DIABETES MELLITUS AND PITUITARY DISORDERS NO insulin production Prone for DKA
Management:
Diet
Exercise
Insulin
Type II (NIDDM)
Maturity – onset, Stable DM, Ketosis – resistant
DM
Onset is 40 years
Common in obese adults
Inadequate insulin production or cells do not
respond to insulin
Prone for HHNKS
Diabetes Mellitus
Management:
a chronic metabolic disease characterized by
hyperglycemia due to disorder of carbohydrate, Diet
fat and protein metabolism Exercise
OHA, Insulin in STRESSFUL situation
Predisposing Factors:
Hyperglycemia Polyuria, Polydipsia, Polyphagia
Heredity: strongly associated with Type II DM
Obesity: Adipose tissues are resistant to insulin, Pathophysiology
therefore glucose uptake by the cells is poor Hyperglycemia
Stress: Stimulates secretion of epinephrine, nor- ↓
epinephrine, glucocorticoids increased serum Large amounts of glucose pass thru kidneys
carbohydrates ↓
Viral infection: increase risk to autoimmune It will exert high osmotic pressure w/in the renal
disorders tubules
Autoimmune Disorders: more associated with ↓
Type I DM Osmotic diuresis
Multigravida Women: with large babies ↓
Polyuria
Types of DM
Type I
Type II
Gestational Diabetes
Diabetes associated with other conditions or
syndromes
o Pancreatic disease, Cushing’s syndrome
o Use of certain drugs
Due to blood osmolarity, water moves from
o Steroids
inside to outside the cell (ICF dehydration)
Type I (IDDM) There will be hypovolemia (ECF dehydration)
Glycosuria will occur if glucose in the blood is
Juvenile – onset, Brittle DM, Unstable DM
>220mg/dl (renal threshold)
Onset is less than 30 years
Common in children or in non-obese adults Glucose Insulin Cell
↓
Cellular o Infections, Periodontal, UTI, Vasculitis,
Starvation Cellulitis, Vaginitis, Furuncles,
↓ Carbuncles, Retarded Wound Healing
Hunger & ↑Appetite Polyphagia
Complications:
Glucose Cell Macroangiopathy
o Brain: Cerebrovascular accident
Cellular o Heart: Myocardial infarction
Starvation o Peripheral arteries: peripheral vascular
Protein disease
Fats Ketones Microangiopathy
Polyphagia o Kidneys: renal failure due to
nephropathy
o Eyes: cataracts due to retinopathy
Neuropathy
o Spinal Cord/ ANS
o Peripheral neuropathy
involves damage to the PNS
affect movement, sensation and
bodily functions (numbness/
tingling)
o Paralysis
o Gastroparesis (delayed gastric
emptying)
o Neurogenic bladder (bladder does not
o empty properly)
o Decreased Libido, impotence
Ketones act as CNS depressants and may
decrease brain pH leading to coma Diagnostic Test
Random Blood Sugar (RBS)
o Blood specimen is drawn without
preplanning
o ≥200mg/dl + symptoms is suggestive of
DM
Fasting Blood Sugar (FBS)
o Blood specimen after 8 hours of fasting
o No DM (70-110 mg/dl)
Postprandial Blood Sugar
o Blood sample is taken 2 hrs after a high
CHO meal
o No DM (70-110mg/dl), DM (≥140)
Oral Glucose Tolerance Test (OGTT)
o Client then fast for 8 hours. A baseline
blood sample is drawn & a urine
specimen is collected
Due to increased blood viscosity o An oral glucose solution is given
o Sluggish circulation
o Proliferation of microorganisms
o Blood is drawn at 30 minutes & 1, 2, Intermediate
and 3 hours after the ingestion of - NPH 1-2 hrs 6-12 hrs 18-24 hrs
glucose solution. Urine is collected - Humulin N 1-2 hrs 8-12 hrs 18-24 hrs
o No DM (glucose returns to normal in 2- - Lente, Humulin L 1-2 hrs 8-12 hrs 12-28 hrs
3 hours & urine is negative for glucose) Long acting
o DM (blood glucose returns to normal - Ultralente 5-8 hrs 14-20 hrs 30-36 hrs
- Lantus UK UK 24 hrs
slowly; urine is positive for glucose)
Glycosylated hemoglobin (HbA1c)
o The amount of glucose stored by the Nursing Responsibilities
hemoglobin is elevated above 7% in the
Insulin Therapy:
newly diagnosed client with DM, in one
who is noncompliant, or in one who is Route: SubQ
Inadequately treated o slow absorption, less painful, 90° (thin)
45° obese clients,
Management
o no need to aspirate, do not massage
Diet site of injection
o Low caloric diet specially if obese o IV insulin: given in emergency cases
o Diet should be in proportion (DKA)
20% CHON Administer insulin at room temperature
30% Fats o Cold insulin can cause lipodystrophy
50% CHO
Lipoatrophy - loss of subcutaneous fat usually caused by
o Consume complex CHO and HIGH fiber
the utilization of animal insulin
diet
inhibits glucose absorption in Lipohypertrophy - development of fibrofatty masses,
the intestines usually caused by repeated use of injection site
Exercise
o Increases CHO uptake by the cells Store vial of insulin in current use at RT
o Decreases insulin requirements o Insulin can be stored at RT for 1 month
o Maintains ideal body weight, serum o Other vials should be refrigerated
carbohydrates & serum lipids Rotate the site of injection
Medications: o To prevent lipodystrophy
o Insulin (for type I and type II) o Lipodystrophy inhibits insulin
o Oral Hypoglycemic Agents (OHA) absorption
For type I Gently roll vial in between the palms to
Sulfonylureas redistribute insulin particles
Nonsufonylureas DO NOT Shake
- Biguanides o bubbles make it difficult to aspirate
- Alpha-glucosidase inhibitors exact amount
- Thiazolidinediones Observe for side effects of insulin therapy
- Meglitinides o Localized: Induration or Redness,
Swelling, Lesion at the site,
Insulin Onset Peak Duration Lipodystrophy
Rapid Acting o Generalized:
- Lispro (Humalog) 5 mins 30 mins-1 2-4 hours Edema: due to sudden
- Aspart (Novalog) hr
resolution of hyperglycemia
Short Acting
Hypoglycemia
- Regular (Humulin 30 min – 2 – 4 hrs 6-8 hrs
Somogyi phenomenon
R, Novolin R, Iletin 1 hr
II regular) Sulfonylureas “insulin releasers”
o Stimulate the beta cells to secrete more o 3-4 oz regular soft-drink, 8 oz fruit
insulin juice, 5-7 pcs lifesaver’s candies, 3-4
o Increases the ability of insulin cell pcs hard candies, 1 tblsp sugar, 5 ml
receptors to bind insulin pure honey/ karo syrup
o SE: weight gain, hypoglycemia, o 10-15 gm CHO
secondary failure of pancreas due to o D5W 20-50 ml IV push ( if unconscious)
overstimulation or 1 mg glucagon
Tolbutamide (Orinase) o Monitor BS (blood sugar)
Acetohexamide (Dymelor)
Diabetes Ketoacidosis (DKA)
Tolazamide (Tolinase)
Chlorpropamide (Diabenese) Acute complication of DM characterized by
Glipizide (Glucotrol) o Hyperglycemia
Glyburide (micronase, Glynase) o accumulation of ketones in the body;
Glimepiride (Amaryl) causes metabolic acidosis
Nonsulfonylureas o frequently occurs in DM Type I (IDDM)
o Biguanides
Metformin (Glucophage) Precipitating factors:
Help tissues use available
undiagnosed diabetes
insulin more efficiently
neglect of treatment
“insulin sensitizers”
infection, cardiovascular disorder
SE: Stomach upset, flatulence,
other physical or emotional stress
diarrhea
no weight gain, no Assessment
hypoglycemia unlike
sulfonylureas 3 P’s
o Alpha-glucosidase inhibitors N&V, abdominal pain
Miglitol (Glyset), Acarbose warm, dry, flushed skin
(Precose) dry mucous membranes; soft eyeballs
Alpha-glucosidase is an Kussmaul’s respirations or tachypnea; acetone
intestinal enzyme that breaks breath or fruity breath
down carbohydrates into Altered LOC
glucose, when this enzyme is Hypotension
inhibited, the process of Tachycardia
forming glucose is slowed and Diagnostic Test
glucose is absorbed more
slowly from the small intestine Serum glucose (up to 600 mg/dL) and ketones
Taken 15 minutes before meal elevated (positive urine ketones)
BUN, Creatinine, Hematocrit are elevated (due
Hypoglycemia
to dehydration)
Causes: Serum sodium decreased, potassium (elevated
due to the acidosis)
Overdose of insulin, omission of meals, ABGs: metabolic acidosis with compensatory
Strenuous exercise, G.I. upset (N&V) respiratory alkalosis
Assessment: Nursing Management
<60 mg/dl Maintain a patent airway.
Management Maintain F&E balance.
o Administer IV therapy as ordered.
Simple Sugars p.o.
Normal saline (0.9% NaCl), then Urine positive for glucose
hypotonic (0.45% NaCl) sodium
chloride
o When blood sugar drops to 250 mg/dl, Nursing interventions:
may add 5% dextrose to IV
o Potassium will be added when the urine treatment and nursing care is similar to DKA,
output is adequate. excluding measures to treat ketosis and
metabolic acidosis
Observe for fluid and electrolyte imbalances,
especially fluid overload, hypokalemia &
hyperkalemia
Administer insulin as ordered.
o ONLY Regular insulin is given IV (drip or
push) and/or subcutaneously (SC).
o If given IV drip, give with small amounts
of albumin since insulin adheres to IV
tubing
o Monitor blood glucose levels frequently.
Check urine output every hour
Monitor vital signs
Assist client with self-care
Provide care for the unconscious client if in a
coma
Discuss with client the reasons ketosis
developed and provide additional diabetic
teaching if indicated
Hyperosmolar Hyperglycemic Nonketotic Syndrome
(HHNKS)
A complication of DM characterized by
o Hyperglycemia
o Hyperosmolar state without ketosis
Occurs in Type II DM
Precipitating factors are:
o undiagnosed diabetes
o Infections, major burns, other stress
o certain medications (Dilantin, Thiazide
diuretics)
o Dialysis, Hyper-alimentation, pancreatic
disease
Assessment findings:
Similar to ketoacidosis but without Kussmaul
respirations and acetone breath
Laboratory tests
Blood glucose level extremely elevated
BUN, creatinine, Hct elevated (due to
dehydration)
