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EP is a 38-year-old female patient that comes in for diabetes education and management. She was diagnosed 12 years ago and states lately she is not able to control her diet although she continues a 1600 calorie diet with appropriate daily carbohydrate intake (per dietitian prescription) and walks 40 minutes every day of the week. She states compliance with all medications. She denies any history of hypoglycemia despite being able to identify signs and symptoms and describe appropriate treatment strategies. PMH: T2DM, HTN, obesity, depression, s/p thyroidectomy due to thyroid cancer FmHx: Noncontributory SHx: (−) Smoking, alcohol use, past marijuana use while in high school Medications: Metformin 850 mg tid, glipizide 20 mg bid, lisinopril 20 mg daily, sertraline 100 mg daily, multivitamin daily Vitals: BP 128/82 mg Hg; P 72 beats/min; BMI 31 m/kg Laboratory test results: Na 134 mEq/L, K 5.4 mEq/L, Cl 106 mEq/L, BUN - - CORRECT ANS- - Exenatide - Exenatide (Bydureon) once weekly has been able to demonstrate weight loss and decrease A1C% by 0.7% to 1.2% in clinical trials; however it is contraindicated for EP due to the self-reported history of thyroid cancer. Dapagliflozin - Dapagliflozin (Farxiga) is contraindicated in this patient due to hyperkalemia which could be made worse by this drug. The package insert does not indicate a specific potassium concentration cut off to no longer use this medication; however, there are better choices in this patient. Sitagliptin - Sitagliptin (Januvia) is able to obtain an A1C goal of less than 7% based on clinical trials and currently the patient does not have any cautionary objective measures to not use this medication. DPP-IV inhibitors are weight neutral. DPP-IV inhibitors can be used in patients taking sulfonylureas; however, it may be recommended to reduce or stop the sulfonylurea dose. Acarbose - Acarbose (Precose) is not recommended for initial management and is associated with significant GI side effects. More information would be needed regarding fasting and post-prandial numbers. In addition, adding acarbose would only lower A1c by 0 .8% at best and therefore would not achieve the desired A1C goal of <7%
JR is a 68-year-old African American man with a new diagnosis of T2DM. He was classified as having prediabetes (at risk for developing diabetes) 5 years before the diagnosis and has a strong family history of type 2 diabetes. JR's blood pressure was 150/92 mm Hg. His laboratory results revealed an A1C of 8.1%, normal cholesterol panel, and normal renal/hepatic function were noted with today's laboratory test results. Past medical history: Hypertension (diagnosed 4 y ago) Hyperlipidemia (diagnosed 2 y ago) Pancreatitis (idiopathic) (acute hospitalization 3 y ago) Family history: Type 2 diabetes Medication: HCTZ 25 mg daily, simvastatin 10 mg daily Allergies: SMZ/TMP Vitals: BP: 150/92 mm Hg P: 78 beats/min RR: 12 rpm Waist Circumference: 46 in Weight: 267 lb Height: 5 ′ 6 ″ BMI: 43.1 kg/m 2 Despite improvements in the past six weeks due to lifestyle changes and exercise, drug therapy is to be started for JR's diabet - - CORRECT ANS- - Metformin is the drug of choice recommended for most patients with diabetes in addition to lifestyle modifications assuming no contraindications or intolerabilities are present upon evaluation. Metformin has also shown to provide positive weight neutral/loss effects in obese patients. It is crucial to know the renal status of patients commencing metformin therapy to limit the risk of lactic acidosis (JR is without contraindication). Since his entry A1C is >7.5%, dual therapy is indicated. There are several potential choices. The second step can be a dipeptidyl peptidase-4 inhibitor, it can be a glucagon-like peptide-1 (GLP-1) receptor agonist, it can be a TZD, it can be a sulfonylurea agent, it can be a SGLT2 inhibitor, or it could be basal insulin. Anything next can be tried depending on what suits the circumstance DPP4 inhibitors are weight neutral bet relatively benign side effect profile. Sitagliptin has been associated with case reports of pancreatitis, so this specific agent should be avoided. $$$ GLP-1 analog and has data to support an A1C reduction necessary to gain glycemic control and may assist with weight loss goals for this patient. New information suggests these
NaHCO3 (as well as ASA). In the presence of HCL it Liberates CO2, that can cause gastric distention, belching and nausea. The reaction is fairly swift allowing little time for dissipation. Tums, its primary ingredient calcium carbonate which when taken cause a reaction with the stomach acid such as production of carbon dioxide gas which can cause bloating and the stomach to stretch to tear the ulcers open. On your way to this examination, you experience the vulnerable feeling that an attack of acute diarrhea is imminent! If you stop at a drug store, which anti-diarrheal drugs could you buy without a prescription even though it is chemically related to the strong opioid analgesic meperidine (but acts only on the peripheral opioid receptor)? - - CORRECT ANS- - Loperamide JA has multiple medical problems and is taking several drugs including theophylline, warfarin and phenytoin. His conditions were well controlled, but recently he started to experience some GI distress for which of his "well intentioned friends" gave him some medication. He presents to you with toxic effects of all his other medications and plasma levels of those medications elevated. What was most likely the medication he took? - - CORRECT ANS- - Cimetidine What lifestyle modifications should be recommended? - - CORRECT ANS- --losing weight if overweight
- elevating head of bed while asleep
- eating smaller meals
- avoid foods/meds that exacerbate gerd
- stop smoking
- stop drinking alcohol What medications / foods can contribute to GERD? - - CORRECT ANS- --Medications: anticholinergics, barbituates, dopamine, estrogen, opioids, progesterone, theophylline, nitrates
- Foods: cirus fruits/juices, coffee, tomatoes, spicy food, carbonated drinks
Fried/fatty foods, garlic, onions, chocolate What is the most effective PPI or H2RA within each of these classes? - - CORRECT ANS- -- PPI- bismuth quadruple therapy combined with proton pump inhibitors
- H2RA- Famotidine 80mg Other products such as antacids are also available. What are some of these and what is their place in therapy? - - CORRECT ANS- --Reflux symptoms <2 times a week (infrequent)
- Effective for immediate relief
- Magnesium/Aluminum Hydroxide (Maalox)- can cause constipation
- Alginic Acid Why would antibiotics be used for PUD caused by H Pylori? What is a typical regimen and duration of therapy? What patient specific factors should be considered and how should treatment be monitored? - - CORRECT ANS- - Considerations before regimen choice:
- penicillin allergy
- previous exposure to macroglide antibiotics Strongest Reccomendation:
- Bismuth Quadruple Therapy 10-14 days do not drink alcohol w/ metronidazole
- Salvage regimen should be different than first regimen Who would be a candidate for prophylaxis of NSAID induced ulcer and what agents are appropriate? What if the patient is on cardio-protective (low dose) aspirin? What if an NSAID induced ulcer does develop. How should it be treated? - - CORRECT ANS- - Candidate:
- Candidates: Chronic Nsaid Use, Hx ulcers, Zollinger-Ellison
Recommended for the treatment of the patient with CKD (modestly elevated (30- 299 mg/24 h) or higher levels (>300 mg/24 h) of urinary albumin excretion), even in those without DM Delay progression of nephropathy in Type 1 with or without HTN and any degree of albuminuria Delay progression of nephropathy in Type 2 with or without HTN and microalbuminuriaReduce development of microalbuminuria (kidney disease) in Type 2 with or without HTN ARBs are considered a reasonable alternative for those intolerant of ACEI - - CORRECT ANS- - Cardioprotective dose ASA (IE baby aspirin or clopidrogel as alternative)For SECONDARY PREVENTION of CV Events- Use in ALL diabetics with CV diseaseFor PRIMARY PREVENTION of CV EventsUSE in: high CV risk patients (10-yr CV risk > 10%) - Typically: male > 50 yo or female >60 yo with 1 additional major risk factor (FH of CVD, HTN, smoker, dyslipidemia or albuminuria)MAY consider: intermediate CV risk patrients 10-yr CV risk of 5 - 10%) - younger patients with 1 or more risk factors, older patients with no risk factorsNOT recommended: low CV risk patients - men <50 yo or women <60 yo without major CV risk factors or 10-yr CV risk < 5%Note - Many authorities consider DM to be an ASCVD risk equivalentThis is basically everyone with DM - - CORRECT ANS- - What are the goals set by ACE /ACCE and are they written in stone for all patients? - - CORRECT ANS- - Primary target for glycemic control is HbA1C Individualize HbA1C goal - based on...Duration of DMAge/life expectancyComorbid conditions Known CVD or advanced comorbid conditionsHypoglycemic unawareness Individual patient considerations Please note when transitioning from oral therapy for type II DM to insulin, metformin is retained! Secretagogues are discontinued possibly when basal insulin is initiated, but definitely when prandial (fast/rapid) insulin is to be added - - CORRECT ANS- - Options to add to basal insulin for prandial coverage...
Fast-acting insulin DPP-4 inhibitors Incretin mimetics Glinides Alpha-glucosidase inhibitors Colesevelam What are the various types of oral and non-insulin medications and what represents a rational combination of medications? - - CORRECT ANS- - Combinations should have different mechanism of action Combinations should avoid overlapping ADRs Combinations should ideally be selected based on need for better basal vs post-prandial control Selection should account for patient specific concerns (eg. weight, CVD risk, etc) What antidiabetic medications have compelling indications: - - CORRECT ANS- - for those with underlying ASCVD or at high risk for CVD for those with CKD for those with a compelling need to avoid hypoglycemia for those where weight is an important consideration (ie which are associated with weight loss, gain or are weight neutral) What are the various insulins and describe the pharmacokinetics (onset, peak, duration)and how are they used (eg basal, basal-bolus, split-mixed, sliding scale (..Ask if you don't understand)). - - CORRECT ANS- - Basal-bolus (long acting basal + rapid/fast acting bolus) provides the greatest flexibility and control of all regimens Sliding Scale Should NOT be used Difficult to do in home setting, requires education and understanding of patient and caregiver
Why are thyroid replacement drugs considered to have a narrow therapeutic index ( NTI )and what does that mean clinically? - - CORRECT ANS- - The therapeutic index (TI) is the range of doses at which a medication is effective without unacceptable adverse events. Drugs with a narrow TI (NTIs) have a narrow window between their effective doses and those at which they produce adverse toxic effects. Oral Bioavailability: (erratic) 40- 80%brand vs generic Highly protein bound (99%)Half-lifeEuthyroid = 6-7 daysHypothyroid = 9 - 10 daysSteady State: @ 6 weeks or 4-5 t1/2 's ... this is the bases for monitoring @ six weeks from start or changes! Consider changes such as brand to generic, different generics manufactures, different pharmacies, etcAny such change will require repeat lab monitoring @ ~ 6 weeks to confirm the same clinical response What are some drug-drug, drug-food interactions associated with thyroid replacement - - CORRECT ANS- - drug binding interactions, di-valent cations, amiodarone, certain antibiotics RECOMMENDATION 13 Methimazole should be used in virtually every patient who chooses antithyroid drug therapy for GD, except during the first trimester of pregnancy when propylthiouracil is preferred, in the treatment of thyroid storm (inhibition of peripheral conversion), and in patients with minor reactions to methimazole who refuse radioactive iodine therapy or surgeryDelayed onset - - CORRECT ANS- - Beta-blockers role in therapy? - - CORRECT ANS- - So .. beta blockers are used for Symptomatic relief of hyperthyroidism until more definative therapy is instituted and thyroid levels retun to normal or near normal.. Reduction of peripheral manifestations Tachycardia, sweating, severe tremor, nervousness Inhibition of peripheral conversion of thyroid hormones at higher doses (propranolol ONLY) Small therapeutic effect in magnitude thyrotoxicosis
Why does amiodarone pose a unique concern to thyroid disorders - - CORRECT ANS- - "Amiodarone-normal thyroid autoregulation is lost because of the relatively high iodine content" .. this fact can lead to a situation where amiodarone can cauase BOTH hyper- and hypo- thyroidism, depending on the patient, through several process blocking thyroid peroxidase blocking proteolysis of Tg and thyroid hormone altering organification, etc What would you recommend if a patient is taking Nexium and Plavix together? - - CORRECT ANS- - As we have seen through our discussions, there is a lot of information (including an FDA issued statement in the package insert) describing the drug interaction and reduced efficacy of clopidogrel if used with a PPI (primarily omeprazole) (or in patients who are genetically slow CYP2C19 metabolizers); however there is also evidence based information indicating the interaction is not as significant as originally thought. Bottom line: Despite pharmacokinetic evidence that omeprazole interferes with clopidogrel metabolism, COGENT trial found addition of omeprazole to clopidogrel reduced gastrointestinal events without increasing cardiovascular events. Note there is no significant difference in efficacy among the H2RAs when given at equipotent dosesCimetidine is associated with numerous clinically significant DIs Dose reduction in renal and hepatic insufficiency and in the elderly Duration of suppression ranges from 6-10 hours and varies with dose Note there is no significant difference in efficacy among the PPIs when given at equipotent doses Food may affect absorption. Given 30-60' before a meal. More flexibility in term of dosing with newer agents (eg. dexlansoprazole)Delayed onset: 3-4 days for full inhibition Duration of action up to 24 hours due to covalent, irreversible inhibition of proton pump - - CORRECT ANS- -
creating a protective layer against acid and pepsinIt may stimulate PG and mucus secretionIt binds bacterial endotoxins and has direct antimicrobial activity against pylori H Pylori eradication - Because of the critical role of H. Pylori in the pathogenesis of peptic ulcer, eradication of this infection is a standard care in patients with gastric or duodenal ulcers All regimens include 2 antibiotics & Acid suppression therapy (PPI or H2RA)May include Bismuth preparation Note especially duration and comments sections of the table below! - - CORRECT ANS- - In patients aged 55 yr or younger with no alarm features, the clinician may consider two approximately equivalent management options: (i) test and treat for H. pylori and a trial of acid suppression if eradication is successful but symptoms do not resolve or (ii) an empiric trial of acid suppression with a proton pump inhibitor (PPI) for 4-8 wk - - CORRECT ANS- - NSAID induced ulcers Prevention: - - CORRECT ANS- - Misoprostol or PPI. H2RAs not recommended for prophylaxis.COX-2 inhibitors are associated with a significantly lower incidence of gastric and duodenal ulcers when compared to traditional NSAIDs. However, this beneficial effect is negated when the patient is taking concomitant low-dose aspirin. The usefulness of these agents has also been reduced by their association with myocardial infarction and other thrombotic CV eventsCOX-2 inhibitors and NSAIDs to be discussed in more detail later in the semester Candidate for prophylaxis Candidate for prophylaxis - - CORRECT ANS- - History of prior gastrointestinal event Age over 60 (5x greater risk) High NSAID dosage Concurrent use of corticosteroids (4x greater risk) Concurrent use of anticoagulants, antiplatelets or low dose ASA (12x greater risk)
Treatment: Discontinue NSAID If possibleEradicate H Pylori if (+)H2RAs or PPIsPPIs heal NSAID-related ulcers more effectively as compared with H2RAs and are therefore the antisecretory drug of choice for treating NSAID-related ulcers, especially when NSAIDs are continuedPatients with NSAID-associated ulcers should be treated with a PPI for a minimum of eight weeksSucralfate is an option for healing only if NSAID will be stopped Constipation - - CORRECT ANS- - Approach to treatment should begin with determination of cause(including medications a patient may be on table 21-1)OpiatesAnticholinergics (eg. tricyclic antidepressant (amitryptiline), diphenhydramine, benztropine, etc.)NDHP-CCB (eg verapamil)Oral iron preparationsCalcium or aluminum antacidsNSAIDsClonidineDiuretics Constipation treatment - - CORRECT ANS- - Non-pharmacological interventions first (diet (fiber), exercise, fluids)Probiotics - limited data Best Pract Res Clin Gastroenterol. 2011;25:119- 126 PharmacologicalBulk forming agents (eg. methylcellulose (Citrucel))Administer 240 mL of water with each dose to prevent esophageal / GI obstruction and worsening symptomPhysical binding of other substances including medicationsSafe in pregnancyEmollients (softeners) (eg. docusate (Colace)Facilitate mixing of aqueous and fatty materials in the intestinal tractUsed for prevention, NOT treatment. Commonly prescribed with medications that may cause constipation (chronic opiate use, iron supplementation)Safe in pregnancyLubricant laxative (mineral oil / castor oil)Coats stool to allow easy passage / Prevents colonic water absorptionSystemic absorption - can generate immune responseAspiration - may lead to lipoid pneumoniaDecreases absorption of fat- soluble vitamins à DO NOT use in pregnancyHyperosmotics (eg. polyethylene glycol (Miralax))Osmotic effects to retain fluid in GI tractSafe in pregnancySaline laxatives - Composed of relatively poorly absorbed ions (Mg+ - sulfate, - phosphate, - citrate)(eg. MOM)Osmotic effects to retain fluid in GI tractMay be used occasionally to treat constipation in otherwise healthy adultADRs: fluid and electrolyte disturbances: Mg (renal dysfunction) or Na (CHF) accumulationStimulant laxatives (Senna, Bisacodyl) (eg Sennokot, Dulcolox)Only recommended for intermittent use - daily use strongly discouragedNew agents available for specific use ONLY (eg. IBS-C, OIC)NOT discussed in this course Summary of constipation recommendations - - CORRECT ANS- - Slow Transit ConstipationHyperosmotic laxativesSenna, Bisacodyl and other stimulants are second line
Probiotics - Help maintain normal GI flora, reduce colonization of disease-causing bacteriaEvidence - Vary based on intended use (acute treatment, prevention, antibiotic associated, adults, children), strain of bacterium and timing of administration Digestive enzymes (lactaid)Use in patients with lactase deficiency who are lactose intolerant We do not routinely use empiric antibiotics in patients with acute diarrhea. Infectious diarrhea: C diff - - - CORRECT ANS- - The initial step in the treatment of Clostridium difficile infection (CDI) is cessation of the inciting antibiotic as soon as possible Therapy for non-severe difficile infection (CDI) consists of oral metronidazole >> oral vancomycinLimitations of metronidazole include dose-dependent peripheral neuropathy and side effects of nausea and metallic taste.Use of oral vancomycin is appropriate for initial therapy of non-severe disease in patients who are pregnant, breastfeeding, or intolerant/allergic to metronidazoleRifaximin— Small case series have suggested that sequential therapy with vancomycin followed by Rifaximin may be effective for the treatment of recurrent CDI Traveler's diarrhea - the classic travelers' diarrhea due to enterotoxigenic Escherichia coli (ETEC) generally produces malaise, anorexia, and abdominal cramps followed by the sudden onset of watery diarrhea. The illness is generally self-limited with symptoms lasting for approximately one to five days. - - CORRECT ANS- - Antibiotics are warranted to treat diarrhea in those who develop severe diarrhea, characterized by more than four unformed stools daily, fever, or blood, pus, or mucus in the stool. In addition, some travelers desire antibiotic treatment for milder disease if the illness is a large burden on a business trip or vacation.For mild to moderate disease, anti-motility drugs(eg. loperamide) may be used as monotherapyFor sever disease, anti-motility drugs(eg. loperamide) may be used cautiously as adjunctive therapyuse in combination with simethicone may provide faster relief of symptoms For adults, several different antibiotic options are effective for travelers' diarrhea. In general, fluoroquinolones (eg ciprofloxacin) are the first choice for their efficacy and tolerability. However, for travelers to Asia, azithromycin is preferable because of increasing resistance to fluoroquinolones among enteric pathogens in that region. Azithromycin is also the preferred agent for pregnant women and children. We only use Rifaximin if a
fluoroquinolone or azithromycin is not available or appropriate because its efficacy for invasive disease is unknown Nausea / Vomiting When choosing an agent - - CORRECT ANS- - Focus on individual patient, evaluate risk factors, and rule out other causes. Agent related variables (efficacy, ADR's, cost) Please review mechanisms, ADRs and Promethazine - Block DA2 receptors in the CTZ + have antihistaminic and anticholinergic effects.ADR's: EPS, sedation, hypotension Place in therapy: "general purpose antiemetics". not very effective in severe n/v (i.e. chemotherapy induced n/v (CINV)Example Lorazepam - Benzodiazepines bind to GABA-A receptors. GABA is the major inhibitory NT in the CNS benzodiazepines are sedatives, not antiemetic agents Sedative and anti-anxiety effects → reduce anticipatory N/V associated with chemotherapy ADRs - CNS - sedation, hallucinations, euphoria; CV - hypotension CINV - Evaluate emetogenic potential of regimen Mono therapy for chemotherapy with low and moderate emetogenic risk Aggressive (combination of agents with different mechanisms) antiemetics for highly emetogenic regimens and delayed CINV Examples Dexamethasone + metoclopramide + diphenhydramine + lorazepam Ondansetron + dexamethasone Ondansetron + metoclopramide Metoclopramide + dexamethasone Ondansetron + dexamethasone + prochlorperazine Ondansetron + dexamethasone + aprepitant Erectile dysfunction - "The inability to attain or sustain an erection adequate for sexual stimulation" - - CORRECT ANS- - Can be the result of age related changes (e.g. diminished testosterone, altered response to NO, etc), comorbidities (e.g. DM, BPH, depression, etc .. Table 51-1), and medications (e.g. 5-alpha reductase inhibitors, beta-blockers, TCAs, etc. .. Table 51-2)
PDE5Is - Often considered drug of choice when pharmacotherapy is necessary. There is no convincing evidence that one agent in this class is superior to another. Choice may be based on patient preference, cost, and formularies - - CORRECT ANS- - There is no drug effect without some type of sexual stimulation because these drugs do not cause penile erections; they only provide the ability of the penis to respond to sexual stimulation. Varying duration of action (most 4-5 h, tadalafil 36h). Headache and flushing most common ADRs. Serious cardiac events possible Significant DIs exist - - CORRECT ANS- - +) nitrates - severe hypotensionIn an emergent situation, a patient who has taken sildenafil may be given a nitrate after 24 hours; for tadalafil, after 48 hours. Vardenafil does not have a suggested time interval, but blood pressure and heart rate did not change when the drug was taken 24 hours before nitrate administration. These suggested intervals are a direct correlation to half-life and duration of action Prolonging of QT interval Serious cardiovascular events have been associated with PDE5 inhibitors; therefore, they should not be used in patients in whom sexual intercourse is inadvisable because of poor cardiac status. Testosterone replacement (Low-T) - - CORRECT ANS- - Testosterone replacement regimens should never be administered to men with normal serum testosterone levels, or in patients with isolated erectile dysfunction as the only sign of hypogonadism. Before initiating any testosterone replacement regimen in patients 40 years and older, patients should be screened for breast cancer, benign prostatic hyperplasia, and prostate cancer. All are testosterone-dependent conditions and theoretically could be worsened by exogenous administration of testosterone Alprostadil - PgE1 analog administered by intracavernosal injection & intraurethral inserts -
- CORRECT ANS- - Because PGs bypass many steps in the erectile cascade, they are quite effective at producing an erection, even in cases where PDE5 inhibitors cannot do so. Most invasive and low patient acceptance. Reserved as second or third line treatment
BPH - - CORRECT ANS- - BPH increases urethral resistance, resulting in compensatory changes in bladder function. Obstruction-induced changes in detrusor function, including smooth muscle hypertrophy, compounded by age-related changes in the functioning of the bladder, lead to urinary frequency, urgency, and nocturia, the most bothersome BPH- related complaints. Not all patients with LUTS have BPH and not all men with BPH have LUTS. BPH diagnosis - - CORRECT ANS- - Diagnosis includes components such as symptom assessment (AUA score), PE and PSA PSA is present in small quantities in the serum of men with healthy prostates, but is often elevated in the presence of prostate cancer or other prostate disorders. PSA is not uniquely an indicator of prostate cancer, but may also detect prostatitis or BPH. PSA correlates with prostate size and can be used as a prognostic marker Non-pharmacologic interventions for BPH - - CORRECT ANS- - Lifestyle modification - limiting EToH, caffeine, avoid certain medications (Table 52-4)(e.g. decongestants, androgens, etc) as well as addressing co-morbidities (weight loss, etc) Watchful waiting is the most conservative approach for patients with mild symptoms or those with moderate symptoms without bother ◦Appropriate option for patients with mild symptoms (AUA-SI score ≤ 7), and for many with moderate to severe symptoms (AUA-SI ≥ 8) if they are not bothered ◦Behavior modification includes restricting fluids close to bedtime, minimizing caffeine, sweetened drinks and alcohol intake, frequent emptying of the bladder during waking hours (to avoid overflow incontinence and urgency), and avoiding drugs that could exacerbate voiding symptoms (e.g. antihistamines, decongestants). ◦At each visit, assess the patient's risk of developing acute urinary retention by evaluating the patient's prostate size or using PSA as a surrogate marker of prostate enlargement The level of symptom distress that individual men are able to tolerate is variable
