pankreas (diabetis mellitus)
TRANSCRIPT
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HEAD
Lies within the curve of the duodenum
Unicate process prolongtion of thehead
UCINATE PROCESS
The part of the head that wrapsbehind the superior mesenteric arteryand vein and comes to lie adjacent tothe ascending part of the duodenum
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CONT,
NECK
A constricted portion to the left of
the head. It abuts the pylorusabove and the beginning of theportal vein behind
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CONT,
BODY Anterior surface separated from the
stomach by the omental bursa
Posteriorly related to the aorta , splenic
vein, left kidney and renal vessels, leftsuprarenal, origin of superior mesentericartery and crura of diaphragm
TAIL
Extends into the lienorenal ligament andabuts the spleen
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FUNCTIONFUNCTION DIGESTIVE - produces digestive
enzymes
HORMONAL - islets of Langerhansproduce insulin needed to controlblood sugar levels
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Hypertrophy of the head portalor bile duct obstruction
Degeration of the islets ofLangerhans DM
Pancreatitis due to seriousinflammatory condition of theexocrine pancreas
CLINICALCLINICAL
CONSIDERATIONCONSIDERATION
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DIABETESDIABETES
( From a Greek work meaning tosiphon , referring to theincreased output of urine. )
MELLITUSMELLITUS
(From a Latin word meaningsweet )
The two words together identify thedisease as an outpouring of sweet
urine.
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DEFINITIONDEFINITIONDiabetes is a metabolic disordercharacterized by inappropriatehyperglycemia ( high levels of
sugar ) caused by a relative orabsolute deficiency of insulin orby a cellular resistance to the
action of insulin.
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MAJOR
CLASSIFICATION OFDIABETES
Type 1 DM insulin-dependentdiabetes mellitus ( IDDM )
Type 2 DM non-insulin-
dependent diabetes mellitus( NIDDM )
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DIABETESIABETESTYPES 1YPES 1INSULIN INSULIN
DEPENDENTDEPENDENT
DIABETES MELLITUSDIABETES MELLITUS( IDDM )
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DEFINATION
Metabolic condition in which thebeta cells of pancrease no longerproduce insulin:
Characterized by hyperglycemia,breakdown of body fats andprotein and development of
ketosis.
CalledJUVENILE onset diabetes or( IDDM )
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SIGN AND SYMPTOMSSIGN AND SYMPTOMS
Hyperglycemia ( elevatedblood glucose levels )
Development of ketosis( an accumulation
of ketone bodies producedduring the oxidation of fattyacids )
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Cont,Result of the destruction of thebeta cells of the islets ofLangerhans in the pancreas ( oncell in the body make insulin ).
When Beta cell destroyed, insulinno longer produced.
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Autoimmune or
Idiopathic Disorder
Begin with insulinitis.
A chronic inflammatory process thatoccurs in response to the autoimmunedestruction of islet cells.
Slowly destroys beta cell productionof insulin.
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Cont,
The onset of hyperglycemia occurring when80% - 90% of beta cell function is lost.
Usually occur over a long preclinical period.
Alpha-cell and Beta-cell function areabnormal, with a lack of insulin a relativeexcess of glucagon resulting inHYPERGLYCEMIA.
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RISK FACTORS Genetic predisposition for increased
susceptibility: Human Leukocyte Antigens(HLA) linkage.
Environmental triggers stimulate anautoimmune response.
Viral infection ( mumps, rubella,
coxsackievirus B4 )Chemical toxins.
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ETIOLOGY
Obesity (overweight) Waist size
Sedentary lifestyle
Age Family history
Ethnicity
Gestational diabetes/high birth weightbaby
High blood pressure/cholesterol
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CLINICAL
MANIFESTATIONS Polyuria( hyperglycemia acts as
osmotic diuretic ) Glycosuria( renal threshold for
glucose: 180mg/dl )
Polydipsia( thirst fromdehydration from polyuria. ) Polyphagia( hunger and eats more
since cell not utilize glucose )
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Cont, Weight loss( body breaking down
fat and protein to restore energysource )
Malaise and fatigue( fron decreasein energy. )
Blurred vision( swelling of lensesfrom osmotic effects. )
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POTENTIALPOTENTIAL
COMPLICATION OFCOMPLICATION OFDM TYPE 1.DM TYPE 1.
DIABETICDIABETIC
KETOACIDOSISKETOACIDOSIS
( DKA )( DKA )
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DEFINITION
Result from breakdown of fat andoverproduction of ketones by the
liver and loss of bicarbonate. Occur when undiagnosed or knowndiabetic has increased energy
needs, when under physical oremotional stress or fails to takeinsulin.
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Y An absolute deficiency of insulin and an increase
in the insulin counterregulatory hormones.
Glucose production by the liver increase,
peripheral glucose use decrease, fatmobilization increase, and ketogenesis is
stimulated.
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Cont, Increased glucagon levels activate thegluconeogenic and ketogenic pathways in
the liver.
Presence of insulin deficiency, hepaticoverproduction of beta-hydroxybutyrateand acetoacetic acid ( ketone bodies)
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Cont, Loss of bicarbonate ( which occurs when the
ketones is formed )
Bicarbonate buffering does not occur and ametabolic acidosis occurs
DKA
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DIABETES TYPES
2
NON-INSULIN-NON-INSULIN-
DIPENDENTDIPENDENT
DIABETESDIABETESMELLITUSMELLITUS
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DEFINITIONDEFINITION
Is a condition of fastinghyperglycemia that occurdespite the availability ofendogenous insulin.
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Sufficient insulin production toprevent DKA
But insufficient to lower bloodglucose through uptake of glucose by
muscle and fat cells.
Cellular resistance to insulinincreased by obesity, inactivity,illness, age, some medication.
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RISK FACTORS History of diabetes in parents or siblings.
Obesity
Physical inactivity.
Race / ethnicityWomen
Hypertension
Metabolic syndrome
CLINICAL
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CLINICAL
MANIFESTATION Not experience weight loss.
Hyperglycemia.
Polyuria
Polydipsia
Blurred vision
Fatigue
Paresthesias
Skin infection
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POTENTIAL
COMPLICATION OF DMTYPE 2.
HYPERSOMOLARHYPERGLYCEMIC
STATE
( HHS ) DEFINITION
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DEFINITION Is characterized by a plasma osmolarity of
340 mOsm/L or greater ( the normal rangeis 280 to 300 mOsm/L.
Greatly elevated blood glucose levels (
over 600 mg/dL and often 1000 to 2000mg/dL), and altered level of consciousness.
HHS is a serious, life-threatening medicalemergency and has a higher mortality rate
than DKA.
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CAUSESTHERAPEUTIC AGENTSGlucocorticoids
DiureticsBeta-adrenergic blocking agent
Immunosuppressant
ChlorpromazineDiazoxide
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Cont,THERAPEUTIC PROCEDURE
Peritoneal dialysis
Hemodialysis
Hyperosmolar alimentation ( oral orparenteral )
surgery
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Cont,ACUTE ILLNESSInfectionGangrene
Urinary infectionBurnsGastrointestinal bleedingMyocardial infarctionPancreatitis
Stroke
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Cont,CHRONIC ILLNESS
Renal disease
Cardiac diseaseHypertension
Previous stroke
Alcoholism
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PATHOPHYSIOLOGY Hyperglycemia leads to increased urine
output and dehydration.
Kidneys retain glucose: glucose and sodiumrise
Severe hyperosmolar state developsleading to brain cell shrinkage.
CLINICALCLINICAL
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CLINICALCLINICAL
MANIFESTATIONSMANIFESTATIONS Altered level of consciousness.
( Lethargy to coma )
Neurological deficits:hyperthermia, motor and sensory
impairment, seizures. Dehydration: dry skin and mucousmembranes, extreme thirst.
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INVESTIGATIONSBlood capillary glucose testRandom blood sugar
Fasting blood sugar2 hours postprandial
Modified oral glucose tolerance test
Renal profileFasting lipid profile
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COMPLICATIONCOMPLICATION
Eye complications (diabetic retinopathy)Kidney damage (kidney disease)
Nerve damage
Heart diseaseStroke (brain attack)
Urinary incontinence (unable to hold urine)
Intestinal disruptions leading to constipation.
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NURSING CARE PLANNURSING CARE PLAN(1)Anxiety related to hospitalization.Goal -Patient will verbalize less anxietyIntervention:
assess patients level of a anxiety explain to patients the important of
completing the treatment. explain to patients regarding procedures.
give emotional support. involve patients when planning nursing care.
C tCont
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Cont,Cont,2)Ineffecive health maintenance
related to management of type 1diabetes mellitus.
Goal:Goal:
patients will describes feeling about self
management of types1 diabetes mellitus.patients will describes disease process.
Interventions:
-evaluate the patients understanding oftypes1 diabetes mellitus and attitudeabout the need to manage it.
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Cont,Cont, correct any misconceptions about type 1
diabetes mellitus and the therapeutic regimen. discuss peer presure.ask the adolescent ifpatients feel social pressure that causes toignore dieter avoid self administering insulin.
ask if patients feel depressed about disorder.
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Cont,Cont,3)Nutrition less than body
requirements related to poor ofappetite.
Goal:
patients will show no further evidence of
weight loss. patients will take in calories daily.
Interventions:
-obtain and record patients weight at thesame time every day to obtain accuratereadings.
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Cont,Cont,maintain parental fluids or
ordered to provide patientswith needed fluids andelectrolytes.
monitor electrolytes level and
report abnormal values.
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Cont,Cont,Intervention:
Monitor vital signs every 15min until theclient condition is stable for 1hour,then4 hourly.
Notify the physician if heart rate is >
120/min,blood pressure is 20mmHg from baseline,CVP is
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Cont,Cont, Monitor the client for fluid volumedeficit: poor skin turgor, dry mucusmembranes sunken and soft eyeballs.
Measure intake and output accurately:report to the physician urine output
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FOOT CAREFOOT CARE
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FOOT CAREFOOT CARE
Check the feet daily.
Monitor for :redareas,cuts,blister,corns,ingrown
toe nails,calluses,cracks in theskin and changes in color. Check the skin for dry and
changes in skin color. Wash feet for lukewarm waterand mild soap.
ContCont
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Cont,Cont,
Do not soak feet. Dry feet thoroughly with a soft toweland pat gently.*DO NOT RUB*
Use moisturizing lotion to prevent skincracking DO NOT APPLY BETWEENTOES-CAN INCREASE RISK OF
INFECTION. Use a pumice stone to remove callus
NUTRITIONNUTRITION
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Advice pt to avoid adding sugar to food Avoid food that sweetened with sugar orhoney
Smoking cessation*** CHECK BLOOD GLUCOSE LEVEL
REGULARLY
*** INCREASE FLUID INTAKE Limit intake of saturated fat andcholesterol in food.
NUTRITIONNUTRITION
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REFERENCEREFERENCE Medical Surgical Nursing Fourth Edition
Pricilla LeMone & Karen Burke ( Page: 562 603 )
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MEMBERSMEMBERSSOLEHAH
IZZATULELLMY
NUR NADIA
TASHA
NUR FARIHAH
LATHA
NURFARAHANIMS
UHAIDA
SITI FATIMAH
NOOR AZIZAH
SHAMINI DEVI
ZURAINI
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