1. Upper gastrointestinal bleeding is a medical emergency caused by bleeding in the upper digestive tract proximal to the duodenojejunal junction. Common causes include esophageal varices, peptic ulcers, and Mallory-Weiss tears.
2. Symptoms include hematemesis (vomiting of blood) and melena (black tarry stools), and clinical assessment focuses on signs of blood loss severity. The Modified Blatchford Score stratifies bleeding risk.
3. Initial management involves intravenous access, fluid resuscitation, gastric lavage, medications, and urgent endoscopy for diagnosis and treatment such as injection therapy or band ligation. Surgery or TIPSS procedure may be needed for
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Approach to patient with upper GIT bleeding
Surgery Resident clinical seminar on the management of a 60yr old male with upper gastrointestinal bleeding presented to the department of surgery, Niger Delta University Teaching Hospital, Okolobiri, Bayelsa State
Seminar present the Upper Gastrointestinal Bleeding problems
Edited by : Dr. Inzar Yassen & Dr. Ammar L. Aldwaf
in Hawler Medical Uni. collage of medicine in 14/01/2014
Iraq - Kurdistan - Erbil
Surgery Resident clinical seminar on the management of a 60yr old male with upper gastrointestinal bleeding presented to the department of surgery, Niger Delta University Teaching Hospital, Okolobiri, Bayelsa State
Seminar present the Upper Gastrointestinal Bleeding problems
Edited by : Dr. Inzar Yassen & Dr. Ammar L. Aldwaf
in Hawler Medical Uni. collage of medicine in 14/01/2014
Iraq - Kurdistan - Erbil
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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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
3. INTRODUCTION
• Medical emergency.
• Bleeding proximal to duodeno- jejunal junction
( Ligament of treitz).
• Presents with hematemesis,melena or both.
12. CLINICAL ASSESSMENT
• Mild blood loss ( <15%)-Resting tachycardia.
• Syncope .
• Orthostatic hypotension, tachycardia .
• Supine hypotension – blood volume loss of atleast 40% .
• Shock supervenes if bleeding continues or recur.
13. FEATURES SUGGESTING SEVERE BLEEDING
• Presence of clots in vomitus.
• Fresh blood in the nasogastric aspirate.
• Hematochezia.
• Hypotension and tachycardia.
• A fall in systolic BP>10 mmHg and rise in a pulse rate
of>20/min on changing from lying to sitting posture.
14. MODIFIED BLATCHFORD SCORE
• Risk scoring system.
• To stratify the risk of needing endoscopic therapy or
of having poor outcome.
• Advantage – Used before endoscopy to to predict the
need for intervention to treat bleeding.
• Low score -> low risk of adverse outcome.
15.
16. DIAGNOSIS
1. History of peptic ulcer.
2. History of alcohol or NSAID ingestion.
3. History of jaundice, pedal edema,abdominal
distension,splenomegaly & other features of liver cell
failure – Variceal bleeding.
4. Hematemesis preceded by retching and blood free
vomitus – Mallory-Wiess tear.
5. History of dysphagia and weight loss prior to bleed
- Malignancy.
17. MANAGEMENT OF NON-VARICEAL BLEEDING
1. INTRAVENOUS ACCESS
Using one large- bore cannula.
2. INITIAL CLINICAL ASSESSMENT
Define circulatory status – severe bleeding >
tachycardia, hypotension,oliguria.
Seek evidence of liver disease – decompensated
cirrhosis> jaundice,hepatosplenomegaly,ascites.
Identify comorbidity –
cardiorespiratory,cerebrovascular and renal diseases.
18. 3.BASIC INVESTIGATIONS
Full blood count –
Chronic or subacute bleeding- anemia.
Hypersplenism – thrombocytopenia.
Urea and electrolytes – Evidence of renal failure.
Severe bleeding – elevated blood urea with normal
creatinine clearance.
Liver function tests – evidence of chronic liver disease.
Prothrombin time.
Cross- matching.
19. 4.RESUSCITATION
Intravenous crystalloid fluid – to raise BP
Blood transfusion – If BP is low& patient is
actively bleeding.
Broad spectrum antibiotics – suspected
chronic liver disease.
Management of comorbidities.
20. 5.GASTRIC LAVAGE.
• Introduce nasogastric tube & aspirate.
• Perform gastric lavage by instilling 500 ml of ice cold water
every 30- 60 min.
• Do not apply vigorous suction.
• Nasogastric tube to be kept for 24 hours after cessation of
the bleed to facilitate detection of fresh blood.
• Gastric aspiration helps to:
✓ to assess the rate of bleeding.
✓clear the stomach prior to endoscopy.
✓dilute acid – pepsin in stomach there by reducing
bleeding from erosion.
21. 6.OXYGEN - to all patients in shock .
7.ENDOSCOPY
✓ Carried out after adequate resuscitation
within 24 hours.
✓ Injection of dilute adrenaline to the bleeding point.
✓Thermal modality treatment by heat probe,
electrocoagulation.
22. 8.MONITORING
Pulse,Blood pressure and urine output.
9.SURGERY
Indications:
✓ Endoscopic hemostasis fails to stop active
bleeding
✓Rebleeding occurs in an elderly or frail patient
or twice in a young patients.
Choice of operation depends on the site and diagnosis of
bleeding lesion.
23. .
•Gastric ulcer biopsy should be taken.
•Local excision.
•Partial gastrectomy.
10.ERADICATION OF H.PYLORI
. Proton pump inhibitors taken simultaneously with
two antibiotics: Amoxicillin,Clarithromycin
Metronidazole. For atleast 7 days.
24. OTHER MANAGEMENT STRATEGIES
• ✓ H2- blockers and proton pump inhibitors.
• ✓Ranitidine 50 mg IV eighth hourly.
• ✓ Pantoprazole 40 mg IV stat followed by 8mg/ hr
infusion.
25. VARICEAL BLEEDING
• The most important consequence of
portal hypertension.
• Esophageal varices > within 3- 5 cm of
gastro esophageal junction.
26. Predisposing factors :
• Large varices.
• High portal venous pressure.
• Salicylates & NSAID’s – mucosal erosion.
• Cherry red spots and stripes on endoscopy.
27. CLINICAL FEATURES
✓Painless massive haematemesis with or without
malena.
✓Mild postural tachycardia to profound shock
depending on the extent of blood loss.
✓ Associated features of liver cell failure, ascites and
Portal hypertension.
28. DIAGNOSIS
• Fibreoptic endoscopy – shows varices& bleeding site.
Done within 8 hours of bleed.
• USG – to confirm patency of portal vein.
• A wedged hepatic venous pressure 25mmHg above
that in IVC support variceal bleeding.
29. MANAGEMENT OF VARICEAL BLEEDING
1.Primary prevention of variceal bleeding.
2.Management of acute variceal bleeding.
3.Secondary prevention of variceal bleeding.
30. PRIMARY PREVENTION OF VARICEAL BLEEDING
If non bleeding varices are identified at endoscopy
Beta blocker therapy – propranolol ( 80- 160 mg/d)
nadolol( 40- 240mg/ d)
Carvedilol(6.25 to 12.5mg/d).
33. PHARMACOLOGICAL REDUCTION OF PORTAL VENOUS
PRESSURE
• Terlipressin – synthetic vasopressin analogue.
Reduces portal blood flow and/ or
intrahepatic resistance & hence
brings down portal pressure.
Dose: 2mg IV 4times daily until bleeding
stops,and then 1mg 4 times
daily for upto 72 hours.
• Octreotide - Somatostatin analogue.
Initial bolus dose is 50 mcg followed by
continuous infusion at a rate
of 50 mcg/ hour.
34. ENDOSCOPIC VARICEAL BAND LIGATION
• Varices sucked into a cap placed on the end of the
endoscope,occluded with a tight rubber band.
• Occluded varix sloughs with variceal obliteration.
• Repeated every 2- 4 weeks until all varices are
obliterated.
• Regular follow up endoscopy required.
• Prophylactic acid suppression with proton pump
inhibitors.
37. BALLOON TAMPONADE
Sengstaken- Blakemore tube.
- Tube introduced into stomach through mouth.
- Has 2 balloons that exert pressure in the fundus
of stomach and in the lower esophagus.
- Gastic balloon is inflated with 200-250 ml air.
- If bleeding does not stop esophageal balloon is
inflated.
- It should be deflated for about 10 min in every 3
hours to avoid esophageal mucosal damage.
39. TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC STENT
SHUNT ( TIPSS)
•A shunt placed between portal vein and hepatic vein
to provide a portosystemic shunt ->
reduce portal pressure.
•Carried out under radiological control via
the internal jugular vein.
•Effective treatment for both esophageal and
gastric varices.
41. PORTOSYSTEMIC SHUNT SURGERY
✓ Prevents recurrent bleeding.
✓ Disadvantages: High mortality rate
Leads to encephalopathy.
ESOPHAGEAL TRANSECTION
✓ As a last resort when bleeding cannot be controlled by
other means.
42.
43. SECONDARY PREVENTION OF VARICEAL BLEEDING
• Bleeding recurs in 65% patients within 1 year after
initial bleed.
• Beta- blockers : Propranolol 80- 60 mg/ day.
• Endoscopic variceal band ligation/ sclerotherapy.
• TIPSS