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CPC Block 1
Case 2 (1) Gout, allergic rhinitis, HTN
| Question | Answer |
|---|---|
| Gout pathohypsiology | Uric acid is a breakdown product of purine degradation. |
| Hyperuricemia is defined as | plasma urate (uric acid) levels >420umol/L (7.0=men) >380umol/L in women |
| Hyperuric acid production is caused by | Over production(chemotherapy), Under excretion (drugs-HCTZ,nictonic acid,ETOH,levodopa) or renal insufficiency, Age |
| Clinical manifestation of gout are | Pain in the 1st metatarsophalangeal, erythema, fever, leukocytosis |
| 4 types of Gout manifestations are | 1. Acute gout arthritis (toe),2. Uric acid nephrolithiasis (Chronic) 3.Acute Gouty Nephropathy (block=ARF) 4. Chronic Gouty nephropathy (tophi deposits) |
| Medications of Acute Gouty arthritis | Dietary modification, NSAIDS, or colchinine, or Prednisone |
| What is the MOA of NSAIDS | Competively inhibits COX 1 and COX2 blocking arachodonic acid production the rate limiting step of inflammatory mediators as well as PG thus afferent constriction occurs-monitor renal |
| What is the MOA of Colchinine | It binds to neutrophile protein microtubules and inhibits the migration and interfers with the inflammatory response. |
| What is MOA of Prednisone | Glucocorticoids are naturally occuring hormones that prevent or suppress inflammation and immune response |
| What is the MOA of Triamincolone | Cortiosteroids produce a peptide (lipocortin) which inhibits the synthesis phospholipase A (membrane protein) thus inhibits the synthesis of arachadonic acid inturn this inhibits inflammation |
| What are drug interactions of NSAIDS | Warfarin, ETOH, methotrexate |
| What does COX 1 express normally | Good PG's for the stomach, intestine, kidney |
| What does COX 2 express normally | PG that mediate pain and inflammation |
| Indomethacin is a NSAID for aucte gouty arthritis why is this prefered? | It is lipophilic and has increased tissue penetration. |
| Dosing of indomethacin | 50mg TID for 1-2 days then 25mg TID prn (max200mg/day) |
| What is the maximum over the counter dose for Ibuprofen and what does this treat? | It is 200mg (1200mg/day) and it is an analgesic and antipyretic dose must be 800mg (2400mg/day) to treat inflammation RX max=3600/day |
| Platelet inhibition does not occur with what NSAID types? | Non-acetylated (sodium salicylate,mag salicylate, salasalate) |
| Contraindications to NSAIDS are | CABG, ASA allergy, GI-bleed |
| What are the side effects of colchinine | Diarrhea, N/V, alopecia, bone marrow suppression, aplastic anemia |
| What are the Drug interactions of colchinine | Clarithromycin,erthyromycin,cyclosporin,tacrolimus |
| Colchinine is contraindicated in | Pregnancy and lactation---Caution is alcholism, and pre-existing Bone marrow suppression |
| At what CrCl must Colchinine be dose adjusted in renal insufficiency | CrCl 10-50ml/min should reduce the dose by 50%-- |
| What are the side effects of Prednisone | Insomnia, dyspepsia, esophigitis, adrenal suppression |
| Chronic gouty arthritis prophylaxis is indicated if | 1. Patient has >2 attacks 2. Patient is undergoing aggressive chemotherapy 3. 1st attack is severe (uric acid>10, kidney stones, urinary excretion >1000/day) |
| Treatment options for chronic gouty arthritis are | Allopurinol, probenecid, or coclhinine |
| What is the MOA of allopurinol | Inhibits xanthaine oxidase which decreases purine catabolism and decreases uric acid synthesis |
| What is the CrCl where allopurinol should be adjusted | CrCl<60=200mg/day and CrCl<40=100mg PO day |
| What are side effects associated with allopurinol | skin hypersensitivities, hepatoxicity, fever |
| What is the MOA of Probenacid | Inhibits renal tubular reabsorption of uric acid at the proximal convuleted tubule |
| What is the CrCl where Probenecid is contraindicated | CrCL <50ml/min |
| What is the pathophysiology of of allergic rhinitis | It is a Type I hypersensitivity. First there is an exposure to antigen, this stimulates IgE production, and upon representation there is binding of antibody to mast cells and degranulation-inflammatory mediators released |
| Signs and symptoms of allergic rhinitis are | Nasal congestion,postnasal drip, itchy eyes,nose or palate |
| What are the treatment options for allergic rhinitis | 1. Topical steroids, 2. Second or 1st generation antihistamines 3. Cromolyn |
| What side effects are seen with topical nasal steroids | Local irritation, mucosal bleeding, and rare septal perforation |
| What is the MOA of antihistamines | They inhibit(antagonist) Histamine receptor thus prevent the release of inflammatory mediators |
| What are a few second generation antihistamines a patient with allergic rhinitis may use | fenofexadine (allegra), loratadine (claritin), cetirizine (zyrtec) |
| 1st genration antihistamines should be avoided in | Patient with narrow angle glaucoma, neonates (paradoxial excitation) |
| What are JNC 7 BP goals for patients without compelling indications | BP<140/90 |
| What are JNC 7 BP goals for patients with a compelling indication for DM or CKD | Bp <130/80-GFR<60, Scr men=1.5, women, 1.3 or macroalbumuria.300 or creatinine >200 |
| What are JNC 7 BP goals for patients with proteinuria >1g/day | 125/75 |
| How do clinicians diagnosis HTN | Must have elevated Bp values on 2 separate days |
| What are the major CVD risk factors (9) | 1. Age (men>55 women>65) 2. DM 3.Dyslipidemia 4. Obesity 5. HTN 6. FHx (male<45,female <55) 7. Microalbuminaria 8. Physical inactivity 9. Smoking |
| 2 types of HTN | 1. Essential HTN (most) 2. Secondary HTN |
| Stages of HTN | Stage I (140-159/90-99) Stage II (>160/>100) 2 drugs exception is those that are >75year old |
| 3 theories of HTN Pathophysiology are | 1. Increased Cardic output due to increase CCA's 2. Chronic HTN causes increased PVR that maintains increased BP-arterioles increase in collagen & calcium -endotheial dysfunction 3. Decrease in renal profusion activates RAAS -Na/water & Preload increase |
| What are the lifestyle modifications that are recommended according to JNC7 (5) | Weight reduction (10kg=5-20 decrease), 2. DASH diet (8-14drop), Sodium (<2.4g= 2-8drop) 4. Physical activity -30min most days (4-9 drop) 5. Moderate ETOH ( 2-4 drop) |
| What is the MOA of HCTZ | At the distal convoluted tubule it inhibits Na/CL cotransporter to secrete Na and water (absorb Calcium) -decrease preload and afterload |
| What are side effects of HCTZ | Hyponatremia, hyperurecemia, hypokalemia, hyperglycemia, hyperlipidemia |
| What are the side effects of ACE inhibitors | Hyperkalemia, dry cough,orthostatic hypotension,angio edema |
| What are the contraindications of ACE inhibitors | Pregnancy, angioedema to any medication, bilateral renal artery stenosis, elevation of Scr >35% from baseline |
| What are the Side effects of ARBS | same as ACE inhibitors: Hyperkalemia, orthostatic hypotension, rare-dry cough, Scr>35% from baseline |
| What is the MOA of non-DHP CCB's | Inhibit Voltage gated Calcium channels in cardiac and smooth muscle arteriole>venous dialation also cause SA node depression (no reflex tachycardia) -excellent for diastolic heart dailure time to fill and artial tachycardia |
| What is the MOA of DHP CCB's | Inhibit voltage operated calcium channels arteriolar> venou, No effect on automacity of SA node, nor chronocity of AV node |
| What are side effects of CCB's | Peripheral edema, flushing, constipation, heartburn |
| What are the contraindications of CCB's | 2nd or 3rd Heart block, systolic heart failure (ok diastolic), (non-DHP) grapefruit, simvastatin,lovastatin are increased=rhabdomylysis |
| What are the side effects of B-blockers | Fatigue, heart block 2nd,3rd (HR,60), execerbate PAD, mask hypoglycemia, rebound HTN if stop suddenly |
| What are the drug interactions of Beta blockers | Cocaine increases angina, Verapamil, diltiazem, digoxin |
| Contraindications of B-blockers are | Non-selective in severe asthma, acute HF, PAD, 2nd or 3rd heart block |
| Furosemide side effects are | hyponatremia, hypokalemia, hypomagnesemia, orthostatic hypotension, ototoxcity, hyperuricemia |
| What are the contraindications of furosemide | Sulfa allergy, azeotemia, dehydration |
| What is the MOA of spironolactone | Competes with aldosterone for the mineral corticoid receptor and causes secretion of Na in the collecting duct |
| What are side effects of spironolactone | hyperkalemia, gynomastica, menstral irregularities |
| What are contraindications of spironolactone | K>5.0, Scr>2.5men, >2.0 women or elderly CrCL,30ml/min, |
| What are the contraindications of Eplerenone | CrCL<50ml/min, Scr men>2.0 Scr women >1.8 or DM + microalbuminuria |
| What is the DI of spironolactone | It interacts with lithium |
| What are the JNC compelling indications for HF (5) | Diuretic (loop), ACE, B-blocker (when hemodynamically stable), spironolactone or eplerenone |
| What are the compelling indications for post MI (4) | ACE, B-blocker, spironolactone or eplerenone |
| What are the compelling indications for High coronary disease risk (4) | Beta blocker, CCB, HCTZ, ACE |
| What are the drugs for the compelling indication of Dm according to JNC7 (5) | ACE (type1, prefer Type II), ARB (Type II -macroalbuminaria, diabetic neuropathy) HCTZ (cannot use CRCl<30, CCB B-blocker |
| What are the Drugs for the compelling indication of CKD | ACE or ARB |
| What are the drugs for the compelling indication of recurrent stroke prevention according to JNC7 | HCTZ + ACE use together |
| Orthostation Hypotension is defined as | a decrease in SBP or DBP greater than 10nnHG from the supine to postural |
| Orthostatic Hypotension is associated with | Diuretics (HCTZ,Loops) nitrates, alpha blockers, PDE inhibitors, ACE inhibitors, ARBS, psychotropics |
| Minority African americans can start 2 drugs according to JNC& when | There BP is > 155/100 or when BP>15/10 |
| Those with CKD, and DM can start 2 drugs if | >145/90 or BP>15/10 |
| BP goal for those with proteinuria (>1g) | <125/75 |
| PAD treatment with | Clopidogrel or clostanzol ( B-blockers worsen due to alpha constriction) |
| Follow up for stable HTN patient is | 2-4 weeks |
| Follow up for an unstable patient with HTN is | 1-7 days |
| When do you screen for dislipidemia | Those with out CHD should be >20 =every 5year, those with CHD or DM-annual |
| Very High Risk -dyslipidemia patients are | Have AVD (+ 1 major risk factor: DM, HTN,smoking, low HDL, FHx, age of onset) , or DM with LDL baseline <100 |
| Very High coronary disease risk must have 1 of these according to NCEP (4) | Multiple major risk factors (DM), poorly controlled risk factors (smoking), Multiple risks for MetSyn, Acute coronary syndrome (acute MI) (goal LDL<70) |
| NCEP lipid goals are | Primary-Lower LDL*** except TG>500 this is goal, secondary -Non-HDL (if TG >200<499), tertiary goal- Increase HDL (if MetSyn) |
| What is the definitaion of High risk for CVD according to NCEP | AVD, or CVD risk equivalent (DM) or Framignham risk >20% +2 risks (smoking, HTN or treat, Low LDL, FHx of CVD( 55, 65) , Age of onset <45, <55 (goal LDL<100) |
| Moderately High risk for CVD according to NCEP are | Framingham risk 10-20% + 2 risk factors (goal LDL <130 with option of <100-if risk) |
| Moderate risk patients according to NCEP are | Framingham risk <10% (goal LDL <130) |
| Low CVD risk according to NCEP are | 0-1 risk factors goal LDL<160 |
| What are 3 disease states that increase LDL | Hypothyroidism, nephrotic syndrom, obstructive liver disease |
| Name 3 drugs that increase LDL | anabolic steroids, oral progestins, B-blockers, HCTZ |
| Name 3 disese states that increase TG | DM, hypothyroidism, severe renal insufficiency |
| Name 3 drugs that increase TG | oral contraceptives, oral retinoids (sccutane), beta-blockers |
| what are non-ISA beta blockers | Carvedilol, Atenolol, Metropolol |
| ISA beta blockers are | Carteolol, penbutolol, pindolol |
| Intrinsic sympathomimetic effets are | They block B1 antagonsit (Decrease CO and renin ) and are Partial B2 agonist (relax smooth muscle and bronchodialation) |
| HMG-COA inhibitors (statins) doubling the dose decreases LDL by___ and the also decrease ____ risk | 6%- |
| What are the side effects of statins | N/V, HA, hepatotoxic, myopathy, rhabdomyolysis |
| Due to a drug interaction with amiodarone and verapamil the dose limits of ____ are | Simvastatin-zocor (20mg) and lovastatin-mevacor (40mg) |
| Due to a drug interaction with cyclosporin there is dose limits with ____ and the doses are____ | simvastatin (10mg ), lovastatin (10mg), rosuvastatin ( 5mg) |
| Due to a drug interaction with gemfibrozil there is dose limits with ____ and the doses are____ | Simvastatin (10mg), Lovastatin (20mg) , Rosuvastatin (10mg) |
| How do you monitor statins | Baseline-FLP, LFT, then 6 weeks and annual |
| What is the MOA of ezetimbe or zetia? | Inhibits enterocyte absorption of cholesterol in the brush border of the small intestine |
| How much does ezetimbe or zetia decrease LDL | 18% or 3 doublings of statin meds |
| What are side effects of ezetimbe or zetia | diarrhea, abdominal pain |
| WHat is the MOA of bile acid sequestrants | Bind to bile acid in the intestine and reduce the amount that are returned to the liver via enterohepatic circulation. |
| What are the side effects of bile acid sequestrants | Decrease absorption of other medications |
| What are the contraindications of bile acid sequestrants | Hx of GI obstruction, dysphagia (large tablets) |
| What is the MOA of niacin | Inhinits the synthesis of VLDL precursors to LDL |
| What are the side effects of Niacin | Flushing, worsening of uric acid levels, flushing, alteration of glucose, hepatotoxic |
| What are the contraindications of Niacin | Active liver disease, active peptic ulcer disease, active gout, poorly controlled DM |
| Monitoring of Niacin includes | FLP and LFT-baseline, 6 weeks and FLP annual |
| What is the MOA of fibrates | Not understood, may involve peripheral lipolysis |
| What are the side effects of fibrates | GI upset, hepatotoxic, rhabdomyolysis(gem) |
| What is the drug interaction with fibrates | warfarin interaction |
| What is the contraindication for fibrates | Active liver disease, gallbladder disease, severe CKD (CRCL<30) |
| Fish oil decreases TG__% the minimum effective dose is ___ | 50% reduction but the minimum effective OTC dose is 6g, Omacor 4g |
| Advicor is a combination of | niacin and lovastatin |
| What are the 5 A's to stop smoking | 1. Ask 2. Advise 3.Assess 4. Assist 5. Arrange follow up |
| How do you dose policrilex gum to stop smoking | How many cigarettes > 25=4mg and <25cigarettes 2mg chew 1 piece each hr (6wks), then 1 piece every 2-4hrs (3wks), 1 piece every 4-8 hrs (2 wks)-DO not eat or drink for 15min before gum |
| How do you choose what patch to select to stop smoking | > 10 cigarettes 14mg (6 wks) then 7mg (2 wks) if >10 cigarettes 21mg (6wk), 14mg (2 wks), 7mg (2 wks) |
| How do you decide what lozenge a patient should use to stop smoking | Based on 1st cigarette if <30mines =4mg and >30minutes=2mg |
| What is the MOA of Bupropion | Stimulates DA and NE |
| What are the contrindications of Buproprion | Seizure disorders, anorexia, bulimina, cocurrent MOA, abpupt D/C of ETOH or sedatives |
| Varenicline (chantix) MOA is | Antagonist of the alpha and beta nicotiinic receptor |
| What is imparied fasting glucose | Glucose >100<126 |
| How do you diagnosis DM | 1 of the following 3 on two separate days. 1. symptoms + random glucose>200 2. Fasting glucose >126 3. Oral glucose tolerance test post 2 hours >200 |
| What is fasting defined as | Greater than 8hrs without food |
| CKD according to JNC7 | GFR<60ml/min, Scr men>1.5, women 1.3 and macroalbuminaria >300albumin or creatinine >200g |
| What are the primary endpoints of the Hot Trial | 1 Established that BP goals are 140/90 or 130/80 2. ASA for prevention of CV event (men reduction in MI and women-stroke reduction) - 3. ASA more nonfatal bleeds 3. Alpha blockers increase HF should not be used as mono HTN therapy |
| Myopathy defined by the national lipid association is | Complaints of myalgia (muscle pain or soreness), weakness, and/or cramps, plusserum CK >10 x the ULN (normal 5-40 so about 400) |
| Rhabdomyolysis defined by the national lipid association is | CK >10,000 IU/L, orCK >10 x the ULN plus an elevation in serum creatinine or medical intervention with IV hydration therapy |
| Guideline for statin therapy from the national lipid association ( 8 remommendations) | 1. Muscle pain/Elevated CK=rule out other etiologies 2.Baseline Ck only risk (elderly) 3.No CK in asymptomatic 4.Counseling of myopathy 5. Ck lab in symptomatic 6.Intolerable pain with or w/o elevated CK-D/C & restart 7.tolerable CK<10 ok 8. Rhab- D/c |
| Rule of thumb for ACE & ARBs with alteration in Scr | Can continue therapy as long as Scr <35% increase. This change maybe reversible in 3-12 months so before dose adjust monitor. ABSOLUTE Contraindication is Scr>3.0 |
| Low dose ASA is indicated in patients with a Framingham 10 year risk of | >10% which for primary reduction (HOT) of MI=men and stroke=women, No mortality change |
| ASA side effects are | GI bleeding (vomit coffee grounds) or Tar stools (dark stools) |
| ALLHAT trial found (3) | 1. Alpha blockers cause more HF 2. CCB vs HCTZ -less HF with HCTZ 3. ACE vs HCTZ- less HF and stroke with HCTZ |
| LIFE trial found (2) | Atenolol vs Losartan in patients with LV dysfunction & HTN - Losartan decreased stroke, MI, and reduced more death than B-blocker |
| CCB extra effects | They dialate the afferent and efferent arteriole in the kidney improving filtration |
| What criteria must be met to have MetSyn | 3 or 5 must be met: 1. TG>150 or treat(Fibrate or Niacin) 2. Low HDL<40men <50 women or treat (Fibrates,Niacin) 3. waist>40men >35women, 4. FPG>100 5.BP>130/85 or treatment |
| LDL= | TC- (TG/5) +HDL |
| Acute gouty arthritis dosing of of colchicine is | 0.6-1.2mg initially the 0.6mg q1hr or 1.2mg q2hr, dose until pain relief or diarrhea-wait minimum of 2 days to repeat courses |
| Allopurinol and pronemicid may precipitate an acute gout attack when they are first started;this can be minimized by | 1.Give it concurrently with low dose NSAID or colchicine 2. Give low dose Allupurinol or Low probenicid 3. Wait before starting therapy |
| Dose of probenecid for chronic gout prophylaxis is | 250mg BID 1-2 weeks then 500mg BID x 2 weeks then increase up 500mg/week- Max dose is 3g/day |
| Side effects of probenecid are | Rash, GI, precipitation of gouty arthritis, kidney stones |
| What are medications that cause increase in serum uric acid | HCTZ, niacin, ethanol, salicylates, levodopa, cyclosporine, cytotoxic agents |
| Treatment goals of acute gouty arthritis are (3) | 1. Terminate acute attack 2. Prevent recurrent attacks of gouty arthritis 3. Prevent complications |
| Acute gout arthritis is treated with NSAIDS what group would you avoid and why | Avoid salicylates since they increase bleed risk and they increase uric acid levels |
| Acute nephrolithiasis is treated with | Hydration to maintain 2-3L/day or urine output + urinary alkalization to maintain pH of 6.0-6.5 with Shohl's solution, Acetazolamide |
Created by:
liza001