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189 Cards in this Set
- Front
- Back
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Cardiac Physiology
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-Electrical conduction (pacemaker, regulator, bundle of his, purkinje fibers)
-electrical current > Ca >released to sarcoplasm > interacts with troponin > actin-myosin coupling > contraction |
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Action potential
what happens in phase : 0, 1, 2, 3, and 4? |
phase 0 - fast sodium channel, Na enters, depolarization
phase 1 - mild repolarization phase 2 - slow Ca channel, contraction phase 3 - repolarization, K enters the cell phase 4 - resting , Na/K pump |
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how can we treat CHF? - (low output failure)
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-diet = weight loss, low Na, low fat
-diuretics (high ceiling loop diuretics) - Cardiac Glycosides - ACE inhibitors (1. vasoconstriction. 2. angiotensin 1/2 or renin/aldosterone system) |
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Cardiac glycosides pharmacology
(Properties) |
-increase contractility of the heart
(increased inotropic effect) --> by not pumping Ca out of cardiac cell, prolongs phase 2. -decrease AV node conduction (decrease chronotropic effect) used in atrial fib. |
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Cardiac glycosides therapeutic monitoring
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-apical pulse
-serum drug level -serum K = caution in hypokalemia -serum Ca = caution in hypercalcemia |
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Pharmacokinetics (Cardiac Glycosides)
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-five half lives leads to steady state
-loading doses required (refers to an initial higher dose of a drug that may be given at the beginning of a course of treatment before dropping down to a lower) * -toxicities -reversed by Digoxin immune fab (Digibind) -HALF LIFE (Digoxin = 24 hrs, Digitoxin = 5 days ) |
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Cardiac Glycosides Toxicities
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-AV block
-sinus bradycardia -arrhythmias -yellow-green halo vision (pre-toxic) -CNS: headaches, weakness, anorexia |
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Cardiac Glycosides Toxicity Therapy
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-discontinue use
-Digoxin immune fab (Digibind) -Correct hypokalemia -antiarrhythmic agents |
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Cadiac Glycosides Therapeutic Uses
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-CHF
-Adjunct therapy for atrial fib. |
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Pharmacologic properties of cardiac glycosides
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-at LOW dose = INOTROPIC effect
-at HIGH dose = CHRONOTROPIC effect |
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Automaticity?
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-all cardiac cells have the potential to be a pacemaker - if it is not the SA node initiating an impulse = arrythmia.
-latent pacemakers fire slower than SA node -causes of ectopic foci = ischemia, acidosis, suppressant drugs.. |
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Mechanism of action of Antiarrhythmics
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-decrease automaticity
-increase the refractory period |
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Quinidine
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-atrial arrhythmia
-different salts (Sulfate = 83% Quinidine, Gluconate = 62% Quinidine) -treatment with Digoxin for atrial arrhythmia until no more automaticity. -IV dilate vessels (hypotension) -Increase conduction thru AV node - bad property |
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Adverse reactions of Quinidine
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-Arrhythmogenic
-Toxicity : Cinchonism -- tinnitus, headache, N/V, vertigo |
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Quinidine usage
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-atrial tachycardia
-atrial fib. - use Digoxin as adjunct therapy |
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Procainamide Pharm.
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-decrease automaticity
-increases refractory period -slows AV conduction - good property |
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Procainamide Adverse reactions
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-lupus-like syndrome (dose related and reversible)
-arrhythmogenic - can cause arrhythmia |
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Procainamide use
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-atrial tachycardia
-atrial fib -ventricular arrhythmia =IV use when lidocaine fails or is contraindicated |
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Disopyramide pharm.
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-decrease automaticity
-increase refractory period -no effect on AV conduction -strong anticholinergic |
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Disopyramide contraindications
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-CHF = decrease cardiac output
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Dysopyramide use
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atrial tachycardia and atrial fib.
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Lidocaine pharm
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-local anesthetics
-antiarrhythmic (IV use only) -high therapeutic index |
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Lidocaine adverse effects
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-CNS toxicity: tinnitus, resp. depression, seizure
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Lidocaine dosing
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-antiarrhythmic = loading dose, IV infusion
-use : ventricular arrhythmias, Digoxin toxicity arrhythmias |
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Class 1B and 1C
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-e.g. :Mexelitine, Tocainide, Flecainide
-oral agents for ventricular arrhythmias -pharmacology similar to Lidocaine |
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Propranolol
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-beta blocker
-decrease atrial/ventricular tachycardia -IV use as an antiarrythmic |
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Amiodarone
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-45 day half life = should be low dose
-use = ventricular arrhythmias -IV form to treat ventricular arrhythmias -adverse reactions (cataract, pulmonary fibrosis, hypothyroid) |
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Verapamil
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-Ca channel blocker
-IV push for antiarrhythmic properties -2nd dose can be repeated in 5 min. -90% effective -use = atrial tachycardia |
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Atropine
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-anticholinergic
-IV push for antiarrhythmic use -Use = sinus bradycardia |
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angina definition
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imbalance between myocardial oxygen requirement versus delivery
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angina etiology
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-atherosclerosis
-vasospasm (prinzmetal) -hypertension -anemia -thyrotoxicosis (An overactive thyroid gland; pathologically excessive production of thyroid hormones or the condition resulting from excessive production of thyroid hormones) -CHF |
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anginal precipitating factors
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-overeating
-exercise -intense emotional stimuli -extremes of heat/cold -medications : sympathomimetics (ex. epinephrine), anorectic agents, antidepressants -smoking |
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Antianginal Pharmacology
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-decrease cardiac workload
-reverse vasospams -does not treat underlying pathology |
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Nitrates
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-coronary artery vasodilation
-peripheral artery dilation -peripheral venous dilation/decreases pre-loading is the DOMINANT mechanism |
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Nitrate use
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-acute angina
-prophylactic |
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Nitrate Caution
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-tolerance develops to constant blood levels (patch*)
-increases intraocular pressure -side effects : headache, syncope, cutaneous flushing |
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Nitrate Acute
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NTG sublingual onset = 3 min., duration = 10 min.
ISDN Dinitrate onset = 2-5 min., duration 1 hour |
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Nitrate Prophylactic
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NTG ointment onset = 1 hr., duration = 4-6 hrs
Isosorbide tab. onset = 1/2 hr., duration 6 hrs NTG patch onset = 24 hrs, duration 24 hrs |
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nitrate sublingual or spray
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-acute
-use lowest dose -administer as tablet or spray -1 dose every 5 min for 3 doses max. - tablets leave burning sensation -store in glass bottle with metal cap -store in cool non-humid place |
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nitrate ointment
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-dosed by the inch every 6 hours
-remove previous application -placed on skin surface with good blood supply -use gloves when applying (to avoid tolerance and hypotension) |
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nitrate patch
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-24 hrs onset (replace once a day)
-to prevent tolerance remove at bed time |
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nitrate injection USE
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-unstable angina
-post-cardiac surgery -administer utilizing non-phthalate injection tubing -decrease pre-load and after-load |
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beta blockers
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-pharmacology : decrease heart rate, decrease cardiac work load, decrease cardiac oxygen demand
-LOW DOSE administration -abrupt withdrawal exacerbates cardiac ischemia |
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Calcium channel blockers USE
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-classical angina = decrease cardiac work load = decrease demand of heart = "atherosclerosis/plaque angina"
-vasospasm angina = increases oxygen supply by dilating coronary arteries = increase delivery |
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Hypolipidemic: etiology , risk factors
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-etiology : atherosclerosis (most prescribed)
-risk factors : (any of these 2) = male > 45 yrs old, female > 55 yrs old , family history of CHD , hypertension , low HDL-C (<40 mg/dl) , smoking |
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hypolipidemic: treatment goals
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-No CHD, < 2 risk factors = < 160 LDL mg/dl
- No CHD, > 2 risk factors = < 130 LDL mg/dl -CHD = <100 LDL mg/dl |
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consequences of hyperlipidemia
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-increase artherosclerosis
-CHD -hypertension -stroke -peripheral vascular disease |
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Lipoproteins
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-VLDL = associated with triglycerides, decreases with lowering saturated fats in diet
-LDL =associated with cholesterol, does not decrease with lowering cholesterol -HDL = increases with exercise = protetant |
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Drug therapy for hyperlipidemia
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-increase elimination of lipoproteins (Colestipol, Cholestyramine )
-decrease production of lipoproteins (Fenofibrate, Gemfibrozil, HMG CoA Reductase (Statins), Nicotinic Acid (Vitamin B3) |
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Bile sequestering agents (increase elimination of lipoproteins)
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-"sandy drug":
- blocks enterohepatic recycling -binds bile acids in GI tract, causing elimination -interaction = binds fat soluble meds. and vitamins, therefore administer at different times |
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HMG-CoA reductase (decrease production of lipoproteins)
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-dyroxymethyl-glutaryl-CoA reductase = decrease production of cholesterol --> LDL
-reduces conversion of HMG - CoA to mevalonic acid (precursor to cholesterol) -muscle cramps/damage = from increase dose of simvastatin -dramatic reduction -monitor LFT's and retina = also damages liver |
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Gemfibrozil
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-decreases triglyceride production
-may increase HDL -may reverse plaque formation -drug interactioin with HMG-CoA reductase = rhabdomyolysis (complete destruction of muscles) |
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Fenofibrate
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-decrease triglyceride production
-may cause rhabdomyolysis when used together with a "statin" |
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Nicotinic Acid (Niacin/Vitamin B3)
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-requires high doses
-side effects include flushing and itching (aspirin lowers these effects) -contraindicated in diabetes - it raises blood sugar |
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Antiplatelets definition
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-inhibits platelets from adhering to fibrin lattice
-USE : TIA, cardiac prosthetic vavle, post MI |
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Anticoagulants definition
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-prevents coagulation cascade
-prevents progression of clot -allow internal plasmin to dissolve clot (takes 6 months to a year!) |
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Thrombolytic definition
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dissolves clot - potential toxicity ? = hemorrhage and pt. can bleed to death
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antithrombin III
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blocks prothrombin from converting to thrombin
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coagulation cascade
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-clotting factors activated
-prothrombin converted to thrombin (blocked by Antithrombin III) -fibrinogen converted to fibrin -fibrin forms a lattice -platelets bind to the lattice |
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Heparin
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-activates antithrombin III
-Injectible administration only = subQ = prevent post operative clotting, or bed ridden pts. clotting = prophilactic ) -heparin flush (line is only for 72 hrs or 3 days) -threaded catheter in vein w/ port outside skin -constant infusion following bolus dose --> tx of deep venous thrombosis, pulmonary embolism. -eventually may switch to warfarin |
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heparin monitoring
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-activated partial thromboplastin time (PTT) --> 1 1/2 to 2 1/2 times control (therapeutic rate)
-bleeding -NO IM injections - pt. can bleed |
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low molecular weight heparins
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-less bleeding reactions
-subQ admin. ONLY -can be utilized for ambulatory care therapy -ex: Enoxaparin (Lovenox) , Dalteparin (Fragmin) |
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Heparin Antidote
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-Protamine Sulfate
=binds excess heparin. =1mg binds 100 units of heparin =excess protamine has anticoagulant properties |
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warfarin
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-decrease production of Vitamn K dependent clotting factors in liver
-high protein binding - leads to many drug interactions -monitor prothrombin time -- INR 2 to 3 -effect of each dose is not seen for 3 days -maintain consistent vitamin K diet |
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warfarin USE
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-continuation therapy of heparin therapy for approx. 6 months
= deep venous thrombosis =pulmonary embolism -cardiac valve replacement, atrial fib., -life long therapy -contraindication - pregnancy |
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warfarin use antidote
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Phytonadione (Vitamin K)
=admin. via subQ route |
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Thrombolytic agents
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-Direct acting (Urokinase, Alteplace) = these drugs by themselves will dissolve clots
-Inderect acting (Straptokinase) = something in hte body will dissolve the clot - it activates plasminogen to plasmin, and plasmin dissolve clots |
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Direct Acting Thrombolytic
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-Urokinase = utilized to open clotted catheters (flush)
-Alteplase = USE : pulmonary embolism, MI, stroke caused by clot |
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Indirect acting thrombolytic
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-stimulates conversion of plasminogen to plasmin
-Streptokinase Use : pulmonary embolism |
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Anemia intro
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-decreased or poor maturation of red blood cells
-multiple etiologies : iron deficiency anemia, megaloblastic anemia, normochromic normocytic anemia |
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Iron deficiency anemia intro
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-hypochromic microcytic anemia - pale, small cell
-decrease RBC's and decreased hemoglobin --> low oxygen binding = increase heart workload = cause HIGH OUTPUT cardiac failure |
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iron deficiency anemia etiology
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-blood loss
-inadequate diet or absorption = low iron in diet / poor absorption |
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iron replacement : oral, IM, IV
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-oral therapy : replacement therapy may require 6 months or more to treat
-IM : Z-track admin. limited daily volume is 100 mg /admin. -IV : guidelines limit use to 100mg/day . required for quick iron replacement (pregnancy, ulcerative colitis) |
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Megaloblastic anemia (large red blood cell)
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-folic acid or cyanocobalamin (vitamin B12) deficiency
-replacement with the wrong vitamin can mask the deficiency -KNOW DEFICIENCY COMPARISON |
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deficiency comparison : cyanocobalamin vs. folic acid
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-cyanocobalamin = irreversible nerve damage , constipation
-folic acid = no nerve damage , diarrhea |
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B12 deficiency
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-cyanocobalamin
-found in red meat -poor diet (vegetarians) -lack of Intrinsic factor (produced in stomach) -onset of symptoms - 1 year -also known as " Pernicious Anemia " |
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B12 deficiency therapy
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-replacement therapy : IM or subQ
- those that lack intrinsic factor will receive monthly injections |
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Folic Acid deficiency
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-onset of symptoms : 2 months
-etiology : poor diet (ex. alcoholic), drug interactions (Phenytoin blocks absorption, BCPs cause folic acid to decrease, Methotrexate, Co-trimoxazole blocks converting to active form of the vitamin tetrahydrofolate) |
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folic acid deficiency therapy
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-oral folic acid supplementation
-Leucovorin (active tetrahydrofolate) is utilized to overcome deficiencies associated with methotrexate and co-trimoxazole |
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Normochromic Normocytic Anemia
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-associated with chronic disease states (renal disease, cancer, HIV)
-Erythropoietin =hormone produced in the kidney to stimulate RBC production in bone marrow =synthetic genetically engineered hormine is commercially available =helps avoid the need for transfusions |
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normochromic normocytic anemia : WBC deficiency
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-associated with cancer chemo
-prone to infections -example of agents that promote production of graulocytes =Filgrastim (Neupogen) |
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2 Digitalis Glycosides
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-Digitoxin (Crystodigin) 25 days to steady state
-Digoxin (Lanoxin) 5 days to steady state |
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1 Digoxin overdose antidote
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Digoxin immune fab (Digibind)
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4 Class 1A antiarrhythmic agents
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-quinidine (Sulfate vs. Glutamate)
-Procainamide (Pronestyl) -Procainamide Sustained Release (Procan SR, Pronestyl SR) -Disopyramide (Norpace) |
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2 Class 1 B Class 1 A antiarrhythmic agents
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-Lidocaine (Xylocaine)
-Mexelitine (Mexitil) |
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1 Class 1C antiarrhythmic agents
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Flecainide (Tambocor)
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which classes are used for ventricular arrhythmia ?
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class 1B, class 1C, and class III
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1 class II antiarrhythmic agent
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Propranolol -for tachycardia, not for fib
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1 class III antiarrhythmic agent
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Amiodarone (Cordarone) -vent. arrhythmia
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1class IV antiarrhythmic agent
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Verapamil (Isoptin, Calan) --> calcium channel blocker - atrial tachycardia
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other antiarrhythmic agents
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Atropine
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1 Antianginal (Nitates) Acute
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-Nitroglycerin Sublingual (Nitrostat)
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6 Antianginal Prophylactic
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-Ntiroglycerin Topical (Nitrol Ointment)
-Isosorbide Dinitrate Tab. (Isordil, Sorbitrate) -Isosorbide Mononitrate Tab (Monoket, Ismo) -Nitroglycerin Oral, Sustained Release caps (NitroBid) -Nitroglycerin Patch (Transderm Nitro) -Nitroglycerin Inj. (Tridil) |
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3 beta adrenergic blocking agents
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-Atenolol (tenormin)
-propranolol (inderal) -nadolol (corgard) |
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3 calcium channel blockers
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-Verapamil (Isoptin, Calan)
-Nifedipine (Procardia XL) -Diltiazem (Cardizem) |
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2 hypolipidemic agents : bile sequestering agents
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-cholestyramine (Questran)
-colestipol (Colestid) |
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2 hypolipidemic agents : fibric acid derivative
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-fenofibrate (tricor)
-gemfibrozil (lopid) |
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5 hypolipidemic agents : HMG CoA reductase inhibitor "statins"
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-Lovastatin (Mevacor)
-Pravastatin (Pravachol) -Simvastatin (Zocor) -muscle damage -Atorvastatin (Lipitor) -Fluvastatin (Lescol) -other : Nicotinic Acid (Nicobid) |
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4 Anticoagulants
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-Warfarin (Coumadin)
-Heparin -Enoxaparin (Levenox) - low molecular weight heparin -Dalteparin (Fragmin) - low molecular weight heparin |
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1 heparin antidote
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-protamine sulfate
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3 antiplatelet drugs
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-aspirin
-dipyridamole (Persantine) -clopidogrel (Plavix) |
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3 thrombolytic agents
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-Streptokinase (Sreptase)
-Urokinase (Abbokinase) -Alteplase (Activase) |
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6 Anemia Tx.
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-Ferrous Sulfate (Feosol)
-Iron Dextran (Imferon) -Cyanocobalamin (Vitamin B12) -Folic Acid -Leucovorin (Welcovorin) -Epoetin Alfa (Epogen) |
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Granulocyte Cology-stimulating factor
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-Filgrastim (Neupogen) for chemo.
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Antidiuretic Hormone (Posterior Pituitary)
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-aka Vasoppresin
-function in the kidneys -conserve water for dehydration -deficiency : diabetes insipidus = does not produce enough ADH -Synthetic replacement therapy =desmopressin, vasopressin |
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Oxytocin (posterior pituitary)
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-induces labor contraction, induces prolactin to start lactin
-drug therapy = labor induction, stops bleeding, post labor |
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Adrenocorticotropin Hormone/ACTH (Anterior pituitary)
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-stimulates adrenal gland to produce adrenocorticosteriod hormoes (Cortisol, Aldosterone)
-Stopped by negative feedback -Drug used to diagnose Addison's disease = adrenal gland not making enough ACTH or Anterior Pituitary not getting the signal |
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Thyroid stimulating hormone/TSH (Anterior Pituitary)
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--stimulates thyroid gland to produce thyroxine
-stopped by negative feedback -drugs used to diagnose hypothyroidism =problem could be pituitary or thyroid, same scenario as ACTH/Anterior Pituitary in Addison's |
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Other Anterior Pituitary Hormones :
-growth hormone (GH) -follicle stimulating hormone (FSH) -luteinizing hormone (LH) -prolactin |
-GH = drug available to treat dwarfism
-FSH -LH = drug available to treat endometriosis by stimulating progesterone production -Prolactin = no medication |
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Adrenocorticosteroids Introduction
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-produced in adrenal cortex
-regulated by ACTH -Synthesized from cholesterol |
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2 Adrenocorticosteroids subgroups
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-Mineralocorticoid = electrolyte homeostasis (ex. mimics aldosterone) so SODIUM RETENSION and POTASSIUM excretion = appearance of pts. blown up
-Glucocorticoid = carbohydrate, fat, and protein metabolism (ex. Cortisol) |
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Adrenocorticosteroids: Disease states
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- Cushing's disease = high output of adrenocorticosteroids, hypertension (Na retension) , fat redistribution --> "moon face" and "buffalo hump"
-Addison's disease (both mineralocorticoid and glucocorticoid) = 1) low production of adrenocorticosteroids decreases blood pressure 2) requires therapy with mineralocorticoids and glucocorticoids |
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Pharma of glucocorticoid ONLY
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*carbs metabolism
-protection under physical stress -protect glucose dependent brain function (gluconeogenesis, reduce peripheral glucose utilization, insensitivity to insulin) |
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Pharma of Glucocorticoid
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gluconeogenesis = producing new glucose from glycogen (stored carb) in the liver
-pt. in stress/trauma have i higher blood sugar = "reduce peripheral glucose utilization" to keep enough sugar in the heart and brain. |
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Lipid Metabolism Glucocorticoid
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-lipogenesis and lipolysis
-fat redistribution = buffalo hump, moon face |
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Electrolyte balance MINERALOCORTICOID
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-sodium and water retention
-increase blood pressure -potassium loss -addison's = opposite effect-hyperkalemia and circulatory collapse --> this is always the diagnosis |
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pharma CNS : Corticosteroids, Addison's disease
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-Corticosteroids --> depression
-Addison's --> apathy (not enough corticosteroids - pt. become psychotic/schizophrenic) |
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Pharma Adrenocorticosteroids 2
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-hematologic = decrease WBC (specifically lymphocytes) = for viruses, it increases viral infection because of low lymphocytes
-decrease immune response ex: transplants -antiinflammatory response ex: RA -retard growth in children (low bone growth) SHOULD NOT BE SYSTEMIC CORTICOSTEROIDS - inhalers are OK or topical creams |
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corticosteroid withdrawal
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-acute adrenal insufficiency --> (once its been "turned off"/on therapy, adrenal gland will be hard to "turn back on" --> fever, myalgia, arthralgia (joint pain), malaise
-avoid by gradual withdrawal of therapy |
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consequences of prolonged therapy of corticosteroids
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-adrenal suppression
-fluid and electrolyte imbalance (increase sodium retention) -peptic ulceration -depression -cataract -osteoporosis |
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Clinical use of corticosteroids
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-adrenal insufficiency (administer both mineralo and gluco-corticoids
-RA = decrease immune response -Allergic disorder (not anaphylactic) = decrease immune response, but is not for acute tx of anaphylactic shock -asthma = decrease immune response and inflammation in the alveoli -Ocular disease = antiinflammation = DO NOT USE corticosteroid in viral infection -skin disorder - antiinflammatory and decrease immune response -lymphocytic leukemia - decrease lymphocyte count |
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Inhibition of adrenocorticoid synthesis
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-aminoglutethimide = decreases production of sterol including sex hormones (in breast cancer, pituitary/testicular cancer)
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Adrenocorticolytic
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-Mitotate = adrenocorticolytic destroys adrenal gland for adrenal cancer
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Female sex hormones : Estrogen
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-always given with progesterone if use in BCPs.
-produced in ovaries, adrenal gland, and testes -regulated by FSH -Stimulates growth and development of sexual organs -stops growth - closes epiphyseal plate -menstrual cycle - growth of endometrium and blood supply |
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Estrogen metabolic effects
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-retention of Na and H2O
-Alter glucose tolerance -prevent negative calcium balance -carcinogenic (uterine** = must take protective drug, progesterone, DES babies with cervical cancer, and breast cancer risks) |
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Estrogen USE
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-oral/patch contraception with a progesterone
-menopausal sympt. (ex. osteoporosis) -increase bone density (no longer approved for this use) = decrease growth faster -atrophic vaginitis (post menopausal) -dysmenorrhea (very painful period - sometimes BCPs are used) -Cancer - prostate (some men take estrogen for their prostate/testicular cancer) |
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Estrogen side effects
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-nausea - tolerance develops
-mid cycle bleeding = esp. from some BCPs =too much estrogen -breast tenderness with BCPs -increased blood clotting (avoid in smokers, avoid BCP over age of 45 |
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what causes menstruation?
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drop of progesterone
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Specific Estrogen receptor modulator (goes to the receptor to prevent osteoporosis without risks of estrogen)
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-non estrogen that stimulates estrogen receptor
-indicated for increased bone density for those who cannot tolerate estrogens -ex. Raloxifene (Evista) |
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Progesterone
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-produced in the corpus luteum AFTER ovulation (ovulation has to take place first, which happens usually on the 14th day)
-regulated by LH -corpus luteum regresses after 14 days if ovum is not fertelized -prepares endometrium for implantaion -increases basal body temp 1 degree C. (if temp. increaes ovulation has occured not a good scenario to prevent pregnancy) |
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corpus luteum stops producing progesterone after day _____ except when there's pregnancy
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after day 28
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Progesterone USE
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-uterine bleed due to ovulatory failure
-dysmenorrhea -contraception with or W/O estrogens -protect uterus from estrogen induced cancer -endometrial cancer |
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Oral/Patch contraceptives (usually lasts for 3 weeks)
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-99% effective (1% = drug interaction, or missing a dose)
-stops ovulation -cervical gland produces mucous so sperm cannot pass -progesterone alone administered daily (3 months no menstruation) -progesterone WITH an estrogen administered for 21 days -21/28 day pills |
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general info on contraceptives
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-not effective during the first month of therapy
-if one dose is missed then double the next dose, if two doses is missed then double for two days -discontinue for three months prior to pregnancy |
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side effects of oral contraceptives
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-nausea/vomiting
-headache -weight gain (tolerance develops to all above) -acne --> lower incidence with tri-phasic birth control pills -melasma --> brown permanent pigment spots |
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long term risks of oral contraceptives
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-decreased fertility
-thromboembolism -cancer-more studies show it protects against breast cancer |
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Male sex hormones : androgens intro.
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-produced in testes, adrenals, and ovaries
-regulated by LH -promotes growth -regulates reproductive organs -spermatogenesis -closes epiphyseal plate =stops growing after puberty! |
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look at menstruation graph
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day 14 =ovulation
day 14 - 28 decrease in progesterone/estrogen progesterone keep producing if there's pregnancy |
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androgens - anabolic properties
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-increase muscle mass --> anabolic steroids (even though it's name says steroids it's not a steroid) IT'S A TESTOSTERONE ! -what athletes abuse
-increase nitrogen balance --> nitrogen = backbone of amino acids = makes protein = makes muscle = increase muscle mass -increase production of RBC's = increase Oxygen (androgens) = decrease in heart workload |
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-therapeutic use for androgens-anabolic
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-hypogonadism (ex. erectile dysfunction in older men)
-promote anabolism in chronic debilitating diseases -tx. of Anemia -tx. of estrogen induced cancers |
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-side effects of androgens-anabolic
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-female masculazation - baldness, atrophy of sex organs
-decrease growth in children = in young age because it closes epiphyseal plate. you don't want to close it that early -sodium and water retention = making a person big |
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Other concerns with androgens - anabolic -
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-hepatic cancer = it's rare for liver cancer to actually start in the liver, usually they metastasize and go to the liver = non treatable
-Contraindications : cancers stimulated by androgens (ex. prostate) |
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all testos/terones are what schedule?
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schedule III because of athlete's abuse potential
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3 posterior pituitary agents
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-desmopressin (DDAVP) inhl. = nasal form of ADH
-vasopressin (Pitressin) -oxytocin (Syntocin) labor inducer and used after |
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4 anterior pituitary agents
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-corticotropin (Acthar, ACTH). used of Addison's
-cosyntropin (Cortrosyn). used for Addison's -Thyrotropin (Thropar) -Somatrem (Protropin) - growth hormone |
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Adrenocorticoids: 1 Mineralocorticoid and 8 Glucocorticoid
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Mineralocorticoid
1. Fludrocortisone (Florinef) -Glucocorticoid 1. Beclomethasone (QVar, Beconase) --> asthma or allergic Rhinitis for inflammation 2. Dexamethasone (Decadron) --> asthma, RA, oncology -leukemia 3. Fluticasone (Flonase) -nasal inhlr. for allergic rhinitis 4. Flunisolide (Aerobid) -inhlr. for asthma 5. Hydrocortisone (Cortef) -also topical = skin inflammation (ex. rashes) = cant be put on the face 6. Methylprednisolone (Medrol) - asthma 7. Prednisone for asthma 8. Triamcinolone (Aristocort, Azmacort) - inhlr. was pulled from the market b/c of CFC' --. inj. can be long acting and injected to the joints. |
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Inhibition of Adrenocorticoid synthesis 1 drug and 1 Adrenocorticolytic
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-Aminoglutethimide (Cytadren)
-Mitotane (Lysodren) |
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Female sex hormones : 6 Estrogens
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-1 Conjugated Estrogen (Premarin) - typically used for post menopausal women
-2. Estrodiol Valerate (Delestrogen) - post menopausal -3. Ethinyl Estradiol (Estinyl) - BCPs -4. Mestranol - for BCPs -5. Estropipate (Ogen) - post menopausal - could be take with progesterone -6. Dienestrol (AVC) topical is used for Atrophic vaginitis |
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5 progesterone
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1. megestrol (megace) - also used to stimulate appetite
2. norethindrone (norlutin) -also used in ovulatory failure 3. medroxyprogesterone (provera) - used with estrogen in post menopausal - inj is long acting for BC. 4. ethynodiol (ovulen) - BCP 5. Norgesterol (ovral) -BCP |
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3 Androgenic male sex hormones
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-still have some anabolic properties
1. fluoxymesterone (Halotestin) 2. methyltestosterone (Oreston) 3. testosterone cypionate (Depo- testosterone) |
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2 anabolic male sex hormones
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1. nandrolone decanoate (deca-durabolin)
2. stanozolol (winstrol) NOT A BETA BLOCKER |
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thyroid introduction
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-regulated by TSH
-uptake of Iodide from diet -production of Thyroxine (T4), a non active hormone -conversion to tri-iodothyronin (T3), the active hormone --> conversion in thyroid gland and periphery |
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consequences of low iodide diet
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-decreased thyroxine (t4) production so also decrease in t3
-decrease blood levels -increased release of TSH from pituitary -HYPERtrophy of thyroid gland - goiter -increased iodide trapping -euthyroid = thyroxine and t3 tests have normalized from trapping but goiter appearance is still present |
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HYPOthyroidism
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-adult (myxedema) = symptoms are : drowsiness, slowed speech, decreased cardiac output, skeletal muscle weakness.
-children (cretenism) : 1. congenital malformation of thyroid gland (child not producing enough hormone) 2. if untreated, permanent mental retardation and failure to grow - this does not have anything to do with IODINE diet . it has to do with HORMONES |
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HYPERthyroidism
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-increase in metabolism = demand on heart increase also = heart risks
degrees of severity -most severe form : Thyrotoxicosis (thyroid storm) = risks in the heart -symptoms include: opthalmalopathy (eye bulge out), high output cardiac failure. |
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physiologic role of thyroid hormone
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-regulate growth and development
-regulate basal metabolic rate -regulate cardiac output - heart = to keep up with metabolic demands -LIPOLYTIC activity on cholesterol - cholesterol increases in blood |
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use of thyroid replacement therapy
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- myxedema
-retenism |
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Thyroid replacement meds.
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1. Levothyroxine = synthetic thyroxine (t4) --> minerals inhibit absorption = should be taken before eating and in the morning)
2. Liothyronine -synthetic t3 (active hormone) = dosed in very low micrograms because it can immediately increase metabolism and can put strain in the heart - this is for severe Hypothyroid 3. Thyroid tab. - dessicated thyroid gland from cattle - mixed t3 and t4 - lot to lot variation |
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tx. of HYPERthyroidism
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-inhibitors of t3 and t4
synthesis = both in the thyroid gland and in the peripheral 1. propylthiouracil (PTU) and Methimazole 2. contraindication: pregnancy, breast feeding 3. 70 to 80 % complete remission and discontinue -potential of curing the pts. 4. 30 % remain on therapy for life or have radioactive therapy |
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tx. of HYPERthyroidism
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-high concentration of Iodide =
1. negative feedback - shuts off thyroid gland for 72 hrs. 2. pre-operative use to prepare pt. for surgery 3. example: super saturated potassium iodide (SSKI) --also used s an expectorant |
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tx. of HYPERthyroidism
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-radioactive Iodide (sodium iodide I-131)
1. onset of action; days to weeks. 2. remission ; 2-3 months 3. 25 to 33 % of pts. cured after first dose 4. advantage; avoid surgery 5. disadvantage ; determine exact dose needed 6. contraindication ; pregnancy, children |
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diabetes mellitus : glucose control intro
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-increase blood glucose --> glucose intake, glucagon ( in the pancrease to liver), corticosteroids
-decreases blood glucose --> insulin (produced in the pancrease), oral hypoglycemic agents |
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Insulin DEPENDENT DM
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-aka . juvenile onset and Type 1 DM
-most severe form of DM --> Complications include; diabetic ketoacidosis= acidic blood pH (normal is 7.4) -decrease synthesis and release of insulin from pancreas |
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NON insulin dependent DM
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-aka as Adult onset or Type 2
-usually overweight -functional beta cells in pancreas (capable of producing insulin but sluggish or peripheral cells have become insensitive to the insulin) -no ketoacidosis associated |
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consequences of DM (if pt is not following therapy/not being compliant)
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-cardiac disease
-renal disease -blindness -peripheral vascular disease -gangrene -polyneuropathy = (can't feel) --> gangrene! = pt. needs physical inspection b/c they're not gonna feel the problem |
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insulins
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-sources = pork, bio-genetic (human). Reactions; Lipodystrophy = "fat sites"
-varieties = U-100 (per mL) versus U-500, Ultra short acting, short acting, intermediate, long acting |
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Regular insulin
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-onset ; less than 1 hour.
-uses : 1. adjunct with longer acting -draw up in syringe first (draw regular/clear first, then cloudy) 2. sliding scale = used around meal time. 3. IV to treat ketoacidosis 4. IV for parenteral nutrition 5. only regular insulin can be administered IV. |
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Intermediate insulins
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-onset; 2 hrs.
-duration; 24 hours. like a sustained release injection |
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long acting insulins
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-onset; 3 hours
-duration ; 30 hours 0 use is usually every 24 hrs. |
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insulin dose variability
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-pt. variability
-diet compliance -complications; (ex. Cortisol = increase blood sugar), infection, physical stress (ex. surgery) |
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type 2 DM therapy
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-diet and weight loss
-oral hypoglycemic agents (Sulfonylureas - 1st and 2nd gen) also....Biguanides, Thiazolidinediones, Misc. |
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Sulfonylureas
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-increases beta cell production of insulin
-first gen. --> f one fails at max. dose, all will fail. switch if side effects. -second gen --> if one fails at max dose, others may be effective |
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Sulfonylurea concerns
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-side effects (ex. tolbutamide = tinnitus, chlorpropamide = cholestatic jaundice)
-hypoglycemia -cardiovascular abnormalities |
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Biguanides
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-could be step 1 or step 2 drug (sulfonylurea)
-increases peripheral cell sensitivity to insulin -avoid use in renal impairment or prior to administration of radiologic dyes....otherwise may lead to lactic acidosis (Metformin) * |
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Thiazolidindiones
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-increases sensitivity of peripheral cells and hepatic cells to insulin (NEVER a step one drug)
-deaths have been associated with Troglitazone - liver failure -associated with causing cardiac abnormalities -not first line therapy -ex. Pioglitazone (Actos), Rosiglitazone (Avandia) |
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Misc.
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-Acarbose (Precose) : --> decreases oral absorption or disaccharides (work in the intestines) , minimal effects on blood sugar, 3rd/4th line agent
-caution ; CANNOT reverse HYPOglycemia with oral dissacharides |
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tx. of HYPOglycemic reactions
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-glucose
-glucagon -Diazoxide (Proglycem) = keeps blood sugar up. .... tx. for NON diabetes with chronic hypoglycemia (low BS) -Drug caution = beta blockers = blocks symptoms of hypoglycemia |
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3 hypothyroidism tx.
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-Levothyroxine (synthroid)
-Liothyronin (cytomel) -Thyroid |
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4 tx. of HYPERthyroidism
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-Propylthiouracil (Propacil)
-Methimazole (Tapazole) -Potassium Iodide (SSKI) -Sodium Iodide I-131 |
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1 Ultra short acting insulin
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-lispro (humalog)
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2 rapid acting insulin
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-insulin (regular)
-prompt insulin zinc suspension (semilente) |
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2 intermediate acting insulin
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-Isophane insulin suspension (NPH)
-insulin zinc suspension (Lente) |
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2 long acting insulin
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-extended insulin zinc suspension (ultralente)
-glargine (Lantus) |
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3 Oral hypoglycemic agents ; 1st gen. Sulfonylureas
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-chlorpropamide (diabenese)
-Tolazamide (Tolinase) -Tolbutamide (Orinase) |
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3 Oral hypoglycemic agents; 2nd gen. Sulfonylureas
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-Glipizide (Glucotrol)
-Glyburide (DiaBeta, Micronase) -Glimepiride (Amaryl) |
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1 Oral hypoglycemic agent; Biguanide
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-Metformin (Glucophage)
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2 Oral hypoglycemic agents; Thiazolidinedione
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-Rosiglitazone (Avandia) = risks = cardio disease
-Pioglitazone (Actos) |
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1 Misc. Oral hypoglycemic agent
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-Acarbose (Precose)
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2 Reverse Hypoglycemia
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- Glucagon
-Diazoxide (Proglycem) |
