Ultrasound is useful for evaluating the pancreas and detecting complications of acute and chronic pancreatitis. In acute pancreatitis, ultrasound can identify changes in the pancreas such as areas of hypoechogenicity and peripancreatic inflammation. Complications like pseudocysts and vascular thromboses are also detectable. Chronic pancreatitis is characterized on ultrasound by ductal dilatation, calcifications, and changes in pancreatic echotexture. Differentiating chronic pancreatitis from pancreatic cancer can be challenging. CT or MRI may be needed when ultrasound findings are inconclusive or to further evaluate necrosis in acute pancreatitis.
Brief description on the benign tumors of liver that includes hemangioma, focal nodular hyperplasia, regenerative nodular hyperplasia, dysplastic foci, dysplastic nodules and focal fatty change.
Brief description on the benign tumors of liver that includes hemangioma, focal nodular hyperplasia, regenerative nodular hyperplasia, dysplastic foci, dysplastic nodules and focal fatty change.
Imaging assessment of malignant focal and diffuse liver lesions from Ultrasound to Mri with overview of interventional modalities and diagnostic snippets,
Pancreatitis -a detailed study ( medical information )martinshaji
Pancreatitis is the Inflammation of the pancreatic parenchyma. Acute condition of diffuse pancreatic inflammation & auto digestion, presents with abdominal pain, and is usually associated with raised pancreatic enzyme levels in the blood &urine. this is a detailed study pancreatitis describing factors such as definition , epidemiology , etiology , pathophysiology , treatment , prevention , imaging techniques , diagnosis , lab investigations , images , drugs , control etc
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Imaging assessment of malignant focal and diffuse liver lesions from Ultrasound to Mri with overview of interventional modalities and diagnostic snippets,
Pancreatitis -a detailed study ( medical information )martinshaji
Pancreatitis is the Inflammation of the pancreatic parenchyma. Acute condition of diffuse pancreatic inflammation & auto digestion, presents with abdominal pain, and is usually associated with raised pancreatic enzyme levels in the blood &urine. this is a detailed study pancreatitis describing factors such as definition , epidemiology , etiology , pathophysiology , treatment , prevention , imaging techniques , diagnosis , lab investigations , images , drugs , control etc
please comment
thank u
The lecture overviews the different situations where cholecystitis can be fatal,if not accurately diagnosed.Different types of dangerous cholecystitis are illustrated with their imaging findings.
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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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
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
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
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.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
1. REFERENCES : RUMACK, RADIOPEDIA,
RADIOLOGY ASSISTANT.
BY : DR. JUHI PATEL
1st Year Resident Doctor
2. ANATOMY.
NORMAL APPEARANCE OF PANCREAS ON
ULTRASOUND.
ACUTE PANCREATITS.
CHRONIC PANCREATITIS.
DIFFENETIAL DIAGNOSIS.
3.
4.
5.
6.
7. Patient position :
• Supine .
• Left lateral decubitus position.
Vascular landmarks are :
• Inferior vena cava (IVC) dorsally.
• SMA and SMV medially.
• GDA and pancreaticoduodenal arcade
anterolaterally.
8.
9. Uncinate process :
Is a portion of the caudal pancreatic head
that wraps behind the SMA and SMV, ending
in a point oriented medially.
The uncinate process is medial and dorsal to
the SMA and SMV.
10. Patient position :
• Supine.
• Left lateral decubitus.
• After water intake (sometimes combined with sitting
position).
Body lies ventral to following vascular
landmarks :
• Splenic vein
• Its confuence with SMV
• SMA
12. Patient position:
• After water intake ask the patient to lie in right
anterior oblique position.
• Right lateral decubitus position (coronal imaging
through spleen and left kidney).
Colour doppler reveals splenic artery and
vein which facilitates identification of tail.
13.
14. Echogenicity : is compared to liver.
• Iso or hyperechoic to liver.
• Echogenicity increases with age.
Texture :
• Homogenous to lobular .
Size :
• Head : 6 to 28 mm.
• Body : 4 to 23 mm.
• Tail : 5 to 28 mm.
Pancreatic duct diameter:
• Head : 3 mm.
• Body : 2.1 mm.
• Tail : 1.6 mm.
22 mm (mean plus 3 standard
deviations)
16. Gall stones : 40 %
Alchoholism : 40 %
Idiopathic : 10%
Other : 10%
• injury (trauma).
• Hereditary.
• high fat levels in the blood.
• Surgery.
17. Blockage of the pancreatic duct leads to increased
pressure in pancreatic duct and rupture.
Pancreatic fluid (proteolytic and lipolytic enzymes)
ruptures into pancreas parenchyma and potential spaces.
18. Targets of Inflammatory spread
in Acute Pancreatitis
1= spread into the
lesser sac
2 = spread into the
transverse mesocolon
3 = spread into the root
of the bowel mesentery
4 = extension into the
duodenum
5= inferior spread into
the remainder anterior
pararenal space
Gore and Levine, Textbook of Gastrointestinal Radiology
21. Look for the changes in pancreas.
Look for secondary peripancreatic
changes.
Try to find out cause of acute pancreatitis
• Gall bladder and bile duct stones.
• Biliary sludge.
22. In Pancreas look for :
1. Echogenicity :
May be normal.
Focal areas of hypo / hyperechogeicity and
inhomogenicity may occur.
2. Size of pancreas : 22 mm (mean plus 3 standard
deviations)
DECREASES INTERSTITIAL EDEDMA
INCREASES HEMORRHAGE, NECROSIS,
FAT SAPONIFICATION
23.
24.
25. Look for peripancreatic pathology :
pancreatitis associated inflammation.
• Extra pancreatic inflammatory changes may be
detected even when the pancreatic contour is
normal and the pancreas is not obviously
enlarged.
• Pancreatic inflammation is typically hypoechoic or
anechoic.
26. • Inflammation is most often seen ventral
and adjacent to pancreas in :
prepancreatic retroperitoneum
Right and left anterior pararenal spaces.
The perirenal spaces.
The transveres mesocolon
28. Peri vascular space :
• Spread of inflammation especially around splenic
vein and spleno portal confluence, is characteristic
of Acute pancreatitis.
• This peri vascular inflammation may explain why
some patients develop thrombosis of portal and
splenic veins.
33. LAB FINDINGS :
Elevated pancreatic enzymes (Amylase and Lipase):
blockage of secretion leads to leakage through
basolateral membrane into circulation
Lipase: sensitivity 86-100%, specificity 50-99%
(Normal value : 0-160 U/L)
Amylase: sensitivity 75-92%, specificity 20-60%
(Normal value : 23-85 U/L. Some lab results upto 140
U/L)
34. LOCAL SYSTEMIC
Acute fluid collections ARDS
Pancreatic abscess Multiple organ dysfunction syndrome
Pseudocysts DIC
Necrosis Hypocalcemia
Infected necrosis Insulin dependent DM
Hemorrhage Pleural effusion
Venous thrombosis GI haemorrhage
Pseudoaneurysms
35. ACUTE FLUID COLLECTIONS :
• The Atlanta Classification suggests that
differentiation between acute fluid collection and
pseudocyst should be made after 4 weeks from
the onset of disease.
• Others studies suggest the fluid collection that
persist for 6 weeks can be considered a
pseudocyst.
38. NECROSIS :
• Cannot be definitely diagnosed on ultrasound.
• CECT : non enhanced pancreatic parenchyma
greater then 3 cm or involving more than 30% of
area of pancreas.
39. ABSCESS :
• There are two different types of acute pancreatitis
associated abscess :
The Atlanta Classification pancreatic abscess : an
infected fluid collection / pseudocyst (which has minimal
necrosis).
Infected necrosis with fluid collection, which arises from
infetion of necrotic pancreatic tissue.
43. Chronic pancreatitis is characterised by
intermittent pancreatic inflammation with
progressive, irreversible damage to gland.
CP ultimately leads to permanent structural
change and deficient endocrine and
exocrine function.
44. Some lasting morphologic changes include :
• Alteration in parenchymal texture.
• Glandular atrophy.
• Glandular enlargement.
• Focal masses.
• Dilatation and beading of pancreatic duct (often
with intra ductal calcification).
• Pseudocysts.
47. HALLMARK OF CP :
• Ductal dilatation.
• Calcifications (look for colour comet tail artifact -
CCTA).
CT is superior to sonography in detecting
calcifications and ductal dilatations.
• Areas of increased and decreased echogenicity are
related to effects of patchy fibrosis. These areas are
subjective and difficult to appreciate.
58. Causes of portal vein thrombosis in CP :
• Intimal injury from recurrent inflammation.
• Chronic fibrosis and inflammation.
• Compression by either a pseudocyst or enlarged pancreas.
Pancreatitis associated thrombus in splenic or
portal vein often results in collaterals different from
those in portal hypertension from liver disease.
These collaterals, rather than conveying blood
away from the diseased liver, conduct blood
towards the liver, bypassing the clot.
59. Splenic vein thrombosis :
Occur more frequently than portal vein thrombosis.
Splenic vein thrombosis often results in left sided
(sinistral) portal hypertension.
This can result in isolated gastric varices. (the
hepatopetal pathway to bypass splenic vein clot
includes short gastric collateral that lead to gastric
mural varices, then flow to liver in coronary vein).
60.
61. It may be difficult or impossible to detect splenic
vein clot or even the splenic vein itself.
Therefore diagnosis of splenic vein clot may
depend on detection of collaterals, such as short
gastric varices or an enlarged coronary vein.
63. Portal vein thrombosis :
When the main portal vein is clotted, blood
flows to the liver around the clot.
If portal vein clot persist, these hepatopetal
collaterals may enlarge, resulting in
cavernous transformation of the portal vein.
Gall bladder varices were present in 30% of
the cases.
66. It is the rare complication of pancreatitis,
much less common than thrombosis.
It can occur in gastroduodenal, spelnic,
superior mesenteric arteries.
It shows ying and yang (red blue) colour
doppler appearance representing the
blood swirling in the lesion.
67.
68.
69. Focal pancreatic masses occur in
approximately 30% CP patients.
Carcinoma and pancreatitis associated
masses are easy to differentiate clinically
and by imaging.
70. CHRONIC PANCREATITIS CARCINOMA
Calcifications are multiple and ductal. Few coarse calcifications, usually
unrelated to ducts.
Multiple dilated branch ducts in
pancreatic head.
Hyperechoic masses even without
discrete calcifications, are usually
related to CP.
Uncalcified iso or hypoehoic mass is
non specific and requires biopsy for
confirmation.
Pseudocysts are more common in CP.
Occur anywhere in the gland, usually
arising in the areas of necrosis.
Usually are peripheral to body and tail
lesions.
73. Autoimmune Pancreatitis (AIP) :
Type of chronic pancreatitis more likely to be
confused for carcinoma.
2 types :
TYPE 1 – older age group, relapse common
TYPE 2 – younger, relapse less likely
Responds to steroids , prednisolone
HYPERIgG4 disease
74. 1. Imaging appearance of pancreatic
parenchyma and pancreatic duct.
2. Serum IgG4 level
3. Other organ involvement with IgG4
related disease
4. Pancreatic histology
5. Response to steroid therapy
78. • Nodular, bulky, enlarged
pancreas due to
infiltration.
• Retroperitoneal
adenopathy.
• Peripancreatic infiltration
(obliteration of fat planes).
• Primary may be seen in
case of metastatic
infiltration.
Lymphoma & Metastases
79. Perforated Duodenal Ulcer :
• Penetrating ulcers may infiltrate anterior
pararenal space, simulating pancreatitis.
• Less than 50% of cases have evidence of
extraluminal gas or contrast medium
collections.
• Pancreatic head may be involved.
80. NBM : atleast for 6 hours is required.
In acute pancreatitis changes may not be
apparent on ultrasound for 24 hours.
Differentiation of certain masses from
pancreatitis associated masses may not be
possible.
Necrosis cannot be definitely diagnosed on
ultrasound.
81. CT Scan:
• Modality of choice in acute and chronic
pancreatitis when ultrasound is not diagnostic.
• In acute pancreatitis to differentiate between
interstitial (80%) and necrotizing pancreatitis
(20%).
• Patients who do not manifest rapid clinical
response within 72hours with conservative
medical therapy.
82. MRI :
• It is particularly helpful in differentiating the fluid
and exudate component.
• When CT is not diagnostic, especially to
distinguish chronic pancreatitis from neoplasm.