Hope Parrocho

Jennylyn Passilan
Jessica Anne Perez
Kenneth Pesarillo
What is Diabetes Mellitus?

 metabolic disorder characterized by

a hyperglycemia or blood sugar
levels are abnormally high.

lack of insulin
lack of insulin effect
both
 3 Classifications
 Type 1
 aka insulin-dependent diabetes or juvenile-
onset diabetes

 Type 2
 aka non-insulin-dependent diabetes or adult-
onset diabetes

 Gestational Diabetes
Definition of Terms:

 Glucose - is a simple sugar found in

food

 Insulin - called the "hunger hormone"

 Hyperglycemia - or raised blood

sugar
HISTORY
 The best early evidence of a
description of the symptoms of
diabetes Ebers papyrus that appears
to date from 1550 B.C
 polyuria to Imhotep

 1674 - Thomas Willis

 discovered (by tasting) that the urine of
individuals with diabetes was sweet
HISTORY
 Matthew Dobson
 boiling urine to dryness had the
appearance and taste of “brown sugar”

 1788- Thomas Cawley

 first published reference to the pancreas
in relation to human diabetes
HISTORY

 1910 - Jean de Meyer

 pancreatic secretion be called “insulin”
to denote its origin from the “insulae” of
Langerhans
 Etiology And Epidemiology
 More than 8% of all adults in the US have diabetes, and
93% of these have Type 2.

 Prevalence of type 1 is higher in white populations in US

 Type 2 is most prevalent in persons of African,

American, Indian, Asian, Hispanic, and pacific Islander
descent

 Most studies of type 1 diabetes have considered only the

disease occurrence in children, typically under the age of
15 years
 Etiology And
Epidemiology
 Early exposure to cow's milk protein

 Risk of developing diabetes (type 2 according to the

current criteria) was higher in obese than nonobese
individuals

 Both a high weight before age 18 years and a large

weight gain during adulthood (after age 18 years)
contributed significantly to the risk of subsequent type
2 diabetes

 Individuals with a modest level of exercise had a

significantly lower risk of type 2 diabetes than did those
who were completely sedentary
 The World Health
Organization (WHO)
 estimates that more than 180 million people
worldwide have diabetes. This number is likely
to more than double by 2030
 In 2005, an estimated 1.1 million people died
from diabetes 1
 Almost 80% of diabetes deaths occur in low
and middle-income countries
 The World Health
Organization (WHO)
 Almost half of diabetes deaths occur in people
under the age of 70 years; 55% of diabetes
deaths are in women.

 WHO projects that diabetes deaths will

increase by more than 50% in the next 10
years without urgent action. Most notably,
diabetes deaths are projected to increase by
over 80% in upper-middle income countries
between 2006 and 2015
 TYPE I DM: a.k.a IDDM
 TYPE II DM: a.k.a NIDDM
 INSULIN RESISTANCE: DECREASE
ABILITY OF PERIPHERAL TISSUES TO
RESPOND TO INSULIN
 B-CELL: INSULIN GENE, REGULATES
INSULIN RELEASE
 KETOACIDOSIS:
TYPE I VERSUS TYPE II DM

TYPE I TYPEII
 ONSET: <20 years  ONSET: >30 years
 Normal weight  Obese
 Markedly decrease  Increase blood insulin
blood insulin (early); normal to
 Ketoacidosis common moderate decreased
insulin (late)
 Autoimmune
destruction of B-cells  Ketoacidosis rare
mediated by T cells and  Insulin resistance in
humoral mediators skeletal mm, adipose
 Absolute insulin tissue and liver
insufficiency  B-cell dysfunction and
 TYPE I DIABETES MELLITUS

VIRAL INFECTIONS
TISSUE DAMAGE AND
INFLAMMATION

RELEASE OF B-CELL ANTIGEN

ACTIVATION OF LYMPHOCYTE AND

OTHER INFLAMMATORY
-
LEUKOCYTES IN THE TISSUES

T LYMPHOCYTES REACT AGAINST B-CELL

ANTIGENS AND CAUSE CELL DAMAGE

T LYMPHOCYTES ALSO SECRETE

CYTOKINES THAT ACTIVATE
MACROPHAGES
 TYPE II DIABETES MELLITUS
(INSULIN RESISTANCE)

USUALLY ASSOCIATED WITH OBESITY

MARKEDLY INCREASE OF TRIGLYCERIDE IN

MUSCLE AND LIVER TISSUES

ABNORMALITIES OF INSULIN SIGNALLING

PATHWAY

INSULIN RESISTANCE STATE

 TYPE II DIABETES MELLITUS
(B-CELL DYSFUNCTION)

INSULIN RESISTANCE

HIGHER INSULIN SECRETION

(HYPERINSULINEMIC STATE)

B-CELL COMPENSATION BECOMES INADEQUATE

INSULIN DEFICIENCY
 Polyuria – frequent and excessive
urination
 osmotic diuresis caused by excess glucose
in urine.
 Polydipsia – excessive thirst associated
with dehydration.
 Polyphagia – cells do not receive
glucose leading to starvation which
triggers excessive eating.
 Weight loss
 Weakness and fatigue
 Muscle cramps – due to electrolyte
imbalance.
 Abdominal discomfort and pain – due
to autonomic neuropathy, causing
gastroparesis and constipation.
 Numbness and tingling – due to
neural tissue damage.
 Vision changes
 Slow healing skin infections or wounds
and itching of skin- due to impaired
peripheral circulation.
 Nausea and diarrhea
 Kussmaul respiration – acetone is
exhaled thus breath has fruity odor.
 excess acids caused increased H+ and CO2
level.
 Stimulate brain to increase rate and
depth of respiration to excrete acid and
CO2.
 Diabetic Ketoacidosis – altered lipid
metabolism
 free fatty acids are shunted into ketone
body formation due to lack of insulin; the
rate of formation exceeds the capacity for
their peripheral utilization and renal
excretion leading to accumulation of
ketoacids and therefore metabolic acidosis.
 Hypercholesterolemia and
atherosclerosis
 Microvascular diseases –
nephropathy (kidney
dysfunction);neuropathy (nerve
dysfunction);retinopathy (vision
problems), microaneurysms,
neovascularisation.
 Macrovascular diseases –including
coronary artery disease,
cerebrovascular accidents, peripheral
vascular disease.
 major risk factor for CAD & MI.
 Diabetic retinopathy - results in changes
in veins, arteries and capillaries
-damage occurs to the fragile blood
vessels in the retina
-could develop cataract and glaucoma
 Non proliferative Diabetic Retinopathy
vs Proliferative Diabetic Retinopathy
 Diabetic Nephropathy -progressive
kidney disease caused by angiopathy
of capillaries in kidney glomeruli.
 Hyperosmolar hyperglycemic
nonketotic syndrome
 Diabetic Neuropathy
 Skin ulcerations
 Hypokalemia and Hyponatremia- lack
of insulin causes depetion of potassium
and sodium
 Based on various chemical test in
urine and blood
 URINARY SUGAR
 TEST used in determining the amount of
gulcose lost in the urine
N:undetactable amount of glucose
With DIABETES: small amount of glucose
 FASTING BLOOD GLUCOSE LEVEL
 Early in the morning
 N: 80-90
 110 highest normal
 (higher than.. Consider diabetes)
 GLUCOSE TOLERANCE CURVE
 1 gram of glucose
 90 to 120 to 140
 Back to normal within 2 hours
Px with diabetes:
Within 4-6 hours, sometimes fail
It indicates normal insulin secretion
 ACETONE BREATH
 SEVERE
 Smell the breath of the patient
 Excessive acetoacetic acid in the blood
 TYPE 1
 Insulin replacement
 Meal planning
 Exercise
 Pancreas transplantation
 TYPE 2
 Oral ant diabetic to stimulate insulin
production
 (other drug combination)
 BOTH TYPES
 Monitor the blood glucose
 Meal plan
 Weight reduction for obese (type2)
 AS A PT:
 Educate the patient
 Diet
 Purpose
 Possible outcome effect of drugs
 Exercise
 Monitoring
 prevention
THANK YOU AND
GOD BLESS!