Endocrine Disorders part 2 Flashcards

1
Q

Peak plasma levels in the…

A

morning or wake time

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2
Q

What zones of the adrenal cortex are aldosterone, cortisol, and androgens produced in?

A

aldosterone - glomerulosa
cortisol - fasciculata
androgens - reticularis

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3
Q

What is the action of aldosterone?

A
  • Kidneys–distal tubules
  • Intravascular volume and RAA system
  • Regulates Na and H20 balance –affects BP
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4
Q

What is the action of cortisol?

A
  • Increases contractility and vascular reactivity to vascoconstriction (results in increased BP)
  • Antagonizes insulin
  • Activates lipolysis – increased FFA
  • Stimulates gluconeogenesis (results in increased sugar, insulin intolerance, and cholesterol)
  • Muscle catabolism – increases glucose
  • Decreases calcium absorption and activates osteoclasts
    — (results in osteoporosis)
  • Inhibits PLA2 and mobilization, migration, function of leukocytes
    — (results in decreased immune response)
  • Increases appetite, suppresses sleep, regulates emotion and memory
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5
Q

What does cortisol do to…
BP
sugar
insulin resistance
immune response
osteoporosis

A

BP - increase
sugar - increase
insulin resistance - increase
immune response - decrease
osteoporosis - increase

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6
Q

What is the action of androgens?

A
  • Gonads
  • Sexual maturation, growth and developmeny
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7
Q

Where is norepinephrine and epinephrine produced?

A

adrenal medulla

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8
Q

What is the action of norepinephrine and epinephrine?

A
  • Fight or flight - stress response
  • Increases BP, peripheral resistance, cardiac output
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9
Q

What is hyperadrenalism?

A

↑ Aldosterone, cortisol, androgen, estrogen isolated or in combination

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10
Q

What is hyperaldosteronism?

A

Hypertension
hypokalemia
edema

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11
Q

What is the most common form of hyperadrenalism?

A

Glucocorticoid excess
- high levels of cortisol

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12
Q

What diseases are associated with glucocorticoid excess?

A
  • Cushing disease (pituitary or adrenal tumor)
  • Cushing syndrome (exogenous corticosteroids)
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13
Q

Wht are the complications associated with glucocorticoid excess?

A

o Diabetes
o Hypertension
o Weight gain
o Moon facies
o Buffalo hump
o Hirsutism
o Acne
o Heart failure
o Osteoporosis
o Delayed wound healing
o Susceptibility to infection
o irregular menses Insomnia
o Psychiatric disorders
o Peptic ulcers
o Glaucoma and cataracts

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14
Q

What does the pneumonic “cushingoid” stand for?

A

C - cataracts
U - ulcers
S - striae and skin thinning
H - hypertension and hirsutism (women)
I - immunosuppressiona nd infections
N - necrosis of femoral heads
G - glucose elevation
O - osteoporosis and obesity
I - impaired wound healing
D - depression and mood changes

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15
Q

What are the cutaneous findings in cushing syndrome?

A
  • increased central adiposity with thin extremities
  • skin thinning and easy brusing
  • violaceous striae
  • acanthosis nigricans
  • increased dermatophyte, candidal skin, and nail infections
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16
Q

What are the related features for cushings syndrome?

A
  • diabetes
  • hypertension
  • osteoporosis
  • irregular menses
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17
Q

How is cushings diagnosed?

don’t really need to know

A
  • measurement of 24-hr urinary free cortisol and late-night salivary control
  • failure to suppress cortisol production with a low-dose dexamethasone suppression test
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18
Q

How do you manage cushings?

don’t really need to know

A
  • endorcine and surgical consult
  • surgical removal of pituitary or adrenal tumor
  • adrenal enzyme inhibitors
  • radiation therapy
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19
Q

How are immediate-acting glucocorticoids (prednisolone, triamcinolone, methylprednisolone) and long-acting glucocorticoids (dexamethasone, betamethasone) different from naturally occuring versions?

A

they are way more potent and require a prescription (not over the counter)

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20
Q

What is primary adrenal insufficiency?

A

addison disease
➢ Destruction of adrenal cortex
o ↓ Cortisol and ↑ ACTH (adrenocorticotropic
hormone)

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21
Q

What is the etiology of addisons disease?

A

o Most commonly autoimmune
o Chronic infectious disease and sepsis
❑ HIV, CMV, fungal infection
o Drugs

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22
Q

What is the problem with people with addison disease getting stressed?

A

Adrenal crisis

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23
Q

How is addison disease managed?

A

o Surgery and stress may require supplemental corticosteroids
o Pain control is important

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24
Q

What are the cutaneous findings in addison disease?

A
  • hyperpigmentation of skin and mucosal membranes
  • longitudinal pigmented bands in nails
  • vitiligo
  • decreased axillary and pubic hair in women
  • calcification of auricular cartilage in men
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25
Q

What are the related features of addison disease?

A
  • abdominal pain
  • electrolyte abnormalities
  • postural hypotension
  • anorexia and weight loss
  • fatigue
  • shock, coma, and death if untreated
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26
Q

How do you diagnose addison disease?

don’t really have to know

A

failure to respond adequately to coricotropin stimulation test

27
Q

How do you manage addison disease?

A

lifelong replacment therapy of glucocorticoids and mineralocorticoids

28
Q

Undiagnosed patient with signs and symptoms of adrenal disease should be…

A

promptly be referred to their primary physician for comprehensive work-up

29
Q

What do you need to do to determine the type and severity of adrenal disease?

A
  • BP and glucose levels
  • Avoid NSAIDs and aspirin → peptic ulcers, GI bleed
  • If osteoporosis and osteopenia
    o More prone to periodontal bone loss - monitor
    o May have history of bisphosphonate use
30
Q

Impaired wound healing may be a consequence of…

A

both hyperadrenalism and adrenal insufficiency

31
Q

Is it necessary to supplement corticosteroids for people with adrenal insufficiency?

A

o Depends on
✓ Type
✓ Severity/ stability/ medical status
✓ Dental procedure being performed (long: >1hr or invasive) /type of stress/dental infection

32
Q

What are the signs of adrenal crisis?

A

o Hypotension - Monitor BP – vasopressors, patient position, fluid replacement
o Abdominal pain
o Myalgia
o Fever
o Supplement with 100 mg of hydrocortisone and send to ED

33
Q

What do you do for pain control in those with adrenal insufficiency?

A

o Adequate anesthesia, long-acting agent at end of procedure
o Good post-up pain control

34
Q

What is the function of the thyroid?

A
  • Involved in developmental and
    metabolic processes
  • Depends on iodide
  • Thyroid produces 3 hormones
    ➢T3 and T4
    ➢Calcitonin
35
Q

What controls T3 and T4 secretion?

A

TSH (pituitary)

36
Q

What is the role of calcitonin from the thyroid?

A

o Regulates circulating calcium and phosphorus levels
o Also influenced by actions of PTH and Vit D

37
Q

What are the target tissues from the thyroid?

A
  • heart
  • adipose tissue (lipolysis)
  • muscle (portein breakdown)
  • bone
  • nervous system
  • gut (increased carb absorption)
  • lipoprotein (formation of LDL receptors)
  • other
38
Q

What are the thyroid disorders?

A
  • Thyroid enlargement = Goiter
  • Thyroid nodules
  • Thyroiditis (hashimoto)
  • Hyperthyroidism (thyrotoxicosis)
  • Hypothyroidism (congenital or acquired)
  • Neoplasia
39
Q

What are the characteristics of thyroid enlargment (goiter)?

A
  • May be functional or non-functional
  • Most are non-functional (euthyroid)
  • Hyperthryoidism goiter – Graves disease
  • Hypothyroidism goiter – Hashimoto thyroiditis
40
Q

What are the causes of throid nodules?

A
  • Hyperplasia
  • Adenoma
  • Carcinoma
41
Q

What is another name for thyroiditis?

A

hasimoto (autoimmune)

42
Q

What are the types of hyperthyroidisim (thyrotoxicosis)?

A
  • Primary – Graves disease (auto-immune disease)
  • Secondary – Pituitary adenoma
43
Q

What are the types of hypothyroidisim (congenital or acquired)?

A
  • Primary – Graves disease (end-stage)
  • Secondary
  • Transient
44
Q

What are the causes of neoplasia of the throid?

A
  • Adenoma
  • Carcinoma (papillary, follicular)
45
Q

What are the symptoms of hyperthyroidism?

A
  • unintentional weight loss
  • heat intolerance/sweating
  • palpitations
  • agitation/emotional lability
  • multiple daily loose stools
  • pruritus
  • weakness
  • oligomenorrhea in women
46
Q

What are the clinical findings of hyperthyroidism?

kinda not important (he didn’t really talk about this)

A
  • goiter
  • tachycardia
  • atrial fibrillation
  • high output cardiac failure
  • fine tremor
  • hot sweaty extremities
  • ophthalmopathy
  • agitation/confusion
  • muscle weakness/wasting
  • exopthalmia (bulging eyes)
  • “thyroid storm” with fever, confusion, dehydration, and eventually death if untreated
47
Q

How do you diagnose hyperthyroidism?

A
  • serum thryoid-stimulating hormone (BEST TEST)
  • serum free thyroxine (T4), total T3, and thyrotropin receptor antibodies
  • radioactive iodine uptake and imaging
48
Q

How do you manage hyperthyroidism?

A
  • endocrine and surgical consult
  • propranolol for symptomatic treatment of tremor, tachycardia, and sweating
  • propythiouracil to inhibit throid homrone metabolism
  • methimazole to inhibit thyroid hormone synthesis
  • radioiodine ablation of the thyroid gland
49
Q

Thyroid storm may be precipitated by…

A

oral infection or surgical procedure in a patient who is poorly controlled

50
Q

What are the symptoms of hypothyroidism?

A
  • unexplained weight gain
  • fatigue
  • constipation
  • cold intolerance
  • dry skin
  • muscle weakness
  • carpal tunnel syndrome
  • hoarseness
  • decrease body temp
  • facial swelling
  • menorrhagia in women
51
Q

What are the clinical findings of hypothyroidism?

he didn’t really talk about this

A
  • goiter
  • cold, doughy skin
  • bradycardia
  • facial and finger swelling
  • slowed relaxation of deep tendon reflexes
  • hair loss/lateral eyebrow loss
  • pericardial effusion
  • myocardial infarction or congestive heart failure with aggressive thyroid hormone replacement
  • coma and death without treatment
52
Q

What are the related features of hypothyroidism?

A
  • macroglossia
  • broadened nose, thickened lips, puffy eyes
  • imparied wound healing
  • cretinism in patients with congential hypothyroisim
  • “myxedema coma”
53
Q

How do you diagnosis hypothyroidism?

A
  • serum thyroid-stimulating hormone (BEST TEST) - should be high
  • other useful tests are T4, T3, and anti-TPO antibodies, and lipid panel
54
Q

What is the management for hypothyroidism?

A
  • endocrine consult
  • oral thyroxine replacement (usually 75-150 ug/day)
  • careful followup for the heart, lungs, adrenal glands
55
Q

How does hyperthyroidism affect dentistry?

A
  • Increased periodontal bone loss
  • Increased susceptibility to caries
56
Q

How does hypothyroidism affect dentistry?

A
  • Delayed tooth eruption and altered bone formation
  • Macroglossia
  • Dysgeusia and burning mouth
  • Salivary gland enlargement
  • Oral lichen planus
57
Q

Patients with both hyper and hypothyroidism may be more susceptible to…

A

infections- treat aggressively

58
Q

Patients with uncontrolled, poorly controlled, suspected hyperthyroidism or hypothyroism should or should not receive dental care until disease is under control?

A

SHOULD NOT

59
Q

Risk of __________ from medications used to treat hyperthyroidism

A

Agranulocytosis
➢ Fever, sore throat, oral ulcers are warning signs

60
Q

What do you do if a patient has a thyrotoxic crisis/storm?

A

➢ CPR and vital signs
➢ Ice packs or wet packs
➢ Administer hydrocortisone 100-300 mg
➢ IV glucose
➢ Administer propylthiouracil
➢ Send to ED

61
Q

What do you do if a patient has myxedema coma?

A

➢ CPR and vital signs
➢ Conserve body heat – blanket
➢ Administer hydrocortisone 100-300 mg
➢ IV saline and glucose
➢ Administer thyroxine
➢ Send to ED

62
Q

What are the drug interactions to be aware of in hyperthyroidism?

A
  • Caution with aspirin and NSAIDS- can increase T4
  • Ciprofloxacin contraindicated – decreases absorption of thyroid hormone
  • Avoid local anesthestics containing epinephrine and ginigval retraction cord with epinephrine in poorly controlled patients
63
Q

What are the drug interactions to be aware of in hypothyroidism?

A
  • Avoid CNS depressants (narcotics, barbituates, sedatives) if patient is poorly controlled
  • Cytochrome p450 inducers (phenytoin, carbamazepine, and rifampin) should be avoided – increases metabolism of levothyroxine