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57 Cards in this Set

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What are the two parts of the adrenal gland?

- Adrenal cortex- Outer part of the adrenal that secrete and synthesize steroid hormone


* Androgens


* Mineralcorticoids (Aldosterone)


* Glucocorticoids (Cortisol)




- Adrenal medulla- inner part of the adrenal that contains neurons and releases neurotransmitters (catecholamines)


* Epinephrine


* Norepinephrine


* Dopamine (very small amount)

What are the three layers of the adrenal cortex and what do they secrete?

- Zona glomerulosa- Outer most layer


* Secretes mineralcorticoid hormones (Salt)




- Zona fasciculata- Middle layer


* Secretes cortisol and other glucocorticoids (Sugar)




- Zona reticularis- Innermost layer


* Secretes adrenal androgenic hormones (Sex)




"The cortex Gets Fun Rewards- Salt, Sugar, Sex"

What is cortisol? What is the physiologic process that causes the adrenal cortex to produce cortisol?

- The prototypical glucocorticoid, accounts for 95% of the glucocorticoids released from the adrenal cortex.




- The hypothalamus synthesizes and releases corticotropin releasing hormone (CRH)




- CRH causes the anterior pituitary to secrete corticotropin (ACTH)




- ACTH stimulated the adrenal cortex to make cortisol

What stimulates ACTH release? What inhibits ACTH release?

Stimulates:


- CRH


- Sleep-waking perioid


- Stress


- Hypoglycemia


- Sepsis


- Trauma


- Decreased plasma cortisol


- Alpha-adrenergic receptor stimulation




Inhibits:


- Elevated plasma cortisol


- Opioids

How is ACTH regulated?

- Direct negative feedback loop on the hypothalamus, which inhibits release of CRH. This decreases ACTH production




- When cortisol levels are high, ACTH production is reduced

What is the importance of cortisol?

- One of the few hormones essential to life.


* Maintains blood pressure


* Maintains normal vascular permeability, tone, and cardiac contractility


* Participates in carbohydrate and protein metabolism


* Participates in fatty acid mobilization


* Participates in electrolyte and water balance


* Participates in the antiinflammatory response


* Facilitates the conversion of norepinephrine to epinephrine in the adrenal medulla



How do the cells respond to cortisol production?

- There is a hyperglycemic response to cortisol secretion




- This reflects gluconeogenesis and inhibition of peripheral use of glucose by the cells.

How does cortisol affect sodium and potassium?

- Retention of sodium




- Excretion of potassium




*Glucocorticoids have some mineralcorticoid and androgenic effects that become apparent with hormone excess or supraphysiologic replacement dosages

How does cortisol affect gluconeogenesis? How does it affect blood glucose?

- Rate of gluconeogenesis increases 6- to 10- fold in the presence of cortisol




- Inhibits peripheral utilization of glucose so it increases blood glucose and worsens diabetic control

How much cortisol is produced daily? When is it typically released?

- 15- 30 mg per day




- Most of this is produced and released in the morning (diurnal)




- Increased levels in relation to stress


* Physical, mental, surgery

What stimulates the hypothalamic- pituitary- adrenal (HPA) axis?

- Surgery




- Degree of activation depends on duration of surgery and type & depth of anesthesia




- CRH, ACTH, and cortisol levels increase during surgery


* Deep general and regional anesthesia will blunt this response

What regulates aldosterone secretion?

- Renin- Angiotensin- Aldosterone- System (RAAS)




- Serum concentrations of potassium

How does aldosterone contribute to fluid and electrolyte balance in the ECF?

- Resorption of Na+ in the distal renal tubules


* Water follows Na+


* Na+ & H2O resorption expands the ECF volume and elevates arterial BP




- Promotes renal excretion of K+ & Hydrogen ions

What stimulates aldosterone secretion?

- Angiotensin II from RAAS


- ACTH secretion


- Hyperkalemia


- Hypovolemia


- Hypotension


- CHF


- Surgery

What innervates the adrenal medulla?

-Innervated by preganglionic cholinergic fibers of the SNS




- Can be thought of as analogous to a postganglionic neuron




- Preganglionic fibers run directly from the spinal cord to the adrenal medulla

What stimulates the adrenal medulla to secrete catecholamines?

- Hypotension


- Hypothermia


- Hypoglycemia


- Hypercapnia


- Hypoxia


- Pain


- Fear

What receptors are stimulated by norepinephrine release? What are the physiologic effects?

- Alpha and beta receptors




- Increase the heart rate


- Inhibit GI function


- Dilate pupils

What receptors are stimulated by epinephrine release? What are the physiologic effects?

- Beta receptors




- Chronotropic and inotropic effects on the heart


- Less vasoconstriction than norepinephrine

What is Conn's syndrome?

- Another name for primary hyperaldosteronism.




- Characterized by an excess of aldosterone due to a functional tumor that acts independently of physiologic stimulus




Can be associated with:


* Adrenocortical hyperplasia


* Pheochromocytoma


* Primary hyperparathyroidism


* Acromegaly


* Unilateral or bilateral adenoma

What is the result of Conn's syndrome?

- Hypokalemic metabolic alkalosis


- HTN (DBP 100- 125 & may be resistant to trx)


- HA


- Polyuria


- Skeletal muscle weakness


- Nocturia


- Muscle cramps


- Hypomagnesemia


- Hypernatremia


- Glucose intolerance

What is secondary hyperaldosteronism? What are causes of it?

- The stimulus for excess aldosterone resides outside the adrenal gland




- Present when there is increased circulating serum renin levels as a result of reduced renal blood flow



- Causes:


* Renovascular HTN


* Obstructive renal artery disease (atheroma, stenosis)


* CHF


* Hepatic cirrhosis w/ acites


* Nephrotic syndrome



What is Bartter's syndrome?

- Aldosteronism causedby hyperplasia of the juxtaglomerular apparatus




- Not accompanied by hypertension

What is the treatment for hyperaldosteronism?

Medical management:


- Supplemental K+




- Treat hypertension if present



- Spironolactone


- Aldosterone antagonist, K+ sparing diuretic with antihypertensive properties




Surgical management:


- Surgical excision if its an aldosterone-secreting tumor




- Bilateral adrenalectomy may be necessary for multiple aldosterone-secreting tumors

What is the anesthesia management for hyperaldosteronism?

- Preop correction of K+ and HTN


- Avoid hyperventilation = decrease K+


- Only use Sevoflurane if kidney function is ok


- Consider CVP or PAC for monitoring volume status


- EKG may show prominent U-waves & arrhythmias


- Low K+ may potentiate muscle relaxants- low and slow


- Assess for hypovolemia with orthostatic BP


- Consider exogenous cortisol if bilateral adrenalectomy

What is hypoaldosteronism? What causes it?

- Hyperkalemia without renal insufficiency suggests hypoaldosteronism.




- Causes


* Atrophy or destruction of both adrenal glands


* Unilateral adrenalectomy


* Diabetes/ESRD


* ACEI therapy

What are s/s of hypoaldosteronism? What is the treatment?

S/S:


* Hyperglycemia


* Hyperchloremic Metabolic Acidosis


* Orthostatic hypotension


* Heartblock




Treatment:


* Treatpreop w/ an exogenously administered mineralocorticoid (fludrocortisone)


* Increase Na+ intake

What is Cushing's syndrome? What are the two forms of Cushing's Syndrome?

- A diverse complex of symptoms, signs, and biochemical abnormalities caused by excess glucocorticoid hormone




- Two forms:


* ACTH dependent


- Inappropriately high ACTH concentrations stimulate the adrenal cortex to produce excessive amounts of cortisol




* ACTH independent


- Excessive production of cortisol by abnormal adrenocortical tissue that is not regulated by secretion of CRH and ACTH


- CRH and ACTH are depressed

What are causes of independent ACTH?

* Exogenous administration of steroid hormones (most common cause)


* Intrinsic hyperfunction of the adrenal cortex (adrenocortical adenoma)


* ACTH production by a non-pituitary tumor (ectopic ACTH syndrome)


* Hypersecretion by a pituitary adenoma ACTH dependent= Cushing’s disease

What is the difference between Cushing's disease and Cushing's syndrome?

The term 'Cushing's disease' refers to Cushing's syndrome that is cause by the oversecretion of ACTH by a pituitary tumor.

What are S/S of Cushing's syndrome?

- Muscle wasting


- Muscle weakness


- Osteoporosis


- Central obesity


- Abdominal striae


- Glucose intolerance


- HTN


- Mental status changes


- Insomnia


- Oligomenorrhea/ amenorrhea


- Moon face

What is the treatment for Cushing's syndrome?

- Transsphenoidal microadenomectomy




- Anterior pituitary resection (85- 90%)




- Pituitary irradiation and bilateral total adrenalectomy may be necessary in some pts.




- Ectopic ACTH-secreting tumor is treated by surgical resection




- Because the contralateral adrenal gland is preoperatively suppressed, exogenous glucocortocoid replacement may be necessary for several months until adrenal function returns.

What are preoperative considerations for Cushing's?

- Correct the hypokalemia


- Correct the blood sugar


- Correct BP


- Correct hypervolemia w/spironolactone

What are the intraoperative considerations for Cushing's?

- At risk for fractures during positioning 2° osteoporosis




- Regional ok may be difficult with osteoporosis




- Etomidate transiently decreases synthesis and release of cortisol




- Muscle relaxants


* Preoperative weakness may indicate sensitivity


* Use muscle relaxants w/different pathways-Cisatricurium




- Once tumor resected may need to start corticosteroids and may see transient Diabetes Insipidus




- Supplemental steroids


* If cause is exogenous, patient’s adrenal glands will not be able to respond to perioperative stress.




- Risk for thromboembolus r/t obesity, HTN, elevated Hct, and increased Factor VIII levels

What is the anesthetic management for an adrenalectomy?

- IV hydrocortisone 100 mg a 8 hours




- Significant blood loss secondary to highly vascularized tumor




- High risk for pneumothorax secondary to unintentional penetration of the pleura

What is adrenal insufficiency? What are the two types of adrenal insufficiency?

- Destruction of the adrenal glands




- Primary


* The adrenal glands cannot produce enough hormones


* Addison's disease is the idiopathic autoimmune destruction of the adrenal gland ( most common U.S. cause)


* Tb is a worldwide cause of adrenal insufficiency


* HIV is the most common infectious disease cause in the U.S.




- Secondary


* Suppression or disease of the hypothalamic/pituitary axis


* Only a glucocorticoid deficiency


* Causes are iatrogenic


- Pituitary surgery


- Pituitary irradiation


- Use of synthetic glucocorticoids (most common)

What are clinical manifestations of adrenal insufficiency?

- Weakness & fatigue


- Weight loss


- Vomiting


- Abdominal pain


- Diarrhea


- Hypoglycemia


- Orthostatic hypotension


- Hypovolemia


- Hyponatremia


- Hyperkalemia


- Metabolic acidosis




* Secondary adrenal insufficiency resembles primary except not associated with hypovolemia, hyperkalemia, or hyponatremia since mineralcorticoid secretion is preserved



Which disease is associated with hyperpigmentation of the skin?

Addison's disease

Which induction agent should NOT be used in individuals with adrenal insufficiency and why?

- Etomidate


* Suppresses adrenal function by inhibiting enzymes that are essential for the production of corticosteroid hormones.




* Even one-time use showed decreased adrenal function

What is Addisonian crisis? What causes it? What are s/s?

- Sudden onset of severe adrenal insufficiency




- Medical emergency with high M & M




- Cause:


* Steroid- dependent pt. who did not receive adequate steroid dose for period of stress, infection, acute illness, sepsis




- S/S:


* Circulatory collapse


* Fever


* Hypoglycemia


* Depressed mentation

How long after discontinuation of long-term steroid use will it take for adrenal function to return to normal?

6 - 12 months for adrenal function to return to baseline

How long after abrupt withdrawal of steroids would symptoms begin to appear in a patient on a long-term exogenous steroid regimen?

24 - 36 hours

What is the required dose of steroid therapy a pt. needs to have received in the past in order to require perioperative steroid supplementation?

- All patients who have received the equivalent of 20 mg/day of prednisone by any route of administration for a period of more than 3 weeks any time in the previous 12 months should be considered unable to respond to surgical stress.




- Doses between 5 and 20mg should be supplemented as well




- >8 mg/day on long term basis should be supplemented

What are the recommended replacement regimens for steroid therapy?

- Bolus option: Administer 100 mg hydrocortisone q 6° IV beginning the evening before or on the morning of surgery for moderate to major surgery




- Continuous infusion option: 100mg IV hydrocortisone at time of induction followed by an infusion of 10 mg/hr during the subsequent 24°.

What are anesthetic considerations for someone with adrenal insufficiency?

- If a pt. is unresponsive to usual therapeutic interventions, they may have adrenal insufficiency




- Treat the cause




- Replace circulating glucocorticoids




- Replace H2O and sodium deficits


* D5NS is best fluid choice




- Hemodynamic support with vasopressors




- Metabolic acidosis and hyperkalemia resolve with fluid and steroid administration




- Use caution with drugs that cause myocardial depression




- Use caution with muscle relaxants

What is pheochromocytoma? What causes it?

- Catecholamine secreting tumor that arises from chromaffin cells of the sympathoadrenal system




- Precise cause is unknown, usually an isolated finding (90% of the cases)




- 10% are inherited as an autosomal dominant trait




- May be a part of multiple endocrine neoplasia (MEN) syndrome or von Hippel- Lindau syndrome

What does a pheochromocytoma commonly secrete? Do pheochromocytomas secrete catecholamines in response to another hormone or physiologic response?

- Mostly they secrete norepinephrine, either alone or with a small amount of epinephrine (85:15)




- 15% secrete epinephine alone




- Small amount secrete dopamine




- Most pheochromocytomas are not under neurogenic control and secrete catecholamines autonomously

What are the s/s of pheochromocytoma?

- Significant hypertension (150- 180s/120s)




- Variable presentation and often dependent on the catecholamine that is being secreted




- May see:


* HA


* Sweating


* Pallor


* Palpitations


* Orthostatic hypotension from hypovolemia




- Norepiphenrine-secreting:


* Systolic and diastolic HTN


* Reflex bradycardia




- Epinephrine-secreting:


* Systolic HTN


* Diastolic hypotension


* tachycardia





How is the cardiovascular system affected by pheochromocytoma?

- Increased SVR


- Normal CO


- Slightly decreased plasma volume




* Desensitized CV system and a downregulation of adrenergic receptors explains the normal findings

What type of cardiomyopathies are seen in pheochromocytoma? What does the EKG look like?

- Both dilated and hypertrophic cardiomyopathies


* Can be reversed if treated early before fibrosis occurs




- LV outflow obstruction




- EKG:


* High or peaked P-waves


* Elevation or depression of ST-segment,


* Flat or inverted Ts


* Prolonged QT


* LAD


* Arrhythmias

Why do individuals with pheochromocytoma have elevated blood glucose?

- Secondary to catecholamine stimulation of glycogenolysis and inhibition of insulin release

How is pheochromocytoma diagnosed?

- 24 hour urine collection for measurement of metanephrine and catecholamines


* > 220 pg/dL




- Plasma-free metanephrine level (most sensitive test)


* > 400 pg/dL




- Clondine suppression test


* Administer clonidine. If it has no effect, positive result




- Glucagon stimulation test (safest provocative test)


* Glucagon acts directly on tumor to stimulate catecholamines.


* > 2000 pg/mL is positive result




- CT or MRI

What is the preoperative management for pheochromocytoma?

- Alpha blockade first


* Phenoxybenzamine- Noncompetitive a1- antagonist with some a2-blocking properties


* Long DOA so d/c 24- 48 hours before surgery




- Goal is normotension




- Eliminate ST-segment and T-wave changes on ECG




- Administer betablocker after alphablocker if tachycardia presents




- CCB and ACEI good for HTN

What is the most common cause of death in the immediate postoperative period after excision of a pheochromocytoma?

Hypotension

What is the preferred vasodilator for hypertensive episodes during surgical excision of a pheochromocytoma?

- Nitroprusside




- Nitroglycerin will reduce the BP, but the amount required to control it often results in tachycardia.

Why is orthostatic hypotension common in patients with pheochromocytoma?

Chronic HTN = hypovolemia and impairment of the vasoconstrictor reflexes.

What alpha blockers may be used in place of phenozybenzamine in the treatment of pheochromocytoma?

Prazosin, doxazosin, and terazosin.

At what point during surgical excision of a pheochromocytoma should you expect hypotension and how should you treat it?

- Following ligation of the vein draining the tumor.




- To prevent hypotension, the patient should undergo volume expansion until a PCWP of 16-18 mmHg is reached prior to ligation of the vein.




- Vasopressors should be utilized only after adequate volume expansion has been achieved.