DIABETES MELLITUS ➢ other clinical manifestations includes: > 3P's

➢ is a group of metabolic diseases characterized by ➔ polyphagia

increased levels of glucose in the blood ➔ polydipsia
(hyperglycemia) resulting from defects in insulin ➔ polyuria
secretion, insulin action, or both ➔ other symptoms includes: fatigue and
weakness, sudden vision changes, tingling
or numbness in hands or feet, dry skin,
PATHOPHYSIOLOGY: INSULIN
skin lesions or wounds that are slow to
➢ a hormone secreted by beta cells, which are one of
heal, and recurreinfections
four types of cells in the islets of langerhans in the
pancreas
➢ an anabolic, or storage, hormone ASSESSMENT AND DIAGNOSIS
➢ insulin secretion increases and moves glucose from
the blood into muscle, liver, and fat cells. in those HISTORY
cells, insulin has the following actions: ➢ symptoms related to the diagnosis of diabetes:
➔ transports and metabolizes glucose for ➔ symptoms of hyperglycemia
energy ➔ symptoms of hypoglycemia
➔ stimulates storage of glucose in the liver ➢ results of blood glucose monitoring
and muscle (in the form of glycogen) ➢ use of tobacco, alcohol and prescribed and
➔ signals the liver to stop the release of over-the-counter medication/drugs
glucose ➢ lifestyle, cultural, psychosocial and economic
➔ enhances storage of dietary fat in adipose factors that may affect diabetes treatment
tissue
➔ accelerates transport of amino acids PHYSICAL EXAMINATION
(derived from dietary protein) into cell
➢ blood pressure (sitting and standing to detect
➔ inhibits the breakdown of stored glucose,
orthostatic changes)
protein, fat
➢ body mass index (height and weight)
➢ foot examination (lesions, signs of infection, pulses)
CLINICAL MANIFESTATION & CHARACTERISTICS ➢ skin examination using monofilament deep tendon
➢ tуре 1: previously classified as juvenile diabetes, reflexes
ketosis-prone diabetes and insulin dependent
diabetes mellitus iddm) DIAGNOSTIC TEST
➔ onset at any age but usually very young ➢ hgb
(<30 y.o) ➢ fasting lipid profile
➔ usually thin at diagnosis; recent weight ➢ test for microalbuminuria
loss ➢ serum creatinine level
➔ etiology includes genetic, immunologic and ➢ urinalysis
environmental factors e.virus ➢ electrocardiogram
➔ little or no endogenous insulin
➢ type 2: (previously classified as Adult-onset
diabetes, Maturity-onset diabetes, Ketosis-resistant
diabetes, stable diabetes, and
non-insulin-dependent diabetes NIDDMI)
➔ onset at any age usually at <30 usually
obese diagnosIs
➔ causes includes obesity, heredity and
environmental factors
➔ decrease in endogenous insulin, or
increased with insulin resistance

TRANSCRIPTED BY: KATRINA ALLYN A. CORDERO

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 ➢ DIABETES MELLITUS CRITERIA DIABETES MELLITUS COMPLICATIONS
➢ symptoms of diabetes plus plasma glucose ➢ hypoglycemia:
concentration equal to or greater than 200 mg/dl ➢ low sugar in the blood. (less than 70mg/dl
(11.1 mmol/l) ➢ manifestations:
➢ fasting plasma glucose greater than or equal to ➔ sweating, tremor, tachycardia, palpitations,
126mg/dl (7.0 mmoll. rasting is defined as no caloric nervousness, hunger
intake for at least 8 hrs ➔ moderate; inability to concentrate,
➢ two-hour postload glucose equal to or greater than headache, lightheadedness, confusion,
200 mg/dl (11.1mmol/l) during an oral glucose numbness of the lips and tongue, slurred
tolerance test. the test should be performed as speech, double vision, drowsiness
prescribed using a glucose load containing the ➔ severe; disoriented behavior, seizures,
equivalent of 75 g anhydrous glucose dissolved in difficulty arousing from sleep, or loss of
water consciousness.

MEDICAL MANAGEMENT MANAGEMENT

➢ administration of insulin ➢ treating with carbohydrates
➔ rapid acting (lispro, asparr, glulisine) ➢ initiating emergency measures
➔ short acting (regular - humalog r, novolin ➢ injection of glucagon 1mg (for px who are
➔ intermediate acting (nph) unconscious)
➔ very long acting (glargine, detemir) ➢ providing patient education
➔ premixed ➔ consistent pattern of eating, administering
➔ inhaled insulin and exercising
➔ oha (oral antidiabetic agents) ➔ snacks between meals
➔ amputation of infected leg/gangrenous
tissue DIABETIC KETOACIDOSIS
➢ ​caused by an absence or markedly inadequate
NURSING MANAGEMENT amount of insulin.
➢ patient education: ➢ 3 main causes of dka
➔ developing a diabetes education plan ➔ decrease or missed dose of insulin
➔ organize informationion ➔ illness / infection
➔ educating patients about survival skills ➔ undiagnosed and untreated diabetes
(must be learned by newly diagnosed type
1 or type < patients who are receiving PREVENTION: “SICK DAY RULES”
insulin) ➢ the most important concept in this is to never
➢ management of glucose eliminate insulin doses when nausea and vomiting
➔ blood glucose targets are 140 - 180 mg/dl occur. instead, patient should take the usual insulin
➔ insulin (subcutaneous or iv) dose
➔ appropriate timing of blood glucose ➢ drinking of fluids every hours is important to prevent
checks, meal consumptions, and insulin dehydration.
dose are all crucial for glucose control and ➢ blood glucose and urine ketones must be assessed
to avoid hypoglycemia. every 3 - 4 hours
➢ storing insulin
➔ whether short or long acting preparation,
MANIFESTATIONS
vials not in use, including spare vials or
➢ hyperglycemia of dka (the 3 p's), and marked
pens should be refrigerated.
fatigue. patient may experience blurred vision,
➢ mixing insulins
headache, weakness, orthostatic hypotension,
➔ when rapid or short acting insulins are to
weak rapid pulse.
be given simultaneously with longer acting
➢ ketosis and acidosis of dka lead to anorexia,
insulins, usually mixed with the same
nausea, vomiting and abdominal pain, px may also
syringe
have acetone breath (truity odor) russmauls
➢ selecting and rotating the injection site
respirations
➔ four main areas are; abdomen, upper arm
➢ mental status: alert, lethargic or comatose.
(posterior surface), thighs (anterior
surface), and hips
➔ the patient should not use the exact same
site

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MANAGEMENT
➢ rehydration:
➔ maintaining tissue perfusion, fluid
replacement enhances the excretion of
excessive glucose by the kidneys
➔ 6 - 10 L of fluid to replace fluid losses
➔ 0.9 % sodium chloride (NSS), half-strength
NS (0.45%)
➔ restoring electrolytes
➔ reversing acidosis

HYPERGLYCEMIC HYPEROSMOLAR SYNDROME

➢  etabolic disorder of type 2 diabetes resulting from
​m
a relative insulin deficiency initiated by an illness
that raises the demand for insulin

MANIFESTATION
➢ hypotension, profound dehydration (dry mucous
membranes, poor skin turgor), tachycardia and
variable neurologic signs (alterations of
consciousness, seizures, hemiparesis)

ASSESSMENT
➢ range of laboratory tests, blood glucose,
electrolytes, bun, complete blood count, serum
osmolality and arterial blood gas analysis (blood
glucose level usually 600-1200 mg/dl and the
osmolality exceeds 320 mosm/kg
➢ mental status changes, focal neurologic deficits and
hallucinations are common

NURSING DIAGNOSIS
➢ risk for deficient fluid volume related to polyuria and
dehydration.
➢ risk for electrolyte imbalance related to fluid loss or
shifts.
➢ deficit knowledge about diabetes self-care skill
information
➢ anxiety related to loss of control, fear or inability to
manage diabetes, misinformation in related to
diabetes, fear of diabetes complications

TRANSCRIPTED BY: KATRINA ALLYN A. CORDERO

Note: For educational use only. No copyright infringement.
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