Cushing's Syndrome
as hypercortisolism that is characterized by hyperactivity of the
adrenal cortex. It results in excessive secretion of
glucocorticoids, particularly cortisol. An increase in
mineralocorticoids and sex hormones may also occur.
CAUSES
➔ Adenoma or carcinoma of the adrenal cortex and pituitary
gland.
➔ Excessive or prolonged administration of glucocorticoids or
corticotropin.
➔ Exogenous secretion of corticotropin by malignant neoplasms
in the lungs or gallbladder
➔ ectopic ACTH syndrome: tumor cells produce ACTH, which
stimulates the adrenal glands to overproduce cortisol
➔ Hyperplasia (increase of cells) of the adrenal glands.
➔ Hypertrophy: enlargement of tissue's size
➔ Hypothalamic (over) stimulation of the pituitary gland.
⬆️
ASSESSMENT FINDINGS
➔ Acne: Testosterone
➔ Amenorrhea: absence of menstruation
- Elevated cortisol levels can suppress gonadotropin-releasing
hormone (GnRH) secretion from the hypothalamus, leading to
decreased secretion of follicle-stimulating hormone (FSH) and
⬇️
luteinizing hormone (LH)
➔ Decreased libido: Androgen
➔ Ecchymosis: walls of blood vessels
⬆️
➔ Edema:
➔ Enlarged clitoris: testosterone
➔ Fragile skin: fluid accumulation
➔ Gynecomastia: in men
➔ Hirsutism: excessive hair
➔ Hypertension: accumulation of salt
➔ Mood swings: imbalance of hormones
➔ Muscle wasting:
➔ Pain in joints: gaining weight
➔ Poor wound healing
➔ Purple striae on abdomen: weakened connective tissue
➔ Recurrent infections: imbalance of cortisol (anti-inflammatory)
➔ Weakness and fatigue: fat deposits
➔ Weight gain, particularly truncal obesity, buffalo hump, and
moonface
DIAGNOSTIC TEST RESULTS
● Blood chemistry shows increased cortisol, aldosterone,
sodium, corticotropin, and glucose levels and a decreased
potassium level
● CT scan shows pituitary or adrenal tumors
● Dexamethasone suppression test shows no decrease in
17-OHCS (hydroxycorticosteroids)
● GTT shows hyperglycemia
● Hematology shows increased WBC and RBC counts and
decreased eosinophil count.
● Ultrasonography shows pituitary or adrenal tumors
● Urine chemistry shows increased 17-OHCS and 17-KS,
decreased urine specific gravity and glycosuria.
● X-ray shows pituitary or adrenal tumor and osteoporosis
● MRI shows pituitary or adrenal tumors
TREATMENT
➔ Hypophysectomy or bilateral adrenalectomy .
➔ Low-sodium, low-carbohydrate, low-calorie, high- potassium,
high-protein diet.
➔ Radiation therapy: instead of removing a tumor if
hypothalamus is affected.
➔ Potassium supplements: potassium chloride (K-Lor).
potassium gluconate (Kaon).
DRUG THERAPY
● Adrenal suppressants: if causative is adrenal. metyrapone
(Metopirone), aminoglutethimide (Cytadren)
● Antidiabetic agents: insulin or oral antidiabetic agents. such as
tolbutamide (Orinase), chlorpropamide (Diabinese),
acetohexamide (Dymelor), tolazamide (Tolinase), glyburide
(DiaBeta, Micronase), glipizide (Glucotrol)
● Diuretics: furosemide (Lasix), ethacrynic acid (Edecrin)
INTERVENTIONS AND RATIONALES
● Perform postoperative care to prevent complications
● Assess fluid balance to detect fluid deficit or overload
● Monitor and record vital signs, intake and output, urine
specific gravity, finger sticks, urine glucose and ketones, and
laboratory studies. Changes parameters may indicate altered
fluid of electrolyte status.
● Assess edema to detect signs of excess fluid volume
● Apply anti embolism stockings to promote venous return and
prevent thromboembolism formation
● Maintain the patient's diet to maintain nutritional status.
● Mantan standard precautions to protect the patient from
infection.
● Provide meticulous skin care and reposition the patient every
2 hours to prevent skin breakdown
● Limit water intake to prevent excess fluid volume
● Weigh the patient daily to detect fluid retention
● Administer medications, as prescribed, to maintain or improve
the patient's condition.
● Encourage the patient to express his feelings about changes
in body image and sexual function to keep him cope
effectively
● Provide rest periods to prevent fatigue
● Provide post radiation nursing care to prevent complications:
Fatigue side effects
TOPIC TEACHINGS
● Recognizing the signs and symptoms of infection and fluid
retention
● Avoiding exposure to people with infections
● Self-monitoring for infection
● Carrying a medical identification card (and immediately
reporting infections, which necessitate increased steroid
dosage)
● Recognizing signs of inadequate steroid dosage (fatigue,
weakness, dizziness) and overdosage (severe ederna, weight
gain
● Avoiding discontinuing steroid dosage
⬇️ADH
Diabetes Insipidus:
- stems from a deficiency ot (vasopressin secreted by the
posterior lobe of the pituitary gland. Decreased ADH reduces
the ability of distal and collecting renal tubules in the kidneys
to concentrate urine, resulting in excessive urination.
excessive thirst, and excessive fluid intake.
CAUSES
➢ Brain injury
➢ Head injury
➢ Idiopathic
➢ Meningitis
➢ Trauma to the posterior lobe of the pituitary gland
➢ Tumor of the posterior lobe of the pituitary gland
➢ Certain drugs that can interfere with ADH secretion/ action
(phenytoin, alcohol, Lithium carbonate)
ASSESSMENT FINDINGS
➔ Dehydration
➔ Fatigue
➔ Headache:
➔ Muscle weakness and pain
➔ Polydipsia (excessive thirst, consumption of 4 to 40L/day)
➔ Polyuria (greater than 50/day): inability of the kidneys to
concentrate urine leads to the excretion of large volumes of
dilute urine.
➔ Tachycardia
➔ Weight loss
DIAGNOSTIC TEST RESULTS
➔ Blood chemistry shows decreased ADH by radioimmunoassay
and increased potassium, sodium, and osmolality levels
- NA+ due to dilutional effects, while potassium levels may rise
due to decreased kidney function and impaired electrolyte
balance regulation.
➔ Urine chemistry shows urine specific gravity less than 1.004,
osmolality 50 to 200 mOsm/kg, decreased urine pH and
decreased sodium and potassium levels.
➔ Increased Osmolality of Plasma: With decreased ADH levels,
the kidneys can't concentrate the urine effectively, resulting in
a dilute urine and increased osmolality of the plasma. This
means that there's more water in the bloodstream compared
to solutes.
TREATMENT
➔ IV therapy hydration (when first diagnosed, intake and output
must be matched milliliter to milliliter to prevent dehydration,
electrolyte replacement.
➔ Regular diet with restriction of foods that exert a diuretic
effect.
DRUG THERAPY
➢ ADH replacement, vasopressin (Pitressin, lypressin Clapid
nasal spray)
➢ ADH stimulant: carbamazepine (Tegretol)
➢ Desmopressin: Administered intranasally; administrations
daily or every 12-24h usually control the symptoms
➢ Vasopressin tannate in oil: Administered intramuscularly every
24-96h
➢ Clofibrate
➢ o Hypolipidemic agent
➢ o Has an antidiuretic effect
INTERVENTIONS AND RATIONALES
➔ - Assess fluid balance to avoid dehydration.
➔ - Monitor and record vital signs, intake and output (urine
output should be measured every hour when first diagnosed),
urine specific gravity (check every 1 to 2 hours when first
diagnosed), and laboratory studies to assess for deficient fluid
volume.
➔ -Maintain the patient's diet to maintain nutritional balance.
➔ Force fluids to keep intake equal to output and prevent
dehydration.
➔ Administer IV fluids to replace fluid and electrolyte loss.
➔ Maintain the patency of the indwelling urinary catheter to allow
accurate measuring of urgency output
➔ Administer medications, as prescribed, to enable the patient
to concentrate urine and prevent dehydration.
➔ Weigh the patient daily to detect fluid loss.
TEACHING TOPICS
➔ Recognizing the signs and symptoms of dehydration
➔ Increasing fluid intake in hot weather
➔ Carrying medication
SYNDROME OF INAPPROPRIATE ADH (SIADH)
➢ Involving oversecretion of ADH, results in excessive water
conservation.
➢ Patient retain fluid and develop a sodium deficiency
➢ Known as DILUTIONAL Hyponatremia:
ETIOLOGY
➢ CNS disorder
➢ Stimulation due to hypoxia/decrease left atrial filling pressure.
➢ Pharmacologic agents
➢ Overuse of vasopressin therapy
➢ Ectopic ADH production associated with some cancers
➢ Nausea/ narcotic use, which can stimulate ADH section
PATHOPHYSIOLOGY
The basic pathologic disturbance are excessive ADH activity,
with water retention and dilutional hyponatremia, and
inappropriate urinary stantion of sodium in the presence of
hyponatremia
LAB FINDINGS
➔ Plasma osmolality and serum sodium levels are decreали
➔ Analysis detects elevated urine sodium and osmolality
➔ Serum ADH level is elevated
MEDICAL MANAGEMENT
➔ Treat the underlying cause
➔ Diuretics (furosemide) and fluid restriction
NURSING MANAGEMENT
➔ Restrict fluid Intake as indicated: may lead to hallucinations
➔ Regularly assess mental status
➔ Careful I&O, dally weight
Diabetes Mellitus
➔ The endocrine pancreas produces hormones necessary for
the metabolism and cellular utilization of carbohydrates,
proteins, and fats.
➔ The cells that produce these hormones are clustered in a
group of cells called the islets of Langerhans.
These islets have 3 different types of cells.
➔ Due to hormones secreted by the placenta, which inhibit the
action of insulin
➔ HPL: Human Placental Lactogen
4. DIABETES ASSOCIATED WITH OTHER CONDITIONS
Described as glucose intolerance caused by other diseases,
drugs or agents.

ALPHA CELLS: Produce the hormone glucagon, which

stimulates the breakdown of glycogen in the liver. The CLINICAL MANIFESTATIONS:
formation of carbohydrates in the liver, and the breakdown of ➔ ALL TYPES: polyuria, polydipsia, polyphagia

⬆️
lipids in both the liver and adipose tissue ➔ Fatigue and weakness
➔ Visual disturbances: Pressure in retina vessels
BETA CELLS: Secrete the hormone insulin, which facilitates the ➔ Recurrent skin, vulva, and urinary tract infections
movement of glucose across cell membranes into cells, ➔ Dry lower part of bodies.
decreasing blood glucose levels ➔ Skin lesions are slow to heal
➔ Tingling/numbness
Insulin prevents the excessive breakdown of glycogen in the ➔ Dry skin
liver and in muscle, facilitates lipid formation while inhibiting
the breakdown of stored fats, and helps move amino acids TYPE 1:
into cells for protein synthesis. ➔ Anorexia, abdominal pains, if DKA developed
➔ Nausea and vomiting
DELTA CELLS: produce somatostatin believed to be a ➔ Weight loss
neurotransmitter that inhibits the production of both glucagon
and insulin. LABORATORY FINDINGS/DIAGNOSTIC TEST FINDINGS:

➔ The brain, Iver, intestines, and renal tubules do not require
insulin to transfer glucose into their cells.
➔ Skeletal muscle, cardiac muscle, and adipose tissue do
require insulin for glucose movement into the cell.
COUNTER-REGULATORY HORMONES:
➔ Epinephrine, growth hormone, tyrosine and
➔ Glucocorticoids/GH, glucagon, cortisol, epinephrine
➔ Stimulate an increase in glucose in times of hypoglycemia,
shess, growth or increase metabolic demand.
HYPERGLYCEMIA
Medical term for an elevated blood glucose level:
➢ In type 1, onset is sudden, with DKA as being the 1st
indication of the disease
➢ In type 2, may develop gradually that some affected people
notice few or no manifestations for a number of years
1.CASTING BLOOD GLUCOSE
➔ A level of 140mg/dl or greater on at least two occasions
confirms DM

TYPES OF DM 2. POSTPRANDIAL BLOOD SUGAR: during an oral glucose

1. TYPE 1
➔ Insulin-dependent DM (IDDM) 5-10%
➔ Typically occurs in persons younger than 25 years old
➔ Characterized by destruction of the pancreatic beta cells
➔ Characterized by hypoglycemia, a breakdown of body fats
and proteins and the development of ketosis (an accumulation
of ketone bodies produced during the oxidation of fatty acids)
2. TYPE 2
➔ Non-insulin-dependent DM (NIDDM) 90%
➔ Most commonly affects persons older than 40 years and
obese adults
2 main problems:
➔ Insulin resistance: not accepting the insulin into cells.
➔ Impaired insulin secretion: impaired (genetics) or resistance
(lifestyle)
3. GESTATIONAL DM
➔ Occurs usually in the 2nd and 3rd trimester
tolerance test.
➔ Normally, blood glucose should return to fasting level within 2
hours. Greater than 200mg/dl.
➔ Using a glucose load containing the equivalent of 75g
anhydrous glucose dissolved in water.
3. GLYCOSYLATED Hgb
➔ Glucose normally attaches itself to the Hgb molecule on a
RBC. Once attached, it cannot dissociate. Therefore, the
higher the blood glucose levels, the higher the levels of
glycosylated Hgb.
➔ The result of times test shows the average blood glucose level
over the previous 3 months.
4. URINE CULTURE & KETONE LEVELS:
Presence of glucose in urine indicates hyperglycemia
5. URINE TEST for the presence of ALBUMIN (albuminuria):
A 24-H urine test for creatinine clearance is used to detect the
early onset of nephropathy
6. SERUM CHOLESTEROL & TRIGLYCERIDE LEVELS:
Indications of atherosclerosis and a increase risk of
cardiovascular impairments
7. SERUM ELECTROLYTES: Levels are measured in clients
who have DKA or HHNS to determine imbalance
MEDICAL MANAGEMENT:
5 components of diabetes management
- Nutritional management
- Exercise
- Monitoring
-Pharmacologic therapy
- Education
A. NUTRITIONAL MANAGEMENT:
➔ Nutrition, diet and weight control are the foundation of
diabetes management.
➔ Carbohydrates:the latest nutritional guidelines recommend
that all carbohydrates be eaten in moderation to avoid high
postprandial blood glucose levels.
Fats:
➔ Reducing the total percentage of calories from fat sources to
less than 30% of the total calories and limiting the amount of
saturated fats to 10% of total calories
➔ This approach may help reduce risk factors such as elevated
serum cholesterol levels, which are associated with the
development of coronary artery disease
➔ The meal plan may include the use if non-animal sources of
protein (legumes and whole grains) to help reduce saturated
fat and cholesterol intake
Fiber
➔ Lowers total cholesterol and low-density lipoprotein
cholesterol in the blood
➔ Increasing fiber also improve blood glucose levels and
decrease the need of exogenous insulin
➔ Fibers increase satiety, which is useful for weight loss
➔ The glucose-lowering effect of fiber may be caused by the
slower rate or glucose absorption.
ALCOHOL CONSUMPTION:
Moderation is recommended
➔ The main danger of alcohol consumption is hypoglycemia,
especially for patients who take insulin.
➔ -Light beer is the recommended alcoholic drink.
➔ To reduce the risk of hypoglycemia, the patient should be
cautioned to eat while drinking alcohol.
➔ Liquors, sweet wine, wine coolers and sweet mixes contain
large amounts of carbohydrates.
➔ Alcohol consumption may lead to excessive weight gain (from
the high calorie content of alcohol), hyperlipidemia and
elevated glucose levels
➔ For patients with type 2 DM treated with sulfonylurea, a
potential side effect of alcohol consumption is a DISULFIRAM
(ANTABUSE) type of reaction, which involves facial flushing,
warmth, headache, nausea and vomiting, sweating, or thirst
within minutes of consuming alcohol.
SWEETENERS
Moderation in the amount of sweetener used is encouraged to
avoid potential adverse effect
2 main types of sweeteners:
O NUTRITIVE
Fructose, sorbitol and xylitol
➔ They provide calories similar to table sugar.
➔ They cause elevation in blood sugar levels more than sucrose
and are often use "sugar-free" foods. Sweeteners containing
sorbitol may have a laxative effect.
O NON-NUTRITIVE
Have minimal or no calories
➔ Produce minimal or no elevation in blood glucose levels and
have been approved safe for people with diabetes.
➔ SACCHARIN, contains no calories
➔ ASPARTAME (NUTRASWEET) is packaged with dextrose; it
contains 4 calories per packet and loses sweetness with heat
➔ ACESULFAME-K (SUNNETTE) is also packaged with
dextrose; contains 1 calorie per packet
➔ SUCRALOSE (SPLENDA) is a newer, non-nutritive, high
intensity sweetener that is about 600x sweeter than.
MISLEADING FOOD LABELS
➔ -Food labeled "sugarless" or "sugar-free" may provide calories
equal to those of the equivalent sugar-conta products if they
are made with nutritive sweeteners
➔ For weight loss these products may not be useful.
➔ -Foods labeled "dietetic" are not necessarily reduced- calorie
foods. They may be lower in sodium but they still contain
significant amount of sugar/fat.
➔ Supposedly healthy snacks frequently contain saturated
vegetable fats (coconut, palm oil), hydrogenated vegetable
fats or animal fats which may be contraindicated in patients
with elevated blood lipid level
B. EXERCISE
➔ Exercise lowers the blood glucose level by increasing the
uptake of glucose by body muscles and by improving insulin
utilization
➔ It also improves circulation and muscle tone.
➔ Reduces stress and tension.
➔ Exercise also alters blood lipid levels, increasing levels of
high-density lipoproteins and decreasing total cholesterol! and
triglyceride levels.
➔ The primary side effect of acute exercise is hypoglycemia.
➔ Patients who have blood glucose levels exceeding 250mg/ di
and who have ketones in their urine should not begin
exercising until the urine tests negative for ketones and blood
glucose level is close to normal.
➔ A patient who requires insulin should be taught to eat a 15-
mg carbohydrate snack or a snack of complex carbohydrate
with a protein before exercise to prevent hypoglycemia. The
exact amount of food needed varies from person to person.
➔ Self-monitor blood glucose before and after exercise.
➔ To avoid post exercise hypoglycemia, the patient may need to ➢ BIGUANIDES
eat a snack at the end of exercise. METFORMIN (GLUCOPHAGE)
➔ Patient should exercise at the same time (preferably when ➔ Decreases hepatic production of glucose
blood glucose levels are at their peak) and in the same ➔ Decrease absorption of glucose in the small intestines
amount each day (20-30 mins) ➔ Decreases triglycerides low-density lipoprotein levels
➔ Muscle strengthening and low-impact aerobic exercise.
> ALPHA-GLUCOSIDASE INHIBITORS
C. MONITORING GLUCOSE LEVELS AND KETONES ACARBOSE (PRECOSE)
MIGLITOL (GLYSET)
Self-monitoring of blood glucose (SMBG) ➔ Delays absorption of glucose in the small intestines, resulting
➔ Allows for detection and prevention of hypoglycemia and in a lower.
hyperglycemia and plays a crucial role in normalizing blood ➔ postprandial blood glucose level
glucose levels, which in turn may reduce the risk of long- term 12
diabetic complications. ➔ Do not enhance insulin secretion
Candidates for SMBG: ➔ Because these meds affect food absorption, they must be
➔ For everyone with diabetes taken immediately before a meal.
Also recommended for patients with ➔ Stimulates beta cells to secrete insulin
➔ Unstable diabetes ➔ Increases tissue response to insulin (insulin sensitizer)
➔ A tendency for severe ketosis/hypoglycemia
➔ Hypoglycemia without wearing symptoms MEGLITINIDES
➔ For patients not taking insulin, SMBG is helpful for monitoring REPAGLINIDE (PRANDIN)
the effectiveness of exercise, diet, and oral antidiabetic agents ➔ Lowers blood glucose level by stimulating insulin release from
Frequency of SMBG the beta cells.
➔ SMBG is recommended 2-4x daily (usually before meals and ➔ It should be taken before each meal to stimulate insulin in
before bedtime for those taking insulin. response to that meal.
➔ For patients who take insulin before each meal. SMBG is
required at least 3x daily before meals to determine each NAGLITINIDES (STARLD)
dose. ➔ Has very rapid onset and short duration
➔ Patients not receiving insulin may be instructed to assess ➔ Should be taken with meals
their blood glucose levels at least 2-3x per week, including a
24 postprandial test. THIAZOLIDINEDIONES
➔ Patient increase frequency of SMBG with changes in meds, ROSIGEITAZONE (AVANDIA)
activity, and with stress or illness DIOGLITAZONE (ACTOS)
➔ Patients are instructed to keep a record/logbook of blood ➔ Increases action at receptors and post-receptor level in
glucose levels so that they can detect patterns hepatic and peripheral tissue (decreases insulin resistance).
➔ Decreases triglyceride
➔ Baseline patterns should be established by SMBG for 1-2 ➔ May lead to pregnancy by decreasing the effect of oral
weeks contraceptive

D. PHARMACOLOGIC THERAPY 2. Insulin therapy

➔ Clients with type 1 depend on exogenous insulin
1. Oral anti-diabetic meds administration on a daily basis.
➔ SULFONYLUREAS: ➔ Type 2 diabetics may supplemental insulin for adequate
➔ Primary exert action by directly stimulating the pancreas to glucose control, especially in times of stress or illness.
secrete insulin.
➔ Therefore a functioning pancreas is necessary for these RAPID ACTING onset peak duration
agents to be effective, and they cannot be used in patients LISPRO (HUMALOG) 10-15min 1h 3h
with type 1 diabetes ASPART (NOVOLOG) 10-15min 40-50min 4-6h
➔ Improve insulin action at the cellular level and may also ➔ Used for rapid reduction of glucose level, to treat postprandial
directly decrease glucose production by the liver hyperglycemia, and/or to prevent nocturnal hypoglycemia.
➔ Because of their onset, patients should be instructed to eat no
First generation: more than 5-15 minutes after injection.
CHLORPROPIZAMIDE (DIABINESE)
➔ Stimulates beta cells to secrete insulin
➔ Mild diuretic

Second generation:
GLIPIZIDE (GLUCOTROL)
➔ Increases tissue response to insulin (insulin sensitizer) >> SHORT ACTING onset peak duration REGULAR
➔ Decreases glucose production by liver (HUMALOG R, NOVOLIN R, 1½-1h 2-3h 4-6h ILETIN II
REGULAR)
➔ Usually administered 20-30mins before a meal
➔ Marked R on the bottle.
➔ Regular insulin is a clear solution and usually administered
20-30 mins before a meal.
> INTERMEDIATE-ACTING onset peak duration
NPH (neutral protamine hagedorn) 2-4h 6-12h 16-20h
(HUMULIN N, ILETIN II LENTE, 3-4h 6-12h 16-20h
ILETIN II NPH, NOVOLIN L (LENTE)
NOVOLIN N (NPH)
➔ Usually taken after meals
➔ Appear white and cloudy
➤ LONG ACTING onset peak duration
ULTRALENTE ("UL") 6-8h 12-16h 20-30h
➔ Used primarily to control fasting glucose level.
➔ Sometimes referred to as peakless insulins because they tend
to have long, slow,sustained action.
VERY LONG-ACTING onset peak duration
➔ GARGLINE (LANTUS) 1h continuous, 24h
➔ no peak
➔ Used for basal dose.
➔ Absorbed very slowly and can be given once a day before
bedtime.
➔ Cannot be mixed with other insulin because this would cause
precipitation.
COMPLICATIONS OF INSULIN THERAPY
1. LOCAL ALLERGIC REACTIONS
➔ Redness, swelling, tenderness and nation or a 2-4cm wheal
may appear at the injection site 1-2h after the insulin
administration.
➔ Usually occur during the beginning stages of therapy and
disappear with continued use of insulin.
➔ The physician may prescribed an antihistamine to be taken 1h
after the injection.
2. SYSTEMIC ALLERGIC REACTIONS
➔ An immediate local skin reaction that gradually spreads into
generalized urticaria (hives).
➔ Treatment is desensitization, with small doses of insulin
administered, gradually increasing its amounts.
3. INSULIN LIPODYSTROPHY
➔ Localized reaction occurring at the site of insulin injections
✓ LIPOATROPHY
➔ Loss of subcutaneous fat and appears as slight climpling or
more serious pitting of subcutaneous fat
LIPOHYPERTROPHY
➔ Development of fibrofatty masses at the injection site, is
caused by the repeated use of an injection site. If insulin is
injected into scarred areas, absorption may be delayed.
4. MORNING HYPERGLYCEMIA
INSULIN WANING
➔ Progressive rise in blood glucose from bedtime to morning
➔ Increase evening (predinner/bedtime) dose of
intermediate/long-acting insulin
✓ DAWN PHENOMENON
➔ A rise in blood glucose between 4-8am
➔ Believed to be related to nocturnal increases in growth
hormone, which decreases peripheral uptake of glucose.
➔ Change time of injection of evening intermediate-acting insulin
from dinnertime to bedtime.
✓ SOMOGYI EFFECT
➔ Normal or elevated blood glucose at bedtime.
➔ A decrease at 2-3AM to hypoglycemic levels
➔ Rebound morning rise in blood glucose to hyperglycemic
levels
➔ The hyperglycemia stimulates the counterregulatory
hormones, which stimulates gluconeogenesis and
glycogenolysis and also inhibit peripheral glucose use.
➔ The patient must be awakened once or twice during the night
to test blood glucose levels. Testing the blood glucose st
bedtime, at 3AM, and on awakening provides information that
can be used in making adjustments in insulin to avoid morning
hyperglycemia caused by dawn phenomenon.
➔ Decrease evening (predinner/bedtime) dose of intermediate
acting insulin/increase bedtime snack
1. INSULIN PENS
➔ Prefilled insulin cartridges that are loaded into a pen-like
holder.
➔ Insulin is delivered by dialing in a dose/pushing a button for
every unit.
➔ Useful for patient with impaired manual dexterity, vision or
cognitive function that makes the use of traditional syringes
difficult.
➔ Advantage of insulin pumps include increased flexibility in
lifestyle (in terms of timing and amount of meals, exercise and
travel.
Disadvantages
➔ Unexpected disruption in the flow of insulin of tubing/ needle
becomes occluded, if supply of insulin runs out or if the
battery is depleted hypoglycemia.
➔ Potential for infection and insertion site.
INSULIN PUMPS
➔ A small portable pump for the continuous administration of
regular insulin.
➔ The small pump, worn externally, injects insulin
subcutaneously into the abdomen through an indwelling
needle site that is usually changed daily.
ALTERNATIVE METHODS OF INSULIN DELIVERY
TEACHING PATIENTS TO SELF-ADMINISTER INSULIN:
 >>STORING INSULIN:
➔ Cloudy insulins should be thoroughly mixed by gently inverting
the vial or rolling it between the hands before drawing the
solution.
➔ Vials of insulin not in use should be refrigerated.
➔ Avoid extremes of temperature, (less than 36°C or greater
than 86°F).
➔ A slight loss of potency may occur after 30 days at room
temperature
➔ The insulin vial in use should be kept at room temperature to
reduce local imitation at the injection site, which may occur
when cold insulin is injected.
➔ If a vial of insulin will be used up in 1month, it may be kept at
room temperature.
➔ Mark the date on the vial when it was initially opened. The
client should always have a spare vial on hand
TEACHING PATIENTS TO SELF-ADMINISTER INSULIN:
STORING INSULIN:
➔ Cloudy insulins should be thoroughly mixed by gently inverting
the vial or rolling it between the hands before drawing the
solution.
➔ Vials of insulin not in use should be refrigerated.
➔ Avoid extremes of temperature, (less than 35°C or ster than
86F)
➔ A slight loss of potency may occur after 30 days at room
temperature
➔ The insulin vial in use should be kept at room temperature to
reduce local irritation at the injection site, which may occur
when cold insulin is Injected
➔ If a vial of insulin will be used up in 1month, it may be kept at
room temperature.
➔ Mark the date on the vial when it was initially opened..
➔ The client should always have a spare vial on hand
➤SELECTING SYRINGES:
Currently, 3 sizes of U-100 insulin syringes are available:
➔ 1ml syringes that hold 100 units
➔ 0.5 ml syringes that hold 50 units
➔ 0.3 ml syringes that hold 30 units
> PREPARING THE INJECTION: MIXING INSULINS
➔ The most important issue is that patients be consistent in how
they prepare their insulin injection from day to day.
➔ If short acting and long acting insulin are given at the same
time, it is recommended that the regular insulin be drawn up
first.
For patients who have difficulty mixing insulins, 2 options are
available:
o Premixed insulins
o Prefilled syringes
➔ Instruct the patient to inject air into the bottle of insulin
equivalent to the number of units of insulin to be withdrawn.
The rationale for this is to prevent the formation of a vacuum
inside the bottle, which would make it difficult to withdraw the
proper amount of insulin
>> SELECTING AND ROTATING THE INJECTION SITE
4 main areas for injection
➔ Abdomen
➔ Arms (posterior surface)
➔ Thighs (anterior surface)
➔ Hips
➔ The speed of absorption is greatest in the abdomen and
decreases progressively in the arm, thigh, and hip.
➔ Pains should be encouraged to use all available injection sites
within one area.
➔ Another approach to rotation is always to use the same area
at the same time of the day.
➔ If the patient is planning to exercise, insulin should not be
injected into the limb that will be exercised, because it will be
absorbed faster, and this may result in hypoglycemia.
1. HYPERGLYCEMIA & DIABETIC KETOACIDOSIS
Dehydration
➔ Electrolyte and acid-base imbalance
➔ In type 1 DM, DKA is a primary complication, it can also affect
clients with type 2 during periods of extreme stress
Common causes:
➔ Taking too little insulin
➔ Skipping doses of insulin
➔ Inability to meet an increased need for insulin created by
surgery, trauma, pregnancy, stress, puberty or infection.
➔ Developing insulin resistance through the presence of insulin
antibodies
Clinical features of DKA:
➔ Hyperglycemia
➔ Dehydration and electrolytes loss
➔ Acidosis
PATHOPHYSIOLOGY:
➔ When the body lacks insulin and cannot use carbohydrate for
energy, it resort to using fats and proteins.
➔ The process of catabolizing fats for fuel gives rise to 3
pathologic events.
KETOSIS
➔ Breakdown of fat (lipolysis) into free fatty acids and glycerol.
The free fatty acids are converted into ketone bodies, by the
liver.
➔ In DKA, there is excessive production of ketone bodies
because of the lack of insulin that would normally prevent this
from occurring.
➔ Ketone bodies are acids, their accumulation in the circulation
leads to metabolic acidosis.
➔ In response to physical and emotional stressors, there is an
increase in the levels of "stress" hormones. These hormones
promote glucose production by the liver and interfere with
glucose utilization by muscle and fat tissue, counteracting the
effect of insulin.
➔ If insulin levels are not increased during times of illness and
infection, hyperglycemia may progress to DK
DEHYDRATION
➔ In an attempt to rid the body of the excess glucose, the
kidneys excrete gicose slong with water and electrolytes. This
 osmotic diere es, which is characterized by excessive ➔ Typically produce long-lasting and more severe
urination (polyuria) leads i dehydration and marked manifestations.
electrolytes loss ➔ Headache
➔ Mental illness
Ketosis and acidosis ➔ Inability to concentrate
➔ Blood glucose and urine ketones must be assessed every ➔ Slurred speech
3-4h; a supply of urine test be available ➔ Confusion
➔ Patients must know how to contact their physician 24h a day ➔ Irrational behavior
➔ strips (for ketones) and blood glucose test strips should be ➔ Lethargy (severe)
available ➔ Loss of consciousness
➔ Coma
MEDICAL MANAGEMENT: ➔ Seizure
✓ REHYDRATION ➔ Death
➔ IV rehydration for clients who are vomiting, unable to drink,
and have acidosis. MANAGEMENT:
➔ IV infusion of isotonic/normal saline. ➔ Immediate treatment must be given when hypoglycemia
Occurs
✓ REVERSE SHOCK
➔ If there's circulatory collapse, the physician may order blood, Usual recommendation is 15g of a fast-acting concentrated
albumin or other plasma volume expanders such as dextran, source of carbohydrate,is given orally:
administered alternately with normal saline. ➔ commercianynared glucose tablets
➔ 4-6 oz of fruit juice/regular
✓ RESTORING ELECTROLYTES ➔ 6-10 lifesavers/other hard candies 27
➔ The major electrolyte of concern during treatment of DKA is ➔ 2-3 tsp of sugar/honey
potassium.
➔ There is a major loss of potassium from body stores and an Initiating emergency measures:
intracellular to extracellular shift of potassium. ➔ For patients who are unconscious and cannot swallow, an
➔ Cautious but timely potassium replacement is vital to avoid injection of glucagon 1mg can be administered either
dysrhythmias subcutaneously or IM
➔ After injection of glucagon, it may take-up to 20min for the
✓ REVERSING ACIDOSIS patient to regain consciousness.
➔ The acidosis that occurs in DKA is reversed with insulin, ➔ In the hospital or ER department, patients who are
which inhibits fat breakdown. unconscious/cannot swallow may be treated with 25-50ml
➔ IV fluid solute such as normal saline solutions are 50% dextrose in water (D50W) administered IV.
administered when blood glucose levels reach 250-300mg/ di
to avoid too rapid a drop in the blood glucose level. Teaching patient self-care:
➔ Hypoglycemia is prevented by a consistent pattern of eating,
2. HYPERGLYCEMIC HYPEROSMOLAR NON-KETOTIC administration of insulin, and exercising.
SYNDROME (HHNS) ➔ Between meal and bedtime sides may be needed to
➔ A variant of diabetic ketoacidosis characterized by extreme counteract the maximum insulin effect.
hyperglycemia (600-2000mg/dl), profound dehydration, mild/ ➔ Vanabie neurologic signs (decrease LOC, seizures,
undetectable ketonuria, and absence of acidosis hemiparesis)
➔ Hallucinations are common secondary to cerebral dehydration
Common in type 2 DM that results from extreme hyperosmolality
➔ The major difference between HHNS and DKA is the lack of
ketonuria with HHNS. In type 2 DM, the mobilization of fats for MEDICAL MANAGEMENT:
energy usually does not occur ➔ Fluid replacement
➔ Correction of electrolyte disturbances
SIGNS AND SYMPTOMS: ➔ Insulin administration
➔ Hypotension
➔ Profound dehydration 3. HYPOGLYCEMIA
➔ Tachycardia ➔ Also known as insulin reaction/hypoglycemic reaction.
➔ Variable neurologic signs (askrsase LOC, seizures, ➔ Usually occurs when blood glucose serum level is less than
hemiparesis) 50-60mg/dl
➔ Hallucinations are common secondary to cerebral dehydration
that results ETIOLOGY AND RISK FACTORS:
➔ Overdose of insulin or less commonly, a sulfonylurea
CNS SYMPTOMS/NEUROGLYCOPENIC SYMPTOMS ➔ Omitting a meal/eating less food than usual
➔ Associated with lack of glucose availability to the brain and ➔ Overexertion without additional carbohydrate compensation
resultant decrease in cognitive functioning.
CLINICAL MANIFESTATIONS:
 Generally divided into 2 categories: ➔ Between meal and bedtime snacks may be needed to
● Adrenergic Symptoms counteract the maximum insulin effect.
● Autoimmune manifestations: ➔ In general, the patient should cover the time of peak activity of
➔ associated with mixing epinephrine levels and are considered insulin by eating a snack and by taking additional food when
"mild" reactions In mild hypoglycemia, as the blood glucose physical activity is increased.
level falls, the SNS is stimulated, resulting in a surge of ➔ Because unexpected hypoglycemia may occur, all the patients
catecholamine treated with insulin should wear an ID bracelet/tag stating that
they have DM.
These manifestations can also occur during other stressful/ ➔ Family members must be aware that any subtle (but unusual)
anxiety provoking events: changes in behavior may be an indication of hypoglycemia.
➔ Shakiness Family members must be taught to persevere and understand
➔ Irritability that hypoglycemia can cause irrational behavior
➔ Nervousness
➔ tachycardia, palpitations
➔ Tremor
➔ Hunger
➔ Diaphoresis
➔ Pallor
➔ paresthesia

CNS SYMPTOMS NEUROGLYCOPENIC SYMPTOMS

➔ Associated with lack of glucose availability to the brain and
resultant decrease in cognitive functioning.

Typically produce long-lasting and more severe

manifestations:
➔ Headache
➔ Mental illness
➔ Inability to concentrate
➔ Slurred speech
➔ Confusion
➔ Irrational behavior
➔ Lethargy (severe)
➔ Loss of consciousness
➔ Coma
➔ Seizure
➔ death

MANAGEMENT
➔ Immediate treatment must be given when hypoglycemia
occurs.
➔ Usual recommendation is 15kg of a fast-acting concentrated
source of carbohydrate is given orally:
➔ ¾ commercially prepared glucose tablets
➔ 4-6oz of fruit juice/regular soda
➔ 6-10 lifesavers. Other hand candies
➔ 2-3tsp of sugar/honey
➔ Initiating emergency measures:
➔ For patients who are unconscious and cannot swallow, an
injection of glucagon 1mg can be administered either
subcutaneously or IM
➔ Alter injection of glucagon, it may take-up to 20min for the
patient to regain consciousness
➔ In the hospital or ER department, patients who are
unconscious/ cannot swallow may be treat with 25-50ml 50%
dextrose in water D50W administered IV.

TEACHING PATIENT SELF-CARE:

➔ Hypoglycemia is prevented by a consistent pattern of eating,
administration of insulin and exercising.