Color Doppler Ultrasound Imaging Course
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Enhance your medical skills with our Doppler Ultrasound Course! Master blood flow assessment and vascular diagnosis with expert-led training, hands-on practice, and cutting-edge techniques. Enroll now to advance your career.
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II. Peptic Ulcer Disease (PUD)
Definition and Epidemiology
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Globally, the prevalence of PUD has declined, largely due to H. pylori eradication, yet NSAID-related ulcers persist, especially among the elderly.
Etiology and Risk Factors
Helicobacter pylori infection – Present in ~90% of duodenal and 70% of gastric ulcers.
NSAIDs – Inhibit prostaglandin synthesis, compromising mucosal defense.
Smoking – Impairs mucosal healing.
Stress (critical illness) – Leads to stress ulcers.
Zollinger-Ellison Syndrome – Gastrinoma with excess acid secretion.
Corticosteroids, alcohol, and genetic predisposition are other contributors.
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The balance between aggressive factors (acid, pepsin, H. pylori, NSAIDs) and defensive mechanisms (mucus, bicarbonate, blood flow, prostaglandins) determines mucosal integrity.
H. pylori causes chronic inflammation and epithelial damage. NSAIDs decrease prostaglandins, reducing mucosal blood flow and bicarbonate production.
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III. Clinical Features of Peptic Ulcer
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Duodenal ulcers: Pain relieved by food, occurs 2–3 hours after meals.
Gastric ulcers: Pain worsens with food intake.
Nausea, bloating, early satiety
Complications:
Bleeding: Hematemesis, melena.
Perforation: Sudden severe abdominal pain.
Gastric outlet obstruction
Penetration into adjacent organs (e.g., pancreas)
---
IV. Diagnosis of Peptic Ulcer
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2. Cyclooxygenase (COX) Pathway:
Converts AA into prostaglandins and thromboxanes.
COX-1: Constitutive enzyme (housekeeping functions).
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Converts AA into leukotrienes and lipoxins.
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12-LOX & 15-LOX: Lead to lipoxins (anti-inflammatory action).
4. Cytochrome P450 (CYP) Pathway:
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5. Endocannabinoid Biosynthesis:
Derived from membrane phospholipids via enzymatic reactions.
Degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL).
Physiological Roles of Lipid Autocoids
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Prostaglandins (e.g., PGE2) modulate fever and pain.
Leukotrienes mediate allergic responses and asthma.
Lipoxins and resolvins promote resolution of inflammation.
2. Cardiovascular System
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PGE2 has bronchodilatory effects.
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P
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DEFINITION:
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INCIDENCE:
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ETIOLOGY:
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Previous abortion history
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Fluid leaking from vagina
Flu like symptoms
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Length of cervix (2.5 cm or more.)
Funneling of internal OS
INVESTIGATIONS:
Blood test
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Serum electrolyte and glucose level
USG
COMPLICATION:
Birth of a pre-term baby
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• Neonatal jaundice
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PREVENTIVE MEASURES:
However, it is not possible to prevent occurrence of preterm labour completely, though its prevalence can be reduced using various measures at following three levels-
1) Prevention at primary level
2) Prevention at secondary level
3) Prevention at tertiary level
1) Prevention at primary level
In this, actions are taken prior to the onset of any disease which reduce or remove the possibility for occurring a disease.
For preventing preterm labour, following measures are applied at primary level.
• Encourage the pregnant, to visit antenatal clinic regularly.
• To identify high risk factors at its incipient stage and to provide appropriate treatment accordingly.
• To provide special care to the women who have history of previous spontaneous abortion or preterm labour.
• Advice the pregnant women regarding:
Not to smoke and use of alcohol
To take well balanced diet
Avoid hard work
Iron folic acid supplementation
Maintaining adequate personal and environmental hygiene
To contact the doctor immediately if any abnormal symptoms arise
2) Prevention at secondary level
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PEPTIC ULCER DISEASE (PUD) , H PYLORI AND GERD TREATMENT BY DR .ANKUSH GOYAL ...
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I. Introduction
Peptic Ulcer Disease (PUD) and Gastroesophageal Reflux Disease (GERD) are distinct yet overlapping disorders of the gastrointestinal system, marked by significant morbidity worldwide. These conditions illustrate the consequence of a disturbed harmony between offensive gastric secretions and the protective barriers of the mucosa. From ancient remedies to modern-day proton pump inhibitors and eradication therapies, the treatment approaches to these disorders represent a triumph of translational medicine.
While PUD typically involves mucosal erosion in the stomach or proximal duodenum due to Helicobacter pylori infection or NSAID use, GERD arises from the reflux of gastric contents into the esophagus due to incompetent lower esophageal sphincter tone. Both conditions necessitate a thorough understanding of their etiopathogenesis for rational therapy and long-term management. This document explores the latest, evidence-based treatment paradigms, structured with clarity and clinical relevance.
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II. Peptic Ulcer Disease (PUD)
Definition and Epidemiology
Peptic ulcers are breaks in the mucosal lining of the stomach or duodenum that penetrate the muscularis mucosa. Gastric ulcers typically occur on the lesser curvature of the stomach, while duodenal ulcers are found in the first part of the duodenum.
Globally, the prevalence of PUD has declined, largely due to H. pylori eradication, yet NSAID-related ulcers persist, especially among the elderly.
Etiology and Risk Factors
Helicobacter pylori infection – Present in ~90% of duodenal and 70% of gastric ulcers.
NSAIDs – Inhibit prostaglandin synthesis, compromising mucosal defense.
Smoking – Impairs mucosal healing.
Stress (critical illness) – Leads to stress ulcers.
Zollinger-Ellison Syndrome – Gastrinoma with excess acid secretion.
Corticosteroids, alcohol, and genetic predisposition are other contributors.
Pathophysiology
The balance between aggressive factors (acid, pepsin, H. pylori, NSAIDs) and defensive mechanisms (mucus, bicarbonate, blood flow, prostaglandins) determines mucosal integrity.
H. pylori causes chronic inflammation and epithelial damage. NSAIDs decrease prostaglandins, reducing mucosal blood flow and bicarbonate production.
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III. Clinical Features of Peptic Ulcer
Epigastric pain: Most common symptom; burning or gnawing in nature.
Duodenal ulcers: Pain relieved by food, occurs 2–3 hours after meals.
Gastric ulcers: Pain worsens with food intake.
Nausea, bloating, early satiety
Complications:
Bleeding: Hematemesis, melena.
Perforation: Sudden severe abdominal pain.
Gastric outlet obstruction
Penetration into adjacent organs (e.g., pancreas)
---
IV. Diagnosis of Peptic Ulcer
Endoscopy: Gold standard for diagnosis and biopsy to rule out malignancy.
Rapid urease test, histology, urea breath test, stool antigen – for H. pylori.
Serologic testing (less preferred).
Barium study
Rheumatology: Understanding Rheumatoid Arthritis & Physiotherapy Management
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Additionally, this presentation focuses on the role of physiotherapy in managing RA. It covers various physiotherapy techniques, including exercise therapy, manual therapy, and modalities such as heat/cold therapy and TENS, which help improve joint mobility, reduce pain, and enhance overall function. It also emphasizes the importance of patient education and the need for a multidisciplinary approach to effectively manage RA.
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Autocoids mcq.ankush goyal gmc patiala punjab
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Introduction
Lipid autocoids, also known as eicosanoids and related lipid mediators, are bioactive molecules derived from polyunsaturated fatty acids (PUFAs). These molecules play crucial roles in inflammation, immunity, hemostasis, cardiovascular function, and various physiological and pathological processes. Unlike classical hormones, lipid autocoids act locally, exerting their effects at or near their site of synthesis.
This document provides an in-depth analysis of lipid autocoids, covering their biosynthesis, classification, physiological roles, and clinical significance.
Classification of Lipid Autocoids
Lipid autocoids are broadly classified into the following categories:
1. Eicosanoids (Derived from Arachidonic Acid)
Prostaglandins (PGs)
Thromboxanes (TXs)
Leukotrienes (LTs)
Lipoxins (LXs)
2. Specialized Pro-resolving Mediators (SPMs)
Resolvins
Protectins
Maresins
3. Endocannabinoids
Anandamide (AEA)
2-Arachidonoylglycerol (2-AG)
4. Platelet-Activating Factor (PAF)
5. Sphingolipid-Derived Mediators
Sphingosine-1-Phosphate (S1P)
Ceramides
Biosynthesis of Lipid Autocoids
Lipid autocoids are derived from membrane phospholipids through enzymatic pathways:
1. Phospholipase A2 (PLA2) Activation:
PLA2 catalyzes the release of arachidonic acid (AA) from membrane phospholipids.
2. Cyclooxygenase (COX) Pathway:
Converts AA into prostaglandins and thromboxanes.
COX-1: Constitutive enzyme (housekeeping functions).
COX-2: Inducible enzyme (inflammation and pain response).
3. Lipoxygenase (LOX) Pathway:
Converts AA into leukotrienes and lipoxins.
5-LOX: Leads to leukotrienes (inflammation, bronchoconstriction).
12-LOX & 15-LOX: Lead to lipoxins (anti-inflammatory action).
4. Cytochrome P450 (CYP) Pathway:
Converts AA into epoxyeicosatrienoic acids (EETs), which regulate vascular tone.
5. Endocannabinoid Biosynthesis:
Derived from membrane phospholipids via enzymatic reactions.
Degraded by fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL).
Physiological Roles of Lipid Autocoids
1. Inflammation and Immune Response
Prostaglandins (e.g., PGE2) modulate fever and pain.
Leukotrienes mediate allergic responses and asthma.
Lipoxins and resolvins promote resolution of inflammation.
2. Cardiovascular System
Thromboxanes (TXA2) induce platelet aggregation and vasoconstriction.
Prostacyclin (PGI2) inhibits platelet aggregation and promotes vasodilation.
EETs regulate blood pressure and vascular homeostasis.
3. Pulmonary Function
Leukotrienes (LTC4, LTD4, LTE4) are potent bronchoconstrictors.
PGE2 has bronchodilatory effects.
4. Renal Function
Prostaglandins regulate glomerular filtration rate and sodium excretion.
EETs contribute to natriuresis.
5. Neurotransmission and Pain
Endocannabinoids modulate pain perception and neuroprotection.
Prostaglandins contribute to central pain sensitization.
6. Reproductive System
P
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DEFINITION:
Pre term labour is defined by WHO as onset of labour prior to the completion of 37 weeks of gestation in a pregnancy beyond 20 weeks of gestation.
INCIDENCE:
Globally, approximately 1 in 10 babies are born preterm (before 37 completed weeks of gestation), with an estimated 13.4 million preterm births annually. This means the incidence of preterm birth is roughly 10-11% worldwide.
In India, about 12% of babies are born preterm, which is higher than neighboring countries.
ETIOLOGY:
In about 50%, the cause of preterm labour is not known- IDIOPATHIC
Some of the high-risk factors are:
HISTORY: previous history of abortion or preterm delivery
Recurrent UTI
Smoking habits
Low socio-economic & nutritional status
Previous abortion history
Malpresentation
COMPLICATIONS IN PRESENT PREGNANCY: it may be due to maternal, fetal and placental.
SIGN AND SYMPTOMS:
Backache
Contractions every 10 minutes, are more often
Cramping in lower abdomen
Menstrual like cramps
Fluid leaking from vagina
Flu like symptoms
Increased pressure in pelvis
Increased vaginal bleeding
Regular uterine activity
Vaginal spotting
DIAGNOSIS:
Regular uterine contractions with or without pain (at least one in every 10 minutes.)
Dilation (2 cm or more) & effacement (80%) of the cervix
Length of cervix (2.5 cm or more.)
Funneling of internal OS
INVESTIGATIONS:
Blood test
Urine analysis, urine culture and sensitivity
Cervicovaginal swab: culture and fibronectin test
Serum electrolyte and glucose level
USG
COMPLICATION:
Birth of a pre-term baby
A pre-term baby usually has following problems:
• Low birth weight
• Birth asphyxia
• Neonatal jaundice
• Underdeveloped organs etc.
PREVENTIVE MEASURES:
However, it is not possible to prevent occurrence of preterm labour completely, though its prevalence can be reduced using various measures at following three levels-
1) Prevention at primary level
2) Prevention at secondary level
3) Prevention at tertiary level
1) Prevention at primary level
In this, actions are taken prior to the onset of any disease which reduce or remove the possibility for occurring a disease.
For preventing preterm labour, following measures are applied at primary level.
• Encourage the pregnant, to visit antenatal clinic regularly.
• To identify high risk factors at its incipient stage and to provide appropriate treatment accordingly.
• To provide special care to the women who have history of previous spontaneous abortion or preterm labour.
• Advice the pregnant women regarding:
Not to smoke and use of alcohol
To take well balanced diet
Avoid hard work
Iron folic acid supplementation
Maintaining adequate personal and environmental hygiene
To contact the doctor immediately if any abnormal symptoms arise
2) Prevention at secondary level
In this level, actions are taken at the incipient stage of the disease so that it can be diagnosed.
Adulterants screening in Herbal products using Modern Analytical Techniques
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Basic types of Adulterations in herbal products.
Modern hyphenated techniques used in determination of adulteration of herbal drugs which includes TLC, HPTLC, HPLC, LC-MS, LC-NMR, SFC, LC-IR,etc.
Various modern analytical techniques used in Quantification of Adulterants present in herbal product.
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