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From Flashcardlet > Endocrine First Aid > Flashcards

Endocrine First Aid Flashcards

Intended for educational purposes only.

0
Q

What connects the thyroid diverticulum to the tongue?

A

thyroglossal duct

This normally disappears, but may persist as pyramidal lobe of thyroid/cystic dilation.

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1
Q

From where does the thyroid diverticulum arise, and to where does it descend?

A

ARISES floor of the primitive pharynx

DESCENDS into neck

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2
Q

What is the foramen cecum?

A

normal remnant of the thyroglossal duct

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3
Q

What is the most common site for ectopic thyroid tissue?

A

tongue

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4
Q

What is the appearance of a thyroglossal duct cyst?

A

anterior midline mass that moves with swallowing

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5
Q

What is the appearance of a branchial cleft cyst?

A

lateral neck mass that does not move with swallowing

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6
Q

What is the anatomy of the fetal adrenal gland?

A

OUTER ADULT ZONE dormant during early fetal life; begins to secrete cortisol late in gestation
INNER ACTIVE FETAL ZONE

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7
Q

In the fetus, what controls cortisol secretion?

A

ACTH and CRH from fetal pituitary and placenta

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8
Q

What is the function of cortisol in the fetus?

A

fetal lung maturation

surfactant production

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9
Q

From what does the adrenal cortex arise?

A

mesoderm

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10
Q

From what does the adrenal medulla arise?

A

neural crest

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11
Q

What is the most common tumor of the adrenal medulla in adults?

A

pheochromocytoma

causes episodic HTN

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12
Q

What is the most common tumor of the adrenal medulla in children?

A

neuroblastoma

does not cause episodic HTN

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13
Q

What is the primary regulatory control and secretory product of the zona glomerulosa of the adrenal medulla?

A

PRIMARY REGULATORY CONTROL renin-angiotensin

PRODUCT aldosterone

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14
Q

What is the primary regulatory control and secretory product of the zona fasciculata of the adrenal medulla?

A

PRIMARY REGULATORY CONTROL ACTH, hypothalamic CRH

PRODUCT cortisol, sex hormones

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15
Q

What is the primary regulatory control and secretory product of the zona reticularis of the adrenal medulla?

A

PRIMARY REGULATORY CONTROL ACTH, hypothalamic CRH

PRODUCT sex hormones (androgens)

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16
Q

What is the primary regulatory control and secretory product of the adrenal medulla at the level of the chromaffin cells?

A 
PRIMARY REGULATORY CONTROL preganglionic sympathetic fibers
PRODUCT catecholamines (Epi, NE)
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17
Q

From capsule to chromaffin cells, what are the secretory products at each level of the adrenal medulla?

A

aldosterone (Na+) –> cortisol (glucocorticoid), sex hormones –> sex hormones –> catecholamines
–the deeper you go, the sweeter it gets–

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18
Q

What is the drainage of the left adrenal gland?

A

left adrenal –> left adrenal vein –> left renal vein –> IVC

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19
Q

What is the drainage of the right adrenal gland?

A

right adrenal –> right adrenal vein –> IVC

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20
Q

From what is the posterior pituitary (neurohypophysis) derived?

A

neuroectoderm

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21
Q

From what is the anterior pituitary (adenohypophysis) derived?

A

oral ectoderm (Rathke’s pouch)

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22
Q

What does the posterior pituitary (neurohypophysis) secrete? Where are these chemicals made, and how do they reach the neurohypophysis?

A

vasopressin/ADH and oxytocin, make in the hypothalamus and shipped to posterior pituitary via neurophysins

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23
Q

What does the anterior pituitary (adenohypophysis) secrete?

A

FSH, LH, ACTH, TSH, ProlactIn, GH, MSH (melanotropin)

–FLAT PiG–

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24
Q

Which hormone subunit is common to TSH, LH, FSH, and hCG?

A

alpha

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25
Q

Which hormone subunit confers specificity?

A

beta

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26
Q

What are the acidophils?

A

GH

prolactin

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27
Q

What are the basophils?

A

FSH, LH, ACTH, TSH

–BFLAT–

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28
Q

From where do pancreatic islets originate, and of what are they composed?

A

ARISE FROM pancreatic buds

COMPOSITION alpha, beta, and delta endocrine cells

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29
Q

Where are alpha endocrine cells located in a pancreatic islet, and what do they produce?

A

peripherally; produce glucagon

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30
Q

Where are beta endocrine cells located in a pancreatic islet, and what do they produce?

A

centrally; produce insulin

–INsulin INside–

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31
Q

Where are delta endocrine cells located in a pancreatic islet, and what do they produce?

A

interspersed; produce somatostatin

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32
Q

What is the major regulator of insulin release? How does this regulator cause insulin secretion?

A

REGULATOR glucose
ACTION glucose enters pancreatic beta cell through GLUT-1 –> glycolysis –> release of ATP –> ATP-sensitive K+ channels close –> depolarization of beta cell membrane –> voltage-gated Ca2+ channels open –> Ca2+ influx –> stimulation of insulin exocytosis –> insulin released to blood

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33
Q

Does insulin cross the placenta?

A

no

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34
Q

How are the alpha and beta chains of proinsulin held together in the protein’s tertiary structure?

A

disulfide bonds

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35
Q

Which organs and cells demonstrate insulin-independent glucose uptake?

A 
Brain
RBCs
Intestine
Cornea
Kidney
Liver
--BRICK L--
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36
Q

Where is GLUT-1 found? Does it require insulin?

A

FOUND brain, RBCs

insulin indepedent

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37
Q

Where is GLUT-2 found? What is the specific property of the transporter?

A

beta islet cells, liver, kidney, small intestine

bidirectional

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38
Q

Where is GLUT-4 found? Does it require insulin?

A

adipose tissue, skeletal muscle

insulin depedent

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39
Q

What are the anabolic effects of insulin?

A

DECREASED glucagon release
INCREASED glucose transport in skeletal muscle and adipose (through GLUT-4), glycogen synthesis and storage, tryglyceride synthesis and storage, Na+ retention (kidneys), protein synthesis (muscles), cellular uptake of K+ and amino acids

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40
Q

What increases release of insulin?

A

hyperglycemia
GH (increases insulin resistance, thus leading to increased insulin release; note that this is not a direct action)
beta-2 agonists (FA Errata)

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41
Q

What decreases insulin release?

A

hypoglycemia
somatostatin
alpha-2 agonists

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42
Q

What effects result when insulin enters a cell?

A

tyrosine phosphorylation –>

(1) phosphoinositide-3 kinase pathway –> glycogen, lipid, and protein synthesis; creation of vesicles containing GLUT-4 receptor –> GLUT-4 on membrane –> glucose entrance into cell
(2) RAS-MAP kinase pathway –> cell growth, DNA synthesis

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43
Q

In starvation, what does the brain use for metabolism?

A

ketone bodies

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44
Q

Why are RBCs always dependent on glucose for metabolism?

A

RBCs lack mitochondria and cannot perform aerobic metabolism

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45
Q

Where is glucagon synthesized?

A

alpha cells of the pancreas

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46
Q

What are the catabolic effects of glucagon?

A

glycogenolysis, gluconeogenesis

lipolysis, ketone production

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47
Q

What stimulates glucagon release?

A

hypoglycemia

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48
Q

What inhibits glucagon release?

A

insulin
hyperglycemia
somatostatin

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49
Q

In hypothalamic-pituitary regulation, what does TRH stimulate?

A

TSH

prolactin

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50
Q

In hypothalamic-pituitary regulation, what does dopamine inhibit?

A

prolactin

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51
Q

In hypothalamic-pituitary regulation, what does CRH stimulate?

A

ACTH
MSH (melanocyte stimulating hormone)
beta-endorphin

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52
Q

In hypothalamic-pituitary regulation, what does GHRH stimulate?

A

GH

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53
Q

In hypothalamic-pituitary regulation, what does somatostatin inhibit?

A

GH

TSH

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54
Q

In hypothalamic-pituitary regulation, what does GnRH stimulate?

A

FSH

LH

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55
Q

In hypothalamic-pituitary regulation, what does prolactin inhibit?

A

GnRH

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56
Q

What is the main source of prolactin?

A

anterior pituitary

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57
Q

What is the function of prolactin?

A

FEMALES simulation of milk production; inhibition of GnRH synthesis and release –> inhibition of ovulation
MALES inhibition of GnRH synthesis and release –> inhibition of spermatogenesis

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58
Q

What increases prolactin secretion?

A 
TRH
dopamine antagonists (most antipsychotics) and estrogens
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59
Q

What inhibits prolactin secretion?

A 
TONIC INHIBITION dopamine from hypothalamus
FEEDBACK INHIBITION increased prolactin --> increased dopamine --> increased inhibition
dopamine agonists (bromocriptine)
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60
Q

What is the treatment of choice for prolactinoma?

A

bromocriptine (dopamine agonist –> increased inhibition of prolactin)

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61
Q

From where is GH (somatotropin) secreted?

A

anterior pituitary

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62
Q

What is the function of GH, and how is it regulated?

A

FUNCTION secretion of IGF-1/somatomedin –> stimulation of linear growth and muscle mass; increased insulin resistance (diabetogenic)
REGULATION pulsatile release by GHRH, increased by exercise and sleep; inhibited by glucose and somatostatin

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63
Q

To what may excess secretion of GH lead?

A

acromegaly in adults or gigantism in children

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64
Q

What effect does 17-alpha hydroxylase deficiency have upon mineralocorticoids, corisol, and sex hormones?

A

MINERALOCORTICOIDS increased
CORTISOL decreased
SEX HORMONES decreased

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65
Q

What is the presentation of 17-alpha hydroxylase deficiency?

A

HTN, hypokalemia
XY: decreased DHT –> variable, ambiguous genitalia; undescended testes
XX: externally phenotypic female with normal internal sex organs, lacking secondary sex characteristics

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66
Q

What effect does 21-hydroxylase deficiency have upon mineralocorticoids, corisol, and sex hormones?

A

MINERALOCORTICOIDS decreased
CORTISOL decreased –> no negative feedback –> INCREASED ACTH
SEX HORMONES increased (production of sex steroids does not require 21-hydroxylase)

67
Q

What is the presentation of 21-hydroxylase deficiency?

A

salt wasting with hypotension, hyperkalemia, increased RAAS, volume depletion
life threatening hyponatremia due to lack of cortisol
masculinization: clitoral enlargement in females or precocious puberty in males

68
Q

What effect does 11beta-hydroxylase deficiency have upon mineralocorticoids, corisol, and sex hormones?

A

ALDOSTERONE decreased
11-DEOXYCORTICOSTERONE increased
CORTISOL decreased
SEX HORMONES increased

69
Q

What is the presentation of 11beta-hydroxylase deficiency?

A

HTN (while aldosterone is absent, 11-deoxycorticosterone is secreted in excess)
masculinization

70
Q

Which congenital bilateral adrenal hyperplasia is most common?

A

21-hydroxylase deficiency

71
Q

Why are 17alpha-hydroxylase deficiency, 21-hydroxylase deficiency, and 11beta-hydroxylase deficiency all categorized as bilateral adrenal hyperplasia?

A

all cause decreased cortisol –> increased ACTH stimulation –> enlargement of both adrenal glands

72
Q

From where is cortisol secreted?

A

adrenal zona fasciculata

73
Q

To what is cortisol bound?

A

CBG (corticosteroid-binding globulin)

74
Q

What are the functions of cortisol?

A
  1. maintains BP: upregulates alpha1 receptors on arterioles –> increased sensitivity to NE and Epi
  2. decreased Bone formation
  3. anti-Inflammatory/Immunosuppressive: inhibits production of leukotrienes and prostaglandins, inhibits leukocyte adhesion –> neutrophilia, blocks histamine release from mast cells, reduces eosinophils, blocks IL-2 production
  4. increased Insulin resistance (diabetogenic)
  5. increased Gluconeogenesis, lipolysis, proteolysis
  6. inhibits fibroblasts (causes striae)
    - -cortisol is BBIIG–
75
Q

What regulates cortisol?

A

STIMULATION chronic stress; CRH from the hypothalamus –> stimulation of ACTH release from the pituitary –> adrenal zona fasciculata produces cortisol
INHIBITION feedback inhibition via excess cortisol (decreased CRH –> decreased ACTH –> decreased cortisol)

76
Q

What secretes PTH?

A

chief cells of the parathyroid

77
Q

What is the function of PTH?

A

INCREASES production of M-CSF, RANK-L in osteoblasts –> stimulation of osteoclasts –> bone resorption of calcium and phosphate; kidney reabsorption of calcium in the DCT; kidney 1alpha-hydroxylase –> 1,25-(OH)2 D3 (calcitol) production –> increased intestinal calcium reabsorption
DECREASES reabsorption of phosphate in the PCT; serum phosphate –> increased converstion of 25-(OH) D3 to 1,25-(OH)2 D3 –> increased intestinal phosphate reabsorption, phosphate release from bone matrix

–PTH=Phosphate Trashing Hormone–

78
Q

What blood changes does PTH cause?

A

increased Ca2+

decreased (PO4)3-

79
Q

What urine changes does PTH cause?

A

increased (PO4)3-

80
Q

What regulates PTH?

A

INCREASES decreased serum Ca2+, moderately decreased serum Mg2+
DECREASES greatly decreased serum Mg2+; PTH (feedback inhibition)

81
Q

What are the common causes of decreased magnesium?

A

diarrhea
aminoglycosides
diuretics
alcohol abuse

82
Q

What are the sources of vitamin D?

A

D3 from sun exposure in skin
D2 from plants

Both are converted to 25-OH in the liver and 1,25-(OH)2, the active form, in the kidney.

83
Q

What are the functions of vitamin D?

A

increases absorption of dietary Ca2+ and (PO4)3- in the gut

increases bone resorption of Ca2+ and (PO4)3-

84
Q

What regulates vitamin D?

A

INCREASED BY increased PTH; decreased Ca2+ and (PO4)3-

INHIBITED BY 1,25(OH)2 (negative feedback)

85
Q

What results from vitamin D deficiency?

A

rickets in kids

osteomalacia in adults

86
Q

If 24,25-(OH)2 D3 active or inactive?

A

inactive

87
Q

From where is calcitonin produced, and what is its function?

A 
SOURCE parafollicular (C) cells of the thyroid
FUNCTION decreased bone resorption of calcium (opposes PTH actions)

–calciTONin TONes down calcium–

88
Q

How is calcitonin regulated?

A

INCREASED BY increased serum Ca2+

89
Q

Which endocrine hormones utilize cAMP in their signaling pathway?

A 
FSH
LH
ACTH
TSH
CRH
hCG
ADH (through the V2 receptor!)
MSH
PTH
calcintonin
GHRH
glucagon
--FLAT ChAMP--

NOTE GHRH also signals through IP3, but its major role of signaling is cAMP

90
Q

Which endocrine hormones utilize cGMP in their signaling pathway?

A

ANP
NO (EDRF)
–think vasodilators–

91
Q

Which endocrine hormones utilize IP3 in their signaling pathway?

A 
GnRH
GHRH
Oxytocin
ADH (through the V1 receptor!)
TRH
histamine (H1)
ATII
gastrin
--GGOAT--

NOTE GHRH also signals through IP3, but its major role of signaling is cAMP

92
Q

Which endocrine hormones utilize a steroid receptor in their signaling pathway?

A 
Vitamin D
Estrogen
Testosterone
T3/T4
Cortisol
Aldosterone
Progesterone
--VETTT CAP--
93
Q

Which endocrine hormones utilize the intrinsic tyrokine kinase in their signaling pathway?

A 
Insulin
IGF-1
FGF
PDGF
EGF
--MAP kinase pathway; think growth factors.--
94
Q

Which endocrine hormones utilize the receptor-associated tyrosine kinase in their signaling pathway?

A

Prolactin
Immunomodulators (cytokines IL-2, IL-6, IL-8, IFN)
GH
–PIG; JAK/STAT pathway; think acidophiles and cytokines.–

95
Q

From serum to nucleus, how are steroid hormones transported?

A

lipophilic steroid hormones bind to specific binding globulins –> solubility in blood increased –> hormone crosses cellular membrane –> hormone binds receptor in nucleus or cytoplasm –> transformation of receptor to expose DNA-binding domain –> steroid binds to enhancer-like element in DNA –> DNA transcription

96
Q

Where are thyroid hormones T3/T4 produced, and what are their functions?

A

SOURCE thyroid follices; most T3 formed in target tissues
FUNCTION bone growth (synergism with GH); CNS maturation; increased B1 receptors in the heart –> increased CO, HR, SV, contractility; increased Na/K ATPase activity –> increased basal metabolic rate –> increased O2 consumption, respiratory rate, body temperature; increased glycogenolysis, gluconeogenesis, lipolysis

–T3 functions are the 4Bs: Brain maturation, Bone growth, Beta-adrenergic effects; Basal metabolic rate increase–

97
Q

What binds T3/T4 in the blood? Is this the active form?

A

TBG (thyroxine-binding globulin) binds most T3/T4; only free hormone is active

98
Q

What change is seen in TBG in pregnancy?

A

increased TBG

This is also seen in oral contraceptive use.

99
Q

What change is seen in TBG in hepatic failure?

A

decreased TBG

100
Q

Where is T4 converted to T3, and what enzyme catalyzes this process?

A

T4 –> T3 in peripheral tissues due to actions of 5’-deiodinase

101
Q

Which binds with greater affinity?

T3 or T4

A

T3

102
Q

What enzyme is responsible for oxidation and organification of iodide? What other reaction requires this enzyme?

A

peroxidase

Also used in coupling of MIT and DIT

103
Q

How do the enzymatic modifications of propylthiouracil and methimazole differ?

A

Propylthiouracil inhibits both peroxidase and 5’-deiodinase; methimazole inhibits peroxidase only.

104
Q

How are the thyroid hormones regulated?

A

INCREASED BY hypothalamic TRH –> pituitary TSH –> stimulation of follicular cells –> increased thyroid hormones; TSI (thryoid-stimulating immunogluobulins, such as those produced in Graves’ disease)
INHIBITION negative feedback of free T3 to anterior pituitary –> decreased sensitivity to TRH

105
Q

What is the Wolff-Chaikoff effect?

A

excess iodine –> temporary inhibition of thyroid peroxidase –> decreased iodine organification –> decreased T3/T4 production

106
Q

What inhibits uptake of iodine into the follicular cells?

A

anions such as perchlorate and pertechnetate

107
Q

What are the various causes of Cushing syndrome?

A

OVERALL MECHANISM increased cortisol

EXOGENOUS iatrogenic steroids –> suppression of ACTH secretion due to negative feedback –> bilateral adrenal atrophy –> decreased ACTH

ENDOGENOUS

  1. Cushing’s disease, 70% of cases: pituitary adenoma –> bilateral adrenal hyperplasia –> increased ACTH secretion
  2. ectopic ACTH, 15% of cases: paraneoplastic syndromes (SCLC, bronchial carcinoids) –> nonpituitary tissue making ACTH –> increased ACTH
  3. adrenal, ACTH independent, 15%: adenoma, carcinoma, nodular adrenal hyperplasia –> atrophy of uninvolved adrenal gland –> decreased ACTH
108
Q

What are the clinical findings and treatment in Cushing syndrome?

A

SYMPTOMS HTN, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance ), skin changes (thinning, striae), osteoporosis, amenorrhea, immune suppression
DIAGNOSIS 24-hour urine cortisol levels
TREATMENT surgery, possible use of steroid synthesis inhibitors

109
Q

How should you interpret the following results of a dexamethasone suppression test?
suppressed with low-dose and high-dose Dex

A

normal system

110
Q

How should you interpret the following results of a dexamethasone suppression test?
not suppressed with low-dose Dex, but suppressed with high-dose

A

ACTH-pituitary tumor

111
Q

How should you interpret the following results of a dexamethasone suppression test?
unsuppressed with both low-dose and high-dose Dex

A

ectopic ACTH-producing tumor (SCLC, bronchial carcinoid)

cortisol producing tumor

112
Q

What is the pathogenesis of primary hyperaldosteronism? How should it be treated?

A

OVERALL CAUSE excess aldosterone
PATHOGENESIS unilateral or bilateral adrenal hyperplasia, adrenal carcinoma, or Conn’s syndrome (aldosterone-secreting adrenal adenoma, most common cause) –> HTN, hypernatremia, hypokalemia, metabolic alkalosis, high aldosterone, WITH LOW plasma renin
TREATMENT surgery and/or spironolactone

113
Q

What is the most common cause of primary hyperaldosteronism?

A

adrenal adenoma

114
Q

What are the overall effects of aldosterone?

A

increase of sodium absorption, secretion of K+ and H+ at the DCT and collecting duct

115
Q

How does spironolactone work? What is the most tested side effect of spironolactone?

A

MOA K+ sparing diuretic; aldosterone antagonist

S/E gynecomastia

116
Q

What is the pathogenesis of secondary hyperaldosteronism? How should it be treated?

A

OVERALL CAUSE excess aldosterone
PATHOGENESIS renal artery stenosis, chronic renal failure, CHF, cirrhosis, nephrotic syndrome –> renal perception of low intravascular volume –> overactive RAAS –> HTN, hypernatremia, hypokalemia, metabolic alkalosis, high aldosterone, WITH HIGH plasma renin
TREATMENT spironolactone

117
Q

What is the pathogenesis of Addison’s disease?

A

OVERALL CAUSE lack of adrenal hormones, atrophy of adrenals
PATHOGENESIS adrenal atrophy (APS1 or APS2) or adrenal destruction by disease (autoimmune process, TB/CMV/histoplasmosis/coccidioidomycosis), metastasis) –> chronic PRIMARY adrenal insufficiency –> deficiency of aldosterone and cortisol –> hypotension (hyponatremic volume contraction), hyperkalemia, acidosis, skin hyperpigmentation (increased ACTH from POMC –> increased MSH), weakness, vomiting, diarrhea

–Adrenal Atrophy, Absence of hormone production, All 3 cortical divisions involves with medullary sparing.–

118
Q

How is Addison’s disease differentiated from secondary adrenal insufficiency?

A

secondary adrenal insufficiency (decreased PITUITARY ACTH) does NOT present with skin hyperpigmentation or hyperkalemia

119
Q

What is APS1?

A

DEFINTION Autoimmune Polyendocrine Syndrome, Type I (also called candidiasis-hypoparathyroidism-Addison’s disease-syndrome)
PRESENTATION chronic mucocutaneous candidiasis, abnormalities of skin, dental enamel, and nails

120
Q

What is APS2?

A

DEFINITION Autoimmune Polyendocrine Syndrome, Type II (most common)
PRESENTATION autoimmune thyroiditis, DM Type I, and Addison’s

121
Q

What is Waterhouse-Friderichsen syndrome?

A

EPIDEMIOLOGY young children
PATHOGENESIS Neisseria meningitidis infection –> DIC, endotoxic shock, adrenal hemorrhagic necrosis –> acute PRIMARY adrenal insufficiency –> lack of cortisol –> exacerbation of hypotension –> death

122
Q

What is the composition of the adrenal medulla?

A

neural crest-derived chromaffin cells

123
Q

What is the pathogenesis of pheochromocytoma, and with what is it associated?

A

PATHOGENESIS tumor of chromaffin cells –> secretion of Epi, NE, Dopamine –> episodic HTN (Pressure, Pain, Perspiration, Palpitations, Pallor)
LABS elevated plasma catecholamines leading to elevated urinary metanephrine and VMA; LM: zellballen in rich vascular network with bizarre cells, EM: membrane bound, electron-dense secretory granules
ASSOCIATIONS NF Type I, MEN 2A and 2B, von Hippel-Lindau

–5 P’s: pressure, pain, perspiration, palpitations, pallor–

124
Q

What is the “Rule of 10s,” and in which disease process is it applicable?

A 
10% malignant
10% bilateral
10% extra-adrenal (blader wall, organ of Zuckerkandl at IMA root)
10% calcify
10% kids
Seen in pheochromocytoma
125
Q

What must be present to declare a pheo malignant?

A

metastases

126
Q

What is the treatment for pheochromocytoma

A

THE FOLLOWING IN ORDER

  1. alpha antagonists: phenoxybenzamine must be given first or HTN crisis may result from cathcholamine leakage into bloodstream
  2. beta-antagonists: slow HR
  3. surgical removal
127
Q

Why is urinary VMA elevated in pheochromocytoma?

A

phenylalanine –> tyrosine –> L-dopa –> dopamine –> HVA, NE
NE –> normetanephrine, VMA, Epi
Epi –> metanephrine, VMA

128
Q

What is the most common type of tumor of the adrenal medulla in children?

A

neuroblastoma

129
Q

Where do neuroblastomas appear?

A

anywhere along the sympathetic chain

130
Q

What is the presentation, association, and laboratory finding of neuroblastoma?

A

PRESENTATION child <2 with abdominal mass
ASSOCIATION N-myc oncogene indicates rapid tumor progression
LABS elevated homovanillic acid in urine (breakdown product of dopamine)

131
Q 
Hyperthyroidism or hypothyroidism?
cold intolerance (decreased heat production)
A

hypothyroidism

132
Q

Hyperthyroidism or hypothyroidism?

chest pain, palpitations, arrhythmias (especially atrial), tachycardia (increased beta-adrenergic receptors)

A

hyperthyroidism

133
Q

Hyperthyroidism or hypothyroidism?

dry, cool skin; coarse, brittle hair

A

hypothyroidism

134
Q

Hyperthyroidism or hypothyroidism?

weight loss, increased appetite

A

hyperthyroidism

135
Q

Hyperthyroidism or hypothyroidism?

diarrhea

A

hyperthyroidism

136
Q

Hyperthyroidism or hypothyroidism?

constipation

A

hypothyroidism

137
Q

Hyperthyroidism or hypothyroidism?

bradycardia, dyspnea on exertion

A

hypothyroidism

138
Q

Hyperthyroidism or hypothyroidism?

increased TSH

A

hypothyroidism, sensitive test

139
Q

Hyperthyroidism or hypothyroidism?

increased free or total T4/T3

A

hyperthyroidism

140
Q

Hyperthyroidism or hypothyroidism?

hypoactivity, lethargy, fatigue, weakness

A

hypothyroidism

141
Q

Hyperthyroidism or hypothyroidism?

hyperactivity

A

hyperthyroidism

142
Q

Hyperthyroidism or hypothyroidism?

weight gain, decreased appetitie

A

hypothyroidism

143
Q 
Hyperthyroidism or hypothyroidism?
heat intolerance (increased heat production)
A

hyperthyroidism

144
Q

Hyperthyroidism or hypothyroidism?

decreased reflexes

A

hypothyroidism

145
Q

Hyperthyroidism or hypothyroidism?

warm, moist skin; fine hair

A

hyperthyroidism

146
Q

Hyperthyroidism or hypothyroidism?

increased reflexes

A

hyperthyroidism

147
Q

Hyperthyroidism or hypothyroidism?

osteoporosis / risk of fracture

A

hyperthyroidism

148
Q

Hyperthyroidism or hypothyroidism?

myxedema (facial/periorbital)

A

hypothyroidism

149
Q

Hyperthyroidism or hypothyroidism?

decreased TSH, if primary

A

hyperthyroidism

150
Q

Hyperthyroidism or hypothyroidism?

pretibial myxedema

A

hyperthyroidism in Graves’ disease

151
Q

Hyperthyroidism or hypothyroidism?

decreased free T4

A

hypothyroidism

152
Q

What is the most common cause of hypothyroidism in regions where iodine is adequate?

A

Hashimoto’s thyroiditis

153
Q

What is the cause, presentation (including histology), and the associations of Hashimoto’s thyroiditis?

A

EPIDEMIOLOGY women 45-65
CAUSE autoimmune disorder of thyroid peroxidase, antithyroglobulin antibodies; may be hyperthyroid early in the course of disease due to thyrotoxicosis during follicular rupture
PRESENTATION moderately enlarged, nontender thyroid
LABS decreased T4, increased TSH; antithyroglobulin and antimicrosomal antibodies; LM: Hurthle cells (eosinophilic metaplasia of cells lining follicles), lymphocytic infiltrate with germinal centers
ASSOCIATIONS HLA-DR5; increased risk of Hodgkin’s lymphoma

154
Q

What is the epidemiology, cause, and presentation of cretinism?

A

EPIDEMIOLOGY neonates, infants; Himalayas, inland China, mountainous areas
CAUSE maternal hypothyroidismduring early pregnancy, thyroid adenesis, dyshormonogenetic goiter, iodine deficiency
PRESENTATION 5P’s: Pot-bellied, Pale, Puffy-faced (coarse facial features), Protruding umbilicus (hernia), Protruberant tongue; marked mental retardation, short stature with skeletal abnormalities

155
Q

What is the most common cause of dyshormonogenetic goiter (seen in cretinism)?

A

congenital defect in thyroid peroxidase

156
Q

What is the cause and presentation (including histology) of subacute / de Quervain’s thyroiditis?

A

EPIDEMIOLOGY women 40-50
CAUSE viral infection (flu-like illness); may be hyperthyroid early in course
PRESENTATION very tender thyroid, jaw pain
LABS increased ESR, early inflammation; granulomatous inflammation

NOTE does NOT progress to hypothyroidism

157
Q

What is the cause, presentation (including histology), and the associations of Riedel’s (fibrosing) thyroiditis?

A

EPIDEMIOLOGY 40s
CAUSE progressive replacement of normal thyroid tissue with fibrous tissue
PRESENTATION fixed, hard (rock or wood-like) painless goiter; may extend to involve local structure such as the airway; clinically mimics anaplastic carcinoma
LABS no malignant cells; chronic inflammation with extensive fibrosis
ASSOCIATIONS considered a manifestation of IgG4-related systemic disease

158
Q

What is the cause and presentation (including histology) of myxedema?

A

EPIDEMIOLOGY children, older adults
CAUSE iodine deficiency, Hashimoto’s thyroiditis, goitrogens (including lithium), surgical removal / radioablation of the thyroid, Wolff-Chaikoff effect, subacute lymphocytic thyroiditis
PRESENTATION decreased basal metabolic rate, decreased SNS activity –> myxedema (accumulation of glycosaminoglycans in the skin and soft tissue –> deepening of voice, large tongue), weight gain despite normal appetitie, slowing of mental activity, muscle weakness, cld intolerance with decreased sweating, bradycardia with decreased CO –> dyspnea, fatigue; oligomenorrhea, hypercholesterolemia, constipation

159
Q

What are the causes, presentation, and treatment of general hyperthyroidism?

A

CAUSES increased level of circulating thyroid hormone –> increased synthesis of Na+/K+ ATPase; increased expression of B1 adrenergic receptors –> increased basal metabolic rate, increased SNS activity
PRESENTATION weight loss despite increased appetite, heat intolerance and sweating, tachycardia with increased CO; arrhythmia (especially atrial fibrillation in the elderly); tremor, anxiety, insomnia, heightened emotions; staring gaze with lid lag; oligomenorrhea; bone resorption with hypercalcemia (risk for osteoporosis); decreased muscle mass with weakness; hypocholesterolemia, hyperglycemia (increased gluconeogenesis and glycogenolysis)
TREATMENT thioamides, iodide; thyroidectomy; beta blocker, glucocorticoids, vitamins

160
Q

What are the epidemiology, pathogenesis, and laboratory findings in Graves’ disease?

A

EPIDEMIOLOGY women 20-40 under stress (childbirth)
PATHOGENESIS thyroid-stimulating immunoglobulins –> IgG stimulation of TSH receptor –> type II hypersensitivity process –> hyperthyroidism, diffuse goiter (constant TSH stimulation –> thyroid hyperplasia, hypertrophy); exopthalmos with “stare” and pretibial myxedema (TSH –> TSH receptor on fibroblasts behind the orbit and overlying the shin activated –> glycosaminoglycan (chondriotin sulfate and hyaluronic acid) buildup, inflammation, fibrosis, edema)
LABS increased total and free T4 and T3; decreased TSH (feedback regulation downregulates TRH receptors in anterior pituitary); hypocholesterolemia, hyperglycemia; LM: irregular follicles with scalloped colloid and chronic inflammation
TREATMENT beta blockers, thioamide, radioiodine ablation

161
Q

What are the cause, presentation, and treatment of thyroid storm?

A

CAUSE exacerbation of Graves’ disease or other hyperthyroid disorders due to stress (surgery, childbirth: elevated catecholamines and massive hormone excess)
PRESENTATION arrhythmia, hyperthermia, vomiting, hypovolemic shock; death due to arrhythmia or pulmonary edema
LABS increased bone turnover –> increased ALP
TREATMENT propylthiouracil, high iodide, beta-blockers, dexamethasone/steroids

162
Q

How does propylthiouracil act?

A

MOA inhibition of peroxidase –> inhibition of oxidation, organification, and coupling steps of thyroid hormone synthesis; inhibition of peripheral conversion of T4 –> T3

163
Q

What are the cause and presentation of nontoxic multinodular goiter?

A

CAUSE relative iodine deficiency

PRESENTATION enlarged thyroid gland with multiple nodules

164
Q

What are the cause and presentation of toxic multinodular goiter?

A

CAUSE mutation of TSH receptor –> focal patches of hyperfunctioning follicular cells working independently of TSH
PRESENTATION enlarged thyroid gland with multiple nodules; hyperthyroidism; rarely malignant
LABS increased release of T3 and T4

165
Q

What is Jod-Basedow phenomenon?

A

thyrotoxicosis if a patient with iodine deficiency goiter becomes iodine replete

166
Q

What is Plummer hyperthyroidism?

A

toxic multinodular goiter without infiltrative opthalmopathy or pretibial myxedema

From Flashcardlet (18 decks)

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