Endocrinology Flashcards

1
Q

Adrenal Gland
Comprised of adrenal cortex and adrenal
medulla
◦ Inner –
◦ Outer –
— Adrenal cortex produces about –
different chemicals
— Those with pharmacologic properties:
(3)

A

medulla
– secretes catecholamines

cortex
– secretes adrenal steroids

50

– Mineralocorticoids
– Glucocorticoids, cortisol
– Androgens

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2
Q

3 layers within cortex
◦ zona glomerulosa: produces —
◦ zona fasciculata produces —
◦ zona reticularis: produces — hormones, mostly
— and small amount of —

A

mineralocorticoids
glucocorticoids
sex, androgens, glucocorticoids

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3
Q

Mineralocorticoids (produced in zona glomerulosa)
— Regulate water and electrolyte balance
(2)

A

◦ Sodium (Na +), Potassium (K+) and fluid balance
◦ Provide important homeostatic functions

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4
Q

Mineralocorticoids
— Aldosterone – main endogenous hormone
(2)

A

◦ essential for blood pressure regulation and electrolyte and fluid
homeostasis - helps to maintain normal blood pressure and
electrolyte balance
◦ acts on the Mineralocorticoid Receptor (MR)

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5
Q

◦ acts on the Mineralocorticoid Receptor (MR)
(3)

A

– MR present in kidneys impacts fluid and electrolyte balance
– Extra-renal MR plays a relevant role in the control of cardiovascular and
metabolic functions
– Overactivation of the MR is implicated in the pathophysiology of aging related
to cardiovascular, metabolic and kidney dysfunction and progress of disease

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6
Q

Aldosterone Basics
(3)

A

— Increases Na+ reabsorption by distal tubules in kidney
with concomitant increased excretion of K + and H +
— Increases BP and blood volume – balance/control the
amount of sodium and fluids in the body
— Work on specific intercellular receptors in kidney

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7
Q

Pharmacotherapeutic use of medications involving
mineralocorticoid effects
(2)

A

— Replacement therapy Addison’s Disease/Adrenal
Insufficiency
◦ Fludrocortisone (Florinef) - mineralocorticoid

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8
Q

— Replacement therapy Addison’s Disease/Adrenal
Insufficiency
◦ Addison’s Disease (autoimmune disease)/Adrenal Insufficiency –

A

adrenal do not produce enough of the steroid hormones, cortisol
and aldosterone.

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9
Q

◦ Fludrocortisone (Florinef) - mineralocorticoid
(4)

A

– Functionally similar to aldosterone
– Most mineralocorticoid effect of available steroids
– Other steroids have much smaller amounts of mineralocorticoid effects
(example: hydrocortisone, prednisone) or no mineralocorticoid effects
(example: dexamethasone, methylprednisolone)
– Other indications: orthostatic hypotension, septic shock

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10
Q

Drugs that Inhibit Aldosterone
— Imbalances in

A

aldosterone and overactivity of the mineralocorticoid
receptor contribute to hypertension, kidney insufficiency, heart failure
and potentially other cardiovascular disease
◦ Due to idiopathic adrenal hyperactivity (most common) or benign tumor (Conn’s
syndrome)

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11
Q

Spironolactone (Aldactone) and Eplerenone (Inspra)
(4)

– Common Indications:
(3)

A

– competitive aldosterone antagonist at receptor sites in distal renal tubules (block higher
concentration of kidney-specific MR), increasing sodium chloride and water excretion while
conserving potassium and hydrogen ions – prevents mineralocorticoid effects of adrenal steroids on
the renal tubule
– Steroidal structure
– Also known as a potassium sparing diuretic

– Hyperaldosteronism (secondary cause of hypertension and causes low potassium)
– Heart failure
– Hypertension

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12
Q

Drugs that Inhibit Aldosterone (Non-steroidal)
— Finerenone (Kerendia)
(4)

A

◦ Blocks Mineralocorticoid receptor (MR) in kidney and heart
◦ Selectively blocks (antagonist) mineralocorticoid receptor-mediated
sodium reabsorption and overactivation of kidney, blood vessel, and heart
tissues, reducing fibrosis and inflammation
◦ MR overactivation is an important factor associated with CV events and
Chronic Kidney Disease (CKD) progression

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13
Q

Drugs that Inhibit Aldosterone (Non-steroidal)
— Finerenone (Kerendia)
◦ Indications:

A

– Chronic kidney disease (CKD) associated with type 2 diabetes
to reduce the risk of kidney function decline, kidney failure,
cardiovascular death, non-fatal heart attacks, and hospitalization for
heart failure in adults with type 2 diabetes and chronic kidney disease

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14
Q

Glucocorticoids (endogenously produced in zona fasciculata)
— Mechanism of action –

A

complex: work through specific
glucocorticoid intracellular receptors to regulate several vital cell
activities
◦ Metabolic
◦ Immune function

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15
Q

Glucocorticoids (endogenously produced in zona fasciculata)
— Widespread actions on intermediate metabolism, affecting
(3) metabolism
— Potent regulatory effects on host defense mechanisms including
(2) function
◦ Glucocorticoid receptors up regulate expression of anti-
inflammatory proteins and down regulate expression of pro-
inflammatory proteins

A

carbohydrate (glucose), protein and fat

inflammation and immune

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16
Q

Glucocorticoids = Corticosteroids
— Main endogenous hormone in humans

A

– hydrocortisone
(also called cortisol)

◦ Produce 24-30 mg endogenous hydrocortisone/cortisol
◦ Use up to 300 mg/day in times of significant stress
— Secreted in circadian rhythm in healthy humans
◦ highest concentrations in early morning

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17
Q

HPA Axis Pathway:

A

◦ Hypothalamus releases Corticotrophin-Releasing Hormone [CRH]
◦ Adrenocorticotropic hormone [ACTH] released from the anterior
Pituitary
◦ Adrenals release glucocorticoids
◦ Negative feedback mechanism to inhibit CRH and
ACTH when glucocorticoid concentrations increase in the
blood

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18
Q

Therapeutic Use of Corticosteroids
— Many have partial mineralocorticoid
and glucocorticoid properties
— Most are used for anti-inflammatory
and immunosuppressive properties
— Common indications:
(5)

A

◦ Addison’s disease/Adrenal
Insufficiency (deficiency in
corticosteroid production)
◦ Cancer therapy (usually in
combination with cytotoxic drugs or
to reduce edema in brain tumors)
◦ Anaphylaxis (use in combination with
epinephrine, antihistamines – note:
steroids have slow onset)
◦ Hypersensitivity states (severe
allergic reactions)
◦ Shock

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19
Q

Therapeutic Use of Corticosteroids
Common indications, continued:
(7)

A

◦ Autoimmune disease
– Systemic Lupus Erythematosus
– Rheumatoid arthritis
– Inflammatory bowel disease
– Connective Tissue Diseases
◦ Asthma (inhaled)
◦ Chronic obstructive pulmonary disease
(inhaled)
◦ Respiratory distress syndrome in infants
◦ Suppressing rejection of skin grafts or graft-
versus-host disease following organ transplant
◦ Acute renal insufficiency
◦ Inflammatory conditions of eyes, ears, nose or
skin /rashes of the skin (topical application)

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20
Q

Use of Steroids in Dentistry
(7)

A

— Use for anti-inflammatory, pain management and auto-immune
properties
— Oral lesions
— Restorative dentistry/pain management
— Bell’s palsy
— Post herpetic neuralgia
— Temporomandibular joint disorder
— Temporal arteritis

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21
Q

— Oral lesions
(7)

A

◦ Aphthous ulcers/stomatitis
◦ Oral lichen planus
◦ Erythema multiforme
◦ Behcet’s disease
◦ Pemphigus
◦ Bullous pemphigoid
◦ Systemic lupus erythematosus

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22
Q

Formulations of Corticosteroids

A

— Dental (topical oral) applications
◦ Pastes, ointments/orabase, gels, lozenges, intralesional therapy, rinses – commercially
available or compounded
◦ Importance of contact time with lesion
◦ Example of commercially available product:
– Kenalog® in Orabase® / Triamcinolone Dental Paste
◦ Patient education:
* Using a cotton swab, press (do not rub) a small amount of paste onto the area to be treated
until the paste sticks and a smooth, slippery film forms. Do not try to spread the medicine
because it will become crumbly and gritty.
* (Usually applied 2-3 times per day – see dosing information of the product). Apply the paste at
bedtime so the medicine can work overnight. The other applications of the paste should be
made following meals.

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23
Q

Formulations of Corticosteroids, continued
— Systemic
(3)
— Others
(3)

A

◦ Oral/IM/IV
◦ Pulse dosing/bursts
◦ Life-long replacement for adrenal suppression

◦ Topical/external (creams/ointments) – skin/joints
◦ Intra-articular – joints
◦ Inhalation – asthma/COPD

24
Q

Steroid Dosing Consideration
(7)

A

— Consider the potency of steroids and formulations
— Weigh pros/cons of oral topical vs. systemic therapy
— Topical/other types of administration may cause systemic effects
◦ Depends on potency, amount, surface area covered, absorption,
permeability of tissue, dosing frequency, site treated, etc.
— Use lowest effective dose for shortest duration
— Monitor for adverse events
— If patient on systemic therapy longer than 14 days, taper dose off.
DO NOT STOP ABRUPTLY – use taper
— Consult with the patient’s provider for management of patients
with Addison’s Disease, chronic steroid use or steroid tapering
plans, when needed

25
Q

Steroid Dosing
— Systemic considerations
(2)
— Prednisone
(3)

A

◦ Low dose < 10 mg prednisone/day
◦ Moderate dose 10-20 mg prednisone/day
◦ High dose > 20 mg prednisone/day

◦ Usually, lowest cost oral steroid
◦ Available in wide range of strength for titration
◦ Morning dosing/can split larger doses to BID, but give earlier in
the day to minimize insomnia and mimic higher endogenous
steroid production in the AM

26
Q

Use of IV Steroids
— Intra-operative administration
(3)

A

◦ Example: 3rd molar extractions with IV sedated patient
– IV dexamethasone or IV methylprednisolone
◦ Provides anti-inflammatory effect (reduces pain and swelling)
◦ Helps reduce post-op nausea from the sedation

27
Q

HPA Axis Suppression/Adrenal Suppression
— When providing supraphysiologic doses of
corticosteroids (> 25-30 mg of hydrocortisone/cortisol
equivalents) X 14 days or more = HPA Axis
SUPPRESSION
(4)

A

— May take weeks to months to fully recover function
— Use of chronic exogenous corticosteroids = suppression of adrenal
gland = atrophy
— Inability of the adrenals to respond to stress can result in adrenal crisis
— Patient may develop chronic adrenal insufficiency (AI) from various
causes

28
Q

Chronic Adrenal Insufficiency (AI)
(4)

A

— Primary Chronic AI – Addison’s Disease (autoimmune)
— Secondary AI – damage/disease of the pituitary or
hypothalamus
◦ Also caused from long-term use of glucocorticoids
— Treatment for chronic primary AI often includes oral
hydrocortisone +/- fludrocortisone
— Other options for treatment of AI – prednisone,
dexamethasone

29
Q

Adrenal crisis prophylaxis
— Acute adrenal crisis = medical emergency (rare)
(4)

A

◦ Life-threatening condition
◦ Predicated in patients with chronic adrenal insufficiency (AI) with
increased significant stress such as from infection, trauma or surgery
◦ Symptoms –fever, abdominal pain, weakness, hypotension, dehydration,
nausea, vomiting, slow, sluggish movement, fatigue, profound weakness,
rapid heart rate, rapid respiratory rate, confusion, loss of
consciousness/coma
◦ Laboratory findings – low K + , low Na + , acidosis, uremia

30
Q

Management of Acute Adrenal Insufficiency (AI)
in Surgery – Steroid Cover
(5)

A

— IV fluids (5% dextrose in Normal Saline)
— Hydrocortisone
— Hydrocortisone – IV initially then change to oral when patient is stable
— Current evidence shows that routine dental care and minor oral surgical
procedures under local anesthesia, including uncomplicated dental extractions,
do not increase stress levels enough to precipitate an adrenal crisis
— Consider 10 mg-25 mg hydrocortisone equivalents orally(po) stress dose cover for
those at highest risk (Addison’s Disease) undergoing major dental surgery with general
anesthesia (steroid cover)

31
Q

— Hydrocortisone
(4)

A

◦ 20-25 mg/day- Primary AI (Addison’s Disease – idiopathic, most commonly auto-immune)
◦ 15-20 mg/day – Secondary AI (exogenous corticosteroids or disease/disorders of hypothalamus or
pituitary)
– Secondary AI selectively causes glucocorticoid deficiency; therefore, mineralocorticoid function is
better maintained
– Adrenal crisis less likely than in primary AI

32
Q

Acute Adverse Effects to Long-term Effects

A

— CV: tachycardia, hypertension
— DERM: acne, delayed wound healing,
facial flushing
— ENDO: hyperglycemia (caution in
diabetes)
— GI: abdominal distention, diarrhea,
constipation, heartburn, increased
appetite, peptic ulcers, and GI bleeds
— INFECTION: suppression of response
to infection, including opportunistic
effects or injury/candidiasis
— NEURO: anxiety, insomnia, mood
swings, euphoria, hallucinations,
depression
— BONE: osteoporosis
— MUSCLE: muscle wasting and weakness
— GROWTH: inhibition in children
— EYES: glaucoma in genetically
predisposed), increased incidence in
cataracts
— Adrenal suppression (sudden
withdrawal – acute adrenal
insufficiency)
— Cushing syndrome

33
Q

Drug interactions/Contraindications
Interactions:
(5)
Contraindications:
(1)

A

— Increased prothrombin time/INR with warfarin
— Risk of hypokalemia with potassium-depleting diuretics
(hydrochlorothiazide, others)
— Increased risk of cardiac toxicity and arrhythmias with cardiac
glycosides (digoxin)
— Interferes with calcium absorption in food
— Absorption of glucocorticoids is decreased in presence of St. John’s
wort

— Severe infections, severe hypertension, severe heart failure, severe
renal impairment

34
Q

Corticosteroids: dental implications summary
— Effective in decreasing swelling/inflammation and pain
◦ Alternative to NSAIDS or opioids for pain in some cases or may decrease need for opioids
— Altered responses to infection and wound healing
— Oral thrush from inhaled steroids (advise patients to rinse mouth after each
inhaler use)
— Contribute to tooth decay, periodontal disease, decreased bone density (long-
term)
— Patients with chronic adrenal insufficiency (AI): risk of developing acute adrenal
crisis when placed in a stressful situation such as major dental procedures
— General Considerations
(5)

A

◦ Pulse steroid/lowest effective dose/shortest duration
◦ Systemic antibiotic therapy – if indicated
◦ For inhaled steroids - rinse/spit and spacers
◦ Anxiety control – for all patients, especially those with AI
◦ Increased administration of glucocorticoids (steroid cover)? - only in patients with AI at high
risk/major dental procedures/surgery

35
Q

Patient Education for Steroid Use
— Purpose:
(3)
— Dose/frequency/dosing instructions:
(4)

A

◦ Relieve the discomfort and redness, swelling/inflammation of some mouth and gum
problems or during/after dental procedures
◦ Useful for pain
◦ Timeframe for expected improvement

◦ Take in AM for systemic administration
– Adjustment if patient to receive steroid prescription (Medrol) in the afternoon to get all tablets
in the first day
– If taper is involved, specifics of taper, what dose to take each day
◦ Length of therapy
◦ Specific instructions for dental paste/topical application
◦ Do not use more often or for a longer time than your medical doctor or dentist
ordered

36
Q

Patient Education for Steroid Use, continued
— Common (short-term) side effects:
(6)

A

◦ Insomnia/difficulty sleeping (one of the most common complaints)
– Taking all in AM may help
– Use of sleep agent for 1-2 nights? (risk vs. benefit)
◦ Agitation/changes in mood/irritability
◦ Leg swelling
◦ Weight gain (more with long-term use)
◦ Risk of increased blood glucose (especially in diabetics)
◦ Risk of increased blood pressure (especially if already elevated)

37
Q

Thyroid Gland
— Secretes 3 main hormones
(5)
– T3 is converted to T4 primarily in the liver and kidney but also in many other tissues
◦ calcitonin
— T3 and T4 (combined are referred to as thyroid hormone)
(3)
— Calcitonin
(1)

A

◦ thyroxine (T4) – large storage – high serum concentrations in body
◦ tri-iodothyronine (T3) – small storage – low serum concentrations in body (fast
turnover rate)
– 80% of T3 daily production is a result of peripheral conversion of T4 →T3

◦ normal growth and development in children (brain and body)
◦ control energy/metabolism
◦ involved in normal functioning of almost every organ system including the brain,
heart, liver, and muscles

◦ control of plasma calcium (Ca2+ )

38
Q

Basics of Regulation of Thyroid Function
(5)

A

— Thyrotrophin releasing hormone
(TRH) stimulated from
hypothalamus
— Thyroid stimulating hormone
(TSH) from anterior pituitary
— Thyroid hormone synthesis
resulting in release of T3 and T4
— Negative feedback on anterior
pituitary with T3 more active than
T4 ( thyroid hormone = TSH)
— Plasma iodine also impacts thyroid
hormone production (decrease of
iodine = hormone production
and TSH)

39
Q

Actions of Thyroid Hormones
— Effects on metabolism
(2)
— Effects on growth and development
(3)

A

◦ increased metabolism on carbohydrates, fats and protein (most
effects in conjunction with other hormones)
◦ T3 3-5X more active than T4

◦ direct action and indirectly influences growth hormone
– skeletal development
– growth and maturation of CNS

40
Q

HYPERthyroidism (Thyrotoxicosis)
— Diffuse toxic goiter (Graves Disease/exopthalmic
goiter)
(2)
— Toxic nodular goiter
(1)

A

◦ autoimmune disease (autoantibodies to TSH receptor)
◦ protruding eyeballs (exophthalmos)

◦ benign neoplasm or adenoma

41
Q

HYPERthyroidism Symptoms
* “Overactive” thyroid
* Common:

A
  • Nervousness or irritability
  • Fatigue
  • Muscle weakness
  • Trouble tolerating heat
  • Trouble sleeping
  • Tremor, usually in your hands
  • Rapid and irregular heartbeat
  • Frequent bowel movements
    and/or diarrhea
  • Weight loss
  • Mood swings
  • Goiter, an enlarged thyroid that may cause
    neck to look swollen.
  • If large, may cause trouble with breathing or
    swallowing
42
Q

HYPERthyroidism treatments

A

— Surgery
— Radioactive Iodine (RAI)- 131 I (destroys thyroid follicles)
◦ hypothyroidism usually results from surgery or RAI
— Drug Therapy (oral)
◦ Propylthiouracil (PTU)
◦ Methimazole (MMI)
– MOA → inhibit biosynthesis of thyroid hormones by blocking the oxidation of
iodine in the thyroid gland; blocks synthesis of thyroxine (T 4) and triiodothyronine
(T 3); does not inactivate circulating T 4 and T 3
– ADRs – neutropenia, agranulocytosis, aplastic anemia, liver toxicity
◦ Beta Blockers (propranolol): symptomatic relief only!
◦ Glucocorticoids for exophthalmos in Graves Disease

43
Q

HYPOthyroidism

A

— General Definition:
◦ Free thyroxine (fT4) is: sub-normal/low (normal range 0.8 – 2.8 mg/dl) and Thyroid-
Stimulating Hormone (TSH) is usually elevated/high (normal range 0.45 mIU/L - 4.12
mIU/L-varies depending on lab)
◦ Myxedema – term used for severe hypothyroidism
– dermatologic changes that can occur (swelling in legs/eyes)
– coma that can occur as an extreme complication
— Subclinical Hypothyroidism (early hypothyroidism)
◦ Free thyroxine (fT4) is: normal
◦ Thyroid-Stimulating Hormone (TSH) is: elevated/high
◦ Mild to no symptoms of hypothyroidism
— Overt Hypothyroidism
◦ Free thyroxine (fT4) is: sub-normal/low
◦ Thyroid-Stimulating Hormone (TSH) is usually: elevated (normally > 10
U/ml)

44
Q

HYPOthyroidism Causes
— Worldwide:
(1)
— Iodine sufficient countries:

A

◦ Iodine deficiency

◦ Chronic Autoimmune Thyroiditis (AITD/Hashimoto’s)
– reaction against thyroglobulin or other thyroid tissue
– Women > Men
– Age
– Other autoimmune disorders
– Goiter may or may not be present

45
Q

Subjective Symptoms
— Causes low metabolic rate
— Common:

A

◦ Dry skin
◦ Cold sensitivity/intolerance
◦ Fatigue
◦ Muscle cramps
◦ Voice changes (hoarseness)
◦ Slow speech
◦ Constipation
◦ Weight gain
◦ Thickened skin (myxedema)

46
Q

Goal of therapy
(4)

A

— Restore euthyroid state
— TSH – usually 0.45 mIU/L - 4.12 mIU/L for reference population
— Alleviate symptoms
— Reduction in size of goiter (if present)
— Avoidance of overtreatment (iatrogenic thyrotoxicosis)

47
Q

Drug Therapy

A

— Levothyroxine/Synthroid (synthetic T4 ) – most common therapy
◦ usual dose 50-100 mcg
◦ lower doses in patients with coronary artery disease
— Liothyronine/Cytomel, Triostat (synthetic T3 )
— Liotrix / Thyrolar (4:1 ratio of synthtic T4 :T3 )
— Thyroid desiccated /Armour Thyroid (“natural” – pig - T4 +T3 )
— Clinical Pearls
◦ Dosing dependent on age, sex and body size
◦ Onset of action 1-2 weeks, full effects 4-6 week
◦ Take on an empty stomach 30-60 minutes before meals (in morning) and before
other medications!
◦ Recommended to a consistent product to minimize variability! (narrow
therapeutic index)
◦ Dangers of using thyroid supplementation for weight loss in euthyroid patients

48
Q

“Adverse Effects” of thyroid treatments

A
  • Too much or too little supplementation/thyroid hormone
49
Q

Drug Interactions with Thyroid Supplementation
— Interference with absorption
(5)
— Decreased hormone
production/secretion
(2)
— Peripheral metabolism of T4
(1)
— Altered secretion of TSH
(5)
— Increased clearance of T4
(2)

A

◦ Bile acid sequestrants
◦ PPIs
◦ Oral bisphosphonates
◦ Iron and calcium supplements
◦ Orlistat

◦ Amiodarone (can also cause
hyperthyroidism - iodine rich)
◦ Lithium

◦ Glucocorticoids, amiodarone

◦ Dopamine (and dopaminergic agonists)
◦ Glucocorticoids
◦ Octreotide
◦ St John’s Wort
◦ Amphetamine

◦ Many antiepileptics
◦ Quetiapine

50
Q

Levothyroxine – Narrow Therapeutic Index Drug
— Narrow therapeutic index (NTI) drugs
◦ Small differences in dose or blood concentration may lead to
serious therapeutic failures and/or adverse drug reactions that are
life-threatening or result in persistent or significant disability or
incapacity
— Evidence from studies hasn’t showing any clinical difference
in brand, generic or switching generic manufacturers
— Because absorption can be decreased by other vitamins,
minerals and/or medications, it’s recommended to be taken

A

on an empty stomach (usually in the morning), 30-60
minutes before food or other medication intake to
avoid erratic absorption

51
Q

Dental Implications
— Undiagnosed –
— Hyperthyroidism
(3)
— Hypothyroidism
(@)

A

be aware of hyper/hypo-thyroid symptoms and refer to
provider
◦ identification of enlarged thyroid/goiter

◦ increased sensitivity to sympathomimetic drugs/vasopressors such as
epinephrine - hypertensive crisis, tachycardia, and/or dysrhythmia
◦ decrease effectiveness of CNS depressants
◦ symptoms mistaken for anxiety

◦ increased respiratory and cardiac depression with benzodiazepines (diazepam,
alprazolam), barbiturates (sodium thiopental), and opioid analgesics
(hydrocodone)
◦ Over supplementation could result in cardiovascular symptoms seen in
hyperthyroidism

52
Q

Dental Implications
(3)

A

— If euthyroid (treated thyroid disorders) – manage normally
during dental interventions /treatment /procedures
— Hyper/hypo-thyroid symptoms - consider decreasing or
avoiding:
◦ sympathomimetics/ vasopressors in symptomatic hyperthyroidism
◦ CNS depressants in symptomatic hypothyroidism
— Severe/uncontrolled hyper/hypo-thyroid condition – consider
postponing dental treatment until consultation from provider
or condition better managed (may take weeks to months)

53
Q

Dental Implications
(2)

A

— On Propylthiouracil (PTU) or Methimazole (MMI) for
hyperthyroidism- caution with bleeding from
agranulocytosis or risk of infection from neutropenia
— Absorption issues or other drug interactions for patients
on thyroid supplementation

54
Q

— Corticosteroids – The good, the bad and the ugly
(3)

A

◦ Useful role in dental practice
◦ Caution with ADRs
◦ Long-term use = HPA Axis suppression

55
Q

— — for adrenal crisis in patients with Adrenal Insufficiency
only needed for patients undergoing major dental surgery
— Both (2) can impact dental care
decisions

A

Steroids
hyperthyroidism and hyperthyroidism

56
Q

◦ Hyperthyroidism
(1)
◦ Hypothyroidism
(2)

A

– Drug therapy may be used as bridge until surgery or radioactive iodine or may be
used long-term

– Levothyroxine mainstay of therapy
– Narrow therapeutic index drug/many drug interactions