PENICILLINS

BEta LACtam aNTibioTics

• Penicillins







• Cephalosporins




• Monobactams






• Carbapenems

PENICILLINS

1. Penicillins

• Penicillin G

• penicillin V

• benzathine penicillin

• procaine penicillin

- active against gram +ve and gram –ve cocci


2. Antistaphyloccocal penicillins

• Dicloxacillin

• Nafcillin

• Methicillin

• Oxacillin

• Cloxacillin

-Resistance against staphylococcal ß- lactamases -Active against staphylococci and streptococci


3. Extended-spectrum penicillins

• Ticarcillin

• Ampicillin

• Piperacillin

• Carbenicillin

• Amoxicillin

-active against gram -VE and gram +VE

Bacterial cell wall

• Composed of peptidoglycan layer

• Peptidoglycan layer consist of polysaccharides and polypeptide called peptidoglycan unit

• Formation of cross linkage of peptide by pentaglysin bridge involved transpeptidase

Mechanism of action of penicillin

• Bind to the specific receptor

• Inhibit transpeptidase, interferes with cross linkage thus inhibit synthesis of peptidoglycan

• Stimulate autolysin, lysis of the bacteria

• BACTERICIDAL

Beta lactamase inhibitor

• Clavulanic acid

• Sulbactams

• Tazobactams

Adverse effects

• Hypersensitivity

• Gastro intestinal upset

• Leucopenia

• Hepatitis

• Pseudomembranous colitis

SULFONAMIDES AND TRIMETHOPRIM

Sulfonamides and trimethoprim are antifolate drugs.
that means, they inhibit the synthesis of folate acid..

they have similar structure to p-aminobenzoic acid (PABA)

SULFONAMIDES

Mechanism of action

• Inhibit dihydroteroate synthase enzyme in bacteria

• Inhibit bacterial growth by reversibly block folic acid synthesis(bacteriosatatic)
• Microorganisms need PABA to form dihydrofolic acid which is essential in production of purine and synthesis of DNA
• Sulfonamides compete with PABA for enzyme and eventually inhibit the enzyme

Spectrum of activity

• Broad spectrum-effective against gram +ve and gram -ve bacteria
• inhibit Chlamydia trachomatis, enteric bacteria, toxoplasma and nocardia sp.

Pharmacokinetics

• Distrubuted widely(CNS and CSF)
• Cross placenta
• Bound to plasma protein
• Exretion by urine so need to reduce dosage in renal failure patients

Clinical uses

• Sulfisoxazole + Sulfamathoxazole = treat urinary track infection
• Sulfadiazine + Pyrimethamine = treat toxoplasmosis
• Sulfadoxine + Pyrimethamine = second line agent for antimalaria
  

Adverse effects

• Hypersensitivity-fever,skin rashes, Steven-Johnson syndrome
• Nausea, vomitting and diarrhea
• Uritary tract disturbances
• Hematopoietic disturbances-can cause kernicterus in newborn baby..be aware!!

TRIMETHOPRIM

Mechanism of action

• Inhibit dihydrofolate reductase enzyme

Clinical used

• oral combination with sulfonamides produces synergistic effect
• Salmonella infection
• Traveller's diarrhea

Adverse effect

• Megaloblastic anemia
• leukopenia
• granulocytopenia
• p/s- to avaoid antifolate adverse effect;administer folinic acid

DRUG INFO: DRUGS FOR COUGH

COUGH

A cough (En-us-cough.ogg pronunciation Latin: tussis), in medicine, is a sudden and often repetitively occurring defense reflex which helps to clear the large breathing passages from excess secretions, irritants, foreign particles and microbes. The cough reflex consists of three phases: an inhalation, a forced exhalation against a closed glottis, and a violent release of air from the lungs following opening of the glottis, usually accompanied by a distinctive sound.[1] Coughing can happen voluntarily as well as involuntarily, though for the most part, involuntarily.

Frequent or severe coughing usually indicates the presence of a disease. Many viruses and bacteria benefit by causing their host to cough, which helps to spread the disease to new hosts. Coughing is classified as acute (of sudden onset) if it is present less than three weeks, subacute if it is present between three and eight weeks, and chronic when lasting longer than eight weeks. A cough can be dry or productive, depending on whether sputum is coughed up. Most of the time, coughing is acute and caused by a respiratory tract infection. Coughing can be triggered by food entering the windpipe rather than the esophagus due to a failure of the epiglottis in patients who have difficulties swallowing. Smoking and air pollution are common causes of coughing.[1] Provided the patient is a non-smoker and has a normal chest X-ray, the three most common causes of chronic cough are asthma, gastroesophageal reflux disease and post-nasal drip. Other causes of chronic cough include chronic bronchitis, heart failure and medications such as ACE inhibitors.

Since cough is a natural protective reflex, suppressing the cough reflex might have deleterious effects, especially if the cough is productive.[2] Nonetheless, coughing might be severe enough (in terms of psychological, physical and social distress) to warrant treatment. This should be targeted towards the cause as much as possible, for example by smoking cessation and discontinuing ACE inhibitors. Some patients may only be worried about serious illnesses, and reassurance may suffice. Cough suppressants (or antitussives) such as codeine or dextromethorphan are frequently prescribed although scientific evidence supporting their use is often of poor quality. Other treatment options may target airway inflammation or may promote mucus expectoration.

gouty attack!!

nk cter sal gout neh...
br je pas pbl....
apekah pbl???
program based learning-
lecturer akan bg satu kes.....
1 patient and prescription for the patient...
tugas kami sbgai pharmacist kononnyer,,,,kene la bincng sal drug 2
their interaction with other drugs,,,patient counselling,,adverse effect,,,dosing,,,mechanism of action,,,n mcm2 lg...
okey,,,stop membebel...


DRUG INFO:Gouty attack


Pathogenesis

• elevation of the serum uric acid levels.Uric acid is the end product of purine metabolism
• Gout is characterized by initial intermittent attack of mono or polyarticular arthritis in the setting of prolonged hyperuricemia
• Marked fluctuation in serum urate levels increase the risk of gout

Factors that increase serum urate

• overproduction of purines.so purines will metabolized to uric acid
  
• reduction in glomerular filtration rate.less uric acid will secrete from blood cause accumulation of uric acid crystal
• lactic acid may competitively inhibit the renal tubular secretion of uric acid..conditions which these will lead to hyperuricemia
• drug induced hyperuricemia.eg;cytotoxic drugs,anhypertensive such as chlorothiazide,diuretics drugs

How gout occurs??

• Monosodium urate crystal(uric acid) precipitate in the joint and initiate an inflammation process
• The realeased crystal are chemotactic to leukocytes and also activate complement leading to inflammation and destructive changes to cartilage and subchondral bone

Guide line to treat Acute Gout Attack

• First line-teratment shoulb be pain relief-NSAIDS-such as indomethacin(not over the counter drugs due to the serious side effect), diclofenac, naproxen and voltaren.Be aware!!!although Aspirin includes under Nsaids, aspirin should not be used as it can worsen the condition.this is because aspirin inhibit uric acid secretion even at low dose.Aspirin also reduces vasodilation due to the inhibition of prostaglandin.
• Second line-Colchicine is given for those unable to tolerate Nsaids .Colchicine inhibits the inflammatory responseand is generally given by mouth but can also be given intravenously.Monitoring the levels of colchicines is necessary due to the narrow theraputic index.
• Third line-Glucocorticoids such as prednisolone.Introduction of these third line drugs must never be during the actual acute attack as they will potentially aggravate the acute episode and prolong it

Antigout

• Allopurinol(inhibit uric acid synthesis)
• Uricosuric agents(incerase uric acis secretion)
• Colchicine(inhibit neutrophil migrate into the joint
• NSAIDS(analgesics and antiinflammatory)

Mechanism of action of allopurinol




-Allopurinol will inhibit the metabolism of purines by inhibiting xanthine oxidase.Hypoxanthine analoque of allopurinol.Allopurinol converted to alloxanthine by xanthine oxidase..Allopurinol and alloxanthine will inhibit xanthine oxidase.So no metabolism of purine

Mechanism of action of Uricosuric agents

-Uricosuric agent will increase the excretion by inhibiting its reabsoption into the proximal tubule

Mechanism of action of Colchicine

-Colchicine inhibits microtubul polymerization by binding to tubulin and preventing its addition to the +ve ends.This binding causes depolymerisation od microtubules so will decreses cell motility and prevent migration of neurophils


Non-pharmacological counseling

• patients must avoid from taking any alcohol while medication because alcohol will reduced the effectiveness of the drugs
• try avaoid from taking high purine diet such as sardine,soya bean,meat,asparagus.

GOUT!!!

testing2

hye...
mcm tersgt hepy sbb berjaya gak buat blog....ngeh2
tp not very sure boley update setiap ari...
frienster pon dh lame xbukak...
very busy n sajer je tangguh keje spy nmpak busy..hahahaha
skang dh rilek sket..
juz tggl repot yg berlambak
asgmnt dh kurng tp stil agak byk..
pray 4 me spy dpt siapkan satu ari nnt..hihiiiii