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This Presentation unravels the complexities surrounding pancreatitis, exploring

the latest insights, diagnostic modalities, and management strategies.
PANCREATITIS
PRESENTATION
TABLE OF
CONTENTS

00 01 02

DEFINATION OF
ETIOLOGY PATHOPHYSIOLOGY
PANCREATITIS
TABLE OF
CONTENTS

03 04 05

SIGNS AND LAB

COMPLICATIONS
SYMPTOMS INVESTIGATIONS
TABLE OF
CONTENTS

06 07

CLINICAL PHYSICAL
EXAMINATIONS ASSESMENT
 DEFINATION OF
PANCREATITIS
PANCREATITIS PANCREAS
Pancreatitis is inflammation The pancreas is a long flat gland
of the pancreas. that's tucked behind the
Inflammation is immune stomach. The pancreas helps the
system activity that can cause body digest food and regulates
swelling, pain and changes in blood sugars.
how an organ or tissues work.
TYPES OF PANCREATITIS

1 2
ACUTE CHRONIC
Emergency Condition Prolonged and frequently
lifelong disorder resulting
from the development of
fibrosis within the pancreas
 DEFINATION OF ACUTE AND CHRONIC
PANCREATITIS
1 2
ACUTE PANCREATITIS CHRONIC PANCREATITIS
• Acute condition of diffuse • Chronic pancreatitis is a progressive

pancreatic inflammation and inflammation disorder that leads to

autodigestion presents with irreversible destruction of exocrine

abdominal part and is usually and endocrine pancreatic.

associated with raised part Pancreatitis caused by atrophy or

enzyme levels in the blood and replacement with fibrotic tissues.

urine.
• Reversible inflammation of the • Functional consequences include

pancreas. severe abdominal pain, diabetes

• Ranges from mild to severe. mellitus, malabsorption.

ETIOLOGY
 ETIOLOGY
• The pancreas has two major roles.
1. It produces insulin which helps the body manage and use sugars.
2. Pancreas also produces dietary juices called enzymes that help with digestion.

• The pancreas makes and stores turned off versions of the enzymes. After the pancreas
sends the enzymes into the small intestines. They are tuned on breakdown protein in
the small intestine.

• If the engines are tuned on too soon, they can start acting like digestive juices inside the
Pancreas.

• The action can irritate, damage, or destroyed. This problem in turn lead to immune
system responses that causes swelling and other events. That affect how the pancreas
works.
1 ETIOLOGY : ACUTE PANCREATITIS
• Blockage in the bile ducts caused
by gallstones.
• Heavy alcohol use.
• Certain medicines.
• High triglyceride levels in the
blood.
• High calcium levels in the blood.
• Pancreas cancer.
• Injuries from trauma or surgery.
2 ETIOLOGY : CHRONIC PANCREATITIS
• Damage from Repeated cause of
acute pancreatitis.
• Heavy alcohol use.
• Inherited genes linked to
pancreatitis.
• High triglyceride levels in the blood.
• High calcium levels in the blood.
• Sometimes a cause of pancreatitis is
never found. This is known as
Idiopathic pancreatitis.
 02
PATHO -
PHYSIOLOGY
 ACUTE PANCREATITIS
❖ The localized destruction characterizes the Pathophysiology in the pancreas and systematic
inflammatory response.

❖ The major inciting event in the premature act of the enzyme trysinogen to trypsin without
acinat cell instead of the duct lumen.

❖ The leading cause is an elevation is duct pressures (such as the duct obstruction) and problem
with calcium homeostalsis and pH

❖ Many toxins responsible for causing Pancreatitis cause ATP depletion, increasing the intra-
acid calcium concentrations that may stimulate the early activation of Trypsinogen to trypsin,
activating enzymes such as elastic and phase lipases.

❖ This premature activation of this zymogenesis causes extensive tissue damage and damage
Associated Molecular Patterns (DAMPs). This release of DAMPs is associated with recruiting
neutrophills and initiating the inflammatory cascade.
 ACUTE PANCREATITIS
❖ The inflammatory cascade then leads to the systematic manifestations of acute pancreas. It
ultimately produces capillary. Permeability and endothelium damage with micro vascular
thrombosis that gives rise to multi organ dysfunction syndrome (MODs) as the main cause of
Morbidity and mortality in the setting of acute pancreatitis.

❖ Some individuals also have a genetic predisposition for pancreatitis and suffer from recurrent
acute pancreatitis. Progressing to chronic pancreatitis.

❖ Not surprisingly, teh associated genes are involved in activating trysiongen to trypsin.

❖ Many genes play a role in recurrent pancreatitis. E.g. - Cystic fibrosis transmembrane
conductance regulator (CETR) gene. Cationic trypsinogen gene (PRSSI) gain of function
mutations. Mutations of trypsin degrading enzyme (CTCR) chymotrypsin C & (SPINKI)
pancreatic secretory trypsin inhibitor.

❖ Furthermore, they are also involved in the increasingly acknowledged spectrum of diseases
from acute to chronic pancreatitis.
 CHRONIC PANCREATITIS
❖ The Pathogenesis of chronic pancreatitis seems involve genetic factors, and environmental factors
studies have identified pancreatitis susceptibility genes associated with loss of function mutation.

❖ There are two main theories on the pathogenesis of Chronic pancreatic disease. One theory is that of
impaired bicarbonate secretion, which cannot respond to the increased secretion of pancreatic
proteins, These abundant proteins subsequently combine to form plugs within the lobules and ducts.
This leads to calcification and stone formation.

❖ The other theory involves intraparenchymal activation of digestive enzymes within the pancreatic
gland, possibly due to genetic or external influences such as alcohol diminishes the cell's ability to
respond Calcium signaling. This alters the feedback mechanism and promotes a cycle leading to cell
death.
SIGNS AND
SYMPTOMS

03
SIGNS – ACUTE PANCREATITIS

Distressed, moving Pale, diaphoretic Low grade fever

continously or confusion
sitting still
SIGNS – ACUTE PANCREATITIS

Tachycardia, Shallow Breathing Hypertension

Tachypnea
SIGNS – ACUTE PANCREATITIS

Mild itchiness Abdominal Grey Tumer's sign,

distinction (ileus, Cullen's sign, Fox's
ascites) sign
SIGNS – ACUTE PANCREATITIS

Rebound Shifting dullness

Tenderness, reduced vowel
Rigidity sounds
 • Upper abdominal pain,
sudden onset, sharp severe
continous radiates to the back
reduced by learning forward.

• Generalized abdominal pain

radiates to the shoulder tips,
patients lies very still.

• Patient lies very still.

• Anorexia.

SYMPTOMS OF • Fever. Weakness.

ACUTE PANCREATITIS
SIGNS – CHRONIC PANCREATITIS

Abdominal Jaundice Biliary obstruction

tenderness
SIGNS – CHRONIC PANCREATITIS

Great Turner and Cullen Abnormal vitals.

sign – • Elevated temperature.
• Ecchymosis in flank • Tachycardia.
• Periumbilical ecchymosis • Hypotension
 • Early symptoms of chronic
pancreatitis are similar to the
acute pancreatitis.

❖ Symptoms occasional and

include :-
• Pain in the upper belly that is
spread into the back.
• Pain in the belly that gets worse
when you eat or drink alcohol.
• Diarrhea and oily stools.
• Nausea and vomiting.
• Severe abdominal pain that may
be constant or that comes back.
SYMPTOMS OF
• Weight loss.
CHRONIC PANCREATITIS
COMPLICATIONS
 COMPLICATIONS OF
ACUTE PANCREATITIS

1. LOCAL 2. REGIONAL 3. SYSTEMIC

• Acute fluid collection. • Vasculer - venous thrombosis • SIRS

• Psecedocyst. bleeding. • MODS

• Intestinal - Paralytic ileus • Respiratory complications.
• Pancreatic Necrosis.
Intestinal ischemia • Cardiovascular complications.
• Pancreatic abscess.
and Necrosis • Metabolic complication –
Cholestasis i. Hypocalcemia
Intestinal obstructions ii. Hyperglycemia
iii. DIC
Encephalopathy.
 COMPLICATIONS OF CHRONIC
PANCREATITIS

Chronic pancreatitis Calcification of the • Diabetes. • bile duct.

damages the insulin pancreas : This • Gall stones • Perforation.
producing cells of means the pancreatic • Kidney failure. • Abscess.
the pancreas. This tissue hardens from • Pancreatic cancer • Gastroparesis.
may cause these deposits of calcium • Stenosis of • Fistula formation.
complications. salts. common
LAB
INVESTIGATIONS
 1. Taste of function - Hormone
stimulation.
• Secretin / secretin CCK test.
• Fecal elastase
• Fecal chymotrypsin
• Serum trypsinogen
• Fecal fat
• Blood glucose.

LAB INVESTIGATIONS
 2. Taste of Structures -
• Endoscopia us
• ERCP.
• MRI / MRCP.
• CT
• Abdominal us
• Plain abdominal film.

LAB INVESTIGATIONS
CLINICAL
EXAMINATIONS
 CLINICAL EXAMINATIONS

• Identify the patient's general symptoms.

06
• Assess for the signs of the deteriorating pancreas.
• Investigate the abdominal pain.
• Collects the patient's family history.
• Review the patient's medical history.
PHYSICAL
ASSESMENT
PHYSICAL ASSESMENT
1. Conduct a through physical examination.
07
• General - Fever, Restlessness
• CNS.- decreased mentation
• HEENT - Yellowish eyes
• Respiratory - Tachypnea, basilar roles upon
auscultation
PHYSICAL ASSESMENT
• Cardiovascular - Tachycardia, hypotension 07
• Gastrointestinal - Abdominal tenderness, Abdominal
guarding distention. Hematemesis black terry stools.
• Abdominal pain that radiates to back, etc.
• Genitourinary - dark urine
• Integumentary - Yellowing skin (Jaundice), itchy skin
(prutitus), Pale skin, diaphoresis
PHYSICAL ASSESMENT
2. Ausculate the Bowel sounds - 07
• Diminished or absent bowel sounds are expected in an ileus
is present during auscultation for acute pancreatitis.

3. Check for pancreatic nercosis or hammorrh aging.

• Cullen sign-bleeding - in the peritoneur causes bluish
discoloration around the umbilious.
PHYSICAL ASSESMENT
07
• Grey tumours and bleeding - At the back of the peritoneum
results in ecchymosis along the flanks commonly seen with
cullens sign.
• Fox's sign - Retroperitoneal bleeding causes brushing over
the inguinal ligament.
 END OF THE
PRESENTATION
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OUR TEAM MEMBERS

RIYAZ ALAM NISHA

B.A.M.S Student B.A.M.S Student
(2nd Year) (2nd Year)