pancreas 25.07 copy nursing
TRANSCRIPT
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13th CNE PROGRAMME
Dept. of MEDICAL SURGICAL NURSING
Presented by
Mrs. E. Sujitha, M.Sc. Nursing,
Lecturer,Faculty of Nursing,
Sri Ramachandra University,
Porur, Chennai-600116
PANCREAS
Two sides of a coin- Collaborative care
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THE PANCREAS
The pancreasis an organlocated in the abdomen
retro-peritoneum, 2ndlumbar vertebral level
tucked behind the stomach.
shaped somewhat like a tadpole
is around 25 cm in length, 60-100 g
surrounded by other organs including the
small intestine, liver, and spleen.
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PARTS
The wide part, -head -toward the center of the abdomen;
the middle section -the neck and the body of the pancreas;
the thin end -the tail and extends to the left side.
Several major blood vessels surround the pancreas, -
superior mesenteric artery,
the superior mesenteric vein,
the portal vein
the celiac axis,
supplying blood to the pancreas and other abdominal organs.
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HORMONAL REGULATION
Pancreas plays an essential role in converting the food we
eat into fuel for the body's cells.
The pancreas has two main functions:
an exocrinefunction that helps in digestion and
an endocrinefunction that regulates blood sugar. ,
Thyroxin- regulates O2 consumption
Growth hormone- protein
Insulin- glucose
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PANCREAS- DUAL ROLES
THE DIGESTIVE SYSTEM
contains exocrine glands that produce enzymesimportantto digestion
Once food has been mulched and partially digested by the
stomach, it is pushed into the duodenum
The pancreas adds its own digestive juices and enzymes to
the food, via a small duct attached to the duodenum.
This process is said to belong to the exocrine role
THE HORMONAL SYSTEM.produces the hormone insulin & glucagon- help to control
the amount of sugar in the blood. (endocrine role)
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PANCREAS
six inches long
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EXOCRINE PORTION- PANCREATIC DUCT
Main duct (Wirsung) runs the entire length ofpancreas
Joins CBD at the ampulla of Vater 24 mm in diameter, 20 secondary branches
Ductal pressure is 1530 mm Hg (vs. 717 inCBD) - preventing damage to pancreatic duct
Lesser duct (Santorini) drains superior portion ofhead and empties into 2ndportion of duodenum
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LIVER AND PANCREAS
The pancreatic duct joins the common bile ductto formthe ampulla of Vater
located at the first portion of the small intestine, called the
duodenum.
The common bile duct originates in the liver and thegallbladderand produces another
important digestive juice called bile.
The pancreatic juices and bile that
are released into the duodenum,
help the body to digest fats,
carbohydrates, and proteins
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HEPATICOPANCREATIC AMPULLA(AMPULLA OF VATER)
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L2
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makes HCO3
PANCREAS- MICROSCOPIC STRUCTURE
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DISORDERS OF THE PANCREAS
Congenitalo Agenesis
o Pancreas Divisum
o Annular Pancreas
o Ectopic Pancreas
Inflammatory
Acute
Chronic Cysts
Neoplasms
Diabetes mellitus
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ACUTE PANCREATITIS
Causes
Alcoholism
Bile reflux
Medications (thiazides) Hypertriglyceridemia,
hypercalcemia
Acute ischemia
Trauma, blunt, iatrogenic
Genes: PRSS1, SPINK1
Idiopathic, 10-20%
Abdominal pain
Extreme emergency
situation
High mortality
But most important lab
test is.Amylase
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MORPHOLOGY
EDEMA
FAT NECROSIS
ACUTE INFLAMMATORY
INFILTRATE
PANCREAS AUTODIGESTION
BLOOD VESSEL
DESTRUCTION
SAPONIFICATION (stearates,
Na+, Ca++)
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CLINICAL FEATURES
Abdominal Pain
Vague abdominal
symptoms
CT calcifications
amylase elevated ( >500
IU/L) chronic diarrhea (chronic
pancreatic insuffiency )
high likelihood of
pseudocysts
Can cause obstruction
Can get infected
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CYSTADENOMA
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SYMPTOMS OF PANCREATICPROBLEMS
The symptoms depend on the underlying cause,
Pain in the upper abdomen
Loss of appetite
Yellowing of the skin and eyes (jaundice)
Back pain
Bloating
Nausea
Vomiting Digestive upsets
Passing foul-smelling and fatty faeces
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DIAGNOSIS OF PANCREATICPROBLEMS
General tests
Ultrasound
Computed tomography (CT) scan Magnetic resonance imaging (MRI)
Endoscopy
Laparoscopy
Biopsy
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TREATMENT FOR PANCREATICPROBLEMS
Acute pancreatitishospitalisation in intensive care;
fasting and intravenous fluids;
surgery to remove gallstones or damaged sections of pancreas;
lifestyle changes, -eliminating alcohol.
Chronic pancreatitislong-term treatment mayreducing dietary fats;
supplementing digestion with pancreatic enzyme tablets;
eliminating alcohol;
taking regular insulin injections for reduced endocrine function.
Pancreatic cancersurgery to remove the cancer and associated tissue;radiotherapy and
chemotherapy.
Diabetesa carefully controlled diet.
regular medications or injections of insulin
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ENDOCRINE FUNCTION-
PANCREASConsists of islet cells that create and release important
hormonesdirectly into the bloodstream.
Two of the main pancreatic hormones are
insulin, which acts to lower blood sugar,
glucagon, which acts to raise blood sugar.
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PRODUCTION OF PANCREATICHORMONES
.Three Cell Types
A - Alpha cells
produce glucagon. B - Beta cells produce
insulin.
D- Delta cells produce
somatostatin
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INSULIN AND GLUCAGON-REGULATE METABOLISM
: Metabolism is controlled by insulin and glucagon
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ROLES OF INSULIN
Acts on tissues except brain (liver, skeletal muscle,adipose) to increase uptake of glucose and amino acids.
Glucose enters the brain by facilitated diffusion
Increases glycogen production (glucose storage) in the
liver and muscle.
Stimulates lipid synthesis from free fatty acids and
triglycerides in adipose tissue.
Also stimulates potassium uptake by cells (role in
potassium homeostasis).
SPECIFIC TARGETS OF INSULIN
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SPECIFIC TARGETS OF INSULINACTION:
CARBOHYDRATES
Moves glucose into cells
Converts glucose to
glycogen.Inhibits gluconeogenesis
LIPIDS
Stimulates production of
free fatty acids from acetyl
CoA.
(increases breakdown of
triacylglycerol in the
circulation
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REGULATION OF INSULINRELEASE
Major stimulus: increased blood glucose levels
1 After a meal, blood glucose
increases
2 Insulin is released
3 Insulin causes uptake of glucose
into tissues
4 Blood glucose levels decrease
5 Insulin levels decline
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INSULIN: SUMMARY AND CONTROLREFLEX LOOP
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INSULIN RELEASE
Stimulated by
Amino acids
Keto acids
Glucagon
negative feedback.
inhibited by
stress-induced increase inadrenal epinephrine
Growth hormone
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GLUCAGON ACTION ON CELLS:DOMINATES IN FASTING STATE
METABOLISM
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TARGETS OF GLUCAGON ACTION
release a glucose molecule off of glycogen.
less glycogen synthesis.
gluconeogenesis
Activates lipases, breaks down triglycerides. decrease free fatty acid formation from acetyl CoA
Result:more production of glucose and substratesfor metabolism
Inhibited by
Increased blood glucose
Insulin
Stimulated by
Stress
Amino acids
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REGULATION OF INSULIN AND GLUCAGONSECRETION (CONTINUED)
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DIABETES MELLITUS
Chronic high blood
glucose.
2 forms of diabetes
mellitus: Type I: insulin
dependent diabetes
(IDDM).
Type II: non-insulindependent diabetes
(NIDDM).
COMPARISON OF TYPE I AND
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COMPARISON OF TYPE I ANDTYPE II DIABETES MELLITUS
Insert table 19.6
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CONSEQUENCES OF UNCORRECTED DEFICIENCY
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CONSEQUENCES OF UNCORRECTED DEFICIENCYIN TYPE I DIABETES MELLITUS
Insert fig. 19.11
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TYPE II DIABETES MELLITUS
Slow to develop.
Genetic factors
Occurs mostly inoverweight.
Decreased sensitivity toinsulin
Do not usually developketoacidosis.
May have high or normalinsulin.
Insert fig. 19.12
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TREATMENT IN DIABETES
Change in lifestyle:
-- Insulin, OHA
Increase exercise:
Increases the amount of membrane GLUT-4 carriers
in the skeletal muscle cells.
Weight reduction.
Increased fiber in diet. Reduce saturated fat.
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HYPOGLYCEMIA
Over secretion ofinsulin.
Reactivehypoglycemia:
Caused by anexaggeratedresponse to arise in bloodglucose.
Occurs inpeople who aregenetically
predisposed to
type II diabetes.
Insert fig. 19.13
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STIMULATION OF PANCREATIC SECRETION DURING THE INTESTINALPHASE
Frank Boumphrey, M.D., wikimedia commons
PANCREATIC BICARBONATE OUTPUT INCREASES IN
http://commons.wikimedia.org/wiki/File:Pancreas_secretion.pnghttp://commons.wikimedia.org/wiki/File:Pancreas_secretion.png -
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PANCREATIC BICARBONATE OUTPUT INCREASES INRESPONSE TO LOW DUODENAL p
Fig. 9-5 Johnson, L. Gastrointestinal Physiology, 6thed. Mosby Elsevier, St. Louis, MO; 2001: 102.
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GLUCOSE CONTENT OF FOOD
What % of the carbohydrates consumed breaksdown into glucose?
100%
What % of the protein consumed breaks down intoglucose?
58%
What % of the fat consumed breaks down intoglucose?
10%
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SOMATOSTATIN
A hormone secreted by the delta cells of the Islets
of Langerhans
Secreted in response toHyperglycemia
Action
Interferes with glucagonInterferes with growth hormone
Has a hypoglycemic effect
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DIAGNOSTIC TESTS
Blood glucose /
Fasting blood glucose
2 hr PPG Glucose tolerance Test
Glycosylated
Hemoglobin Assay
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FASTING BLOOD GLUCOSE
Measures blood
glucose levels after
fasting
Results
Normal70-115 mg/dL
Diabetic level > 126
mg/dL Critical > 400 mg/dL
Critical < 50 mg/dL
Nurses Role
Fast 6-8 hours
Water OK No insulin or anti-
diabetic meds
Exercise will affectresults
Meds that interfere`
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2-hours post-prandial glucose
Measure blood
glucose 2 hours after a
meal
Normal
70-140 mg/dL
Diabetic level
> 140 mg/dL
Nurses Role
Eat entire meal
Dont eat anythingmore until blood draw
Water OK
Notify lab when mealis finished
Exercise with effect
results
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ORAL GLUCOSE TOLERANCE TEST
Measurement of theability of b cells tosecrete insulin.
Ability of insulin tolower bloodglucose.
Normal persons
rise in blood[glucose] afterdrinking solution isreversed to normalin 2 hrs.
Insert fig. 19.8
GLUCOSE TOLERANCE TEST
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GLUCOSE TOLERANCE TEST
Normal
Blood glucose
S < 140mg/dL at 2 hours Urine negative for
glucose (all times)
Diabetic level
Blood glucose > 140mg/dL at 2 hours
Glucose in urine
Nursing responsibility
6-8 hours before test
Hold meds that interfere
A glucose load
Evaluates blood glucoseand urine glucose
30 minutes before
1 hour after
2 hours after 3 hours after
4 hours after
Administer meal and meds
afterwards
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EMBRYOLOGICAL DEVELOPMENT OF PANCREAS
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EMBRYOLOGICAL DEVELOPMENT OF PANCREAS
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Ventral Bud
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Use of glycated haemoglobin (HbA1c) in
the diagnosis of diabetes mellitus
Abbreviated report of a WHO consultation
Editors: WHOPublication date: 2011
Conclusion: WHO has concluded that Hb A1C can be used as
a diagnostic criteria for DM with cut off value 6.5%
I di J E d i l M b 2014 M 18(3) 379 85 d i 10 4103/2230
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Indian J Endocrinol Metab.2014 May;18(3):379-85. doi: 10.4103/2230-
8210.131191.
Knowledge and awareness of diabetes in urban and rural India: The IndianCouncil of Medical Research India Diabetes Study (Phase I): Indian Council
of Medical Research India Diabetes 4(Dr. Mohan et al.,)
Only 43.2% (6160/14,274) of the overall study population
had heard about a condition called diabetes. Overall urban
residents had higher awareness rates (58.4%) compared torural residents (36.8%) (P < 0.001). About 46.7% of males
and 39.6% of females reported that they knew about a
condition called diabetes (P < 0.001). Of the general
population, 41.5% (5726/13,794) knew about a conditioncalled diabetes
N k ti Th d J l 24 2014
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Newyork times: Thursday, July 24, 2014
Diabetes Diet - Type I
Carbohydrates should provide 45 - 65% of total daily calories. The type andamount of carbohydrate are both important. Best choices are vegetables, fruits,
beans, and whole grains. These foods are also high in fiber.
Fats should provide 25 - 35% of daily calories. Monounsaturated (such asolive, peanut, and nuts) and omega-3 polyunsaturated (such as fish, flaxseed
oil, and walnuts) fats are the best types. Limit saturated fat (red meat, butter) to
less than 7% of daily calories. Choose nonfat or low-fat dairy instead of whole
milk products. Limit trans-fats (such as hydrogenated fat found in snack foods,
fried foods, and commercially baked goods) to less than 1% of total calories.
Protein should provide 12 - 20% of daily calories, although this may varydepending on a patients individual health requirements. Patients with kidney
disease should limit protein intake to less than 10% of calories. Fish, soy, and
poultry are better protein choices than red meat.
Lose weight if body mass index (BMI) is 25 - 29 (overweight) or higher
(obese).
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