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
2
Q
what is the typical presnetation of papillary thyroid cancer
A
usually early lymphatic spread is the first finding. there are usually microcalcifications
3
Q
what is the first step after finding a thyroid nodule
A
ultrasound
4
Q
what is the second step after finding a thyroid nodule
A
measuring TSH.
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.
6
Q
what is more likely to be malignant hot or cold nodules
A
cold nodule s
7
Q
what is the second most common type of thyroid cancer
A
follicular
8
Q
what are the characteristics of follicular thyroid cancer
A
blood vessel invasion with capsular invasion
usually no lymph node involvement
9
Q
what does orphan annie nuclei suggest on thyroid biopsy
A
papillary carcinoma
10
Q
is lymphoma of thyroid rare or common
A
very rare and usually arises due to hashimotos thyroiditis
11
Q
what does psammoma bodies on thyroid biopsy suggest
A
papillary carcinoma
12
Q
what are the most likely findings on biopsy of papillary thyroid cancer
A
psammoma bodies and orphan Annie nuclei
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
14
Q
what does high prolactin do to FSH and LH
A
decreases them. it has an inhibitory effect on GnRH
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
16
Q
where are LH and FSH made
A
pituitary
17
Q
where is GnRH made
A
hypothalamus
18
Q
what is the consequence of GnRH secretion
A
increases LH and FSH which then stimulate the ovaries to secrete estrogen
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
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
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
22
Q
does a prolactinoma produce galactorrhea in men
A
Very rarely
23
Q
what does a proalctinoma usually cause in men
A
erectile dysfunction
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.
25
what is the name from reduced GnRH that impacts gonadal function
hypogonatropic hypogonadism
26
elevated calcitonin is indicative of what
medullary carcinoma of the thyroid
27
where are pheochromocytomas located
within the adrenal medulla
28
what hormones are produced within the adrenal gland and where
cortex -corticoids and androgens
| medulla -catecholamines + somatostatin and substance P
29
what are the subdivisions of the adrenal cortex and what do they produce
glomerulosa -mineral corticoids
fasciculata -glucocorticoids
reticular -androgens
30
what is the next step after a pheochromocytoma is found
provide phenoxbenzamine
31
can you give beta blockers to someone with a pheochromocytoma
NO. you know why. same reason for cocaine use
32
what is the therapy for neuroblastoma or pheochromocytoma tumors that cannot be resected or are inoperable
Metaiodobenzylguanidine (MIBG) is similar in structure to norepinephrine, so it is taken up by sympathetic nerve cells throughout the body
33
what is the treatment of choice for thyroid cancer that is less than 1 cm
lobectomy
34
does aripriprazole cause hyperprolactinemia
no. it is unique as it acts as a partial agonist under hypodopaminergic conditions
35
can hypothyroidism cause hyperprolactinemia and galactorrhea
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.
36
what endocrinolgical is the RET gene mutation associated with
MEN2A and B
37
what is the presentation of MEN2A
medullary thyroid (95-100% of cases); pheochromocytoma 40%; primary hyperparathyroid 20-30
38
what is the presentation of MEN2B
medullary thyroid (95-100% of cases); pheochromocytoma 40%
marfanoid habitus
multiple neurinomas
39
what is the presentation of MEN1
primary hyperparathyroidism 90%, pancreatic tumors
| gastrinoma and insulinoma, pituitary adenoma carcinoid tumors.
40
what must be checked in someone with MEN2 before surgery and why
metanephrines. this can cause hemodynamic instability during surgical procedures
41
what is the most common cause of adrenal insufficiency and what is another cause
autoimmune adrenalitis
| Tuberculosis
42
signs or symptoms of acromegaly
(e.g., bitemporal hemianopsia, coarsened facial and skull features, amenorrhea, or hypertension)
43
what is the cause of diabetic nephropathy, retinopathy, or neuropathy.
microvascular damage
44
what is thyroid storm
It presents very acutely with hyperpyrexia, tachycardia, hypertension, nausea, vomiting, and severe agitation. life threatening complicated hyper metabolic state
45
treatment for toxic adenoma
beta blockers and thioamides (PTU, methamazole)
46
presentation of cushings
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,
47
what are three tests for diagnosing cushings and how is the diagnosis made
low-dose dexamethasone suppression test along with a midnight salivary cortisol test and 24-hour urinary cortisol
need two positive tests
48
after Cushing's diagnosis what is the next step
high dose dexamethasone test to determine if this is ectopic or pituitary produced ACTH.
49
what type of ACTH production will be sensitive to high dose dexamethasone
pituitary. ectopic is resistant
50
what is the most likely cause of ectopic ACTH/cushings
small cell lung cancer
51
what is the presentation of adrenal crisis and what is the treatment
abdominal pain, emesis, shock (hypotension, tachycardia), and fever immediately after surgery
glucocorticoids --high dose hydrocortisone
52
whaat is the firstline treatment for pituitary adenoma
cabergoline; bromocriptine and other dopamine agonists can be used as well
53
what is the second line therapy for pituitary adenoma
transsphenoidal surgery
54
what does cabergoline do
shrinks tumors and reduces the prolactin secretion
55
what is a treatment of GBM
temozolamide
56
how does cabergoline work on pituitary adenomas
it is a dopamine agonist and acts to suppress prolactin release and reduces the size fo the tumor
57
what is the etiology of toxic adenoma
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
what tis the presentation of hashimotos
hypothyroidism and a generally enlarged painless thyroid or goiter
59
what are the positive lab findings for hashimotos
Thyroid peroxidase (TPO) and thyroglobulin (Tg) antibodies
60
what antibodies are found in Graves
anti TSH and thyroglobulin
61
why dont we immediately remove thyroglossal cysts
because they may be the only thyroid tissue that the person has
62
what does deficiency of ACTH cause
hypotension, hypoglycemia --loss of glucocorticoids
63
Cerebral salt wasting syndrome is what
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
what are some commonly used agents for neuropathic pain
SNRIs, gabapentin, carbamazepine, tramadol
65
what is perinaud syndrome
Includes vertical gaze abnormalities, nystagmus, impaired convergence, upper eyelid retraction, ptosis, and pupillary abnormalities.
66
Weight loss, headache, insomnia, and Parinaud syndrome suggest
a tumor of the pineal gland (pinealoma).
67
what is an endocrinological consequence of pinealoma
precocious puberty due to the preoduction of bhcg from germinoma which is the most common type off pinealoma
68
what is a malignant neuroendocrine tumor in children that produces catecholamines and crosses the midline
neuroblastoma
69
what is opsoclonus-myoclonus
rapid jerky eye and feet movements
70
what is the presentation of hashimotos
lymphocytic infiltrate on biopsy, hypothyroidism, nontender mass in the neck,
71
what is the presentation of 21b-hydroxylase deficiency f
essentially congenital adrenal insufficiency with virilization.
this means that the adrenal glands cannot appropriately produce steroids and must be titrated appropriately.
72
what is the treatment for 21B-hydrox def
hydrocortisone and fludrocortisone
73
what is congenital adrenal hyperplasia
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
what is the most common form of CAH
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
what are the rare forms of CAH
| and what is the treatment
(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
why do breasts still develop in androgen insensitivity syndrome
because the adipose tissue converts androgens into estrogen and that causes breast development
77
what is the treatment for androgen insensitivity
gonadectomy
78
what is the a consequence of acromegaly
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
what are the endocrinological findings for prader willi and the treatment
hypogonadism and short stature.
| treat with testosterone and growth hormone
80
how does 17alpha hydroxylase present
with decreased androgens and elevated 11 deoxycorticosterone
81
what is the presentation of 21 hydroxylase def
decreased cortisol, aldosterone and 11 deoxycorticosterone with elevated androgens
female pseudohermaphordism and precocious puberty in males
82
what is 11B hydroxylase def
decreased cortisol and aldosterone, with increased 11deoxycorticosterone and increased androgens
83
what is the main difference between 21hydroxylase, 11beta hydroxylase and 17alpha deficiency
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
what is the presnetation of neuroblastoma
raccoon eyes or periorbital bruising/bleeding with bulging, nausea, fever, failure to thrive, cardiac symptoms, posterior mediastinal mass
85
what gene is mutated in neuroblastoma
N-myc
86
is there is a risk to the baby in graves disease
yes 5% have thyrotoxicosis
| the toxicosis usually resolves within 12 weeks after the antibodies are out of the system
87
what is the treatment for infantile thyrotoxicosis
methimazole and propanolol
88
what is the greatest risk of diabetic keto acidosis
cerebral edema
89
what is the presentation of cretinism
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
what does obesity in children do the reproductive systme
causes precocious puberty through pusatile GnRH due to the overproduction of leptin
91
what is the presentation of constitutional growth delay
short stature, decreased bone age (2-4 years), later puberty, family history
92
what is the presentation of hypocalciuric hypercalcemia of the newborn
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
what is the treatment of precocious puberty
Leuprolide therapy. the hyperstimulation will lead to reduction in LH and FSH
this is FUCKING STUPID
94
what is the treatment for lead poisoning
succimer
95
what is the presentation of lead poisoning
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
what is the presentation of hypocortisolism
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
what is recommended for all types of adrenal insufficiency
glucocorticoids
98
what do glucocorticoids treat in adrenal insufficiency
hypocortisolism
99
what is the LH/FSH in PCOS
ratio is increased.
100
In a patient with type 2 DM who presents with a UTI, blurred vision and signs of dehydration should raise suspicion of a
hyperosmolar hyperglycemic state (HHS).
101
what do you give to someone activity seizing from hypoglycemia
IV dextrose
102
what else other than dextrose can you give to someone with hypoglycemia
glucagon
103
what is the treatment of choice for gigantism
transphenoidal adenomectomy
104
what is the treatment for hyperthyroidism
propanolol therapy for symptomatic treatment first. then start on antithyroidals
105
what is the cause of exophthalmus in graves
fibroblast secretion and accumulation of glycosaminoglycan in the orbit
106
what is the treatment of choice for acute symptomatic hypercalcemia
IVF and calcitonin
107
what is the presentation of glucagonoma
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
what is the treatment for glucagonoma
octreotide. this will bring the symptoms under rapid control
109
what is Hawthorne bias
principle that states that people modify their behavior when they think they ar being observed
110
what does pooling studies together do
increases the precision of the results; reduces the likelihood of a type II error based on increased statistical power
111
can pooling data from individual studies overcome the limitations of those studiees
no. the data out is only as good as the data in
112
the risk is calculated how
cases/people in question
113
what is the relative risk
risk of X/risk in general pop = (a/(a+b))/(c/(c+d))
114
when do you use anova
when you are comparing the averages of threee or more groups
115
when do you use a t test
when you are comparing the averarges of two groups
116
when do you use the Kaplan meier analysis
when you are looking to compare the incidence of something over time
117
what is cancer anorexia-cachexia syndrome treated with
megestrol acetate or glucocorticoids
118
what causes cancer anorexia-cachexia syndrome
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
megestrol acetate can be used for stimulating appetite in what disorders
cancer. HIV
120
people with hep B are Moree likely to get what renal disease
membraneous nephropathy
121
what is the physiological result of nasogastric tube/vimiting
hyopkalemic, hypochloremic metabolic alkalosis
122
what is necessary for diagnosing metabolic acidosis
anion gap
123
what is necessary for diagnosing metabolic alkalosis
uirine chloride
124
what is it called and what are the causes of metabolic alkalosis with normal urine chloride
this is chloride responsive metabolic alkalosis or responsive to fluids. this is secondary to volume loss or diuretic use.
125
what is it called and what are the causes of metabolic alkalosis with elevated urine chloride
this is chloride-resitant alkalosis.
| associated with mineralocorticoid excess and hypertension and increased extracellular volume
126
what is the first thing you do when someone has hyperkalemia
ECG
127
what is the treatment for hyperkalemia without e\cg changes
furosemide and saline
128
what should SLE patients with proteinuria have
renal biopsy to rule out lupus nephritis
129
what is the presentation of scurvy
bruising, coiled hairs deficient wound healing.
