Care of Patients with Endocrine Conditions d.

MSH - stimulates pigmentation of the

skin; the more melanocytes, the darker
PITUITARY GLAND e. ACTH - stimulates production of
corticosteroids
f. ICTH - stimulates testosterone
g. Prolactin - stimulates production of milk
h. GH - stimulates growth of bone, muscles
and soft tissue
2. Posterior Pituitary Gland/PPG (Neurohypophysis)
● Storage and releasing of hormones
● Hypothalamus produces the hormones
Hormones:
a. Oxytocin
- uterine contraction (induce labor
at 5cm)
- Milk let-down reflex
b. ADH/Vasopressin
(pons and medulla for respiratory/pulmonary pattern) - conserves ALL fluids (not only
● Master gland of most of your hormones urine) directly to 2 areas:
● Brain controls this gland vascular area and kidney
● Direct or indirect effect to most of your hormones - potent vasoconstrictor
● Found on the base of your brain below - BP regulation (increases)
hypothalamic: “hypophysis”
● Hypophysectomy: removal of the pituitary gland
○ common route: transsphenoidal
○ common manifestation of bleeding:
frequent swallowing
● All hormones in pituitary are for stimulation
activated via negative feedback (will only be
activated if there is a deficiency)

Diabetes Insipidus/D.I.
● Due to deficiency or actual absence of ADH
● Dry inside
Symptoms:
- Polyuria
- Polydipsia
- Hypovolemia
- Hypotension
Parts of the Pituitary Gland: - Weight loss
1. Anterior Pituitary Gland/APG (Adenohypophysis) - Poor skin turgor
● Produces stimulating hormones - Sunken eyeball
Hormones: - Dry skin
a. TSH - stimulates thyroid; converts T3 to - Prone for hypovolemic shock
T4
b. FSH - stimulates follicles; stimulates egg
cells
c. LH - helps in ovulation
 - Causes cell damage; cells can
regenerate (mitosis)

Syndrome of Inappropriate Antidiuretic

Hormone/SIADH
● Syndrome of Increased levels ADH
Symptoms:
- Anuria
- Water retention/fluid overload
- Hypervolemia
Diabetes Insipidus Syndrome of
- Hypertension Inappropriate ADH
- Weight gain
- No edema because fluid goes to the blood due to deficiency/ due to excess production
vessel (vascular) absence or high of ADH
Fluid compartments/spaces: resistance to ADH
a. Vascular
Types: Causes:
- Most important
1. Neurogenic - Primary reason:
- Where ADH acts; water stays here - Most common adenoma
- Connected to all your vital organs type of D.I. (benign tumor in
b. Cellular - Problem in the vital organs)
c. Interstitial hypothalamus or causing
- Largest PG overactivity in
- “Under/Absent PG or
- Edema occurs here
Activity” - no/slow hypothalamus
Classification of Dehydration: function - Hypertrophy/Hyp
a. Vascular Idiopathic so causes may erplasia
- More severe and life threatening since be: - Hyperpituitarism
vital organs may die; organs cannot - Atrophy - Inflammation
regenerate - Autoimmune - Overtreatment
b. Cellular damage (ex. HRT)
 - Hypopituitarism/S - Best test: Test (Increased in
immond’s Specific Gravity SIADH)
Disease test (Urinalysis); - Serum
- Genetics/Congeni (Decreased/Dilut Osmolarity
tal ed) (Decreased)
- Cancer - Serum osmolarity
- Overtreatment test
(radiation) (Increased/Conce
- Surgery ntrated)
(accidental/intenti
onal)
2. Nephrogenic
- Kidney has high *WDT: with DI, urine is
resistance to still increased at the end
ADH *Hypertrophy: increase of the shift even w/o fluid
- Cause: renal size of cell *SGT: checks urine
failure (infection, *Hyperplasia: increase concentration/ability of
genetic, diabetes, number of cells kidney to concentrate
autoimmune etc.) *Hyperpituitarism excess urine (1.010 - 1.030); if
so can cause gigantism less = diluted, if more =
concentrated
Clinical manifestations: Clinical manifestations: *SOT: blood
- Polyuria - Oliguria/anuria concentration (280-295
(>4L/day) - Water retention mosm)
- Polydipsia - Concentrated
- Diluted urine urine Management: Management:
- Water loss - Fluid - DOC: Hormone - Diet: high sodium
- Fluid deficit excess/overload replacement but limit fluid
- Hypovolemia - Hypervolemia therapy for life - Diuretics
- Hypotension - Vascular (ex. Vasopressin (Furosemide -
- Hemoconcentrati distention (JVD) “pressins”) wasting)
on - Hypertension - Route: intranasal - Antihypertensive
- Viscous blood - Weight gain (maintenance), drug
(poor circulation) - No body edema intravenous - Anticonvulsants
- Metabolic - Organ congestion (emergency) (Diazepam,
Acidosis (ex. - Hydration Valium)
- Dehydration Hepatomegaly, (increase oral or - Anti-arrhythmia
(vascular) splenomegaly, IVF) (Amiodarone)
- Weight loss hydronephrosis) - Anticoagulants - Sodium
Cause of death: - Hemodilution “parin/farin” replacement
Hypovolemic Shock Watch Out For: - Monitor I&O - Monitor I&O
(multiple organ failure, Dilutional Hyponatremia - Weigh daily (AM, - Weigh patient
systemic) (may lead to seizures and same time and daily (AM, same
arrhythmia) clothing) time and clothing)
*No insulin problems but - Monitor and - Seizure
has similar symptoms to correct precaution
D.M electrolytes - DOC:
- Inotropic drugs demeclocycline
Diagnostic tests: Diagnostic tests: PRN (increases (decreases ADH
- CT Scan/Mri to - CT contraction of production)
visualize pituitary Scan/MRI/PET heart) “cycline”
and Scan for tumor - Chlorpropamide - Surgery (last
hypothalamus - Kidney function (Diabinese) option) of choice:
- Kidney Function test - Sodium hypophysectomy
Test - ABG (met. bicarbonate (transsphenoidal)
- ECG alkalosis) (Antacid) or infratentorial
- ABG (met. - ECG/EGG craniotomy
acidosis) (arrhythmia, *most important thing is “burrhole”
- Water deprivation seizures) to replace the hormone
test - Specific Gravity *anticoagulants since risk
 for clotting due to viscous
blood
*best time to weigh: AM
*inotropic d/t risk for
shock; “mine”
*chlorpropamide: oral
hypoglycemic agent for
off-label effect (low dose)
*Diabinese stimulates
ADH release, lowers
resistance to ADH,
*Antacid since DI is
acidosis
*low sodium because of a. Calcium
delusional hyponatremia - form of mineral
*Fast food and canned - the more calcium, the more fibrinogen,
goods are okay since the more clots
high in sodium - Important for the production of
*loop diuretics - fibrinogen (clotting factors)
potassium wasting
- Acts as cement/concrete as it makes
*Amiodarone: potassium
blocker so elevate our bones hard, teeth, blood etc.
sodium (inversely Parathyroid Hormone/Parathormone (PTH)
proportional)
*mouthpiece during aura
*”cycline”- antibiotic
*after infratentorial
craniotomy place patient
flat

- Regulates calcium and phosphate level

Urinalysis and Serum Osmolarity test: - PTH withdraws calcium from the bone and
transfers it to the blood
- “Bone to blood”
- Activates during
hypocalcemia/hyperphosphatemia

HYPERPARATHYROIDISM
- Too little calcium in the bone
- More calcium in blood

HYPOPARATHYROIDISM
- Too little calcium in the blood
- More calcium in bone

*calcitonin - calcium from the blood to the bone

*calcium and phosphate inversely proportional

PARATHYROID GLAND Hyperparathyroidism Hypoparathyroidism

● Posterior to the thyroid gland (PTG)
Due to Due to absence/low
● Butterfly shaped organ; composed of four overproduction/excess of production of PTH
nodules - two in each side PTH
● Only produces PTH
 Leads to excessive
demineralization of bones
and overaccumulation of
calcium in the blood
Leads to excessive stenosis hypocalcemia
calcium deposits in the - Renal
bone and inability to calculi/stones Watch out for:
replace calcium in the (Calcium oxalate) - laryngobronchosp
blood - asm

Causes: Causes: *pathological fracture: *either hypo/hyper, still

- Leading cause: Idiopathic atrophy of from a medical condition triggers arrhythmia
adenoma in PTG PTG: *osteoporosis: systemic; *need calcium to produce
- Hypertrophy/Hyp - Under/absent primary - natural; clotting factor fibrinogen
erplasia in PTG activity secondary -
(overactivity) - Cancer disease/conditions
- Genetic problem - Overtreatment *smallest: ear stapes;
- Inflammation (radiation) largest: femur
(autoimmune - Surgery *sensorineural: inner ear
condition, (accidental/intenti is affected, caused by
infection) onal) nerve damage (CN8)
- Overtreatment - Damaged PTG *conductive: bone
(HRT) (Infection, structural problem; outer
autoimmune) or middle ear is affected
- Genetics/congeni *”lith” means stones
tal

*iatrogenic: if a medical Diagnostic Tests:

treatment causes an - X-ray
illness - CT/MRI
- Bone Scan “Densimeter”
Clinical Manifestations: Clinical manifestations: - ECG (arrhythmia)
- Weak, brittle, - Big, heavy, rigid, - Bleeding and clotting parameters
soft, spongy hard bones - Serum PTH level
bones - Weight gain - Serum electrolytes (calcium and phosphorus)
- decrease bone - Bone deformity - Hearing test
density “thickening” - ALP (Alkaline Phosphatase) levels
- Risk for - Pain (due to
fractures/osteopo thickening of Management: Management:
rosis (Pathologic bone) - Diet: low calcium - Diet: High
fracture; - Hearing loss - DOC: Calcitonin calcium, high Vit.
secondary (conductive) (hormone D, high fiber, low
osteoporosis) - Hypocalcemia/Hy replacement; phosphate
- Hearing loss perphosphatemia depositor) - DOC: HRT of
(conductive - Risk for bleeding, - Hydration PTH for life
hearing loss) bruising, etc. (OFI/IVF) - Calcium
- Bone deformity - Tetany (viscous blood supplements
“bowing”/bend - Twitching and risk for renal (calcium lactate,
- pain muscles calculi) ca gluconate)
- Abnormal posture - Paresthesia - Analgesics - Analgesics (pain)
(kyphosis/Dowag - Chvostek’s Sign - Mild to moderate - Antiarrhythmia
er’s hump-most (stroking or activities/ Handle - Tranexamic acid
common, tapping the cheek extremities gently (hemostan)
lordosis, scoliosis face/eyes will (prone fractures) Oral/IV
- hypercalcemia/hy twitch d/t irritation - Antihypertensive - Steroids PRN if
pophosphatemia of CN7 - Anticoagulants autoimmune
=arrhythmia - Trousseau's sign (prone bleeding) - Weigh patient
- Viscous blood; (inflate bp cuff - Anti Arrhythmia daily (wt. gain)
poor circulation tremors will occur - Radiation Tx - ET/Tracheostomy
- Risk for clotting then arm will PRN (d/t set/bag valve
- Vascular/valvular lock) adenoma) mask (ready in
calcification *Chvosteks and - Antineoplastic the bedside)
which causes Trousseaus: for PRNtreat - Antacid and

underlying cause
- Treat underlying
cause
- Hearing aid PRN
Surgery:
Parathyroidectomy
(subtotal/total)
*Calcitonin deposits
calcium from blood to
bone
*subtotal more popular
*total surgery: HRT for life
● Leads to an unnecessary and excessive
phosphate
binder: Amphojel production of catecholamines even without
(Al Hydroxide) emergency
● Leads to excessive sympathetic effect
● More common in women
● Tumor (internal)- produces both E and N
● Tumor (external) - produces epinephrine only
*high calcium cause
constipation
*Maintenance: oral;
emergency: IV
*ET/Tracheostomy
set/bag valve mask in
case of breathing difficulty
*Amphojel decreased
phosphorus

Benign without biopsy:

● No metastasis
● Tumor is encapsulated
Cause:
● Main cause: Genetics/Hereditary
● Can be a part of another condition MEN IIA
(multiple endocrine neoplasia/Sipple’s Disease)
-multiple tumors
● MEN IIA - Autosomal dominant condition
● Common in women

ADRENAL GLAND ➢ x-link: sex chromosome problem

● Above kidneys, 2 parts ○ Common for women
○ More severe symptoms in men
Basic Parts: ➢ autosomal: 46 chromosomes problem
1. Adrenal cortex ○ Autosomal Dominant- with
- Produces corticosteroids: physical/anatomical changes in the body
Hormones of AC: with your naked eye or CT, MRI etc;
● Mineralocorticoid (Aldosterone); salt level need only 1 parent that carries the trait
● Glucocorticoids (cortisol/cortisone) = stress ○ Autosomal Recessive - without physical
hormones; sugar level changes that can be seen with the
● Gonadotrocorticoids = sex hormones; secondary naked eye; can only be confirmed by a
sexual characteristics blood test; both parents must have a
2. Adrenal medulla genetic problem for it to be passed on
- Produces catecholamines: Clinical Manifestations:
Hormones of AM: ● Cardinal sign: triad sign (pheochromo triad)
● Epinephrine and norepinephrine (Adrenaline) ○ Palpitations
- sympathetic effect; fight or flight ○ Hypertension (systolic >180, dia >120;
response; “adrenaline rush” hypertensive crisis)
- Sympathetic: up, elevated, fast EXCEPT ○ Excessive sweating (Diaphoresis;
GI/GU (constipation, urine retention) parasympathetic)
● Hyperthermia
PHEOCHROMOCYTOMA ● Hyperhidrosis
● Benign adrenal medulla tumor (adenoma) ● Headache (occipital d/t hypertension)
● “Chromaffin Tumor” ● Hyperglycemia
● Hyperactivity: tremors/insomnia/agitation
 ● Hyperventilation
● Hypermetabolism: polyphagia
● Weight loss
● Water retention
● Constipation
Diagnostic tests:
● Confirmatory test: MRI/CT Scan/Pet Scan
picture; biopsy is optional
● Screening test:
1. VMA Test: vanillylmandelic acid test
- Checks for urine
catecholamines
- It is a 24 hr urine test
- C/I: vanilla, chocolate, nuts as it
can cause false positive result
2. Serum catecholamines
- Checking the blood for
epinephrine and norepinephrine
Management:
- Diet: high calorie, high carbohydrates, high
protein since these are all fast in metabolism; no
stimulants
- Hydration
- Radiation
- Antineoplastic
- Antihypertensives (propranolol)
*beta blockers: decrease blood pressure and
palpitations
- Laxatives
- Place patient in cold and comfortable low
stimulus environment; far from the nurse’s
station
- DOC: Phentolamine (Regitine) -direct acting
vasodilator through IV and lowers BP
significantly
- Surgery: Adrenalectomy (last option) in which
client will have HRT (steroids) to prevent
Addison’s Disease