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 insulin-
dependent diabetes; onset before age 40
-Type 2: formerly called maturity-onset or non-
insulin-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- 2 hours after meal blood specimen is withdrawn- blood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

< 200 mg/dl > 200 mg/dl

(11.1 > (11.1
mmol/L) mmol/L)
Consider taking 2hr DIABETES MELLITUS
PG Confirm with FPG or
> 200 mg/dl OGTT
< 140 mg/dl 140-199 mg/dl
> 11.1 On a different days if
< 7.8 7.8-11.0
mmol/L condition of the
mmol/L mmol/L
Repeat 2hr patient allows
PG
LIFESTYLE
NORMAL DIABETES MELLITUS
MODIFICATION
Anatomy and Physiology
Insul in
*Insulin increases glucose transport into cells & promotes con-
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

Glucose is
rise in uptake of
metabolized
blood glucose into
generating ATP
pancreatic B
glucose w/n the cell
cells

This cause
secretion activation of the
B cell & influx of
of Calcium into the
cell
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 LIVER

the cell membrane of
SKELETAL MUSCLE
CELLS
CELLS and FAT
CELLS
INSULIN

Stored as
GLYCOGEN
 BLOOD GLUCOSE
Decreased
KIDNEYS water in
cells
increased glucose in blood
CELLULAR
increased blood DEHYDRATION
glucose
Osmotic effect of
glucose when blood send
passes thru kidney
SIGNAL to
tubules
the BRAIN
HYPERGLYCEMIA Decreased water Body experiences
that goes back to excessive THIRST
blood
Increased water in the
POLYURIA kidney tubules
POLYDIPSIA
 BLOOD GLUCOSE

Cells become
X
INSULIN

hungry
able to pass through

X
the cell membrane
of SKELETAL
MUSCLE CELLS
and FAT CELLS

INCR EA SED
APP ET ITE
 BLOOD GLUCOSE

Cells become
X
INSULIN

hungry
able to pass through

X
the cell membrane
of SKELETAL
MUSCLE CELLS
Brain
and FAT CELLS
interprets this
as LACK OF

send signal to

LIVE R
 FATS in PROTEI NS in
ADIPOSE MUSCLES
BREAKDOWN

Increased FATTY ACIDS AMINO ACIDS

amount in the
blood
Formation of
KETONE bodies

KETOACIDOSIS
LIV ER
GLUCONEOGENESIS

GLUCOSE
 FATS in PROTEI NS in
ADIPOSE MUSCLES
BREAKDOWN

FATTY ACIDS AMINO ACIDS

LIV ER
GLUCONEOGENESIS

GLUCOSE
 FATS in PROTEI NS in
ADIPOSE MUSCLES
PROTEINS from
BREAKDOWN
LENS

FATTY ACIDS AMINO ACIDS

decreased lens CHONs

BLURRING OF VISION
LIV ER
GLUCONEOGENESIS

GLUCOSE
 BLOOD GLUCOSE

Increased
glucose in the
X
INSULIN

blood
Blood vessels LIPID
later, will produce
function accumulates in
damage in blood
abnormally the walls of the
vessels walls
damaged blood
vessels
MYOCARDIAL
INFARCTION
decreas size of lumen of ATHEROMA
ANGINA ed blood vessels formation
STROKE blood are reduced
POOR HEALING supply
PROCESS
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 Serum glucose &
Secondary choices: thiazolidinediones
HbA1c remain
or an alpha-glucosidase inhibitor
elevated

Serum glucose Serum glucose

Add second oral agent or
& HbA1c normal & HbA1c remain
bedtime insulin
elevated

Add second oral agent, Serum glucose

Continue bedtime insulin, or other & HbA1c remain
insulin regimen elevated
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
 
Pr eventiv
*Prevent e
moisture from accumulatingFootbetween toes Car e
*Wear loose socks & well-fitting (not tight) shoes & instruct
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
Inst
*Meticulous skin r uctio
care & proper foot care ns

*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 Education During
*Take insulin or oral hypoglycemic agents as prescribed.

*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 magazine-
January 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!