Is alcohol beneficial in cardiovascular disease ??

Alcohol exerts several effects on lipid levels, including raising the serum triglyceride and HDL cholesterol levels. Its effect on LDL cholesterol appears to be minimal. Since excessive alcohol causes numerous adverse effects, including hepatic toxicity, cardiomyopathy, motor vehicle crashes and extensive psychosocial consequences, it is not recommended for the prevention of coronary heart disease

Comorbid conditions associated with metabolic syndrome

Gout (Hyperuricemia)
Polycystic ovarian disease
Nonalcoholic fatty liver disease
Osteoarthritis
Obstructive sleep apnea

Which type of obesity is more dangerous- apple shaped or pear shaped ??

Differences in body-fat distribution (i.e., gynecoid versus android) associated with an altered metabolic profile were documented in the medical literature 50 years ago. Android or apple shaped obesity is more dangerous as compared to gynecoid or pear shaped obesity. Apple shaped obesity lead to more deposition of body fat in the visceral organs, that is why it is more dangerous

Is artificial sweetener used by diabetic safe ?

Saccharin: increase risk of cancer bladder
Sorbitol: produce diarrhoea
Aspartame: destroyed by heat so can not be used in baking or cooking
Acesulfame: can be used in cooking & baking
Fructose: is effective but can increase blood cholesterol
So artificial sweeteners should be avoided.

Are protein supplements safe ?

Protein supplements supplied by gym owners are very dangerous. They may contain steroids, heavy metals & other toxic ingredients. These can damage kidneys, bones & other vital organs if used for months.These products are promoted by gym owners for body building. Standard protein supplements may be used for some medical conditions like burns, malnutritions etc when prescribed by a qualified doctor.

New antidiabetic drugs

Insulin like growth factor-1 (Mecasermine): tried in patients with severe insulin resistance

Aldose reductase inhibitors- Alconil, Sorbinil. They prevent diabetes complications

Amylin analogue (Pramalinitide): It improve glycemic control

Incretins: GIP (glucose dependant insulinotropic polypeptide) & GLP-1 (glucagon like peptide-1) increase glucose dependant insulin secretion but rapidly metabolized by DPP IV (Dipeptidyl peptidase)

Exenatide is a GLP-I agonist that resist DPP IV & has a good glycemic control.
Sitagliptin & Vidagliptin are DPP IV inhibitors which prolong the effect of incretins

Circumcision:

Now it is confirmed scientifically that circumcised people have a very low incidence and prevalence of developing cancer penis. So circumcision has very protective role in the prevention of cancer penis. It was observed that cancer penis was very rare in Muslims and jews because they are circumcised at an early age.
Compelling evidence has shown that newborn circumcision prevents urinary tract infection (UTI) in infancy, balanoposthitis and phimosis in childhood and adolescence, human immunodeficiency virus (HIV) infection, and certain other sexually transmitted diseases (STDs) in young adults and invasive penile cancer (IPC) in middle and old age. (Reference:"Pediatrics-The Highly Protective Effect of Newborn Circumcision Against Invasive Penile Cancer")
According to a study published in NEJM, "Male circumcision is associated with a reduced risk of penile HPV infection and, in the case of men with a history of multiple sexual partners, a reduced risk of cervical cancer in their current female partners"

Hospital waste management

Hospital waste include all waste arising from healthcare establishments.
Large hospital’s generate 2.0 kg of waste, per bed per day. Of this, 0.5 kg can be categorized as biomedical risk waste.
Improper disposal practices results in reuse of discarded
syringes, IV tubes, blood bags and other equipment which
is not 0designed for either sterilization or reuse.
If hospital waste is not properly managed and disposed of,
it can result in injury by contaminated sharps and infection
with Hepatitis B, C, and
Hospital waste can be broadly be defined into 2 categories- risk & non risk waste.
Risk waste: Infectious, Pathological, Sharps, Pharmaceutical, Chemical & radioactive waste
Non- risk waste: Paper, Packaging, food waste
Methods:
Treatment:
• Incineration
• Chemical Disinfection
• Autoclaving
• Encapsulation
• Microwave irradiation etc.,
Final Disposal
• Landfill
• Burying inside Premises
• Discharge into Sewer etc.,
Waste not to be Incinerated
• Pressurized gas containers
• Large amounts of reactive chemical waste
• Radioactive waste
• Silver salts or radiographic waste
• Halogenated plastics (e.g. PVC)
• Mercury or cadmium
• Ampoules of heavy metals

How vultures become endangered species in india ?

Diclofenac is a non-steroidal anti-inflammatory drug (NSAID) taken to reduce inflammation and as an analgesic reducing pain in conditions such as arthritis or acute injury. It can also be used to reduce menstrual pain, dysmenorrhea.
Diclofenac is available as a generic drug in a number of formulations. Over the counter (OTC) use is approved in some countries for minor aches and pains and fever associated with common infections.
Veterinary use of diclofenac has been linked to a crash in vulture populations across Asia, many of which are now endangered. A vulture will die of acute kidney failure within a few days of consuming meat from the carcass of livestock recently treated with the drug.
Use of diclofenac in animals has been reported to have led to a sharp decline in the vulture population in the Indian subcontinent, 95% decline in 2004, 99.9% decline as of 2008. The mechanism is probably renal failure, a known side-effect of diclofenac. Vultures eat the carcasses of livestock that have been administered veterinary diclofenac, and are poisoned by the accumulated chemical. At a meeting of the National Wildlife Board in March 2005, the Government of India announced that it intended to phase out the veterinary use of diclofenac. Meloxicam is a safer candidate to replace use of diclofenac. It is more expensive than diclofenac, but the price is coming down as more drug companies begin to manufacture it.
"The loss of tens of millions of vultures over the last decade has had major ecological consequences across the Indian subcontinent that pose a potential threat to human health. In many places, populations of feral dogs (Canis familiaris) have increased sharply from the disappearance of Gyps vultures as the main scavenger of wild and domestic ungulate carcasses. Associated with the rise in dog numbers is an increased risk of rabies" and casualties of almost 50,000 people The Government of India cites one of those major consequences as a vulture species extinction A major shift in transfer of corpse pathogens from vultures to feral dogs and rats can lead to a disease pandemic causing millions of deaths in a crowded country like India.
The loss of vultures has had a social impact on the Indian Zoroastrian Parsi community, who traditionally use vultures to dispose of human corpses in Towers of Silence, but are now compelled to seek alternate methods of disposal
Diclofenac has been shown also to harm freshwater fish species such as rainbow trout

(Reference: From Wikipedia, the free encyclopedia)

Health benefits of dark chocolates

Chocolate is made from plants, which means it contains many of the health benefits of dark vegetables. These benefits are from flavonoids, which act as antioxidants. Antioxidants protect the body from aging caused by free radicals
Two heart health benefits of dark chocolate are:
Lower Blood Pressure: Studies have shown that consuming a small bar of dark chocolate everyday can reduce blood pressure in individuals with high blood pressure.
Lower Cholesterol: Dark chocolate has also been shown to reduce LDL cholesterol (the bad cholesterol) by up to 10 percent
Other health benefits of dark chocolates
* it tastes good
* it stimulates endorphin production, which gives a feeling of pleasure
* it contains serotonin, which acts as an anti-depressant
* it contains theobromine, caffeine and other substances which are stimulants

Doesn't Chocolate Have a lot of Fat?
The fats in chocolate are 1/3 oleic acid, 1/3 stearic acid and 1/3 palmitic acid:

* Oleic Acid is a healthy monounsaturated fat that is also found in olive oil.
* Stearic Acid is a saturated fat but one which research is shows has a neutral effect on cholesterol.
* Palmitic Acid is also a saturated fat, one which raises cholesterol and heart disease risk.
That means only 1/3 of the fat in dark chocolate is bad for you.

Why chocolate should be avoided for those patients who are taking antidepressants ?

Some foods like cheese, bear, wines, yeast extracts & chocolates have high content of tyramine & other catecholamines. If these foods are taken by those patients who are taking some antidepressant drugs like monoamine oxidase inhibitors (MAOI), it will lead to sudden rise in blood pressure, tachycardia & palpitations. This is known as cheese reaction. So those patients who are taking these medication should avoid these foods.If this cheese reaction happen, it should be treated by giving i.v. injection of some alpha blockers like phentolamine, prazocin etc

Obesity

Obesity is a multifactorial disorder of energy balance in which chronic calorie intake is greater than energy output
Body mass index (BMI) The BMI is body mass (kg) divided by the square of the height (metres); it is highly correlated with body fat. 'Healthy' people have a BMI of 20-25, those with a BMI of 25-30 are deemed to be 'overweight', those with a BMI of >30 are said to be obese and those with a BMI >40 to be morbidly obese.
In our body there are two types of hormones which affect food intake
1. Hormones which decrese food intake (anorexigenic peptide) e.g. leptin, MSH etc
2. Hormones which increase food intake (orexigenic peptide) e.g. neuropeptide Y & agouti related protein which increase food intake

Pharmacological approaches for obesity
Orlistat is a pancreatic lipase inhibitor, preventing the breakdown of dietary fat to fatty acids and glycerols

Sibutramine, originally intended to be used as an antidepressant, has recently been shown to have anti-obesity action. Sibutramine is an inhibitor of neuronal 5-hydroxytryptamine (5-HT)/noradrenaline reuptake at the hypothalamic sites that regulate food intake
POTENTIAL NEW ANTI-OBESITY DRUGS
mazindol (adrenergic agonist
sertraline (a selective serotonin uptake inhibitor
pegylated leptin
β3-adrenoceptor agonist

Some other uncategorized antiarrhythmics

Atropine: for sinus bradycardia
Adrenaline: for cardiac arrest
Isoprenaline: for heart block
Digoxin: for atrial fibrillation
Adenosine: for PSVT
Calcium chloride: for ventricular tachycardia due to hyperkalemia
Magnesium chloride: for ventricular fibrillation, digoxin toxicity, & torsade de pointes

Classification of antiarrhythmic drugs (Vaughan & Williams)

Class I – sodium channel blocker
Ia: Procainamide, quinidine, disopyramide, moricizine (PQDM)
Ib: Lignocaine, mexilitine, phenytoin (LMP)
Ic: Propafenone, Flecainide (PF)
Class II: Beta Blockers (BB) e.g. metoprolol, propanolol, esmolol, sotalol
Class III: K channel blockers e.g. amiodarone, bretylium, dofetilide (BAD)
Class IV: Calcium channel blockers (CCB) e.g. verapamil

Factors that precipitate arrhythmias

Ischemia
Hypoxia
Acidosis
Alkalosis
Electrolyte imbalance
Sympathetic overactivity
Digitalis toxicity
Overstretching of cardiac fibres
Presence of scarred or diseased tissue

Etiology of cardiac arrhythmias

MI- commonest cause
Cardiomyopathy
Congenital e.g. congenital long QT syndrome d/t mutation in the gene encoding K channels
Myocarditis
Cardiac dilatation
Thyroid disorders
Electrolyte imbalance e.g. hypo or hyperkalemia
Drug induced e.g. cisapride, terfenadine etc

Approach to a patient of erectile dysfunction

The physical examination is an essential element in the assessment of ED. Signs of hypertension as well as evidence of thyroid, hepatic, hematologic, cardiovascular, or renal diseases should be sought. An assessment should be made of the endocrine and vascular systems, the external genitalia, and the prostate gland. The penis should be carefully palpated along the corpora to detect fibrotic plaques. Reduced testicular size and loss of secondary sexual characteristics are suggestive of hypogonadism. Neurologic examination should include assessment of anal sphincter tone, the bulbocavernosus reflex, and testing for peripheral neuropathy.
The other test may be done to rule out common causes

1. studies of nocturnal penile tumescence and rigidity;
2. psychological diagnostic tests.
3. vascular testing (in-office injection of vasoactive substances, penile Doppler ultrasound, penile angiography, dynamic infusion cavernosography/cavernosometry)
4. neurologic testing (biothesiometry-graded vibratory perception; somatosensory evoked potentials)
Depending upon cause following steps should be taken
1. Patient counselling & education
2. Oral agents: Sildenafil, tadalafil, and vardenifil are the only approved and effective oral agents for the treatment of erectile dysfunction
3. Androgen therapy
4. Vacuum Constriction Devices: Vacuum constriction devices (VCD) are a well-established, noninvasive therapy.
They are a reasonable treatment alternative for select patients who cannot take sildenafil or do not desire other interventions.
VCD draw venous blood into the penis and use a constriction ring to restrict venous return and maintain tumescence.
Adverse events with VCD include pain, numbness, bruising, and altered ejaculation. Additionally, many patients complain that the devices are cumbersome and that the induced erections have a nonphysiologic appearance and feel.
5. Intraurethral Alprostadil: If a patient fails to respond to oral agents, a reasonable next choice is intraurethral or self-injection of vasoactive substances. Intraurethral prostaglandin E1 (alprostadil), in the form of a semisolid pellet (doses of 125–1000 g), is delivered with an applicator
6. Intracavernosal Self-Injection: Injection of synthetic formulations of alprostadil is effective in 70–80% of patients with ED, but discontinuation rates are high because of the invasive nature of administration.
Surgery: A less frequently used form of therapy for ED involves the surgical implantation of a semirigid or inflatable penile prosthesis. These surgical treatments are invasive, associated with potential complications, and generally reserved for treatment of refractory ED. Despite their high cost and invasiveness, penile prostheses are associated with high rates of patient and partner
satisfaction.
7. Sex therapy : A course of sex therapy may be useful for addressing specific interpersonal factors that may affect sexual functioning. Sex therapy generally consists of in-session discussion and at-home exercises specific to the person and the relationship. It is preferable if therapy includes both partners, provided the patient is involved in an ongoing relationship.

Common causes of erectile dysfunction

Vasculogenic
Neurogenic
Endocrinological
Diabetes
Psychogenic
Drugs e.g. thiazides, methyldopa, calcium channel blockers, SSRI, Cimetidine, estroge, progesterone, cytotoxic drugs, ethanol, coccaine, marijuana etc.

Sildenafil

Inhibits PDE5 in the corpus cavernosa of the penis
50mg, p.o. 1 h before sexual activity
potentiate nitrate’s hypotension activity
ketoconazole & erythromycin increases its level
renal & hepatic disease increases its level
Side effects: headache, flushing, dyspepsia, myalgia

Classification of purgatives

Purgative are drugs that induce defecation
They are divided into
Laxative & cathartics
Laxative: help in production of soft, formed stool
Cathartics: help in rapid, intense fluid evacuation of bowel
Ther are classified into following groups (BOSS)
B-Bulk forming e.g. methylcellulose, psyllium
O-Osmotic purgatives e.g. lactulose, magnesium salts
S-Stimulant e.g. castor oil, bisacodyl,
S- Surfactant e.g. bile acid, docusate salts

Comorbid conditions associated with metabolic syndrome

Nonalcoholic Fatty Liver Disease
Hyperuricemia (Gout)
Polycystic Ovary Syndrome
Obstructive Sleep Apnea
Osteoarthritis

Pathogenesis of metabolic syndrome

Insulin resistance
Inflammation
Prothrombotic state
Endothelial dysfunction
Obesity & abnormal body fat distribution

Monoclonal Antibodies

Both polyclonal and monoclonal antibodies against cell-surface antigens are widely used for prevention and treatment of various diseases

The advent of hybridoma technology to produce monoclonal antibodies was a major advance in immunology
Both polyclonal and monoclonal products have a place in immunosuppressive therapy
Based on origin, monoclonal antibodies may be murine, humanized, human or chimeric
Following is the list of some monoclonal antibodies

Trastuzumab- used in Ca breast

Rituximab- used in Non Hodgkins lymphoma (tu for tumour)

Infliximab- used in rheumatoid arthritis

Omalizumab- used in bronchial asthma ((li suffix for monoclonal antibodies, used in disorders of immunity)

Absciximab- used as antiplatelet antibody in thromboembolic disorders (Ci suffix for circulatory system)

Tefibazumab- for staphylococcal infections (ba suffix for bacterial disease)

Natalizumab- multiple sclerosis

Denosumab- osteoporosis (os suffix for osteoporosis)

Palivizumab- for respiratory syncitial virus infection (vi suffix for viral infection)

Daclizumab- to prevent graft rejection

Ezetimibe

Ezetimibe: inhibit intestinal absorption of cholesterol & phytosterols

Interfere with specific cholesterol transport protein in intestinal mucosa

Reduce absorption of both dietary & biliary cholesterol

Compensatory ↑ in cholesterol synthesis, which can be blocked by statins

Statins + ezetimibe: synergistic CH lowering effect

Weak hypocholestrolemic drug

no major side effects

Fibrates

stimulate the beta-oxidative degradation of fatty acids
- liberate free fatty acids for storage in fat or for metabolism in
striated muscle

- increase the activity of lipoprotein lipase,
hence increasing hydrolysis of triglyceride in chylomicrons
and VLDL particles

reduce hepatic VLDL production and increase hepatic LDL
uptake
The fibrates act through paroxysome proliferator activated receptor (PPAR-alpha) which is gene transcription regulating receptor
PPAR-alpha are present in liver, adipocytes & muscle cells.
Activation of PPAR alpha enhances lipoprotein lipase synthesis & fatty acid oxidation
PPAR alpha also mediate enhanced LDL receptor expression in liver
Compare from PPAR gamma agonist glitazones, on which insulin sensitizer act
LDL ↓5-20 %, may ↑ LDL when TG is high
HDL ↑ 10-20 %
TG ↓ 20-50 %
With clofibrate there is risk of gall stones, so not used now a days
Gemfibrozil + statin ↑the risk of myopathy
Fenofibrate is most suitable fibrate for combining with statins
O t h e r e f f e c t s :
improve glucose tolerance
inhibit vascular smooth muscle inflammation
A d v e r s e e f f e c t s:
In patients with renal impairment myositis (rhabdomyolysis) myoglobulinuria, acute renal failure
Fibrates should be avoided in such patients and also in alcoholics)
Mild GI upset
Uses: Mixed dyslipidemia
Diabetic dyslipidemia
Patients with low HDL & high risk of atheromatous disease

Metabolic Syndrome

The National Cholesterol Education Program’s Adult Treatment Panel III report (ATP III) identified the metabolic syndrome as a multiplex risk factor for cardiovascular disease (CVD) that is deserving of more clinical attention
The various synonyms exist for metabolic syndrome are insulin resistance syndrome, Syndrome X, Beer Belly syndrome, Dysmetabolic syndrome, Reaven syndrome

ATP III Definition of Metabolic Syndrome

1. Abdominal obesity, given as waist circumference (Men > 40 in or women >35 in)
2.TG > 150 mg %
3. HDL cholesterol < 40 mg % in males & < 50 mg % in females 4. BP > 130/85 mmHg
5. Fasting blood glucose > 110 mg%
When ≥ 3 out of 5 listed characteristics are present, with or without treatment, a diagnosis of metabolic syndrome can be made.

Complementry & Alternative Medicines for Dyslipidemias

Gugulipid
Omega-3-fatty acids
Policosanol
Plant stanols sterols
Flaxseed
Red yeast rice
Garlic fiber
Almonds
Soy
Black seed (Nigella sativa)

Statins

HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors. The reductase catalyses the conversion of HMG-CoA to mevalonic acid
Simvastatin + pravastatin + atorvastatin decrease hepatic CHO synthesis
LDL ↓20-55%
HDL ↑ 5-15 %
TG ↓ 10-35 %
All statins produce peak LDL CH lowering after 1-2 weeks of therapy
Statins are effective in both primary & secondary dyslipidemias
Statins are given at bed time to obtain maximum effect.
Not necessary for atorvastatin & rosuvastatin which have long plasma half life
All statins except rosuvastatins are metabolized by CYP3A4
Pleiotropic actions:
improved endothelial function
reduced vascular inflammation and platelet aggregability
antithrombotic action
stabilisation of atherosclerotic plaques
increased neovascularisation of ischaemic tissue
enhanced fibrinolysis
immune suppression
osteoclast apoptosis and increased synthetic activity in
osteoblasts
Pharmacokinetics
well absorbed when given orally
extracted by the liver (target tissue), undergo extensive presystemic biotransformation

Simvastatin is an inactive pro-drug
C l i n i c a l u s e s
Secondary prevention of myocardial infarction and stroke in patients who have symptomatic atherosclerotic disease (angina, transient ischemic attacks) following acute myocardial infarction or stroke
Primary prevention of arterial disease in patients who are at high risk because of elevated serum CHO concentration, especially it there are other risk factors for atherosclerosis
Atorvastatin lowers serum CHO in patients with homozygous familiar hypercholesterolemia
A d v e r s e e f f e c t s:
mild gastrointestinal disturbances

increased plasma activities in liver enzymes

severe myositis (rhabdomyolysis), muscle tenderness & rise in Creatine phosphate kinase (CPK) levels, myopathy
and angio-oedema (rare), myopathy is more common when enzyme inhibitors are used simultaneously

Calcineurin inhibitors

Cyclosporine:
cyclic polypeptide, obtained from fungus
Highly selective immunosuppressant which markedly increased the success of organ transplantation
Selectively inhibit T lymphocyte proliferation, IL-2 & other cytokine production without affecting suppressor T cells
Tacrolimus
Sirolimus
Mechanism
Cyclosporine enter target cells, bind to cyclophilin
The complex then bind & inactivate calcineurin
Calcineurin is membrane associated serine/ threonine phosphatase enzyme, present in T lymphocytes
Calcineurin help in transcription of cytokine genes, leading to production of IL-2, GM-CSF, TNF alpha & interferons
Selectively suppress CMI, humoral immunity remains intact
Recipient is able to deal with bacterial infection
No toxicity of bone marrow & RES
Adverse effects
Nephrotoxicity
Hypertension
Precipitate diabetes
Impair Liver functions
Hyperkalemia
Gum hyperplasia
Opportunistic infections
Hirsutism
Anorexia, lethargy
Tremor
seizures
Therapeutic uses
Kidney, liver, heart, and other organ transplantation (First line drug) along with other immunosuppressant
Second line drug in autoimmune disorders, when not controlled by primary drugs
Severe rheumatoid arthritis
Psoriasis
Behcet’s acute ocular syndrome
Endogenous uveitis,
Atopic dermatitis,
Inflammatory bowel disease
Nephrotic syndrome, when standard therapies have failed

Toxicity of Imatinib

The most frequently reported drug-related adverse events are nausea, vomiting, edema, and muscle cramps
Most events are of mild-to-moderate grade, and only 2% to 5% of patients permanently discontinue therapy, most commonly because of skin rashes and elevations of transaminases
Edema can manifest at any site, most commonly in the ankles and periorbital tissues. Severe fluid retention (pleural effusion, pericardial effusion, pulmonary edema, and ascites) is reported in 1% to 2% of patients taking imatinib.
Neutropenia and thrombocytopenia are consistent findings in all studies in leukemia patients, with a higher frequency at doses ³750 mg.
(Reference : Goodman & Gillmans 11th edition)

Imatinib- Mechanism of action

Imatinib has inhibitory activity against ABL and its activated derivatives v-ABL, BCR-ABL, and EVT6-ABL
Cellular studies showed that imatinib specifically inhibited the proliferation of myeloid cell lines that express the BCR-ABL fusion protein associated with CML
Similar concentrations of imatinib inhibit the proliferation of cells dependent on KIT or PDGFR for proliferation. This includes cells expressing mutant KIT isoforms associated with gastrointestinal stromal tumors (GISTs)

Terbutaline

Terbutaline is beta 2 agonist adrenergic drug. It is used as a bronchodialtor drug. Given by oral, s.c. & inhalational route.
Uses of terbutaline
1. Bronchial asthma
2. Refractory asthma
3. Status asthmaticus
Adverse effects: Tremors, palpitation & rarely arrythmias

Therapeutic uses of metoclopramide

1. As antiemetic in postoperative, drug induced, disease associated, radiation induced vomitting
2. As gastrokinetic agent in emergency GA, before giving spinal anesthesia for cesarian operation, postvagotomy or diabetes associated gastric paresis, to facilitate duodenal intubation
3. Dyspepsia
4. Gastroesophageal reflux disease

How beta blocker propanolol is effective in hypertension ?

1. Reduction of cardiac output (CO) leads to reduce total peripheral resistance (TPR). Due to reduction in TPR both systolic & diastolic BP falls.
2. Decrease renin from kidney leading to decrease plasma renin activity
3. Decrease NA release from sympathetic nerves
4. Decreased central sympathetic outflow

How haloperidol is effective in schizophrenia ?

According to dopamine theory of schizophrenia, it occurs due to overactivity of dopaminergic neurones in the limbic area of brain. Haloperidol antagonize dopaminergic activity in brain by blocking D2 receptors in brain which are located in corpus striatum & limbic system.In this way haloperidol is effective in schizophrenia.

Similarities in insulin & sulfonylureas

1. Both cause weight gain.
2. Both are secretogogue.
3. Both cause hypoglycemia.

Difference between insulin & sulfonylurea

1. Insulin is given by subcutaneous route while sulfonylureas are given orally.
2. Insulin is used predominately in type I diabetes, while sulfonylureas are used predominately in type II patients.
3. Insulin is a peptide hormone synthesized in body by beta cells of pancreas, while sulfonylureas are synthetic sulfa group of drugs.
4. Insulin stimulate glucose transport across the cell by ATP dependent translocation of glucose transportes GLUT 1 & GLUT 4, while sulfonylureas release insulin by blocking ATP dependent K channels in beta cells of pancreas.

Advantages of clarithromycin over erythromycin

1. Clarithromycin covers Mycobacterium avium complex (MAC), other atypical mycobacteria, M. leprae & some anaerobes.It also covers Legionella, M.pneumonae & H. pylori, while erythromycin is not active against these microbes.
2. Clarithromycin is more acid stable than erythromycin, rapidly absorbed, better gastric tolerance as compared to erythromycin
3. Clarithromycin has better tissue penetration.
4. Erythromycin is given four times a day while clarithromycin is given twice daily