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PREPARED BY: MUHAMMAD ARIFF B. MAHDZUB
BACHELOR MEDICINE AND SURGERY (MBBS)
UNIVERSITY COLLEGE SHAHPUTRA, KUANTAN
MD-2508 (DIGESTIVE SYSTEM)
PROBLEM BASED LEARNING (PBL)
ACUTE
PANCREATITIS
TRIGGER 1
• Man
• 44 Y/O
• 160 pound (72 kg)
• Suffer epigastric pain (last 3 hour), radiate to
back
• Anatomical organ related
• Differential diagnose related
TRIGGER 2 (History)
• Already vomited clear material three times
• Alcoholic
• Likes fatty meal & has elevate fat in blood
TRIGGERS 3 (physical examination)
• Pulse 110/min
• Bp: 120/70 mmHg (normal)
• Esp. rate: 16/min (normal)
• temp: 38.3 C
• Exm abdomen
• Distension epigastrium, bowel sound are hypoactive,
percussion tenderness, involuntary guarding, referred
tenderness
• No diabetes, htn
• Sister had gallbladder removed
d/word
• percussion tenderness: Pain feel at area of
percussion
• involuntary guarding: abdominal muscle
spasm, caused by retroperitoneal
inflammation
• referred tenderness: Called reflex pain, pain
at other site
Trigger 4 (investigation)
• X-ray : dilated transvers colon with no-free air
• Hemoglobin: 15 g/dl
• Wbc: 15,000/ ul
• Serum amylase: 2,000 units/l (high)
• Acute pancreatitis
• Site of tenderness
• Onset of tenderness (when)
• Associating factor (symptom)
• Duration of pain (how long)
• Does it radiate to other part
• Characteristic of pain (crushing, burning,
palpate)
• What make pain worst
• How patient react to relieve the pain
ABDOMINAL REGION
TRANSPYLORIC PLANE : An upper
transverse line also known as Addison's
Plane, located halfway between the
jugular notch and the upper border of
the pubic symphysis. The plane in most
cases cuts through the pylorus of the
stomach, the tips of the ninth costal
cartilages and the lower border of the
first lumbar vertebra.
TRANSTUBECULAR PLANE : passing
through the iliac tubercles; behind, its
plane cuts the body of the fifth lumbar
vertebra.
Abdomen
Regions
Organs
Right
Hypochondriu
m
Liver, Gallbladder, Right Kidney, Small Intestine
Left
Hypochondriu
m
Spleen, Colon, Left Kidney, Pancreas
Epigastrium Stomach, Liver, Pancreas, Duodenum, Spleen,
Adrenal Glands
Right Lumber
Region
Gallbladder, Liver, Right Colon
Left Lumber
Region
Descending Colon, Left Kidney
Umbilical
Region
Umbilicus, Jejunum, Ileum, Duodenum
Right Iliac
Fossa
Appendix, Cecum
Left Iliac Fossa Descending Colon, Sigmoid Colon
Hypogastrium Urinary Bladder, Sigmoid Colon, Female
Reproductive Organs
What is Abdominal Pain?
• the term abdominal pain generally is used to
describe :
– pain originating from organs within the abdominal
cavity.
– Organs of the abdomen include the stomach, small
intestine, colon, liver, gallbladder, spleen, and
pancreas.
– Abdominal pain can range in intensity from a mild
stomach ache to severe acute pain.
– The pain is often nonspecific and can be caused by a
variety of conditions.
What Causes Abdominal Pain?
• Inflammation (appendicitis, diverticulitis, colitis),
• Stretching or distention of an organ (obstruction
of the intestine, blockage of a bile duct by
gallstones, swelling of the liver with hepatitis)
• Loss of the supply of blood to an organ (ischemic
colitis).
• Constipation
• Diarrhoea
• Acid reflux
Pancreas: type of cell and
secretion
THE PANCREAS
• Combination of two glands
a. Exocrine pancreas
o Secrete substances into the intestine
o enzymes
b. Endocrine pancreas
o Secrete substances into the bloodstream
o hormones
The exocrine pancreas
• It has 2 types of cells:
–Acinar cells :
• Produce digestive
enzymes:
–Protease, amylase,
lipase and peptidases
–Duct cells :
• Alkaline Fluids
–Bicarbonate ions
–Water
The endocrine pancreas
• Part of pancreas that made up endocrine
function is Islets of Langerhans
• 4 main types of cells:
– α alpha cells : Glucagon
– β beta cells : Insulin
– Δ delta cells : Somatostatin
– PP cells (γ (gamma) cells) : Pancretic polypeptide
• The islets of Langerhans play an imperative role
in glucose metabolism and regulation of blood
glucose concentration
 GALLSTONES
Hard pieces of stone-like
Produced in the gallbladder
Block the bile duct
Stopping pancreatic enzymes from traveling to the small intestine
Forcing them back into the pancreas
It begin to irritate the cells of the pancreas
Causing the inflammation
ALCOHOLISM
 How alcohol actually triggers the inflammation in the pancreas
is not clear.
 The molecules in alcohol interfere with the cells of the
pancreas.
 Causing the enzymes to start digesting it.
 Stopping them working properly.
 INJURY TO PANCREAS
 Car accident or bad fall leading to abdominal trauma.
 accidental damage during a procedure to remove gallstones or examine
the pancreas
 AUTOIMMUNE DISEASE
 own immune system attacks healthy cell
 Associated with lupus or Sjogren's syndrome
 INFECTION
 Viral – mumps virus , HIV
 IDIOPATHIC
 Idiopathic pancreatitis
 No obvious cause was identified
Pathophysiology of Acute
Pancreatitis
Pathogenesis of acute pancreatitis
Interstitial oedema
Impaired blood flow
Ischaemia
Acinar cell injury
Interstitial inflammation
oedema
Gallstone
Chronic alcoholism
Release of intracellular
proenzymes and
lysosomal hydrolases
Activation of enzymes
ACTIVATED ENZYMES
Delivery of proenzymes to
lysosomal compartment
Intracellular activation of
enzymes
Proteolysis
(proteases)
Fat necrosis
(lipase, phospholipase)
Haemorrhage
(elastase)
Alcohol, drugs
trauma, ischaemia,
viruses
Metabolic injury
(experimental)
Alcohol, duct obstruction
DUCT OBSTRUCTION ACINAR CELL INJURY DEFECTIVE INTRACELLULAR
TRANSPORT
pathogenesis
progression
Acute Pancreatitis; Haemorrhage and necrosis
Normal pancreas
Acute pancreatitis
MARIA
INTRODUCTION OF VOMITTING
• Known as emesis / throwing up
• Involuntary, forceful expulsion of the contents of
one's stomach through the mouth and sometimes
the nose.
• Not same as regurgitation.
MARIA
WHAT CAN YOU EXPECT FROM THE
VOMITUS?
QUANTITY COLOUR
CONTENTS
ONSET &
DURATION
MARIA
•Large amount.
•Small amount.
MARIA
GREEN/DARK
YELLOW
FRESH
BRIGHT RED
BROWNISH -
RED
FROTHY PINK
COLOUR
COFFEE-
GROUND
GREEN/DARK
YELLOW
FRESH BRIGHT
RED
BROWNISH
RED
FROTHY PINK COFFEE
GROUND
MARIA
MARIA
Undigested
food
Blood
Bile Fecal
MARIA
4.Onset and duration
MARIA
AMYLASE
• enzyme
• begins the chemical process of digestion
• catalyses the hydrolysis starch—sugars
• 3 type-α-Amylase, β-Amylase, γ-Amylase
• Pancreas, salivary gland -alpha amylase
• hydrolyse dietary starch -
disaccharides ,trisaccharides converted by other
enzymes to glucose -energy
• Foods large amounts of starch, little sugar,
( rice,potatoes) -slightly sweet taste as chewed- amylase
degrades starch – sugar
• producing salivary amylase-gene AMY1,-originated in
pancreas
amylase
The normal range is 23
to 85 units per liter
(U/L). Some
laboratories give a
range of 40 to 140 U/L
pancreas damage @
inflamed-amylase in
blood
urine
By blood@urine sample
Some can affect
amount of detectable
amylase
Amylase
blood test
• Some medications that could heighten the amount of
amylase in the blood include:
• asparaginase
• aspirin
• birth control pills
• cholinergic medications
• ethacrynic acid
• methyldopa
• opiates (codeine, meperidine, morphine)
• thiazide diuretics (chlorothiazide, hydrochlorothiazide,
indapamide, metolazone)
Indication of high amylase count
• Acute or chronic pancreatitis: enzymes - help break down food in
intestines -malfunction - begin breaking down the tissues of the
pancreas. Acute pancreatitis - sudden - not last long, chronic
pancreatitis does improve , worsens over time.
• Cholecystitis: inflammation of the gallbladder. Cholecystitis is
usually caused by gallstones. Gallstones are deposits of hardened
cholesterol or other substances that can form in the gallbladder,
and cause blockages. This condition can also sometimes be caused
by tumors.
• Macroamylasemia: the presence of macroamylase in the blood.
This is an abnormal compound of the enzyme and a protein.
• Gastroenteritis: inflammation of the gastrointestinal tract.
• Tubal pregnancy: the fertilized egg (embryo) is
in one of the fallopian tubes (tubes that
connect the ovaries to the uterus) instead of
in the uterus. This is also called an ectopic
pregnancy, which is a pregnancy that takes
place outside the uterus.
• Other conditions: can also cause elevated
amylase counts, including salivary gland
infections, or intestinal blockages.
Indications of low count of amylase
• preeclampsia: a condition in pregnant
women, also called toxemia of pregnancy.
Signs of this condition also include high blood
pressure.
• damaged pancreas
• kidney disease
FAT METABOLISM
• The body has limited supply of glucose.
• 3 sources of fatty acid for energy metabolism
- dietry tryacylglycerol
- tryacylglycerol that synthesize in liver
- tryacylglycerol stored in adipocytes
• When foods enter the stomach, it will breakdown
into components such as carbohydrates, proteins
and fats.
• Dietry tryacylglycerol comes from the fat in the foods
we eat and the process of breakdown start to occurs
in small intestine not in the stomach.
In the small intestine,
bile salt from the gall
bladder will emulsify the
realtively insoluble
dietry fat to form
micelles.
The micelles have non-polar
core and surrounded by bile
salts.
R-group are non-polar and
so they point towards the
centre of the micelles.
After that, as micelles moving
downwards the small
intestine, pancreatic lipase will
degrades the triacylglycerol
into fatty acids and glycerol.
Then, the 3 Fatty acids and 1
glycerol packaged with
apoprotein and cholesterol
into blood-soluble-complex
called chylomicrons.
The chylomicrons will
cross blood vessel
membrane and move
into blood stream.
From here on, the
chylomicrons will have 2
possible pathways:
-Stored in adipocytes
-Move to muscle cells
For fat storage in adipocytes,
the triacylglycerol is cleaved
on the wall of blood vessel
by lipoprotein lipase into
fatty acid and glycerol.
Then it will move to
adipocyte cells and stored as
fat droplets.
However, if the person
exercise or do hard
chorus after that, the
fat then will be utilized
by muscle cells as
energy through beta-
oxidation
to form carbon dioxide
and ATP.
Up to this point we have
described dietry fatty acid
pathway either stored in
the adipocytes or
immediately utilized.
During strenous exercise,
muscle use up the small
amount of the body’s stored
glycogen. So, in order to
compensate that insufficient
energy, the energy that
stored as fat droplets in
adipocytes is released.
Epinephrin or glucagon leaves
bloodstream and binds to
adipocytes receptor.
This will allow adenylate cyclase
to convert ATP into cAMP.
Then, cAMP will bind to protein
kinase and activates it.
Activated protein kinase will
Proceeds to bind to
triacylglycerol lipase and
activating it.
Once activated, the
triacylglycerol lipase is able
to break triacylglycerol into
fatty acid and glycerol.
Then fatty acid molecules are
pick up by the protein albumin
in the blood stream.
Serum albumin travels through
the blood vessels and release
the fatty acid molecules into
myocytes.
Finally, the fatty acid will
undergo beta-oxidation to
produce carbon dioxide and ATP
Complication of Pancreatitis.
Early
complications
infections
Malnutrition
Abdominal swelling
Systemic inflammatory response
High blood glucose
Severe respiratory failure
Late
complications
Recurrent pancreatitis
Pancreatitic pseudocyst
Acute necrotizing pancreatitis
Early complications
Infection.
• make pancreas vulnerable to bacteria and infection  inflammations 
interruption to blood supply  necrosis
• require intensive treatment, such as surgery to remove the infected tissue.
Diabetes.
• Damage to insulin-producing cells in pancreas
• from chronic pancreatitis can lead to diabetes
• affects the way our body uses blood sugar.
Kidney failure
• can be treated with dialysis if the kidney failure is severe and persistent.
Malnutrition.
• Both acute and chronic pancreatitis can cause pancreas to produce fewer of the
enzymes that are needed to break down and process nutrients from the food
• lead to malnutrition, diarrhea and weight loss, even though patient may be eating
the same foods or the same amount of food..
Pleural effusion pain
Shallow
breathing
Breathing
problems.
Lung collapse
Severe
respiratory
complications
Pancreatic enzymes may
attack the lungs
inflammation
Severe inflammation
lead to intra-abdominal
hypertension
and abdominal
compartment syndrome
impaired renal and
respiratory function
Late complications
Recurrent pancreatitis
• Pancrease permanently damaged & chronic pancreatitis develops
Pseudocyst.
• fluid and debris to collect in cyst-like pockets in pancreas and walled off by scar tissue
• may cause pain, become infected, rupture and bleed
• May cause bloating, indigestion and a dull abdominal pain
Acute necrotizing pancreatitis
• pancreatic abscess (a collection of pus caused by necrosis, liquefaction and infection)
• Hypovolemic shock (ascites  decreasing the blood volume & BP)
• Prone to infection  bacteremia  multiple organ failure
Pancreatic cancer.
• Long-standing inflammation in pancreas caused by chronic pancreatitis is a risk factor
for developing pancreatic cancer
Treatment and management of acute
pancreatitis
Aim of treatment
1. Focus on relieving the symptoms
2. Preventing further complication
3. Support body functions
Treatment & management
• Determine and treat etiology (avoid alcohol)
• No solid food should be taken by mouth for a
few days (bowel rest)
• Adopt a liquid diet consisting of foods like
soups. These simple foods may allow the
inflammation process to get better.
• Administration of pain killer
• IV replacement of fluids
• If the attack lasts longer than a few days,
nutritional supplements are administered
through an IV line.
Treatment & management
• Nasogastric (NG) tube. The thin, flexible plastic tube
is inserted through the nose and down into the
stomach to suck out the stomach juices. This suction
of the stomach juices rests the intestine further,
helping the pancreas recover
• By giving antiemetic
• Prevent infection by antibiotic
• Indication to surgery if pancreatitis not respond to
treatment
INVESTIGATION OF ACUTE
PANCREATITIS
PANCREATIC ENZYME
• Amylase
- after 2 to 12 hours
- 23-85 U/L (normal range)
- Most accurate diagnosed when at least twice
of normal range
• Lipase
– 4 to 8
– 0-160 U/L (normal range)
– Increased sensitivity in alcohol-induced
pancreatitis
– more specific and sensitive than amylase for
detecting acute pancreatitis
Complete blood count (CBC) and
hematocrit;
• Normal hematocrit value
Male: 38.8-50.0 percent
Female: 34.9-44.5 percent
• To evaluate RBC count
• To evaluate WBC count
Trypsinogen activation peptide
• Within a few hours
• Early marker for acute pancreatitis and close
correlation to severity
Blood glucose test
• Pancreas released insulin to handle level of
blood glucose
• In pancreatitis,
- pancreas may does not make enough insulin
- The insulin does not work properly
• Using fasting blood glucose level
• Normal value (3.9 to 5.5 mmol/L)
Why do abdominal X-ray?
• Acute pancreatitis
- low sensitivity
- localised ileus (blockage of intestine)
- colon cut-off sign ( dilated colon to colon
with no air seen beyond the splenic flexure.
This is due to extension of inflammation along
mesocolon)
- pleural effusion
• Chronic pancreatitis
- calcification
Acute Pancreatitis
Acute Pancreatitis

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Acute Pancreatitis

  • 1. PREPARED BY: MUHAMMAD ARIFF B. MAHDZUB BACHELOR MEDICINE AND SURGERY (MBBS) UNIVERSITY COLLEGE SHAHPUTRA, KUANTAN MD-2508 (DIGESTIVE SYSTEM) PROBLEM BASED LEARNING (PBL) ACUTE PANCREATITIS
  • 2. TRIGGER 1 • Man • 44 Y/O • 160 pound (72 kg) • Suffer epigastric pain (last 3 hour), radiate to back
  • 3. • Anatomical organ related • Differential diagnose related
  • 4. TRIGGER 2 (History) • Already vomited clear material three times • Alcoholic • Likes fatty meal & has elevate fat in blood
  • 5. TRIGGERS 3 (physical examination) • Pulse 110/min • Bp: 120/70 mmHg (normal) • Esp. rate: 16/min (normal) • temp: 38.3 C • Exm abdomen • Distension epigastrium, bowel sound are hypoactive, percussion tenderness, involuntary guarding, referred tenderness • No diabetes, htn • Sister had gallbladder removed
  • 6. d/word • percussion tenderness: Pain feel at area of percussion • involuntary guarding: abdominal muscle spasm, caused by retroperitoneal inflammation • referred tenderness: Called reflex pain, pain at other site
  • 7. Trigger 4 (investigation) • X-ray : dilated transvers colon with no-free air • Hemoglobin: 15 g/dl • Wbc: 15,000/ ul • Serum amylase: 2,000 units/l (high) • Acute pancreatitis
  • 8. • Site of tenderness • Onset of tenderness (when) • Associating factor (symptom) • Duration of pain (how long) • Does it radiate to other part • Characteristic of pain (crushing, burning, palpate) • What make pain worst • How patient react to relieve the pain
  • 10. TRANSPYLORIC PLANE : An upper transverse line also known as Addison's Plane, located halfway between the jugular notch and the upper border of the pubic symphysis. The plane in most cases cuts through the pylorus of the stomach, the tips of the ninth costal cartilages and the lower border of the first lumbar vertebra. TRANSTUBECULAR PLANE : passing through the iliac tubercles; behind, its plane cuts the body of the fifth lumbar vertebra.
  • 11. Abdomen Regions Organs Right Hypochondriu m Liver, Gallbladder, Right Kidney, Small Intestine Left Hypochondriu m Spleen, Colon, Left Kidney, Pancreas Epigastrium Stomach, Liver, Pancreas, Duodenum, Spleen, Adrenal Glands Right Lumber Region Gallbladder, Liver, Right Colon Left Lumber Region Descending Colon, Left Kidney Umbilical Region Umbilicus, Jejunum, Ileum, Duodenum Right Iliac Fossa Appendix, Cecum Left Iliac Fossa Descending Colon, Sigmoid Colon Hypogastrium Urinary Bladder, Sigmoid Colon, Female Reproductive Organs
  • 12. What is Abdominal Pain? • the term abdominal pain generally is used to describe : – pain originating from organs within the abdominal cavity. – Organs of the abdomen include the stomach, small intestine, colon, liver, gallbladder, spleen, and pancreas. – Abdominal pain can range in intensity from a mild stomach ache to severe acute pain. – The pain is often nonspecific and can be caused by a variety of conditions.
  • 13. What Causes Abdominal Pain? • Inflammation (appendicitis, diverticulitis, colitis), • Stretching or distention of an organ (obstruction of the intestine, blockage of a bile duct by gallstones, swelling of the liver with hepatitis) • Loss of the supply of blood to an organ (ischemic colitis). • Constipation • Diarrhoea • Acid reflux
  • 14.
  • 15.
  • 16. Pancreas: type of cell and secretion
  • 17. THE PANCREAS • Combination of two glands a. Exocrine pancreas o Secrete substances into the intestine o enzymes b. Endocrine pancreas o Secrete substances into the bloodstream o hormones
  • 18.
  • 19. The exocrine pancreas • It has 2 types of cells: –Acinar cells : • Produce digestive enzymes: –Protease, amylase, lipase and peptidases –Duct cells : • Alkaline Fluids –Bicarbonate ions –Water
  • 20. The endocrine pancreas • Part of pancreas that made up endocrine function is Islets of Langerhans • 4 main types of cells: – α alpha cells : Glucagon – β beta cells : Insulin – Δ delta cells : Somatostatin – PP cells (γ (gamma) cells) : Pancretic polypeptide • The islets of Langerhans play an imperative role in glucose metabolism and regulation of blood glucose concentration
  • 21.
  • 22.
  • 23.  GALLSTONES Hard pieces of stone-like Produced in the gallbladder Block the bile duct Stopping pancreatic enzymes from traveling to the small intestine Forcing them back into the pancreas It begin to irritate the cells of the pancreas Causing the inflammation
  • 24. ALCOHOLISM  How alcohol actually triggers the inflammation in the pancreas is not clear.  The molecules in alcohol interfere with the cells of the pancreas.  Causing the enzymes to start digesting it.  Stopping them working properly.
  • 25.  INJURY TO PANCREAS  Car accident or bad fall leading to abdominal trauma.  accidental damage during a procedure to remove gallstones or examine the pancreas  AUTOIMMUNE DISEASE  own immune system attacks healthy cell  Associated with lupus or Sjogren's syndrome  INFECTION  Viral – mumps virus , HIV  IDIOPATHIC  Idiopathic pancreatitis  No obvious cause was identified
  • 27. Pathogenesis of acute pancreatitis Interstitial oedema Impaired blood flow Ischaemia Acinar cell injury Interstitial inflammation oedema Gallstone Chronic alcoholism Release of intracellular proenzymes and lysosomal hydrolases Activation of enzymes ACTIVATED ENZYMES Delivery of proenzymes to lysosomal compartment Intracellular activation of enzymes Proteolysis (proteases) Fat necrosis (lipase, phospholipase) Haemorrhage (elastase) Alcohol, drugs trauma, ischaemia, viruses Metabolic injury (experimental) Alcohol, duct obstruction DUCT OBSTRUCTION ACINAR CELL INJURY DEFECTIVE INTRACELLULAR TRANSPORT
  • 28.
  • 33. MARIA
  • 34. INTRODUCTION OF VOMITTING • Known as emesis / throwing up • Involuntary, forceful expulsion of the contents of one's stomach through the mouth and sometimes the nose. • Not same as regurgitation. MARIA
  • 35. WHAT CAN YOU EXPECT FROM THE VOMITUS? QUANTITY COLOUR CONTENTS ONSET & DURATION MARIA
  • 39. MARIA
  • 43. • enzyme • begins the chemical process of digestion • catalyses the hydrolysis starch—sugars • 3 type-α-Amylase, β-Amylase, γ-Amylase • Pancreas, salivary gland -alpha amylase • hydrolyse dietary starch - disaccharides ,trisaccharides converted by other enzymes to glucose -energy • Foods large amounts of starch, little sugar, ( rice,potatoes) -slightly sweet taste as chewed- amylase degrades starch – sugar • producing salivary amylase-gene AMY1,-originated in pancreas amylase
  • 44. The normal range is 23 to 85 units per liter (U/L). Some laboratories give a range of 40 to 140 U/L pancreas damage @ inflamed-amylase in blood urine By blood@urine sample Some can affect amount of detectable amylase Amylase blood test
  • 45. • Some medications that could heighten the amount of amylase in the blood include: • asparaginase • aspirin • birth control pills • cholinergic medications • ethacrynic acid • methyldopa • opiates (codeine, meperidine, morphine) • thiazide diuretics (chlorothiazide, hydrochlorothiazide, indapamide, metolazone)
  • 46. Indication of high amylase count • Acute or chronic pancreatitis: enzymes - help break down food in intestines -malfunction - begin breaking down the tissues of the pancreas. Acute pancreatitis - sudden - not last long, chronic pancreatitis does improve , worsens over time. • Cholecystitis: inflammation of the gallbladder. Cholecystitis is usually caused by gallstones. Gallstones are deposits of hardened cholesterol or other substances that can form in the gallbladder, and cause blockages. This condition can also sometimes be caused by tumors. • Macroamylasemia: the presence of macroamylase in the blood. This is an abnormal compound of the enzyme and a protein. • Gastroenteritis: inflammation of the gastrointestinal tract.
  • 47. • Tubal pregnancy: the fertilized egg (embryo) is in one of the fallopian tubes (tubes that connect the ovaries to the uterus) instead of in the uterus. This is also called an ectopic pregnancy, which is a pregnancy that takes place outside the uterus. • Other conditions: can also cause elevated amylase counts, including salivary gland infections, or intestinal blockages.
  • 48. Indications of low count of amylase • preeclampsia: a condition in pregnant women, also called toxemia of pregnancy. Signs of this condition also include high blood pressure. • damaged pancreas • kidney disease
  • 50. • The body has limited supply of glucose. • 3 sources of fatty acid for energy metabolism - dietry tryacylglycerol - tryacylglycerol that synthesize in liver - tryacylglycerol stored in adipocytes • When foods enter the stomach, it will breakdown into components such as carbohydrates, proteins and fats. • Dietry tryacylglycerol comes from the fat in the foods we eat and the process of breakdown start to occurs in small intestine not in the stomach.
  • 51. In the small intestine, bile salt from the gall bladder will emulsify the realtively insoluble dietry fat to form micelles.
  • 52. The micelles have non-polar core and surrounded by bile salts. R-group are non-polar and so they point towards the centre of the micelles.
  • 53. After that, as micelles moving downwards the small intestine, pancreatic lipase will degrades the triacylglycerol into fatty acids and glycerol.
  • 54. Then, the 3 Fatty acids and 1 glycerol packaged with apoprotein and cholesterol into blood-soluble-complex called chylomicrons.
  • 55. The chylomicrons will cross blood vessel membrane and move into blood stream. From here on, the chylomicrons will have 2 possible pathways: -Stored in adipocytes -Move to muscle cells
  • 56. For fat storage in adipocytes, the triacylglycerol is cleaved on the wall of blood vessel by lipoprotein lipase into fatty acid and glycerol. Then it will move to adipocyte cells and stored as fat droplets.
  • 57. However, if the person exercise or do hard chorus after that, the fat then will be utilized by muscle cells as energy through beta- oxidation to form carbon dioxide and ATP.
  • 58. Up to this point we have described dietry fatty acid pathway either stored in the adipocytes or immediately utilized.
  • 59. During strenous exercise, muscle use up the small amount of the body’s stored glycogen. So, in order to compensate that insufficient energy, the energy that stored as fat droplets in adipocytes is released.
  • 60. Epinephrin or glucagon leaves bloodstream and binds to adipocytes receptor. This will allow adenylate cyclase to convert ATP into cAMP. Then, cAMP will bind to protein kinase and activates it.
  • 61. Activated protein kinase will Proceeds to bind to triacylglycerol lipase and activating it. Once activated, the triacylglycerol lipase is able to break triacylglycerol into fatty acid and glycerol.
  • 62. Then fatty acid molecules are pick up by the protein albumin in the blood stream. Serum albumin travels through the blood vessels and release the fatty acid molecules into myocytes.
  • 63. Finally, the fatty acid will undergo beta-oxidation to produce carbon dioxide and ATP
  • 65. Early complications infections Malnutrition Abdominal swelling Systemic inflammatory response High blood glucose Severe respiratory failure Late complications Recurrent pancreatitis Pancreatitic pseudocyst Acute necrotizing pancreatitis
  • 66. Early complications Infection. • make pancreas vulnerable to bacteria and infection  inflammations  interruption to blood supply  necrosis • require intensive treatment, such as surgery to remove the infected tissue. Diabetes. • Damage to insulin-producing cells in pancreas • from chronic pancreatitis can lead to diabetes • affects the way our body uses blood sugar. Kidney failure • can be treated with dialysis if the kidney failure is severe and persistent. Malnutrition. • Both acute and chronic pancreatitis can cause pancreas to produce fewer of the enzymes that are needed to break down and process nutrients from the food • lead to malnutrition, diarrhea and weight loss, even though patient may be eating the same foods or the same amount of food..
  • 67. Pleural effusion pain Shallow breathing Breathing problems. Lung collapse Severe respiratory complications
  • 68. Pancreatic enzymes may attack the lungs inflammation Severe inflammation lead to intra-abdominal hypertension and abdominal compartment syndrome impaired renal and respiratory function
  • 69. Late complications Recurrent pancreatitis • Pancrease permanently damaged & chronic pancreatitis develops Pseudocyst. • fluid and debris to collect in cyst-like pockets in pancreas and walled off by scar tissue • may cause pain, become infected, rupture and bleed • May cause bloating, indigestion and a dull abdominal pain Acute necrotizing pancreatitis • pancreatic abscess (a collection of pus caused by necrosis, liquefaction and infection) • Hypovolemic shock (ascites  decreasing the blood volume & BP) • Prone to infection  bacteremia  multiple organ failure Pancreatic cancer. • Long-standing inflammation in pancreas caused by chronic pancreatitis is a risk factor for developing pancreatic cancer
  • 70. Treatment and management of acute pancreatitis
  • 71. Aim of treatment 1. Focus on relieving the symptoms 2. Preventing further complication 3. Support body functions
  • 72. Treatment & management • Determine and treat etiology (avoid alcohol) • No solid food should be taken by mouth for a few days (bowel rest) • Adopt a liquid diet consisting of foods like soups. These simple foods may allow the inflammation process to get better. • Administration of pain killer • IV replacement of fluids • If the attack lasts longer than a few days, nutritional supplements are administered through an IV line.
  • 73. Treatment & management • Nasogastric (NG) tube. The thin, flexible plastic tube is inserted through the nose and down into the stomach to suck out the stomach juices. This suction of the stomach juices rests the intestine further, helping the pancreas recover • By giving antiemetic • Prevent infection by antibiotic • Indication to surgery if pancreatitis not respond to treatment
  • 75. PANCREATIC ENZYME • Amylase - after 2 to 12 hours - 23-85 U/L (normal range) - Most accurate diagnosed when at least twice of normal range
  • 76. • Lipase – 4 to 8 – 0-160 U/L (normal range) – Increased sensitivity in alcohol-induced pancreatitis – more specific and sensitive than amylase for detecting acute pancreatitis
  • 77. Complete blood count (CBC) and hematocrit; • Normal hematocrit value Male: 38.8-50.0 percent Female: 34.9-44.5 percent • To evaluate RBC count • To evaluate WBC count
  • 78. Trypsinogen activation peptide • Within a few hours • Early marker for acute pancreatitis and close correlation to severity
  • 79. Blood glucose test • Pancreas released insulin to handle level of blood glucose • In pancreatitis, - pancreas may does not make enough insulin - The insulin does not work properly • Using fasting blood glucose level • Normal value (3.9 to 5.5 mmol/L)
  • 80. Why do abdominal X-ray? • Acute pancreatitis - low sensitivity - localised ileus (blockage of intestine) - colon cut-off sign ( dilated colon to colon with no air seen beyond the splenic flexure. This is due to extension of inflammation along mesocolon) - pleural effusion
  • 81. • Chronic pancreatitis - calcification

Hinweis der Redaktion

  1. Under a microscope, stained sections of the pancreas reveal two different types of parenchymal tissue. The lightly-staining clusters of cells are called islets of Langerhans, which produce hormones that underlie the endocrine functions of the pancreas. The darker-staining cells form acini, connected to ducts. Acinar cells belong to the exocrine pancreas and secrete digestive enzymes into the gut via a system of ducts.
  2. Peptidases are secreted in an inactive form (zymogen) and only activated as it reach the duodenum. Bicarbonate ion: To neutralize acidic chyme Fluids: Flushes enzymes and zymogens into large pancreatic duct Acinar cells : majority of pancreatic cell , The pancreas is also the main source of enzymes for digesting fats (lipids) and proteins. (The enzymes that digest polysaccharides, by contrast, are primarily produced by the walls of the intestines.) The cells are filled with secretory granules containing the precursor digestive enzymes. The major proteases which the pancreas secretes are trypsinogen and chymotrypsinogen. Secreted to a lesser degree are pancreatic lipase and pancreatic amylase. The pancreas also secretes phospholipase A2, lysophospholipase, and cholesterol esterase. The precursor enzymes (termed zymogens or proenzymes) are inactive variants of the enzymes; thus autodegradation, which can lead to pancreatitis, is avoided. Once released in the intestine, the enzyme enteropeptidase (formerly, and incorrectly, called enterokinase) present in the intestinal mucosa activates trypsinogen by cleaving it to form trypsin. The free trypsin then cleaves the rest of the trypsinogen, as well as chymotrypsinogen to its active form chymotrypsin. Defect in duct cell secretion in cystic fibrosis Secretion of bicarbonate by duct cells depends upon the protein CFTR. In the fall, we learned that CFTR is a chloride channel that provides the rate limiting step in fluid secretion in the small intestine (see webpage on Epithelial Transport). But it turns out the CFTR protein is also a bicarbonate channel. When the CFTR protein is defective, as it is in patients with cystic fibrosis, duct cell secretion is disrupted. This causes a lack of fluid secretion to flush out pancreatic zymogens, blockage of pancreatic ducts, and inappropriate activation of trypsin in the pancreas. The result is inflammation with damage to acinar and duct cells, which may be replaced by connective tissue. Patients with severe mutations of CFTR (little or no CFTR function) are often born with pancreatic insufficiency, meaning their pancreas does not release sufficient quantities of digestive enzymes. They will have have a failure to thrive, and need to be treated with digestive enzyme supplements. Less severe mutations in CFTR (with some channel function) still increase the risk for pancreatitis.
  3. The islets of Langerhans are the regions of the pancreas that contain many endocrine (i.e., hormone-producing) cells. Hormones produced in the islets of Langerhans cells are secreted directly into the blood flow by at least five different types of cells: alpha, beta, delta, PP and epsilon. The hormones produced are insulin, glucagon and somatostatin. The islets of Langerhans can influence each other through paracrine and autocrine communication. The paracrine feedback system is based on the following correlations: the insulin hormone activates beta cells and inhibits alpha cells. The hormone glucagon activates alpha cells which, in turn, activates beta cells and delta cells. Somatostatin hormone inhibits alpha cells and beta cells. insulin A polypeptide hormone that regulates carbohydrate metabolism. somatostatin A polypeptide hormone, secreted by the pancreas, that inhibits the production of certain other hormones. glucagon A hormone, produced by the pancreas, that opposes the action of insulin by stimulating the production of sugar.
  4. The islets are a compact collection of endocrine cells arranged in clusters and cords and are crisscrossed by a dense network of capillaries. The capillaries of the islets are lined by layers of endocrine cells in direct contact with vessels, and most endocrine cells are in direct contact with blood vessels, either by cytoplasmic processes or by direct apposition. According to the volume The Body, by Alan E. Nourse,[10] the islets are "busily manufacturing their hormone and generally disregarding the pancreatic cells all around them, as though they were located in some completely different part of the body."
  5. Inflammation of the pancreas
  6. Malnutrition=malabsorption=weight loss=happens becoz pancreas inflamed, so the gland not releasing enough enzymes to break down food Diabetes=high glucose level=insulin producing cells of the pancreas are damaged Abd may be become swollen & painful due to stomach being distended or misplaced by a mass in the pancreas. Swelling may also be caused by abnormal mv of the intestinal content
  7. Pancreatic infections are serious and require intensive treatment, such as surgery to remove the infected tissue.
  8. Breathing problems. chemical changes in body that affect lung function, causing the level of oxygen in blood to fall to dangerously low levels
  9. Abd compartment syndrome= occurs when the abdomen becomes subject to increased pressure Specific cause is unknown. Sometimes can be sepsis & severe abd trauma Increasing pressure reduced bf to abd organs & impairs pulmonary renal cvs & git fx causing multiple organ dysfx syndrome & death
  10. Hypovolemic shock=in severe cases,parts of the pancrease die (necrotizing pancreatitis). Cause pancreatic fluid & blood to leak into abd cavity (ascites), decreasing the blood volume & bp. So jd lah hypovolemic shock