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Pharmacology Test 3 > thyroid and adrenal conditions > Flashcards

thyroid and adrenal conditions Flashcards

1
Q

what is mild deficiency of thyroid hormone referred to as in adults?

A

hypothyroidism

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2
Q

what is severe deficiency of thyroid hormone referred to as in adults?

A

myxedema

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3
Q

what is hypothyroidism called in infants?

A

cretinism

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4
Q

clinical presentation of hypothyroidism in adults

A
  • S/S depend on dz severity
  • face is pale, puffy, expressionless
  • skin is cold and dry
  • hair is brittle and hair loss occurs
  • HR and temp are decreased
  • lethargy, fatigue
  • intolerance to cold
  • goiter is reduced levels of T3 and T4 promote excessive release of TSH
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5
Q

causes of hypothyroidism in adults

A
  • due to malfunction of the thyroid itself
    • in iodine sufficient countries, the cause is often chronic autoimmune thyroiditis (Hashimoto’s thyroiditis)
    • insufficient iodine in the diet
    • surgical removal of thyroid
    • destruction of thyroid by radioactive iodine
    • insufficient secretion of TSH, TRH
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6
Q

therapeutic strategy for hypothyroidism in adults

A
  • requires replacement therapy with thyroid hormones
  • tx is lifelong
  • std regimen is often levothyroxine (T4) alone
    • also can combne with liothyronine (T3)
    • but have seen no advantage of T3 with T4 OVER T4 alone
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7
Q

hypothyroidism in pregnancy

A
  • can result in permanent neuropsychologic deficits in the child
    • impact mostly limited to first trimester when fetus is unable to produce thyroid Hs of its own
      • so to prevent any problems, should be diagnosed early, but often S/S are nonspecific
      • so, some recommend to routinely check for hypothyroidism
  • congenital hypothyroidism can cause developmental problems
  • when women taking thyroid supplements become pregnant, dosage requirements often inc by as much as 50%
    • need for inc begins at 4-8 weeks gestation, and levels off around week 16
  • must monitor TSH closely
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8
Q

clinical presentation of hypothyroidism in infants

A
  • can be permanent or transient
  • delay in mental development
  • derangement of growth
  • large and protruding tongue
  • potbelly
  • dwarfish stature
  • development of nervous system, bones, teeth, and muscles is impaired
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9
Q

causes of hypothyroidism in infants

A
  • failure of thyroid development
  • autoimmune disease
  • severe iodine deficiency
  • TSH deficiency
  • exposure to radioactive iodine in utero
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10
Q

therapeutic strategy of hypothyroidism in infants

A
  • requires replacement therapy with thyroid Hs
  • if initiated w/in a few days of birth, physical and mental development will be normal
    • but if delayed beyong 3-4 weeks, some permanent disability will be evident
  • tx should continue for at least 3 years, then stop for 4 weeks to determine if deficiency is transient or permanent
    • if TSH rises, then we know thyroid production is low, and deficiency is permanent, so need replacement therapy
    • if TSH and T4 normalize, we know deficiency is transient, and no further replacement therapy
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11
Q

2 types of hyperthyroidism

A
  • Graves disease
    • more common
    • can cause exophthalmos
  • toxic nodular goiter
    • does not cause exophthalmos
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12
Q

Graves disease: population

A
  • women ages 20-40 years
    • incidence in females is 6x greater than males
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13
Q

Graves disease: clinical presentation

A
  • most result from elevated levels of thyroid hormone
    • heartbeat is rapid and strong
    • dysrhythmias
    • angina
    • CNS is stimulated–>nervousness, insomnia, rapid thought flow, rapid speech
    • skeletal muscles weaken and atrophy
    • metabolic rate is inc–>inc heat production, inc body temp, intolerance to heat, warm/moist skin
    • inc appetite
    • weight loss
      • all of the above are called thyrotoxicosis
    • exophthalmos
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14
Q

Graves disease: cause

A
  • caused by thyroid stimulating immunoglobulins (TSIs) which are antibodies produced by an autoimmune process
    • TSIs inc thyroid activity by stimulating receptors for TSH on the thyroid gland
      • so, TSIs mimis theeffects of TSH on thyroid fcn
    • TSIs are not responsible for exophthalmos
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15
Q

Graves disease: treatment

A
  • directed at dec the production of thyroid hormones
    • surgical removal of thyroid tissue
    • destruction of thyroid tissue w/ radioactive iodine
    • suppression of thyroid hormone synthesis with an antithyroid drug (methimazole or PPU)
      • preferred to use radiation for adults and antithyroid drugs for younger pts
  • can also use beta blockers (to suppress tachycardia) and nonradioactive iodine (to inhibit release of thyroid Hs) as adjunctive therapy
  • exophthalmos is not result of hyperthyroidism so can’t treat by lower thyroid H levels
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16
Q

Toxic Nodular Goiter (Plummer’s Disease)

A
  • result of a thyroid adenoma
  • S/S: same as Graves Dz, except no exophthalmos
  • persistent condition that rarely undergoes spontaneous remission
  • tx: same as Graves dz
    • if antithyroid drug is used, symptoms return rapidly when the drug is withdrawn
    • use sugery or radiation for long term control
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17
Q

Thyrotoxic Crisis (Thyroid Storm): S/S

A
  • can occur in pts with severe thyrotoxicosis when they undergo major surgery or develop a severe intercurrent illness
  • syndrome characterized by profound hyperthermia, tachycardia, restelessness, agitation, and tremor
    • may also have unconsciousness, coma, hypoTN, HF
      • all produced by excessive levels of thyroid Hs
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18
Q

Thyrotoxic Crisis: tx

A
  • can be life threatening
    • need to suppress thyroid H release by using potassium iodide or a strong iodine soln
    • methimazole is given to suppress thyroid H synthesis
    • beta blocker given to reduce HR
19
Q

Cushing’s Syndrome: causes

A
  • hypersecretion of ACTH by pituitary adenomas
  • hypersecretion of glucocorticoids by adrenal adenomas and carcinomas
  • administering glucocorticoids in large doses used to treat arthritis
    • S/S are due to excess levels of glucocorticoids
20
Q

Cushings Syndrome: clinical presentation

A
  • hyperglycemia
  • glycosuria
  • HTN
  • fluid and electrolyte disturbances
  • osteoporosis
  • muscle weakness
  • myopathy
  • hirsutism
  • menstrual irregularities
  • dec resistance to infection
  • stretch marks
  • inc susceptibility to injury
  • fat goes to abdomen (potbelly), face (moon face), and back (buffalo hump)
21
Q

Cushings Syndrome: treatment

A
  • for adrenal adenoma/carcinoma: surgical removal of adrenal gland
    • if have to remove both adrenal glands, then need to give glucocorticoids and mineralocorticoids
  • if inoperable, use mitotane which is an anticancer drug to destroy adrenal cells
  • for pituitary adenoma: surgical removal of part of pituitary
  • can use drugs along with surgery but not by themselves
    • most effective is ketoconazole which blocks glucocorticoid synthesis
22
Q

Primary Hyperaldosteronism: clinical presentation

A
  • hypokalemia
    • muscle weakness
    • EKG changes
  • metabolic alkalosis
  • HTN
  • inc risk for HF
23
Q

Primary Hyperaldosteronism: causes

A
  • aldosterone producing adrenal adenoma
  • bilateral adrenal hyperplasia
24
Q

Primary Hyperaldosteronism: diagnosis

A
  • diagnosed by determining the ratio of plasma aldosterone concentration to plasma renin activity
25
Q

Primary Hyperaldosteronism: treatment

A
  • mgmt depends on the cause:
    • adrenal adenoma: surgical resection
    • bilateral adrenal hyperplasia: aldosterone antagonist, usually spironolactone
  • may need a diuretic to help with HTN
26
Q

adrenal hormone insufficiency

A
  • can result from destruction of the adrenals, inborn deficiencies of enzymes required for glucocorticoid synthesis, or reduced secretion of ACTH/CRH
  • need lifelong therapy:
    • REQUIRES a glucocorticoid
      • prednisone, hydrocortisone, and dexamethosone are the best
    • some may require a mineralocorticoid
      • fludrocortisone is the best
27
Q

adrenal hormone insufficiency: replacement therapy

A
  • the therapy needs to mimic normal patterns of glucocorticoid secretion
    • levels of glucocorticoids normally peak in the morning
      • so take the entire dose immediately after waking up
      • alternative: to divide daily dose giving 2/3 in the morning and 1/3 in afternoon
  • give mineralocorticoids 1x daily
28
Q

adrenal hormone insufficiency: stress

A
  • with normal healthy adrenals inc their output of glucocorticoids in response to stress
    • for pts with adrenal insufficiency, need to give extra glucocorticoids in times of stress
  • for mild or febrile illness, the 3 by 3 rule applies
    • take 3x the usual dosage for 3 days
29
Q

adrenal hormone insufficiency: glucocorticoids in emergencies

A
  • to ensure availability of glucocorticoids in amergencies, pts should carry an adequate supply at all times
    • supply should be an injectable preparation and an oral preparation
  • pt should wear a medic alert bracelet
30
Q

what is Addison’s Disease?

A

primary adrenocortical insufficiency

31
Q

Addison’s Disease: causes

A
  • adrenal glands are damaged and unable to make glucocorticoids
  • most cases caused by autoimmune destruction of adrenal tissue
    • the other 15% is caused by TB
  • other causes: hemorrhage, cancer, certain drugs (ketoconazole)
32
Q

Addison’s Disease: clinical presentation

A
  • anorexia
  • nausea
  • vomiting
  • diarrhea
  • weight loss
  • weakness
  • emaciation
  • abdominal pain
  • hypotensive crisis
  • hyperkalemia
  • hyponatremia
  • hyperpigmentation of the skin/mucous membranes
  • excessive production of ACTH in an attempt to restore depressed levels of glucocorticoids
33
Q

Addison’s Disease: tx

A
  • replacement therapy with adrenocorticoids
    • hydrocortisone is drug of choice
  • if need additional mineralocorticoid activity, fludrocortisone is added
34
Q

secondary adrenocortical insufficiency: cause

A
  • decreased secretion of ACTH
    • adrenal secretion of glucocorticoids is diminished
35
Q

tertiary adrenocortical insufficiency: cause

A
  • decreased secretion of CRH
    • adrenal secretion of glucocorticoids is diminished
36
Q

secondary and tertiary adrenocortical insufficiency: S/S

A
  • hypoglycemia
  • malaise
  • loss of appetite
  • reduced capacity to respond to stres
37
Q

secondary and tertiary adrenocortical insufficiency: tx

A
  • replacement with glucocorticoids
    • ie. hydrocortisone
38
Q

acute adrenal insufficiency (adrenal crisis): clinical presentation

A
  • hypoTN
  • dehydration
  • weakness
  • lethargy
  • GI symptoms: vomiting, diarrhe
  • can progress to shock and death
39
Q

acute adrenal insufficiency (adrenal crisis): causes

A
  • adrenal failure
  • pituitary failure
  • failure to provide patients receiving replacement therapy with adequate doses of glucocorticoids
  • abrupt withdrawal from high dose glucocorticoid therapy
40
Q

acute adrenal insufficiency (adrenal crisis): treatment

A
  • rapid replacement of fluid, salt, and glucocorticoids
  • also need glucose for energy
    • inject 100 mg of hydrocortisone followed by IV infusion of normal saline with dextrose
41
Q

congenital adrenal hyperplasia: clinical presentation

A
  • in females: inc androgen levels cause masculinization of external genitalia, but ovaries/uterus/fallopian tubes are not affected
  • in males: inc androgen levels may cause precocious penile enlargement
  • in children, linear growth is accelerated
    • but adult height is usually diminished b/c androgens cause premature closure of the epiphyses
42
Q

congenital adrenal hyperplasia: causes

A
  • result from an inborn deficiency of enzymes needed to make glucocorticoids
    • especially 21 alpha hydroxylase
  • ability to make glucocorticoids is reduced
  • in order to try to enhance glucocorticoid synthesis, pituitary releases large amts of ACTH which acts on adrenals –> inc growth of adrenal tissue and inc synthesis of glucocorticoids and androgens
    • amts of ACTH required for normalization are so large that synthesis of adrenal androgens becomes excessive
43
Q

congenital adrenal hyperplasia: treatment

A
  • goal is to ensure adequate levels of glucocorticoids while preventing excessive production of adrenal androgens
    • so use lifelong glucocorticoid replacement: hydrocortisone, dexamethasone, prenisone
  • by giving glucocorticoids endogenously, we can suppress secretion of ACTH
    • so adrenals no longer stimulated to produce excessive quantities of androgens
  • so suppression of ACTH achieved by daily doses of hydrocortisone equivalent to twice the amt secreted by normal adrenals
44
Q

congenital adrenal hyperplasia: screening

A
  • recommends universal screening of newborns for 21 alpha hydroxylase deficiency
    • if positive, follow up testing to confirm CAH deficiency

Pharmacology Test 3 (10 decks)

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