Adrenal Flashcards
What role does cortisol play
Cortisol- stress hormone
Released during stress to help body deal w/ stressor
Cortisol metabolizes glucose- increased BG, break down fats, proteins, and carbs
regulates sodium, potassium
Describe negative feedback loop related to adrenal glands/cortisol
Hypothalamus released CRH–> causes pituitary gland to release ACTH–> causes adrenal cortex to release cortisol
any issues with release of ACTH will cause issues with cortisol
what can cause Addisonian crisis
Stressors- sickness, infection, increased stress, trauma
Not taking glucocorticoid steroids
Adrenalectomy- Adrenal gland is remove so body is not producing cortisol anymore- needs to take steroids Life long
Pituitary gland damage r/t negative feedback loop- not releasing enough ACTH
S/S of Addisonian crisis
5 s's super low BP- can NOT be brought up i.e. fluids, vasopressors sudden pain in stomach, back, legs syncope shock r/t low BP, dehydration severe V/D/Ha
3 H’s
hyponatremia <135
hypoglycemia <70 r/t cortisol which metabolizes glucose (brings into blood)
hypERkalemia 5.2
What s/s are present in Addison’s disease and Addisonian crisis
3 h’s
Hyponatremia
Hypoglycemia
Hyperkalemia
How does cortisol affect BG levels
Cortisol will metabolize glucose which brings it into the circulatory system, low cortisol = low BG levels
Which of the following below is NOT a sign or symptom of Addisonian Crisis?
A. Low blood pressure
B. Severe pain in the stomach, legs, and lower back
C. Hypokalemia
D. Hyponatremia
C- you will see HYPERkalemia
Which of the following abnormal electrolyte imbalances is EXPECTED with Addisonian Crisis? A. Potassium level of 3.2 B. Sodium level of 112 C. Blood glucose level of 120 D. Phosphate level of 1.2
B- sodium level of 112
3 H’s- hyponatremia
You will also have low BG d/t low cortisol and high potassium d/t low sodium
** remember sodium and potassium are opposite
which disorder is r/t hypo in adrenal disorders
Addison disease, adrenal insufficiency
What are causes of Addison’s disease
Primary: Damage to adrenal cortex- cannot produce sufficient amount of cortisol R/T autoimmune or idiopathic atrophy
infection- TB, fungal (histoplasmosis)
Secondary-Damage to pituitary glands- pituitary glands release ACTH which stimulates adrenal glands to release cortisol
also….
removal of both adrenal glands (adrenalectomy)
sudden cessation of steroids
What does steroid therapy do to the body and what education must be provided
Steroids suppress the body’s normal respond to stress by releasing cortisol and interferes with the normal negative feed back mechanism
Steroids must be tapered to allow adrenal cortex to start producing efficient levels of cortisol
Dx of Addison’s disease Lab findings
decreased 17-hydroxycorticosteroids
Decreased 17- ketocorticosteroids
Decreased serum cortisol
Increased ACTH
non specific to Addison’s disease but r/t
hypoglycemia d/t decrease cortisol
hyponatremia
HYPERkalemia r/t hyponatremia
S/S Addison disease
think low steroids LOW BP- most critical Low weight Low energy- fatigue low BG Low muscle ability- muscle weakness
HIGH P
Hyperkalemia- potassium
Hyperpigmentation- bronzed color
Addison disease treatment
LIFE LONG- corticosteroids
prednisone, hydrocortisone, methyl prednisone
will need to increase dependent upon stress, surgery etc.
If excessive sweating- salt tab or salty foods
physical exercise alt w/ periods of rest, no strenuous activity
Addisonian crisis treatment
1ST- give cortisone- usually solu cortef
Stabilize BP- Fluids, vasopressor?
Stabilize BG levels fluids such as D5NS- which will also stabilize sodium
PO steroids such as prednisone etc…teaching
What is crushing’s disease/syndrome
Syndrome- usually caused by external factor- corticosteroids
Disease- usually caused by internal factor- tumor, hyperplasia, malignancy
Excessive cortisol release
d/t
Adrenal tumor of hyperplasia
Pit tumor which over secretes ACTH which oversecretes cortisol
Non pituitary tumor, neoplasm that stimulates ACTH or cortisol
Small cell lung cancer
long term steroid use
Iatrogenic
prolonged steroid use
s/s Cushing’s
Think BIG
Truncal obesity w/ striae
Moon face, with redness, acne and thing skin
Buffalo hump with thin muscle wasted extremities
increased hair production esp. on face for women
Increased risk of Cataracts d/t steroid use
Osteoporosis d/t increased steroid causing osteoclast and inhibit osteoblast which leads to R/F of fractures
Decreased immune R/F for prolonged wound healing, infections
Hypernatremia, hyperglycemia. hypokalemia
Tx of cushing’s
Treat cause
prolonged steroid use- decrease dose or alt days
If r/t tumor- removal of tumor
Adrenal- will need life long replacement if bilateral involvement
Pituitary- hormonal replacement etc
Monitor salt intake- diet is low in salt, high in potassium; supplement
Monitor hyperglycemic states d/t increased cortisol = ^ BG levels
Let patient talk! disturbed body image etc
What is Pheochromocytoma
Functioning tumor of adrenal medulla
10% are malignant, usually benign
What does epinephrine do?
Acts as a vasoconstrictor on the blood vessels
What does a pheochromocytoma do?
Secretes excessive levels of epinephrine and norepinephrine, causing hypertension d/t vasoconstrition
Who is most at risk of pheochromocytoma?
25-50 year old
equally men and women
High risk if family member dx- familial
s/s of pheohromocytoma
non specific hypertension
Usual triad- HA, diaphoresis and palpations
tachy, dilated pupils, cold extremities
Hyperglycemia
