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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- 2 hours after meal blood specimen is withdrawn- blood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
Glucagon
*Hormone secreted by the alpha cells of the islets of Langerhans
in the pancreas
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
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
KETOACIDOSIS
LIV ER
GLUCONEOGENESIS
GLUCOSE
FATS in PROTEI NS in
ADIPOSE MUSCLES
BREAKDOWN
LIV ER
GLUCONEOGENESIS
GLUCOSE
FATS in PROTEI NS in
ADIPOSE MUSCLES
PROTEINS from
BREAKDOWN
LENS
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
*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
N= 6-12hrs. R= 3-4hrs.
TREATMENT
APPROACH TO DIABETES
MELLITUS:
DIET
EXERCISE
*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 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