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Mar: Sem 2 - Health Assessment > Exam 4: Endocrine part II > Flashcards

Exam 4: Endocrine part II Flashcards

1
Q

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

A

0.5%-0.8%
myxedema

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2
Q

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

A

Primary
Low T3 and T4 despite adequate TSH

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3
Q

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

A

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

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4
Q

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

A

hashimoti thyroiditis
goitrous
middle-aged women

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5
Q

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

A

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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6
Q

Hypothyroidism S/S chart
HEENT
Neuro
GI
Psych
Skin
Cardiac

A

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7
Q

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

A

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

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8
Q

What is controversial in subclinical hypothyroid disease?

A

Throid replacement

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9
Q

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

A

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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10
Q

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?

A

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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11
Q

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

A

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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12
Q

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

A

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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13
Q

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

A

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

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14
Q

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

A

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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15
Q

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

A

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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16
Q

In most cases, goiter is associated with what?

A

A compensated euthyroid state

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17
Q

How are goiter and thyroid tumors treated?

A

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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18
Q

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

A

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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19
Q

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

A

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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20
Q

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

A

13%
Recurrent Laryngeal Nerve (RLN)

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21
Q

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

A

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

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22
Q

During thyroid surgery, what may lead to permanent hoarseness?

A

ligation or transection of the RLN

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23
Q

Bilateral complications of thyroid surgery may lead to what?

A

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

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24
Q

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

A

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

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25
Q

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

A

hematoma
trach-set

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26
Q

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

A

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

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27
Q

Adrenal gland normal function and release of hormones?

A

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, reflectinggluconeogenesis and inhibition of glucose uptake by cells
Together, cortisol & aldosterone cause sodium retention & K+ excretion

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28
Q

What is pheochromocytoma?

A

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

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29
Q

uncontrolled catecholamine release can cause what 3 things?

A

malignant HTN, CVA, and MI

Slide 40

associated with pheochromocytoma

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30
Q

What is the cause of pheochromocytoma?
Is it genetic?

A

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

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31
Q

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

A

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)

32
Q

Where do malignant pheochromocytomas spread?

A

Through venous and lymph systems

Slide 40

33
Q

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, ____

A

85:15, inverse
higher, dopamine

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34
Q

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

A

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

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35
Q

Sx of pheo

A

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

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36
Q

How do we diagnose Pheo’s?

A

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

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37
Q

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

A

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

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38
Q

Why would we give Prazosin and Doxazosin instead of phenoxybenzamine?

A

pure alpha 1 blockers, shorter acting w/ less tachycardia

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39
Q

What should tachycardia after a blockade be treated with?

With pheo

A

Beta blockers

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40
Q

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

A

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

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41
Q

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

A

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

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42
Q

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

A

Cushing Syndrome
ACTH dependent and ACTH independent

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43
Q

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

A

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

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44
Q

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

A

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

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45
Q

Sx and Dx of Cushings?

A

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

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46
Q

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

A

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 isuseful for determining tumor location, but isn’t helpful ingaugingadrenal function

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47
Q

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

A
  • 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

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48
Q

S/S of Cushings plus a picture :)

A
  • 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

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49
Q

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

A
  • 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

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50
Q

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

A
  • 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

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51
Q

Hyperaldosteronism (Conn Syndrome) Diagnosis and treatment

A
  • 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

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52
Q

Hypoaldosteronism Signs and symptomes

A
  • 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

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53
Q

Hypoaldosteronism
* lack of aldosterone is caused by

A

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

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54
Q

Hypoaldosteronism Treatment

A

Treatment of hypoaldosteronism includes liberal sodium intake and daily administration of fludrocortisone

Slide 50

55
Q

Primary Adrenal Insufficiency

A

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

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56
Q

Secondary Adrenal Insufficiency

A

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

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57
Q

Adrenal Insufficiency: Diagnosis and treatment

A

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

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58
Q

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

A
  • 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

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59
Q

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

A
  • Present when secretion of PTH is increased
  • Serum calcium concentrations may be increased, decreased, or unchanged
  • Classified as Primary, secondary, or Ectopic

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60
Q

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

A
  • 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

61
Q

Secondary Hyperparathyroidism
* cause
* treatment

A

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

62
Q

Hypoparathyroidism
* causes
* Diagnosis

A

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

63
Q

Hypoparathyroidism
* S/S
* treatment

A
  • 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

64
Q

Pituitary Gland Dysfunction
* Anatomy and what gland releases what

A

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

65
Q

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

A

osmoreceptors in the hypothalamus that sense plasma osmolarity

Slide 57

66
Q

Overproduction of anterior pituitary hormones is often associated with…

A

hypersecretion of ACTH (Cushing syndrome) by anterior pituitary adenomas

Slide 57

67
Q

Acromegaly
* due to
* how to diagnose

A
  • 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

68
Q

Acromegaly Anesthesia considerations

A
  • 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

69
Q

Acromegaly Treatment

A

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

Slide 58

70
Q

Acromegaly (Upper airway anesthesia implications)

A
  • 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

71
Q

Diabetes Insipidus
* definition
* S/S

A

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

72
Q

Diabetes insipidus
* Treatment for each type
* Anesthesia considerations

A
  • 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

73
Q

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

A

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

74
Q

SIADH treament

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

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Mar: Sem 2 - Health Assessment (32 decks)

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