Simple and Algorthymic approach ,covering all aspects of gastrointestinal hemorrhage.
A concise discussion of the diagnostic approach to obscure
bleeding.
Fundamental principles of initial evaluation and management followed with a welldefined and logical approach to the patient with GI hemorrhage
is outlined.
Simple and Algorthymic approach ,covering all aspects of gastrointestinal hemorrhage.
A concise discussion of the diagnostic approach to obscure
bleeding.
Fundamental principles of initial evaluation and management followed with a welldefined and logical approach to the patient with GI hemorrhage
is outlined.
G I bleeding with radiological interventions(ACR Appropriateness Criteria).Tc-99m RBC scintigraphy,Catheter-directed Angiography,Pharmacological control,Embolization,Arterial interventions,Endoscopy,CT Angiography
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
Atls fatmawati semua sooal pre tes Assalamu'alaikum wr. wb.
Selamat Pagi Bapak/Ibu Dokter.
Alhamdulillah hingga 31 Desember 2022, total responden untuk Riset Stunting PB IDI adalah 727 responden.
Kami dari tim peneliti mengucapkan banyak terima kasih atas partisipasi dan bantuan Bapak/Ibu Dokter sekalian🙏
Untuk reward yang dijanjikan, secepatnya kami akan mengirimkan nama-nama yang telah bersedia untuk berpartisipasi ke PB IDI untuk selanjutnya diproses.
Demikian kami sampaikan, atas perhatian dan bantuannya kami ucapkan terima kasih
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_Kepala bidang Riset, Pengembangan Ilmu, dan Publikasi PB IDI_
Acute abdoment contains all traumatic and non traumatic routine workup done at radiology center along with all the causes regarding abdominal pain refrence takent from manorama berry book of radiology
Endoscopic Hemostasis - for Endoscopy NursesJarrod Lee
Endoscopic hemostasis is an important first line treatment modality in bleeding from the gastrointestinal tract. It is also a prerequisite skill for anyone performing therapeutic endoscopy, where bleeding is the most common intra-procedural endoscopic complication. This lecture is aimed at endoscopy nurses assisting the endoscopist, and gives an overview of endoscopic hemostasis in routine endoscopy today.
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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 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
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.
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
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).
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
2. CME:1
• 1. Acute lower GI Bleeding constitutes what % of all acute GIB:
• A. 10%.
• B. 20%.
• C. 30%.
• D. 40%.
• E. 50%.
3. CME:2
• 2. What % of presumed acute lower GI Bleeding are found to have
upper GI source:
• A. 10%.
• B. 15%.
• C. 20%.
• D. 30%.
• E. 50%.
4. CME:3
• 3. What % of acute GI bleeding is due to small intestinal source:
• A. 1%.
• B. 5%.
• C. 10%.
• D. 15%.
• E. 20%.
5. CME:4
• 4. Bleeding from which colonic areas can present with melena
rather than hematochesia:
• A. Cecum.
• B. Transverse colon.
• C. Descending colon.
• D. Rectum.
• E. Splenic flexture.
6. CME:5
• 5. What % of melena could be from the colon:
• A. 10%.
• B. 20%.
• C. 30%.
• D. 40%.
• E. 50%.
7. CME:6
• 6. In acute lower GIB & hemodynamic instability, an upper GIT
source is best explored by:
• A. upper GI endoscopy.
• B. NT tube.
• C. Capsule endoscopy.
• D. RBC scan.
• E. CT Angio.
8. CME:7
• 7. The following should be the goal in patients with acute lower GIB
before enedoscopic evaluation except:
• A. Normal BP.
• B. Normal heart rate.
• C. Hb > 7 gms in low risk patients.
• D. Hb > 9 gram in high risk patients.
• E. Hb > 9 grams in all patients.
9. CME:8
• 8. In acute LGIB endoscopic hemostasis can be done safely without
the use of reversal agents , with INR up to:
• A. 3.
• B. 4.
• C. 2.5.
• D. 5.
• E. 6.
10. CME:9
• 9. In patients with acute LGIB, endoscopic intervention can be
carried out safely with platelet counts:
• A. 50000.
• B. 10000.
• C. 20000.
• D. 30000.
• E. 5000.
11. CME:10
• 10. Colonic preparation in acute LGI bleeding should be
adminstered over:
• A. One hour.
• B. Two hours.
• C. Three hours.
• D. Five hours.
• E. Six hours.
12. CME:11
• 11. In patients with ongoing acute LGI bleeding, colonoscopy should
be performed after stabilization & adequate preparation within:
• 6 hours.
• B. 12 hours.
• C. 24 hours.
• D. 36 hours.
• E. 48 hours.
13. CME:12
• 12. In patients with acute LGI bleeding but not ongoing,
colonoscopy should performed after stabilization & adequate
preparation within:
• 6 hours.
• B. 12 hours.
• C. When next available.
• D. 36 hours.
• E. 48 hours.
14. CME:13
• 13. Endoscopic interventions indications for acute LGI bleeding compared to
acute UGI bleeding is:
• A. The same.
• B. Different.
• C. Only done for spurting vessels.
• D. Done done for adherent clot.
• E. Contact thermal modalities are preferred.
15. CME:14
• 14. The preferred endoscopic intervention indicated for acute LGI
bleeding due to diverticulosis is:
• A. Clips.
• B. Bands.
• C. Thermal.
• D. APC.
• E. Saline injection only.
16. CME:15
• 15. The preferred endoscopic intervention indicated for acute LGI
bleeding due to angiodysplasia is:
• A. Clips.
• B. Bands.
• C. Thermal.
• D. APC.
• E. Saline injection only.
17. CME:16
• 16. The preferred endoscopic intervention indicated for acute LGI
bleeding post-polypectomy is:
• A. Clips.
• B. Bands.
• C. Thermal.
• D. APC.
• E. Saline injection only.
18. CME:17
• 17. The preferred endoscopic intervention indicated for acute LGI
bleeding from post-polypectomy if through the scope clips are not
available is:
• A. Over the scope clips.
• B. Bands.
• C. Thermal contact therapy.
• D. APC.
• E. Saline injection only.
19. CME:18
• 18. Before surgery is considered for acute LGI Bleeding , the most
important point is:
• A. Localize the bleeding site.
• B. Risk stratification.
• C. Anesthesia tolerance.
• D. Good history taking.
• E. Hb level.
20. CME:19
• 19. The diagnostic modality to localize the bleeding site in acute LGI
Bleeding before angiography is:
• A. CT Angio.
• B. RBC scan.
• C. MRI Angio.
• D. CT Colonography.
• E. Barium enema.
21. CME:20
• 20. Radiographic intervention is indicated for acute LGI bleeding
with all the following characteristics except:
• A. Ongoing bleeding.
• B. High risk patient.
• C. Preparation intolerants.
• D. Colonoscopy intolerants.
• E. All massive bleeders.
22. CME:21
• 21. In the majority of patients with acute LGI bleeding the initial
diagnostic modality is:
• A. Colonoscopy.
• B. CT Angio.
• C. Angiograpy.
• D. Barium enema.
• E. CT colonography.
23. Introduction:
• Acute overt LGIB accounts for ~20% of all cases of GIB.
• Usually leads to hospital admission with invasive diagnostic
evaluations& consumes significant medical resources.
• Most patients with ALGIB stop bleeding spontaneously with
favorable outcomes, morbidity / mortality are increased in older
patients & those with comorbid medical conditions.
• ALGIB classically presents with the sudden onset of hematochezia
(maroon or red blood passed per rectum).
• In rare cases, patients with bleeding from the cecum/right colon can
present with melena (black, tarry stools)
• Hematochezia can be seen in patients with brisk UGIB.
• 15% with ALGIB are ultimately found to have an UGI source.
• LGIB: from the colon or the rectum, SIB (middle GIB) is distinct from
colonic bleeding in terms of presentation, management &
outcomes.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39. Conclusion:
• Hemodynamic status should be initially assessed with intravascular
volume resuscitation started as needed.
• Risk stratification based on clinical parameters should be performed
to help distinguish patients at high&low-risk of adverse outcomes.
• Hematochezia associated with hemodynamic instability may be
indicative of UGI bleeding source &warrants an upper endoscopy.
• In the majority of patients,colonoscopy should be the initial
diagnostic procedure performed within 24 h of patient presentation
after adequate colon preparation.
• Endoscopic hemostasis therapy should be provided to patients with
high-risk endoscopic stigmata of bleeding including active bleeding,
non-bleeding visible vessel, or adherent clot.
• The endoscopic hemostasis modality used (mechanical, thermal,
injection, or combination) is most often guided by the etiology of
bleeding, access to the bleeding site&endoscopist experience.
40. Conclusion:
• Repeat colonoscopy, with endoscopic hemostasis performed if
indicated, should be considered for evidence of recurrent bleeding.
• Radiographic interventions (tagged RBC scintigraphy, CT
angio&angiography) should be considered in high-risk patients with
ongoing bleeding who do not respond adequately to resuscitation &
who are unlikely to tolerate bowel preparation&colonoscopy.
• Strategies to prevent recurrent bleeding should be considered:
NSAIDs use should be avoided in patients with a history of ALGIB,
particularly if secondary to diverticulosis or angioectasia.
• Patients with established CVD who require aspirin (2ndary
prophylaxis) should resume aspirin ASAP after bleeding ceases at
least within 7 days, exact timing depends on bleeding severity,
perceived adequacy of hemostasis& risk of a thromboembolism.
• Surgery for prevention of recurrent LGIB should be individualized&
source of bleeding should be carefully localized before resection.
41. CME:1
• 1. Acute lower GI Bleeding constitutes what % of all acute GIB:
• A. 10%.
• B. 20%.
• C. 30%.
• D. 40%.
• E. 50%.
42. CME:2
• 2. What % of presumed acute lower GI Bleeding are found to have
upper GI source:
• A. 10%.
• B. 15%.
• C. 20%.
• D. 30%.
• E. 50%.
43. CME:3
• 3. What % of acute GI bleeding is due to small intestinal source:
• A. 1%.
• B. 5%.
• C. 10%.
• D. 15%.
• E. 20%.
44. CME:4
• 4. Bleeding from which colonic areas can present with melena
rather than hematochesia:
• A. Cecum.
• B. Transverse colon.
• C. Descending colon.
• D. Rectum.
• E. Splenic flexture.
45. CME:5
• 5. What % of melena could be from the colon:
• A. 10%.
• B. 20%.
• C. 30%.
• D. 40%.
• E. 50%.
46. CME:6
• 6. In acute lower GIB & hemodynamic instability, an upper GIT
source is best explored by:
• A. upper GI endoscopy.
• B. NT tube.
• C. Capsule endoscopy.
• D. RBC scan.
• E. CT Angio.
47. CME:7
• 7. The following should be the goal in patients with acute lower GIB
before enedoscopic evaluation except:
• A. Normal BP.
• B. Normal heart rate.
• C. Hb > 7 gms in low risk patients.
• D. Hb > 9 gram in high risk patients.
• E. Hb > 9 grams in all patients.
48. CME:8
• 8. In acute LGIB endoscopic hemostasis can be done safely without
the use of reversal agents , with INR up to:
• A. 3.
• B. 4.
• C. 2.5.
• D. 5.
• E. 6.
49. CME:9
• 9. In patients with acute LGIB, endoscopic intervention can be
carried out safely with platelet counts:
• A. 50000.
• B. 10000.
• C. 20000.
• D. 30000.
• E. 5000.
50. CME:10
• 10. Colonic preparation in acute LGI bleeding should be
adminstered over:
• A. One hour.
• B. Two hours.
• C. Three hours.
• D. Five hours.
• E. Six hours.
51. CME:11
• 11. In patients with ongoing acute LGI bleeding, colonoscopy should
be performed after stabilization & adequate preparation within:
• 6 hours.
• B. 12 hours.
• C. 24 hours.
• D. 36 hours.
• E. 48 hours.
52. CME:12
• 12. In patients with acute LGI bleeding but not ongoing,
colonoscopy should performed after stabilization & adequate
preparation within:
• 6 hours.
• B. 12 hours.
• C. When next available.
• D. 36 hours.
• E. 48 hours.
53. CME:13
• 13. Endoscopic interventions indications for acute LGI bleeding compared to
acute UGI bleeding is:
• A. The same.
• B. Different.
• C. Only done for spurting vessels.
• D. Done done for adherent clot.
• E. Contact thermal modalities are preferred.
54. CME:14
• 14. The preferred endoscopic intervention indicated for acute LGI
bleeding due to diverticulosis is:
• A. Clips.
• B. Bands.
• C. Thermal.
• D. APC.
• E. Saline injection only.
55. CME:15
• 15. The preferred endoscopic intervention indicated for acute LGI
bleeding due to angiodysplasia is:
• A. Clips.
• B. Bands.
• C. Thermal.
• D. APC.
• E. Saline injection only.
56. CME:16
• 16. The preferred endoscopic intervention indicated for acute LGI
bleeding post-polypectomy is:
• A. Clips.
• B. Bands.
• C. Thermal.
• D. APC.
• E. Saline injection only.
57. CME:17
• 17. The preferred endoscopic intervention indicated for acute LGI
bleeding from post-polypectomy if through the scope clips are not
available is:
• A. Over the scope clips.
• B. Bands.
• C. Thermal contact therapy.
• D. APC.
• E. Saline injection only.
58. CME:18
• 18. Before surgery is considered for acute LGI Bleeding , the most
important point is:
• A. Localize the bleeding site.
• B. Risk stratification.
• C. Anesthesia tolerance.
• D. Good history taking.
• E. Hb level.
59. CME:19
• 19. The diagnostic modality to localize the bleeding site in acute LGI
Bleeding before angiography is:
• A. CT Angio.
• B. RBC scan.
• C. MRI Angio.
• D. CT Colonography.
• E. Barium enema.
60. CME:20
• 20. Radiographic intervention is indicated for acute LGI bleeding
with all the following characteristics except:
• A. Ongoing bleeding.
• B. High risk patient.
• C. Preparation intolerants.
• D. Colonoscopy intolerants.
• E. All massive bleeders.
61. CME:21
• 21. In the majority of patients with acute LGI bleeding the initial
diagnostic modality is:
• A. Colonoscopy.
• B. CT Angio.
• C. Angiograpy.
• D. Barium enema.
• E. CT colonography.