Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DIT topics > endocrine > Flashcards

endocrine Flashcards

1
Q

stimulates bone and muscle growth

A

growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

stimulates milk production

A

prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

stimulates milk secretion during lactation

A

oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

responsible for female 2° sex characteristics

A

estrogen (primarily estradiol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

stimulates metabolic activity

A

thyroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

↑ blood glucose level

↓ protein synthesis

A

glucocorticoids: cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

responsible for male 2° sex characteristics

A

testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

prepares endometrium for implantation/maintenance of pregnancy

A

progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

stimulates adrenal cortex to synthesize and secrete cortisol

A

ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

stimulates follicle maturation in females + spermatogenesis in males

A

FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

↑ plasma calcium

↑ bone resorption

A

PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

↓ plasma calcium, ↑ bone formation

A

calcitonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

stimulates ovulation in females + testosterone synthesis in males

A

LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

stimulates thyroid to produce TH and uptake iodine

A

TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

anterior pituitary hormones

A 
FLAT PiG
FSH
LH
ACTH
TSH
Prolactin
intermediate: MSH
GH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

made in hypothalamus and stored in

posterior pituitary hormones

A

ADH (supraoptic nucleus)

oxytocin (paraventricular nucleus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

adrenal cortex hormones

A

deeper you go, sweater it gets:

1) zona glomerulosa (salt): mineralcorticoids (aldosterone: Na+ retention)
2) zona fasciculata (sugar): glucocorticoids (cortisol)
3) zona reticularis (sex): androgens (testosterone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

sex gland hormones

A

ovaries: estradiol, progesterone, testosterone
placenta: estriol, progesterone
testes: testosterone, estrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

stimulates production of IGF-1

A

growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

thyroid hormones

A

T3/T4

calcitonin: parafollicular cells of thyroid (C cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

heart hormones

A

antrial natriuretic hormone (ANH) = atria of heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

pancreatic hormones

A

α cells: glucagon
ß cells: insulin
delta cells: somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

adrenal medulla hormones

A

Catecholamines: NE + epi (Chromaffin cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

fat cell hormones

A

estrone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

formed from rathke’s pouch (ectodermal diverticulum of primitive mouth that invaginates upward)

A

anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

formed from invagination of hypothalamus (neuroectoderm)

A

posterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

causes of hyperprolactinemia

A

pregnancy/nipple stimulation
stress (physical or pyschological)
prolactinoma (associated with bitemporal hemianopia = peripheral vision loss)
dopamine antagonist: antipsychotics (haloperidol, risperidone), domperidone, metoclopramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

premenopause female with hypogonadism sx:
infertility
oligo/amenorrhea
rarely galactorrhea (not hypogonadism sx)

A

hyperprolactinemia:

↑ prolactin → inhibits GnRH → no FSH, LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

postmenopausal female with hyperprolactinemia presents with

A

NOTHING (may have galactorrhea) - already hypogonadal (ovaries don’t respond to GnRH anyways - so inhibition of GnRH provides same action)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q 
male with hypogonadism (low T):
↓ libido
impotence
infertility: low sperm count
gynecomastia
rarely galactorrhea
A

hyperprolactinemia:

↑ prolactin → inhibits GnRH → no FSH, LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

most common pituitary adenoma

A

prolactinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q 
cause of:
amenorrhea
galactorrhea
low libido
infertilty
lesion the optic chiasm: bitemporal hemianopia
A

hyperprolactinemia from pituitary adenoma:

↑ prolactin → inhibits GnRH → no FSH, LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

treatment of pituitary adenoma

A

dopamine agonist: bromocriptine or cabergoline
↑ dopamine →↓ prolactin
surgical resection if visual sx severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q 
large tongue: deep furrows, indentations
increase spacing of teeth
deep voice
large hands + feet
coarse facial features (nose, ears)
impaired glucose tolerance (insulin resistance) → can lead to diabetes
A

acromegaly: excess GH in adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

excess bone growth of linear bones

tall + big children

A

gigantism: excess GH in kids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

diagnosis of acromegaly/gigantism

A 
IGF-1 (screening test, stable during day, downstream hormone)
if high IGF-1, oral glucose tolerance test (check GH: if ↑ glucose doesn't affect GH level = tumor)
not GH (pulsatile, highest at night)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

treatment of acromegaly/gigantism

A

resection of pituitary adenoma

then, octreotide (somatostatin analog)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

postpartum hemorrhage → underperfusion of pituitary → pituitary necrosis → hypopituitarism

A

sheehan syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q 
agalactorrhea (↓ prolactin)
amenorrhea after delivery
2° hypothyroidism: fatigue, cold intolerance, weight gain
acute hyponatremia (rare)
A

sheehan syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

replacement of tissue in sella turcica (= pituitary) with CSF would cause

A

called empty sella:
asymptomatic (enough residual pituitary tissue outlining sella turcica) or symptoms of pituitary hormone deficiency (1 or more hormones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

adrenal cortex and medulla derived from

A

adrenal cortex: mesoderm

adrenal medulla: neural crest = ectoerm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

most common tumor of adrenal MEDULLA in adults

A

pheochromocytoma: chromaffin cell tumor (neural crest cell)→catecholamines: ↑ NE, epi, dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q 
EPISODIC of:
sweats
severe HTN (episodic) + headache
tachycardia 
palpitations
A

pheochromocytoma: chromaffin cell tumor →↑ NE, epi, dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

most common tumor of adrenal MEDULLA in kids

A

adrenal neuroblastoma: tumor of sympathetic ganglion cells (can develop anywhere along chain, 40% in adrenals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

secrete little dopamine, VMA, HVA:

kid with mild SUSTAINED HTN

A

adrenal neuroblastoma: tumor of adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

fetal type 2 pneumocytes can’t mature and secrete surfactant without

A

fetal cortisol (wk 34 GA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

no aldosterone: HYPOTENSION, hyponatremia (salt wasting), hyperkalemia
no cortisol: ↑ ACTH
↑17-OH progesterone
shunt pathway to ↑ androgens: masculinization, virilization

A

21 α hydroxylase deficiency: congenital adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

diagnosis of 21 α hydroxylase deficiency

A

screening test: ↑↑ 17-OH progesterone
if no screening test is done:
infant girl: masculinization is obvious
infant boy: salt wasting is life-threatening (↓Na, ↑K)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

no aldosterone
no cortisol
↑ DOC = deoxycorticosterone (seak MC that causes Na +H20 retention → HTN)
shunt pathway to ↑ androgens: masculinization, virilization

A

11 ß hydroxylase deficiency: congenital adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

no cortisol
no testosterone, estrogen: default pathway: phenotypic female (since default) unable to mature; ambiguous genitalia with undescended testes, if male
ONLY aldosterone: Na + H20 retention →HTN, hypokalemia

A

17α hydroxylase deficiency: congenital adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

complication of 21α hydroxylase, 11 ß hydroxylase deficiency, 17 α hydroxylase deficiency

A

all cause NO cortisol →↑↑ ACTH → hyperplasia of adrenal gland in order to make more cortisol

52
Q

no aldosterone: Na+ excretion in urine (salt wasting) → early death if untreated
no cortisol
no testosterone, estrogens: phenotypic female (since default) unable to mature; ambiguous genitalia with undescended testes, if male
↑ pregnenolone, DHEA

A

3ß-HSD deficiency

53
Q

causes of cushing syndrome: ↑ cortisol

A

1) exogenous steroid use (glucocorticoids)

2) Cushing disease: ACTH-producing pituitary adenoma
3) non-pituitary tumor/cancer that produces ectopic ACTH: small cell lung cancer
4) adrenal overproduction of cortisol: adrenal adenoma

54
Q

symptoms of Cushing syndrome (4 stars)

A 
BAM, CUSHINGOID
Buffalo hump
Amenorrhea
Moon facies
Crazy: psychosis, agitation
Ulcers (PUD)
Skin changes: acne, thinning of skin, bruising, purple striae
HTN
Infection 
Necrosis of femoral head
Glaucoma, cataracts
Osteoporosis
Immunosuppresion
Diabetes
55
Q

diagnosis of cause of cushing syndrome requires

A 
dexamethasone suppression test: 
low dose of dexamethasone (only glucocorticoid that doesn't interfere with cortisol assay)
check cortisol in morning
high dose of dexamethasone
check cortisol next morning
56
Q

Conn syndrome

A

aldosterone-secreting adrenal tumor: 1° hyperaldosteronism

57
Q

triad:
HTN: Na, H20 retention
hypokalemia
metabolic alkalosis: low K+ stimulates H+ urinary excretion + H+ moves intracellularly in exchange for K+ out of cells
low plasma renin: ↑ aldo →↓ renin (- feedback)

A

aldosterone-secreting adrenal tumor: 1° hyperaldosteronism (Conn syndrome)

58
Q

kidneys sense low intravascular volume → RAAS system

↑ renin → ↑ aldo

A

2° hyperaldosteronism

59
Q

causes of 2° hyperaldosteronism

A

*(kidneys sense low intravascular volume= ↓ renal perfusion:
renal artery stenosis
low output heart failure: low LV EF
*low protein state, compensatory ↑ renin due to low intravascular volume:
nephrotic syndrome
cirrhosis

60
Q

treatment of 1° hyperaldosteronism

A

surgical resection of tumor
if both adrenals secreting or no surgery:
aldosterone antagonist: spironolactone, eplerenone

61
Q

no cortisol AND aldosterone: hypotension
hyponatremia
hyperkalemia
generalized fatigue
anorexia
weight loss (opposite of excess cortisol)
skin hyperpigmentation: ↑ ACTH → stimulates MSH R

A

1° adrenal insufficiency: addison disease

62
Q

causes of 1° adrenal insufficiency: addison disease

A

1) autoimmune destruction of adrenal cortex

2) met cancer
3) TB
4) Waterhouse-Friderichsen syndrome

63
Q

skin hyperpigmentation

A

1° adrenal insufficiency: addison disease ONLY

64
Q

acute 1° adrenal insufficiency due to adrenal hemorrhage from severe N. meningococcal sepsis (petechial rash) or DIC (coagulopathy)

A

Waterhouse-Friderichsen syndrome

65
Q

treatment for 1° adrenal insufficiency: addison disease

A

treat low cortisol AND aldosterone:

glucocorticoid: prednisone, etc.
mineralcorticoid: fludrocortisone

66
Q

↓ACTH → ↓ cortisol
NORMAL aldosterone (stimulated by renin!): NO hyperkalemia, hypotension
+ weakness, malaise, weight loss

A

2° adrenal insufficiency

67
Q

↓ CRH from hypothalamus due to abrupt withdrawal of long-term exogenous steroid use (must wean)
suppression of HPA axis: ↓ CRH, ACTH, cortisol
NORMAL aldosterone: no hyperkalemia, hypotension

A

3° adrenal insufficiency

68
Q

diagnosis of pheochromocytoma

A 
urine test for byproducts:
VMA: vanillylmandelic acid
↑serum catecholamines:
metanephrine
normetanephrine
69
Q

rule of 90’s for pheochromocytoma

A 
90% benign
90% unilateral
90% adrenal medulla 
90% no calcification
90% adults
70
Q

MEN 2A and 2B AND neurofibromatosis I are associated with what adrenal pathology

A

pheochromocytoma

71
Q

EPO-secreting tumors → polycythemia

A

pheochromocytoma
renal cell carcinoma
hemangioblastoma: vascular tumor of CNS
hepatocellular carcinoma

72
Q

treatment of pheochromocytoma

A

surgical resection
before surgery, medically-treat HTN, tachycardia:
epi stimulates α + ß receptors
α blocker for HTN!!! (nonselective, irreversible: phenoxybenzmine)
then, ß blocker for tachycardia!!!
if only ß blocker with α blocker: epi stimulates α R (vasoconstrict) → ↑ bp even more

73
Q

diagnosis of adrenal neuroblastoma

A

urinary VMA and HVA

74
Q

n-myc oncogene

A

adrenal neuroblastoma

75
Q

bombesin tumor marker

A

adrenal neuroblastoma

76
Q

neurofilament stain

A

adrenal neuroblastoma

77
Q

Homer Wright rosettes: radial arrangement of tumor cells around central tangle of fibrils

A

adrenal neuroblastoma

78
Q

thyroid gland makes excess T3/T4

A

hyperthyroidism

79
Q

general term for excess thyroid hormone due to exogenous drug or thyroid inflammation

A

thyrotoxicosis

80
Q 
tachycardia
palpitations
anxiety
weight loss
heat intolerance
hyperactivity
warm skin
A

thyrotoxicosis (includes hyperthyroidism)

81
Q

diagnosis of thyrotoxicosis (includes hyperthyroidism)

A

screen: serum TSH (increases exponentially, sensitive)

confirmation/determine extent of disease: free T4/T4 (increases linearly)

82
Q

autoimmune disorder
TSI (thyroid stimulating immunoglobulin = IgG) binds to TSH receptor on thyroid gland → stimulates free T3/T4 secretion →↓ TSH
may have goiter: swelling of thyroid gland
4:1 female predominance

A

hyperthyroidism: Graves’ disease

83
Q

associated with HLA-DR3 and HLA-B8

A

graves’ disease

84
Q

diagnosis of hyperthyroidism: Graves’ disease

A

↑ uptake on radioactive iodine study (diffuse)

thyroid uptakes LOTS of iodine to keep up with T3/T4 production

85
Q 
warm dry skin, thin hair
tachycardia, palpitations
muscle atrophy
weight loss
bowel hypermobility
↓ or absent menstrual flow
\+/- goiter
exophthalmos: abnormal CT deposition in orbit + EOM
pretibial myxedema: ↑ deposition of CT components: glycosamino glycans, mucopolysaccharides, thickening of skin on shins
thyroid bruit
A

hyperthyroidism: Graves’ disease

86
Q

treatment of hyperthyroidism: Graves’ disease

A

antithyroid: propylthiouracil, methimazole
B blocker: ↓ HR, anxiety
definitive treatment: surgical resection or radioactive iodine: iodine taken up into thyroid gland → destroyed by high dose iodine of next several mo (with need thyroid replacement meds)

87
Q

causes of hyperthryoidism

A 
Graves disease
toxic adenoma (single nodule) /toxic multinodular goiter
iodine-induced hyperthryoidism
subacute thryoiditis
thyroid storm
struma ovarii teratoma: thyroid tissue
88
Q

focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH R →↑ free T3/T4
hyperthyroidism sx
rarely malignant

A

toxic adenoma (single)/toxic multinodular goiter

if wasn’t associated with hyperthyroidism - called “non-toxic” adenoma

89
Q

diagnosis of toxic adenoma/toxic multinodular goiter

A

radioactive uptake and scan: ↑ iodine uptake only in nodules (“hot nodules”)

90
Q

goiter

A

can be hyperfunctioning, hypofunctioning or normal

91
Q

common if iodine deficiency goiter who receives iodine or iodide (IV iodine contrast agent, amiodirone)
↑ risk if Graves disease or toxic multinodular goiter: ↑ hyperthyroidism

A

iodine-induced hyperthryoidism (Jod-Basedow phenomenon)

92
Q

occurs after viral URI: coxsackie, echovirus, adenovirus, measles, mumps
acute fever + rapid PAINFUL goiter
early: transient elevation in T3/T4 - follicular release of pre-stored hormone (HYPERthyroid)
late: HYPOthyroidism (due to focal destruction of thyroid + granulomatous inflammation)
or transient thyroiditis: NEVER progresses to hypothyroidism, SELF-LIMITED
3:1 female predominance

A

subacute thyroiditis (granulomatous infiltration, hypothyroidism + PAINFUL goiter)

like hoshimoto’s thyroiditis - (lymphocytic infiltration, hypothyroidism + PAINLESS goiter)

both: hyperthyroid → hypothyroid

93
Q

associated with HLA-B35

A

subacute thyroiditis

94
Q 
most dangerous type of thyrotoxicosis
complication of Graves disease (most common) or other hyperthyroid states
SURGE of T3/T4 + catecholamines
↑ body temp
AMS
tachycardia
vomiting
diarrhea
dehydration
coma
death
A

thyroid storm

95
Q

treatment of thyroid storm

A

ß blocker: ↓ catecholamine effect

PTU or methimazole: ↓ T3/T4

96
Q

causes of hypothyroidism

A

destruction of thyroid gland:
congenital hypothyroidism
autoimmune Ab-mediated destruction (Hoshimoto’s)
iodine deficiency or excess
subacute granulomatous thyroidits (late course)
tx of hyperthyroidism by radiation
surgical removal of thyroid
idiopathic
meds: amiodarone, tyrosine kinase inhibitors (chemo), lithium
CANCER

97
Q 
cold intolerance
weight gain
constipation
menorrhagia
slowed mental/physical function
dry skin
coarse brittle hair
reflexes showing slow return phase
A

hypothyroidism

98
Q

treatment of hypothyroidism

A

levothyroxine: T4 (most common)
triiodothyronine: T3

99
Q

cause of congenital hypothyroidism

A

thyroid dysgenesis: complete agenesis, hypoplasia, ectopic (failed to descend)
thyroid-related enzyme deficiency
dysfunctional TH production, transport, function
TSH resistance
transfer of anti-thyroid meds or anti-thyroid antibodies from mom
leading cause outside US: iodine deficient mom during pregnancy (supplemented in US diet)

100
Q 
newborn screen for this
if untreated child has:
impaired physical growth
ID
enlarged tongue
enlarged/distended abdomen
A

congenital hypothyroidism

101
Q

autoimmune: infiltrate of lymphocytes into thyroid → eventual destruction of hormone production
hypothyroidism + PAINLESS goiter
early: EUthyroid, + ab, normal TH/TSH, asymptomatic (may never progress to thyroid dysfunction with + ab)
inflammation begins: destruction of thyroid follicle cells → spill T3/T4 = transient HYPERthryoidism (lasts few mo)
destruction of thyroid: HYPOthyroid (goiter → scarred, shrunken gland)
5:1 female
↑ incidence with age

A

hoshimoto’s thyroiditis: most common cause of hypothyroidism in US

102
Q

diagnosis of hoshimoto’s thyroiditis

A 
TH
TSH
thyroglobulin antibodies
thyroid peroxidase antibodies
presence of Abs doesn't mean will become hypothyroid
103
Q

HLA-DR5

HLA-B5

A

hoshimoto’s thyroiditis

104
Q

autoimmune thyroid diseases can be associated with

A 
other autoimmune diseases:
addison's disease
type 1 DM
pernicious anemia
vitiligo
sjogren syndrome
105
Q

↑risk B cell lymphoma of thyroid gland (RAPIDLY enlarging thyroid mass)

A

hoshimoto’s thyroiditis

106
Q

treatment of subacute thyroiditis

A

relief of thyroid pain
NSAID
corticosteriods
if hypothyroidism:thyroid hormone replacement

107
Q

YOUNG patient with:
chronic inflammation of thyroid → replaced by fibrous tissue (can extend into airway)
histo: fibrosis, MACROPHAGES, EOSINOPHILS
hypothyroid or euthyroid
FIXED, HARD, ROCK-LIKE PAINLESS goiter

A

riedel thyroiditis

108
Q

thyroid nodules/goiter

A

isolated or multiple (multinodular goiter)

can be associated with normal thyroid function, hyperthryoidism, hypothyroidism

109
Q

evaluation of thyroid nodule

A

US: size, location, abnormal lymph nodes in neck
can’t determine if benign or malignant
biopsy by fine needle aspirations: determine if benign or malignant
thyroid cancers are never HOT nodules = not making normal or overproducing TH (iodine uptake + scan)

110
Q

papillary shaped cells
no follicles/colloid
ground glass appearance of cytoplasm with large nuclei with nuclear grooves or empty appearing nuclei “orphan annie nuclei”
“psammoma bodies”: concentric calcifications

A

papillary thyroid cancer: most common type of thyroid cancer

111
Q

papillary thyroid cancer risk factors

A

tobacco use
radiation exposure: treatment dose radiation to neck
possibly hereditary: RET gene mutation or BRAF

112
Q

activation of tyrosine kinase receptor

A

papillary and medullary thyroid cancer

113
Q 
30-50 yo
 "orphan annie nuclei"
"psammoma bodies"
good prognosis
may reoccur
3:1 female predominance
A

papillary carcinoma of thyroid

114
Q

treatment of thyroid cancer

A

1) total thyroidectomy
followed by radioactive
2) papillary or follicular:
iodine treatment (higher dose if treating hyperthryoidism because of increased need for iodine to make TH)
3) medullary: no radioactive iodine (not a carcinoma of thyroid producing cells)

115
Q

uniform cuboidal cells lining follicles
cancer of follicle cells surrounded by fibrous capsule - cells INVADE fibrous capsule
can spread in blood (unique to thyroid cancer - most carcinomas spread by lymph nodes)
3:1 female prodominance

A

follicular thyroid carcinoma: 2nd most common type

116
Q

uniform cuboidal cells lining follicles

A

follicular adenoma OR follicular thyroid carcinoma (but invasive - invade fibrous capsule)

117
Q

associated with RET gene mutation or BRAF gene mtuation

A

papilllary thyroid carcinoma

118
Q

associated with RAS mutation

or PAX8-PPAR gamma 1 rearragment

A

follicular thyroid carcinoma

119
Q

proliferation of parafollicular C cells in medulla (secrete calcitonin)

A

medullary carcinoma of thyroid

120
Q

associated with MEN 2A and MEN 2B

A

medullary carcinoma of thyroid

if have cancer - must remove screened for pheochromocytoma BEFORE removal of thyroid

121
Q

associated with RET gene mutation

A

papillary or medullary thyroid carcinoma

122
Q

undifferentiated neoplasm
more common in elderly
FIXED, HARD, ROCK-LIKE PAINLESS goiter WITH local extensions
very poor prognosis

A

anaplastic thyroid carcinoma

123
Q

surgical complications of thyroidectomy

A

remove/damage parathyroid: ↓ Ca (perioral tingling, myalgia/cramping → tetany, seizures in POST-OP period), can have transient hypoglycemia that recovers over wks
damage to recurrent laryngeal nerves (vagus nerve - innervates thyroid + vocal cords): hoarseness

124
Q

complications of hypothyroidism

A

↑ LDL

↑ total cholesterol

125
Q

complications of hyperthryoidism

A

atrial fibrillation: need rate-control drug
use ß blocker (not CCB): treat HR + adrenergic sx of hyperthyroidism
tx hyperthyroidism: methimazole

DIT topics (115 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions