ENDOCRINE

DISORDERS
Overview
The endocrine system is a collection of cells and glands which release hormones. It is quite like a
nervous system. The nervous system is fast, direct, and short-acting but the endocrine system is
slow, indirect, and long-acting.
The Hypothalamus extension of the hypothalamus is called the Pituitary gland. Hypothalamus is
a master regulator of the endocrine system. It produces and releases several important hormones
and these are:
 Thyrotropin-releasing hormone
 Corticotropin-releasing hormone
 Growth hormone
 Prolactin hormone
 Gonadotropin-releasing hormone
Hypothalamus released hormone and travel to the blood supply to the
anterior lobe of the pituitary gland Which stimulates a hormone in the
anterior pituitary to be produced and released.

 Thyrotropin-releasing hormone—— thyroid stimulating hormone

 Corticotropin-releasing hormone—- adrenocorticotropic hormone
 Growth hormone-releasing hormone—growth hormone
 Prolactin releasing hormone——prolactin
 1. Thyroid hormone travel to the thyroid gland
The thyroid gland produces T3 (triiodothyronine), T4 (thyroxine), and calcitonin.
These hormone functions are:
 Metabolism (when food is being broken into components, such as breaking of protein
into amino acids).
 Development (embryo)
 Catecholamine (epinephrine or norepinephrine)
When these hormone levels are high in the body, they go back to the hypothalamus and have
inhibitory effects on releasing hormones called negative feedback.
2. When the corticotropin-releasing hormone is released from the hypothalamus it travels
through the bloodstream to the anterior pituitary and then travels to the adrenal gland to
secrete hormones.
Adrenal gland (Triangular shaped gland)
 Cortex
cortisol (glucocorticoid): It increases blood glucose levels and suppresses the immune
system.
Aldosterone mineralocorticoid
It increases sodium reabsorption and also retains water.
Increase blood volume=increase BP
Androgen (male sex hormones)
 Medulla (norepinephrine/epinephrine)
Control sympathetic and parasympathetic hormones like it increase in flight and fight mode.
3. Growth hormone
It increases growth by increasing protein synthesis.
4. Prolactin
Increase milk production
5. Gonadotropins
It promotes reproductive cycles.
In females: the pituitary produces luteinizing hormone and follicle-stimulating hormone.
It increases estrogen, Progesterone, and ovulation and prepares the uterine lining.
In males, the pituitary produces luteinizing hormone and follicular stimulating hormone,
increasing testosterone and sperm production.

Posterior pituitary gland:

It releases oxytocin because the hypothalamus does not release hormones but send nerve signal
to the posterior.
Oxytocin: increase milk injection and you try and contract because oxytocin does contraction
and pushes off smooth muscles. It strengthens bonds of both positive and negative relationships.
Anti diuretic hormone: (vasopressin)
During the time of shock, vasopressin is released.

Syndrome of inappropriate antidiuretic

hormone (SIADH)

Soaked inside= ADH increases

It is the condition in which the posterior pituitary gland
starts hyperfunctioning and releasing an excess of ADH.

Excessive secretion of ADH causes the syndrome of

inappropriate antidiuretic hormone (SIADH). In SIADH,
the kidneys retain water, urine becomes concentrated,
output drops, and extracellular fluid volume is increased
The syndrome results in water intoxication, and delusional
hyponatremia

Causes:
 Trauma, stroke
 Malignancies
  Medications and stress
 Small cell lung cancer.
 Sepsis
Signs and symptoms:
7’s:
S: stop urination (low urine output)
S: sticky and concentrated “urine” high specific gravity
S: low and liquid labs. (hyponatremia)
S: Sodium low (early signs: headache, seizures, death).
S: Seizures
S: Severe high BP (but sometimes normal also)
S: Stop all fluids – Give salt + (diuretics (only if sodium level is 125mg/dl or more).
(NO IV or drinking fluids. Only provide IV fluids 3% saline to increase Na).
Keynote: In SIADS no peripheral edema occur because before peripheral edema cerebral
edema occur and the patient died).
Pharmacology:
 Vasopressin antagonist
 Lithium- Therapeutic range- 0.6- 1.2 meq/L Toxicity occurs over- 1.5 meq/L 25
 Old client and client with impaired renal function (creatinine over 1.3) are at higher risk
for lithium toxicity.
 Client with stomach flu (vomiting, diarrhea) are at higher risk of toxicity as it causes
dehydration
 Client are advice for regular blood test (blood sample should be taken after 12 hour of
last dose) Lithium is contraindicated in pregnancy.
 Client is advice to increase fluid intake and sodium intake (contraindicated in
dehydration and hyponatremia) Teach client to avoid performing exercise for any other
activity outdoor in hot days.
 Demeclocycline
 Tolvaptan
Interventions:
  Monitor vital signs of the patient with neurological and cardiac status.
 Monitor intake/ output of the patient and fluid and electrolyte balance.
 Provide a safe environment because of loss of consciousness.
 Monitor for signs of increased ICP and implement seizure precautions.
 Check daily weight monitoring (not weekly)
 Weight gain = water gain.
 Elevate the head of the bed at least 10 degrees
 Monitor urine osmolality

Diabetes Insipidus
It is a condition in which the bodies dry from the inside due to low ADH by the posterior
pituitary gland caused by stroke, trauma, or any surgery. In this condition, kidney tubules fail to
reabsorb water. There are two types of diabetic insipidus: central or nephrogenic.
In central diabetic insipidus, there is decreased ADH production.
In nephrogenic diabetes insipidus, ADH production is adequate, but kidneys do not respond
appropriately to ADH.
Cause
 Damage to the brain due to any trauma, tumors, or
surgery

 Signs and symptoms:
7 D’s:
D: Diuresis “drain fluid” high urine output 20 Lt/day.
D: Diluted urine (low specific gravity 1.005)
D: Dry inside high and dry labs
Hyper osmolality and hypernatremia over 145
D: Drinking a lot “thirsty”
D: Dehydrated dry mucosa and skin
D: Decrease BP postural hypotension
D: Desmopressin “vasopressin” (ADH subcutaneous/
IV/ orally)
 Fatigue, muscle pain, and weakness
 Headache
 Tachycardia
Diagnostics:
 Water deprivation test (DDAVP) Desmopressin acetate: It includes not drinking any
liquid for several hours (8 HOURS) to see body response. If urine output is nil means
psycho genic. If urine output is more mean diabetic insipidus. To check whether central
or nephrogenic we give desmopressin. If urine output decrease after giving desmopressin
it means central DI [problem with pituitary gland (ADH production)]
Treatment:
For nephrogenic medication given are:
 Carbamazepine
 Chlorpropamide
Interventions:
 Monitor vital signs, and neurological and cardiac status.
 Because the patient is at risk for seizures provide a safe environment.
  Monitor intake and output, Serum osmolality, and specific gravity
 Daily weight monitoring should be done.
 Weight loss= Water loss.
 Avoid cola, caffeine, and tea.
 Maintain client intake of adequate fluids, IV hypotonic saline may be prescribed
 Instruct the client to wear a medic alert bracelet all the time.

Adrenal Gland Disorders

Addison’s disease is an adrenocortical insufficiency. It is caused by damage or dysfunction of
the adrenal cortex.
Mineralocorticoids – Aldosterone (increases sodium absorption, causes potassium excretion in
the kidney)
◯ Glucocorticoids – Cortisol (affects glucose, protein, and fat metabolism; the body’s response
to stress; and the body’s immune function)
◯ Sex hormones – Androgens and estrogens
Definitive diagnosis is made using an ACTH stimulation test.

Addison Disease-
Primary adrenal insufficiency is known as a decent disease because in this Pituitary is
ok but the problem is the adrenal gland.
In Addison disease ACTH increases but hypo-secretion of:
 Glucocorticoid hypoglycemia
 Mineralocorticoid hyponatremia and hyperkalemia.
It requires lifelong replacement of glucocorticoid and mineralocorticoid If hyposecretion occurs,
the condition is fatal if left untreated.
 Secondary adrenal insufficiency is caused by hyposecretion of ACTH from the anterior
pituitary gland.
Test Normal reference Interpretation of Nursing actions
range Finding
ACTH stimulation If no increase in ACTH stimulation Two consecutive
test cortisol occurs after test determines the collections of 24-hr
administration of functioning of the urine are used, one
ACTH, the test is pituitary gland in prior to and one after
positive for relation to stimulating the administration of
Addison’s disease or the secretion of ACTH.
hypocortisolism. adrenal hormones of
cortisol.

 Adrenocorticotropic hormone (ACTH) stimulation test – ACTH is infused, and the

cortisol response is measured. With primary adrenal insufficiency, plasma cortisol levels
do not rise.

Signs and symptoms:

Everything is low except 2P and C
Potassium, pigmentation (bronze color skin), Ca
GI disturbance due to hypercalcemia
 Weight loss
 Hyperkalemia
 Hypoglycemia, hyponatremia
 Hyperpigmentation of skin (bronzed skin) due to
increase ACTH, because it gives color to the skin.
 Low BP
 Slow or absent periods (amenorrhea)
 Low energy (fatigue) and low temperature
 Low hair (alopecia)
  Low mood (depression)
Interventions:
 Monitor vital signs, weight loss, and intake output chart.
 Check patient about weight loss
 Observe for Addisonian crisis. Already patients have Addison disease and if the patient
has stress, sepsis, or surgery hormones are zero called a crisis.
Client education:
 Ask the patient to take lifetime therapy of glucocorticoid or mineralocorticoid and
corticosteroid replacement and insulin will need to be increased during stress.
 Each patient there is no cure
 Because in times of stress corticosteroids are necessary and if glucocorticoid increases,
glucose increases in the body, so insulin is needed.
 Ask the patient to never abruptly stop medication because it causes death
 Avoid themselves from infection and never take over-the-counter drugs
 High calcium and high vitamin diet should be provided to the patient because
corticosteroid-induced osteoporosis occurs.
 High protien
 Avoid stranger’s exercise and stressful situations.
 Wear a medic alert bracelet.

Addisonian crisis
It is a life-threatening disorder caused by acute adrenal insufficiency because of stress, infection,
surgery, and trauma or abruptly stopping corticosteroids can cause hyponatremia, hypoglycemia,
and shock.
Causes:
 The autoimmune body kills adrenals or pituitary.
 Diseases cancer, infection
  Damage adrenal hemorrhage
Signs and symptoms:
 Severe abdominal, leg, and lower back
pain occur.
 Fluid replacement should be done
 Vital signs and neurological status
should be checked
 Monitor intake output and lab values of
the patient
 Protect patients from infection
 provide proper bed rest and a quiet environment.
Key point: Steroids always give with food or with antacids never given on empty stomach.
Treatment:
 Prepare to administer corticosteroids Iv as prescribed. Teach the client to increase the
doses during surgery, strenuous activity, or sepsis.
 Administer Iv fluids as prescribed to replace fluids and restore electrolyte balance.
 Provide a diet high in protein, carbohydrates, and sodium
 Never abruptly stop steroids
 Don’t believe this medicine will cure you. It will only slow the progression
 It is lifelong hormone replacement therapy.
7’S steroid precautions:
S: Sugar increased hyperglycemia
S: skinny muscle and bones osteoporosis
S: site cataract risk refers to the optometrist
S: swollen (weight gain= water gain)
Key terms: sudden, excess, rapid. Report 1LB in one day or 2-3 liter in a few days.
S: sepsis (infection or illness)
Low WBC fever is a priority
Prevent crisis:
S: slowly taper off
S: Stress and surgery increase dose.
Treatment for Addisonian crisis:
 Add steroids- IV push
 Key point steroids cause psychosis.
 Provide IV NS 0.9%
Key point: Addison’s disease is characterized by the hyposecretion of adrenal cortex
hormones, whereas Cushing’s syndrome and Cushing’s disease are characterized by
hypersecretion of glucocorticoids.

Cushing Syndrome
It is a metabolic disorder resulting from the chronic and excessive production of cortisol by the
adrenal cortex from the administration of glucocorticoids in a large dose for several weeks or
longer.
Sodium retention in the body results in water retention and weight gain.
Diagnostics:
 To check Cushing syndrome: a dexamethasone suppression test should be done. In this
test give 1MG dexamethasone at night and draw a sample in the morning. If plasma
cortisol level is normal (<5MG/ DL) Means a normal adrenal response.

Cushing disease is a disorder characterized by abnormally increased secretion of

cortisol caused by an increased amount of ACTH by the pituitary gland.
Causes 4’S:
 Surgery
 Stress
 Sepsis
 Strenuous activity
 Small cell lung cancer
Signs and symptoms: (everything is big)
 Severe headache and diaphoresis
 Increased BP and blood volume
 Hyperglycemia
 Heat intolerance
 Big belly “truncal obesity”
 Big face “moon-face”
 Big Buffalo hump “fat pad”
 Big hair “hirsutism”
 Big stretch marks “purple striae”
 Big red face “rosy cheeks”
 Big infection “slow wound healing”
 The big risk of fracture and acne
Intervention:
 Monitor vital signs and blood pressure
 Monitor intake and output, weight monitoring of the patient
 Check lab values and electrolytes
 Administer chemotherapeutic agents or radiation therapy if the problem is adrenal
tumors.
 Prepare the client for removal of a pituitary tumor (hypophysectomy, sublabial
transsphenoidal adenectomy) If the condition results from increased ACTH.
 Teach the client that lifelong glucocorticoid replacement should be taken and increased
during the time of stress
 Protect the patient from postoperative thrombus formation
 Ask the client to wear a medic alert bracelet all the time
 Allow the client to discuss feelings related to body appearance.
Primary hyperaldosteronism (Conn’s syndrome)
It is the tumor of the cortex in which hypersecretion of mineralocorticoids from the adrenal
cortex of the adrenal gland. Excess secretion cause sodium and water retention but potassium
excretion and H+ ions excretion increase resulting in hypertension and hypokalemic alkalosis.
Signs and symptoms:
 Symptoms related to hypokalemia, hypernatremia, and hypertension
 Headache, fatigue
 Muscle weakness
 Cardiac dysrhythmias
 Polydipsia (excessive thrust)
 Swollen dry tongue
 Increased muscle tone
 DTR decreases
 Visual changes
 Glucose intolerance
Nursing interventions:
 Monitor vital signs of the patient frequently
 Monitor for intake and output of the patient and urine-specific gravity
 Administer potassium supplements as prescribed to treat hypokalemia.
 Advise patient to take potassium-sparing diuretics.
 Maintain a sodium restriction diet strictly.
 Instruct the client regarding the need for glucocorticoid therapy after adrenalectomy.
 Instruct the client to wear the medic alert bracelet all the time.
Pheochromocytoma
It is the tumor of the medulla in the adrenal gland. Excess amounts of epinephrine and
norepinephrine are secreted.
Diagnostic tests include 24-hour urine collection for venial medallic acid. Its ph should be less
than 3 so HCL is used as preservation.
Sign and symptoms:
  Proximal or sustained hypertension
 Severe headaches
 Palpitations
 Flushing and profound diaphoresis
 Heat intolerance, weight loss
 Pain in the chest or abdomen with nausea and
vomiting
 Tremors
 Hyperglycemia
Complications:
 Hypertensive crisis
 Hypertensive retinopathy and nephropathy
 Cardiac enlargement and dysrhythmias.
Intervention:
 Monitor vital signs of the patient
 Monitor for hypertensive crisis or complications with hypertension crisis such as stroke,
cardiac dysrhythmias, and myocardial infarction.
 Instruct the client not to smoke, drink caffeine-containing beverages, or change position
suddenly.
 Prepare to administer alpha-adrenergic blocking agents and beat adrenergic blocking
agents to control hypertension
 Monitor blood glucose levels
 Promote rest and provide a quiet environment.
 Provide a diet high in calories, vitamins, and minerals.
 Prepare the client for an adrenalectomy.
Key point: Bleeding is a priority because the adrenal gland is a highly vascular organ.
Thyroid gland disorders
Hypothyroidism (Hashimoto’s disease)
Everything is low and slow, low T3 and T4.
Hypothyroidism is a state in which hyposecretion of thyroid hormones decreases the rate of body
metabolism.
T3 is low and TSH is elevated.
Test Tip: Always focus on T3 and T4 levels first. Because it’s always the opposite of T3 and
T4.
In primary hypothyroidism, the source of dysfunction is the thyroid gland because the thyroid is
not able to produce the necessary amount of hormones. But in secondary hypothyroidism, this
gland is not being stimulated by the pituitary to produce hormones.
Signs and symptoms:
 Low energy, fatigue, weakness, muscle pain, intolerance to cold.
 Low metabolism —weight gain
 Face puffiness (edema around eyes)
 Low digestion— Constipation
 Low hair loss —alopecia “not hirsutism
 Mental fatigue, Altered level of consciousness
 Low mood—depression, apathy, Confusion
 Low libido, sexual desire, in fertile
 Slow dry skin turgor
 Low and slow mensuration or very heavy mensuration.
Always monitor for an overdose of thyroid medications, Characterized by tachycardia, chest
pain, Restlessness, nervousness, and insomnia.

Myxedema Coma:
This very low respiratory rate cause respiratory failure. Priority is to place a tracheostomy kit by
the bedside of the patient
 Endotracheal intubation setup ready
 Low BP and heart rate Hypotension, Bradycardia
 Low-temperature cold intolerance
 No electric blankets
 Coma
 Hypothermia and hyponatremia, hypoglycemia
 Ivy fluid administration and provide levothyroxine Iv
Risk factor of myxoedema coma:
 Post thyroidectomy
 Abruptly stop levothyroxine
Interventions:
 Maintain the patent airway of the patient.
 Administer Iv fluids to the patient
 Provide a diet low in calories, cholesterol, and
fats
 Provide frequent rest periods to patient
 Provide roughage to prevent Constipation
 Check vital signs regularly and institute aspiration precautions.
 Administer corticosteroids as prescribed
 Keep the client warm
Diet:
 Low calories
 Low cholesterol and fats
Treatment: levothyroxine
Release T3 and T4 in the body
Lifelong is taken and taken early morning on an empty stomach at least one hour before
breakfast, one tablet a day.
Assess for:
  Very hyper increase BP or heart rate
 Report agitation confusion
 Never abruptly stop
 No double doses
 No cure-only treatment
 It reacts with sunlight. Avoid sunlight
 Exercise —walking

Hyperthyroidism
Hyperthyroidism is a state resulting from the hypersecretion of thyroid hormones T3 and T4,
characterized by an increased rate of body metabolism. It is also known as Graves’ disease.
Causes:
 Autoimmune disorder
 Iodine excess
 Levothyroxine excess
 Priority is thyrotoxicosis (thyroid Storm)
 Extreme high agitation and confusion are an early sign
 Temperature extreme above 105
 High heart rate and BP
 Maintain patent airway and adequate ventilation
 Tremor, delirium, and coma

Signs and symptoms:

 Grape eye (exophthalmos)
 Use an eye patch or tape your eyelid down for sleeping
 Apply artificial tear
 Ask the patient to exercise intra-ocular muscles.
  Golf ball in throat “goiter”
Key point: never palpate goiter in
hyperthyroidism.
 High BP— Hypertension crisis over 180/100
 High heart rate tachycardia
 Heart palpitations and atrial fibrillation
 Hot and sweaty skin “diaphoresis
 Heat intolerance
 Fast GI diarrhea
 Provide cooling blankets
Diet:
 Diet should be high in calories 4000 to 5000 per day and provide high protein and
carbohydrates.
 Frequent meals and snacks should be provided
 6 to 8 meals per day
 Avoid
 No high fiber
 No caffeine or stimulants
 No spicy food
Treatment:
 Methimazole— Not safe for baby
 Propylthiouracil— Baby safe
 The report, a fever sore throat
 Help the patient to rest well and sleep at night.
 SSKI potassium iodide
 It shrinks the thyroid before removal
 It stains teeth use a straw and juice
 Keep one hour before or after other meds
 Beta-blockers for low BP and heart rate
  RAIU radioactive iodine uptake Destroys the thyroid But may take radioactive cautions.
(Permanent hypothyroidism is a major complication). It may take several weeks to see
the full benefits of treatment.
Before RAIU:
 A negative pregnancy test should be done
 Remove neck jewelry and dentures
 Five to seven days before holding anti-thyroid
medications
 Awake no anesthesia or sedation is given
 NPO two to four hours before and one to two hours
after (Not 12 hours).
After:
 Avoid everyone 1-3 days
 No pregnant people
 No crowds
 No same restroom or washroom flush three times
 Not use the same food utensils
 Not the same laundry as their family
 No cuddling or kissing.
Priority after surgery thyroidectomy
 Airway
 Laryngeal stridor, Noisy breeding, and even hoarseness or weak voice.
 Priority bedside endotracheal tube or tracheostomy set ready
 Breathing
 Noisy, monitor voice strength and quality
 Circulation
 Bleeding around the pillow and suctioning site
 Neutral head and neck alignment
 Not supine head of bed 30 to 45 degree
 No flexing or extending neck
 Calcium check
 Below 8.6, check for tingling around the mouth because when the thyroid is removed,
some parathyroid gland is also removed which results in a decrease in calcium.

Parathyroid gland disorder

Parathyroid gland produces and secretes PTH (parathyroid hormone) which
controls the level of calcium in the blood.

Hypoparathyroidism-
Condition caused by the hyposecretion of parathyroid hormone by the parathyroid gland.
 Causes- Exposure to radiations
 Can occur due to accidental removal of parathyroid while thyroidectomy
Sign and symptoms-
Hypercalcemia or hyperphosphatemia
Numbness and tingling on the face
Muscle cramps and cramps in the abdomen
Positive trousseau’s and Chvostek sign
Nursing interventions-
Monitor for signs of hypocalcemia and tetany.
Initiate seizure precautions.
Place a tracheotomy set, oxygen, and suctioning equipment at the bedside.
Prepare to administer calcium gluconate intravenously for hypocalcemia.
Provide a high-calcium, low-phosphorus diet.
Instruct the client in the administration of calcium supplements as prescribed.
Instruct the client in the administration of vitamin D supplements as prescribed;
vitamin D enhances the absorption of calcium from the Gl tract.
Instruct the client in the use of thiazide diuretics if prescribed, to protect the
kidney if vitamin D is also taken.
Instruct the client in the administration of phosphate binders as prescribed to
promote the excretion of phosphate through the GI tract.
 Instruct the client to wear a Medic Alert bracelet.
Exam Hint If two or more parathyroid glands have been removed, the chance of
tetany increases dramatically. • Monitor serum calcium levels (9.0 to 10.5 mg/dL is
normal range).

Hyperparathyroidism-
Condition caused by hypersecretion of parathyroid hormone (PTH) by parathyroid gland
Causes-
Tumor of parathyroid gland
Chronic kidney failure
Sign and symptoms-
STONES: Kidney stones (increase calcium)
• BONES:
• Skeletal pain
• Pathological fractures
from bone deformities
Abdominal MOANS
- Nausea, vomiting, and abdominal pain
- Weight loss / anorexia
- Constipation
Psychic GROANS
- Mental irritability
• Confusion
Nursing interventions-
a. Monitor vital signs, particularly blood pressure.
b. Monitor for cardiac dysrhythmias.
c. Monitor intake and output and for signs of renal stones.
d. Monitor for skeletal pain; move the client slowly and carefully.
e. Encourage fluid intake.
f. Administer furosemide as prescribed to lower calcium levels.
g. Administer NS intravenously as prescribed to maintain hydration.
 h. Administer phosphates, which interfere with calcium reabsorption, as prescribed.
i. Administer calcitonin as prescribed to decrease skeletal calcium release and increase
renal excretion of calcium.
J. Administer IV or oral bisphosphonates to inhibit bone resorption.
k. Monitor calcium and phosphorus levels.
1. Prepare the client for parathyroidectomy as prescribed.
m. Encourage a high-fiber, moderate-calcium diet.
n. Emphasize the importance of an exercise program and avoiding prolonged inactivity.

Diabetes mellites-
A metabolic disorder characterized by high levels of glucose resulting from defects in insulin
production, insulin action (insulin resistance) or both

Types-
 Type- 1 (IDDM) – No insulin production
 It is an autoimmune disorder in which body kills it own pancreas. Because of that there is
no insulin production.
 Usually diagnosed in childhood
 The cells are starved of glucose since there is no insulin to bring glucose into the cells.
 Cells use protein and fats for energy, causing ketones to build up those leads to diabetes
ketoacidosis.
 Sign and symptoms- Polyuria, polydipsia, polyphagia, weight loss
 Only has one treatment insulin. Oral hypoglycemic agents will not work
Type- 2 (NIDDM) Insulin resistance)
 Type 2, problem is you
 In this type because of ugly lifestyle cells become resistance to insulin that led to
hyperglycemia.
 Causes- HTN, High cholesterol over 200, obesity
 Sign and symptoms- Polydipsia, polyuria, polyphagia, weight loss, fatigue,
frequent infections, blurred vision, acanthosis nigricans (brownish skins on
neck and armpits) impotence eventually led to diabetic foot
  Treatment- Typically a stepwise approach Diet, exercise Oral agents’ Oral
agents and insulin, Insulin

Causes- Stress (physical-surgery, emotional), Sepsis (infection) lead to

Normal Random Fasting Hba1c

70-140 Upto 100 Under 5.7

Prediabetic 140-199 100-125 5.7-6.4

hyperglycemia. Insulin must be administered either patient has eaten or not, because
in case of any stress. Stress hormone (cortisol) over function and can lead to
hyperglycemia
Steroids- Prednisone can lead to hyperglycemia

Diagnosis-
Diabetic 200+ 126+ 6.5+

Complications-

Rules of insulin-
Peak+plates- Give food during the peak time of insulin
No peak no mix
Regular insulin – IV only (direct into the veins)
Give clear to cloudy or Regular insulin than NPH (RN is for syringe)
Rotate location every 2-3 weeks, best location is on abdomen near umbilical area
Always monitor for DKA- we give insulin even in sick days, even patient hasn’t eaten
anything (but closely monitor the client)
TYPES OF INSULIN AND HYPOGLYCEMIA LIKHNA AAE
Type Name Peak Action Duration Nursing implementation
Long acting Detemir No Peak 24 hour Not to be given IV
Glargine No peak no need of food
Recommended-Give once
daily (subcutaneous) at
bedtime
Acts as a basal insulin
(present in the body acts
like normal insulin,
whenever body needs
insulin works)
Do not infuse insulin
Do not shake insulin
Do not mix with another
insulin

Intermediate NPH 5-6 HRS 16-18 Not to be given IV

HRS Given two time a day
Mis clear to cloudy
Short acting Regular 2-4 HRS 5-8 HRS Can be given IV
insulin If patient feels shake give candy
Rapid Aspart 15-30 min 30-90 min Never given until plate is on bed
acting Lispro
Glulisine
Oral hypoglycemic agent-
When diet and exercise fail then OHA given
Never given with Iron, Ca and antacid that contain Ca
Oral hypoglycemic agents are contraindicated in pregnancy

Drugs Adverse Nursing implications

reaction
Metformin (Reduces  Abdominal  Discontinue 48 hours before and
the production of discomfort wait 48 hours to restart after
glucose through  Diarrhoea diagnostic studies with iodine
suppression of  Lactic contrast media
gluconeogenesis) acidosis  Instruct the client to contact the
provider if signs of lactic acidosis
(myalgia, hyperventilation) are
experienced.
 Can lead to vit b12 deficiency
 Use cautiously with pre-existing
renal (creatinine over 1.3) and
liver disease
Sulfonylureas  Weight gain  Alcohol is contraindicated
 Glyburide  Sunburn  Instruct the client to avoid alcohol
 Glipizide due to disulfiram effect.
 Glimepiride  Toxic for heart patient specially in
old patient
Thiazolidinediones  Pitting edema 
Rosiglitazone  Crackle
Pioglitazone sounds
 Rapid weight
gain
Care of Diabetic foot-
Wash feet daily (use lukewarm water, use thermometer to check temp of water not hands)
Gently pat feet dry with cotton towel (no heavy powder, light is ok)
Feet should not be moisturised no oil or cream
Inspect feet daily with a mirror, check any cuts, blisters, or sores. Educate client not to remove
callous (dead skin)
Cut toenails straight across (no angles). If in hospital only physician is allowed to cut nails.
Educate client to avoid flip flops, high heels, nylon socks (only cotton)
Wear close toe comfortable, supportive, leather shoes
Shake shoes before wearing.
DKA VS HHNS