1
Q
a form of congenital hypothyroidism where a child is born with an underactive or absent thyroid gland
A
cretinism
2
Q
a state of normal thyroid gland functioning
A
euthyroid
3
Q
a visible enlargement of the thyroid gland
A
goiter
4
Q
an autoimmune disorder that leads to hyperthyroidism, where antibodies stimulate the thyroid, causing excessive hormone production
A
graves’ disease
5
Q
a condition marked by the overproduction of thyroid hormones, often with an enlarged thyroid gland
A
hyperthyroidism
6
Q
a condition in which the thyroid gland produces insufficient thyroid hormones
A
hypothyroidism
7
Q
a form of hypothyroidism occurring after childhood, characterized by a range of symtpoms; more common in women
A
myxedema
8
Q
a life-threatening complication of severe hypothyroidism
A
myxedema coma
9
Q
a rare, life-threatening condition of extreme hyperthyroidism symptoms, often triggered by stress or inadequate treatment
A
thyroid storm/crisis
10
Q
inflammation of the thyroid gland, often autoimmune in origin, and a common cause of hypothyroidism
A
thyroiditis
11
Q
hormones produced by thyroid gland
A
- thyroxine (T4)
- triiodothyronine (T3)
- calcitonin
T3 is more potent and biologically active, with a faster onset but shorter duration than T4
12
Q
regulate metabolism, growth, and development, especially influencing the heart, skeletal muscles, liver, and kidneys
A
thyroid hormones
13
Q
Caused by excessive synthesis of thyroid hormones, often due to Graves’ disease or nodular thyroid goiter
A
hyperthyroidism
14
Q
- results from diminished thyroid hormone secretion. It may be primary (thyroid gland dysfunction) or secondary (pituitary or hypothalamic dysfunction)
- common causes include Hashimoto’s thyroiditis, treatment for hyperthyroidism, and certain medications like amiodarone or lithium.
A
hypothyroidism
15
Q
Growth of thyroid nodules causing hormone overproduction
A
nodular thyroid goiter
16
Q
caused by excessive thyroid drug therapy, functioning thyroid carcinoma, or pituitary adenomas
A
thyroiditis
17
Q
Characterized by reduced TSH levels and normal T3/T4 levels, typically caused by excess thyroid hormone therapy
risk factors: osteoporosis in postmenopausal women and AFib in individuals 60+
A
subclinical hyperthyroidism
18
Q
symptoms
- severe tachycardia
- fever
- dehydration
- heart failure
- coma
A
thyroid storm/crisis
19
Q
Occurs after ingestion of iodine-rich foods (e.g., seafood, kelp) or radiographic contrast dyes
A
iodine-induced hyperthyroidism
20
Q
- purpose: treats hyperthyroidsism, including graves’ disease, before surgery and after radioactive iodine therapy, and during thyroid storm
- action: inhibits thyroid hormone and conversion of T3 to T4, but doesn’t affect previously stored hormones, so effects take time (days to weeks)
may use a beta blocker like propanolol as adjunct for heart palpitations
A
anti-thyroid drugs
- propylithouracil (PTU)
- Methimazole
21
Q
adverse effects of antithyroid drugs
A
- adverse effects: signs of hypothyroidism - fatigue, slow HR, weight gain
- serious effects: liver toxicity, agranulocytosis (low wbc ct), rash, joint pain
22
Q
pt teaching for thyroid drugs (levothyroxine)
A
- lifelong therapy: don’t stop w/o consulting provider
- take med on empty stomach, avoid switching brands
- report sx of chest pain or heart palpitations
22
Q
pt teaching for antithyroid drugs
A
- therapy may take 1+ yr
- report any signs of fever, sore throat, or liver problems (dark urine, yellow skin)
23
Q
cautions for use of thyroid drugs (levothyroxine)
A
- dosage may change w/ growth in children
- start w/ lower doses to avoid CV risks in older adults
- monitor drug metabolism as it may be slower in liver-impaired pts
24
* **purpose:** a synthetic form of T4 used as replacement therapy for hypothyroidism
* **action:** increases metabolism, oxygen use, heart rate, and growth processes
levothyroxine (synthroid)
25
adverse effects of levothyroxine
* **adverse effects:** signs of hyperthyroidism (rapid HR, nervousness)
* **serious effects:** chest pain, heart issues, weight loss, heat intolerance
26
# caused by:
* chronic (hashimotos) thyroiditis
* treatment of hyperthyroidism
* radiation exposure, drugs like amiodarone, lithium, or iodine preparations
primary hypothyroidism
27
results from decreased TSH production by the anterior pituitary or decreased TRH from the hypothalamus
secondary hypothyroidism
28
* occurs when a child is born w/ a poorly functioning or absent thyroid gland; symptoms develop gradually in infancy/early childhood
* poor growth and development, lethargy, slow pulse, constipation, and subnormal temperature
* untreated cases can lead to irreversable mental retardation
congenital hypothyroidsim (cretinism)
29
* occurs after early childhood, more common in women
* can be subclinical (mildly elevated TSH w/ normal hormone levels) or clinical
* over time, may lead to a goiter d/t overstimulation of the thyroid gland by TSH
myxedema (adult hypothyroidism)
30
* a life-threatening complication of severe hypothyroidism
* pre-disposing factors: exposure to cold, infection, trauma, respiratory disease, and CNS depressants
myxedema coma
31
* coma
* hypothermia
* cardiovascular collapse
* hypoventilation
* severe metabolic disorders (hyponatremia, hypoglycemia, lactic acidosis)
myxedema coma
32
release of adrenal hormones is controlled by
* hypothalamic-pituitary-adrenal (HPA) axis
* renin-angiotensin-aldosterone system (RAAS)
33
* “Stress hormone” with 1:1 Glucocorticoid:Mineralocorticoid effect
* Both ACTH and cortisol levels rise to a peak in the morning (6:00
AM to 8:00 AM) and decline throughout the day, reaching their
nadir at around midnight
* Mineralocorticoid effects
* Glucocorticoid effects
cortisol
34
Maintains blood pressure by increasing sensitivity of blood
vessels to catecholamines (epinephrine and norepinephrine)
which narrow blood vessel lumen
mineralocorticoid effects of cortisol
35
glucocorticoid effects of cortisol
* Creates energy substrates -Increases gluconeogenesis, proteolysis, and lipolysis
* Dampens inflammatory and immune response: Reduces production of prostaglandins and interleukins; Inhibits T-lymphocytes
36
inactive prodrug that is converted into hydrocortisone, or cortisol, in the liver
cortisone
37
endogenous cortisol =
exogenous hydrocortisone
38
inactive prodrug that is converted into its active form, prednisolone, by liver enzymes
prednisolone
| In people with severe liver disease, prednisolone is usually preferred
39
considerations for cortisol treatment
* treatment: replacement or pharmacologic
* routes: topical, inhaled/nasal, oral, parenteral
* glucocorticoid vs mineralocorticoid action
40
* Immunologic (weakens immune system)
* Calcium wasting
* anti-inflammatory
* Neurologic
glucocorticoid effects
41
* Na+ retention
* K+ secretion
| controls BP
mineralocorticoid effects
42
* Pure glucocorticoid activity
* Useful for severe inflammation and/or nausea
* Ex: Meningitis or anti-emetic regimen
dexamethasone
43
* High glucocorticoid activity
* Useful for immunologic flares
* Ex: Multiple sclerosis, transplant rejection
* methylprednisolone
* prednisone
44
* Equal action (1 Glucocorticoid: 1 Mineralocorticoid)
* Useful for adrenal insufficiency
* Ex: Sepsis, Addison’s
hydrocortisone
45
* Only synthetic mineralocorticoid
* Useful for Addison’s disease:
* Treat hyperkalemia and
hypotension
| waste K+ and retain Na+
fludrocortisone
46
adverse effects of supraphysiological doses of glucocorticoids
* **short term use:** Na+ retention, water retention, psychosis, mood changes, poor wound healing, insomnia, hyperglycemia, ulcers (GI upset), increased appetite (weight gain)
* **long term use:** HTN, HLD, weight gain, adrenal suppressiion (needs tapered), cataracts, osteoporosis (Ca2+ wasting), acne, elevated insulin = fat accumulation
47
* supraphysiologic concentrations of glucocorticoids
* possible causes: Endogenous excess production of cortisol (Pituitary corticotrope adenoma = Cushing disease, Ectopic secretion of ACTH by nonpituitary tumor, Adrenocortical adenoma or carcinoma)
* Iatrogenic causes: (Supraphysiologic administration of exogenous glucocorticoids)
cushing syndrome
48
* mood disorders
* weakness and fatigue
* moon face
* redness of cheeks
* buffalo hump
* immunosuppression
* hypertension
* osteoporosis (increased ca2+ reabsorption from bone)
* adrenal hyperplasia
* amenorrhea
* easy bruising and thin skin
* hirsutism
* truncal obesity
* violaceous striae
* skin ulcers
* muscle loss
cushing syndrome
49
treatment of cushing syndrome (caused by endogenous reasons)
* First line = surgery (resection of tumor), chemotherapy, or radiation
* Pharmacotherapy -used to stabilize patients prior to surgery; used in patients waiting for potential response to chemotherapy or radiation; used if surgery is ineffective
50
pharmacotherapy options for treatment of cushing syndrome
* Drugs that inhibit adrenal hormone synthesis (prototype = Ketoconazole)
* Drugs that destroy adrenocortical cells (prototype = Mitotane)
* Drugs that inhibit ACTH secretion (prototype = Pasireotide)
* Glucocorticoid Receptor Antagonists (prototype = Mifepristone)
51
* **Drug Class:** antifungal agent, but Steroidogenesis Inhibitor at higher dose
* **MOA:** blocks production of cortisol and aldosterone, antiandrogenic activity
* Formulation: Oral (2-3 times daily); Take with acidic drinks to enhance absorption (do not take at same time as antacids); Take with food to prevent GI upset
* **Side effects:** elevation of hepatic transaminases / hepatotoxicity (biggest side effect), N/V; can cause gynecomastia and hypogonadism in men; teratogenic
Ketoconazole
*drugs that inhibit adrenal hormone synthesis*
52
* **Drug Class:** Adrenolytic Agent
* **MOA:** cytotoxicity – destroys cells within the adrenal gland; also increases extra-adrenal metabolism of exogenously
administered corticosteroids
Formulation: oral medication (taken three or four times daily) for at least 2 years
**Side effects:** significant neurologic and GI side effects; high doses of steroid replacement therapy often needed after therapy (prednisone or dexamethasone); avoid in pregnancy and breastfeeding
Mitotane
*drugs that destroys cells w/in the adrenal gland (antineoplastics)*
53
* **Drug Class:** Glucocorticoid-Receptor Blocking Agent
* **MOA:** Progesterone receptor antagonist used to terminate pregnancy; Also, a nonselective antagonist of glucocorticoid receptors - Causes INCREASE in ACTH and cortisol levels!!
* Formulation: Oral
* **Side effects:** Increases endogenous cortisol and ACTH levels; Fatigue, nausea, vomiting, arthralgias, headache, hypertension, hypokalemia, edema, endometrial thickening
mifepristone
*glucocorticoid receptor antagonists*
54
* Damage to adrenal glands themselves
* Effects both glucocorticoid and mineralocorticoid production (needs replacement)
primary adrenal insufficiency
| addison's disease
55
* Low ACTH causes reduced cortisol
* Effects JUST glucocorticoid production; aldosterone is normal
* pituitary
secondary adrenal insufficiency
56
* Decreased cardiac output
* Dehydration
* Weakness and fatigue
* Hypoglycemia
* Craving for salt
* Postural dizziness
* Women have diminished axillary and pubic hair (men do not have these effects as androgens produced in testes)
* hyperpigmentation in palmar creases, nail beds, mucous membranes
adrenal insufficiency
57
* GI sx (n/v, abd pain
* hyponatremia
* hyperkalemia
* hypotension
adrenal crisis
58
addison's disease treatment
## Footnote
primary adrenal insufficiency
Glucocorticoid plus Mineralocorticoid Replacement
59
treatment of secondary (pituitary) or teritiary (hypothalamic) adrenal insufficiency
glucocorticoid replacement
60
physiologic dosing of glucocorticoid replacemnt
* Hydrocortisone or cortisone
* initial dosing schedule: AM and then 8 hours later; Can be used two or three times daily
* **Goal:** establish lowest effective dose while mimicking the
normal diurnal adrenal rhythm
* **Monitor:** body weight, postural blood pressures, subjective energy levels, and signs glucocorticoid excess every 6 to 8
weeks to assess proper glucocorticoid replacement; Disappearance of hyperpigmentation and the resolution of electrolyte abnormalities are indicators of adequate replacement
61
* Triggered by anything that increases adrenal requirements dramatically
* Stressful situations, surgery, infection, and trauma
* HPA-axis suppression brought on by abrupt withdrawal of chronic glucocorticoid use
adrenal crisis
62
how do we prevent an adrenal crisis
* Additional 5 to 10 mg of hydrocortisone shortly before strenuous activities (exercise)
* Patients should be told to double their daily dose during times of severe physical stress such as febrile illnesses or injury
* For major trauma, surgery, or in critically ill patients, larger doses, up to 10 times the usual daily dose may be required.
63
mineralocorticoid replacement adrenal insufficiency
* Only needed for primary adrenal deficiency (Addison’s)
* Fludrocortisone acetate 0.05 to 0.2 mg once a day
* **Adverse effects** must be monitored closely and
include gastric upset, edema, hypertension, hypokalemia, insomnia, excitability, and diabetes mellitus. In addition, patient weight, blood pressure, and electrocardiogram should be monitored regularly
64
* Less than 20% produced in thyroid
* Majority is formed from breakdown of T4 in peripheral tissue
* More potent than T4
* More rapid onset but shorter duration of action
T3 (triiodothyronine - 3 atoms of iodine)
65
* Prohormone
* ONLY source is secretion from thyroid
T4 (thyroxine - 4 atoms of iodine)
66
production of thyroid hormones in thyroid depends on
presence of iodine and tyrosine
67
TRH
thyrotropin-releasing hormone (acts in hypothalamus)
68
TSH
thyroid-stimulating hormone (thyrotropin)
## Footnote
acts in pituitary gland
69
* Affects function of every organ system
* Critical for normal growth and development in childhood
* Maintains metabolic stability in adults
thyroid hormones
70
* overproduction of thyroid hormone by thyroid gland
* high T3 and T4
hyperthyroidism
71
high T3 and T4, low TSH
primary hyperthyroidism (Graves disease)
72
high T3 and T4, high TSH
secondary hyperthyroidism
## Footnote
maybe d/t a pituitary tumor
73
* caused by tissue exposure to excessive levels of T3 and T4
* symptomatic to high levels of these hormones
thyrotoxicosis
74
* **symptoms:** hyperactivity/irritability/dysphoria, heat intolerance/sweating palpitations, fatigue/weakness, weight loss w/ increased appetite, diarrhea, polyuria, menstrual disturbances/loss of libido, nervousness, anxiety, emotional lability
* **signs:** tachycardia - AFib, tremor of tongue or hands, thyromegaly/goiter, warm moist skin, muscle weakness/proximal myopathy, lid retraction/lag, gynecomastaia, fine hair, onycholysis, hyperactive DTRs, opthalamopathy/exopthalamos, pretibial myxedema
thyrotoxicosis
75
treatment goal for hyperthyroidism
* Reduce amount of thyroid tissue: Radioactive iodine, Thyroidectomy
* Reduce thyroid hormone synthesis – antithyroid medications
* Reduce symptoms: β-Blockers (propanolol, atenolol)
76
pros and cons to antithyroid meds
* Advantages: noninvasive, low initial cost, low risk of permanent hypothyroidism, possible remission due to immune effects
* Disadvantages: low cure rate (40-50%), adverse drug
reactions, adherence
77
how do we monitor levothyroxine tx in the lab
* Gradual dose increases until symptoms relieved and TSH is normal (driver of if dose is right)
* Check TSH and T4 no sooner than every 6 weeks after dose changes to assess effectiveness - Allows for steady state
78
levothyroxine interactions
* **Decreased absorption:** Acid suppression with antacids, histamine blockers and proton pump inhibitors, Ferrous sulfate, Sucralfate
* **Increased clearance:** Rifampin, Carbamazepine, Phenytoin
* **Block conversion of T4 to T3:** Amiodarone, Selenium deficiency
79
PK of levothyroxine
* Half-life: approximately 7 days; Stable pool of prohormone, Once daily dosing
* Food impairs absorption of T4 – Traditionally administered on empty stomach to increase absorption; Take 30 minutes prior to breakfast for new starts
* Reformulation allows for improved bioavailability: about 80%
* If patient’s TSH is stable on a dose taken with meals, do
not change time of administration
* Metabolized in liver and excreted in urine
* **Side Effect** = Signs and symptoms of hyperthyroidism
* Formulations: Oral and IV
80
hypothyroid tx
* Replacement of thyroid hormone is cornerstone of treatment
* Drug of choice: Levothyroxine (synthetic T4)
81
elevated TSH and low T3 and T4
hypothyroidism
82
* **symptoms:** Dry skin, Cold intolerance, Weight gain, Constipation, Weakness
* **signs:** Weakness – proximal muscles affected more than distal; Slow relaxation of deep tendon reflexes; Coarse skin and hair; Cold/dry skin; Periorbital puffiness; Bradycardia; Speech: slowed and hoarse; Reversible neurologic syndromes; Goiter – due to overstimulation of TSH
hypothyroidism
83
* **Used for β-adrenergic mediated symptoms: palpitations, anxiety, tremor, heat intolerance**
* Propranolol dose: 20-40 mg every 6-8 hours - 240-480 mg/day may be required for younger or severely toxic patients
* Atenolol preferred by some providers for once daily dosing
* **Contraindications:** Decompensated heart failure unless caused solely by tachycardia, Sinus bradycardia, MAOI or TCA therapy, Spontaneous hypoglycemia
* **Side effects**: n/v, anxiety, insomnia, light-headedness, bradycardia, hematologic disturbances
beta blockers
84
adverse effects of antithyroid medications
* Signs and symptoms of hypothyroidism
* Benign transient leukopenia (WBC <4,000/mm3)
* Pruritic maculopapular rash
* Arthralgias
* Fever
* Agranulocytosis – serious - D/c therapy and contact provider for flulike sx (fever/malaise/sore throat) and get labs
85
* Inhibit both the organification of iodine to tyrosine and
therefore new formation of thyroid
hormone in the thyroid
PTU also inhibits peripheral conversion of T4 to T3
antithyroid medications
thionamide class
* methimazole (MMI)
* propylthiouracil (PTU)
## Footnote
Therapeutic effect in 1-2 weeks, but euthyroid state may not occur for 6-8 weeks
86
* first-line pharmacotherapy for hyperthyroidism
* once a day dosing
* long half-life
methimazole (MMI)
87
* second line pharmacotherapy for hyperthyroidism
* Use limited by hepatotoxicity
* Requires dosing 3-4 times per day
* Preferring first trimester of pregnancy (less teratogenic)
propylthiouracil (PTU)
88
Which of the following agents has glucocorticoid activity and lacks mineralocorticoid activity?
dexamethasone
89
Which of the following is an adverse effect you might expect after taking Prednisone 60 mg (a supraphysiologic dose) for 3 days?
hyperglycemia
90
Your patient is diagnosed with a tumor in his adrenal gland and he is prescribed mifepristone since he is currently not stable for surgery. Which of the following best describes the mechanism of action of mifepristone?
acts as a glucocorticoid receptor antagonist
91
Which of the following is a clinical manifestation of Addison's disease but not secondary adrenal insufficiency?
hyperpigmentation
92
If a patient with Addison's disease is going for major surgery, which of the following orders would you expect?
give a dose of hydrocortisone that is 8-10x the patient's usual dose prior to surgery
93
Which of the following is always true in patients with hyperthyroidism?
T4 levels will be high
94
Which of the following best describes the primary mechanism of action of radioactive iodine?
reduce amount of thyroid tissue
95
Which of the following is associated with hepatotoxicity as an adverse effect?
propylithiouracil
96
Which of the following best describes levothyroxine?
synthetic T4
97
When should someone who is newly started on levothyroxine ideally be educated to take it?
At least 30 minutes before breakfast
Pharm
flashcards
Decks in class (19)
# Cards
-
Chapter 150
-
Cell and Pharmacokinetic/Dynamic Basics79
-
Autonomic Nervous System150
-
medication administration, ATL, immunizations74
-
dosage calc12
-
cardiovascular agents and anti-hypertensives101
-
lipid-modifying agents pharmacology39
-
pharmacology of antiplatelets, anticoagulants, and fibrinolytics62
-
diabetes106
-
endocrine98
-
respiratory181
-
GI146
-
liver/renal57
-
neuro pathophys70
-
az/pd53
-
anti-epileptics72
-
anti-psychotics67
-
pain and opioids62
-
immune/heme38
