This document provides an overview of peptic ulcer disease (PUD). It defines PUD and describes the types, epidemiology, etiology, pathophysiology, clinical manifestations, complications, diagnosis, and treatment. PUD is a disruption of the gastric or duodenal mucosa caused by acid and pepsin. Risk factors include H. pylori infection, NSAID use, smoking, and stress. Symptoms include abdominal pain and dyspepsia. Complications are bleeding, perforation, and anemia. Treatment involves eradicating H. pylori, healing ulcers, and preventing recurrence using proton pump inhibitors, H2 receptor antagonists, and lifestyle modifications.
This presentation is to help readers to be equipped with knowledge on predisposing factor to peptic ulcer disease and how it can be managed in the clinical/hospital setup.
This ppt is suitable for b.pharma students. This ppt is prepared according to b.pharma IInd semester syallbus. In this ppt we provide all topics related to pathophysiology of peptic ulcer. In this ppt we covered introduction, types, sign & symptoms, pathophysiology, diagnosis, complications and treatments.
This presentation is to help readers to be equipped with knowledge on predisposing factor to peptic ulcer disease and how it can be managed in the clinical/hospital setup.
This ppt is suitable for b.pharma students. This ppt is prepared according to b.pharma IInd semester syallbus. In this ppt we provide all topics related to pathophysiology of peptic ulcer. In this ppt we covered introduction, types, sign & symptoms, pathophysiology, diagnosis, complications and treatments.
This presentation is about Peptic Ulcer Disease. I presented it in 2017 to my colleagues at Al Ain hospital. Information provided is up to date. I allow you to use it for educational purposes.
A circumscribed ulceration of the GI mucosa occurring in areas exposed to acid and pepsin with a defect in the mucosa that extends through the
Muscularis mucosa into the
Submucosa or deeper.
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.
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
3. Definition
• PUD is one of the most common gastroenterologic disease affecting
the upper GI tract.
• An ‘ulcer’ is defined as disruption of the mucosal integrity of the
stomach or duodenum leading to a local defect due to active
inflammation.
• The term ‘peptic ulcer’ describes a condition in which there is a
discontinuity in the entire thickness of the gastric or duodenal
mucosa that persists as a result of acid and pepsin in the gastric
juice.
4. (Or)
• A peptic ulcer is an abnormal area of mucosa that has been damaged
by the pepsin and hydrochloric acid of gastric juice, with consequent
inflammation of the underlying and surrounding tissue.
5. Types of inducer in peptic ulcer:
H. pylori Induced peptic ulcer
NSAID Induced peptic ulcer
Stress related mucosal damage ulcer
Types of peptic ulcer depending on sites:
Gastric ulcers: which appear in the stomach lining.
Esophageal ulcers: which appear in the long tube like structure that
connects the stomach with the mouth.
Duodenal ulcers: which appear in a section of the small intestine
known as the duodenum.
6. Epidemiology
Acid peptic disorders are very common in the United States, with 4
million individuals (new cases and recurrences) affected per year.
The prevalence of H. pylori is more common in developing
countries than in industrialized countries H. pylori prevalence
exceeds 80% in adults.
The prevalence of H. pylori in the United States is 30% to 40%, but
remains higher in ethnic groups such as African and Latin
Americans.
7. Etiology
Previous peptic ulcer.
Dyspepsia (Indigestion )
H. pylori (80–85% of gastric ulcers are associated with H. pylori)
NSAIDs induced.
Concomitant use of anticoagulant (warfarin).
Concomitant use of Antiplatelet drug such as Clopidogrel.
Concomitant use of oral Bisphosphonates.
Concomitant use of Selective Serotonin Reuptake Inhibitor (Citalopram).
Corticosteroids
8. Cigarette smoking
Alcohol consumption
Hypersecretion of acid which occurs in the rare Gastrinoma
(Zollinger–Ellison) syndrome.
Gastric acid hypersecretion and severe ulcer disease.
Viral infections (e.g., cytomegalovirus)
Radiation
Chemotherapy
Psychologic stress (feeling of strain and pressure)
Emotional stress; head injury, spinal cord injury, burns, multiple
trauma.
9.
10. Risk factors:
Crowded living conditions, unclean water.
Consumption of raw vegetables.
Coffee, tea, cola beverages, beer, milk, and spices may cause
dyspepsia, but do not increase the risk for PUD.
14. Stress induced peptic ulcer:
Circulatory disturbances of the gastro-intestinal blood supply with
necrosis of the apical mucosal cells
Increased gastric acidity (increased histamine release, vagal stimulation
and increased production of glucocorticoids)
Changes in the mucosal barrier (e.g. gastro-duodenal reflux)
15. Cigarette smoking induced peptic ulcer:
Cigarette smoking potentiated ethanol-induced gastric mucosal
damage
The reduction of mucus secretion, increase in Leukotriene B4 level
Increased activities of inducible Nitric oxide synthase, Xanthine oxidase
and Myeloperoxidase
Adhesion molecules in the gastric mucosa
Potentiating effects.
16. Zollinger-Ellison syndrome (ZES)
Caused by a non–beta islet cell
Gastrin-secreting tumor of the pancreas that stimulates the acid-
secreting cells of the stomach to maximal activity
Leads gastrointestinal mucosal ulceration
The overproduction and secretion of gastrin by the gastrinoma
(tumor in the pancreas)
stimulates hypersecretion of hydrochloric acid
17. Alcohol induce peptic ulcer:
Affect to mucosal barrier
Ulcerogenic effects
Result in altering gastric mucosal defense mechanisms
18. Clinical manifestations
Upper abdominal pain occurring 1–3 h after meals
Dyspepsia (discomfort in the upper abdomen).
Anorexia (eating disorder)
weight loss
Nausea
Vomiting
Heartburn
A typical nocturnal pain that awakens the patient from sleep
(especially between 12 AM and 3 AM)
Belching (allowing air in the stomach to come up through the
mouth)
Bloating (uncomfortable sensation of a very full stomach)
19.
20. Complications
Upper GI bleeding (erosion of an ulcer into an artery)
Melena/ black-colored stool
Hematemesis/ vomiting of blood
Perforation (second to bleeding)
Anaemia
21. Diagnosis
Rapid Urease Test:
• Considered “gold standard” for detection of H. pylori infection;
>95% sensitivity and >95% specificity.
• Results are not immediate; not recommended for intitial diagnosis;
more expensive than rapid urease test.
Culture test:
• Permits sensitivity testing to determine antibiotic choice or
resistance.
• Results are not immediate; not recommended for initial
diagnosis; more expensive than rapid urease test.
22. Urea Breath Test:
• Results usually take about 2 days
• Less expensive than tests that utilize gastric mucosal biopsy but
more expensive than serologic tests.
• Availability and reimbursement is inconsistent.
Serologic Antibody Tests:
• Detects IgG antibodies to H. pylori in serum, whole blood or urine.
• Qualitative in office tests; provide results quickly (usually
within 15 minutes) but yield more variable results.
• Tests are widely available and inexpensive.
24. DESIRED OUTCOME:
Overall treatment is aimed at relieving ulcer pain, healing the ulcer,
preventing ulcer recurrence, and reducing ulcer-related
complications.
Successful eradication heals ulcers and reduces the risk of
recurrence to less than 10% at 1 year
GOAL OF THE TREATMENT:
The goal of therapy in H. pylori-positive patients with an active
ulcer, a previously documented ulcer, or a history of an ulcer-related
complication, is to eradicate H. pylori, heal the ulcer, and cure the
disease.
The goal of therapy in a patient with a NSAID-induced ulcer is to
heal the ulcer as rapidly as possible.
28. Non-pharmacological
• Regular small meals are advisable.
• Smoking and alcohol should be avoided.
• Avoid stress
• Coffee or tea should be taken only in moderation, because they are
strong stimulants of acid secretion.
• Late snacks are best avoided, because they stimulate nocturnal
gastric secretion.
• Drink water.
• Patients with PUD should discontinue NSAIDs.
30. H2 receptor antagonists
These were the first truly effective drugs for the therapy of acid-
peptic disease, and their long history of safety and efficacy.
Rimetidine .Ranitidine, Famotidine, and Nizatidine are less potent
than proton pump inhibitors but still suppress 24-hour
Their efficacy appropriate in suppressing nocturnal acid secretion.
Dosage form:
oral administration. Intravenous and intramuscular preparations of
Cimetidine, Ranitidine, and Famotidine are available.
31. Dose:
Evening dosing of H2 receptor antagonists is adequate therapy in
most instances.
single night-time or twice-daily dose, though gastric ulcers may
need larger doses and more prolonged treatment.
There is some evidence that dosing after the evening meal gives
superior results to bedtime dosage.
These doses provide healing in about 70% of gastric ulcer patients
after 1 month and in about 80% after a further 2–4 weeks, but
treatment may need to be extended to 12 weeks.
Therapeutic levels are achieved rapidly after intravenous dosing
and are maintained for 4–5 hours (Cimetidine), 6–8 hours
(Ranitidine), or 10–12 hours (Famotidine).
32. Precaution :
Reduce doses of H2 receptor antagonists in patients with decreased
creatinine clearance.
Interaction:
Cimetidine, uniquely among the H2-RAs, potentiates the actions of
Warfarin, Theophylline, Phenytoin, beta-blockers and many other
drugs, by inhibiting cytochrome P450-mediated liver metabolism.
Half life: 2–3 hr
Pregnancy category: B
33. Adverse effects:
Diarrhea, headache, drowsiness, fatigue, muscular pain, and constipation.
Less common adverse effects include those affecting the CNS (confusion,
delirium, hallucinations, slurred speech, and headaches), which occur
primarily with intravenous administration or in elderly subjects.
Long-term use of Cimetidine at high doses decreases testosterone
binding to the androgen receptor and inhibits a CYP that hydroxylates
estradiol.
Clinically, these effects can cause galactorrhea in women and
gynecomastia, reduced sperm count, and impotence in men.
Several reports have associated H2 receptor antagonists with various blood
dyscrasias, including thrombocytopenia.
H2 receptor antagonists cross the placenta and are excreted in breast
milk.
34. Drug Dose and frequency
Ranitidine 300 mg at bed time or 150 mg BD; for maintenance
150 mg at bed time.
Parenteral dose—50 mg, i.m. or slow i.v. inj. every 6–
8 hr (rapid i.v. injection can cause hypotension), 0.1–
0.25 mg/kg/hr by i.v. infusion has been used for
prophylaxis of stress ulcers.
Famotidine 40 mg at bed time or 20 mg BD (for healing); 20 mg
at bed time for maintenance; upto 480 mg/day in ZE
syndrome;
parenteral dose 20 mg i.v. 12 hourly or 2 mg/hr i.v.
infusion
Cimitidine Dose: 150 mg at bed time or 75 mg BD; maintenance
75 mg
at bed time.
35. Proton pump inhibitors (PPIs)
Drugs of first choice.
These are prefer either complicated or unresponsive to treatment
with H2 receptor antagonists.
These are FDA-approved for treatment and prevention of recurrence
of NSAID associated gastric ulcers in patients who continue NSAID
use and for reducing the risk of duodenal ulcer recurrence associated
with H. pylori infections.
In children, omeprazole is safe and effective for treatment of erosive
esophagitis
36. Dosage forms:
Omeprazole, Esomeprazole, and Lansoprazole available as Enteric-
coated drugs contained inside gelatin capsules.
Lansoprazole enteric-coated granules supplied as a powder for
suspension.
Pantoprazole, Rabeprazole, and Omeprazole available as enteric-
coated tablets.
Powdered drug combined with sodium bicarbonate Omeprazole.
Pantoprazole is available in intravenous form
Dose:
Pantoprazole is directed to gastric ulcers in 8 weeks, but
Rabeprazole takes rather longer (6 and 12 weeks, respectively).
37. Interaction:
Proton pump inhibitors can interact with warfarin & diazepam
Esomeprazole and Omeprazole and pantoprazole interacts
Cyclosporine inhibits CYP2C19
Decreasing the clearance of Disulfiram, Phenytoin,
These are induces the expression of CYP1A2, thereby increasing the
clearance of imipramine, several antipsychotic drugs, tacrine, and
theophylline).
Contraindication:
Hypersensitivity reactions, including anaphylaxis, anaphylactic
shock, angioedema, bronchospasm, acute interstitial nephritis, and
urticaria
Pregnancy category: B
38. Precaution:
Care should be taken patient who has Renal impairment , liver
disease and hypersensitivity to IV.
ADR:
The most common are nausea, abdominal pain, constipation,
flatulence, and diarrhea.
Subacute myopathy, arthralgias, headaches, and rashes also have
been reported. Gynaecomastia (breast enlargement).
Half life:
Oral or IV, 1 hour
Oral or IV, slow metabolizers, 3.5 to 10 hours
Pediatrics, 0.7 to 5.34 hours
39. Drug Dose and frequency
Omeprazole 20–40 mg OD
Lansoprazole 15–30 mg OD
Pantoprazole Dose: 40 mg OD
Rabeprazole 20 mg OD; ZE syndrome — 60 mg/day
40. Mucosal protectents
Sucralfate
It is a basic aluminium salt of sulfated sucrose.
Sucralfate may offer an advantage over proton pump inhibitors and
H2 receptor antagonists for the prophylaxis of stress ulcers
The process can be inhibited by sulfated polysaccharides. acid-
induced damage, pepsin-mediated hydrolysis of mucosal proteins
contributes to mucosal erosion and ulcerations.
Dose :
Stress ulcer; Prophylaxis:1 gram NG or ORALLY empty stomach
1 hour before the 3 major meals and at bed time for 4–8 weeks.
Infant, 40 mg/kg/day NG or ORALLY in 4 divided doses
Children, 40 to 80 mg/kg/day NG or ORALLY in 4 divided doses;
maximum 4 g/day
41. Half life: 2-4 hr
Precaution:
Care should be taken patient with chronic renal failure.
Contraindication:
Hypersensitivity to sucralfate or any of its excipients.
Adverse drug reaction:
Common :Constipation (2% )
Serious: Hyperglycemia, In diabetic patient
Pregnancy category: B
42. ANTACIDS
These are indicated as sole therapy in young patients (under 40
years) and those with chronic, stable, mild symptoms.
sodium bicarbonate effectively neutralizes acid.
Contraindication:
chloride loss, by vomiting
Precaution:
renal impairment and sodium-restricted diet patients.
ADR:
Cellulitis, Injection site extravasation, Skin ulcer, Tissue necrosis,
Metabolic alkalosis.
Pegnancy category: C
43. H Pylori treatment
High eradication rates are achieved by a short course of triple
therapy consisting of a PPI, clarithromycin and amoxicillin or
metronidazole in a twice-daily simultaneous regimen.
European guidelines recommend 1 week of therapy.
US guidelines recommend 10–14 days of therapy and achieve 7–9%
better eradication rates.
Triple therapy consists of:
OCA: omeprazole 20 mg, clarithromycin 500 mg and amoxicillin 1
g or
OCM: omeprazole 20 mg, clarithromycin 250 mg and
metronidazole 400 mg.
44. Amoxicillin is preferred over clarithromycin for initial eradication
because bacterial resistance is almost absent and it has fewer
adverse effects.
Substitution of Clarithromycin 250 to 500 mg four times a day for
tetracycline yields similar results after unsuccessful initial treatment
with a PPI–amoxicillin– Clarithromycin regimen.
Second-line therapy should be instituted with bismuth subsalicylate,
Metronidazole, tetracycline, and a PPI for 14 days.
A lower dose of clarithromycin (250 mg twice daily) is effective and
recommended when combined with Metronidazole 500 mg twice
daily to achieve consistency.
In patients with hypersensitivity to penicillin, the OCM regimen or
substitution of amoxicillin from the OCA regimen with tetracycline
500 mg twice daily is used.
45. • Recommended second-line triple therapy regimens include a PPI,
amoxicillin or tetracycline and Metronidazole.
AMOXICILLIN:
Half life: immediate-release, 61.3 minutes, extended-release, 1.5
hours.
Precaution:
Severe renal impairment, erythematous skin rash.
Contraindication:
Serious hypersensitivity reactions, such as anaphylaxis and Stevens-
Johnson syndrome, to amoxicillin or other beta-lactam antibiotics.
46. Pregnancy category: B
ADR:
Tetracyclines (decreased antibacterial effectiveness)
Warfarin (increased risk of bleeding)
Methotrexate (methotrexate toxicity)
Piperine (increased bioavailability of amoxicillin)
Venlafaxine (increased risk of serotonin syndrome).
47. CLARITHROMYCIN
Dose:
(Immediate-release, triple therapy) Clarithromycin 500 mg,
omeprazole 20 mg, and amoxicillin 1 g orally twice daily for 10
days, followed by an additional 18 days of omeprazole 20 mg once
daily when ulcer present at time of initiation of therapy
Half life: Clarithromycin (250 mg every 12 hours): 3 to 4 hours; (500
mg every 12 hours): 5 to 7 hours
Precaution:
renal impairment, severe, with or without hepatic impairment
48. Contraindication:
cholestatic jaundice and/or hepatic dysfunction.
hypersensitivity to clarithromycin or any component of the product,
erythromycin, or any macrolide antibiotics.
QT prolongation or ventricular cardiac arrhythmias.
Interaction:
Colchicine may result in increased colchicine plasma concentrations
and increased risk of toxicity.
Ergot derivatives and Macrolide antibiotics may result in an
increased risk of acute ergotism (nausea, vomiting, vasospastic
ischemia).
Simvastatin may result in an increased risk of myopathy or
rhabdomyolysis.
Fluconazole may result in increased clarithromycin exposure and an
increased risk of cardiotoxicity
51. Contraindication:
hypersensitivity to Metronidazole.
pregnancy, first trimester, in patients being treated for
trichomoniasis.
Interaction:
Mesoridazine and QT interval prolonging drugs may result in
increased risk of QT-interval prolongation.
Disulfiram may result in CNS toxicity (psychotic symptoms,
confusion).
Ziprasidone may result in increased risk of QT-interval
prolongation.
WARFARIN may result in increased risk of bleeding
Gonadotropin Releasing Hormone Agonists may result in increased
risk of QT-interval prolongation.
52. ADR:
Common
• Gastrointestinal: Abdominal discomfort , Abnormal taste in mouth
, Diarrhea , Nausea
• Immunologic: Jarisch Herxheimer reaction
• Neurologic: Dizziness
Serious
• Stevens-Johnson syndrome, Toxic epidermal necrolysis,
Leukopenia
Hepatic failure, acute, Hepatotoxicity. Ototoxicity, Disorder of
optic nerve.
Pregnancy category:
Fetal risk has been demonstrated
53. BISMUTH SUBSALICYLATE
Dose:
Quadruple therapy, 300 mg orally 4 times per day in combination
with tetracycline 500 mg orally 4 times per day, metronidazole 500
mg orally 3 or 4 times per day OR 250 mg orally 4 times per day,
and standard-dose proton pump inhibitor orally twice daily.
Continue regimen for 10 to 14 days.
Half life:
2-5 hours
Precaution:
colitis or other gastrointestinal mucosa abnormalities
anticoagulants, gout, or diabetes medications
previous hypersensitivity
54. Contraindications:
children or teenagers with or recovering from influenza or varicella.
hypersensitivity to the bismuth subsalicylate or salicylates.
ADR:
Serious
Neurotoxicity (rare).
Pregnancy category: B
55. Proton Pump Inhibitor–Based Three-Drug Regimens:
Drug Dose Frq Days
Clarithromycin 500 mg BID 10–14 days
PPI Standard dose BID 10–14 days
Amoxicillin 1 gm BID 10–14 days
Metronidazole 500 mg BID 10–14 days
56. Bismuth-Based Four-Drug Regimens:
Drug Dose Frq Days
Bismuth subsalicylate 525 mg QID 10–14 days
Metronidazole 250–500 mg QID 10–14 days
Tetracycline plus 500 mg QID 10–14 days
PPI Standard dose QID 10–14 days
H2RA Standard dose BID 4–6 wks
57.
58. References:
1. Manual of pharmacology and therapeutics by Goodman and
gilman’s Drugs affecting Gastrointestinalfunction Pg: 621-27.
2. Clinical pharmacy and therapeutics by roger walker Peptic ulcer
disease Pg: 162-173.
3. Pathology and therapeutics for pharmacist by Russell J Greene,
peptic ulcer disease, Pg: 97-107.
4. Applied therapeutics by Marry Anne Koda Kimble upper gastro
intestinal disorder.
5. Pharmacotherapy a Phathophysiologic approach by Joseph T
Dipiro, Peptic ulcer disease, Pg: 570-85.
6. Micromedex.
7. Pubmed.
8. Medscape.