Diabetes Mellitus
• Hyperglycemia [wt loss, fatigue, 3P and
• Group of metabolic diseases characterized by
increased levels of glucose in the blood
(hyperglycemia) resulting from defects in
insulin secretion, insulin action or both.
• Most common endocrine disorder
• Basic etiology = unknown
• Insulin = hormone produced by pancreas
secreted by the beta cells of the islets of
Langerhans that controls the level of glucose in
the blood by regulating the production and
storage of glucose.
Cardinal Signs [3P and Wt loss]
• Polydipsia = thirst being a sign of dehydration
r/t polyuria
• Polyuria = due to secretion of glucose
(glycosuria) and ketones (ketonuria) that exerts
osmotic pressure.
• Polyphagia = due to cellular starvation
• Weight loss = due to unavailability of energy
for cellular use, protein and fat stores are used
up.
Classification
• Type 1 diabetes = (IDDM and juvenile DM)
insulin-producing pancreatic beta cells are
destroyed by the autoimmune process. As a
result, little or no insulin produced.
Characterized by acute onset usually before 30.
= in the absence of insulin, glucose
accumulation in the blood and urine leading to
hyperglycemia and glycosuria.
• Type 2 diabetes = (NIIDM) people have insulin
resistance and relative insulin deficiency results
in decreased insulin production.
= etiology: strong hereditary component,
commonly associated with obesity
= middle-aged and obese adults, 99% of
all cases in the Philippines
• Prediabetes = abnormality in glucose values
intermediate b/w normal and overt diabetes.
• Gestational diabetes = carbohydrate
intolerance occurring during pregnancy
Laboratory tests
• Blood Glucose
• Fasting Blood Sugar = [N=70-110 mg/dL]
8 hour fast overnight
• Random Blood Sugar = 200 mg/dL
• Postprandial test = 2 hours after meals.
• Glucose tolerance test [best method] = after
normal diet, FBS and urine sample is taken in
the morning then ingestion of glucose load then
blood sugar and urine is monitored after
1,2,and 3 hours.
• Glycated Hgb = measures glycemic control
over previous 3 months
• C-peptide assay and fructosamine assay
General Procedures and Treatment Modalities
• Blood Glucose Monitoring
• Insulin Therapy
Clinical Manifestations
blurred vision]
• Altered tissue response [poor wound healing,
recurrent infx]
Management
• Diet [considered as cornerstone] = caloric
restriction to carbohydrates and saturated fats
[to maintain IBW}
• Goal of meal planning = control blood
glucose and lipid levels.
• Wt reduction = primary tx for type 2 DM.
• Carbo [50-60%], proteins [20%], fats [30%
which 90% unsat fat]
• Don’t skip or delay meals ; small frequent
meals
• Measure amount of food given
• Increase intake of soluble and insoluble
fiber
• Avoid salt, limit refined sugars, high
fructose sources, food and bevs with
concentrated sucrose
• Exercise =lowers BS, facilitates wt reduction,
enhance insulin action, decrease BP and
stress, improves CV fitness.
• Medication = oral antidiabetic agents [for
type2] – sulfonylureas [ stimulates pancreas to
secrete insulin; for type 2 only], metformin
[biguanides – facilitates action of insulin on
peripheral receptor sites; contraindicated w/
renal dse]; AGI- delays glucose absorption;
thiazolidinediones
• Insulin therapy = abdomen [fastest
w/shortest duration, arms, thighs,
buttocks.
= sources – pork, beef, human stored at
cold temp.
= [categories] rapid acting [lispro,
aspart], short acting [regular], intermediate
acting [NPH, lente], long-acting [ultralente],
very long acting [glargine]
= complications – hypoglycemia,
lipodystrophy [localized rxn prevented by
rotating sites], somogyi effect [rebound
hypoglycemia], dawn phenomenon
[increase of blood sugar at 5-6am]
• Hypoglycemic agents = drug that act
either to stimulate the islet cells to secrete
more insulin (oral) or act as insulin
rplacement when pancreatic function
ceases.
=sfx= hypoglycemic rxns, GI
distress, neurological symptoms, alcohol
intolerance, allergic rxns.
Complications
• Acute = hypoglycemia [insulin rxn]
= DKA [absence or markedly
inadequate amount of insulin;
hyperglycemia, dehydration and
electrolyte loss and acidosis]
= Hyperglycemic hypersmolar
nonketotic syndrome (HHNS) [relative
insulin deficiency inititated by an
intercurrent illness that raises the
 demand for insulin assoc w/ polyuria Pathophysiology
and dehydration]
• Chronic = Macrovascular complications
[CVD, CAD, Peripheral artery dse]
= microvascular [Retinopathy –
deterioration of the small blood vessels
that nourish the retina
= nephropathy = damaged kidney cells;
characterized by microalbuminuria in
early stages.
= neuropathy = group of dse that
affectsall types of nerves [ peripheral or
autonomic neuropathy]
Nephropathy = renal dse 2ndary to diabetic
microvascular changes in the kidney.
= if blood glucose are elevated consistently for
a significant period of time, the kidney’s filtration
mechanism is stressed, allowing blood proteins to leak
in the urine. As a result, increase pressure in the blood Modifiable factors
vessels of the kidney.
• Large vessels [ aorta, coronary artery, basilar
artery to the brain and etc] eventually become
sclerosed and tortous
• Lumen narrow resulting to decreased blood
flow to the heart, bladder and the lower
extremities.
• Vessel completely occluded or rupture
• Rupture to the intima of the blood vessel is the
cause of local edema and intravascular clotting
Classifications
• Essential HPN [benign, idiopathic,
primary]
• Renal HPN
• Malignant HPN
• HPN crisis
• Stress, obesity, diet

Assessment Non-modifiable factors

• evidence of increased glomerular filtration rate • Family history, age, gender, ethnic group
• microalbuminuria = 1st clinical sign of renal dse.
• Elevation of BUN and creatinine. [ creatinine = Non-pharmacologic intervention
• Wt reduction
0.7-1.4 mg/dL or 62-124 umol/L; BUN = 10-20
mg/dL or 3.6 – 7.2 mmol/L] • Caffeine, Na restriction
• gross proteinuria. • Low fat diet
• Relaxation, exercise
Management/ intervention • Smoking cessation, alcohol limitatiom
• Control of HPN [DOC= ACE inhibitors or • K and Ca supplementation
calcium channel blockers] and blood glucose
• Prevention or tx of UTI Pharmacologic intervention
• Avoidance of nephrotoxic substances • Diuretics
• Adjustment of medications as renal fxn changes • Vasodilators
• Low Na and protein intake • Beta blockers
• Alpha adrenergic inhibitor
Hypoglycemia = <60; cold and clammy • Central acting adrenergic inhibitor
Hyperglycemia = >110; hot and dry • Calcium channel blocking agents

Antidiabetics and glucagons Management

• Acarbose alpha- glucosidase inhibitor • Lifestyle modifications
• Chlorpropamide -sulfonylureas • Drug therapy
• Exenatide – incretin mimetic
• Glimepiride -S Objective cues
• Elevated BP
• Glipizide - S
• Retinal changes
• Glucagon – S/ antihypoglycemic
• Possible hematuria
• Glyburide - S • Epistaxis
• Insulin – pancreatic hormone • Cardiac hypertrophy
• Metformin Hcl - biguanides
• Miglitol - AGI Diagnostic evaluation
• Nateglinide – meglitnide derivative • ECG
• Pioglitazone Hcl • Chest x-ray
• Pramlintide acetate • Prteinuria, creatinine and BUN
• Repaglinide • Serum K
• Rosiglitazone maleate- TZD • u/a
• Sitagliptin phosphate
Complications
• Angina pectoris or MI
Hypertension [silent killer] • LVH and heart failure
= persisted elevated BP [systolic >140 and • Renal failure
diastolic >90] • TIAs, stroke, cerebral hemorrhage
• Retinopathy