Proton pump inhibitors (PPIs) like omeprazole irreversibly inhibit the gastric H+/K+-ATPase enzyme to reduce acid secretion. They are effective for treating acid-related disorders like GERD and peptic ulcers. PPIs have high bioavailability but require acidic conditions for activation. Common side effects include diarrhea and headache, while long term use may increase risks of infections, fractures, and nutrient deficiencies. Drug interactions are rare due to short half-lives, but some PPIs inhibit CYP2C19 and decrease clopidogrel effectiveness.
Presentation on Antacids and antiulcer drugs. Introduction to ulcers, classification of antiulcer drugs, their pharmacological actions, uses and adverse effects.
Proton pump inhibitors (PPIs) block the gastric H,K-ATPase, inhibiting gastric acid secretion. This effect enables healing of peptic ulcers, gastroesophageal reflux disease (GERD), Barrett's esophagus, and Zollinger-Ellison syndrome, as well as the eradication of Helicobacter pylori as part of combination regimens.Proton-pump inhibitors (PPIs) are a class of medications that cause a profound and prolonged reduction of stomach acid production. They do so by irreversibly inhibiting the stomach's H+/K+ ATPase proton pump.[1]
They are the most potent inhibitors of acid secretion available.[2] Proton-pump inhibitors have largely superseded the H2-receptor antagonists, a group of medications with similar effects but a different mode of action, and antacids.[3]
PPIs are among the most widely sold medications in the world. The class of proton-pump inhibitor medications is on the World Health Organization's List of Essential Medicines.[4][5] Omeprazole is the specific listed example.[4][5]
Mechanism of action
The activation of PPIs
Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase, or, more commonly, the gastric proton pump) of the gastric parietal cells.[71] The proton pump is the terminal stage in gastric acid secretion, being directly responsible for secreting H+ ions into the gastric lumen, making it an ideal target for inhibiting acid secretion.[citation needed]Because the H,K-ATPase is the final step of acid secretion, an inhibitor of this enzyme is more effective than receptor antagonists in suppressing gastric acid secretion.[72] All of these drugs inhibit the gastric H,K-ATPase by covalent binding, so the duration of their effect is longer than expected from their levels in the blood.[73]
Targeting the terminal step in acid production, as well as the irreversible nature of the inhibition, results in a class of medications that are significantly more effective than H2 antagonists and reduce gastric acid secretion by up to 99%.[2
A brief description on proton pump inhibitor.In simple words, Proton-pump inhibitors are a group of medications whose main action is a pronounced and long-lasting reduction of stomach acid.
ANTIDIARREHAL AGENTS, therapy,ORS, DRUGS used ,
IBD DRUGS, loperamide, probiotics,antisecreatory drugs, antimotility
mechanism of each drugs used in diarrhea
Presentation on Antacids and antiulcer drugs. Introduction to ulcers, classification of antiulcer drugs, their pharmacological actions, uses and adverse effects.
Proton pump inhibitors (PPIs) block the gastric H,K-ATPase, inhibiting gastric acid secretion. This effect enables healing of peptic ulcers, gastroesophageal reflux disease (GERD), Barrett's esophagus, and Zollinger-Ellison syndrome, as well as the eradication of Helicobacter pylori as part of combination regimens.Proton-pump inhibitors (PPIs) are a class of medications that cause a profound and prolonged reduction of stomach acid production. They do so by irreversibly inhibiting the stomach's H+/K+ ATPase proton pump.[1]
They are the most potent inhibitors of acid secretion available.[2] Proton-pump inhibitors have largely superseded the H2-receptor antagonists, a group of medications with similar effects but a different mode of action, and antacids.[3]
PPIs are among the most widely sold medications in the world. The class of proton-pump inhibitor medications is on the World Health Organization's List of Essential Medicines.[4][5] Omeprazole is the specific listed example.[4][5]
Mechanism of action
The activation of PPIs
Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase, or, more commonly, the gastric proton pump) of the gastric parietal cells.[71] The proton pump is the terminal stage in gastric acid secretion, being directly responsible for secreting H+ ions into the gastric lumen, making it an ideal target for inhibiting acid secretion.[citation needed]Because the H,K-ATPase is the final step of acid secretion, an inhibitor of this enzyme is more effective than receptor antagonists in suppressing gastric acid secretion.[72] All of these drugs inhibit the gastric H,K-ATPase by covalent binding, so the duration of their effect is longer than expected from their levels in the blood.[73]
Targeting the terminal step in acid production, as well as the irreversible nature of the inhibition, results in a class of medications that are significantly more effective than H2 antagonists and reduce gastric acid secretion by up to 99%.[2
A brief description on proton pump inhibitor.In simple words, Proton-pump inhibitors are a group of medications whose main action is a pronounced and long-lasting reduction of stomach acid.
ANTIDIARREHAL AGENTS, therapy,ORS, DRUGS used ,
IBD DRUGS, loperamide, probiotics,antisecreatory drugs, antimotility
mechanism of each drugs used in diarrhea
Gastrointestinal drugs used for their effects on the gastrointestinal system, as to control gastric acidity, regulate gastrointestinal motility, water flow, and improve digestion.
Omeprazole 20mg gastro resistant capsules smpc taj pharmaceuticalsTaj Pharma
Omeprazole - Drug Information - Taj Pharma, Omeprazole dose Taj pharmaceuticals Omeprazole interactions, Taj Pharmaceutical Omeprazole contraindications, Omeprazole price, Omeprazole Taj Pharma Omeprazole 20mg Gastro-resistant Capsules SMPC- Taj Pharma . Stay connected to all updated on Omeprazole Taj Pharmaceuticals Taj pharmaceuticals Hyderabad.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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3. Pharmacokinetics
• Omeprazole and lansoprazole are
racemic mixtures of R- and S-isomers.
• Esomeprazole is the S-isomer of
omeprazole and dexlansoprazole the R-
isomer of lansoprazole.
• All are available in oral formulations.
• Esomeprazole and pantoprazole are
also available in intravenous
formulations.
4. Pharmacokinetics
• PPIs are administered as inactive
prodrugs.
• Oral products are formulated for
delayed release as acid-
resistant, enteric-coated
capsules or tablets.
5. Pharmacokinetics
• After passing through the stomach
into the alkaline intestinal lumen, the
enteric coatings dissolve and the
prodrug is absorbed.
• For children or patients with
dysphagia or enteral feeding tubes,
capsules may be opened and the
microgranules mixed with juice.
6. Pharmacokinetics
• Lansoprazole is also available
as a tablet formulation that
disintegrates in the mouth.
• It may be mixed with water
and administered via oral
syringe or enteral tube.
7. Pharmacokinetics
• Omeprazole is also available as a
powder formulation (capsule or
packet) that contains sodium
bicarbonate (1100-1680 mg
NaHCO3: 304-460 mg of sodium) to
protect the naked drug from acid
degradation.
8. Pharmacokinetics
• When administered on an empty
stomach by mouth or enteral
tube, this immediate-release
suspension results in rapid
omeprazole absorption (within 30
minutes) and onset of acid
inhibition.
9. Pharmacokinetics
• PPIs are lipophilic weak
bases (pKa 4-5).
• After intestinal absorption
diffuse readily across lipid
membranes into acidified
compartment: the parietal cell
canaliculus.
10. Pharmacokinetics
• The prodrug rapidly becomes
protonated within the canaliculus
and is concentrated more than
1000-fold by Henderson-
Hasselbalch trapping.
• It rapidly undergoes a molecular
conversion to the active form.
11. Pharmacokinetics
• The active form is a reactive
thiophilic sulfenamide cation that
forms a covalent disulfide bond
with the H+/K+-ATPase.
• The active form irreversibly
inactivates the enzyme.
13. Pharmacokinetics
The bioavailability of all agents is
decreased approximately 50% by
food.
The drug should be administered
on an empty stomach, 1 hour
before meal.
14. Pharmacokinetics
• In a fasting state, only 10% of
proton pumps are actively
secreting acid and susceptible to
inhibition.
• That is why PPIs should be
administered 1 hour before a
meal (usually breakfast).
15. Pharmacokinetics
• The drugs have a short serum half-
life of about 1,5 hours.
• Acid inhibition lasts up to 24 hours
owing to the irreversible inactivation
of the proton pump.
• About 18 hours are required for
synthesis of new H+/K+-ATPase
pump molecules.
16. Pharmacokinetics
Up to 3-4 days of daily
medication are required before
the full acid-inhibiting potential is
reached.
After stopping the drug, it
takes 3-4 days for full acid
secretion to return.
17. Pharmacokinetics
• PPIs undergo rapid first-pass and
systemic hepatic metabolism and
have negligible renal clearance.
• Dose reduction is not needed for
patients with renal insufficiency
or mild to moderate liver disease.
18. Pharmacokinetics
• To provide maximal inhibition
during the first 24-48 hours of
treatment, the intravenous
formulations of esomeprazole
and pantoprazole must be given
as a continous infusion or as
repeated bolus injections.
19. Pharmacodynamics
PPIs inhibit both fasting and
meal-stimulated secretion.
In standard doses, PPIs inhibit
90-98% of 24-hour acid secretion.
21. GERD
PPIs are the most effective agents for
the treatment of:
• nonerosive and erosive reflux
disease
• esophageal complications (peptic
stricture, Barrett´s esophagus)
• extraesophageal manifestations of
reflux disease
23. GERD
• GERD symptoms recur in over 80%
of patients within 6 months after
discontinuation of a PPI.
• For patients with erosive esophagitis
or esophageal complications, long-
term daily maintenance therapy with
full or half-dose is needed.
26. GERD
Sustained acid suppression with twice-
daily PPIs for at least 3 months is used
to treat extraesophageal complications:
• asthma
• chronic cough
• laryngitis
• noncardiac chest pain
27. Peptic ulcer disease
All PPIs heal more
than 90% of
duodenal ulcers
within 4 weeks and
a similar
percentage of
gastric ulcers within
6-8 weeks.
28. H. pylori associated ulcers
Therapeutic goals are: heal the
ulcer and eradicate the
microorganism.
2 AB + PPI +/- bismuth salts!
29. H. pylori associated ulcers
PPIs promote eradication of H. pylori
through these mechanisms:
• direct antimicrobial properties
(minor)
• raising intragastric pH
• lowering the minimal inhibitory
concentrations of AB (antibiotics)
30. H. pylori associated ulcers
14-day regimen of triple therapy:
• PPI twice daily
• clarithromycin 500 mg twice daily
• amoxicillin 1 g twice daily or
metronidazole 500 mg twice daily
Bismuth quadruple therapy with
bismuth subcitrate.
31. H. pylori associated ulcers
After completion of triple
therapy, PPI should be
continued once daily for a
total of 4-6 weeks to ensure
complete ulcer healing.
32. H. pylori associated ulcers
Sequential treatment for 10 days:
• first 5 days PPI twice daily plus
amoxicillin 1 g twice daily
• other 5 days PPI twice daily plus
clarithromycin 500 mg twice daily
plus tinidazole 500 mg twice daily
33. NSAID-associated ulcers
• In patients with NSAID-
induced ulcers who require
continued NSAID therapy,
treatment with once or twice
daily PPI promotes ulcer
healing.
34. NSAID-associated ulcers
• Asymptomatic peptic ulceration
develops in 10-20% of people
taking frequent NSAIDs.
• Ulcer-related complications
(bleeding, perforation) develop in
1-2% of persons per year.
35. NSAID-associated ulcers
• PPIs taken once daily are
effective in reducing the
incidence of ulcers and ulcer
complications in patients
taking aspirin or other
NSAIDs.
36. Prevention of rebleeding from peptic ulcers
• Rebleeding of high-risk ulcers is
reduced significantly with PPIs
administered for 3-5 days either
as high-dose oral therapy
(omeprazole 40 mg orally twice
daily) or as a continuous
intravenous infusion.
37. Prevention of rebleeding from peptic ulcers
• Intragastric pH higher than 6 may
enhance coagulation and platelet
aggregation.
• Initial bolus administration of
esomeprazole or pantoprazole 80 mg
followed by constant infusion 8 mg/h
is recommended.
38. Prevention of stress-related mucosal bleeding
• Oral immediate-release omeprazole
formulation is administered by
nasogastric tube twice daily on the
first day, then once daily.
• For patients without a nasoenteric
tube or with significant ileus, iv. H2
antagonists are preferred.
39. Gastrinoma, other hypersecretion
• Isolated gastrinomas: surgical
resection.
• In patients with metastatic or
unresectable gastrinomas, massive
and hypersecretion results in peptic
ulceration, erosive esophagitis and
malabsorption.
40. Gastrinoma, other hypersecretion
• With PPIs, excellent acid suppression
can be achieved.
• Dosage is titrated to reduce basal
acid output to less than 5-10 mEq/h.
• Typical doses of omeprazole are
60-120 mg/day.
42. General
• Diarrhea, headache and abdominal
pain are reported in 1-5% of
patients.
• Increasing cases of acute interstitial
nephritis have been reported.
• Safety during pregnancy has not
been established.
43. Nutrition
• Acid is important in releasing vitamin
B12 from food.
• A minor reduction in oral
cyanocobalamin absorption occurs
during PPIs therapy.
• Subnormal B12 levels may occur with
prolonged therapy.
44. Nutrition
Acid also promotes absorption
of food-bound minerals:
• non-heme iron
• insoluble calcium salts
• magnesium
45. Nutrition
PPIs may reduce calcium
absorption or inhibit osteoclast
function, especially in the case of
long term therapy:
• bone density control
• calcium supplements
46. Nutrition
Cases of severe, life-
threatening
hypomagnesemia with
secondary hypocalcemia
have been reported.
47. Respiratory and enteric infections
• Gastric acid is an important barrier to
colonization and infection of the
stomach and intestine from ingested
bacteria.
• There may be increased risk of both
comunity-acquired respiratory
infections and nosocomial
pneumonia.
48. Respiratory and enteric infections
• There is a 2 to 3-fold increased risk
for hospital and community acquired
Clostridium difficile infection.
• There is also a small increased risk
of other enteric infections:
Salmonella, Shigella, E. coli and
Campylobacter.
49. Increased serum gastrin
• Gastrin levels are regulated by
intragastric activity.
• Acid suppression alters normal
feedback inhibition so that
median serum gastrin levels rise
1,5 to 2-fold in patients taking
PPIs.
50. Increased serum gastrin
• Upon stopping the drug, the levels
normalize within 4 weeks.
• The rise in serum gastrin level may
stimulate hyperplasia of ECL and
parietal cells which may cause
transient rebound acid
hypersecretion.
51. Other
• Among patients infected with
H. pylori, long-term acid
suppression leads to
increased chronic
inflammation in the gastric
body and decreased
inflammation in the antrum.
52. Other
Long-term PPI therapy is associated
with the development of small benign
gastric fundic-gland polyps in a small
number of patients.
53. Drug interactions
Decreased gastric acidity may alter
absorption of drugs for which
intragastric acidity affects drug
bioavailability:
• ketoconazole, intraconazole
• digoxin
• atazanavir
54. Drug interactions
• All PPIs are metabolized by
hepatic P450 cytochromes,
including CYP2C19 and CP3A4.
• Because of the short half-lives of
PPIs, clinically significant drug
interactions are rare.
55. Drug interactions
• Omeprazole may inhibit the
metabolism of warfarin, diazepam
and phenytoin.
• Esomeprazole may decrease
metabolism of diazepam.
• Lansoprazole may enhance
clearance of theophylline.
56. Drug interactions
Rabeprazole and pantoprazole
have no significant drug
interactions!
They are appropirate choice, for
example, in patients taking
warfarin.
57. Drug interactions
• Clopidogrel is a prodrug that requires
activation by the hepatic P450
CYP2C19 isoenzyme.
• PPIs (especially omeprazole,
esomeprazole, lansoprazole and
dexlansoprazole) could reduce
clopidogrel activation and its
antiplatelet action.
58. Drug interactions
• Patients on clopidogrel should
take PPIs with minimal CYP2C19
inhibition (pantoprazole,
rabeprazole) if necessary:
increased risk of gastrointestinal
bleeding, chronic GERD or peptic
ulcer disease.