DIABETES

MELLITUS
MOHD WAFIY ARIFFIN BIN
ANWAR
1090273
 Review of Anatomy and
Physiology
PANCREAS
HORMONES:

INSULIN BY BETA CELLS

GLUCAGON BY ALPHA CELLS

 Pancreas secretes 40-50
units of insulin daily in two
steps:
Secreted at low levels during
fasting ( basal insulin
secretion)
Increased levels after eating
(prandial)
An early burst of insulin occurs
within 10 minutes of eating
Then proceeds with increasing
release as long as
hyperglycemia is present
 The role of insulin
Uptake of glucose from blood into muscle
& fat cells
Stops hepatic gluconeogenesis
Increases glycogen production in liver &
muscle
Stimulates fat & protein synthesis
DIABETES MELLITUS
is a chronic disorder of
carbohydrate, protein,
and fat metabolism
resulting from insulin
deficiency or abnormality
in the use of insulin
Types
1.Type I
formerly known as Insulin
Dependent Diabetes Mellitus (IDDM)
Autoimmune (Islet cell antibodies)
Early introduction of cows milk and
cereals
Intake of medicine during pregnancy
Indoor smoking of family members
destruction of beta cells of the
pancreas little or no insulin
production
requires daily insulin admin.
may occur at any age, usually appears
below age 15
2. Type II
formerly known as Non Insulin
Dependent Diabetes Mellitus (NIDDM)
probably caused by:
disturbance in insulin reception in the
cells
number of insulin receptors
loss of beta cell responsiveness to
glucose leading to slow or insulin
release by the pancreas
occurs over age 40 but can occur in
children
common in overweight or obese
w/ some circulating insulin present,
often do not require insulin
Risk Factors
Obesity
Race
History of CVD
HTN
Physical inactivity
Familial history
Polycystic Ovary Syndrome
Gestational Diabetes

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Clinical Manifestations ( Signs and Symptoms)

- Polyuria - weakness
- Polydipsia - fatigue
- Polyphagia - blood sugar / glucose level
- weight loss - (+) glucose in urine (glycosuria)
- nausea / vomiting
Diagnostics
Interventions for Diabetes Mellitus
A.Dietary Management

1. Follow individualized meal plan and snacks as

scheduled
Balanced diabetic diet 50% CHO, 30% fats, 20%
CHON, vitamins and minerals
diet based on pts. size, wt., age, occupation and
activity
2. Pt. must have adequate CHO intake to correspond to
the time when insulin is most effective
3. Routine blood glucose testing before each meal and at
bedtime is necessary during initial control, during
illness and in unstable pts.
4. Do not skip meals
5. Measure foods accurately, do not estimate
6. Less added fat, fewer fatty foods and low-cholesterol
Interventions for Diabetes Mellitus
A.Dietary Management

7. Advise use of complex carbohydrates to help

stabilize blood sugar. Meal should include more
fiber and starch and fewer simple or refined
sugars.
8. Avoid concentrated sweets, high in sugar
(jellies, jams, cakes, ice cream)
9. If taking insulin, eat extra food before periods of
vigorous exercise
10.Avoid periods of fasting and feasting
11.Keep weight at normal level, obese diabetics
should be on a strict weight control program
and should lose weight.
B. Teach pt. on correct administration of insulin
and other hypoglycemic agents.
1. insulin in current use may be stored at room
temp., all others in ref. or cool area
2. avoid injecting cold insulin lead to tissue
reaction
3. press (do not rub) the site after injection
(rubbing may alter the rate of absorption of
insulin)
4. avoid smoking for 30 mins. after injection
(cigarette smoking absorption)
5. Rotate sites
Failure to rotate sites may lead to
Lipodystrophy
Lipodystrophy localized
disturbance of fat metabolism
Ex. Lipohypertrophy thickening of
subcutaneous tissue at injection site,
feel lumpy or hard, spongy
result to absorption of
insulin making it difficult to
control the pt.s blood glucose
 Insulin
injection
sites
Insulin
Factors that influence the bodys
need for insulin

1. need : trauma, infection, fever, severe

psychological or physical stress, other
illnesses
2. need : active exercise
ACUTE COMPLICATIONS OF
DIABETES MILLETUS
DIABETIC KETO-ACIDOSIS (DKA)

INSULIN SHOCK

HYPERGLYCEMIC, HYPEROSMOLAR,
NONKETOTIC (HHONK) COMA

DAWN PHENOMENON
 D.K.A.
PATHOPHYSIOLOGY
NO INSULIN

OSMOTIC
DEHYDRATION MARKED HYPERGLYCEMIA

GLUCOSURIA LIPOLYSIS CELLULAR

HUNGER
OSMOTIC
DIURESIS WEIGHT
LOSS
POLYPHAGIA
POLYURIA
POLYDIPSIA
D.K.A.
S/SX:
S/SX OF DM +
KETONURIA
METABOLIC ACIDOSIS
KUSSMAULS RESPIRATION
ACETONE BREATH
TACHYCARDIA
CIRCULATORY COLLAPSE
COMA DEATH
The biochemical criteria for the diagnosis of DKA
are :
Hyperglycaemia: blood glucose > 11 mmol/L
(> 200 mg/dL).
Ketonaemia and ketonuria.
Venous pH < 7.3 or bicarbonate <15 mmol/L.

Goals of therapy
Correct dehydration.
Correct acidosis and reverse ketosis.
Restore blood glucose to near normal.
Avoid complications of therapy.
Identify and treat any precipitating event.
CHRONIC COMPLICATIONS OF DIABETES
MILLETUS
DEGENERATIVE CHANGES IN THE
VASCULAR SYSTEM
UNDERNOURISHMENT
ATHEROSCLEROSIS
NEUROPATHY FROM:
VASCULAR INSUFFICIENCY
HYPERGLYCEMIA
EYE COMPLICATIONS FROM ANOXIA
CATARACT
DIABETIC RETINOPATHY
RETINAL DETACHMENT
Hypothyroidism
 Physiology
In utero:
Small amount of thyroxine deliver to fetous
Fetal thyroid predominantly produce inactive T3
After birth:
TSH , T3 and T4.
TSH after several weeks to normal adult level
Preterm may have low T4 for several weeks, TSH normal range
Its important for
brain dev. and intellectual f(x) during prenatal and early post-natal.
For bones and foetal lungs.
 Overview
Common : 1/4000
In Malaysia, 1/3666

One of preventable cause of learning difficulties

Types:
Congenital
Juvenile
 Causes
Maldescent of thyroid and athyrosis
Failure of desecend frm sublingual below larynx
Partially or incomplete development of thyroid
May stay as lingual mass or uni-lobular small gland
Cause: unknown
Dyshormonogenesis
Inborn error of thyroid synt, (1-5%)
Common in certain ethnic with consanguineous marriage.
Iodine def.
Commonost cause worlwide, prevented with iodinized salt.
2ry to TSH def.
Rare ( <1%)
Ass with panhypopituitarism
Clinical features
Congenital Acquired

Usually asymptomatic and picked Females > males

up on screening. Short stature/growth failure
Otherwise: Cold intolerance
Failure to thrive Dry skin
Feeding problems Cold peripheries
Prolonged jaundice Bradycardia
Constipation Thin, dry hair
page 442
Pale, cold, mottled dry Box
skin Pale,
25.7 Clinical features puffy eyes with loss of
of hypothyroidism page 443

Coarse facies eyebrows

Large tongue Goitre
Hoarse cry Slow-relaxing reflexes
Goitre (occasionally) Constipation
Umbilical hernia Delayed puberty
Delayed development Obesity
Slipped upper femoral epiphysis
Deterioration in school work
Learning difficulties
 D(x)
On routine neonatal biochemical screening ( Guthries test).
TSH in blood except in hypothyroidism 2ry to TSH def. ( TSH
)
 Treatment
Urgent treatment once diagnose
Treatment is life-long unless suspect transient hypothyroidism
Treatment: L-thyroxine crashed and mixed with breast, formula
milk or water
Caution : not to give with soy beans and iron containing
product.
Goal of post- therapy: