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PharmTest#4
Ca++blockers/antidysryhtmics/chemo drugs/digitalis/hormone drugs
| Question | Answer |
|---|---|
| Calcium Channel Blockers-Phenylalkylamines | verapamil |
| Calcium Channel Blockers - Dihydropyramidines | Nifedipine, Nicardipine, Nimodipine, Isradipine, felodipine, amlodipine, clevidipine |
| Calcium Channel Blockers - Benzothiazipines | Diltiazem |
| Calcium Channel Blockers Mechanism of action | Calcium ion influx through L-type channels results in phase 2 of cardiac action potential. Affects SA and Av node firing and coronary and vascular smooth muscle. Can affect L, N, ant T type channels. Alpha subtype 1 is blocked which prevents calcium. |
| Where are voltage gated calcium ion channels located in the body | cell membranes of skeletal, vascular smooth muscle, cardiac muscle, mesenteric muscle, glandular cells, and neurons. |
| Do CCBs exert negative inotropic effects? | Yes, especially dilt and verapamil |
| Verapamil | phenylalkylamine, synthetic of papaverine, when open occludes channel, more selective to AV node (marked), will moderately dilate both peripheral and coronary arteries. Active metabolite norverapamil (antidysrythmic also). 80-160mg PO;75-150mck/ |
| Verapamil side effects | major depressant of AV node, negative chronotropic effect on SA, Negative inotropic effect on cardiac muscle (more exaggerated with preexisting LV issues), may precipitate dysrythmias in WPW, use caution with patients on betablockers |
| Ventricular pre-excitations syndromes | accessary pathways that bypass normal conduction pathways (i.e. remnants of fetal AV muscular connections left by incomplete annulus fibrosus |
| WPW | both pre-excitation and tachydysrythmia must exist for diagnosis, characterized by an earlier than normal defelction of QRS (delta wave). AVNRT most common tachy in WPW. |
| orthrodromic | narrow QRS, goes through normal pathway then returns to atria via accessary |
| antidromic | goes from atria to ventricles via accessary pathway then returns to atria via normal pathway |
| WPW treatment | orthodromic-vagal maneuvers, adenosine, verapamil, b-blockers; antidromic-blcok accessary pathway, drugs that slow AV node conduction not effective in antidromic AVNRT |
| WPW treatment antidromic AVRNT | dont give drugs that slow AV conduction (may increase ventricular HR). if stable then procainamide may actually stop conduction via the accessary pathway; if uncontrolled then cardiovert. |
| Afib in WPW | can produce extreme ventricular response rates and/or VF if anterograde conductions through accessary. dont give verapamil or dig because can lead to acceleration through accessary. |
| Clinical uses of Verapamil | SVTs, vasospastic angina pectoris, essential HTN, symptomatic hypertrophic cardiomyopathy, maternal and getal tachydysrythmias and premature labor. |
| Dihydropyramidines | prevent Ca++ entry into vascular smooth muscle by extracellular allosteric modulation of L channels, selective for arteriolar beds, Nimodipine favors cerebral, everything else prefer peripheral arterioles, reflex SNS/baroreceptor activity |
| Which two dihydropyramidines are particularly helpful in management of patients with residual HTN despite b-blocker therapy? | nifedipine and nicardipine |
| NIfedipine | greater coronary and peripheral arterial vasodialator properties than verapamil, minimal SA and AV node depression, negative inotropic, chronotropic, and dromotrop[ic effects (offset by SNS) |
| NIfedipine dose | 10-30mg oral, 5-15 mcg.kg IV |
| Nicardipine | possesses the greatest vasodilating effects of all CCBs. Most prominent in coronaries, no affect to AV and SA nodes (good for using with b-blocker therapy), useful as tocolytic |
| Nimodipine | lipid soluble analogue of nigedipine, crosses BBB, affects cerebrals, prevention of vasospasm in SAH patients, also valuable in cerebral protection following global ischemic events (i.e. MI) |
| Amlodipine | oral only, most valuable for combo therapy with beta blocker for myocardial ischemia, produces minimal effects on myocardial contratility |
| Clevidipine | ultra short acting CCB metabolized by nonspecific esterase in blood and tissues (hydrolysis). 0.3-3mcg/kg/min max of 16, careful in psudocholinesterase deficiency, reduces gastric emptying |
| Benzothiazepines - Diltiazem | acts on L-type channel by unknown way, may also act on Na-K pump thhus decreasing sodium available to exchange with extracelular Ca++, may inhibit calcium-calmodulin binding, selective to AV node, first for SVTs, good for essential HTN and chest pain |
| Diltiazem dose | 60-90mg PO; 0.25-0.35mg/kg over 2 minute bolus then 10mg/hr IV |
| CCBs and drug interactions | Dig and beta blockers: patients with preexisting cadiac conduction abnormalities experience greater AV heart block with concurrent administration of CCBs. B-adrenergic agonists can counter CCB effects, CCB may decrease plasma clearance of digoxin |
| Volatile anesthetics to CCBs | may exaggerate myocardial depression (halothane and enflurane > iso, sevo, or des) and peripheral vasodilation. hypotension may be profound, AV nodal effects with dilt and verapamil warrant caution |
| CCbs and local anesthetics | verapamil and dilt exhibit inhibitory properties upon Na ions. This increases the risk of local anesthetic toxicity with regional anesthesia combined with CCBs. |
| CCBs and NMBAs | CCBs potentiate NMBA, use nerve stimulation to guide therapy. |
| CCBs and K | CCBs slow intracellular movement of K, administration of whole blood or expgenous K (for hypokalemia) mat result in exaggerated elevations of K in patients on CCBs. |
| Dantrolene and CCBs | TheoreticallyCCBs would be helpful in treatment of MH yet not proven in animal studies. Verapamil has been associated with hyperkalemia when administered concurrently with dantrolene, |
| Risks of CCBs | greater with dihydropyrimidines, risks include: cardiovascular complications, increased perioperative bleeding, GI bleeding, speculated development of CA, |
| Diltiazem increases sedative effect of what drug | midazolam |
| Classifications and mechanisms of cardiac dysrythmias | according to HR and site of abnormality (SR/tachy, V-tach, A-fib), ectopic dysrythmias (impulse formation(no SR, other area acting as pacemaker), impulse trasmission (reentr(accessary)), triggering afterdepolarizations |
| causes of dysrythmias | arterial hypoxemia, electrolyte or acid/base balance(alkylosis>acidosis), myocardial ischemia, increased SNS lowers threshold for VF, bradycardia, certain drugs (hypokalemia and hypomagnesemia predispose pts to dysrythmias and be suspected with diuretics |
| phase 0 cardiac action potential | depolarization; big rapid Na+ influx |
| phase 1 cardiac action potential | Cl- influx |
| Phase 2 cardiac action potential | Ca++ influx; K+ efflux |
| Phase 3 Cardiac action potential | K+ efflux |
| Phase 4 cardiac action potential | RMP -90mv up the threshold of -70mv, Na+ influx |
| Class 1A antidysrythmics | Quinidine, procainamide, disopyramide, moricizine; lengthen AP duration and effective refractory period also lengthen repolarization owing the K+ channel blockade (similar to Class 3s) |
| Class 1B antidysrythmcs | Lidocaine, tocainide, mexiletine,phenytoin; less powerful Na blocking drugs, differ from 1A by shortening Ap duration and refractory period in normal cardiac ventricular muscle |
| Class 1C antidysrythmics | Flecainide, propafenone; potent Na+ channel blockers and markedly decrease phase 0 and speed of conduction of cardiac muscle, shortens AP duration in purkinje fibers , no lengthening of AP or refractory period |
| Class 2 antidysrythmics | betablockers; esmolol, propanolol, metoprolol, acebutolol; decrease rate of phase 4 depolarization, duration of AP in ventricular myocardium is not altered, decreased O2 requirments, effective in decreasing incidence of dysrythmia related morbid&mortal |
| Class 3 antidysrythmics | block K+ channels, amiodarone, sotalol, ibutilide, dofetilide, bretylium; prolong repolarization by prolonging duration of Ap and effective refractory period, decrease proportion of cardiac cycle in which cells are excitable to triggering events. |
| Class 4 antidysrythmics | CCBs, inhibit slow inward calcium channels, useful for tx of VT. |
| prodysrythmics effects | typically manifest from proloning QTc, hypokalemia, hypomagnesemia, pool LV function, concurrent use of other QTc prolonging drugs, types include, torsades, incessant VT, and wide complex ventricular dysrythmias |
| Normal QTc | <0.47 sec, should be less than 1/2 the preceding R-R interval, sevo and iso have hx of proloning QTc also antiemetics and antibiotics; consider preoperatice b-blocker therapy in at risk pts, have defibrillator ready, QTc also increasd by up SNS |
| Medical tx for prolonged QTc | beta blocker therapy, discontinue prodysrythmic, cardiac pacing, ICD therapy |
| good, bad, and ugly of antidysrythmics | suppression of ventricular ectopy with a cardiac antidysrythmic does not prevent future life-threatening dysrythmias and may increase mortality; Class 1C drug treated pts have higher incidence of sudden cardiac arrest; betablockers decrease mortality |
| good, bad, and ugly of antidysrythmics continued | class 1A and 1C not good for CHF pts d/t prodysrythmias and negative inotropic; amio good for CHF. |
| Magnesium prophylaxis | likely beneficial, produces systemic and coronary vasodilation, inhibits platelet aggregation, decrease myocardial reperfusion injury, first-line therapy for torsades |
| Lidocaine prophylaxis | likely not so beneficial, not recommended for MIs for ventricular ectopy prophylaxis, may actually increas mortality d/t badydysrythmias andasystole; yet lowers chance of VF and mortality |
| VT tx | lidocaine or amiodarone |
| SVT tx | adenosine or verapamil or dilt |
| what drugs help decrease mortality after MI | beta blockers |
| lidocaine | delays phase 4 by decreasing Na+ influx, used primarily for ventricular activity (very good with reentry (PVCs and VT); therapeutic range from 1-5mcg/ml; toxic>5mcg/ml |
| procainamide | broad spectrum antidysrythmic; reduces phase 0, prolongs AP duration and effective refractory period partly d/t K= channel blocking properties (class 3 property), preferred over amio for mono VT, max load dose 17mg/kg; active metab NAPA; |
| procainamide side effects | discontinue if QRS begins to widen more than 50% or hypotension develops; lengthening of QTc can precipitate torsades, chronic administration can lead to systemic lupus erythmatous-like syndrome. |
| Amiodarone | primarily K+ blocker(class3), also Na+ blocker(class 1), beta blocker(class 2), and CCB(class 4);prolongs effective refractory period in ALL cardiac tissue; good for SVT, Afib, VT, and WPW; decreases mortality /p MI |
| Amiodarone (furthermore) | exhibits antiadrenergic effects through noncompetitive blockade of alpha and beta receptors; minor inotropic effect; potent vasodilator; 1/2 life 29 days;active metab=desethylamiodarone has 60day 1/2 life |
| Amiodarone side effects | photosen, rash, cyan discolor, periph neuropathy, tremors, sleep issues, HAs, PROXIMAL SKELETAL WEAKNESS, corneal microdeposits, prolonged QTc, ATROPINE RESISTANT BRADY, down SNS response to catechola, pulm toxicity, PNEUMONITITS give lowest level of O2 |
| Amiodarone side effects continued | containes iodine which may affect hyper to hypothyroidism, inhibits p-450 enzymes thus increased concentrations of other drugs in the body, depress vit K dependant clotting factors, |
| Sotalol | Class 3 K+ blocker, also non-selective beta blocker, prolongs AP in the atria, ventricles, and accessary paths; good for VT or VF of AFIB following bypass, prolongs QTc, typically reserved for life-threatening ventricular dysrythmias. |
| Chemotherapy (a must) | know as much as possible about CA and tx (type of chemo, number o treatments, date of last, total amount received, may need to go to other places other than pt for info gathering) |
| Chemotherapy drug classes | alkylating agents, antimetabolites (necleic acid synthesis inhibitors), antitumor antibiotics (DNA topoisomerase inhibitors), Vinca alkaloids, and miscellaneous (drug doesn't fall under a typical class). |
| Alkylating agents | affect DNA, cuase cross-link and abnormal nucleic acid base pairing, intracellular imbalance and cell death(DNA structure altered and replication and transcription inhibited) |
| Antimetabolites | nucleic acid synthesis inhibitors, subclasses include folate analogs, pyramidine analogs, and purine analogs. Mess up replication by substitution of metabolites needed for cell reproduction (occurs in S phase of cell cycle when DNA is synthesized) |
| Antitumor Antibiotics | DNA topoisomerase inhibitors, inhibits DNA and RNA synthesis, anthracycline antibiotics (doxorubicin & daunorubicin), actinomycin D (dantinomyocin) for Wilms tumor in children, Bleomycin (pulm toxicity) |
| Vinca Alkaloids | interact with microtubular proteins needed for cell division, active ingredients from periwinkle; vincristine; Taxanes also interact at microtubles (paclitaxel from pacific yew tree) |
| Hormones (signal transduction modulators) | estrogens and androgens (side effect hypercalcemia), Antiestrogens (tamoxifen binds to tumor estrogen receptors, increased risk of DVT, also exhibit meopausal symptoms, also lowers cholesterol levels and increases bone density) |
| Antiandrogens | tx for hormone dependant prostate CA, can develop gynecomastia, hot flashes, facial hair loss, skeletal muscle weakness, osteoporosis. Flutamide (methemoglobinemia) |
| Toxic effects of chemotherapy drugs | effects related to specific drug, cumulative dose, and dosing schedule. N&V, mucositis and diarrhea, myelosuppression and alopecia, secondary malignancies with DNA alkylating drugs and topoisomerase drugs. |
| Chemo and N/V | one of top 3 side effects, acute onset within 12-24 hrs, delayed /p 24 hrs may last 6-7 days, risk factors same as for PONV, cisplatin in high doses causes vomiting in 24hrs in 90% of pts. |
| CNS effects of Chemo | seizures (may occur with busulfan up to 24hrs /p last dose); vincristine toxicity includes numbness, tingling of extremities, loss of deep tendon reflexes, and weakness of dital limb muscles |
| CNS effects of chemo continued | neuropathies (cisplatin, taxanes, oxaliplatin); vinca alkaloids (vocal cord paralysis, loss of extraocular muscle function); CNS toxicities usually disappear /p drug discintinued or dose reduced |
| Chemo drug classes that produce CNS issues | alkylating agents, vinca alkaloids, natural and miscellaneous agents (taxane, docetexal, nab-paclitaxel, paciltaxel) |
| Chemo cardiotoxicity drug class | cytostatic anthecycline antibiotics are main problematic drug class (subset of antibiotic chemo drugs); -rubicins |
| 3 classes of cardiotoxicity | acute,chronic,late; acute st-t wave or prolonged QTc, arrythmias; chronic occur within 1 yr, include dilation, tachy, pulm congestion, chf and down LV function;late occurs yrs after therapy stopped (as child) |
| risk factors that increase incidence of cardiotoxicity from chemo drugs | radiation therapy to medistinum or left chest wall, previous tx with cyclophosphamide, higher incicdence at younger ages, preexisting cardiac disease, obesity, LV EF <50% |
| pulmonary toxic effects of chemo drugs | direct lung damage and indirect inflammatory processes, interstitial pneumonitis, acute pulmonary edema, bronchospasm, pleural effusion, dyspnea, cough, tachypnea, bibasilar rales, fever, pneumonitits induces fibroblast activity leading to pulm fibrosis. |
| What chemo agent is most associated toxicity leading to pulmonary fibrosis? | bleomyocin; nearly 25% tx with this drug develop postop respiratory insufficiency |
| Risk factors for pulm toxicity | > 70 yrs old, total drug dose, O2 therapy, preexisting pulmonary disease, smoking hx, thoracic radiation, genetic prediposition for respiratory insufficiency |
| What are the 2 primary concerns for anesthesia in reguards to pulmonary toxic effects of chemo drugs? | intraoperative O2 and fluid balance; minimal fluid for hemodynamic stability and kidney function; <30%FiO2, may need mixed venous serials; bleomyocin tx sensitizes lung tissue to O2 |
| Nephrotoxicity of chemo drugs | impairs GFR, proximal and distal tubular function, CO 20% to kidneys (lots chemo agent to kidneys); methotrexate and cisplatin; hemolytic uremic syndrome, prerenal perfusion deficits, non-oliguric renal failure |
| Nephrotoxicity of cisplatin | toxic effects occur 3-5 days /p start of tx, increased BUN and creatinine, proteinuria, hyerureicemia, magnesium wasting, ATN then ARF; electrolyte disturbances, ototoxic, N/V, allergic reactions=facial edema, bronchocontrict, tachycardia, hypotension |
| Hepatoxicity chemo drugs | methotrexate(hepatic cirrhosis and coag disorders), flutamide(anitandrogen rarely causes hepatotoxicity /c jaundice and dark urine), GAs can worsen hepatocellular damage, careful /c aminosteroids NDNMBAs, avoid halothane |
| myelosuppresion of chemo agents | neutropenia 8-10 days, anemia, coag problems |
| CYP-450 enzymes induce or inhibit with chemo agents | induced; rapid metabolism of anesthetic drugs |
| Which chemo drugs reduce psuedocholinesterase activity | thiopenta and cyclophosphamide (prolongs drugs such as sux, ester locals, mivacurium); plasma cholinesterase levels may not return to normal for weeks /p being suppressed. |
| Cardiac glycosides and nonglycoside/noncatecholamine inotrops | digoxin, digitoxin, quabain; occur naturally in plants; inotropics; nonglycoside and noncatecholamine agents include phosphodiesterase inhibitors and Ca++, glucagon, and myofiliment calcium sensitizers |
| Clinical uses of cardiac glycosides | managment of SVT dysrythmias associated with RVR (paroxysmal atrial tachy, a-fib, a-flutter); useful in CHF but not used as much d/t ace inhibitor therapy. |
| Cardiac glycoside mechanism of action | selectively and reversibly inhibit Na-K ATP ion transport resulting in increased NA inside cell which decreases CA++ efflux by the Na+ pump= increased Ca++ to interact with contractile proteins, thus increased inotropy |
| Indirect effects of cardiac glycosides | relfex alterations in ANS: up parasympathetic d/t sensitization of SA node and activation of vagal nuclei, negative chrontropy and dromotropy; net effect is slow HR; decrease RMP d/t loss of NA-K pump; up phase 4; down phase 0;decreased phase 2 |
| Cardivascular effects of cardiac glycosides | increased stroke volume, decreased heart size, decreased LVEDP; decreased SVR thus increased forward flow; inotropic induced diuresis.Direct:down LV preload, afterload, LV wall tension, and O2 consumption. Indirect:slow HR(suppress Atrial dysrythmias) |
| ECG effects of cardiac glycosides | prolonged PR, Shortened QTc, ST depression d/t decreased slope of phase 3 depolarization, diminished amplitude or Twave inversion, ST and Twave changes may indicate myocardial ischemia |
| dysrythmogenesis | advanced age >60, CAD, cardiomyopathies, valvular disease, CHF, HTN, chronic pulm disease, hypomag, hypokalemia or hyper, hypoxemia, hypercarbia and acidosis, myocardial ischemia, pulm embolus, elevated catecholamine states, low depth of anesthesia |
| Digoxin | slows AV conduction, combo /c betablocker for SVT lessens doses of both drugs; decreased risk of death from heart failure but increase risk of sudden death(dysrythmogeneic)(consider other drugs before cardiac glycosides(i.e.ACE); careful with WPW |
| Dig metabolism | 1/2 life 31-33hrs therapeutic range 0.5-2ng/ml; primarily renal excretion; primary inactive resivoir is skeletal muscles (FOPs exhibit higher plasma levels d/t less muscle mass) |
| Digitoxin | more lipid solube than digoxin, thus greter absorption /p oral dosing; 1/2 life 5-7 days; therapeutic range 10-35ng/ml; hepatic clearance |
| Digitalis and drug interactions | sympathomimetics with beta adgrenergic agonist effects as well as pancuronium may increase the likelihood of cardiac dysrythmias. Calcium combined /c cardiac glycosides may precipitate dysrythmias; hypokalemia bad |
| Digitalis toxicity | hypokalemia, hyperventilation decreases K 0.5 for q 10mmHg decrease in PaCO2, hypercalcemia, hypomagnesemia, arterial hypoxemia (increased SNS) |
| Signs of digitalis toxicity | anorexia, N/V, transitory amblyopia and scotomata, trigeminal neuralgia-like pain, Atril and ventricular cardiac dysrythmias leading to possible heart block(atrial tach /c block is most common). VF is most common cause of death from dig tox. |
| Digitalis toxicity tx | correct prediposing electrolyte issue, administer drugs (phenyutoin, lidocaine, atropine), insert temp pacing wire if complete heart block, administer antibiotics(fab fragments) will lead to glycosides binding with antibodies and not cell membranes |
| Phophodiesterase inhibitors PDE III mechanism of action | PDE II inhibition results in increased cAMP and CGMP in myocardium and vascular smooth muscle, thus increased Ca++ for contractile activation, also facilitation of diastolic relaxation by enhancing calcium removal from myoplasm. |
| PDE III physiological effects | enhacement of catecholamine responses, positive inotropy, vascular smooth muscle relaxation, airway smooth muscle relaxation, tidbit(can be used with cardiac glycosides because no increase to dig tox) |
| Amrinone | controversy as to wether primarily inotropic or vasodilatory, posses neither antidysrythmic nor prodysrythmics properties, kidney excretion, no tachyphylaxis, can exacerbate hypotension and core temp loss, chronic theraoy leads to thrombocytopenia |
| Milrinone | useful for L ventricular dysfunction /p bypass, chronic dosing may increas morbid and mortal in pts /c severve CHF, kidney excretion |
| PDE III imidazole derivatives | enoximone & piroximone |
| PDE III bypyridine derivatives | amrinone & milrinone |
| Theophylline (recommended only when beta-2 adrenergic agonists and corticosteroids have proven ineffective for bronchospasm in asthma) | noncompetitive inhibitors of all PDE (I-V), also competitive antagonism of adenosine receptors, metabol by liver, crosses placenta, relaxes gastroesophageal sphincter, toxic levels + volatile anesthestics=dysrythmias |
| pentozifylline (trental) | PDE III nonselective inhibitor; methylxanthine derivative that increases flexibility of erythrocytes and decreases blood viscosity, not an anticoag, can cause hypotension, angina, and cardiac dysrythmias |
| Calcium | intense positive inotropic effect for 10-20minutes; HR and SVR are decreased, enhanced effect in hypocalcemia, dysrythmogenic if given to pt on dig (especially if hypokalemic) |
| Glucagon | polypeptide hormone produced by alpha cells of pancrease, anhances formation of cAMP, increases myocardial contractility and HR in presense of beta blockade(functions independantly of adrenergic receptors, enhances automacity of SA and AV, carefulAfibupHR |
| Side effects of glucagon | N/V, hyperglycemia (sometimes pardoxical hypoglycemia d/t not enough glycogen to offsett increased insulin release), hypokalemia, HTN(especially with undiag pheo), glucagon stimulates release of catecholamines |
| Anterior pituitary hormones | growth hormone (prolactin), Gonadotropins (LSH and FSH; can be given as drug), Adrenocorticotropic hormone(can be given as drug), thyroid stimulating hormone, |
| Growth Hormone | stimulates release of somatosedins from liver( a family of insulin-like growth factors), IGF with GH and TSH stimulate linear growth in children |
| Growth hormone in adults | stimulates protein synthesis in muscle and release of fatty acids from adipose; inhibits reuptake of glucose by muscle and stimulate uptake of amino acids; AA used in protein formation ; muscle uses FAs as energy |
| Where is GH produced in the anterior lobe | somatotropic cells; stimulate most cells but specifically bone and skeletal muscle; promote protein sunthesis and encourages use of FAs; most effects are indirect through somatomedins |
| GH stimulates liver, skeletal muscle, bone, and cartilage to do what? | produce IGF and direct action to promote lipolysis and inhibit glucose uptake |
| IGF I (somatomedin C) | produced in liver in response to GH; stimulates chondrocytes (linear growth), stims myocytes & amino acid uptake and protein synth for muscle growth; structure and receptors of insulin; inhibits GH release; plasma protein bound |
| metabolic effects of GH | proteins=anabolism, increase amino acid uptake, inc protein synth, decreased oxidation of proteins; fat metab=increased FAs breakdown; Carbs=anti insulin activity to let glucose into cell, up glucose synth, paradoxical increase insulin release, up BS. |
| Deficiency of GH in children and adults | in children=leads to dwarfism; in adults=indicative of panhypopituitarism or tumor formation |
| Dwarfism | panhypopytuitarism in chilhood results in proper growth proportions yet rate decreased. only 1/3 secrete everything but GH-this group has sexual function yet others do not. |
| African pygmy and levi-lorain dwarf | rate of GH normal or high yet lacks hereditary ability to form somatomedin C(IGF I). |
| Adult hypopituitarism caused by | brain tumors, thrombosis of pituitary blood supply(often occurs when new mother develops circulatory shock /p childbirth), general effects (hypothyroidism, down glucocorticoid production, loss of sexual function), lethargic /c weight gain. |
| gigantism | excess GH as child, hyperglycemia, general deficiency of pituitary hormones results in death in early adulthood, Robert Wadlow |
| GH supplementation | usually IM at weekly intervals, biosynthetic version from recombinant DNA technology |
| octreotide (somatostatin analogue) | trade name is Sandostatin, mimics endogenous hormone somatostatin(growth hormone-inhibiting hormone (GHIH) that is synthesized in hypothalamus, tx of acromegaly, also tx for diarrhea and flushing in carcinoid syndrome |
| octreotide side effects | long term use (>1 month)=cholesterol gallstones; hyperglycemia, decreased glucose tolerance; bolus for carcinoid crisis may result in bradycardia and 2 or 3 heart block |
| ACTH | stimulates adrenal cortex to secrete glucorticoid hormones (cortisol); exogenous use for dx of primary adrenal insufficieny (addisons disease) |
| T3 and T4 | regulate metabolism, affect growth, affect function of most body systems, essential component is iodine; thyroid also produces calcitonin for calcium homeostasis; thyroid hormones eat up Vit K dependent clotting factors |
| Levothyroxine | synthetic T4, replacement for hypothyroidism |
| Liothyronine | isomer of T3, much more potent than levothyroxine, much faster onset and shorter duration of action, not used for long term therapy |
| Calcitonin | produced by parafollicular cells of thyroid, reduces calcium levels and opposes effects of parathyroid hormone, unique effect on bone pain associated with joint disease |
| Inhibitors of thyroid hormones | antithyroid hormones, inhibitors of iodide transport, iodide, radioactive iodide |
| Propylthiouracil (PTU) and methimazole | interfere with the addition of iodide to tyrosine residues on the hormone precursor, thyroglobulin, thus preventing formation of thyroxine; also prevents conversion of T4 to T3; used to tx hyperthyroidism |
| PTU and methimazole side effects | urticarial or papular skin rash, granulocytopenia, arganulocytosis (can develop rapidly), earliest signs may be fever of pharyngitis |
| Thiocyanate and perchlorate | inhibitors of iodide transport mechanisms, interfere with uptake of iodide ions by thyroid, percholate can cause aplastic anemia (rare) |
| Iodide | tx for hyperthyroidism, inhibits endogenous release of thyroid hormone, used with propanolol to tx hyperthyroid prior to elective thyroidectomy, also decreases vascularity of thyroid |
| Radioactive iodine (131I) | quickly trapped by thyroid gland cells, emits beta rays that destroy thyroid gland, little or no damage to surrounding tissues; fairly effective /c one dose, may need 1-2 more, not recommended <30yrs old, used for FOPS and heart issues, no to prego |
| Radioactive iodine precautions | no sex for one month /p tx, women told not to get prego for 6 months, don't hold or hug children when radiactiviy is high, radiation detectors at airports may be triggered up to 12 weeks /p tx |
| synthetic corticosteroids | used for antiinflammatory effect, but suppress HPA axis, cause weight gain, and skeletal muscle wasting |
| mineralcorticoid receptors | distal renal tubules and hippocampus |
| glucocorticoid receptors | found virtually everywhere, selective to glucocortocoids only, inhaled drug often first line therapy for controlling symptoms of asthma, may cause dysphonia(hoarse) and candidiasis |
| corticosteroids | corticosteroids should be given 1-2 hrs before induction, these drugs also enhance duration and response to beta agonists, can help suppress allergic reactions |
| other benefits of glucocorticoids | help prevent PONV, reduce surgery inflammation, increses release of endorphins to up mood and appetite, inhibit phospholipase enzyme thus reducing transduction of pain signals, decrease cerebral edema |
| side effects of chronic steroid therapy | suppression of HPA axis, electrolye/metabolic changes, osteoporosis, peptic ulcer disease, skeletal muscle myopathy, CNS dysfunction, peripheral blood changes, inhibition of normal growth, increase risk to infection, decreased effectiveness of anticoags |
| HPA axis supplementation | supplement if actively tx with corticosteroids or > 1 month in past 6-12 months |
| signs of acute adrenal insufficiency | persistent hypotension, hyponatremia, hyperkalemia, abdominal pain, N/V, altered mental satus |
| metabolic changes of steroids | fat distrubution in back of neck(buffalo hump), supraclavicular area and moon face, loss of fat in extremities, also mobilze amino acids from tissues results in decreased muscle mass, osteoporosis, thinning of skin, and negative nitrogen balance |
| Chlorpropamide (an oral hypoglycemic) | sensitizes renal tubules to effects of AVp, beneficial in pts with DI, believed to do this by inhibiting prostaglandin production which will increase renal tubule sensitivity to AVp, no effect to pts with nephrogenic DI, will cause hypoglycemia |
| side effects of vasopressin | increased BP, increased PA pressure, coronary vasocontriction (angina), GI peristalsis, decreasd plt count |
| DDAVP | antidiuretic effect, decreased pressor effect, release of VWf promote plts adhesiveness, tissue type plasminogen activator, prostaglandins |
| oxytocin | induce labor, 10mU/ml via a constant infusion beginning at 1-2 mU per minute, infusion rate increased 1-2 mU/min q 15-30min until optimal response (contraction q 2-3 minutes). up to 40mU/min for uterine atony, decreased BP, relaxes vascular smooth muscle |
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