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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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