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First Aid Chapters > Endocrine > Flashcards

Endocrine Flashcards

1
Q

where does the thyroid come from

A

floor of the primitive pharynx

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2
Q

what initially connects the thyroid to the tongue

A

the thyroglossal duct

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3
Q

what is the normal remnant of the thyroglossal duct

A

foramen cecum

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4
Q

most common ectopic thyroid tissue site

A

tongue

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5
Q

presentation of a thyroglossal duct cyst

A

anterior mid line neck mass that moves with swallowing or protrusion of the tongue. this is different from a persistent cervical sinus leading to brachial cleft cyst in the lateral neck

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6
Q

adrenal cortex is derived from

A

mesoderm

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7
Q

adrenal medulla is derived from

A

neural crest

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8
Q

most common tumor of adrenal medulla in kids

A

neuroblastoma. rarely causes hypertension

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9
Q

most common tumor of adrenal medulla in adults

A

pheochromocytoma

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10
Q

where does left adrenal vein drain to

A

left renal vein

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11
Q

where does right adrenal vein drain to

A

IVC

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12
Q

what is the posterior pituatary derived from

A

neuro-ectoderm

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13
Q

what is the anterior pituatary derived from

A

oral ectoderm (rathke’s pouch)

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14
Q

what does the posterior pituatary make

A

NOTHING

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15
Q

what does the posterior pituatary secrete

A

ADH and oxytocin. these are made in the hypothalamus and shipped to the posterior pituatary via neurophysins.

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16
Q

what do the acidophiles in the anterior pituatary make

A

GH and prolactin

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17
Q

what 4 hormones have the alpha subunit from the anterior pituitary in common

A

TSH, LH, FSH and Beta HCG

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18
Q

position of the cell types in the islets of the endocrine pancreas

A

alpha cells- make glucagon- periphery

beta cells- make insulin- in the center

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19
Q

where is pre-pro insulin made

A

in the rough ER

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20
Q

what type of insulin is stored in the granules

A

pro insulin

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21
Q

what type of insulin gets exocytosed

A

just regular insulin. the proinsulin is cleaved and insulin an C peptide are released

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22
Q

what is unique about C peptide

A

it is made in the body but exogenous insulin does not contain this

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23
Q

does glucose cross the placenta

A

YES

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24
Q

does insulin cross the placenta

A

NO

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25
Q

Glut 4

A

adipose tissue and skeletal muscle. it is the only insulin dependent transporter

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26
Q

Glut5

A

this is for fructose

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27
Q

Glut1

A

this is for RBCs, brain and cornea

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28
Q

Glut2

A

this is bidirectional- beta islet cells, liver, kidney and small intestine.

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29
Q

growth hormone relationship to glucose

A

growth hormones increases insulin release

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30
Q

beta blockers and insulin

A

beta blockers increase insulin

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31
Q

how is insulin secreted

A

glucose is brought into the cells, ATP is generated from glucose metabolism, this closes K+ channels, this depolarizes the cell membrane, this opens voltage gated calcium channels, resulting in Ca influx, this then stimulates exocytosis of insulin.

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32
Q

relationship between GnRH and prolactin

A

prolactin regulates GnRH secretion. high prolactin levels decrease GnRH. inhibits both GnRH synthesis and release

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33
Q

what does somatostatin do

A

decreases GH and TSH

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34
Q

what is the relationship between TRH and prolactin

A

TRH increases both TSH and prolactin

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35
Q

dopamine and prolactin

A

the hypothalamus secretes dopamine and this suppresses prolactin secretion from the anterior pituitary on a normal basis.

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36
Q

how does Growth hormone work

A

by stimulating linear growth and muscle mass trough IGF1 and somatomedin secretion. increases insulin resistance (can cause diabetes).

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37
Q

when is growth hormone secretion increased

A

during exercise and sleep. secretion is inhibited by glucose and somatostatin

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38
Q

where is ADH made

A

in the supra-optic nucleus, released by the posterior pituatary

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39
Q

what is the function of ADH

A

V1- regulates blood pressure and V2- regulates osmolarity by acting on free water. does this in the principal cells of renal collecting duct.

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40
Q

what disease has low ADH

A

diabetes insipidus

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41
Q

where is the mutation in nephrogenic diabetes insipidus

A

in the V2 receptor

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42
Q

what is a drug that is an ADH analog

A

Desmopressin.

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43
Q

what is elevated in 21 hydroxylase deficiency

A

androgens. you therefore see salt wasting and precocious puberty in boys and virilization of girls

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44
Q

what is elevated in 17 alpha hydroxylase deficiency

A

increased mineralocorticoids. you see low potassium and increased blood pressure. low androgens means ambiguous genitalia and lack of secondary sex deveopment

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45
Q

what is elevated in 11 beta hyroxylase deficiency

A

increased androgens and weak increased mineralocorticoids. looks like 21 but without the salt wasting. precocious puberty and virilization of girls

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46
Q

which andrenal cortex enzyme deficiency leads to increased 17 hydroxy progesterone

A

21 hydroxylase deficiency

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47
Q

what do the adrenal glands look like in enzyme deficiencies

A

increased or hyperplasia because of increased AcTH simtulation from low cortisol

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48
Q

function of cortisol on blood pressure

A

increases blood pressure by upregulating the lapha 1 receptor on arterioles so that increases sensitivity to epi and nor epi

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49
Q

how does cortisol mediate immune response

A

inhibits leukotriene and prostaglandin production
inhibitrs leukocyte adhesion- neutrophilia
blocks histamine release from mast cells
reduces eosinophils
blocks IL2 so can’t activate T cells

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50
Q

adrenal gland size with exogenous steroid use

A

both are small

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51
Q

adrenal size with adrenal adenoma or carcinoma that secretes cortisol

A

the one secreting the stuff is big and the other is small.

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52
Q

what causes both adrenal glands to be large

A

both increased AcTH from a pituatary adenoma and from paraneoplastic syndrome. can distinguish by giving cortisol which will suppress the pituatary adenoma but not the paraneoplastic from like small cell lung cancer.

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53
Q

which cells secrete PTH

A

chief cells of the parathyroid gland

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54
Q

function of PTH

A

increase bone resorption of Ca and phosphorus
increase kidney re-absorption of Ca in distal convoluted tubule and dumping of phosphourus (decreased re-absorption in the proximal convoluted tubule)
increase vitamin D production by stimulating kidney 1-alpha hydroxylase

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55
Q

function of RANK-L

A

this is increased by PTH. it binds to RANK on the osteoblasts which then gets osteoclast stimulation and increased calclium. increases through NfKb ligand

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56
Q

common causes low magnesium

A

diarrhea, aminoglycosides, diuretics, and alcohol use

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57
Q

how does pH effect Ca

A

increase in pH means incrased affinity of albumin for calclium which means effective hypocalcemia. symptoms of low calclium

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58
Q

where is D3 from

A

the sun

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59
Q

where is D2 from

A

vegetables and oral intake

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60
Q

how is vitamin D made

A

first brought in and converted in the liver to 25-OH and then goes to the kidney to make 1,25 OH2

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61
Q

function of vitamin D

A

increases absorption of dietary Ca and phosphorous

increased bone resorption of calcium and phosphorous

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62
Q

what is 24,25 (OH)2

A

this is an inactive form of D3

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63
Q

where is calcitonin made

A

parafollicular cells- C cells- of the thyroid

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64
Q

how do thyroid hormones increase basal metabolic rate

A

increase the K/Na ATPase function (this increases O2 consumption) and increase beta 1 adrenergic receptors so increase sympathetic activity in the body. also increases glycogenolysis and gluconeogenesis

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65
Q

where is most T3 formed

A

in the tissues of the body- in the target areas

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66
Q

Wolff Chaikoff effect

A

this is when excess iodine temporarily inhibits thyroid peroxidase and this decreases iodine organification and then this ultimately decreases T3/T4 production.

67
Q

thyroxin binding globulin

A

this binds most T3/T4 in the blood. only free hormone is active

68
Q

birth control pills and thyroid function

A

birth control pills increase thyroxin binding globulin so decreased thyroid hormone that is free

69
Q

how to convert T4 to T3

A

5’ deiodinase

70
Q

what causes the striae with cushing syndrome

A

weak collagen and ruptured vessels

71
Q

how does cortisol cause hypertension

A

increases alpha receptors on vessels- specificlaly arterioles and this leads to increased effect of norepi and hypertension

72
Q

primary hyper-aldosteronism

A

this is caused by an aldosterone secreting tumor of the adrenal gland or just adrenal hyperplasia. an adenoma is called Conn syndrome. hypertension, hypokalemia, LOW renin, but normal Na because of aldosterone escape. treatment is surgical or spironolactone to decrease aldosterone

73
Q

secondary hyper-aldosteronism

A

this is when the kidneys sense low volume and INCREASE renin so that they increase aldosterone. often due to renal artery stenosis (fibromuscular dysplasi) or CHF, cirrhosis etc. treatment- spironolactone. remember high renin here unlike primary hyper-aldosteronism

74
Q

conn syndrome

A

aldosterone secreting adrenal adenoma

75
Q

addison disease

A

adrenal insufficiency

76
Q

3 causes of addison’s disease

A 
autoimmune
TB
Metastatic carcinoma (lung cancer loves the adrenal)
77
Q

what is addison’s disease

A

basically a deficiency in aldosteron and cortisol such that you get hypotension and hyperkalemia. they also get acidosis and skin and mucosal hyper pigmentation. this is from the increased AcTH that is turned into MSH from POMC. get bilateral adrenal atrophy. spares the medulla.

78
Q

secondary adrenal insuficiency

A

this is from decreased AcTH. no skin pigmentation in this disease and no hyperkalemia

79
Q

infectious agent assocaited with Waterhouse Friderichsen syndrome

A

acute primary adrenal insufficiency due to adrenal hemorrhage assocaited with Neisseria meningitidis septicemia, DIC and endotoxic shock. severe hypotension.

80
Q

neuroblastoma

A

most common tumor of adrenal medulla in CHILDREN
occurs anywhere along sympathetic chain.
abdominal distension and a firm, irrgeular mass that can cross the midline (vs. Wilms tumors that do not cross).

81
Q

how to diagnose neuroblastoma

A

homovanillic acid (HVA) - a breakdown product of dopamine- found in the urine.
bombesin positive.
associated with overexpression of N-myc oncogene

82
Q

pheochromocytoma

A

tumor of chromafin cells. brown tumor. most common tumor of adrenal medulla in adults. derived from chromafin cells which arise from neural crest. cyclic hypertension, diarrhea, perspiration, palipitations, headache etc.

83
Q

how to diagnose pheochromocytoma

A

increased urinary VMA (breakdown product of norepi and epi) and plasma catecholamines are elevated

84
Q

what do patients with a pheo need before surgery

A

they need an alpha blocker like phenoxybenzamine (irreversible) and beta blockers to prevent any hypertensive issues when the tumor is removed.

85
Q

patient has symptoms of a pheo when they pee?

A

check the bladder wall. 10% met and they love the bladder wall.

86
Q

what is associated with myxedema (facial/periorbital)

A

this is associated with HYPOthyroidism. increased glycosaminoglycan in the larynx and throat can cause deepening of the voice.

87
Q

what is associated with pre tibial myxedema

A

HYPERthyroidism. graves disease. can also see periorbital edema.

88
Q

hyperthyroidism causes… (cholesterol levels)

A

Hypocholesterolemia.

89
Q

Hashimotos thyroditis

A

hypothyroidism. anti thyroid peroxidase and anti-thyroglobulin antibodies. enlarged, non tender thyroid

90
Q

genetic association HLA with hashimotos

A

HLADR5

91
Q

cancer risk with Hashimotos

A

non hodgkin lymphoma. this is because there is chronic inflammation and formation of germinal centers.

92
Q

hashimoto thyroid levels

A

may by hyperthyroid early on from toxicosis and rupture of cells and then become hypothyroid

93
Q

histological findings in hashimoto

A

hurthle cells, lymphoid aggregate with germinal centers

94
Q

congenital hypothyroidism

A

this is also known as cretinism. this is due to severe maternal hypothyroidism, thyroid agenesis, thyroid dysgenesis iodine deficiency or dyshormonogenic goiter.

95
Q

most common congenital thyroid enzyme deficiency

A

thryoid peroxidase

96
Q

findings of congenital thyroid deficiency

A 
Pot bellies
Pale
Puffy Faced
Protruding umbilicus (hernia)
Protuberant tongue
Poor brain development
97
Q

subacute de Quervain thyroditis

A

self limited hypothyroidism usually after a viral infection (flu like illness). may be hyperthyroid early in the course. classic is TENDER thyroid. this is unique. histology shows granulomas.

98
Q

findings in subacute de Quervains thyroiditis

A

tender thyroid
elevated ESR
jaw pain,
early inflammation

99
Q

Riedel thyroiditis

A

disease of young females generally
thyroid replaced by fibrous tissue- become hypothyroid
fibrosis can extend to local structures like airway.
mimics anaplastic carcinoma.
classic is a hard as wood non tender thyroid. IgG systemic disease.

100
Q

what drugs can cause hypothyroidism

A

lithium

101
Q

multinodular goiter

A

this is toxic when the cells make thyroid hormone regardless of TSH stimulation. hot nodules are rarely malignant. this is due to a mutation in the TSH receptor.

102
Q

Jod Basedown phenomenon

A

thyrotoxicosis is a patient with iodine deficiency goiter is given enough iodine to replenish it

103
Q

what causes graves disease

A

auto antibodies (IgG) stimulate TSH receptors on thyroid. get a diffuse goiter. these antibodies also stimulate retro-orbital fibroblasts giving pre-tibial myxedema. often presents during stress such as childbirth

104
Q

thyroid storm

A

complication of hyperthryoid conditions. stress induced catecholamine surge. can see increased alk phos from increased bone turnover. presents with agitation, delirium, fever, diarrhea, coma and tacchyarythmia.

105
Q

treatment of thyroid storm

A

three Ps
propanalol (beta blocker)
propylthiouracil
Prednisone

106
Q

scalloping of the colloid on histology

A

this is graves disease.

107
Q

increased thyroid uptake on a scan

A

this means its probbaly graves or a nodular goiter.

108
Q

decreased thyroid uptake on a scan

A

this is likely an adenoma or carcinoma.

109
Q

how to biopsy the thyroid

A

FNA. they will bleed if you do an open biospy. be careful and always do a fine needle aspiration.

110
Q

papillary carcinoma of the thyroid

A

most common thyroid cancer. empty or white appearing nuclei- orphan annie, psammoma bodies, nuclear grooves. good prognosis. increased risk with REt and BRAF mutations. goes to the cervical nodes but still good prognosis. can be seen in children who have had ionizing radiation.

111
Q

follicular carcinoma of the thyroid

A

carcinoma if it invades the capsule

adenoma if it does not invade the capsule

112
Q

medullary carcinoma of the thyroid

A

from parafollicular C cells, make calcitonin, see sheets of cells in an amyloid stroma.

113
Q

what genetic conditions are associated with medullary carcinoma of the thyroid

A

MEN2A, MEN2B, ret mutations

114
Q

anaplastic carcinoma of the thyroid

A

bad diagnosis. older patients. invades local structures. this is different from reidel thyroditis because of the age group. both can cause invasion of local structures and dysphagia

115
Q

what does elevated alk phos tell you

A

tells you there is osteoblast activity

116
Q

primary hypoerparathyroidism

A

this is usually from an adenoma. causes hypercalcemia and hypercalciuria and low phosphate. get increased cAMP in the urine (because PTH works via Gs signaling). presents as stones, bones, moans and groans. can cause acute pancreatitis- HY

117
Q

osteitis fibrsoma cystica

A

secondary to primary hyperparahtyroidism. when the bone gets replaced with fibrous tissue and cystic spaces. causes bone pain

118
Q

secondary hyperparathyroidism

A

this is from decreased gut absorption of Ca most often from chronic renal disease (reduced vitamin D). high PTH but LOW calclium. high phosphate if it is from renal disease. low phosphate from anything else.

119
Q

renal osteodystrophy

A

this is bone lesions due to secondary or tertiary hyperparathyroidism due in turn to renal disease. increased phosphate in the blood means it can bind calcium, which lowers free calcium levels

120
Q

tertiary hyperparathyroidism

A

this is refractory or autonomous PTH production in the presence of chronic renal disease

121
Q

Chovstek sign

A

tap on the facial nerve and contraction of the muscles. low calcium. often in hypoparathyroidism

122
Q

trousseau sign

A

occlusion of the brachial artery with BP cuff leading to carpal spasm. this is a sign of low calcium from hypoparathyroidism

123
Q

pseudohypoparathyroidism

A

also known as albright hereditary osteodystrophy
kidney is not responsive to PTH.
hypocalcemia, shortened 4th and 5th digits (if due to AD mutation in Gs), short stature.

124
Q

shortened 4th and 5th digits, short stature and low calcium

A

this is pseudohypoparathyroidism. it is from an AD mutation in the G stimulatory protein that is used to signal through PTH. it makes the kidney unresponsive to PTH that is secreted.

125
Q

what is the most common type of pituatary adenoma

A

prolactinoma

126
Q

treatment for prolactinoma

A

dopamine agonist like bromocriptine or cabergoline

127
Q

what other symptoms of prolactinoma other than galloctorrhea?

A

remember that prolactin decreases GnRH so you can get amenorhea in females and decreased libido in men. remember that women get gallactorrhea but men should not because they do not have any lobular units. only have terminal ducts and cant make milk.

128
Q

excess GH in children

A

gigantism

129
Q

excess GH in adults

A

acromegaly

130
Q

most common cause of death from excess GH

A

cardiac failure

131
Q

insulin and GH relationship

A

too much GH causes insulin resistance. nrmally oral glucose can reduce GH secretion

132
Q

how to medically treat acromegaly

A

octreotide- this blocks the response to growth hormone releasing hormone
pegvismant- growth hormone receptor blocker

133
Q

what is missing in diabetes insipidus

A

to little ADH

134
Q

how to treat central diabetes insipidus

A

intranasal DDAVP and hydration

135
Q

how to treat nephrgenic diabetic insipidus

A

HCTZ, indomethacin, amiloride, hydration

136
Q

causes of siADH

A

ectopic ADH from small cell lung cancer, CNS disorders/head trauma, pulmonary disease, drugs like cycloposphamide

137
Q

classic finding in siADH

A

urine osmolarity > serum osmolarity

138
Q

dangerous complications of siADH

A

seizures and cerebral edema from the hyponatremia. must correct this slowly because need t prevent central pontine myelinolysis.

139
Q

treatment of siADH

A

no water, democlocycline (ADH blocker)

140
Q

two drugs that can cause nephrogenic diabetes insipidus

A

lithium and democlocycine

141
Q

pituitary tumor in children

A

craniopharyngioma

142
Q

sheehan syndrome

A

this is ischemic infarct to the pituatary usually following post partum bleeding- patients prevent with no lactation and important- LOSS OF PUBIC HAIR

143
Q

genetic HLA association with type 1 diabetes

A

HLA DR3 and HLA DR4

144
Q

complications of diabetes

A

non enzymatic glycosylation of the large vessels- atherosclerosis, small vessels- hyline arteriolosclerosis esp in the kidney and of hemoglobin- Ha1c elevation.

also get osmotic damage to the schwann cells and pericytes in the retina. the lens also accumulates sugar causing cataracts

145
Q

what is classic finding in the kidney with diabetes

A

arteriolosclerosis of kidney. increased efferent involvement. nephrotic syndrome- sclerosis of the mesangium= kimmel steil wilson nodules

146
Q

aldose ruductase

A

this turns glucose into sorbitol. sorbital dehydrogenase is not in every tissue to reduce the sorbital. this happens in the lens, pericytes, schwann cells. neuropathy and cataracts.

147
Q

does type 1 or type 2 diabetes have a stronger genetic predominance

A

type 2

148
Q

which diabetes causes hyper-osmolar non ketotic coma

A

type 2

149
Q

which type of diabetes causes DKA

A

type 1 only!

150
Q

how does obesity increase diabetes

A

decreases the number of insulin receptors on adipose tissue and skeletal muscle. this makes the tissue more resistant to insulin

151
Q

which type of diabetes shows islet leukocyte infiltrate

A

type 1

152
Q

which type of diabetes shows islet amyloid polypeptide (IAPP) deposits

A

type 2

153
Q

what are kussmal respirations

A

rapid, deep breathing seen in DKA

154
Q

potassium situation in DKA

A

they have hyperkalemia but this is because there is no insulin to put any into the cells and the reality is that the cells intracellularly are severely depleted of K+

155
Q

treatment of DKA

A

fluids, insulin and K+ to replete the intracellular stores. if necessary give glucose to prevent hypoglycemia

156
Q

lab findings in DKA

A

hyperglycemia, increased H+, decreased bicarb, (anion gap metabolic acidosis). increase ketones, hyperkalemia

157
Q

whipple triad of episodic CNS symptoms with insulinoma

A

lethargy, syncope, and diplopia

158
Q

somatstatinoma

A

this means too much stomatostatin.
decreased gastrin, decreased CCK
leads to low acid, gallstones, steatorrhea

159
Q

VIPoma

A

this causes watery diarrhea, decreased K+, decreased gastric acid

160
Q

gastrinoma

A

this is a gastrin secreting tumor of the pancreas or duodenum. causes too much acid to be secreted- zollinger ellison syndrome. recurrent ulcers in distal duodenum and jejunum. presents with abdominal pain, diarrhea. can be seen in MEN1

161
Q

MEN1

A

parathyroid
pituatary adenoma
pancreatic endocrine tumor (gastirnoma, insulinoma, VIPoma, glucagonoma)

can present with kidney stones and stomach ulcers

162
Q

MEN2a

A

parathyroid
phoechromocytoma
medullary carcinoma of the thyroid

163
Q

MEN2b

A

pheochromocytoma
medullary carcinoma of the thyroid
oral or intestinal ganglineuromatosis- neuromas

associated with marfinoid habitus

164
Q

what gene is assocaited with Men2a and 2b

A

ret gene

First Aid Chapters (8 decks)

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