15 cm in length, 60-140 gm, consists of head, body & tail; pancreatic duct empty into duodenum or common bile duct
Histologically, consists of 2 components:
1) Exocrine: 80-85%, consists of numerous glands (acini) lined by columnar basophilic cells containing zymogen granules, which form lobules; ductal system
Trypsin, chemotrypsin, aminopeptidase, amylase, lipase
2) Endocrine: islets of Langerhans, which are invaded by capillaries. Islets consist of:
4 main cell types: B (insulin), A (glucagon), D (somatostatin), PP cells (pancreatic polypeptide)
2 minor cell types: D1 (VIP) & enterochromaffin cells (serotonin
Management of Acute Pancreatitis By Dr. Dhaval Mangukiya
https://drdhavalmangukiya.com/
http://www.youtube.com/c/DrDhavalMangukiyaGastrosurgeonSurat
https://gastrosurgerysurat.blogspot.com/
severe acute pancreatitis has high mortality rate and there is always confusions in between physicians. This topic is about management of acute pancreatitis its complications and ongoing controvercies. hope this will help and clear the doubts among physicians, residents and medical students
Management of Acute Pancreatitis By Dr. Dhaval Mangukiya
https://drdhavalmangukiya.com/
http://www.youtube.com/c/DrDhavalMangukiyaGastrosurgeonSurat
https://gastrosurgerysurat.blogspot.com/
severe acute pancreatitis has high mortality rate and there is always confusions in between physicians. This topic is about management of acute pancreatitis its complications and ongoing controvercies. hope this will help and clear the doubts among physicians, residents and medical students
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
- 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
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.
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.
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
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.
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The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
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Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
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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.
2. ANATOMY & HISTOLOGY OF THE
P A N C R E A S
• 15 cm in length, 60-140 gm, consists of head, body & tail; pancreatic duct empty
into duodenum or common bile duct
• Histologically, consists of 2 components:
• 1) Exocrine: 80-85%, consists of numerous glands (acini) lined by columnar
basophilic cells containing zymogen granules, which form lobules; ductal
system
• Trypsin, chemotrypsin, aminopeptidase, amylase, lipase
• 2) Endocrine: islets of Langerhans, which are invaded by capillaries. Islets
consist of:
• 4 main cell types: B (insulin), A (glucagon), D (somatostatin), PP cells
(pancreatic polypeptide)
• 2 minor cell types: D1 (VIP) & enterochromaffin cells (serotonin)
3. Mortality/Morbidity:
• The overall mortality rate of patients with acute pancreatitis is 10-15%.
• In patients with severe disease, the mortality rate is approximately 30%.
• In the first week of illness, most deaths result from multi organ system
failure. In subsequent weeks, infection plays a more significant role, but
organ failure still constitutes a major cause of mortality.
• Sex:
• In general, acute pancreatitis affects males more often than females.
• The etiology in males is more often related to alcohol; in females, to
biliary tract disease.
4. AUTO PROTECTION
• First, proteins are translated into an inactive form called
pro enzymes.
• The pro enzymes are packaged in a para- crystalline
arrangement with protease inhibitors(zymogens
granules)
• Zymogen granules have an acidic pH and a low calcium
concentration, which are factors that guard against
premature activation
6. Pathogenesis:
• Autodigestion of pancreatic tissue by inappropriately activated pancreatic enzymes
• Trypsin has a major role:
• Activates other proenzymes (proelastase , prophospholipase )
• Converts prekallikrein to kallikrein (Kinin system)
• Hageman factor is activated
• Mechanisms of pancreatic enzyme activation:
• Pancreatic duct obstruction
• Primary acinar cell injury
• Defective intracellular transport of proenzymes within acinar cells
7.
8. ETIOLOGY
• REMEMBER -I GET SMASHED
• : Although pancreatitis has numerous etiologies, alcohol
dependence and biliary tract disease cause most cases. In 10-30%
of cases, the cause is unknown, and careful evaluation may
identify a rare etiology in 10% of cases.
• Metabolic: alcohol, hyperlipoproteinemia, hypercalcemia, drugs (e.g.
thiazides), genetic
• Mechanical: gallstones, traumatic & perioperative injury
• Vascular: shock, atheroembolism, polyarteritis nodosa
• Infections: Mumps, Coxsackie virus, Mycoplasma
• Idiopathic : 10-20% ; ? Genetic basis
I-idiopathic,G-gallstone(micro harrison),E-ethanol,T-trauma,S-
mumps,A-autoimmune dse,S-scorpion bite,H-
hyperkalemia/hypertryglyceridaemia,E-ercp(endoscopic retrograde
cholangiopancretography),D-drugs(NRTIS,protease inhibitor)
9.
10. SYMPTOMS
• History:
• The cardinal symptom of acute pancreatitis is abdominal pain, which is characteristically
dull, boring, and steady. Most often, it is located in the upper abdomen, usually in the
epigastric region, but it may be perceived more on the left or right side, depending on
which portion of the pancreas is involved.
• The pain radiates to the back in approximately half of cases.
• The duration of pain varies but typically lasts more than a day.
• The pain may be aggravated by eating or lying supine and it may be alleviated by
fasting or lying on the left side with the knees and hips flexed.
• Associated symptoms (eg, anorexia, nausea, vomiting) are common, and some patients
experience diarrhea due to indigestion.
• Avulsion to fatty foods may be reported
11. Physical exam:
• Distressed anxious patient
• Low grade fever
• Tachycardia
• Shock-(i)due to exudation of blood and plasma proteins into
retroperitoneal space. (ii)kininins- vasodilation, increased vascular
permeability (iii)systemic effects of lipolytic enzymes released into
circulation
• Jaundice-infrequent-edema of head of pancreas
• Erythematous skin nodules-subcut fat necrosis
• 10-20 %→ pulmonary findings-rales, atelectasis, pleural effusions
• Decreased bowel sounds
• Pancreatic pseudocyst-palpable in upper abdomen
• Cullens sign-faint blue discolouration around umblicus due to
hemoperitoneum
• Turner”s sign → blue-red-purple discolouration or green brown
discolouration in the flanks-Tissue catabolism of hemoglobin-Latter 2
rare. If present-necrotising pancreatitis
12. Diagnosis of acute pancreatitis
Amylase and lipase-elevations of 3 times above reference range
considered diagnostic
Amylase not specific for pancreatic dis-can occur in small intestine
obstruction, mesenteric ischaemia, tubo-ovarian disease, renal insufficiency,
parotitis
Serum T ½ of amylase is short-elevations return to ref range
within a few days.
Lipase-longer half life more specific to the pancreas. Note-levels of
the two do not correlate with prognosis
REF-Lipase-56-239
-Amylase-0-260U/L(under 18 years)
-35-115U/L(over 18years)
13. ….Diagnosis
Liver enzymes-ALP, total bil, AST, Alanine aminotransferase-
search for gall stone pancreatitis if elevated
Alanine aminotransferase >150U/L-gallstone pancreatitis
Calcium levels-hypercalcemia as aetiolgy or saponification if
hypocalcemia- correlates well with severity of disease. Levels
lower than 7 mg/dL (when serum albumin is normal) are
associated with tetany and an unfavorable prognosis.
Cholesterol, TGs, if elevated search for aetiology
(Hyperlipidimia) -fasting triglyceride levels above 1000
mg/dL.
Baseline TGs can be lower in acute pancreatitis
14. ….Diagnosis…
C.B.C –Hct >47 proposed as a sensitive measure of more
severe disease, however this has subsequently been shown
to have value only as a negative predictor of severe disease
i.e. lack of severe hemoconcentration rules out severe
disease
Leukocytosis-inflammation or infection
CRP-higher levels-organ failure. CRP not specific.
BGAs if patient is dyspnoic
Trypsin and its precursor trypsinogen 2 in both urine and
peritoneal fluid-not widely used
15. ….DIAGNOSIS
Imaging-Radiologic findings are inconstant and non-
specific. CXR, K.U.B- exclude other diagnosis
CT scan may confirm impression of acute pancreatitis
and severity (esp. Contrast Enhanced CT-CECT) .
Abdominal ultrasonography-detects gall stones-
Sensitivity in acute pancreatitis 70-80 %
MRCP-emerging role.T2 weighted images provide a
non invasive image of the biliary and pancreatic
ducts
Endoscopic ultrasonography-more details than
transcutaneous U/S-Principal role –evaluating
microlithiasis, biliary sludge, periampulary lesions
16. Diagnostic procedures
ERCP- evaluates biliary and pancreatic ductal
system. Should be used with caution in pts with
acute pancreatitis.Never to be used as a first line
tool in this disease.
Used in suspected choledocholithiasis and biliary
pancreatitis with worsening jaundice
CT-guided needle aspiration-diff sterile from
infected necrosis. Evaluate specimen for culture
and sensitivity and gram stain
19. ASSESSMENT OF SEVERITY
• Ranson's criteria- are generally used in assessing the severity
of acute alcoholic pancreatitis on presentation (pancreatitis
due to other causes is assessed by similar criteria).
1. When three or more of the following are present on
admission, a severe course complicated by pancreatic
necrosis can be predicted with a sensitivity of 60–80%:
• Age over 55 years.
• White blood cell count over 16,000/mcL.
• Blood glucose over 200 mg/dL.
• Serum LDH over 350 units/L.
• AST over 250 units/L.
20. 2. Development of the following in the first 48 hours
indicates a worsening prognosis:
• Hematocrit drop of more than ten percentage points.
• BUN rise greater than 5 mg/dL.
• Arterial Po2 of less than 60 mm Hg.
• Serum calcium of less than 8 mg/dL.
• Base deficit over 4 mEq/L.
• Estimated fluid sequestration of more than 6 L.
22. TREATMEMT OF ACUTE
PANCREATITIS
• 85 -90 % of patients the disease is self limited, subsides in 3 to 7 days
of rx
• Conventional measures
• (i) analgesics- meperidine, up to 100–150 mg intramuscularly every 3–4
hours as necessary
• (ii) IV fluids and colloids
• (iii) no oral intake
• (iv) NG suction to decrease gastrin release and prevent gastric contents from
entering duodenum.
Anticholinergics-no therapeutic advantage
• Antibiotics-used but RCTs have shown no benefit in mild to
moderate severity disease
Current evidence- prophylactic antibiotics in necrotizing acute
pancreatitis-decreases sepsis and mortality
23. ….TREATMENT…
• Surgery-infected pancreatic necrosis.
Data support delaying surgical debridement of
necrotic tissue for at least 2 weeks for viable
pancreatic tissue to become evident
Patients with severe gall stone induced pancreatitis
may improve if papillotomy is done within 36
to 72 hours
Studies show that only those pts with gall stone
pancreatitis who are in the very severe group
should be considered for ERCP
24. …TREATMENT…
• Hypertryglyceridemia associated
acute pancreatitis-
• (i)wt loss
• (ii)Lipid restricted diet
• (iii)exercise
• (iv)avoid alcohol and drugs e.g. vitamin
A, thiazides, beta blockers
• (v) control DM
25. INFECTED PANCREATIC NECROSIS
• Diffuse infection of acutely inflamed, necrotic
pancreas occurs in the first 1 to 2 weeks of
onset of acute pancreatitis
• Treated by surgical debridement.
• Mostly gram negative bacteria of gut origin.
• Early diagnosis-CT guided needle aspiration
• Imipenem-cilastatin 500 mg TID for 2 weeks-
prophylactic
26. Pancreatic abscess
• Ill defined collection of pus, evolves over
longer period 4 to 6 weeks
• Life threatening but lower rate of surgical
mortality
• Treated surgically or in selected cases
percutaneous drainage
27. PANCREATIC PSEUDOCYST
• Collection of tissue, fluid, debris, pancreatic
enzymes, and blood. Develops over 1-4 weeks.
Forms in 15% of patients
• Wall consists of necrotic tissue, granulation tissue,
fibrous tissue
• Preceded by pancreatitis in 90% of cases, trauma in
10% of cases
• May be two or more.
• 85% located in body or tail.15% head
28. …Pseudocyst…
• Abdominal pain with or without radiation to
the back.
• Palpable tender mass in the middle or left upper
abdomen
• Serum amylase elevated in 75% of patients at
some point during illness
• Sonography reliable in detecting pseudocysts.
Serial u/s indicates resolution or not
• CT complements U/S in diagnosis
• Recent studies show non interventional,
expectant management is the best course in pts
with minimal symptoms with no alcohol use
29. Pseudocyst….
• Complications-pain caused by expansion, rupture,
hemorrhage, abscess
• Increase in size, localized bruit over mass, sudden
drop in Hb/Hct-possibility of hemorrhage from
pseudocyst
• U/S or CT guided repeated needle aspiration/
catheter drainage-success rate 45-75 % success rate
30. Pseudoaneurysm-
• In 10% of pts. Reflects distribution of pseudocyst
and fluid collections.
• Splenic artery most commonly involved, followed by
inferior and superior pancreatico duodenal arteries
• Thin cut CT usually reveals a contrast enhanced
lesion within or adjacent to suspected pseudocyst.
Arteriography is necessary to confirm diagnosis
35. THANK YOU let meet in surgery
References:
HARRISON’S PRINCIPLES OF INTERNAL
MEDICINE.
ROBBINS AND COTRAN PATHOLOGICAL BASIS OF
DISEASES 9TH EDITION
William F. Ganong
eMedicine
36. • I-idiopathic
• G-gallstones-the bigger it is the lesser it cause and vice versa
• E-ethanol
• T-trauma
• S-mumps
• M-auto immune dise
• S-scorpion bite
• H-hyperkalemia/hypertryglyceridaemia
• E-ercp(endoscopic retrograde cholangiopancreatography)
• D-drugs-NRTI and protease inhibitors