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05/09/2014

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MS ABNORMALS

Endocrine Disorders

Let’s observe SILENCE!

“Showmanship muna, mamaya ang Testmanship!”

Gabriel, Joy

Garcia, John Diego

Gayo, Jacqueline

Ilumin, Jeffrey

Jacinto, Jayson -Emcee-

Jugo, Domingo Jr.

Junatas, Benjo Roy

Lagrata, Venesse

Landingin, Alvin

Leyva, Mark Philip

Liwanag, Mark Louie

Magliba, Veronica

DIABETES MELLITUS

General Information
Chronic disease caused by improper metabolic interaction of carbohydrates, protein, fats and insulin Interaction of pregnancy and diabetes may cause serious complications of pregnancy A CHRONIC DISORDER OF IMPAIRED GLUCOSE INTOLERANCE AND CARBOHYDRATE, PROTEIN & LIPID METABOLISM; CAUSED BY A DEFIECIENCY OF INSULIN

Major Types:
1. INSULIN-DEPENDENT DIABETES 2. NON-INSULIN DEPENDENT DIABETES Classifications of Diabetes mellitus: -Type 1: formerly called juvenile-onset or insulindependent diabetes; onset before age 40 -Type 2: formerly called maturity-onset or noninsulin-dependent; onset after age 40 -Type 3: formerly called gestational; onset during pregnancy; reversal after termination of pregnancy -Type 4: formerly called secondary; occurs after pancreatic infections or endocrine disorder

RISK FACTORS
Family History of diabetes (i.e. parents or siblings with diabetes) Overweight (BMI= 23kg/m) and obesity (BMI >30 kg/m) Sedentary lifestyle Hypertension HDL cholesterol <35 mg/dl (0.90 mmol/L) and/or triglyceride level >250 mg/dl (2.82 mmol/L) History of Gestational Diabetes Mellitus (GDM) or delivery of a baby weighing 9 lbs (4.0kgs) Previously identified to have Impaired Glucose Tolerance (IGT)

DIAGNOSTIC PROCEDURES
FBS (Fasting Blood Sugar) - Diabetes is detected by measuring the amount of glucose
in the blood after an individual has fasted (abstained from food) for about eight hours.

2 hour PPBS (2 hour Post Prandial Blood Sugar) - 2 hours after meal blood specimen is withdrawn- blood
sugar returns to normal level

OGTT/ GTT (Oral Glucose Tolerance Test) Glycosylated Hgb- Most accurate

Diagnostic criteria
Classical symptoms of Diabetes Mellitus
Random blood sugar

Consider taking 2hr PG < 140 mg/dl 140-199 mg/dl < 7.8 7.8-11.0 mmol/L mmol/L LIFESTYLE MODIFICATION > 200 mg/dl > 11.1 mmol/L Repeat 2hr PG

< 200 mg/dl (11.1 mmol/L)

> 200 mg/dl > (11.1 mmol/L)
DIABETES MELLITUS Confirm with FPG or OGTT On a different days if condition of the patient allows

NORMAL

DIABETES MELLITUS

Anatomy and Physiology

Insul in glucose transport into cells & promotes con*Insulin increases
version of glucose to glycogen, decreasing serum glucose levels *Primarily acts in the liver, muscle, adipose tissue by attaching to receptors on cellular membranes & facilitating transport of glucose, potassium & magnesium

Glucagon
*Hormone secreted by the alpha cells of the islets of Langerhans in the pancreas *Increase blood glucose by stimulating glycogenolysis in the liver *given SC, IM or IV routes *Used to treat insulin-induced hypoglycemia when semiconscious/

INS ULIN
GLU COSE - the mo st i mport ant st imu lu s fo r synt he si s
rise in blood glucose
uptake of glucose into pancreatic B cells Glucose is metabolized generating ATP w/n the cell This cause activation of the B cell & influx of Calcium into the cell

secretion of

PATHOPHYSIOLOGY OF DIABETES MELLITUS
Deficient insulin production  Hyperglycemia  Inc. concemtration of blood glucose  Glucosuria  Excess glucose excreted in urine  Excess fluid loss

Insulin deficiency  Impaired metabolism of CHON and fats  Weight loss  Decreased storage of calories  Polyphagia

BLOOD

GLUCOSE INSULIN
able to pass through the cell membrane of SKELETAL MUSCLE CELLS and FAT CELLS

LIVER CELLS
INSULIN

Stored as GLYCOGEN

BLOOD

GLUCOSE
KIDNEYS increased glucose in blood

Decreased water in cells
CELLULAR DEHYDRATION

increased blood glucose

Osmotic effect of

HYPERGLYCEMIA

glucose when blood passes thru kidney tubules

Decreased water that goes back to blood
Increased water in the kidney tubules

send SIGNAL to the BRAIN Body experiences excessive THIRST

POLYURIA

POLYDIPSIA

BLOOD

GLUCOSE INSULIN

Cells become hungry

X

able to pass through the cell membrane of SKELETAL MUSCLE CELLS and FAT CELLS

X

INCR EA SED APP ET ITE

BLOOD

GLUCOSE INSULIN

Cells become hungry

X

Brain interprets this as LACK OF

able to pass through the cell membrane of SKELETAL MUSCLE CELLS and FAT CELLS

X

send signal to

LIVE R

FATS in ADIPOSE

PROTEI NS in MUSCLES

BREAKDOWN

Increased amount in the blood

FATTY ACIDS

AMINO ACIDS

Formation of KETONE bodies

KETOACIDOSIS
LIV ER

GLUCONEOGENESIS

GLUCOSE

FATS in ADIPOSE

PROTEI NS in MUSCLES

BREAKDOWN

FATTY ACIDS

AMINO ACIDS

LIV ER

GLUCONEOGENESIS

GLUCOSE

FATS in ADIPOSE

PROTEI NS in MUSCLES
PROTEINS from LENS

BREAKDOWN

FATTY ACIDS

AMINO ACIDS decreased lens CHONs

BLURRING OF VISION
LIV ER

GLUCONEOGENESIS

GLUCOSE

BLOOD

GLUCOSE INSULIN

Increased glucose in the blood later, will produce damage in blood vessels walls

X

Blood vessels function abnormally

LIPID accumulates in the walls of the damaged blood vessels

MYOCARDIAL INFARCTION

POOR HEALING PROCESS

ANGINA STROKE

decreas ed blood supply

size of lumen of ATHEROMA blood vessels formation are reduced

Medical Pathophysiology

Getting BORED and SLEEPY?! It’s time for

Signs and Symptoms
POLYPHAGIA POLYDIPSIA POLYURIA HYPERGLYCEMIA WEIGHT LOSS BLURRED VISION SLOW WOUND HEALING VAGINAL INFECTIONS WEAKNESS & PARESTHESIAS SIGNS OF INADEQUATE FEET CIRCULATION

COMPLICATIONS
*HYPOGLYCEMIA *DIABETIC KETOACIDOSIS (DKA) *HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME (HHNS)

ACU TE COMPL ICA TI ON S
DIABETIC KETOACIDOSIS
precipitating factors: a. omission of insulin doses b. injuries c. emotional stress d. excessive alcohol intake e. intercurrent illness Pathogenesis : a. hyperglycemia – decreased insulin, increased glucagon resulting in increased glucose synthesis, breakdown of glycogen, and protein breakdown b. osmotic diuresis – increased glucose in the urine that attract water and electrolytes thus increasing urine volume c. ketogenesis – free fatty acids in the blood will form excess ketones d. acidosis – ketone bodies in the blood is not

Signs of Hypoglycemia
*sweating *tremor *tachycardia *palpitations *nervousness *hunger

HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC SYNDROME vs. DIABETIC KETOACIDOSIS (DKA)

Chronic Complications
- Chronic Renal Disease (Nephropathy) - Blindness (Retinopathy) - Coronary Artery Disease/ Stroke - Neuropathy - Foot Ulcers

Possible Nursing Diagnosis
- Altered Nutrition: due to

imbalanced less than body requirements

  - Knowledge deficit: disease process
 

 

PREVENTION AND CONTROL Maintain body weight and prevent obesity through
proper nutrition and physical activity/ exercise. Encourage proper nutrition- Eat more Dietary Fiber, reduce salt and fat intake, avoid simple sugars like cakes and pastries; avoid junk foods.

 

  Promote regular physical activity and exercise to prevent obesity, hypercholesterolemia and enhance insulin action in the body.   Advise smoking cessation for active smokers and prevent exposure to second- hand smoke. Smoking among diabetics increases risk for heart attack and

Health Teachings (Meds)
Oral Hypoglycemic Agents
  Sulfonylureas   Chlorpropamide (Diabinase) Tolbutamide (Orinase) Glimepinide (Solosa) Acetohexamide (Dymelor)   Prandial Glucose Regulator   Repaglinide (Novonorm) Rosiglitazone (Avandia)   Non-sulfonylureas   Metphormine (Glucophage) Precose (Acarbose) Rosiglitazone (Avandia)

70/30- mixture of Humulin N(cloudy) & Humulin R(clear)

Air (N)—Air(R)—Aspirate(R)—Aspirate(N)
N= 6-12hrs. R= 3-4hrs.

TREATMENT
APPROACH TO DIABETES MELLITUS:
DIET EXERCISE ORAL HYPOGLYCEMIC AGENTS/INSULIN

TREATMENT OF TYPE 2 DM
Encourage lifestyle modification (diet, exercise)
Treat with sulfonylurea or metformin Secondary choices: thiazolidinediones or an alpha-glucosidase inhibitor

Serum glucose & HbA1c remain elevated

Serum glucose & HbA1c normal

Add second oral agent or bedtime insulin Add second oral agent, bedtime insulin, or other insulin regimen

Serum glucose & HbA1c remain elevated Serum glucose & HbA1c remain elevated

Continue therapy

NURSING MANAGEMENT
D- IET: 50-60% CHO, 20-30% FATS, 10-20% CHON I- NSULIN A-NTIDIABETIC AGENTS B-LOOD SUGAR MONITORING E-XERCISE T-RANSPLANT OF THE PANCREAS E-NSURE ADEQUATE FOOD INTAKE S-CRUPULOUS FOOT CARE

Simple Carbohydrate to Treat Hypoglycemia
*3 or 4 commercially prepared glucose tablets CHILD: 2-3 GLUCOSE TABS   *4-6 ounces of fruit juice or regular soda CHILD: ½ CUP OR 120 ML OF ORANGE JUICE OR SUGAR-SWEETENED JUICE   *6-10 Life Savers or hard candy CHILD: 3-4 HARD CANDIES OR 1 CANDY BAR   *2-3 teaspoons of sugar or honey CHILD: 1 SMALL BOX OF RAISINS  

*Prevent moisture from accumulating between toes Car Pr eventiv e(not tight) shoes & instruct e Foot *Wear loose socks & well-fitting client not to go barefoot *Change into clean cotton socks daily *Wear socks to keep feet warm *Do not wear the same shoes 2 days in a row *Do not wear open toed shoes or shoes with strap that goes between toes *Check shoes for tears or cracks in lining & for foreign objects before putting them on *Break in new shoes gradually *Cut toenails straight across & smooth nails with an emery board *Do not smoke

Pr eventiv e F oot Car e *Meticulous skin care & proper foot care ns Inst r uctio
*Inspect feet daily & monitor feet for redness, swelling or break in skin integrity *Avoid thermal injuries from hot water, heating pads & baths *Wash feet with warm (not hot) water & dry thoroughly (avoid foot soaks) *Do not soak feet *Do not treat corns, blisters or ingrown nails *Do not cross legs or wear tight garments that may constrict

Client hypoglycemic agents as prescribed. Education During *Take insulin or oral
*Test blood glucose & test the urine for ketones every 3-4 hours *If meal plan cannot be followed, substitute with soft food 6-8 x per day *If vomiting, diarrhea or fever occurs, consume liquids every ½ to 1 hour to prevent dehydration & to provide calories *Notify doctor if vomiting, diarrhea, or fever persists, if blood glucose levels are greater than 250 to 300 mg/dL, when ketonuria is present for more than 24 hours, when unable to take food or fluids for a period of 4 hours, when illness persists for more than 2 days

NURSING CARE PLANS

DRUG STUDY

UPDATES!

AMPALAYA (MOMORDICA CHARANTIA)   Ampalaya (Bittern Melon) or it’s scientific name, Momordica Charantia has been a folkloric cure for generations but has now been proven to be an effective herbal medicine for many ailments. Most significant of which is Diabetes. The Philippine variety has proven to be most potent. Ampalaya contains a mixture of flavanoids and alkaloids make the Pancreas produce more insulin that controls the blood sugar in diabetics. Aside from Ampalaya’s medicinal value, it is good source of vitamins A, B and C, iron, folic acid, phosphorus and calcium.   Ampalaya has been for used even by the Chinese for centuries. The effectivity of Ampalaya as an herbal medicine has been tried and tested by many research clinics and laboratories worldwide. In the Philippines, the Department of Health has endorsed Ampalaya as an alternative medicine to help various ailments including diabetes, liver problems and even HIV.

Seen and heard online (comments coming from reader’s digest magazineJanuary 2008 issue) via rdasia.com
Q: What should be done to curb the rising trend of diabetes in Asia? - Government, media and health sectors should increase people’s awareness of the disease such as it’s cause, symptoms and effects and how to prevent its onset. -grampa_hann - Some guidelines about healthy diets will be useful, especially for families with high risk of diabetes - alberthahaha6 - Taking taheebo, ampalaya leaves and sambong helps - auriel769 - Kids spend the most time in school so that’s where the battle against diabetes should begin. - cintiazinha

THANK YOU!

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