This document discusses gastrointestinal bleeding (GIB), summarizing its main causes and approaches to management. It notes that upper GIB accounts for 80% of cases, with the most common causes being peptic ulcer disease, esophageal varices, esophagitis, and Mallory-Weiss tears. Lower GIB is more common in the elderly and can be caused by conditions like diverticulosis, colitis, ischemia, and hemorrhoids. Small intestinal bleeding is relatively uncommon but can now be identified in most patients using video capsule endoscopy, deep enteroscopy, or radiological imaging. The document provides guidance on assessing severity, differentiating upper from lower sources, initial resuscitation measures, the role of endoscopy,
Colonoscopy is one of the most common procedures in medicine today. This lectures covers the complications associated with colonoscopy, including the risk factors and management.
Recent Update on Management of Ulcerative ColitisDr Amit Dangi
Recent update on the surgical and medical management of ulcerative colitis, including various controversies regarding IPAA and recent medical management incorporating the role of biologicals
Nutrition in Acute Pancreatitis (According to ESPEN guidelines 2002 and ACG g...Jibran Mohsin
This presentation compares the European Society of Parenteral & Enteral Nutrition (ESPEN) 2002 guidelines and American College of Gastroenterology (ACG) 2013 guidelines regarding nutrition in patients of acute pancreatitis
Colonoscopy is one of the most common procedures in medicine today. This lectures covers the complications associated with colonoscopy, including the risk factors and management.
Recent Update on Management of Ulcerative ColitisDr Amit Dangi
Recent update on the surgical and medical management of ulcerative colitis, including various controversies regarding IPAA and recent medical management incorporating the role of biologicals
Nutrition in Acute Pancreatitis (According to ESPEN guidelines 2002 and ACG g...Jibran Mohsin
This presentation compares the European Society of Parenteral & Enteral Nutrition (ESPEN) 2002 guidelines and American College of Gastroenterology (ACG) 2013 guidelines regarding nutrition in patients of acute pancreatitis
Management of Acute Variceal Bleeding based on American Association for The Study of Liver Disease (AASLD) and European Association for The Study of Liver (EASL) guidelines.
Some slides are taken from different textbooks of medicine like Davidson, Kumar and Clark and Oxford, and some from other presentations made by respected tutors. I'm barely responsible for compilation of various resources per my interest. These resources are free for use, and I do not claim any copyright. Hoping knowledge remains free for all, forever.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
micro teaching on communication m.sc nursing.pdfAnurag Sharma
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.
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
2. Introduction:
• Upper :80%
• Lower :15%
• SIB:5%
• Proximal or distal to the ligament of Treitz.
3. UGIB:
• Presents with:
• Hematemesis (bright-red or “coffee-ground” emesis)
• Melena (black, tarry-appearing stool)
• Or very rarely hematochezia or bright red blood per rectum due to
briskly UGIB, which is associated with increased mortality.
4. UGIB : Causes
• 80% is due to 4 causes:
• PUD
• EV
• Esophagitis
• Mallory-Weiss tear.
• Bleeding in 80% stops spontaneously
• 20% have persistent or recurrent bleeding, increasing mortality.
5. UGIB causes: slow & or chronic causes
• Suggested by history of IDA.
• Typical of erosive disease: tumor, esophageal ulcer, portal
hypertensive gastropathy, Cameron lesion (5%, eroded large hiatal
hernias)& angiodysplasia.
6. UGIB: causes
Causes of brisk&/or severe upper GIB that increase mortality.
• Peptic ulcer
• Esophagogastric varices
• Dieulafoy lesion
• Aortoenteric fistula
• Hemobilia: usually from liver or biliary procedural complication or
gallstone complications, tumors &angiodysplasia.
• Hemosuccus pancreaticus: (pseudoaneurysm/aneurysm)
• Neoplasm
• Esophageal lesions
• Gastric GIST
7. UGIB: History
H/O chronic alcohol abuse: a clue to the possibility of VH.
• Chronic dyspepsia: PUD.
• NSAIDs use: PUD.
• H/O Aortic aneurysm repair: aortoenteric fistula.
Predictors of severe GIB are:
• Hematemesis
• Comorbidities (such as cirrhosis or malignancy)
• HD instability
• Hb <8 g/dL (80 g/L).
• bleeding source.
8. Management aims:
Assessing severity.
Differentiating upper from lower GIB sources.
Determining the need for interventions.
9. Assessing severity:
Outpatient management is usually appropriate when the following criteria
are met:
• BUN<18.2 mg/dL (6.5 mmol/L)
• Normal Hb
• Systolic BP>109 mm Hg
• PR< or equal to 100/min
• Absence of: melena, Syncope,Liver disease,Cardiac failure.
11. Assessing severity:
Severity scoring:
Best validated &most useful is Glasgow-Blatchford score (0-23), of 9
variables: BUN (0-6 points), Hb (0-6), SBP(0-3), PR(0-1), melena (0-
1), syncope (0-2), hepatic disease (0-2 points)& HF(0-2).
• Has a nearly 100% NPV for severe GIB& the need for hospital-based
intervention (blood transfusion, endoscopic therapy, TC arterial
embolization, surgery).
UGIB is most reliably predicted by 4 variables: melena, NGT with blood or
“coffee grounds,” BUN/ Cr > 30 & absence of blood clots in the stool.
12. Management:
1. Pre-endoscopic care (resuscitation, hemodynamic monitoring, PPI
therapy, attention to coagulopathy)
• 2. Early endoscopic evaluation (with excellent endoscopic vision) &
treatment.
• 3. Postendoscopic care & risk reduction.
13. Management: pre-endoscopic care
1.Resuscitated with crystalloids to reach physiologic endpoints (PR
<100/min, SBP>100 mm Hg&resolution of orthostasis).
• 2.Blood transfusion indicated:
• A. HD instability &ongoing bleeding or susceptibility to complications
from hypoxia (for example IHD).
• B. Target Hb < 7 g/dL, if HD stable with no active or massive bleeding.
• 3.Early (pre-endoscopic) PPI does not improve clinical outcomes
(bleeding, surgery, mortality) but is safe & reduces the likelihood of
detecting ulcers with high-risk stigmata & need for endoscopic trt.
• 4.Coagulopathy (INR >1.5) corrected with FRP not vit K (delayed full
therapeutic effect) in actively bleeding receiving anticoags.
• 5.Octreotide & antibiotics should be given before endoscopy for
suspected variceal bleeding.
14. Management: pre-endoscopic care
NGT is not required for diagnosis, prognosis, visualization, or therapeutic
effect.
Beneficial for excluding UGI bleeding source before proceeding to lower
GIB management in HD unstable patients with Hematochesia.
Routine use of prokinetics is not recommended except when patients are
suspected of having large amounts of blood in the UGIT; in such cases, IV
erythromycin can be given prior to upper endoscopy.
15. Management: endoscopic care
Upper endoscopy within 24 hours of presentation in patients with features
of UGIB.
Endoscopy within 12 hours is generally recommended only for patients
with suspected variceal bleeding.
Low-risk ulcers not requiring endoscopic intervention are clean-based or
have a non-protuberant pigmented spot.
Intermediate-risk ulcers have adherent clots can be left without
intervention or vigorously irrigated to dislodge the clot & reclassified
based on appearance.
High-risk ulcers that require endoscopic treatment: active arterial
spurting or a non-bleeding visible vessel & visible vessel at ulcer base.
Routine second-look endoscopy is not required after UGIB unless
rebleeding occurs or the initial examination was incomplete.
16.
17. Management: post-endoscopic care
Post endoscopic PPI improves outcome after endoscopic interventions.
PUD tested for H pylori &If positive, eradication done &confirmed.
If negative, re-testing done with an alternative method BZ of false-negative
results from bleeding, PPI, or concomitant antibiotics.
Aspirin should be resumed within 3 - 5 days for patients with established
CVD.
Long-term PPI may not be necessary for aspirin users who undergo H.
pylori testing &eradication.
Long-term, daily PPI should be offered to aspirin users who are H. pylori
negative or those who use concomitant NSAIDs, anticoagulants,
glucocorticoids, or other antiplatelets.
18. Management: variceal bleeding
10% of UGIB.
Octreotide / telipresin infusion & antibiotics are given even if this is
suspected.
FLuid resuscitation is preferred with crystaloids.
Endoscopic intervention can be done safely even with INR up to 2.5 &
above that, correction done with FFP.
Endoscopic band ligation is preferred over sclerotherpay for acute
esophageal variceal bleeding.
Special eso stents used when above fail.
For bleeding gastric varices cyanoacrylate sclerotherpay is preferred over
band ligation.
When the above measures fail, temponade with esophgeal balloons as
Baltimore-Sengestaken tube is used as bridge to more definitive therapies
as TIPS or surgery.
NS Beta-blockers are used after the control of the bleeding.
19.
20.
21. Lower GIB:
Typically occurs in elderly.
• Presents with hematochezia; acute bright red blood per rectum or red- or
maroon-colored stool.
• HD instability is less common but, if present, raises the possibility of a
briskly bleeding UGI source.
23. Lower GIB: causes of severe type
• Diverticulosis
• Aortoenteric fistula
• Colonic or rectal varices
• Dieulafoy lesions
• Neoplasm
• Colitis
• Ischemic
• IBD
• Infectious
• Intussusception
• Meckel diverticulum
• Angiodysplasia
24.
25.
26. Small GIB:
Relatively uncommon ; 5–10% of GIB.
With advances in SI imaging(VCE, deep enteroscopy& radioimaging) the
cause of bleeding in SI identified in most patients.
OGIB should be reserved for patients in whom a source of bleeding cannot
be identified anywhere in the GI tract.
SIB should be considered in patients with GI bleeding after performance
of a normal upper & lower endoscopic exams.
Second-look exams using upper endoscopy, push enteroscopy&/or
colonoscopy can be performed if indicated before SB evaluation.
VCE should be considered a first-line procedure for SIB& should be
performed before deep enteroscopy if there is no contraindication.
Any method of deep enteroscopy can be used when endoscopic
evaluation& therapy are required.
27. Small GIB:
CTE should be performed in patients with suspected obstruction before
VCE or after negative VCE exams.
When there is acute overt hemorrhage in the unstable patient,
angiography should be performed emergently.
In patients with occult hemorrhage or stable patients with active overt
bleeding, multiphasic computed tomography should be performed after
VCE or CTE to identify the source of bleeding & guide further
management.
If a source of bleeding is identified in the small bowel that is associated
with significant ongoing anemia and/or active bleeding, the patient should
be managed with endoscopic therapy.
Conservative management is recommended for patients without a source
found after SB investigation, whereas repeat diagnostic investigations are
recommended for patients with initial negative SB evaluations & ongoing
overt or occult bleeding.