PITUITARY GLAND
Anterior Posterior
(Adenohypophysis) (Neurohypophysis)
Growth hormone Oxytocin
TSH (thyroid stimulating hormone) ADH (anti-diuretic hormone)
Prolactin
ACTH (adrenocorticotropic hormone)
LH (luteinizing hormone)
FSH (follicle stimulating hormone)
MSH (melanocyte stimulating hormone)
Growth Hormone
Stimulates growth
Increases glucose levels
Hypersecretion (Adult) – acromegaly
Hypersecretion (Child) – gigantism
o DOC: Sandostatin (Octrocotide) somatostatin anti-GH
Hyposecretion – dwarfism
o DOC: Humatrope (Somatropin) increases GH
Thyroid Stimulating Hormone
TSH stimulates the thyroid gland, which produces: T3 (metabolism/catabolism), T4 (heat), &
Calcitonin (lowers serum Calcium & increases bone calcium) thyroid hormones increases the
action of epinephrine & norepinephrine (sympathetic)
Hyperthyroidism
o Grave’s Disease (Toxic Diffused Goiter) autoimmune disease the immune system
stimulates the production of thyroid hormone while attacking the fat pads behind the
eyes, causing inflammation causes exophthalmos (Graves’ ophthalmopathy)
o More common with females, 40 years old
o Increased appetite, decreased weight, increased body temperature, heat intolerance,
diaphoresis, increased v/s complication: cardiovascular; hyperactivity (restlessness,
irritability), increased LOC; all are increased except body weight, TSH, and menses
o Negative feedback mechanism: if there’s an increase; there’s a decrease somewhere
(e.g. increase in T3 & T4 causes decrease in TSH, FSH, & LH which may cause
amenorrhea)
o Management:
Weight loss – high calorie
Heat intolerance – provide cool environment
Hyperactivity – non-stimulating environment
Diarrhea – low fiber diet, increase OFI
Exophthalmos – eye drops (artificial tears); sunglasses
o Medications
Iodides – prevent releases of TH
Lugol’s solution
Saturated solution of potassium iodide (SSKI)
Bitter take with milk or fruit juice/ice
Staining provide straw
Thioamides – decreases production of TH
Methimazole
Propylthiouracil (PTU)
A/E: agranulocytosis decreased WBC increased risk for
infection report any form of infection (fever/sore throat)
WOF signs and symptoms of hypothyroidism
GI irritation take with meals
Increase in weight reflects effectivity of medication
o Surgery (Thyroidectomy)
Total
Subtotal – leaves 5/6; 2 grams of thyroid is removed
Pre-operative intervention:
Give Lugol’s solution two weeks prior to promote eurothyroid state,
decrease size, and decrease vascularity (decreases chances of bleeding).
Post-op
Monitor for:
Hypocalcemia and tetany caused by the accidental removal
of the parathyroid gland leading to decrease in PTH
Chevostek’s – cheek twitching
Trosseau’s – carpopedal spasms
DOC: Calcium gluconate
Thyroid storm – severe form of hyperthyroidism due to leakage
of TH in the circulation
Severe signs & symptoms (all increased)
DOC: Thioamides
Laryngospasm – caused by decreased calcium or inflammation
Prepare tracheostomy set at bedside
Laryngeal Nerve Damage
Hoarseness
Tell the client to speak every hour
Signs of Bleeding
Decreased BP, increased PR, increased RR
Inspection: dressing anterior and posterior of the
neck
Neck and head: avoid flexion and hyperextension
can cause increased pressure at the suture line which
can cause bleeding
Position
Semi-Fowler’s – increased breathing
Hypothyroidism
o Adults – myxedema (severe form) caused by decreased metabolism production of
mucopolysaccharides which move under the skin & attracts fluid leading to the puffing
of the face and the hands
o Children – cretinism accommodated by mental retardation
o Causes: Hashimoto’s disease (autoimmune disease which destroys the thyroid gland),
thyroidectomy, antithyroid drugs
o Increased weight, anorexia, constipation, decreased temperature, cold intolerance,
hypoactive, decreased v/s; all are decreased except weight
o Management
Monitor daily weight – decreased weight = effectiveness
Low calorie diet
High fiber diet
Increase fluid intake – due to constipation
Provide warm environment – due to cold intolerance
Medication: Levothyroxine (TH replacement in the AM with empty stomach)
Parathyroid Glands
Hyperparathyroidism – increased PTH
o Hypercalcemia & Hypophosphatemia
Decreased neuromuscular irritability muscle weakness, decreased peristalsis
(constipation)
Bones weakened; at risk for pathologic fractures
Blood pressure increased
Heart cardiac dysrhythmia
Kidneys high risk for renal calculi
o Management:
Low calcium diet
High phosphate food rich in protein
High fiber & increase OFI
Exercise
Safety
Monitor v/s
Increase fluid
DOC: Calcitonin
Hypoparathyroidism
o Hypocalcemia & hyperphosphatemia
Increased neuromuscular irritability – can cause tetany spasms, seizures;
diarrhea
Blood pressure – decrease BP
Heart – cardiac dysrhythmia
o Management:
High calcium and low phosphorus diet
Calcium gluconate
Decrease fiber & increase OFI
Seizure precaution
Tracheostomy set
Monitor v/s
Aluminum hydroxide (Ampogel) – phosphate binder binds with phosphorus
so that it can be excreted instead of being in the circulation; (taken with meals)
Adrenal Glands
Adrenal Medulla
o Epinephrine & Norepinephrine
o Pheochromocytoma
Benign tumor in the adrenal medulla
Classic sign: increased BP
Triad
Headache
Palpitation
Diaphoresis
DOC: Phentolamine (anti-adrenergic)
Complication: cardiovascular complication
Adrenal Cortex endogenous steroids
o Glucocorticoids – cortisol: stress, increased glucose, breakdown of protein; anti-
inflammatory
o Mineralocorticoids
RAAS (trigger: low BP) [renin-angiotensin-aldosterone-system] hypovolemia
decreased BP kidney releases renin liver releases angiotensinogen
which is activated by renin to Angiotensin I lungs will produce ACE ACE
converts Angiotensin I to Angiotensin II which causes vasoconstriction
Angiotensin II triggers Adrenal Cortex to produce aldosterone to correct
hypovolemia by excreting potassium
ACE inhibitor: -pril (Captopril) (anti-HPN)
Angiotensin II receptor blocker: -sartan (Losartan) (anti-HPN)
Potassium-sparing diuretic: Aldactone
o Androgen
Testosterone
Estrogen
Cushing’s Syndrome
o Causes:
Adrenal adenoma
Prolonged steroid therapy
o Cortisol:
Increases glucose – detected by pancreas increase in insulin which
aggregates increase of adipose tissues (face, dorsocervical area, trunk)
Breakdown of protein – thin extremities; weak bones; thin skin easy bruising
stretch marks
Immunosuppressive action – increased risk for infection
o Aldosterone:
Hypernatremia
Increased fluid retention
Hypokalemia
Increased BP
Weight gain
o Androgen
Estrogen
Gynecomastia in males
Decreased libido
May lead to impotence
Testosterone
Viralization in females (male appearance dominance)
Hirsutism
Amenorrhea
Deepening of voice
o Management
Monitor
V/S
I&O
Weight
Decrease sodium diet
Aseptic technique
Allow client to verbalize feelings
Medications: MMK
Mitotane
Metyrapone
Ketoconazole
Addison’s Disease
o Low cortisol & low aldosterone
o Autoimmune disorder may destroy adrenal cortex
o Cortisol
Hypoglycemia
Poor/decreased response to stress
o Aldosterone
Poor retention of sodium and water
Hyperkalemia: cardiac dysrhythmia
Decreased body weight
o Propriomelanocortin APG ACTH adrenal cortex decreased steroids positive
feedback increase in MSH bronze-like skin
o Management
Monitor
Vital signs – BP & HR
Weight
I&O
Fluid intake – increase
Potassium intake – decrease
Administer steroids for life
Hydrocortisone
Dexamethasone
Betamethasone
Prednisone
Taken in the AM to mimic release of cortisol
Take with/after meals
Do not stop abruptly may cause addisonian crisis
SIADH
Excess in ADH
Oliguria
Concentrated urine
Increased fluid retention increased BP, increased weight, distended neck veins, diluted blood
dilutional hyponatremia due to high solvent:solute ratio check for cerebral edema
(increased ICP, N&V, headache, lowered LOC, seizures)
Management:
o Decrease fluid intake
o Monitor fluid status: weight, I&O
o DOC: diuretics (Mannitol, Lasix; except Thiazide will cause opposite effect);
declomycin (blocks ADH in the kidney)
Diabetes Insipidus
Decreased ADH
Types
o Central/Neurogenic – decreased ADH
o Nephrogenic – kidneys are resistant to ADH
Signs & symptoms
o Polyuria, diluted urine, DHN polydipsia (3-5L)
o Flat neck veins
o Decreased BP
o Decreased body weight
Management
o Neurogenic -> vasopressin
o Nephrogenic thiazide; chlopropramide
o Increase fluid
o Monitor v/s, i&o, weight
Water Deprivation Test
o H2O is withheld for 1-8H
o (+) urine is dilutes
o (-) urine is concentrated
Desmopressin Stimulation Test
o Neurogenic – signs & symptoms will disappear
o Nephrogenic – signs & symptoms will persist
Diabetes Mellitus
A chronic disorder of carbohydrate, fat, and protein
Cause is unknown
Predisposing factors:
o Stress – increase in cortisol increased blood glucose
o Heredity
o Obesity – increased fat may lead to insulin resistance
o Autoimmune – immune system attacks pancreas decreased insulin
Types:
DM1 DM2
Juvenile onset Adult onset
Thin Obese
DKA – 250mg/Dl HHNKS (hyperosmolar hyperglycemic non-
ketotic syndrome) – 600mg/dL
Management: “DIE” Management: “DIE+OHA”
Diet modification Diet modification
Insulin Insulin
Exercise Exercise
Oral hypoglycemic agent
Diagnostic tests
o Fasting Blood Glucose (FBS)
70-110mg/dL
NPO 8H prior
o Capillary blood glucose
80-120mg/dL
SELF-MONITORING: report if blood glucose reaches 250mg/dL
o Glycosylated Hgb (HgbA1c)
Most accurate
Blood glucose for the past 3 months
Compliance
Normal: 4-6%
If with DM: goal is <7%
DM1
o Increased viscosity narrowing of blood vessels macrovascular (HPN, MI,
CVA)/microvascular (-pathy: retinopathy, nephropathy, neuropathy)
o Hyperglycemia kidney glycosuria polyuria DHN polydipsia
o Breakdown of proteins “thin”
o Breakdown of fats ketone (acidic) DKA (metabolic acidosis)[brain], fruity odor
(acetone breath)[lungs] lungs will compensate by expelling carbonic acid (CO2)
through hyperventilation & labored breathing (Kussmaul’s)
DM2
o No breakdown of fats because of the presence of insulin no ketone presence
o Hyperosmolar
o Increased viscosity micro & macrovascular complications
o Hyperglycemia kidney glycosuria polyuria DHN polydipsia coma
DKA & HHNS
o Causes:
Stress
Surgery
Trauma
Illness (infection)
o Management:
IV NSS to correct DHN
IV with regular insulin
Diet
Protein (20%), fats (30%), carbohydrates (50%)
Complex carbohydrates pasta, rice, root crops, bread
High fiber slows down gastric emptying controls blood glucose
Exercise controls the progression of complications (moderate exercise at
least 3x a week) – increased uptake of glucose by the cells; increased risk for
hypoglycemia eat complex carbohydrates before exercise
OHA
Sulfonylureas avoid alcohol = can cause disulfiram-like reactions
Increases insulin production by the pancreas
Glimepiride
Chlorpropramide
Glipizide
Alpha glucosidase inhibitors
Blocks absorption of glucose
Acarbose
Biguanide
Prevents production of glucose in the liver
Metformin
S/E: lactic acidosis
Meglitinide
Increases insulin production by the pancreas
Nateglinide
Thiazolidinediones / glitazone
Increases insulin sensitivity
Rosiglitazone
Insulin – never skip
LOG rolls rapidly – novolog, humalog
Short-acting “R” – regular, humulin R, novolin R
Intermediate “NL” – NPH, Lente, Humulin N/L, Novolin N
Long acting “U” – Ultralente, LantUs
Route: SQ
Areas: abdomen, arms, thighs, buttocks
Do not massage injection site
Rotation site: reuse site after or at least 2-3W
1 or ½ inch apart from previous injection site
Administer at room temperature; no cold insulin (unopened vial: ref
body; opened vial: room temperature)
Two insulin in one syringe: NPH(cloudy):Regular(clear); 80:20; N-air,
R-air, R-asp, R-asp; never shake
Hypoglycemia
Blood glucose below 60mg/dL
Signs & symptoms
o Sweating moist skin
o Tremors
o Light headedness
o Tachycardia
Management
o Give 15-30g of fast acting carbohydrates; 15/15 rule 15g will not cause
hyperglycemia
o Hard candy, 4t of sugar, 1/2c of fruit juice or soda; Low-fat milk
o If unconscious – IV, IM, SQ glucagon
o Foot care:
Inspect feet daily
Wash feet with warm water & mild soap
Wear properly fitted shoes (leather or canvas)
Do not wear open toed shoes
Do not wear the same shoes for 2days in a row
Break-in new pair of shoes for 1-2H only until it becomes comfortable
Wear cotton socks – white.
Clip toenails straight across or following contour of toe
Do not apply lotion in between the toes
Avoid self-treatment of corns, blisters, or ingrown toenails