thyroid and adrenal conditions Flashcards
1
Q
what is mild deficiency of thyroid hormone referred to as in adults?
A
hypothyroidism
2
Q
what is severe deficiency of thyroid hormone referred to as in adults?
A
myxedema
3
Q
what is hypothyroidism called in infants?
A
cretinism
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
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
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
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
- impact mostly limited to first trimester when fetus is unable to produce thyroid Hs of its own
- 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
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
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
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
11
Q
2 types of hyperthyroidism
A
- Graves disease
- more common
- can cause exophthalmos
- toxic nodular goiter
- does not cause exophthalmos
12
Q
Graves disease: population
A
- women ages 20-40 years
- incidence in females is 6x greater than males
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
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
- TSIs inc thyroid activity by stimulating receptors for TSH on the thyroid gland
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
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
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
- may also have unconsciousness, coma, hypoTN, HF
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
- REQUIRES a glucocorticoid
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
- levels of glucocorticoids normally peak in the morning
- 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
