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amboss endocrine Flashcards

1
Q

what is the most common type of thyroid cancer

A

papillary carcinoma of the thyroid accounts for 80% of thyroid cancers

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2
Q

what is the typical presnetation of papillary thyroid cancer

A

usually early lymphatic spread is the first finding. there are usually microcalcifications

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3
Q

what is the first step after finding a thyroid nodule

A

ultrasound

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4
Q

what is the second step after finding a thyroid nodule

A

measuring TSH.

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5
Q

what to do if thyroid nodule and normal or elevated TSH

A

regular monitoring in case the tumor grows to more than 1cm and then fine needle aspiration.

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6
Q

what is more likely to be malignant hot or cold nodules

A

cold nodule s

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7
Q

what is the second most common type of thyroid cancer

A

follicular

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8
Q

what are the characteristics of follicular thyroid cancer

A

blood vessel invasion with capsular invasion

usually no lymph node involvement

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9
Q

what does orphan annie nuclei suggest on thyroid biopsy

A

papillary carcinoma

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10
Q

is lymphoma of thyroid rare or common

A

very rare and usually arises due to hashimotos thyroiditis

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11
Q

what does psammoma bodies on thyroid biopsy suggest

A

papillary carcinoma

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12
Q

what are the most likely findings on biopsy of papillary thyroid cancer

A

psammoma bodies and orphan Annie nuclei

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13
Q

what is the treatment for papillary thyroid cancer

A

total thyroidectomy; partial resection is possible with tumors <1 cm with no lymph node involvement t

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14
Q

what does high prolactin do to FSH and LH

A

decreases them. it has an inhibitory effect on GnRH

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15
Q

what is the presentation of hyperprolactinemia

A

can have milk productive effects, decreases estrogen which causes vaginal atrophy, oligo/amonorrhea, endometrial atrophy. decreased LH/FSH

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16
Q

where are LH and FSH made

A

pituitary

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17
Q

where is GnRH made

A

hypothalamus

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18
Q

what is the consequence of GnRH secretion

A

increases LH and FSH which then stimulate the ovaries to secrete estrogen

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19
Q

what does estrogen do to LH and FSH in a normal system

A

they inhibit the release as a negative feedback system at the pituitary gland

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20
Q

what happens to estrogen/LH/FSH in primary ovarian failure

A

there is decreased estrogen production in response to pulsatile GnRH and thus FSH and LH will be HIGH due to the lack of response from the ovaries

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21
Q

what does prolactin do to the GnRH axis

A

it inhibits the production release of LH and FSH from the pituitary gland and thus reduces estrogen at the ovaries. this is what happens in pituitary adenoma

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22
Q

does a prolactinoma produce galactorrhea in men

A

Very rarely

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23
Q

what does a proalctinoma usually cause in men

A

erectile dysfunction

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24
Q

why does a prolactinoma cause erectile dysfunction in men

A

because the high levels of prolactin will inhibit the release of GnRH from the hypothalamus and thus the release of FSH and LH from the testicles. this will reduce the testosterone levels The resulting manifestations include erectile dysfunction, decreased libido, reduced testicular volume, infertility, gynecomastia, and loss of axillary hair.

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25
Q

what is the name from reduced GnRH that impacts gonadal function

A

hypogonatropic hypogonadism

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26
Q

elevated calcitonin is indicative of what

A

medullary carcinoma of the thyroid

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27
Q

where are pheochromocytomas located

A

within the adrenal medulla

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28
Q

what hormones are produced within the adrenal gland and where

A

cortex -corticoids and androgens

medulla -catecholamines + somatostatin and substance P

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29
Q

what are the subdivisions of the adrenal cortex and what do they produce

A

glomerulosa -mineral corticoids
fasciculata -glucocorticoids
reticular -androgens

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30
Q

what is the next step after a pheochromocytoma is found

A

provide phenoxbenzamine

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31
Q

can you give beta blockers to someone with a pheochromocytoma

A

NO. you know why. same reason for cocaine use

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32
Q

what is the therapy for neuroblastoma or pheochromocytoma tumors that cannot be resected or are inoperable

A

Metaiodobenzylguanidine (MIBG) is similar in structure to norepinephrine, so it is taken up by sympathetic nerve cells throughout the body

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33
Q

what is the treatment of choice for thyroid cancer that is less than 1 cm

A

lobectomy

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34
Q

does aripriprazole cause hyperprolactinemia

A

no. it is unique as it acts as a partial agonist under hypodopaminergic conditions

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35
Q

can hypothyroidism cause hyperprolactinemia and galactorrhea

A

yes. In primary hypothyroidism, decreased T3 and T4 levels stimulate the hypothalamus to release TRH (thyrotropin releasing hormone), which in turn increases TSH secretion by the anterior pituitary. In addition to increasing TSH production, excessive TRH also stimulates the lactotroph cells of the anterior pituitary to release prolactin, thus resulting in a state of hyperprolactinemia.

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36
Q

what endocrinolgical is the RET gene mutation associated with

A

MEN2A and B

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37
Q

what is the presentation of MEN2A

A

medullary thyroid (95-100% of cases); pheochromocytoma 40%; primary hyperparathyroid 20-30

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38
Q

what is the presentation of MEN2B

A

medullary thyroid (95-100% of cases); pheochromocytoma 40%
marfanoid habitus
multiple neurinomas

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39
Q

what is the presentation of MEN1

A

primary hyperparathyroidism 90%, pancreatic tumors

gastrinoma and insulinoma, pituitary adenoma carcinoid tumors.

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40
Q

what must be checked in someone with MEN2 before surgery and why

A

metanephrines. this can cause hemodynamic instability during surgical procedures

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41
Q

what is the most common cause of adrenal insufficiency and what is another cause

A

autoimmune adrenalitis

Tuberculosis

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42
Q

signs or symptoms of acromegaly

A

(e.g., bitemporal hemianopsia, coarsened facial and skull features, amenorrhea, or hypertension)

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43
Q

what is the cause of diabetic nephropathy, retinopathy, or neuropathy.

A

microvascular damage

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44
Q

what is thyroid storm

A

It presents very acutely with hyperpyrexia, tachycardia, hypertension, nausea, vomiting, and severe agitation. life threatening complicated hyper metabolic state

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45
Q

treatment for toxic adenoma

A

beta blockers and thioamides (PTU, methamazole)

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46
Q

presentation of cushings

A

hypertension, hypokalemia, (mild) hypernatremia, fatigue, muscle weakness, and depression, weight gain (central obesity, moon facies, and buffalo hump), bruisable skin and stretch marks, hirsutism, acne, and hyperglycemia,

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47
Q

what are three tests for diagnosing cushings and how is the diagnosis made

A

low-dose dexamethasone suppression test along with a midnight salivary cortisol test and 24-hour urinary cortisol
need two positive tests

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48
Q

after Cushing’s diagnosis what is the next step

A

high dose dexamethasone test to determine if this is ectopic or pituitary produced ACTH.

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49
Q

what type of ACTH production will be sensitive to high dose dexamethasone

A

pituitary. ectopic is resistant

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50
Q

what is the most likely cause of ectopic ACTH/cushings

A

small cell lung cancer

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51
Q

what is the presentation of adrenal crisis and what is the treatment

A

abdominal pain, emesis, shock (hypotension, tachycardia), and fever immediately after surgery
glucocorticoids –high dose hydrocortisone

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52
Q

whaat is the firstline treatment for pituitary adenoma

A

cabergoline; bromocriptine and other dopamine agonists can be used as well

53
Q

what is the second line therapy for pituitary adenoma

A

transsphenoidal surgery

54
Q

what does cabergoline do

A

shrinks tumors and reduces the prolactin secretion

55
Q

what is a treatment of GBM

A

temozolamide

56
Q

how does cabergoline work on pituitary adenomas

A

it is a dopamine agonist and acts to suppress prolactin release and reduces the size fo the tumor

57
Q

what is the etiology of toxic adenoma

A

arise from gain-of-function mutations in the TSH receptor. this causes autonomous functioning of cells with that receptor which are not susceptible to feedback regulation and the thyroid follicular cells to hypertrophy and eventually become a toxic adenoma

58
Q

what tis the presentation of hashimotos

A

hypothyroidism and a generally enlarged painless thyroid or goiter

59
Q

what are the positive lab findings for hashimotos

A

Thyroid peroxidase (TPO) and thyroglobulin (Tg) antibodies

60
Q

what antibodies are found in Graves

A

anti TSH and thyroglobulin

61
Q

why dont we immediately remove thyroglossal cysts

A

because they may be the only thyroid tissue that the person has

62
Q

what does deficiency of ACTH cause

A

hypotension, hypoglycemia –loss of glucocorticoids

63
Q

Cerebral salt wasting syndrome is what

A

may occur in patients after neurosurgical procedures, is a hypovolemic, hypotonic hyponatremia. Patients with cerebral salt wasting syndrome have a low serum osmolality, as seen here, but also present with symptoms of hypovolemia (e.g., hypotension, tachycardia) and paradoxical polyuria.

64
Q

what are some commonly used agents for neuropathic pain

A

SNRIs, gabapentin, carbamazepine, tramadol

65
Q

what is perinaud syndrome

A

Includes vertical gaze abnormalities, nystagmus, impaired convergence, upper eyelid retraction, ptosis, and pupillary abnormalities.

66
Q

Weight loss, headache, insomnia, and Parinaud syndrome suggest

A

a tumor of the pineal gland (pinealoma).

67
Q

what is an endocrinological consequence of pinealoma

A

precocious puberty due to the preoduction of bhcg from germinoma which is the most common type off pinealoma

68
Q

what is a malignant neuroendocrine tumor in children that produces catecholamines and crosses the midline

A

neuroblastoma

69
Q

what is opsoclonus-myoclonus

A

rapid jerky eye and feet movements

70
Q

what is the presentation of hashimotos

A

lymphocytic infiltrate on biopsy, hypothyroidism, nontender mass in the neck,

71
Q

what is the presentation of 21b-hydroxylase deficiency f

A

essentially congenital adrenal insufficiency with virilization.
this means that the adrenal glands cannot appropriately produce steroids and must be titrated appropriately.

72
Q

what is the treatment for 21B-hydrox def

A

hydrocortisone and fludrocortisone

73
Q

what is congenital adrenal hyperplasia

A

group of disorders that are characterized by low cortisol, high levels of ACTH, and adrenal hyperplasia. the exact clinical manifestations depend on the exact defect.

74
Q

what is the most common form of CAH

A

a deficiency of 21β-hydroxylase and manifests with hypotension, ambiguous genitalia, virilization (in the female genotype), and/or precocious puberty (in both males and females).

75
Q

what are the rare forms of CAH

and what is the treatment

A

(e.g., 11β-hydroxylase and 17α-hydroxylase deficiencies) manifest with symptoms of mineralocorticoid excess (e.g., hypertension) and therefore require spironolactone (aldosterone receptor inhibitor) in addition to glucocorticoid replacement.

76
Q

why do breasts still develop in androgen insensitivity syndrome

A

because the adipose tissue converts androgens into estrogen and that causes breast development

77
Q

what is the treatment for androgen insensitivity

A

gonadectomy

78
Q

what is the a consequence of acromegaly

A

cardiomyopathy, which may progress to congestive heart failure and manifest with reduced cardiac output. Cardiovascular complications such as hypertension and ventricular hypertrophy are the most common complications and the cause of death in ∼ 60% of patients with acromegaly.

79
Q

what are the endocrinological findings for prader willi and the treatment

A

hypogonadism and short stature.

treat with testosterone and growth hormone

80
Q

how does 17alpha hydroxylase present

A

with decreased androgens and elevated 11 deoxycorticosterone

81
Q

what is the presentation of 21 hydroxylase def

A

decreased cortisol, aldosterone and 11 deoxycorticosterone with elevated androgens
female pseudohermaphordism and precocious puberty in males

82
Q

what is 11B hydroxylase def

A

decreased cortisol and aldosterone, with increased 11deoxycorticosterone and increased androgens

83
Q

what is the main difference between 21hydroxylase, 11beta hydroxylase and 17alpha deficiency

A

21 has decreased 11-deoxycorticosterone while the others have decreased.
17 is the only one with decreased androgens
11beta os the only one with both elevated androgens and elevated 11-deoxycorticosterone

84
Q

what is the presnetation of neuroblastoma

A

raccoon eyes or periorbital bruising/bleeding with bulging, nausea, fever, failure to thrive, cardiac symptoms, posterior mediastinal mass

85
Q

what gene is mutated in neuroblastoma

A

N-myc

86
Q

is there is a risk to the baby in graves disease

A

yes 5% have thyrotoxicosis

the toxicosis usually resolves within 12 weeks after the antibodies are out of the system

87
Q

what is the treatment for infantile thyrotoxicosis

A

methimazole and propanolol

88
Q

what is the greatest risk of diabetic keto acidosis

A

cerebral edema

89
Q

what is the presentation of cretinism

A

enlarged tongue, hypotonia, poor feeding, raspy crying, neonatal jaundice, umbilical hernia.
this presents similar to Beckwith-weideman syndrome but the patient will not display symptoms at birth becuase maternal will cover them

90
Q

what does obesity in children do the reproductive systme

A

causes precocious puberty through pusatile GnRH due to the overproduction of leptin

91
Q

what is the presentation of constitutional growth delay

A

short stature, decreased bone age (2-4 years), later puberty, family history

92
Q

what is the presentation of hypocalciuric hypercalcemia of the newborn

A

shortly after birth the infant will become jittery and have severe tachycardia. there will be low PTH and calcium because the maternal hypercalcemia suppressed the parathyroid glands

93
Q

what is the treatment of precocious puberty

A

Leuprolide therapy. the hyperstimulation will lead to reduction in LH and FSH
this is FUCKING STUPID

94
Q

what is the treatment for lead poisoning

A

succimer

95
Q

what is the presentation of lead poisoning

A

abdominal pain, fatigue (which may be a sign of anemia and lead-induced encephalopathy), and bluish-black discolorations of the gums. Moving to another house prior to the start of symptoms could also indicate exposure to lead-based paint that was used in houses built before 1978. However, the gum discoloration due to lead exposure (i.e., the Burton line) appears as a thin line along the gums rather than generalized gum hyperpigmentation.

96
Q

what is the presentation of hypocortisolism

A

include lethargy, weight loss, anorexia, gastrointestinal complaints, hypotension (due to decreased catecholamine‑induced vasoconstriction and myocardial contractility), decreased serum glucose (due to increased peripheral glucose utilization and decreased gluconeogenesis), and dilutional hyponatremia (due to increased secretion of antidiuretic hormone). Hyperpigmentation of the skin and gums is caused by increased production of melanocyte-stimulating hormone, which is cleaved from the same precursor peptide as ACTH;

97
Q

what is recommended for all types of adrenal insufficiency

A

glucocorticoids

98
Q

what do glucocorticoids treat in adrenal insufficiency

A

hypocortisolism

99
Q

what is the LH/FSH in PCOS

A

ratio is increased.

100
Q

In a patient with type 2 DM who presents with a UTI, blurred vision and signs of dehydration should raise suspicion of a

A

hyperosmolar hyperglycemic state (HHS).

101
Q

what do you give to someone activity seizing from hypoglycemia

A

IV dextrose

102
Q

what else other than dextrose can you give to someone with hypoglycemia

A

glucagon

103
Q

what is the treatment of choice for gigantism

A

transphenoidal adenomectomy

104
Q

what is the treatment for hyperthyroidism

A

propanolol therapy for symptomatic treatment first. then start on antithyroidals

105
Q

what is the cause of exophthalmus in graves

A

fibroblast secretion and accumulation of glycosaminoglycan in the orbit

106
Q

what is the treatment of choice for acute symptomatic hypercalcemia

A

IVF and calcitonin

107
Q

what is the presentation of glucagonoma

A

increases gluconeogenesis and inhibits glycolysis, causing hyperglycemia and/or mild diabetes. Anemia may be a result of anemia of chronic illness or directly related to the inhibitory effect of glucagon on erythropoiesis. As seen here, patients with glucagonoma can also present with neuropsychiatric symptoms (e.g., depression, dementia, ataxia). Necrolytic migratory erythema is characterized by the occurrence of multiple, centrifugally spreading erythemas, located predominantly on the face, perineum, and lower extremities, which develop into painful and pruritic crusty patches with central areas of bronze-colored induration.

108
Q

what is the treatment for glucagonoma

A

octreotide. this will bring the symptoms under rapid control

109
Q

what is Hawthorne bias

A

principle that states that people modify their behavior when they think they ar being observed

110
Q

what does pooling studies together do

A

increases the precision of the results; reduces the likelihood of a type II error based on increased statistical power

111
Q

can pooling data from individual studies overcome the limitations of those studiees

A

no. the data out is only as good as the data in

112
Q

the risk is calculated how

A

cases/people in question

113
Q

what is the relative risk

A

risk of X/risk in general pop = (a/(a+b))/(c/(c+d))

114
Q

when do you use anova

A

when you are comparing the averages of threee or more groups

115
Q

when do you use a t test

A

when you are comparing the averarges of two groups

116
Q

when do you use the Kaplan meier analysis

A

when you are looking to compare the incidence of something over time

117
Q

what is cancer anorexia-cachexia syndrome treated with

A

megestrol acetate or glucocorticoids

118
Q

what causes cancer anorexia-cachexia syndrome

A

progressive wasting of skeletal muscle mass with or without the loss of body fat that occurs in patients with cancer. Results from decreased appetite and the hypercatabolic state that is generated by pro-inflammatory cytokines and tumor-derived factors.

119
Q

megestrol acetate can be used for stimulating appetite in what disorders

A

cancer. HIV

120
Q

people with hep B are Moree likely to get what renal disease

A

membraneous nephropathy

121
Q

what is the physiological result of nasogastric tube/vimiting

A

hyopkalemic, hypochloremic metabolic alkalosis

122
Q

what is necessary for diagnosing metabolic acidosis

A

anion gap

123
Q

what is necessary for diagnosing metabolic alkalosis

A

uirine chloride

124
Q

what is it called and what are the causes of metabolic alkalosis with normal urine chloride

A

this is chloride responsive metabolic alkalosis or responsive to fluids. this is secondary to volume loss or diuretic use.

125
Q

what is it called and what are the causes of metabolic alkalosis with elevated urine chloride

A

this is chloride-resitant alkalosis.

associated with mineralocorticoid excess and hypertension and increased extracellular volume

126
Q

what is the first thing you do when someone has hyperkalemia

A

ECG

127
Q

what is the treatment for hyperkalemia without e\cg changes

A

furosemide and saline

128
Q

what should SLE patients with proteinuria have

A

renal biopsy to rule out lupus nephritis

129
Q

what is the presentation of scurvy

A

bruising, coiled hairs deficient wound healing.

step II (22 decks)

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