pankreas (diabetis mellitus)

8/14/2019 Pankreas (Diabetis Mellitus)

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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.

C tC t


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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.

C tC t


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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.

C tC t


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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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pankreas (diabetis mellitus)

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