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*Endocrine > Endocrine Prodigy > Flashcards

Endocrine Prodigy Flashcards

1
Q

What is acromegaly and what is the most common cause?

A

Acromegaly is the excessive release of growth hormone.

It is most commonly due to an adenoma in the anterior pituitary gland.

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2
Q

What are the most common clinical features of acromegaly? (3)

A
  1. Enlargement of the jaw, hands, and feet
    >increased GH levels stimulate release of insulin-like growth factor I.
    >These hormones increase proliferation of cartilage, bone, protein synthesis, and lipolysis.
  2. DM
    >d/t decreased insulin sensitivity
  3. HTN
    >promotion of sodium retention
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3
Q

what are the cardiac manifestations of acromegaly? (4)

A

chronic HTN leads to
>ventricular dysfunction
>enlarged heart
>ischemic heart disease
>dysrhythmias

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4
Q

How does acromegaly affect the peripheral nervous system?

A

Overgrowth of soft tissue traps peripheral nerves
>carparal tunnel syndrome is common
>from decreased ulnar artery flow due to compression by soft tissue

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5
Q

How does acromegaly affect the integumentary system?
(2)

A

thick, oily skin & hyperhidrosis

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6
Q

How does acromegaly affect the respiratory system? (2)

A

increased lung volumes & VQ mismatching

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7
Q

How is the musculoskeletal system affected by acromegaly?

What’s the effect on NMB on these patients?

A

Osteoarthritis & Osteoporosis

*skeletal muscle weakness and increased sensitivity to muscle relaxants

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8
Q

Symptoms of Addison’s disease (9)

A

weakness
hypotension
hypovolemia
hyponatremia
hyperkalemia
anorexia/n/v
hyperpigmentation

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9
Q

What are the 2 types of adrenal insufficiency?

A

Primary and Secondary

Primary- adrenal glands cannot produce enough hormones (Addison’s)

Secondary- due to suppression or disease of the HPA

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10
Q

How do the effects of primary adrenal insufficiency differ from secondary insufficiency?

A

Primary adrenal insufficency results in the inadequate release of glucocorticoid, mineralocorticoid, and androgen hormones.

Secondary adrenal insufficiency results in the inadequate release of glucocorticoid only.

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11
Q

What is the most potent mineralocorticoid produced by the adrenal gland?

A

Aldosterone

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12
Q

Which is the most potent endogenous glucocorticoid and produced by the adrenal cortex?

A

Cortisol

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13
Q

What are the most common causes of secondary adrenal insufficiency? (3)

A

administration of synthetic glucocorticoids

-pituitary surgery
-radiation

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14
Q

What patients are at risk for adrenal insufficiency?

A

Pt’s on chronic steroid therapy during periods of stress such as surgery.

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15
Q

*Which induction agent would be least appropriate for a patient in acute Addisonian crisis?

A

*Etomidate - can supress the HPA axis and even a single dose should be avoided in patients prone to adrenal insufficiency

*Nagelhout

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16
Q

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

A

6-12 months.

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17
Q

What is carcinoid syndrome and what are its 2 most common symptoms?

A

a massive release of serotonin, histamine, and kinins/killikreans

*Flushing and diarrhea

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18
Q

What diagnostic test is usually indicative of carcinoid syndrome?

A

5-hydroindoleacetic acid in the urine

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19
Q

*Not all patients with a carcinoid tumor experience side effects from the release from the tumor. Why not?

A
  • Usually, hepatic-first pass metabolism elimates the hormones from the circulatory system before they can exert any deleterious effects

*Nagelhout

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20
Q

Carcinoid syndrome often causes right-sided cardiac lesions and typically spares the left-side (unless a shunt is present) - why?

A
  • elevated serotonin levels can result in right-sided heart failure.

-the lungs metabolize serotonin and therefore spare the left side of the heart.

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21
Q

What are the cardiac manifestations of carcinoid syndrome?

A

Pulmonic Stenosis and TR

> from fibrosis of the endocardium (on the right side of the heart- remember serotonin gets metabolized in the lungs and wont affect left unless shunt)

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22
Q

How can carcinoid syndrome mimic an allergic reaction?

A

Histamine and kallikrein release
>hypotension
>tachycardia
>bronchospasm

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23
Q

What medications relieve the diarrhea associated with carcinoid syndrome?

A

5-HT3 antagonists

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24
Q

*What anesthetic drugs should be avoided in patients with carcinoid syndrome?

A

Sympathomimetics
>Ephedrine, Epi, NE, dopa, isoproterenol

Histamine releasing drugs
>MMAST

*Nagelhout

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25
Q

*Why shouldn’t hypotension be tolerated in someone with carcinoid tumors?

A

It can trigger the release of hormones from the tumor.

*Nagelhout

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26
Q

*Which agent is an analog of somatostatin that is administered to blunt the bronchoconstriction and vasoactive effects of carcinoid tumor products?

A

Octreotide

*Nagelhout

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27
Q

Is Cushing’s Disease the same as Cushing’s Syndrome?

A

“Cushing’s disease” refers to “Cushing’s syndrome” that is caused by oversecretion of ACTH by the anterior pituitary.

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28
Q

What are the 2 types of Cushing’s Syndrome?

A

ACTH-dependent and ACTH-independent Cushing’s syndrome

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29
Q

What are the three zones of the adrenal gland and what hormones does each produce?

A

innermost= zona glomerulosa (produces mineralocorticoids such as aldosterone)

the zona fasciculata (produces glucocorticoids such as cortisol)

the zona reticularis (which produces sex steroids such as androgens).

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30
Q

What is the pathophysilogy behind ACTH-depedent Cushing’s syndrome?

A

-extremely high plasma ACTH levels which stimulate the adrenal gland to produce excessive amounts of cortisol

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31
Q

What is the pathophysilogy behind ACTH-independent Cushing’s syndrome?

A

Excessive production of cortisol is due to an abnormal adrenal gland and suppresses secretion of corticotropin releasing hormone and ACTH

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32
Q

What are the anesthetic considerations for a patient undergoing bilateral adrenalectomy for Cushing’s disease?

A

increased cortisol levels = hypokalemia, hyperglycemia, and skeletal muscle relaxation.

> this may require a decreased NON-depolarizing dose of MR.

-low dose etomidate infusion may be helpful.

-steroid replacement before or during surgery

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33
Q

What is the difference between type I and type II diabetes?

A

Type I diabetes is caused by a T cell-mediated destruction of beta cells in the pancreas.

Type II diabetes is not immune-related and results from a deficiency of insulin and/or a defect in insulin receptors.

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34
Q

Why should you be cautious in administering a high neuraxial block to a patient with chronic hepatic disease?

A

High (T5) neuraxial blocks are associated with a decrease in hepatic blood flow that may not be reversed with the administration of catecholamines.

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35
Q

What percent of patients with diabetes mellitus are type I?

A

5-10%

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36
Q

What is the function of insulin?

A

Insulin facilitates the transport of glucose and potassium into the cell, and is important for the cellular uptake of glucose with the exception of the brain and liver where it does not affect glucose transport.

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37
Q

How is insulin metabolized?

A

Insulin is metabolized by both the liver and kidneys

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38
Q

What is the normal insulin production in a day?

A

40 to 50 units per day

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39
Q

*How do sulfonylureas help control glucose?

A

increase insulin secretion by beta cells*

*Nagelhout

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40
Q

Which oral diabetic agents work by decreasing postprandial glucose absorption?

A

Alpha-glucosidase inhibitors

Arcabose & miglitol

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41
Q

*What are the sympathetic symptoms of hypoglycemia?

A

*HTN, tachycardia, diaphoresis, lacrimation

*Nagelhout

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42
Q

Elective surgery should be postponed if there is an acute rise in glucose to what value?

A

400mg/dL

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43
Q

What percent of type I and type II diabetics develop end-stage renal disease?

A

30-40% of type I diabetics and about 5-10% of type II diabetics develop end-stage renal disease.

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44
Q

What is the hallmark sign of severe glomerulosclerosis in the diabetic patient?

A

Proteinuria

(pt’s can be asympatomatic for as long as 15 years)

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45
Q

What percentage of diabetics will develop peripheral neuropathy?

A

~50% of diabetics over the course of 25 years

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46
Q

How does diabetic retinopathy occur and how can it be prevented?

A

result of microvascular pathologies. Strict maintenance of glucose within normal ranges helps prevent these alterations.

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47
Q

*How does blood glucose affect global ischemia?

A

*Studies have correlated elevated glucose levels with poor short-term and long-term outcomes in patients with brain damage from global ischemia.

*Nagelhout

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48
Q

*What are the symptoms of autonomic neuropathy due to diabetes and why is this important? (4)

A

*lack of orthostatic change in heart rate
-early satiety
-lack of sweating
-impotence

*these pts are at increased risk for gastroparesis and silent MI

*Nagelhout

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49
Q

What laboratory values are consistent with diabetic ketoacidosis? (5)

A

serum glucose > 300mg/dL
pH < 7.3
Bicarb < 18
Serum os < 320mOsm/L
elevated serum and urine ketones

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50
Q

What is different about the serum os in DKA vs hyperosmolar syndrome?

A

DKA- <320mOsm/L
HH- >340mOsm/L

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51
Q

What are 2 significant risks in HHS?

A

intravascular coagulation and mesenteric thrombosis

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52
Q

What athe the diagnostic features of HHS? (4)

A

Glucose > 600
pH > 7.3
Bicarb > 15
Serum Os > 350

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53
Q

Over what period of time does hyperglycemic hyperosmolar syndrome occur?

A

over days to weeks

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54
Q

What electrolye abnormalities usually occur with diabetic ketoacidosis? (4)

A

Hyperglycemia results in:
-hyponatremia
-hypophosphatemia
-hypokalemia (?)
-hypomagnesemia

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55
Q

Cushing disease is distinct from Cushing syndrome in that it Cushing disease is a direct result from what?

A

An anterior pitutiary tumor

Cushing syndrome refers to any condition involving corticosteroid excess.

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56
Q

incidence of PE in patient’s with Cushing’s Disease

A

3%

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57
Q

The hallmark signs of DI are:

Urine SG:
Urine Os:

A

Urine SG < 1.005
Urine Os < 200mOsm/kg

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58
Q

Which oral diabetic agent can increase ADH levels in someone with DI?

A

chlorpropamide (sulfonyurea)

-hypoglycemic effects limits it’s usefulness clinically

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59
Q

Type II diabetes accounts of ___% of all cases of diabetes

A

90%

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60
Q

What is a normal A1C?

A

Between 4-6%

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61
Q

Treatment of hypoglycemia

A

10-25g of IV D50 to prevent irreversible brain damage

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62
Q

What 3 things characterize HHS?

A

-severe hyperosmolarity
-hyperglycemia
-dehydration

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63
Q

On average, pt’s with HHS have a water deficit of what?

A

9 Liters!

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64
Q

HHS carries of mortality rate of ____%

A

15%

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65
Q

What is Grave’s disease?

A

An autoimmune disorder where thyroid-stimulating antibodies produce hyperplasia of the thyroid gland.

*most common cause of hyperthyroidism, accounting for 60-80% of all cases

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66
Q

What are the symptoms of hyperthyroidism mosty related to?

A

The hypermetabolic state

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67
Q

Where are the parathyroid glands located?

A

Behind the thyroid gland
>2 superior, and 2 inferior

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68
Q

What are the two types of cells found in the parathyroid glands?

A

Chief cells (secrete PTH)
& Oxyphil cells (?)

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69
Q

What is the primicpal function of the parathyroid glands?

A

PTH release to regulate calcium balance.

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70
Q

How does parathyroid hormone decrease serum phosphate?

A

By increasing the renal excretion of phosphate.

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71
Q

How does parathyroid hormone act on the kidneys?

A

Parathyroid hormone can cause a rapid loss of phosphate ions in the urine by its effect on the proximal tubule. As more phosphate is excreted, calcium is retained.

The increased calcium reabsorption takes place primarily in the collecting tubules and the late distal tubules.

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72
Q

What are the cardiac signs and symptoms of hyperparathyroidism? (3)

A
  1. HTN
  2. Prolonged PR
  3. Shortened QT
73
Q

What are the renal signs and symptoms of hyperparathyroidism? (6)

A

Polyuria
Polydyspia
Decreased GFR
hypophos
hyperchloremic acidosis
renal stone

74
Q

What is the cause of primary hyperparathyroidism 90% of the time

A

Benign tumor

75
Q

*What is secondary hyperparathyroidism?

A

*a normal, compensatory increase in parathyroid hormone secretion in response to a disease process or condition that produces hypocalcemia, such as the increased parathyroid hormone secretion associated with chronic renal disease.

Because it is a compensatory mechanism, it rarely produces hypercalcemia.

(Nagelhout)

76
Q

*How should you adjust your anesthetic for the patient with primary hyperparathyroidism?

A

*should be aimed at dealing with underlying hypercalcemia. Because of this, hydration with normal saline and monitoring of urinary output is essential.

Because hypercalcemia is associated with somnolence, the anesthetic requirement may be decreased.

If personality changes due to chronic hypercalcemia are present, then ketamine may need to be avoided.

Baseline skeletal weakness may necessitate a decreased dose of nondepolarizing muscle relaxants, however the increased calcium can antagonize muscle relaxants–in short, hyperparathyroidism is associated with an increased sensitivity to succinylcholine and a resistance to nondepolarizing muscle relaxants.

Acidosis increases the serum calcium level, so hypoventilation should be avoided.

As with thyroidectomy, there is a risk of damage to the recurrent laryngeal nerve during surgery, so a Nim(Registered) tube or similar device should be used to monitor nerve function during surgery.

It is important to position patients with a risk of pathologic fractures carefully. Normal saline is preferred over Lactated Ringer’s solution for fluid management.

The patient may be more sensitive to the effects of digoxin.

*Nagelhout

77
Q

S/S Hypoparathyroidism (4)

A
  • same as hypocalcemia
  1. Prolonged QT
  2. Muscle spasm
  3. Hypotension
  4. Decreased responsiveness to beta agonists
78
Q

Treatment options for hypoparathyroidism (3)

A

-aimed at restoring low calcium levels to normal

  1. 10mL of Calcium gluconate 10% IV until NM irritability resolves
  2. Resp or metabolic alkalosis should be normalized
  3. Thiazide diuretics
    >they deplete sodium without the loss of potassium which tends to increase calcium levels
79
Q

What is the primary function of aldosterone?

A

Promotes sodium reabsorption and secretion of potassium in the renal tubule.

80
Q

What is Conn’s syndrome another name for?

A

Primary hyperaldosteronism due to excess aldosterone secretion due to a functional tumor.

81
Q

What are your concerns cardiac-wise for a patient with hyperaldosteronism?

A

they have a high incidence of ischemic heart disease and preop eval should be aimed at that with close monitoring during procedure.

82
Q

Should patients undergoing surgery for excision of an aldosteronoma receive supplementary exogenous corticosteroids?

A

A patient undergoing surgery for an isolated adenoma of the adrenal gland that is secreting aldosterone probably will not need exogenous corticosteroids. A patient presenting for excision of bilateral aldosteronomas, however, will likely need supplementation with corticosteroids.

83
Q

What are the signs and symptoms of hyperaldosteronism?

A
  1. HTN and headache
    >from sodium retention
  2. Polyuria, skeletal muscle weakness, nocturia, and muscle cramps, hypokalemic metabolic acidosis
    >from potassium loss
  3. hypomagnesemia and abnormal glucose tolerance test may be present
84
Q

What is the most common cause of primary hyperaldosteronism?

A

unilateral adenoma in the adrenal gland. About 25% of these patients, though, may exhibit bilateral adenoma.

85
Q

How can hyperaldosteronism affect the use of nondepolarizing muscle relaxants?

A

The resultant hypokalemia can result in skeletal muscle weakness and potentiation of NONdepolarizing muscle relaxants .

86
Q

How is hyperaldosteronism treated? (2)

A

K+ supplement and an aldosterone antagonist such as spironolactone.

87
Q

What lab findings are associated with HYPOaldosteronism (2)

A
  1. Hyperkalemia in pts with normal renal function
  2. Hyponatremia
88
Q

2 cardiac symptoms of HYPOaldosteronism?

A
  1. Heart block
  2. Orthostatic hypotension
89
Q

5 Potential causes of HYPOaldosteronism

A
  1. Adrenalectomy
  2. Prolonged heparin administration
  3. Diabetes
  4. Renal failure
  5. Congential condition
90
Q

How is acid-base balance affected by HYPOaldosteronism?

A

it produces a hyperkalemic metabolic acidosis

91
Q

How are plasma renin levels affected by hypoaldosteronism?

A

-decreased renin levels

92
Q

How is hypoaldosteronism treated? (2)

A

Fludrocortisone and a high sodium diet

93
Q

What’s the most common cause of hypoparathyroidism?

A

Surgical removal of the parathyroid glands

94
Q

What acid-base state should be avoided in pts with HYPOparathyroidism

A

Respiratory alkalosis

(an increased pH further decreases ionized calcium levels)

95
Q

What electrolyte abnormality is associated with hypothyroidism?

A

Hyponatremia and impaired free water excretion

96
Q

Why are patients with hypothyroidism more prone to respiratory depression from anesthetics and narcotics?

A

Due to their decreased ventilatory response to hypoxia and hypercarbia

(everything slowsssss down)

97
Q

What are the integumentary changes seen with hypothyroidism? (3)

A

Thick skin, periorbital and peripheral edema

98
Q

What are the ECG changes often seen with hypothyroidism? (3)

A
  1. Flattened or inverted T-waves
  2. Low voltage P’s and QRS’s
  3. sinus bradycardia

(also more prone to ventricular dysrhythmias)

99
Q

What is another name for hypothyroidism?

A

Myxedema

100
Q

Normal TSH level

A

0.5-5.0mU/L

101
Q

What is the typical TSH level in a patient with hypothyroidism?

A

5-15 mU/L

-normal= 0.5-5

102
Q

How does hypothyroidism affect mental status?

A

Mental sluggishness: slow speech, apathy, and listlessness

103
Q

How does hypothyroidism affect cardiac status?

A

-decreased CO due to reductions in both HR and SV.

-pericardial effusions are common

104
Q

How is peripheral vascular resistance affected by hypothyroidism?

A

PVR is INCREASED and blood volume is reduced

105
Q

What is the best approach for treating hypotension following induction of a patient with hypothyroidism?

A

-Epi, ephedrine, or dopamine

(No neo due to decreased contracility)

106
Q

How is secondary hypothyroidism diagnosed?

A

decreased T3, T4, R-T3U
increased TSH

107
Q

Is the cardiomyopathy seen with hypothyroidism reversible?

A

Yes - pts who take levothyroxine will exhibit improvement in myocardial function within 2-4 months.

108
Q

How do patients with hypothyroidism respond to anesthetic drugs?

A

they are highly sensitive to the effects of narcotics, sedatives and inhalational agents

109
Q

Airway concerns in a patient with hypothyroidism?

A
  • more prone to airway compromise:
  1. edema of airway and vocal cords
  2. possible goiter
  3. prolonged gastric transit time (aspiration risk)
110
Q

How does hypothyroidism affect temp maintenance under anesthesia?

A

More prone to hypothermia which occurs quickly and is difficult to correct once it does occur.

111
Q

What is myxedema coma? (7 sxs)

A

an uncommon and severe form of hypothyroid which the patient exhibits
1. change in MS
2. unconsciousness
3. Hypothermia
4. hypoventilation
5. Bradycardia
6. hypotension
7. dilutional hyponatremia

112
Q

In what population of patients does myxedema most commonly occur?

A

elderly females with a longstanding history of hypothyroidism

113
Q

What is the cardinal feature of myxedema coma?

A

NOT unconsciousness (relatively uncommon suprinsingly)

–>Hypothermia which may be as low as 80 degrees F

114
Q

What is the only indication for IV levothyroxine?

A

Myxedema coma.

300-500mcg load
+50-200mcg/day

115
Q

What is a goiter?

A

hypertrophy of the follicular epithelium of the thyroid gland that occurs in response to a reduction in thyroid gland function.

116
Q

What is primary hypothyroidism?

A

A decrease in the amount of thyroid hormone produced despite adequate levels of TSH

117
Q

What are the 3 most common causes of HYPERthyroidism?

A
  1. Graves disease
  2. Toxic multinodular goiter
  3. Toxic adenoma
118
Q

What population is most affected by HYPERthyroidism?

A

females between 20-40

119
Q

a patient exhibits thyroid storm postop, what interventions should you take? (4)

A
  1. tx dehydration with D5NS
  2. cooling measures
  3. betablockers titrated to HR < 90
  4. Steroids and antithyroid medications
120
Q

At what point during the perioperative period is a patient with hyperthyroidism most likely to experience thyrotoxicosis?

A

it can occur any time during the anesthetic but is most likely to occur in the post-op period.

121
Q

What is thyroid storm?

A

A life-threatening exacerbation of hyperthyroidism

122
Q

What is the most important goal in the anesthetic management of the thyrotoxic patient?

A

-To render the patient euthyroid prior to surgery

123
Q

Is the onset of hypothyroidism in adults usually acute or insidious?

A

slow, insidious progression

124
Q

What drug regiment is typically used in thyrotoxic patients prior to surgery to gain control of their symptoms? (2)

A

Propanolol &
Potassium iodine

125
Q

What are the general s/s of hyperthyroidism?(8)

A
  1. anxiety
  2. emotional lability
  3. heat intolerance
  4. insomnia
  5. fatigue
  6. tremors
  7. exopthalmos
  8. weight loss
126
Q

What is the origin of graves disease?

A

-autoimmune syndrome where thyroid stimulating ANTIBODIES attach to TSH receptors and stimulate the hyperplasia of thyroid tissue

127
Q

How is hyperthyroidism diagnosed? (3)

A

elevated T3, T4, R-T3U;
increased radioactive iodine uptake
3. low TSH

128
Q

How does hyperthyroidism affect the hematocrit and platelet count?

A

anemia and thrombocytopenia

129
Q

First-line treatment for hyperthyroidism?

A
  1. Propylthiouracil or methimazole (block the synthesis of thyroid hormone)
130
Q

What is an insulinoma?

A

An insulin secreting adenoma of the pancreatic beta cells

131
Q

What are the presenting symptoms of insulinoma known as and what are they ? (3)

A

Whipple’s triad

-Hypoglycemia with fasting,
-gluclose level < 50
-relief of symptoms with glucose administration

132
Q

What does preoperative medical mangement usually require for patients with insulinoma?

A

Diazoxide

(inhibits the release of insulin from beta cells)

133
Q

During the perioperative period, at which point is a patient with insulinoma most likely to exhibit hypoglycemia?

A

intraoperatively.

134
Q

*What are the principal manifestations of an insulinoma?

A

sever hypoglycemia resulting in depression, seizures, and coma

*Nagalhout

135
Q

*What is the primary treatment for an insulinoma?

What about in advanced cases?

A

-surgical excision of the metastatic tumor.

in advanced cases, the entire distal pancreas may have to be excised, referred to as Child procedure

*Nagalhout

136
Q

Do pheocrhomocytomas primarily secrete epi or norepi?

A

Norepi

137
Q

What is the most sensitive test for pheo?

A

a measurement of plasma free metanephrines.

138
Q

Two important things preop for pheo patients

A
  1. alpha blockers
  2. correct hypovolemia
139
Q

What factors should be avoided in pheo patients?

A

any factors that stimulate release of catecholamines: anxiety, shivering, hypoxia, hypercarbia.

140
Q

For patients who’s pheo primarily secretes epinephrine, what are the preferred “downer” agents?

A

labetalol and esmolol

141
Q

In pheo patients, is the patient at greatest risk for significant hypotension?

A

when the tumor vein is ligated

142
Q

What is the most common cause of death following resection of a pheo?

A

hypotension

143
Q

What is pheochromocytoma?

A

a catecholamine secreting tumor that occurs from neural crest cells.

144
Q

Where are pheo’s located?

A

At any location that’s derived from the neural crest ranging from the neck to the inguinal ligament

145
Q

What are 2 s/s indicative of pheo?

A
  1. Extremely labile HTN
  2. HTN/sweating/HA combo
146
Q

Where are most pheo’s located?

A

in the medulla of one of the adrenal glands (85%)

-other places: spleen, ovary, right atrium, bifurcation of the aorta

147
Q

Incidence of pheo’s according to age and gender

A

equally between men and females

ages: 30-50

148
Q

what complex disorders are pheo’s associated with (5)

A
  1. multiple endocrine neoplasia (consists of thyroid cancer and parathyroid hyperplasia)
  2. neurofibromatosis
  3. tuberous sclerosis
  4. Sturge-Weber syndrome
  5. von Hippel-Lindau disease
149
Q

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

A

Nitroprusside

(nitroglycerin will decrease BP but the amount required to control the BP often results in reflex tachycardia)

150
Q

How does phenoxybenzamine affect alpha-1 and alpha-2 receptors?

A

it produces NONcompetitive alpha-1 blockade with mild blockade of alpha-2 receptors

151
Q

What side effect can occur from the alpha-2 receptor blockade produced by phenoxybenzamine. What is the recommended treatment for this side effect?

A

Tachyarrhythmias
>betablockers

152
Q

In what proprotions do pheochromocytomas release NE and epi?

A

85% epi
15% Ne

153
Q

What is the ost sensitive test for pheo?

A

Plasma free metanephrine levels > 220pg/mL

or

free normetanephrine levels > 400pg/mL

154
Q

What condition is expressed by elevated vasopressin levels?

A

SIADH

155
Q

What are the hallmark clinical manifestations of SIADH? (3)

A
  1. decreased UOP with high osmolality
  2. decreased serum osmolality
  3. hyponatremia
156
Q

What is the typical indication for thymectomy?

A

tx of myasthenia gravis patients

157
Q

*Where do T-lymphocytes mature vs B- lymphocytes?

A

*T- thymus
B- bone marrow

*Nagalhout

158
Q

What type of anesthetic is used for thymectomy?

A

GA

159
Q

Anesthetic concerns for a patient undergoing thymectomy pertain to what underlying disease?

(depolarizers vs nondepolarizers)

A
  • myasthenia gravis

*HIGH RESISTANCE TO SUX
*HIGH SENSITIVITY TO NDMR
*AVOID NMB ENTIRELY WHENEVER POSSIBLE

160
Q

What type of incision is typically made for thymectomy?

A

A complete sternotomy if thymoma is present.

otherwise, a transcervical incision or video-assisted thoracoscopy.

161
Q

A patient with carcinoid syndrome demonstrates left-sided cardiac complications as a result. You would suspect that this patient also has
A. Cushing’s syndrome
B. increased venous return
C. tricuspid stenosis
D. a right-to-left shunt

A

D. a right-to-left shunt

162
Q

Which agent is an analog of somatostatin that is administered to blunt the bronchoconstrictive and vasoactive effects of carcinoid tumor products?
A. Octreotide
B. Neuropeptide
C. Pancreatic polypeptide
D. Prostaglandins

A

A. Octreotide

163
Q

You are performing a general anesthetic on a patient undergoing a parathyroidectomy. Which of the following signs and symptoms would be most closely associated with hyperparathyroidism?
A. Hypotension
B. Hyperreflexia
C. Metabolic alkalosis
D. Shortened QT interval

A

D

164
Q

What is the cause of Graves’ disease?
A. Toxic adenoma
B. Thyroid-stimulating antibodies
C. Decreased T3 levels
D. Decreased T4 levels

A

B

165
Q

A patient with a diagnosis of incomplete diabetes insipidus is treated with chlorpropamide 500 mg per day. Which laboratory test would be the most appropriate to assess prior to surgery?
A. Glucose
B. Serum potassium
C. Arterial blood gas
D. Chest x-ray

A

A. Glucose

166
Q

What is the most potent mineralocorticoid produced by the adrenal gland?
A. Aldosterone
B. Cortisol
C. ACTH
D. PTH

A

A. Aldosterone

167
Q

Which of the following is caused by an anterior pituitary tumor?
A. Hepatocellular syndrome
B. Cushing’s disease
C. Cushing’s syndrome
D. Conn’s syndrome

A

B. Cushing’s disease

168
Q

Administration of synthetic glucocorticoids is one of the most common causes of
A. hypoglycemia
B. secondary adrenal insufficiency
C. iatrogenic thyroiditis
D. primary adrenal insufficiency

A

B. secondary adrenal insufficiency

169
Q

What drug would be preferred for the treatment of hypertension under anesthesia for a patient with a pheochromocytoma if the tumor secretes primarily epinephrine rather than norepinephrine?
A. Clonidine
B. Verapamil
C. Nitroglycerin
D. Esmolol

A

Esmolol - short acting

Not sure why this matters in regards to primarily epi vs norepi secreting but ok

170
Q

What alteration in anesthetic response would you expect to see in a patient who suffers from Conn’s syndrome (hyperaldosteronism)?
A. Decreased MAC
B. Decreased nondepolarizing muscle relaxant dose requirements
C. Increased nondepolarizing muscle relaxant dose requirements
D. Increased MAC

A

B. Decreased nondepolarizing muscle relaxant dose requirements

171
Q

What medical treatment may be used as a temporizing measure prior to surgical excision of an insulinoma?
A. potassium
B. diazoxide
C. spironolactone
D. regular insulin

A

B. diazoxide

172
Q

The most common symptom of carcinoid syndrome is
A. flushing
B. tachycardia
C. jaundice
D. hypotension

A

A. flushing

173
Q

During induction for a parathyroidectomy for relief of hyperparathyroidism, which ECG alteration would you most expect to see?
A. Shortened QT Interval
B. Prominent U wave
C. Shortened PR Interval
D. Prolonged QT Interval

A

A. Shortened QT Interval

174
Q

What electrolyte abnormality is associated with hypothyroidism?
A. Hyperkalemia
B. Hypermagnesemia
C. Hypophosphatemia
D. Hyponatremia

A

D. Hyponatremia

175
Q

Which of the following symptoms is consistent with Addison’s disease?
A. hyperkalemia
B. hypocalcemia
C. hypernatremia
D. polycythemia

A

A. hyperkalemia

176
Q

Which of the following respiratory changes occurs with hypothyroidism?
A. The ventilatory response to hypercarbia is increased
B. Minute ventilation increases slightly
C. Diffusion capacity is increased
D. The ventilatory response to hypoxia is decreased

A

D. The ventilatory response to hypoxia is decreased

177
Q

You are preparing to induce a patient undergoing general anesthesia for resection of a carcinoid tumor. If possible, all of the following drugs should be avoided in this patient except:
A. Atracurium
B. Vecuronium
C. Morphine
D. Pancuronium

A

B. Vecuronium

178
Q

Metabolic alkalosis can be the result of
A. renal failure
B. aspirin intoxication
C. hyperaldosteronism
D. cyanide poisoning

A

Not D…

Renal failure?

C i think- increased aldosterone = increased sodium, decreased potassium and hydrogen ions

*Endocrine (2 decks)

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