Adrenal Disorders Flashcards
What are the adrenal glands?
Two pyramid-shaped organs located above the kidneys.
Adrenal glands stimulated by
Stimulated by ACTH. Avg. size = 3x5x10cm
Adrenal cortex weight
80% of gland’s wgt.
What are the 3 layers of the Adrenal Glands?
Three Layers:
Zona glomerulosa
Zona fasciculata
Zona reticularis
What does the Zona Glomerulosa regulate?
Mineralocorticoids
Na+, K+ Aldosterone
Zona Glomerulosa regulated by
All and K+
Zona Fasciculata is regulated by
ACTH
Zona Fasciculata secretes
Glucocorticoids , Cortisol, Cortisone, Corticosterone
Zona Reticularis is regulated by
ACT and unknown factors
Zona Reticularis secretes
DHEA
DHEA sulfate
DHEA
Precursor to testosterone
Aldosterone on Na+ and K+ and H+
- Na+ retention
* K+ and H+ ion secretion
What is the primary stimulant of aldosterone synthesis and secretion?
Angiotensin II
What is renin activated by?
- ↓ Na+, ↓H2O
- ↓ blood volume
- ↑ K+
Regulates Na+ and K+ balance
Aldosterone
Where does Aldosterone act on the nephron?
Distal tubule
Aldosterone regulated by
RAAS
Cortisol action
↑ blood glucose in response to stress (↑gluconeogenesis,
↓insulin
Cortisol Causes_________ and has _______, -________
protein breakdown
Has anti inflammatory, growth-suppressing effects
Cortisol on the immune system
↓ immune response (eosinophils, neutrophils, lymphocytes) which increases likelihood for infection and poor wound healing
ANDROGENS____
Converted by ___
DHEA
converted by peripheral tissues to stronger androgens
such as testosterone and estrogen
What happens to the Conversion of androgens to estrogen?
increased in aging (post-menopause osteoporsis)
Catecholamines : Name 3
Norepinephrine
Epinephrine
Dopamine
What are catecholamines secreted by?
Secreted by chromaffin cells of medulla
Catecholamines are Synthesized from
phenylalanine
Catecholamines induce this response
“fight-or-flight” response
Catecholamines and blood glucose
Promote Hyperglycemia
Adrenergic Receptor Effects
Blood Vessels: α1 & 2 =
vasoconstriction
Adrenergic Receptor Effects β2 =
vasodilation
At low doses of Epinephrine, which effects dominates
β
At high doses of Epinephrine, which effects dominates
α
β2 on bronchi =
Relax
Cholesterol
Leads to progesterone => Cortisol and aldosterone
Heart: β1&2 = action
↑ rate and contraction
Aldosterone tell kidneys to
Reabsorb sodium and K+ and H+ secretion
ADDISON DISEASE
(adrenal insufficiency)
Addison’s Most often seen in adults
30-60
Addison’s disease: when you see clinical manifestations
90% of gland destroyed before clinical manifestations = atrophy of adrenal gland
Gluconeogenesis
Produce glucose from non- carb sources
Addison disease caused by PSD
Due to:
Pituitary Failure(↓ACTH)
Suppression of HPA Axis
Damage to Adrenal Gland (Autoimmune)
Other causes of Addison (READ)
Other Causes:
Infections (**Tuberculosis, HIV, Fungal)
Infiltrative Ds. (Amyloidosis, Metastatic CA)
Assoc’d. w/ development of **Autoimmune Disease
ADDISON DISEASE (adrenal insufficiency) hormone decrease
↓ Aldosterone, ↓ Cortisol
Addison Disease metabolic effects
Hyponatremia, Hypotension, Hyperkalemia,
Hypoglycemia, Metabolic Acidosis
Signs and symptoms of Addison Disease
WeSAV
Signs & Symptoms: ***Weakness/Fatigability Eosinophilia **** Skin Hyperpigmentation (or Vitiligo) ***** Anorexia N/V Diarrhea ***Vascular Collapse & Shock
Addison’s Disease Treatment
Treatment: Hormone replacement
Anesthesia Considerations for adrenal insufficiency/Addison’s –>During surgery
Normal expectation is a rise in cortisol and
aldosterone during anesthesia and surgery.
Pt.s with adrenal failure/Addison’s have
absence of steroid response resulting in hypotension, diminished response to vasopressors and low C.O.
Addison’s May be exacerbated by
hyperkalemia.
Addison’s Pre-op mgmt.
w/ fluid replacement, 0.9% NS and glucocorticoid replacement
CONN’S SYNDROME
Due to:
↑ Aldosterone (Hyperaldosteronism)
Due to: Adrenal Adenoma (Primary)
↑ Renin/Angiotensin Angiotensin II (Secondary)
Conn’s pseudohyperaldosteronism:
licorice, chewing tobacco)
What differentiates Primary vs Secondary Conn’s syndrome?
Elevated Renin levels differentiate Secondary from
Primary
CONN’S SYNDROME
BP and K+ what happens
↑ Aldosterone
Hypertension, Hypokalemia (< 3.0 mEq/L)
Results in: Muscle Weakness, Cardiac Dysfunction
Hypervolemia
CONN’s results in (acid base imbalance)
Metabolic Alkalosis (K+ moves from intracellular to extracellular space in exchange for H+ ions. Also, ↑H+ excretion at the kidneys)
CONN’s syndrome: Edema does not occur because of:
ANP release –↑ Na+ excretion
Pressure natriuresis- ↑ Renal hydrostatic pressure promotes Na+ excretion
Aldosterone escape – nephron compensates by
↑Na+excretion at proximal tubule
Conn’s Tx
Treatment: with aldosterone receptor antagonist
Spironolactone
Anesthesia Considerations for Conn’s Syndrome Pre-op
replacement of K+ and Mg++
Conn’s disease: What should be avoided and why?
Hyperventilation should be avoided as respiratory alkalosis may worsen hypokalemia and preexisting metabolic
alkalosis
ANP is opposite
Aldosterone
ANP tell kidneys
Get rid of sodium
Keep potassium
Cushing: Cortisol
In a normal individual there is circadian release pattern of Cortisol
Cushing pts. lack circadian pattern
Cushing syndrome is due to (2)
1) Due to: overproduction of ACTH from pituitary adenoma or less commonly adrenal tumor
2) High doses exogenous steroid
Cushing Signs & Symptoms:
Weight gain Trunk Obesity, “Moon Face”, “buffalo hump” Muscle wasting (extremities) Skin atrophy, Acne, Alopecia Easy bruising
Cushing electrolytes and other abnormalities , BG
CHOSH
↑ Cortisol
Hyperglycemia (insulin resistance & ↑ gluconeogensis)
Suppressed Immunity (susceptible to infx. & poor healing)
HTN (↑ Cortisol = ↑vascular sensitivity to catecholamines =
↑vasoconstriction)
Osteoporosis (pathologic fractures & renal calculi)
Anesthesia Considerations for Cushing Syndrome
Airway
Increased neck size secondary to facial changes may
increase difficulty of intubation.
Anesthesia Considerations for Cushing Syndrome
CV
Increased risk of Cardiovascular complications (CAD,
heart failure, stroke).
Anesthesia Considerations for Cushing Syndrome
Patient handling
Careful attention to handling/positioning of pt. to avoid
risk of fracture secondary to osteoporosis.
Attention to aseptic technique if performing an epidural
or spinal tap (immunosuppression).
Cushing
For Cushing–> If adrenalectomy performed laparoscopically,
be aware of risk of diaphragmatic injury and possible tension pneumothorax.
ANDROGEN IMBALANCE
Caused by tumors
syndrome depends on the hormone, gender and age of patient
Androgen imbalance with high estrogen
causes feminization with development of female sex characteristics
↑ Androgens causes
virilization with development of male sex characteristics
Androgen imbalance Tx
Treatment for these conditions is surgical excision. No specific requirements for anesthesia in these patients.
Pheochromocytoma
↑ Norepi/Epi screted by chromaffin cell tumors of
medulla
Pheochromocytoma population
Most common in pts. 40 – 60 yrs.
Men and women affected equally
Can be sustained or paroxysmal.
Pheochromocytoma Can be trigged by
ARBY
ingestion of foods containing tyrosine (ex. Aged cheese, red wine, beer, yogurt).
“True” pheochromocytomas secreting epi/norepi arise from.
adrenal medulla
“Paraganglionomas” a.k.a. ________arise from
extra-adrenal pheochromocytomas secreting epi/norepi arise from the sympathetic chain.
↑ Norepi/Epi Signs/Symptoms: (5)
HHH , TPDS
HTN Severe HA Tachycardia Palpitations Diaphoresis Hyperglycemia
Pheochromocytoma : triad
At least one of a triad of diaphoresis, headaches and
palpitations occurs in over 90% of these patients
Why does Hyperglycemia occurs with Pheochromocytoma?
via catecholamine induced inhibition of insulin
Treatment with pheochromocytama:
Phenoxybenzamine and/or surgical excision palpitations occurs in over 90% of these patients.
Pheochromocytoma Crisis Presents with:
Severe pounding HA Sweating Pallor Palpitations Anxiety
Ionized contrast media can precipitate
crisis
Catecholamine induced Cardiomyopathy
Notched P wave “P-mitrale” indication of left atrial hypertrophy left ventricular diastolic dysfunction.
Mitral valve stenosis may or may not be present.
Catecholamine induced Cardiomyopathy
•CXR with
cardiac failure and pulmonary edema. This patient had ejection fraction of 24%.
Catecholamines and their oxidation products have
direct toxic effect on the myocardium.
•Cerebral ischemia and stroke may also occur with
cardiomyopathy.
Anesthesia Considerations in Pheochromocytoma
These tumors are very
Control HTN crisis with alpha blockers essential.
vascular, excision = significant blood loss.
Assessment of volume status difficult.
As a guide, a difference in
Systolic pressure between peak inspiration and expiration >10mmHg suggests inadequate volume regardless of actual arterial pressure.
Phenoxybenzamine action
non-selective α-blocker forms irreversible bond with
α-receptor.
Cannot be overcome during catecholamine surge.
Favored for pre-op hemodynamic control.
High doses can result in post-op hypotension.
Anesthesia Considerations in Pheochromocytoma (CHAD)
Catecholamine-sensitizing anesthetics
Histamine-releasing agents
Anticholinergics
Droperinol
Anticholinergics to avoid in pheochromocytoma
Atropine
Pancuronium
Histamine-releasing agents
Morphine Fentanyl & Sufentanil on to use Succinylcholine Atracurium Mivacurium, cisatracurium
How does droperidol act in pheochromocytoma
Inhibits catecholamine reuptake
Catecholamine-sensitizing anesthetics
Desflurane
Halothane – rarely used now
Careful patient positioning essential -
Metastatic lesions have predilection for bone, particularly vertebral bodies and long bones – pathologic fractures common late in course of illness.
Pathway of steroid synthesisa
Cholesterol -> Pregnenalone –> Progesterone –>Aldosterone (CPREPROGA)
PREG->DEHYDROEPIAN(DHEA) –>Testosterone –>Estradiol
Endemic goiter caused by this deficiency
Iodine
