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***Pharmacotherpay of Diarrhea+conspitationI-Diahrea:-Antimotility Aents: -Tx the Cause: Ax/ antiparasites!-Diahrea is a Sx it can be managed non X-Loperamide 2.4mg4x/day-Coedine phosphate 15-330 mg2/d-Correct electrolyte disutbance-Blood idahrreea=C difficil-Antidiahrea X ↑ Risk of Hemolytic urenmic syndrome
Replacement Tx(mainly lipasE)-pancreatic enzyme used in exocrine ancreatic enzyme deficient!-Fat absprtion of protien, madigestion occuyr when pancreaseloss >90%Goal: prevent malabsrption+ pallaiation of Pain1II-Conspitaption (phamacotherpy)Osmatoic Laxatives:-Sorbital OP -Lactulose 10-20mg/d-Sodiumphophate 10hg/day-Polyethelem glycol 17g/dayIII-Emmolients:
-Omega-2 DA-Fibrates^^ Monitering for effectiness :-Lipid Panel ( total cholesterol/LDL/HDL/TGL)-↓ BO^^Moniter for Safety :-Rhabdomyolysis( myoglobiuria/serum CK)-Liver moniterong(AST/ALT/ bilirubin/albumin)^^Target cholesterol values in CVD ptstotal Cholesterol <5.2mmol/LLDL <1/8 mmol/LHDL >1/6mmol/LTGL <1.7 mmol/L
| Acute:-OP huydration-Underlying disease-pharmacologicalt | Chronic:Underlying disease TX-Loperamdie-Anticholenrgic agents1 |
Glycerin 2-3g suppositories 1/d
Mineral oil 15-45mL 1/d
Docusate Na 100mg 2-3x/d
Mineral oil 15-45mL 1/d
Docusate Na 100mg 2-3x/d
IV-Stimulants:
Bisacodyl 10mg suppositories up to x3/week
Tegaserod 6mg x2/d
Bisacodyl 10mg suppositories up to x3/week
Tegaserod 6mg x2/d
Diarrhea: |
***13-Lipid Levering X, Classification Monitering of effectiness!
-Statins : Lower cholesteron (atovastatin)-Nian: Decrease Hepatic Synthetis of cLDLD and LDL-Bile acid Regimen: dirupts bile avid reabsotpion and D(-) cholesterol level esp LDLD-Nicottie acid, omega 3 Datty acid-Effectiness of total cholesterol : LDL /HDL .TGL-Sagery: Rhabdomyolsys K/myoglovin /liver moniteirng Biirubin-Target:very High risk group (DM/CKD)50% LDLD reduction when target levelcannot be achieved HDL TGL <1.7mmolLTotal Cholesterol <5.2 mmol/L
^^Classification(3 most common)| Statins | Niacin | Bile-Acid Resins |
| -Low Cholesterol level by(-) Enzyme HMG-CoA reductase! | -↓ hepatic synthesis of CLDL and LDL | -disrupts bile acid reabospriton -Decrease Choldestol Level |
***14algorythm for HBP :
(GRAPH)
(GRAPH)
-Duiretics/ BB/ ACE(-)/ARB are suitable for initiation + mainaitain of therpy-Choice depends on pts previousexperience/ Cost/risk /profile-aget organ damage/ DVC/CKD-The goal of BP <140/90 is approtpate for general prevention-PTs with DM are high for risk of CV evens
Diuretics, betablockers, ACEI, ARBS are suitable for initiation and maintenance of therapy. The choice depends on patient’s:
-previous experience,
- cost
- risk factors
- target organ damage,
- CVD
- CKD
- DM
- LUNG DISORDE
-previous experience,
- cost
- risk factors
- target organ damage,
- CVD
- CKD
- DM
- LUNG DISORDE
***Eradication of H pylori:-Single Ax is ineffective!-Combinination of 2-3 Ax+ ACid suppresion therpay!-PPI or H2 BLocker+ (amoxicillin or carlithromycin)-10-14 Days not less- triple Theray (14 days) : PPI + clarithromycin 600mg + metronidazole 500mg/amoxillin 1g 2x/day-Quaterary therapy(14 days: PPI 2/dat+ nmetronidazole 500mg x3/day+ bismuth 535mg+tetracyline 500 mg x4/day!^^GERD:-change lfiestyle: Lose Kg/HEad of bed elevation/ small infrequent meals!-Phamacological = PPI, omerpazole,H2 lbockers(cimetidine,ranititne), antacid!!
***H pylori: |
***10-Ca Channel blockers:^^classification
-Calcuim CB act selectively on cardiovascular tissues.-Dihydropyridines are selective vasodilators (with increased affinity for vascular ca channels than cardiac ca channels)
Angina----->immediate short actign Calcium Channel can icnrease risk of Cardiac event and are contraindicated!
***11-Angiostensin Covnerting Enzyme inihibiot(ACE_ and Angio II Blockers:
^^ Adverse reactions:
1. Severe hypotension ( after initial dose )
| Non Dihydropyridinise | Dihydopyridine |
| -Verapmil=Carcian and vascular muscle effect-Dilitazem= effect on carddiac and smooth muscle | -Nifepine ( CVD disease)-Amlopine=Felodipine-Isradipine-Uicardipine |
-& non Dihydropyridines are equipotent for cardiac tissue.
^^Short+long acting Formulation:-most have short hald lives following an oral dose!-Tx is 3 x a day use-amiodropine has veyr long hald life!Examples:
- Amlodipine 5 mg tablets
- Diltiazem 60 mg tablets
- Adizem-SR (diltiazem SR) 90 mg capsules
- Adizem-XL 120 mg capsules
- Nifedipine 5 mg capsules
- Adlat Retard (nifedipine retard) 10 mg tablets
- Adipine SR (nifedipine SR) 10 mg capsules (SR=slow release)
- Amlodipine 5 mg tablets
- Diltiazem 60 mg tablets
- Adizem-SR (diltiazem SR) 90 mg capsules
- Adizem-XL 120 mg capsules
- Nifedipine 5 mg capsules
- Adlat Retard (nifedipine retard) 10 mg tablets
- Adipine SR (nifedipine SR) 10 mg capsules (SR=slow release)
| ^^ADR:iconstpitation in 10%-Dizziness-headache-ausea-peripheral edema-fatigue-Veramil ( not for Congestive HF)-Cardiac depression ( if Cablocker in high dose | ^^Clinical use:- Cardiac: HTN, SVTS,AP - Non cardiac: migraine, raynauds phenomenon, cluster headaches. - Nifedipine does not decrease atrioventricular conduction and therefore can be used more safely than verapamil or diltiazem in the presence of atrioventricular conduction abnormalities |
| ^^clssiciation:1 -Dihydropyridines(Nifedipine)2- Phemylalklyamines(Verapamil)3-Benzothiazepine( Ditixan)-CCB act selectively on CVD Tissue , Dihydropuridine are selective Vasodialators! &Non dihydrapyrimidine are Equipotent for Cardiac tissue !-Short+ong Acting Forumation ... Oral short acting 3-8 hours half life!-advere Reaction : excessive use----->Cardiac depression , cardiac arrest , BRdy ,AVB,HF |
| Similarities | Differences |
| -Same efficacy in Tx HBP-Delay progression of CM neuropathy-Tx of HF | -Angiosten Rector Antogniist less cough -ACE(-) , inhibit degradation of substance like bradykinin/substance/enkephalins-angio Recpetor antagonist is more selectiveBlock of ACE receptor |
^^ Adverse reactions:
1. Severe hypotension ( after initial dose )
in patients who are hypovolemic due to diuretics, salt restriction
2. Acute renal failure ( particular in patients with renal artery stenosis)
3. Hyperkalemia ( more common in patients with renal insufficiency or diabetes )
4. Dry cough ( less common in angiotensin receptor blocker)
5. Fetal anuria, hypotension , renal failure (contraindicated in 2nd and 3rd trimester)
6. Alter sense of taste , allergic skin rash
^^ Practical recommendations for use and monitoring:
-Start with very low dose as possible.
- Be careful if the pts is on diuretics because of risk for hypotension.
- Wait to effect 3-5d, than double the dose.
- Each change in the dose check for K levels
^^practical recommendation:-start with lowest dose possibl-Be careful if pts is on Duiretc( hypotension risk)-Wait for effect -3-5 Day-Each change in dose, check K levels!!
^^ADR:Severe hypotension (after 1st dose hypokalemia)^^REcommended:-Start with low dose if pts takes Doiuretics---> may cause Hypotension-In 3-5 Days double the Dose-Montering Check for K level , Kindey function test
2. Acute renal failure ( particular in patients with renal artery stenosis)
3. Hyperkalemia ( more common in patients with renal insufficiency or diabetes )
4. Dry cough ( less common in angiotensin receptor blocker)
5. Fetal anuria, hypotension , renal failure (contraindicated in 2nd and 3rd trimester)
6. Alter sense of taste , allergic skin rash
^^ Practical recommendations for use and monitoring:
-Start with very low dose as possible.
- Be careful if the pts is on diuretics because of risk for hypotension.
- Wait to effect 3-5d, than double the dose.
- Each change in the dose check for K levels
^^practical recommendation:-start with lowest dose possibl-Be careful if pts is on Duiretc( hypotension risk)-Wait for effect -3-5 Day-Each change in dose, check K levels!!
| Similarities: | Diff |
| -Same Efficacy in Tx of HBP-delay progression of Diabetic nephropathy -Both used for H Tc | ACE(-) Cause--->cough ,angioedemaARB case----> Dizziness |
***35-Antiepilectic X:Def: Chronic brain disoder of various etiologies!, Characterized by reccuent epileptic seizured!^^Anti epiliectic X classification:-According ot MOA , Or by the classification of seizure to determine Tx!-given as monotherapy you give combination in case :1-Failure monotherapy!2-2 Different types of epilepsy!-MOA: aim to prevent spread of Abnormal Electricl disacharge!1-Block Na/Ca channel2-↑ Inihibitory GABAergic impulses3-interference with excitatory glutate transmission
^^Efficacy:First Drug-50%Second X-20%Combination 10%Rsstance toTx -20%^^Duration of antiepiletpic Tx:-After Dx 5 YHears from last attack-After stopping the natiepilectic X reccuirence 15-40% of pts!
^^ADR:-(+)Risk of Suicidal behavior-Nausea+Vommiting-Drowsiness-sedation-Ataxia-rash-Hyponatremia-Weight gain /weight loss-Teratogenicty-osteoporosis!^^Interactions:Toxicity may (+) without icnreasing antiepletic effect!!interaction by hepatic enzyme induction or inhibition-Are compelx and may (+) toxicity without (+) in epileptic effect!1-Carbamazepine---> ¯plasma concentration of lamotrigine2-Ethosuximide---->↑plasma concentration of phenytoin.3-Lamotrigine------>↑ plasma concentration of an active metabolite of carbamazepine.^^Driving antiepletic use:-patients cna drive if they been epilepsy free for 1 years-patiwent with drowziness should not dive-1st siezure must not drive for 6 M^^Pregnancy women:-Antieplectic X increase Teratogeneicity-Valoprate associte with congenital malformation,so should be avoided unless no safer alternative-No (+) teratogencity with Phenytoin,primidone,phenoarobtal,lamotrigine!-Foalte supplementsation to decrease Neural tube defects!-Routin Vitamine K at bith minize risk of Neonatal hemorrhage! -Breast feeding is ok normal doses exception barbiturates!^^Rational pharmacotherpy Epilepsy(C) Rest(PART 2):1-Obbject of Tx is to prevent occurance of sieure by mainint an effecitve dose of X2-when choosing X , The sieuzre type, cocominent medication3-Dosagfe Frequnecy determined by plasma Half life [C]4-when used in ussualt dose can be given 2x day!5-Lamotgine,phenoribtal have long Half life cna be given at bedtime6-Young children metabolize nati Epilesy X faster!may need more frequent dose7-change of X should be caution , by slow withdrawl8-concurrent anti epilectic increase risk of ADR^^STatus epilecpticus Therapy:1-immeidate measure of epilectic status:-Position thatpts to avoid injudr-supprot respitation-mainting BP-Hypoglycemaia correction2-PArantral thiamine should be be considered3-Tx urgently with IC lorazepan , repeat once after 10 min4-Clonazepan can be used as alt
-The decision to initiate symptomatic medical therapy in
patients with PD is determined by the degree to which
the patient is functionally impaired.
– The effect of disease on the dominant hand
– The degree to which the disease interferes with work,
activities of daily living, or social and leisure function
– The presence of significant bradykinesia or gait
disturbance
– Patient values
^^Levodopa:-Most effective Drug for Sx Tx on PD-X of first choice SX particulary Bradykinesia!-should be introduced when Akinetic Sx become disabiling fo pts -Trmor and rigidity can also repond to Levodopa but Postural instability is less likely!-It is Reasonable to initiate therapy with levodopa in older pts-Must be combined with peripheral decarboxylase(-) =Carbidopa!-Carbidopa blocks concersation in systemic circulation+ liver-After metabolism process BBB to preven: N+V, Orthostatic Hypotension-DO NOT stop suddenly!
^^levodopa ADR:
^^Dopamine Agonist:-Monotherap in combination with other anti parkinsong Xfor more advanced Disease-ineffective in pts who show no response to levodopa-Delay the need to initiate levodopa Tx-use in assiacited increased impulse control disorder-Dopamine agonist associte with fewe motor fluctuation then levodopa-It is reasonable to start therpy with dopamin agonist in younger(<65 Years)^^Dopamin agonist ADR:-N+V-Sleepiness, orthostatic hypotension-Confusion, hallucination-Can be avoided by intitiating Tx with very small doses and tirating to Tx level!-MAO B (-) (elegiline and rasagiline) may be useful in pts with early PD but only have modest SX Benefit as Monoptherapy-Anticholnergic X are most useful as monotherpay in pts <70 pots with disturbing tremor with no signiicant bradykinesia!-used in pts with more advanced disease who have persisten tremor despite Tx with leveopaor dopamina agonsit!
***Migraine:
-More Effective when Gives Early in the course of heafache-LArge Dose> Small doses repetitive-Oral Agent poor effectivenss due to low absorption^^General Recommendation:-Use migraine specific agents (eg, triptans) in patients with
more severe migraine and in those whose headaches
respond poorly to NSAIDs or combination analgesics
- Select a nonoral route of administration for patients
whose migraines present early with significant nausea or
vomiting
- Consider a selfadministered rescue medication for
patients with severe migraines that do not respond well to
other treatments
- Guard against medication overuse headache by educating
patients about risk and using prophylactic medications in
patients with frequent headaches
^^:Mild to moderate:Simple analgesics (NSAIDs, acetaminophen) or
combination analgesics are 1st choice agents.
üeffective,
üless expensive,
üless likely to cause adverse effects
• When associated with severe nausea or
vomiting, an oral or rectal antiemetic drug can
be used in conjunction.
^^Moderat to Severe:-Oral migraine specific agents are firstline,
including oral triptans and the combination of
sumatriptan-naproxen.
• If vomiting or severe nausea is present -
nonoral migraine specific medications
including sumatriptan s/c, nasal sumatriptan
and zolmitriptan, nonoral antiemetic agents,
and dihydroergotamine i/v.
^^Variable attacks
-Two or more options for self management of
acute migraine are required:
– oral medications for mild to moderate attacks
– nonoral medications (eg, subcutaneous or nasal
triptans) for more severe attacks or those
associated with vomiting or severe nausea.
^^Erogotamina:-structually similar to amines/Serotonon/NE/Dopamine-Interact wih x Recptros-Casuye vasconstirction-Wede range of effect-problems :avoid for coronay disease
^^5-hydrozytryptamine (5-HT)
^^SMBG is helpful for DM :1-To Detect High or Low gluvose level!+ adjust A1C2-Folllowing pts for comfirmation of acute hypo or hyperglycemia!3-Technology facilitates educations!4-SMBG helps motivate people ^^DM II Tx for Oral Hypoglycemia and incretins!I-Insulin Secreagogue:Sulgonylurea:
^^NPH based concvnetional analgue:-T FM to provide insulin in psychologioc manner-Insulin replacement by giving preprandial insulin!-Long acting( glargine or determir)-Intermediate acting (NPH)regiments:1-Split/Mixed(NPH with rapid acting or regular) before breakdfast)2-Split /ixed variant(NPH with rapidacting or eular before breakdgast)3-Multiple daily injection(long acting once a day in morning or evening)(Rapid actng insulin Before Meals or snacks)4-continous subcutanous insulin infusion:(rapid acting insulin infused continously 24 hours a day , via insuline pump)***Antithyroid X:
V-Adenorecpeotre Blocking agents:^^Efficacy :-Beta blockers---->(metorolol/propranlo/atenolol) are effective theraputic adjuvents in Thyrodixcodsis manafement!-beta blockers can cause clinical improvement of hyperthyroid Sx!-At big dose ropanolol reduce T3 levels!^^Rational Tx of Thyrotoxicosis:Goal is to Decrease synthesis or release of additional hormone , This may be accomlished by:1-remvoing art of gland!2-(-) synthesis of hormone bby blocking release of horone from follicle!***cliniccal aspects of hypothyrodism:
***Inefficacy of Ax:-When ts has inadwequate (WBC/CRP/ fever) clinical or microbiological response ot Ax , --->Systemic invetigation shouldbe done^^Causes may include:1-errors in suspectiblity test( repeat the test)2-X doses and absorption( test serum emasurments)3-Abnormalities in immune system!4-Developmen t of infection and superinfection!(follow up culture)------>after Test AAx therapy muyst be adjusted!***Pharmacotherpay of Diarrhea+conspitationI-Diahrea:-Antimotility Aents: -Tx the Cause: Ax/ antiparasites!-Diahrea is a Sx it can be managed non X-Loperamide 2.4mg4x/day-Coedine phosphate 15-330 mg2/d-Correct electrolyte disutbance-Blood idahrreea=C difficil-Antidiahrea X ↑ Risk of Hemolytic urenmic syndrome
Replacement Tx(mainly lipasE)-pancreatic enzyme used in exocrine ancreatic enzyme deficient!-Fat absprtion of protien, madigestion occuyr when pancreaseloss >90%Goal: prevent malabsrption+ pallaiation of Pain1II-Conspitaption (phamacotherpy)Osmatoic Laxatives:-Sorbital OP -Lactulose 10-20mg/d-Sodiumphophate 10hg/day-Polyethelem glycol 17g/dayIII-Emmolients:
***Clinical Pharmacology of antimicrobial X :speicific aspects of rational use:1. Precise efficacy
- Empyric treatment against most probable m/o or its group
- Excluded resistance
- Colonization not treated
- Dosage – according to SmPC (Summary of Product
Characteristics or EBM based recommendations)
– Goal
• Sufficient exposure at the site of infection:
– Precise sensitivity of m/o in vitro,
– Minimal concentraitons at the site of infection (in-vivo)
– Managed risk of biofilms
• This can be acheaved following SmPC 4.2 or vis modeling
PK/PD with kinetic softwares
2-Selected Ax should have Narrowest sepctrum Grou:-Empeirici Tactic-Escalaltory or desclaalotry-According to BAG-Consisdered PK/PD features( penetration), IV Dose, Inteaction)-X Conctration in urine and prenchyma is not same3-In the Group ,We choose Safest+Cheaprst X:-In addition totoxicity ,Estimate biological activity as weelll-2nd (R) Quiniline>IV-III>II Gen Cephalosorin-Local Guidlines-if doses aare not effective, Consider Dosages4-More Conveneint Ax( More exp) Chosen when pluses( Lower risk for non comopliance) is more important then price.5-Early Evaluation -First evalauation in case of acute infective Process timely therpay (measure Temp every 2 hours)6-Main duration of course is in SmPC and RUD recommendations!
| PArtial:-Carbamazepin-Oxcarbazepin-Gabapentin-Tiagabin-Pregabalin-Vigabalin | Partial/generalized:valrpoic Acid-Topiramate-Levetricetam-Nitrazepam-Diazepam |
| ^^Na Channel Blocker:-Carbamazepine(Alwas check for hyponitramia)-Phenytoin(↑ Liver enzyme!)-Oxcarbazepine-->(Similar to carbazepine , they (+) hepatic enzyme) | ^^Ca Channel Blocker: |
| ^^GABA receptor Agonist:-Clobazam-Clonadzepam-Phenobarbital-Primidone! | ^^GAMA reuptake (-):Tiagabine^^GABA Transaminase (-):-Vigabatrin |
| ^^AED with potential GABA MOA:-Gebapentin-Pregablin-Valporate | ^^Glutamate blockers:-Felbamate-Topiramate^^K Channel opener:-retigabine! |
^^Principle of antiepletics:
1-Selection depends on seizure type2-Monotherapy is possible3- dose (+) 1-3W4-moniter serum concentration5-Duration of therpay 5 years after last seizure6-Grandual withdrawa of Tx7-Minoter DDI^^Interaction:-Oxacrarpazapine+ valporic/phenotyn= (+)Fever-carapamazapine+ Phenotyn/Phenovalposic= -Valporic Acids+ Phenoarbital=(+) effect of phenoarbital-Gabaphentin -LAmatrgine+Carpamabine= ^^Comparison:-AED are made to modify the process to favor(-) of Excitation and stop seziure activity!-Main action include : Na channel blocker/ CCB Gaba(+) Glutmate blocker/Carbonic anhydrase(-) / Hormones /X^^indication| 1-Partial Seizures:-Simple Partial seizure-Complex partieal seizure | 2-Generalized Seizures:-Generalized Tonix-clonic Seizures-Status epilepticus |
***36-Parkinson:
^^Classification:1-Levodopa and Carbidopa2-Monoamine oxidase inihibots (MAO)-Selegilline-Rasagilline3-Catechol-O-Methyltrasnfferase(-)(COMT):-Tolcapone-Entacapone!4-Dopamine-receptor Agoniost:-Bromocriptine-Apocmoprhine5-Amantadine6-Antimuscarinic agent:-Enztropine-Triexypheniyl-Procyclidine-biperiden^^General Principle:-The decision to initiate symptomatic medical therapy in
patients with PD is determined by the degree to which
the patient is functionally impaired.
– The effect of disease on the dominant hand
– The degree to which the disease interferes with work,
activities of daily living, or social and leisure function
– The presence of significant bradykinesia or gait
disturbance
– Patient values
^^Levodopa:-Most effective Drug for Sx Tx on PD-X of first choice SX particulary Bradykinesia!-should be introduced when Akinetic Sx become disabiling fo pts -Trmor and rigidity can also repond to Levodopa but Postural instability is less likely!-It is Reasonable to initiate therapy with levodopa in older pts-Must be combined with peripheral decarboxylase(-) =Carbidopa!-Carbidopa blocks concersation in systemic circulation+ liver-After metabolism process BBB to preven: N+V, Orthostatic Hypotension-DO NOT stop suddenly!
| ^^Levodopa pros: -Most effective drug -Well tolerated (with carbidopa) -Rapid effect -Cheap -Potential neuroprotective effects | Levodopa Cons: -Motor fluctuations -On-off phenomenon -Potential neurotoxic effects -Special diet - avoid taking levodopa with high protein meals. |
| Most common Mostserious: Nausea Somnolence Dizziness Headache | Most Serious: Confusion Hallucinations Delusions Agitation Psychosis Orthostatic hypotension |
| Dopamine agonist Pro | Dopamin agonsit con |
| -Effective -Less motor fluctuations -Potential neuroprotective effects -No special diet | -Dose titration is essential - Side effects – gastrointestinal, mental disorders - Sudden sleep attacks - Monotherapy not always possible - Swollen ankles |
^^Anticholinergic Agents adverse effects
-Xerostomia
-Glaucoma
-Blurred vision
-Xerostomia
-Glaucoma
-Blurred vision
-Tachycardia
-Constipation
-Urinary retention
-Anticholinergic psychosis
^^Choice:-X Tx does Not Prevent diease progression -Pts with parkisnon disease need to be refered to a specilist to confirm the Dx!-Reviews every 6-12 M-Tx is not started until Sx cause significant Disruption of faily activities!-Levodopa, non ergot Dopamine receptor agonist-Tx with 2+3 anti parkisnon x maybe necessary!-Eldely antiparkisonian X , low doses andto increase the dose gradually!^^Interaction:1-Vitamine pyriodoxine (B6)----> ↑peirpheral breakfown of Levoopsa+ ↓2-Concomitat of Levodopa+ MAO (-) ----->Hypersenstivie Crises caused by (+) Catecholamine production!3-In GLaucoma, The X can cause ↑ intraocular pressure4-Cardiac pts---->can develop aRR5-Antipsychotric x are counter CI in parkinon syndeome!^^Levodopa and carbidopa:-Levodopa---->Because parkisonim results in insuffience dopamine in brain-Dopamine does nto cross BBB but levodopa(precursor) Does^^ADR:-Constipation
-Urinary retention
-Anticholinergic psychosis
| Peripheral Effects | CNS Effects |
| -Anerixa-N+V-Hypotension-Adrenergic action on iris | -Visual And auditory hallucination-Dyskinesisas |
| ^^COMT ADR:-Diahrea-postural hpoyesion-hepatic necorsis-dyskiensis-sleep disorder | ^^Dopamine-receptor agonists (ADR): - Sedation - Hallucinations - Confusion - Anorexia, Nausea, vomiting - Postural Hypotension - Dyskinesia | ^^Antimuscarinic agents: ADR -mood changes -dry mouth -visual problems -pupillary dilation -confusion -hallucination -sinus tachycardia -urinary retention -constipation |
| Non Specific | Specific |
| -Aspirin-PAracetamol ,NSAID-Antiemetic-Acetaminophen | I-Triptans-Sumatriptan-Naratriptan-RizatriptanII-Ergot alkaloid:-Dihydroergotamine-ergotamine |
more severe migraine and in those whose headaches
respond poorly to NSAIDs or combination analgesics
- Select a nonoral route of administration for patients
whose migraines present early with significant nausea or
vomiting
- Consider a selfadministered rescue medication for
patients with severe migraines that do not respond well to
other treatments
- Guard against medication overuse headache by educating
patients about risk and using prophylactic medications in
patients with frequent headaches
^^:Mild to moderate:Simple analgesics (NSAIDs, acetaminophen) or
combination analgesics are 1st choice agents.
üeffective,
üless expensive,
üless likely to cause adverse effects
• When associated with severe nausea or
vomiting, an oral or rectal antiemetic drug can
be used in conjunction.
^^Moderat to Severe:-Oral migraine specific agents are firstline,
including oral triptans and the combination of
sumatriptan-naproxen.
• If vomiting or severe nausea is present -
nonoral migraine specific medications
including sumatriptan s/c, nasal sumatriptan
and zolmitriptan, nonoral antiemetic agents,
and dihydroergotamine i/v.
^^Variable attacks
-Two or more options for self management of
acute migraine are required:
– oral medications for mild to moderate attacks
– nonoral medications (eg, subcutaneous or nasal
triptans) for more severe attacks or those
associated with vomiting or severe nausea.
^^Erogotamina:-structually similar to amines/Serotonon/NE/Dopamine-Interact wih x Recptros-Casuye vasconstirction-Wede range of effect-problems :avoid for coronay disease
| Ergotamine1-2mgOP | ADR:-N+V-Cold extrmeieis-ISchemia-vasospams | CI:Coronary artery disease-hepatic /renal problems-HBP-Sepsis |
| Dihiroergotamine12-Mg/IM | -N+V-Cold extrmeieis-ISchemia-vasospams |
-A group of drugs known as triptans bind the
serotonin 5-HT1B receptors in the walls of blood
vessels
-Leads to constriction of arteries, particularly at
cerebral and dura arteries
-Triptans also inhibit inflammation of vessels of the
dura matter that are stimulated by the trigeminal
ganglion
-Do this by acting as a 5-HT1D receptor agonist
Smatriptan (1-2 hours)(Half life 1-2)(MAO-A)Sumatriptam (12 min)(1-2 hours)(MAO-A)Sumatriptan(12 min)(1-2H )(MAO-A)NAratriptan(2-3 Hours)(6hours)^^Prophylaxis:Considered in PTs ->2-3 Attack/monthserotonin 5-HT1B receptors in the walls of blood
vessels
-Leads to constriction of arteries, particularly at
cerebral and dura arteries
-Triptans also inhibit inflammation of vessels of the
dura matter that are stimulated by the trigeminal
ganglion
-Do this by acting as a 5-HT1D receptor agonist
-↑Frequency attacks
-suffer despite suitable Tx-Cant take Suitable Tx for Migraine!x are taken daily although mechnism unkown:1-Propranolol2-Ca C blocker3-Gabapentin4-Valproic acid4-Antiderpessent(amitripytaline/Nortriptylline)Doses shoudl be as low as possible!^^ADR:Triptan--->Dizziness/muscle weakenss/neck pain!!^^interaction:1-Triptan + ergot derivation--->(+) Coronary artery vasocontriciton----->(+) DRisk of HBP2- Propanolol ---> icnrease Triptan [C]^^interactions:1Triptans:Combination with ergot derivatives (_) risk of coronary artery vasoconstriction and hypertensive effect-Concentration of triptan may be increased by concomitant administration of propranolol
2. Ergo-derivatives: all this drugs increase the risk of ergotism (vasoconstriction, convulsions, GI effects)
Macrolides
Macrolides
Tetracycline
Imidazoles
Triazoles
Antivirals
Imidazoles
Triazoles
Antivirals
^^Preventive migraine treatment
indications
• Frequent or long lasting migraine headaches
• Migraine attacks that cause significant disability
or diminished quality of life despite appropriate
acute treatment
• Contraindication to acute therapies
• Failure of acute therapies
• Serious adverse effects of acute therapies
• Risk of medication overuse headache
• Menstrual migraine
indications
• Frequent or long lasting migraine headaches
• Migraine attacks that cause significant disability
or diminished quality of life despite appropriate
acute treatment
• Contraindication to acute therapies
• Failure of acute therapies
• Serious adverse effects of acute therapies
• Risk of medication overuse headache
• Menstrual migraine
^^Drug classes used for the prevention of
migraine:
-Beta blockers (metoprolol, propranolol,
timolol)
-Antidepressants (amitriptyline, venlafaxine)
-Anticonvulsants (valproate, topiramate)
***DM Goals:- Blood sugar Control :-the goal to keep Blood sugar level at normal / Near normal levels!-Control of blood ushar can prevent long -term effect-level:1-Fasting=<7mmol/L2-Postprandial Glucose <9mmol/L-Home Blood sugar testing can be done!=Normal Fasting blood sugar is <100mg/dl (5.6mmol/L)althought some people have difference gols:migraine:
-Beta blockers (metoprolol, propranolol,
timolol)
-Antidepressants (amitriptyline, venlafaxine)
-Anticonvulsants (valproate, topiramate)
| A1C | CVD |
| -Goal of A1C ofor most people is to keep AC <7% | Most common Complication of DM II can lead to Heart atack , chest pain ,stroke ,death(-) risk by :1-Quitting smokng2-BP <130/80-Lipids Choldrestol <5mmol/LTAG>1.7..HDL >1.6LSL <1.8 |
1. 1 st generation:older generation
-Tolbutamide 0.5-2g/d duration of action 6-12h
- Chlorpropamide 0.1-0.5g/d, duration of action <60h
2. 2 nd generation most commonly used because less A/E and drug interaction then 1 st generations
- glyburide <20mg/d duration of action 10-24h
- glipizide <40mg/d duration of action 10-24h
Main MOA is (+) Insulin Secretion from Pancreatic B cells by closure ofPotassium channels---->depolarization---->(+) insulin Realise (-) Glucagon!I-Meglitinide:--->Modulate B-cell insuline release by regulating K channel!II-D-Phenylanine Derivative:----->newest x /(+) release by regulating K eflux.2-Biguandies(500 mg-2.55g/d)-MOA ?? , but it slows Glucose absorption! From GIT!+↑ (+) of glycolysis!-Metofrmine half life 1.5-3 H!3-Thiaolidinediones:-Plotgitazone (15-45 mg/d) -Rosiglitazone (2-8 mg/d)-Tolbutamide 0.5-2g/d duration of action 6-12h
- Chlorpropamide 0.1-0.5g/d, duration of action <60h
2. 2 nd generation most commonly used because less A/E and drug interaction then 1 st generations
- glyburide <20mg/d duration of action 10-24h
- glipizide <40mg/d duration of action 10-24h
-↓ Insuline (R) .
-TZD are ligant of peroxisome !-steriod and thyroid uperfamilt of nuclear receptor-PPAR -gamam receptors module the expression of gene involved in lipid + glucose metabolism!-TZD action is adipose tissue , modulate syntehsis of lipid hormone!4-Alpha Glucosidas (-) :-Acarbose 25-100 mg before meal-M glittol 25-100 mg before meal-acarose+ miglitil are cumilative"(-) of intetinal glucosidas!-↓post meal glucose exursion by delay abs+ digestion of stach!6-Incretins:Pramlintide 15-120mg-SC--->Pramlinite syntheitc analog of amylin!---->is injectable antihyperglucemia aent--->Modulate Postptandial glucose levels!-Adminsitere with insulin-for pts who cannto acheive post prnadial target glucose level!EXeNATIDE:-↓ Body weight-Synthetic analog of glucagon -like-polypeptide!-approved as injectable,adjuvent Tc for DMII with metformin!SITAGLIPTIN:↑ Body weight:
-(-) of DDP- enzyme that degrates incretic and GLP-1 lime molcules!-Effect : (+) level og GLP-1 and GIP in blood!-Decreaes Postprandial glucose excurtion!****Insulin:I-Rapid Acting:---->rapid onset and short duration-insuline Lipro-insulin Aspart-.. Glilisine-Human insuline Recombinant (inhaled)Durection 3-5 HII-Short acting Insulin:-Soluble moledcule -Idnetical to human insuline-appear withing 30 min and peask between 2-3 H-Last 5-8 HRegular insulin should be administed 30-45 min before meal to avoid postprandial hyperglycemia!III-Intermediate Acting-Isophane:-Insuline+ protamine-After SC injection eunzme degradeprotamine to permit absrption of insulin-NPH onset 2-5H ,-Duration 4-12HIV- Long acting:| Glargine | Determir |
| -ulta long action-onset 1-1.5H-max effect 4-5 H-durecton 11-24H | -1-2 H->24 H |
-Agents: propylthiouracil, methimazole
-Indications: hyperthyroidism
- As definitive treatment, to control the disorder in anticipation of a spontaneous remission in Graves disease
- In conjunction with radioactive iodine, to hasten recovery while awaiting the effects of radiation
- To control the disorder in preparation for surgical treatment
-Indications: hyperthyroidism
- As definitive treatment, to control the disorder in anticipation of a spontaneous remission in Graves disease
- In conjunction with radioactive iodine, to hasten recovery while awaiting the effects of radiation
- To control the disorder in preparation for surgical treatment
Prior to initiating thionamides, we obtain baseline blood tests, including a
complete blood count (white count with differential) and a liver profile
(bilirubin and transaminases)
We do not use thionamides in patients with a baseline absolute neutrophil
count <1000 cells/microL or elevated liver transaminases (more than
fivefold the upper limit of normal) except in selected patients after careful
assessment of alternatives and risks
^^Dosing:complete blood count (white count with differential) and a liver profile
(bilirubin and transaminases)
We do not use thionamides in patients with a baseline absolute neutrophil
count <1000 cells/microL or elevated liver transaminases (more than
fivefold the upper limit of normal) except in selected patients after careful
assessment of alternatives and risks
| Free T4 to 1.5 x of upper notmrmal limit | ...To 2 x of upper nromal | ..To 3 x the upper limit |
| -5-10 mgof methimazole/daily-dose can be (+) if hyperthyrodism is not ameliorated ithin 4-6 W | -10-20 mg of ,methimazole once daily!-The dose is rapered to maitnence levels | 20-40 mg of methamzole dailt in diided doses |
^^EFFECTIVENESS MONITORING
-Improvement in clinical signs and symptoms indicates efficacy
-free T4 and total T3, TSH shoul be initially assessed at 4 to 6 week intervals until stabilized on
maintenance thionamide therapy.
-Once the patient is euthyroid, the dose of methimazole can be decreased by 30 to 50 percent.
-Thyroid tests (TSH, fT4) should be repeated 4 to 6 weeks after each dose adjustment.
-Whena stable maintenance dose is achieved, thyroid (TSH, fT4) tests can be performed every 6
months
-It is important to measure both serum free T4 and total T3 because serum T3 concentrations may
remain high even though serum free T4 concentrations become normal.
^^ADR of PRopylithiouracil:-Improvement in clinical signs and symptoms indicates efficacy
-free T4 and total T3, TSH shoul be initially assessed at 4 to 6 week intervals until stabilized on
maintenance thionamide therapy.
-Once the patient is euthyroid, the dose of methimazole can be decreased by 30 to 50 percent.
-Thyroid tests (TSH, fT4) should be repeated 4 to 6 weeks after each dose adjustment.
-Whena stable maintenance dose is achieved, thyroid (TSH, fT4) tests can be performed every 6
months
-It is important to measure both serum free T4 and total T3 because serum T3 concentrations may
remain high even though serum free T4 concentrations become normal.
I-Common
Rash
Serious
Vasculitis
Agranulocytosis (0.2% to 0.5% ), Aplastic anemia
Hepatotoxicity, Liver failure
Nephritis
^^Safety monitering:-CBC-Liver fucntion-hepatic function-prothrombin^^Clinical Pharmacologgy :Rash
Serious
Vasculitis
Agranulocytosis (0.2% to 0.5% ), Aplastic anemia
Hepatotoxicity, Liver failure
Nephritis
| I-Thiomides:-Methimazole-ProphythioracilEfficarcy:-Action to ito prevent hormone synthesis --->(-) Thyroid peroxidas enzyme!1-blocks iodone oxidartion2-(-) incorporation of indion to tyrosne3-Stops coupling of T3+T4 compoudsDO Not stop iodine uptake by glands!-->used to lower thyroid hormone levels , but do not block target organ!-->TY (-) converstion of T4 to T3 since the synthesis rather thenrealease hormone is affecte the onset of afent is slow^^Safety:ADR 3-12%1-Heptitis and choelstatic jaundice( Methimazole) --->Need ot moniter transaminase level(AST, ALT)2-Agranulocytosis---> infreuqnecty but fatal (tiomides) |
| II-Anion(-):Efficacy :-Perchlar/pertecnetate. Thiocyanate---> block uptake of Iodine by gland!-competitive (-) of iodine trnasprot mechanism ! |
| III-Iodides:^^Efficacy :(-) organification and hormone release and decrease the size of vasculairy of hyerplastic gland!^^Safety:-Iodine increase intraglandular sotreage, delay onset of thiomade therapy!-should be used alone, because glad will escae from iodide block in 2-8 Wleading to thyrotoxicosis exacerbationb!-Acoid in preganacy |
| IV-adioactive iodine:Efficacy:-in few weks can destroy Thyroid parenchhyma visible by epithlial sweeling and necrosis!Safety:-NMot for nursing mother ( crosses lacenta and destroy fetal thyroid gland)-may lead to hypothyroidism--->moniter TH4+ TSH level( in case of hypothyrdosim give 50-150 mcg of levothyroxine) Safety:-NMot for nursing mother ( crosses lacenta and destroy fetal thyroid gland)-may lead to hypothyroidism--->moniter TH4+ TSH level( in case of hypothyrdosim give 50-150 mcg of levothyroxine) |
| Congenital | Acquired |
-Early Dx is very important!! - New born needed to be screened on his 2 nd week of life. - Tx with L-thyroxine(for life) - In infants a&children with congenital hypothyroidism and juvenile myxedema, the dose of levothyroxine should be titrated according to clinical response, growth assessment, and measurements of plasma thyroxine and TSH. - The target – TSH slightly elevated then the lower limit | #1 Most often due to autoimmune Hashimoto's thyroiditis. #2 It is require long-term replacement therapy for thyroid hormone (levothyroxine=T 4 , Triiodothyronine = T 3 ). #3Baseline ECG because changes induced by hypothyroidism can be confused with ischemia.#4 The dosage needed to be small -> if improvement -> slowly increasing dosage. 5) The optimal dose in the treatment of hypothyroidism is determined by the patient's well-being and TSH level (within the normal limit=0.5-5.7mu/L) and T4 (the upper limit of normal=70-140nmol/L) in |
| uncomplicated Adult | 1.61.7mcg/kg/d averge replacement dose | Onset of action:2-3 WeeksMax Effect:4-6W-Reversal of skin and hair changes , may take several mnth-Th4 and TSH should be checked 6-8 W after inititation of Tx!- doses before steady state are mislading |
| Elderly | <1/6mcg/ kg/d | -initiate Th4 cautiona,ly-Eldely may require less then young- prs >60 , need <50 mcg/d |
| Cardiovascur isease(Angina , CAD) | -Start with 12.5-25 mcg/d-(+) by 25 mcg/day every 4-6 W | -sensitive to Cardiovascular effecto f T4 -Steady state may be delayed becayse of ↓clearance |
| Preganancy | Most ↑ in dose to ensure eurothyrodiasm | -Evaluate TSH/ TTH00 |
| ediatric (0-3M) | 10-15 mcg/kg/day | Hypothyroid kids can exihibi skin mottlets, lethary |
| Acute:-OP huydration-Underlying disease-pharmacologicalt | Chronic:Underlying disease TX-Loperamdie-Anticholenrgic agents1 |
Glycerin 2-3g suppositories 1/d
Mineral oil 15-45mL 1/d
Docusate Na 100mg 2-3x/d
Mineral oil 15-45mL 1/d
Docusate Na 100mg 2-3x/d
IV-Stimulants:
Bisacodyl 10mg suppositories up to x3/week
Tegaserod 6mg x2/d
Bisacodyl 10mg suppositories up to x3/week
Tegaserod 6mg x2/d
Diarrhea: |
- Empyric treatment against most probable m/o or its group
- Excluded resistance
- Colonization not treated
- Dosage – according to SmPC (Summary of Product
Characteristics or EBM based recommendations)
– Goal
• Sufficient exposure at the site of infection:
– Precise sensitivity of m/o in vitro,
– Minimal concentraitons at the site of infection (in-vivo)
– Managed risk of biofilms
• This can be acheaved following SmPC 4.2 or vis modeling
PK/PD with kinetic softwares
2-Selected Ax should have Narrowest sepctrum Grou:-Empeirici Tactic-Escalaltory or desclaalotry-According to BAG-Consisdered PK/PD features( penetration), IV Dose, Inteaction)-X Conctration in urine and prenchyma is not same3-In the Group ,We choose Safest+Cheaprst X:-In addition totoxicity ,Estimate biological activity as weelll-2nd (R) Quiniline>IV-III>II Gen Cephalosorin-Local Guidlines-if doses aare not effective, Consider Dosages4-More Conveneint Ax( More exp) Chosen when pluses( Lower risk for non comopliance) is more important then price.5-Early Evaluation -First evalauation in case of acute infective Process timely therpay (measure Temp every 2 hours)6-Main duration of course is in SmPC and RUD recommendations!
Peculiarities of algoritms for AB usage:
- Represent national and local experience;
- Represent various components of RUD (pvz.,
benefit or economy)
- Applicability for HI is limited
7-To Assure Ax Safety (including inefficacu) seek higher colaoration with pts and nurse-Fluoroquinolone used for UTI prophylactic -Upper UTI Treates with Lower/rarer amoxicillin-Treat Urinary Test But Not Pts-Galenic X used in too msall doses-Ax are veyr improtant for Tx! Of infection -also help in complciation as Cancer/chemotx/ surgery!-they are hwoever ovepescribed! A- Due ot overprescibrition,over or underuse there is a Resistance develpment!-Resistance limits our option for Txcx lfie htratinign ifnection which evolved!Quesiton to ASk for Ax therpay:-is Ax indicated on basis of Clinical finding?-have appropirate microbiolgoical test been made?-what are leiky etiolgoical agents?-how to protect the indicual exsoed to the index case to prevent 2nd cases!?-how ot prevent further exposure-is there any clincial evidence that suggest Ax will not be beneficialOne you establish the cause , further test must be done!:-can wer substitue narrow spectured for empireical?-is it 1 Ax of cominbation neded?-what is optimal ,dose, Routes. Duration?-what adjuvent therapy must be added to eradicate thei nfection(fex surgery to remvoe forieng body ,/drainage of abscess/ infusion of aAx into an area)( is it ossible to reduce mrotality by reducing the host immunolgical response to the infeciton)***Risk of Bacteiral (R) to Ax and its managment:-(r) may be inherent to a specifis or maybe acquired ivia genesfor Ax (R)!-resisance genes between 2 bacteiral cell follow this:- Represent national and local experience;
- Represent various components of RUD (pvz.,
benefit or economy)
- Applicability for HI is limited
1- Transformation (uptake of naked DNA from another organism)
2- Transduction (infection by a bacteriophage)
3- Conjugation (exchange of genetic material in the form of either plasmids, which are pieces of independently replicatingextrachromosomal DNA,)
-Ax elimiante non(R) vbacteira, but increases proortion of (R) bacteria that remains !-Ax has effectn ot only on pathogens but also on Normal Flora!-To prevent (R) has to be used onle where is it required!-spectrum should be as narrow ass possible!2- Transduction (infection by a bacteriophage)
3- Conjugation (exchange of genetic material in the form of either plasmids, which are pieces of independently replicatingextrachromosomal DNA,)
Q: Why are bacteria becoming resistant to antibiotics?A: Overuse and misuse of antibiotics allows the development of antibiotic-resistant bacteria. Every time a person takes antibiotics, sensitive bacteria (bacteria that antibiotics can still attack) are killed, but resistant bacteria are left to grow and multiply. This is how repeated use of antibiotics can increase the number of drug-resistant bacteria. Antibiotics are not effective against viral infections like the common cold, flu, most sore throats, bronchitis, and many sinus and ear infections. Widespread use of antibiotics for these illnesses is an example of how overuse of antibiotics can promote the spread of antibiotic resistance. Smart use of antibiotics is key to controlling the spread of resistance. Q: How do bacteria become resistant to antibiotics?A: Bacteria can become resistant to antibiotics through several ways. Some bacteria can “neutralize” an antibiotic by changing it in a way that makes it harmless. Others have learned how to pump an antibiotic back outside of the bacteria before it can do any harm. Some bacteria can change their outer structure so the antibiotic has no way to attach to the bacteria it is designed to kill. After being exposed to antibiotics, sometimes one of the bacteria can survive because it found a way to resist the antibiotic. If even one bacterium becomes resistant to antibiotics, it can then multiply and replace all the bacteria that were killed off. That means that exposure to antibiotics provides selective pressure making the surviving bacteria more likely to be resistant. Bacteria can also become resistant through mutation of their genetic materia |