Exam 4: Endocrine part II

Question 1

Hypothroidism affects ____ to ____% of adults and is also known as

Answer 1

0.5%-0.8%
myxedema

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Question 2

95% of cases of hypothyroidism are ____ hypothyroidism.
What labs are expected

Answer 2

Primary
Low T3 and T4 despite adequate TSH

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Question 3

What is the most common cause of hypothyroidism?
2nd most common cause?

Answer 3

1) ablation of the gland by radioactive iodine or surgery
2) idiopathic and probably autoimmune with antibodies blocking TSH receptors

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Question 4

____ ____ is an autoimmune disorder characterized by ____ enlargement and hypothyroidism that usually affects ____

Answer 4

hashimoti thyroiditis
goitrous
middle-aged women

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Question 5

What does the progression of hypothyroidism look like in adults?
S/Sx?
What are other common co-existing problems?

Answer 5

slow, progressive course in adults
Sx: cold intolerance, weight gain, nonpitting edema
Other: SIADH is common along with fluid overload, pleural effusions and dyspnea. GI function is slow and adynamic ileus may occur

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Question 6

Hypothyroidism S/S chart
HEENT
Neuro
GI
Psych
Skin
Cardiac

Answer 6

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Question 7

____ women > ____y/o have subclinical hypothyroid, which is associated with increased risk of what?

Answer 7

20%, 60y/o
CAD if TSH is >10millunits/L

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Question 8

What is controversial in subclinical hypothyroid disease?

Answer 8

Throid replacement

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Question 9

How is secondary hypothyroidism characterized?
How do we differentiate b/w types of hypothyroidism

Answer 9

disease by reduced levels of T3, T4, and TSH
A TRH stimulation test can confirm if the pituitary is the cause by measuring pituitary responsiveness to IV TRH
In primary hypothyroidism, TRH further elevated TSH
W/ pituitary dysfunction, there is no response to TRH

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Question 10

what is the name for abnormal thyroid function tests in critically ill pts?
What do labs look like in this population?
why does this happen?

Answer 10

Euthyroid sick syndrome
Low T3 and T4 w/ normal TSH level
likely a response to stress, and it can be induced by surgery

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Question 11

What is the treatment for hypothyroidism?
Pre-op implications?

Answer 11

Tx: L-thyroxine is DOC
Pre-op:
Assess for airway compromise d/t swelling, edematous vocal cords, goitrous enlargement
Expect slower gastric emptying, aspiration rx
Cardiovascular system may be hypodynamic
Respiratory function may be compromised
More prone to hypothermia
Electrolyte imbalances possible
If elective case, Thyroid tx should be initiated at least 10 days prior
If emergent surgery: IV Thyroid replacement along with steroids ASAP

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Question 12

What is myxedema coma?
This occurs most commonly in what population?

Answer 12

Rare, sever form of hypothyroidism characterized by delirium, hypoventilation, hypothermia, bradycardia, HoTN, and severe dilutional hyponatremia
elderly women w/ a long hx of hypothyroidism

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Question 13

What triggers myxedema coma?
What is a cardinal feature of myxedema coma?

Answer 13

triggers: infection, cold, and CNS depressants
cardinal feature: hypothermia d/t impaired thermoregulation

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Question 14

Myxedema coma is a ____ ____ with a mortality rate > ____%
Tx?
how long does is take which vital signs to improve?

Answer 14

medical emergency
50%
Tx: IV L-thyroxine or L-triiodothyronine
IV hydration w/glucose-saline solutions, temp regulation, correction of e-lyte imbalances, and stabilization of cardiac & pulmonary systems are necessary
Mechanical ventilation is frequently required
HR, BP & temp usually improve within 24 h

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Question 15

What are goiter and thyroid tumors?
What causes goiter and thyroid tumors?

Answer 15

Swelling of the thyroid gland d/t hypertrophy and hyperplasia of follicular epithelium
Causes: lack of iodine, ingestion of goitrogen (cassava, phenylbutazone, lithium), or a defect in the hormonal biosynthetic pathway

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Question 16

In most cases, goiter is associated with what?

Answer 16

A compensated euthyroid state

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Question 17

How are goiter and thyroid tumors treated?

Answer 17

most cases are treated with L-thyroxine
surgery indicated only if medical therapy is ineffective, and goiter is compromised airway or cosmetically unacceptable

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Question 18

Pre-op implications of goiter or thyroid tumors?
What testing should be done prior?

Answer 18

pre-op hx of dyspnea in upright or supine position is predictive of possible airway obstruction during GA.
CT scan must be examined to assess the extent of the tumor
PFT- flow volume loop
Echocardiogram in the upright and supine positions can indicated degree of cardiac compression

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Question 19

what do Flow volume loops look like in goiter and thyroid tumors?

Answer 19

Flow-volume loops in the upright and supine positions will demonstrate the site and degree of obstruction
Limitations in the inspiratory limb of the loop indicate extra-thoracic obstruction
Delayed flow in the expiratory limb indicates an intra-thoracic obstruction

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Question 20

Morbidity related to thyroid surgery approaches ____%
____ injury may be unilateral or bilateral and temporary or permanent

Answer 20

13%
Recurrent Laryngeal Nerve (RLN)

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Question 21

If thyroid surgery causes a unilateral RLN injury, the patient experiences what?

Answer 21

hoarseness but no airway obstruction, and function usually returns in 3-6months

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Question 22

During thyroid surgery, what may lead to permanent hoarseness?

Answer 22

ligation or transection of the RLN

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Question 23

Bilateral complications of thyroid surgery may lead to what?

Answer 23

It is more serious than unilateral and may cause airway obstruction and difficults coughing.
May warrant a tracheostomy

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Question 24

What other endocrine disorder can occur as a complication of thyroid surgery? When will symptoms begin and what will they be?

Answer 24

Hypoparathyroidism may result from inadvertent parathyroid damage. Sx of hypocalcemia occur in the first 24-48 hours postoperatively

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Question 25

____ may lead to tracheal compression. what should be kept at bedside during the immediate post-op period?

Answer 25

hematoma trach-set | Slide 38

Question 26

Each adrenal gland consists of what? What is the function of these parts?

Answer 26

a cortex and a medulla the cortex synthesizes glucocorticoids, mineralocorticoids (aldosterone), and androgens | Slide 39

Question 27

Adrenal gland normal function and release of hormones?

Answer 27

Hypothalamus sends corticotropin-releasing hormone (CRH) to the anterior pituitary, which stimulates corticotropin (ACTH) release from the anterior pituitary ACTH stimulates the adrenal cortex to produce cortisol, which facilitates the conversion of NE to EPI in the adrenal medulla Cortisol also induces hyperglycemia, reflecting gluconeogenesis and inhibition of glucose uptake by cells Together, cortisol & aldosterone cause sodium retention & K+ excretion | Slide 39

Question 28

What is pheochromocytoma?

Answer 28

Catecholamine-secreting tumors that arise from chromaffin cells of the sympathoadrenal system | Slide 40

Question 29

uncontrolled catecholamine release can cause what 3 things?

Answer 29

malignant HTN, CVA, and MI | Slide 40 ## Footnote associated with pheochromocytoma

Question 30

What is the cause of pheochromocytoma? Is it genetic?

Answer 30

Precise cause is unknown 90% are an isolated finding, 10% inherited (familial) | Slide 40

Question 31

____ %of pheochromocytoma's occur in the ____. ____% in ____, and ____ %in the ____

Answer 31

80% occur in the adrenal medulla, 18% in organ of Zuckerkandle, 2% neck/thorax | Slide 40 (Organ of Zuckerkandle is at the bifurcation of the aorta)

Question 32

Where do malignant pheochromocytomas spread?

Answer 32

Through venous and lymph systems | Slide 40

Question 33

Most pheochromocytomas secrete NE:Epi in a ratio of ____, which is ____ of normal adrenal secretion Some pheo's secrete ____ levels of Epi and more rarely, ____

Answer 33

85:15, inverse higher, dopamine | Slide 40

Question 34

Pheochromocytoma attacks range from ____ to ____ and may last b/w ____ to ____ What causes a pheochromocytoma attack?

Answer 34

occasional to frequent 1min to several hours may occur spontaneously or triggered by injury, stress, or meds | Slide 41

Question 35

Sx of pheo

Answer 35

H/A, pallor, sweating, palpitations, orthostatic HoTN Coronary vasoconstriction, cardiomyopathy, CHF, and EKG changes | Slide 41

Question 36

How do we diagnose Pheo's?

Answer 36

24hr urine collection for metanephrines and catecholamines CT and MRI, I-metaiodobenzylguanidine (MIBG) scintagraphy help localize the tumor | Slide 41

Question 37

What should be given pre-op for pheo and why? What is the most frequent one given? MOA?

Answer 37

Preop: α blocker to lower BP, decrease intravascular volume, allow sensitization of adrenergic receptors, and decrease myocardial dysfunction Phenoxybenzamine- most frequently used preop α-blocker noncompetitive α1 antagonist with some α2-blocking properties | Slide 42

Question 38

Why would we give Prazosin and Doxazosin instead of phenoxybenzamine?

Answer 38

pure alpha 1 blockers, shorter acting w/ less tachycardia | Slide 42

Question 39

What should tachycardia after a blockade be treated with? | With pheo

Answer 39

Beta blockers | Slide 42

Question 40

Never give ____ before α blocker b/c blocking vasodilatory β2 receptors results in ____

Answer 40

nonselective BB unopposed α agonism, leading to vasoconstriction and hypertensive crises | Slide 42

Question 41

what other medication may also be used for pheo besides alpha and bb? What is its MOA?

Answer 41

CCBs also used to control HTN. Calcium triggers catecholamine release from the tumor, and excess calcium entry into myocardial cells contributes to a catecholamine-mediated cardiomyopathy | Slide 42

Question 42

Hypercortisolism is also known as what? What are the 2 forms?

Answer 42

Cushing Syndrome ACTH dependent and ACTH independent | Slide 44

Question 43

What is ACTH-dependent Cushing's? What is it associated with?

Answer 43

ACTH-dependent Cushings: high plasma ACTH stimulates the adrenal cortex to produce excessive cortisol  Acute ectopic ACTH syndrome is a form of ACTH-dependent Cushings that is most often assoc w/small cell lung carcinoma | Slide 44

Question 44

What is ACTH-independent Cushing's? What is the most common cause of this type of cushings?

Answer 44

ACTH-independent Cushings: excessive cortisol production by abnormal adrenocortical tissue that is not regulated by CRH and ACTH CRH and ACTH levels are actually suppressed  Benign or malignant adrenocortical tumors are the most common cause of ACTH-independent Cushing syndrome | Slide 44

Question 45

Sx and Dx of Cushings?

Answer 45

Sx: sudden weight gain, usually central w/↑facial fat(moon face), ecchymoses, HTN, glucose intolerance, muscle wasting, depression, insomnia  Dx: 24 hr urine cortisol  ****We Might Eat Hyper Goats More During Intercourse | Slide 45

Question 46

How do we determine what type of cushings the patient has? What is imaging useful for?

Answer 46

Determining whether Cushing's is ACTH dependent or independent requires reliable measurements of plasma ACTH using immunoradiometric assays The high-dose dexamethasone suppression test distinguishes Cushings from ectopic ACTH syndrome Imaging is useful for determining tumor location, but isn't helpful in gauging adrenal function | Slide 45

Question 47

Hypercortisolism (Cushing Syndrome) * Treatment of choice and alternative tx * other treatment in some patients * surgical treatment * Preop

Answer 47

* Treatment of choice: transsphenoidal microadenomectomy if microadenoma is resectable * Alternatively, pts may undergo 85-90% resection of the anterior pituitary * Pituitary irradiation and bilateral total adrenalectomy are necessary in some pts * Surgical adrenalectomy is the treatment for adrenal adenoma or carcinoma * Preop: evaluate/treat BP, e-lyte imbalance, and blood glucose *Consider osteoporosis in positioning* | Slide 46

Question 48

S/S of Cushings plus a picture :)

Answer 48

* Fat pad buffalo hump * thin arms and legs * thin skin with bruising * stretch marks on the tumtum * thinning hair on head * extra face and body hair * "moon" face * Red cheeks | Slide 47

Question 49

Hyperaldosteronism (Conn Syndrome) * Primary Hyperaldosteronism = * which gender is more affected? * What 3 additional diseases can be associated with Conn?

Answer 49

* Primary hyperaldosteronism: Excess secretion of aldosterone from a functional tumor (aldosteronoma) that acts independently of a physiologic stimulus * women>men * Occasionally assoc w/pheochromocytoma, hyperparathyroidism, or acromegaly | Slide 48

Question 50

Hyperaldosteronism (Conn Syndrome) * Secondary hyperaldosteronism * s/s

Answer 50

* Secondary hyperaldosteronism: presents when serum renin is increased, stimulating the release of aldosterone * S/S: nonspecific, some are asymptomatic, but can have: HTN, hypokalemia, hypokalemic metabolic alkalosis | slide 48

Question 51

Hyperaldosteronism (Conn Syndrome) Diagnosis and treatment

Answer 51

* Spontaneous hypokalemia in presence of systemic HTN is highly suggestive of hyper-aldosteronism * With Primary: plasma renin is suppressed * with Secondary: the renin is high * *Long term ingestion of licorice can cause a syndrome that mimics the features of hyperaldosteronism (HTN, hypokalemia, suppression of RAAS)* * Treatment: competitive aldosterone antagonist (**Spironolactone**), K+ replacement, antihypertensives, diuretics, tumor removal, possible adrenalectomy | Slide 49

Question 52

Hypoaldosteronism Signs and symptomes

Answer 52

* Hyperkalemia in the absence of renal insufficiency suggests hypoaldosteronism * Hyperkalemia may be enhanced by hyperglycemia * Hyperchloremic metabolic acidosis is common * Pts could have heart block because of hyperkalemia, orthostatic hypotension, and hyponatremia | Slide 50

Question 53

Hypoaldosteronism * lack of aldosterone is caused by

Answer 53

Lack of aldosterone can be a congenital deficiency of **aldosterone synthetase** or **hyporeninemia** due to defects in the **juxtaglomerular apparatus** or ACE inhibitors * Hyporeninemic hypoaldosteronism typically occurs in pts >45 w/CRF or DM * Indomethacin-induced prostaglandin deficiency is a reversible cause of hypoaldosteronism | Slide 50

Question 54

Hypoaldosteronism Treatment

Answer 54

Treatment of hypoaldosteronism includes liberal sodium intake and daily administration of fludrocortisone | Slide 50

Question 55

Primary Adrenal Insufficiency

Answer 55

AKA: Addisons Disease * Adrenal glands unable to produce enough glucocorticoid, mineralocorticoid, and androgen hormones * Most common cause: autoimmune adrenal dstruction * >90% fo the glands must be involved before signs appear | Slide 51

Question 56

Secondary Adrenal Insufficiency

Answer 56

hypothalamic-pituitary dz or suppression leading to failure in the production of CRH or ACTH * Unlike Addison's, **there is only a glucocorticoid deficiency** * In most of cases the cause is iatrogenic, such as with the use of synthetic glucocorticoids, pituitary surgery, or radiation * These pts lack hyperpigmentation and may demonstrate only mild electrolyte abnormalities | Slide 51

Question 57

Adrenal Insufficiency: Diagnosis and treatment

Answer 57

Diagnosis: baseline cortisol <20mcg/dL and remains <20mcg/dL after ACTH stimulation * A positive test demonstrates a poor response to ACTH and indicates an impairment of the adrenal cortex * **Absolute AI** is characterized by a low baseline cortisol level and a positive ACTH stimulation test * **Relative AI** is indicated when the baseline cortisol level is higher but the ACTH stimulation test is positive * Treament: Steroids | Slide 52

Question 58

Parathyroid Dysfunction: * location * what stimulates the release of PTH? * how does PTH maintain normal plasma calcium?

Answer 58

* The 4 parathyroid glands are located behind the upper & lower poles of the thyroid gland and produce parathyroid hormone (PTH), which is released into the circulation by a negative feedback that depends on plasma calcium level * **Hypocalcemia** stimulates the release of PTH, whereas **hypercalcemia** suppresses hormonal synthesis and release * PTH maintains normal plasma calcium levels by promoting the movement of calcium across GI tract, renal tubules, and the bone | Slide 53

Question 59

Hyperparathyroidism: * Happens when? * what happens to Calcium? * Classificiations

Answer 59

* Present when secretion of PTH is increased * Serum calcium concentrations may be increased, decreased, or unchanged * Classified as Primary, secondary, or Ectopic | Slide 54

Question 60

Primary Hyperparathyroidism * cause * s/s * diagnosis * treatment

Answer 60

* benign parathyroid adenoma (90%) carcinoma (<5%) parathyroid hyperplasia * S/S: sedation, N/V, decreased strength, polyuria, renal stones, Peptic ulcer disease, cardiac disturbances * Diagnosis: Plasma calcium, 24 hour urinary calcium * Treatment: surgical removal of abnormal portions of the gland | Slide 54

Question 61

Secondary Hyperparathyroidism * cause * treatment

Answer 61

compensatory response of the parathyroid glands to counteract a separate disease process producing hypocalcemia s/a CRF - *Because secondary hyperparathyroidism is adaptive, it rarely produces hypercalcemia* * Treatment: controlling the underlying disease, normalizing phosphate levels in pts with renal disease by administering a phosphate binder | Slide 55

Question 62

Hypoparathyroidism * causes * Diagnosis

Answer 62

Present when PTH is deficient or peripheral tissues are resistant to its effects * Absence or deficient PTH is almost always iatrogenic, reflecting inadvertent removal of parathyroid glands, as may occur during thyroidectomy * **Pseudohypoparathyroidism** is a congenital disorder where PTH is adequate, but the kidneys are unable to respond to it * Diagnosis: Hypocalcemia <4.5mEq/L and iCal <2mg/dL, along with decreases of PTH, and increased phosphate | slide 56

Question 63

Hypoparathyroidism * S/S * treatment

Answer 63

* S/S will depend on the speed of onset * Acute: hypocalcemia seen after accidental removal of parathyroid during thyroidectomy may cause inspiratory stridor reflecting irritability of the laryngeal musculature * Chronic: hypocalcemia is associated with fatigue, cramps, prolonged QT interval, lethargy, cataracts, SubQ calcifications, thickening of the skull, neurologic deficits *CRF is the most common cause of chronic hypocalcemia* * Treatment: Calcium replacement, Vit D | Slide 56

Question 64

Pituitary Gland Dysfunction * Anatomy and what gland releases what

Answer 64

Pituitary gland, located in the **sella turcica at the base of the brain**, consists of the anterior pituitary & posterior pituitary * Anterior pituitary secretes 6 hormones under the control of the hypothalamus: GH, ACTH, TSH, FSH, LH and prolactin * Vasopressin and Oxytocin are synthethized in the hypothalamus - then transported and stored in the posterior pituitiary | Slide 57

Question 65

Piruitary Glad: The stimulus for the release of the pituitary hormone from the posteior pituitary araises from...

Answer 65

osmoreceptors in the hypothalamus that sense plasma osmolarity | Slide 57

Question 66

Overproduction of anterior pituitary hormones is often associated with...

Answer 66

hypersecretion of ACTH (Cushing syndrome) by anterior pituitary adenomas | Slide 57

Question 67

Acromegaly * due to * how to diagnose

Answer 67

* Due to: Acromegaly is due to **excessive secretion of growth hormone** in adults, most often by an adenoma in the anterior pituitary gland * **Serum insulin-like growth factor 1 (IGF-1) is elevated** * Diagnosed: by an **oral glucose tolerance test**- measure plasma growth hormone which remains above 1ng/mL 2hours after ingestion of 75g of glucose | Slide 58

Question 68

Acromegaly Anesthesia considerations

Answer 68

* Overgrowth of soft tissues make pts susceptible to upper airway obstruction * Hoarseness & abnormal movement of vocal cords or Right laryngeal nerve paralysis may result from overgrowth of the surrounding cartilaginous structures * Peripheral neuropathy is common d/t nerve trapping by connective tissues | Slide 58

Question 69

Acromegaly Treatment

Answer 69

Transsphenoidal surgical excision of pituitary adenoma * If surgery not feasible, treatment is a LA somatostatin analogue | Slide 58

Question 70

Acromegaly (Upper airway anesthesia implications)

Answer 70

* Distorted facial anatomy may interfere with placement of a face mask * Enlarged tongue and epiglottis = airway obstructions and may interfere with vocal cord visualization * Mandible overgrowth = increase distance between lips and vocal cords * narrowed glottic opening because of vocal cord enlargement * *May require smaller ETT, VL, awake fiberoptic intubation* | slide 59

Question 71

Diabetes Insipidus * definition * S/S

Answer 71

Absence of vasopressin (ADH) from: destruction of posterior pituitary (neurogenic DI) or failure of renal tubules to respond to ADH (nephrogenic DI) * Neurogenic and nephrogenic DI are differentiated with **response to desmopressin**, which causes urine-concentration in neurogenic, but not nephrogenic, DI * S/S: polydipsia and high output of poorly concentrated urine despite increased serum osmolarity | Slide 60

Question 72

Diabetes insipidus * Treatment for each type * Anesthesia considerations

Answer 72

* Initial treatment: IV e-lytes to offset polyuria * Neurogenic DI treatment: DDAVP * Nephrogenic DI treament: low-salt, low-protein diet, diuretics, and NSAIDs * Anesthesia: Monitor UOP and e-lytes | slide 60

Question 73

Syndrome of Inappropriate ADH * How can this occur? * Inappropriately increased _ _ and _ in the presence of hyponatremia and decreased serum osmolarity are highly suggestive of SIADH

Answer 73

SIADH can occur in the presence of diverse pathologies, including intracranial tumors, hypothyroidism, porphyria, and lung carcinoma * elevated ADH levels likely occue in most pts following major surgeries * Inappropriately increased **urinary sodium** and **osmolarity** in the presence of hyponatremia and decreased serum osmolarity are highly suggestive of SIADH * Abrupt decreases in serum sodium concentration can result in cerebral edema and seizures | Slide 61

Question 74

SIADH treament

Answer 74

* Treatment: fluid restriction, salt tablets, loop diuretics & ADH antagonists-Demeclocycline * Hyponatremia may be treated with hypertonic saline: <8 mEq/L over 24-hrs | Slide 61