Endocrine: Thyroid + Adrenal D/o Flashcards
1
Q
Normal amount of thyroid hormone is produced via daily absorption of:
A
150 - 200 micrograms of iodide
2
Q
Functional units of the thyroid
A
Follicles
Tiny, saclike structures that comprise the thyroid gland, a shield-like structure below the larynx.
3
Q
What hormone?
Increases metabolism and protein synthesis in most tissues.
Necessary for brain development + growth.
Only the free hormone enters cells and regulates pituitary feedback mechanisms.
A
Thyroid hormones.
TRH is made in the hypothalamus and controls release of TSH.
4
Q
Thyroid hormone actions on metabolism
A
Increase glucose absorption. Increase glycogenolysis Increase gluconeogenesis Increase lipolysis Increase protein synthesis + degradation (net catabolic)
5
Q
Thyroid lab used to differentiate b/n primary and secondary thryoid d/o
A
TSH
6
Q
Active thyroid hormone
A
T3
7
Q
Inactive thyroid hormone; what does it need to be converted to?
A
T4 = inactive; needs to be converted to T3
8
Q
Thyroid lab that measures unbound T4 that is free to enter the cells
A
Free T4
9
Q
TSH levels in primary hypothyroidism
A
Increased
10
Q
TSH levels in primary hyperthyroidism
A
Decreased
11
Q
TSH levels in secondary hypothyroidism
A
Decreased
12
Q
T3, T4, and free T4 decreased in:
A
primary hypothyroidism
13
Q
Free T4 levels in hyperthyroid
A
Increased
14
Q
FNA biopsy used to differentiate
A
between benign vs malignant thyroid disease
15
Q
Causes of hypofunction of endocrine glands
A
Congenital defects
Ischemia, Infx, Inflammation, autoimmune, neoplasms, age, atrophy d/t drugs, receptor defects, inactive hormones
16
Q
Causes of hyperfunction of endocrine glands
A
Excess hormone production d/t stimulation + hyperplasia, exogenous hormone use
17
Q
T4+T3 and TSH levels for: Primary Hyperthyroidism
A
Increased T4+T3
Decreased TSH
18
Q
T4+T3 and TSH levels for: Secondary Hyperthyroidism
A
Increased T4+T3
Increased TSH
19
Q
T4+T3 and TSH levels for: Primary Hypothyroidism
A
Decreased T4+T3
Increased TSH
20
Q
T4+T3 and TSH levels for: Secondary Hypothyroidism
A
Decreased T4+T3
Decreased TSH
21
Q
Clinical manifestations of hypothyroidism
A
Hair loss, apathy, lethargy, dry skin, muscle aches + weakness, constipation, intolerance to cold, receding hairline, facial + eyelid edema, dull-blank expression, extreme fatigue, thick tongue-slow speech, anorexia, brittle nails + hair, menstrual disturbances
22
Q
Late clinical manifestations of hypothyroidism
A
Subnormal temp, bradycardia, weight gain, decreased LOC, thickened skin, cardiac complications
23
Q
Neonatal hypothyroidism treatment
A
Thyroid replacement (esp T4) needs to be initiated w/in first 6 weeks of life to avoid cretinism, mental retardation + growth retardation
24
Q
Acquired hypothyroidism causes
A
- Hashimoto’s thyroiditis: autoimmune; Ab against TPO + TG
- Iodide deficiency: decreases thyroid hormone synthesis ,neg feedback and increases TSH production; can cause goiter
- Primary Hypothyroidism: more common than 2o or 3o; may result from radioablation; Hashimoto’s is a subset of primary hypothyroidism
25
Hashimoto's is a subset of:
Primary hypothyroidism
26
Most common cause of hypothyroidism
Hashimoto's disease. F>M, increase w/ age. Other causes: thyroidectomy, RAI tx. 2o hypothyroidism uncommon.
27
Dx of acquired hypothyroidism. Clinical sx, Lab findings in primary vs secondary?
Clinical sx, diffuse goiter, prior hx of RAI or thyroid surgery.
- Primary: Increased TSH, Decreased free T4, Increased cholesterol.
- Secondary: low or normal TSH, decreased free T4
28
Treatment of acquired hypothyroidism
Levothyroxine (synthroid): usual starting dose in healthy adult: 100 mcg. Elderly 50 mcg. Cardiac dz: 25-50 mcg.
29
In primary hypothyroidism, monitor therapy w/:
TSH
30
In secondary hypothyroidism, monitor therapy w/:
free T4
31
Hashimoto's thyroiditis treatment:
T4 (levothyroxine, synthroid) 75-150 mcg PO QD. Take 30 min before meal.
32
Life-threatening, end stage hypothyroidism. Sx: coma, hypothermia, lactic acidosis, CV collapse, metabolic d/o.
Myxedematous coma
33
Three aspects of myxedematous coma
CO2 retention + hypoxemia, fluid + electrolyte imbalance, hypothermia. Most often in elderly women w/ chronic hypothyroidism; most often in winter
34
Tx of myxedematous coma
Supportive therapy; tx electrolyte abnormalities, thyroid replacement therapy, PASSIVE rewarming
35
Sx include: finger clubbing, tremors, increased diarrhea, menstrual changes, intolerance to heat, fine-straight hair, bulging eyes, facial flushing, enlarged thyroid, tachycardia, increased systolic BP, breast enlargement, weight loss, muscle wasting, localized edema
Hyperthyroidism
36
Causes of hyperthyroidism
1. thyroid over-secreting thyroid hormone (MC Graves)
2. pituitary over-stimulates thyroid
3. some exogenous source of thyroid hormone is being produced or iodide-containing agents being taken/ administered
37
MC etiology of hyperthyroidism
Graves disease
38
PE findings for Graves Dz
diffuse goiter +/- thyroid bruit; ophthalmopathy or dermopathy
39
What antibodies in Graves disease?
anti-TSH receptor antibodies
40
Decreased RAI uptake in?
thyroiditis + hypothyroid d/o
41
Which hyperthyroid drug blocks conversion of T4 to T3 in tissues?
PTU
42
Tx of Graves dz
Beta blockers (Propranalol) for tachycardia; temp tx w/ methimazole or PTU. Definitive tx: RAI - followed by T4
43
Tx of Toxic MNG or adenoma
RAI except in pregnancy
44
Thyroid nodule that becomes independent of the pituitary and secretes excess thyroid hormone
Toxic nodule; another cause of hyperthyroidism
45
Ovarian tumor that secretes thyroid hormone
Struma ovarii; another cause of hyperthyroidism
46
Life-threatening thyrotoxicosis. Rare but when it does occur, its in pts who have not been dx or those who are not being tx'd after dx
Thyroid storm
47
Sx: high fever, tachycardia, CHF, angina, severe CNS effects. High mortality rate
Thyroid storm
48
Thyroid Storm tx
Peripheral cooling (avoid shivering), supportive measures, IVFs, correct electrolyte d/o, beta blocker, glucocorticoids, PTU or methimazole
49
What drug to avoid in thyroid storm
ASA
50
Inflammation; can cause hypo or hyperthyroidism. Can cause px + enlargement of thyroid
Thyroiditis. Can be Hashimoto's but also can be caused by viral infx, radiation, amiodarone, autoimmune and delivery of baby
51
Tx of thyroiditis
NSAIDs, steroids, treat hypo- or hyper-thyroidism
52
MC thyroid cancer
Papillary carcinoma 75%, then follicular; well-differentiated
53
Thyroid cancer that originates from parafollicular cells in thyroid gland
Medullary carcinoma; genetic component; tx: total thyroidectomy + LN dissection; tumor does not concentrate iodine thus RAI not used
54
Thyroid cancer w/ poorest prognosis
Anaplastic carcinoma
55
Adrenal glands secrete what hormones
Aldosterone, Glucocorticoids (cortisol), adrenal androgens(DHEA + DHEAS), NE + epi
56
Zona glomerulosa secretes
aldosterone (a mineralocorticoid)
57
Zona fasciculata secretes
cortisol (a glucocorticoid)
58
What secretes EPI + norepi
Adrenal medulla
59
Aldosterone is regulated by:
RAA system and/or hyperK+
60
Cortisol secretion is stimulated by
secretion of ACTH from pituitary
61
What is given in suppression testing for adrenal function?
dexamethasone (glucocorticoid) -- to measure negative feedback suppression of ACTH
62
What is given in stimulation testing for adrenal function?
ACTH - to assess response of adrenal cortex to stimulation
63
What test is the gold standard for assessing HPA Axis?
Insulin-induced hypoglycemic test
64
Dexamethasone Suppression Testing is used to assess
Cushing dz vs syndrome.
| Types of testing include: low-dose overnight, standard low-dose, High-dose overnight and standard high-dose
65
Clinical manifestations of glucocorticoid excess; elevation in cortisol
Cushing Syndrome. Most commonly d/t iatrogenic causes, 2o to exogenous use of prednisone
66
Endogenous form of Cushing Syndrome w/ bilateral adrenal hyperplasia and increased cortisol and adrenal androgens. What type of tumor and what is the treatment?
Cushing disease; pituitary adenoma secreting ACTH. Tx: transsphenoidal resection
67
Endogenous form of Cushing Syndrome caused by small cell lung carcinoma; this type of tumor usually obvious.
Ectopic ACTH-secreting tumors. Tx: chemo
68
Endogenous form of Cushing Syndrome with increased cortisol, negative feedback inhibits ACTH. What type of tumor and what is the tx?
Adrenocorticol tumor. Tx: surgery
69
Cushing Syndrome xray will reveal:
osteoporosis w/ vertebral fractures
70
Cushing Syndrome labs: (BS, K+, pH?)
increased blood sugar
decreased K+
alkalosis
71
Cushing Syndrome labs:
- 24 hr urine collection for free cortisol
- Saliva cortisol test at night
both elevated
72
Cushing Syndrome ACTH serum level (independent vs dependent)
Decreased in ACTH-independent.
| Elevated in ACTH-dependent Cushing syndrome/ dz
73
What is an abnormal low dose dexamethasone suppression test?
No change in ACTH = Cushing syndrome. but won't know source unless do high dose test.
74
Suppression test results for ACTH-hypersecreting pituitary
Low ACTH from high dose dexamethasone suppression + High cortisol
75
Suppression test results for ectopic site? (ACTH, cortisol)
Normal ACTH and high cortisol
76
Normal values for overnight and standard high dose dexamethasone suppression test
Overnight: higher than 50% reduction in plasma cortisol.
Standard: higher than 90% reduction in urinary free cortisol.
77
High dose dexamethasone suppression test for Cushing syndrome caused by an adrenal tumor:
ACTH level: low; in most cases, high-dose test is not needed
78
High dose dexamethasone suppression test for Cushing syndrome caused by an ectopic ACTH-producing tumor:
High-dose test: ACTH no change
79
High dose dexamethasone suppression test for Cushing syndrome caused by a pituitary tumor:
High-dose test: ACTH low
80
Cushing syndrome tx
Surgical removal or radiation of offending tumor, maybe RADn, or tapering of glucocorticoid therapy if Cushings is iatrogenic. Meds that block steroid synthesis can be used: mitotane, ketoconazole, metyrapone
81
Meds that block steroid synthesis in Cushing Syndrome:
mitotane, ketoconazole, metyrapone
82
Hypercortisolism resulting from ACTH-secreting pituitary adenoma. And Tx?
Cushing Disease. Tx: transsphenoidal removal then replacement of cortisol for 6-12 months +/- pituitary radiation
83
Labs for primary adrenal failure (ACTH, cortisol, aldosterone):
Increased ACTH
Low cortisol
Low aldosterone
84
Labs for secondary adrenal failure (ACTH, cortisol, aldosterone)
Decreased ACTH
Low cortisol
Normal aldosterone
85
Adrenal insufficiency causes
1. problem w/ one or both glands (primary)
2. lack of ACTH stimulation from pituitary (secondary)
3. lack of CRH from hypothalamus (tertiary insufficiency)
86
Cortisol levels for adrenal insufficiency are:
LOW
87
Aldosterone level in primary and secondary insufficiency
Primary: low
Secondary: normal
88
Why is aldosterone normal in secondary insufficiency?
Because RAA axis still works.
89
MC cause of secondary adrenal insufficiency
withdrawal from steroids
90
Adrenal insufficiency sx
fatigue, weakness, LH, hair loss, dehydration, HYPOGLYCEMIA, anemia and weight loss
91
Adrenal insufficiency - ACTH stimulation "Cort stim" test. If cortisol levels increase it means? If it doesn't increase?
If it does increase, means the problem is 2o or 3o because gland wasn't being stimulated. If it doesn't increase, means problem is 1o because gland isn't able to respond.
92
Primary or Secondary insufficiency?
Low cortisol, low aldosterone, increase ACTH, hyperpigmentation, increased K+ w/ volume depletion, hyponatremia d/t lack of aldosterone + orthostatic HoTN d/t sodium wasting
Primary
93
Primary or Secondary insufficiency?
| Decreased ACTH, aldosterone is normal
Secondary
94
Primary or Secondary insufficiency? Melanocyte stimulating hormone (MSH) is increased.
Primary. bc/ of the increase of ACTH (the two share the same precursor)
95
Primary adrenal insufficiency treatment
Replace cortisol (prednisone 5mg PO QAM and 2.5 mg PO QPM) PLUS replace aldosterone (fludrocortisone 0.1 mg PO QD) regulated according to volume status, BP and K.
96
Secondary or tertiary adrenal insufficiency treatment
No need for mineralocorticoid replacement. Replace glucocorticoid (ex hydrocortisone w/ increased dose for stress
97
Mild illness treatment for adrenal insufficiency
Double or triple replacement of cortisol
98
Severe illness tx for adrenal insufficiency
10x regular dose ("stress doses") hydrocortisone 50 mg IV Q8H
99
Life threatening. Usually precipitated by illness or stress. Onset may be sudden or over several days. S/S: n/v, weakness, HoTN, dehydration, vascular collapse
Acute adrenal crisis
100
Acute adrenal crisis labs
Low cortisol
Low aldosterone
High ACTH
101
Acute adrenal crisis treatment
IVFs (D5NS), glucocorticoids IV then advance to PO as tolerated; once the initial doses of glucocoricoids are being reduced, then add a mineralocorticoid as well; cover w/ abx
102
Tumor w/ oversecretion of catecholamines (epinephrine) --> vasoconstriction + HTN
Pheochromocytoma
103
Adrenal medulla pheochromocytoma
usually benign unilateral and intra-adrenal
104
Episodes of sweating, palpitations, HA, tremor + tachycardia occurring paroxysmally. Increased BP during attack; only 10% normotensive b/n attacks
Pheochromocytoma
105
Labs: Increased blood sugar and urine catecholamines
Pheochromocytoma
106
Pheochromocytoma tx
SURGERY. Req pre-op alpha adrenergic blocker (phenoxybenzamine) + beta blocker (propranolol/ labetalol/ metoprolol)
107
What happens if you give beta antagonist alone in pheochromocytoma?
Causes worsening HTN d/t vasodilation being inhibited + alpha receptors not being stimulated; must give BB + alpha adrenergic blocker to prevent worsening rebound sx
108
Rules of 10%?
10% bilateral, 10% not in adrenal gland, 10% malignant. Pheochromocytoma.
109
Increase in aldosterone. Occurs if the adrenal glands themselves hypersecrete or if the adrenal glands are stimulated by the RAA system, hyperK, hypoNa, or HoTN. Can cause hyperNa, hypoK, and HTN
Hyperaldosteronism
110
MC cause of primary hyperaldosteornism
Conn's syndrome. one or both of adrenal glands are hyperactive. Causes Na+ and water retention w/ volume expansion and increase BP. No edema.
111
What should you be suspicious of in patient w/ increased BP and low K+ (not on diuretic)
Primary hyperaldosteornism. Order CT scan r/o tumor.
Tx for adenoma: surgery.
Tx for bilateral hyperplasia: Aldactone, an aldosterone antagonist
112
Dx labs: increased aldosterone, normal cortisol and ACTH, decreased renin
Primary hyperaldosteronism
113
Problem from RAAS. Causes include: hyperK, hypoNa, HoTN
Secondary hyperaldosteronism.
114
Decrease in aldosterone. Occurs in adrenal failure or in decreases of RAA system, HypoK, HyperNa, HTN, from drugs that cause aldosterone resistance (spironolactone) or if renal aldosterone receptors are not re: to aldosterone. Can cause hyponatremia and hyperkalemia.
Hypoaldosteronism
115
Hypoaldosteronism can cause what regarding Na+ and K+
Hyponatremia and hyperkalemia.
116
Tx of choice for 2o HTN (renovascular). What will you find on PE?
ACE. Abdominal bruits.
117
PE findings for coarcation of aorta
systolic murmur b/n scapulae; decreased systolic BP in legs
118
MEN 1 tumors
pituitary, parathyroid and pancreas. 3 Ps
119
MEN2a tumors
parathyroid, pheochromocytoma, medullary thyroid carcinoma
120
MEN 2b tumors
pheochromocytoma, MTC, marfanoid body habitus (2 tumors + an abnormality)
121
What happens to MEN1 if untreated?
50% probability of death by 50 years of age
122
Tx of MEN
depends on sites; surgery, chemo, radiation, +/- hormones
