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Acute:-OP huydration-Underlying disease-pharmacologicalt | Chronic:Underlying disease TX-Loperamdie-Anticholenrgic agents1 |
Mineral oil 15-45mL 1/d
Docusate Na 100mg 2-3x/d
Bisacodyl 10mg suppositories up to x3/week
Tegaserod 6mg x2/d
Diarrhea: |
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 |
(GRAPH)
-previous experience,
- cost
- risk factors
- target organ damage,
- CVD
- CKD
- DM
- LUNG DISORDE
***H pylori: |
Non Dihydropyridinise | Dihydopyridine |
-Verapmil=Carcian and vascular muscle effect-Dilitazem= effect on carddiac and smooth muscle | -Nifepine ( CVD disease)-Amlopine=Felodipine-Isradipine-Uicardipine |
- 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 )
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 |
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! |
1-Partial Seizures:-Simple Partial seizure-Complex partieal seizure | 2-Generalized Seizures:-Generalized Tonix-clonic Seizures-Status epilepticus |
-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 |
-Xerostomia
-Glaucoma
-Blurred vision
-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 |
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
Macrolides
Imidazoles
Triazoles
Antivirals
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
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 |
-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
Glargine | Determir |
-ulta long action-onset 1-1.5H-max effect 4-5 H-durecton 11-24H | -1-2 H->24 H |
-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
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 |
-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.
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 |
Mineral oil 15-45mL 1/d
Docusate Na 100mg 2-3x/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!
- Represent national and local experience;
- Represent various components of RUD (pvz.,
benefit or economy)
- Applicability for HI is limited
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 |