risk factors for NAFLD? Obesity, metabolic syndrome, genetic risks, and family histry. What are the emerging risk factors associated with NAFLD? PCOS, hypothyroidism, OSA, hypopituitarism, hypogonadism, pancreato-duodenal resection List common causes of NAFLD Hepatitis C, Wilson's disease, lipodystrophy, TPN, medications (amiodarone, methotrexate, tamoxifen, steroids), Reye's syndrome, acute fatty liver of pregnancy, HELLP syndrome, malnutrition What are the most common clinical manifestations of NAFLD? Elevated LFTs, fatigue, pain in the RUQ, central obesity, hepatomegaly, acanthosis nigricans, and presence of dorsocerviccal hump. What are the s/s of decompensated cirrhosis? Ascites, icterus, nail changes, splenomegaly, asterixis, variceal bleeding, and hepatic encephalopathy. Labs: platelets 150,000, elevated INR, and low albumin. What test is diagnostic of Hep A? Anti-HAV IgM What test is diagnostic of Hep B? HBsAg (surface antigen) What test is diagnostic of Hep C? Anti-HCV with reflex PCR What test is diagnostic of Hep D? Anti-HDV IgM (acute) or IgG (past exposure) Type I diabetes is characterized by _______ . autoimmune destruction of pancareatic beta cells and total lack of insulin production Type II diabetes is characterized by _______ . insulin resistance and a defect in pancreatic beta cell secretion Name the 3 factors contributing to insulin resistance 1) impaired binding to receptors 2) fewer receptors 3) post-receptor defects Stage I of Type II diabetes progression Pancreatic beta cells make more insulin (hyperinsulinemia) to combat insulin resistance, which results in temporary restoration of normal glucose homeostasis Stage 2 of Type II diabetes progression Fat lipolysis begins, increased free fatty acids. More insulin resistance and impaired glucose uptake. Hyperinsulinemia continues but beta cells become exhausted. Postprandial hyperglycemia, although fasting blood glucose is fine. Stage 3 of Type II diabetes progression Even more free fatty acids, even more insulin resistance, even more hyperinsulinemia. More gluconeogenesis from liver, resulting in postprandial and fasting hyperglycemia. There's down regulation of insulin receptors and impairment of post-receptor events. Accumulates in major hyperglycemia, eventual decreased insulin secretion, and diagnosis of Type II diabetes. List the signs and symptoms of diabetes Polydipsia, polyuria, polyphagia. Also dry mouth, drowsiness, frequent bed wetting, stomach pains (ketone bodies), and possible weight loss (breakdown of fat). What cells don't require insulin for glucose to enter? Hepatocytes, neurons, erythrocytes, and endothelial cells What are the normal results of an oral glucose tolerance test (75g glucose)? Fasting blood glucose: 80-100 One hour later: 120 Back to baseline: within two hours What are the diagnostic results for prediabetes? Fasting blood glucose: 100-125 Two hours after OGTT: 140-199 HbAlc: 5.7-6.4% What are the microvascular complications of diabetes? Retinopathy, neuropathy, and nephropathy (cells do not require insulin to transport glucose) What are the macrovascular complications of diabetes? Accelerated cardiovascular disease, accelerated peripheral vascular disease, and stroke The absence of _______ leaves cells in the retina, kidney, and nervous tissue susceptible to intracellular oxidative stress. glutathione Chronic hyperglycemia results in ______ , which alters protein structures and results in the development of ______ that interfere with structure and function of the cell. glycation; irreversibly advanced glycation end products (AGEs) List three prevailing theories behind the pathogenesis of hyperglycemia complications Lack of glutathione and increased intracellular oxidative stress, glycation end products (AGEs), and altered second messenger systems that activate protein kinase C Why are diabetics taking SQ insulin or oral agents at risk for hypoglycemia? Insulin and glucagon normally work together in balance. But when a pt has SQ insulin or oral agents on board, insulin can't naturally back off and glucagon can't provide enough of a response. Signs and symptoms of hypoglycemia Sweating, trembling, dizziness, mood changes, hunger, headaches, blurred vision, and extreme tiredness and paleness. What are three main end results of DKA? Loss of water/electrolytes and dehydration, metabolic acidosis, and net loss of body K+ What is a normal blood osmolality? 280-294 mOsm What primarily differentiates hyperglycemia hyperosmolar syndrome from DKA? The small amount of insulin available in HHS prevents lipolysis and the formation of ketones, so there is no metabolic acidosis. HHS is a longer, slower progression that mimics the imaired carbohydrate metabolism from insulin deficiency in DKA. What are the main steps in the pathogenesis of HHS? Insulin deficiency, decreased glucose utilization, glycogenolysis from the liver, hyperglycemia, glycosuria and osmotic diuresis, loss of H2O/electrolytes and dehydration, hyperosmolar state (up to 400 mOsm), shock, coma, and death. What is the connection between nephropathy and diabetes? The glomerular capsule has many endothelial cells, which don't require insulin for glucose transport. Hyperglycemic states cause damage. Signs and symptoms of hyperthyroidism Tachycardia, palpitations, wide pulse pressure, arrythmias (afib), systolic murmurs, possible heart failure, warm, moist skin with velvety texture, palmar erythema, vitiligo, fine and silky hair texture, temporal baldness, prominent stare, lid lag, failure of convergence, failure to wrinkle brow, tremors, excessive swewating, heat intolerance, hyperreflexia, weight loss, proximal muscle weakness, emotional lability, anorexia, n/v/d, menstrual abnormalities Signs and symptoms of hypothyroidism Lethargy, constipation, cold intolerance, weight gain, arthralgias, deep hoarse voice, general weakness, dry hair that falls out, cool and tough doughy skin, obesity, diminished auditory acuity, cardiomegaly, prolonged relaxation phase of deep tendon reflexes Normal TSH level 0.4-4.5 mIU/mL Normal T4 level 5.0-11.0 ug/dL Lab results for primary hyperthyroidism Low TSH and high T4 Etiology of Grave's disease (hyperthyroidism) Autoimmune process in which antibodies act like TSH and stimulate the thyroid gland, resulting in a diffuse goiter, exophthalmos, and dermopathy Etiology of Toxic Multinodular Goiter (hyperthyroidism) The patient had a past goiter in which certain areas are now nodular and secreting thyroid hormone independently Etiology of Thyroid Adenoma (hyperthyroidism) One nodular spot in the thyroid is secreting thyroid hormone Possible etiologies of hypothyroidism Congenital defects, idiopathic, iodine deficiency, drugs (lithium), chronic thyroiditis, removal of pituitary gland Etiology of Hashimoto's Thyroiditis (hypothyroidism) Autoimmune disorder in which the body makes antibodies that attack the cels of the thyroid. Most common symptom is a goiter. Which is the more metabolically active thyroid hormone? T3. 80-90% of T4 is converted to T3 in the peripheral tissues. Only free (unbound) hormone is responsible for activity. A primary cause of thyroid hormone disruption is an issue with the ______ . Lab results ______ . Thyroid; Low T4 but high TSH and TRH. A secondary cause of thyroid hormone disruption is an issue with the ______ . Lab results _____ . Anterior pituitary; Low T4 and TSH, but high TRH. A tertiary cause of thyroid hormone disruption is an issue with the ______ . Lab results ______ . Hypothalamus; Low T4, TSH, and TRH. List causative and risk factors for the developnment of cancer. Tobacco, alcohol, obesity, red meat, post-menopause, infections (STIs), ionizing radiation, occupational hazards, reproduction, sun exposure and tanning beds, and lack of fruits and vegetables, fiber, and physical exercise. What are the three leading causes of cancer deaths in men? Lung and bronchus, prostate, and colorectal. What are the three leading causes of cancer deaths in women? Lung and bronchus, breast, and colorectal. List characteristics of benign tumors. 1) Well-differentiated 2) Glow slowly in a well-defined capsule; not invasive 3) Low mitotic index 4) Do not metastasize What is a benign tumor? Non-cancerous abnormal growth that serves no physiologic function. Only life-threatening if it enlarges in a critical location. Ex: lipoma, adenoma, etc. List characteristics of malignant tumors. 1) Poorly differentiated (anaplasia) 2) Grow rapidly 3) Not encapsulated 4) High mitotic index 5) Capable of metastasizing and spreading through blood vessels and lymph What are two major characteristics of cancer cells in the laboratory? 1) Do not exhibit contact inhibition and continue to divide, piling up on each other, and 2) are anchorage independent and can proliferate suspended in soft agar Anaplasia The loss of cellular differentiation, a microscopic hallmark of cancer cells. What are proto-oncogenes? Genes that encode components of receptor-mediated pathways designed to regulate normal cellular proliferation. Cancerous cells characteristically express mutated or overexpressed proto-oncogenes, which are referred to as _______ . oncogenes Oncogenes are ______ in cancers, and tumor suppressor genes must be _______ to allow cancer to occur. activated; inactivated "the guardian of the genome" p53 tumor suppressor gene TP53 monitors intracellular signals related to stress and activates ______ which are responsible for the maintenance of genomic integrity and DNA repair caretaker genes List common tumor suppressor genes that, if mutated, may result in cancer BRCA1 (breast cancer), APC (familial adenomatous polyps), p53, and RB1 (retinoblastoma) List major mechanisms of genomic instability in the development of cancer 1) mutations in caretaker genes and tumor suppressor genes 2) epigenetic silencing altering the promoter region region of tumor suppressor genes 3) bad microRNAs (oncomirs) that decrease the stability and expression of other genes 4) chromosome instability In cancer cells, the _____ gene is switched on, producing an enzyme that rebuilds the telomere caps. As a result, cancer cells (like germ cells and adult stem cells) are _____ . This mechanism of cancer cell survival is known as _____ . telomerase; immortal; resisting apoptosis In what ways can cancer cells prevent the activation cytotoxic T cells, thus hiding from the immune system? 1) By not displaying an antigen on the MHC protein 2) by getting rid of the MHC protein entirely 3) by producing immunosuppressive proteins Carcinoma in situ (CIS) Preinvasive epithelial tumors that have not yet penetrated the local basement membrane; not malignant. Three fates: remain stable for a long time, progress to invasive and metastatic cancers, or regress and disappear. If caught early, could prevent metastasis. Cancer cells utilize ______ for energy metabolism, a competitive advantage that allows for a more efficient production of building blocks for rapid cell growth aerobic glycolysis (glycolysis even in the presence of adequate oxygen, also known as the Warburg effect) Angiogenesis and cancer cell survival Tumor cells can grow their own blood supply by secreting growth factors that recruit new vascular endothelial cells and initiating the proliferation of existing blood vessels A prerequisite for metastasis is _____ . Invasion (local spread) of the primary tumor. Includes recruitment of macrophages and other cells that digest the connective tissue capsule and other structural barriers. What are tumor markers? How do we use them? Substances produced by both benign and malignant cells that either are present in or on tumor cells, or are found in blood, spinal fluid, or urine. They could be hormones, enzymes, genes, antigens, and antibodies. Ex: prostate-specific antigen (PSA). We can collect and measure this data to aid in diagnosis or treatment evaluation. TNM Staging System T = Tumor spread/size N = Node involvement M = Metastases Tumor grading G1: well differentiated (low grade) G2: moderately differentiated (intermediate grade) G3: poorly differentiated (high grade) G4: undifferentiated (high grade) What are paraneoplastic syndromes? Symptom complexes triggered by the release of biologic substances from the tumor (ex: hormone) or immune response triggered by the tumor (ex: antibodies). This might result in the earliest symptoms of an unknown cancer. Examples of paraneoplastic syndromes (clinical syndrome, causal mechanism, and underlying cancer) 1) Hypoglycemia caused by insulin released from fibrosarcoma and hepatocellular carcinomas 2) Hypercalcemia caused by parathyroid hormone-related protein released from squamous cell carcinoma of the lung, breast and renal carcinoma 3) DVT/PE caused by mucins that activate clotting released from pancreatic and bronchogenic carcinomas