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Endocrine Flashcards

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1
Q

what 8 organs make up the endocrine system

A 
pancreas
pituitary
thyroid
parathyroid
adrenal
thymus
ovary/testis
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2
Q

what is the difference between endocrine and exocrine

A

endocrine glands secrete hormones that go into the bloodstream, which are then carried to their targest to induce specific action

exocrine glands secrete products into ducts

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3
Q

which gland is considered the “master gland” and why

A

pituitary gland

this gland controls/regulates most other endocrine glands

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4
Q

where is the pituitary gland anatomically

A

at the base of the brain

lies in the sella turcica of the sphenoid bone

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5
Q

how does the hypothalamus and pituitary work together in function

A

the pituitary is connected to the hypothalamus via a stalk

–>the hypothalamus releases factors that regulates the release of trophic hormones from the pituitary

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6
Q

embryologically where are the anterior and posterior lobe of the pituitary derived

A

anterior–>the primitive oral cavity (Rathke’s Pouch)

posterior–>neuroectoderm

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7
Q

what shape cells make up the anterior pituitary and how are they organized

A

round cells arranged in cords and nests

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8
Q

what cells are present in the anterior pituitary and what hormones do they secrete

A 
somatotroph-->growth hormone (GH)
lactotroph-->prolactin (PRL)
coritcotroph-->corticotropin (ACTH)
gonadotroph-->LH and FSH
thyrotroph-->Thyrotropin (TSH)
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9
Q

what is the anatomic size of the pituitary

A

size of a pea

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10
Q

what type of cells make up the posterior pituitary

does the posterior pituitary secrete hormones?

A

modified glial cells w/ axonal processes extending from the hypothalamic neurons

NO; but the hypothalmic neurons secrete oxytocin and antidiuretic homrone (ADH)

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11
Q

what is almost always associated pathologically with anterior lobe hyperfunction

A

pituitary adenoma

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12
Q

what are 2 etiologies of anterior pituitary hyperfunction

A
  1. hormone production

2. mass effect

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13
Q

what is the associated syndromes for overproduction of:

  1. ACTH
  2. GH
  3. Prolactin
  4. Prolactin & GH
  5. TSH
  6. FSH, LH
A
  1. Cushings
  2. Gigantism, Acromegaly
  3. Galactorrhea/amenorrhea–>sexual dysfunction, infertility
  4. combinations of prolactin and GH excess
  5. hyperthyroidism
  6. hypogonadism
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14
Q

what are 2 main symptoms of hyperfunction of the pituitary (hyperpituitarism)

A
  1. pressure on the optic n causing visual disturbances

2. increased intracranial pressure–>headache, nausea, vomiting

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15
Q

in which gender are prolactinomas more noticeable

A

women

in men they have to grow to be very larger before symptoms

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16
Q

with GH adenomas, what determines the clinical manifestation

–>what are some manifestations that present

A

when epiphyses closes

  • -prognathic mandible
  • -spacing of dentition
  • -large sausage-like fingers
  • -hypertension and CHF
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17
Q

what happens in hypofunction of the pituitary (Hypopituitarism)

A

deficiency of one or multiple hormones

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18
Q

causes of hypopituitarism

A
  • nonfunctional pituitary adenoma
  • postpartum ischemic necrosis (75% of gland must be compromised to show symptoms)
  • ablation/destruction by surgery, radiation, adjacent tumor
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19
Q

what syndromes are associated with the underproduction of these hormones:

  1. GH
  2. Gonadotropin
  3. Prolactin
  4. TSH
  5. ACTH
A
  1. pituitary dwarfism
  2. amenorrhea and infertility in women
    - ->decreased libido, impotence, lack of pubic/axillary hair in men
  3. no post partum lactation
  4. hypothyroidism
  5. hypoadrenalism
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20
Q

what hormone causes pathology with the posterior pituitary gland and what are the complications?

A

ADH

normal fxn: to help kidney resorb water

hypofunction: if not enough ADH then body retains less water
- ->develops diabetes insipidus: excessive thirst and diluted urine

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21
Q

gigantism

  • -etiology
  • -onset
  • -clinical features
  • -tx
  • -prognosis
A

ETIOLOGY: pituitary adenoma in anterior lobe that secretes GH (hyperfxn)

ONSET: before epiphyseal plates close in long bones

CLINCIAL FEATURES: generalized increase in size, disproportionately long arms and legs

TX: surgical removal of adenoma

PROGNOSIS: fair to good

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22
Q

ACROMEGALY

  • -etiology
  • -onset
  • -clincial features
  • -tx
  • -prognosis
A

ETIOLOGY: pituitary adenoma producing excess GH

ONSET: after epiphyseal plates close

CLINCIAL FEATURES: enlarged bones of hands, feet, face; prognathism, diastema; hypertension, CHF

TX: surgical removal of adenoma

PROGNOSIS: guarded–>because of hypertension and CHF

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23
Q

Pituitary Dwarfism

  • -etiology
  • -clinical features
  • -tx
  • -prognosis
A

ETIOLOGY: lack of production of GH -OR- pts tissues don’t respond to GH

CLINICAL FEATURES: short stature, small jaws/teeth

TX: hormone replacement therapy (if lack of production is problem)

PROGNOSIS: Good

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24
Q

Thyroid–embryology

-where does thyroid gland originate and where does it migrate to

A

arises at the base of the tongue from invagination of endoderm (in region of foramen cecum)

migrates down to its permanent anatomic location anterior to the thyroid cartilage

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25
Thyroid--histology | -cells that exist
follicles filled with colloid and lined by cuboidal follicular cells C-cells scattered between follicles
26
what is a lingual thyroid
remnant of tissue in thyroid's original position before migration to its permanent anatomical position tissue remaining at the base of the tongue
27
what is the shape of a thyroid gland? | can you palpate it?
"bow tie" shape | cannot always palpate a healthy thyroid during head and neck exam
28
what is the thyroid's job
regulate the RATE that the body carries out necessary functions -->"thermostat"
29
Hyperthyroidism etiologies (5)
Diffuse toxic hyperplasia-->graves disease hyperfunctional multinodular goiter hyperfunctinoal thyroid adenoma TSH-secreting pituitary adeonoma (rare) ingestion of exogenous thyroid hormone-->synthroid
30
diagnosis of hyperthyroidism | -->on hormonal level
elevated TH and decreased TSH
31
hyperthyroidism clinical behavior
hypermetabolic - ->GI hypermobility, malabsorption, diarrhea - ->weight loss; although increase appetite increased activity of symp nervous system - ->irritable, nervous, tremor, palpations - ->can't sit still (hypermobile) - ->tachycardia
32
hyperthyroidism clinical features
- ->weight loss - ->exophthalmos--buldging of the eyes - ->wide eye gaze, eyelid lag - ->excessive sweating (always hot) - ->flushed warm skin
33
what is thyroid storm trigger? complication?
thyroid storm is sudden onset of hyperthyroidism symptoms triggered by stress MEDICAL EMERGENCY-->pts that are not treated will die of cardiac arrythmias
34
tx of thyroid storm prognosis
reactive iodine used to destroy overactive thyroid tissue good prognosis if tx
35
what gender is predominantly affected by graves disease
females | 7:1
36
what are clinical presentations of graves disease
- ->hyperthyroidism symptoms - ->exophtalmos (40% of cases) - ->skin lesion--pretibial myxedema - ->diffuse enlargement of thyroid gland
37
what is another name for graves disease
diffuse toxic hyperplasia
38
what is happening on the hormonal level during graves disease
autoimmune complication that causes autoantibodies to TSH receptor-->constantly stimulated get increase TH and decrease TSH
39
what happens to the follicles in graves disease
hyperplasia of the follicles with lymphoid infiltrates
40
what is pretibial myxedema?
scaly skin thickening over the shin that presents in graves disease
41
hypothyroidism
lack of thyroid hormone production
42
etiologies of hypothyroidism
iodine deficiency autoimmune destruction of thyroid (hasimoto's thyroiditis) ablation by surgery or radiation
43
what are two ways that hypothyroidism can manifest clincially and what is the major difference between these two classes
cretinism vs myxedema age cretinism-->infants and young children myxedema-->older children and adults
44
cretinism clinical manifestations
- impaired development of skeleton and CNS - short stature - severe mental retardation - protruding tongue **rare--due to iodine supplementation
45
myxedema clinical manifestations
- generalized apathy - mental sluggishness - obesity - cold intolerant - enlarge tongue - deepen voice - constipation - late cardiac effects **accumulation of mucopolysaccharide rich edema
46
what happens to levels of TSH in hypothyroidism
TSH increase in primary hypothyroidism-->loss of feedback inhibition TSH does not increase in primary hypothalamic or pituitary disease
47
tx of hypothyroidism
exogenous thyroid hormone replacement therapy | -->synthroid
48
prognosis of hypothyroidism
good unless tx is delayed
49
hashimoto thyroiditis
most common cause of hypothyroidism autoimmune destruction of the thyroid gland -->usually these patients are normal and progress to hypothyroidism
50
hasimotos affects what gender
predominantly females; older | significant genetic component
51
complications of hashimotos
pts usually at risk from other autoimmune disease and B-cell non hodgkin lymphomas no risk for thyroid neoplasm
52
what is the most common clinical manifestation of thyroid disease
goiter
53
if there is a diffuse mutlinodular goiter on a pt what could you suspect
there is impaired synthesis of thyroid hormone
54
impaired synthesis of thyroid hormone is most often caused by
diet deficiency
55
clinical problems w/ goiter
- cosmetic - airway obstruction - compression of vessels - dysphagia
56
when do you see a hyperfunctional "toxic" goiter
hyperthyroidism
57
thyroid nodules are commonly detected but how many are cancerous
1% are carcinomas most are non neoplastic if male and younger-->more likely to be neoplastic
58
what is the main risk factor for a thyroid nodule to be cancerous
exposure to radiation in the first 2 decades of life
59
follicular adenoma - presentation - pathology - histology
- presents as a solitary nodule; 3-5 cm in diameter - separated from thyroid by thin capsule - composed of follicles w/ varying amounts of colloid
60
thyroid neoplasma (5) - ->most common - ->worst prognosis
1. follicular adenoma 2. papillary thyroid carcinoma--most common 3. follicular carcinoma 4. anaplastic thyroid carcinoma--worst prognosis 5. medullary thyroid carcinoma
61
onset of papillary thyroid carcinoma
3rd-5th decade
62
gender affected most by papillary thyroid carcinoma
female
63
etiology of papillary thyroid carcinoma
radiation exposure | possible mutation of RET proto-oncogene
64
pathology of papillary thyroid carcinoma
characterized by papillary projections
65
histology of papillary thyroid carcinoma
nuclear changes | -->clear nucleus "orphan annie nuclei"
66
papillary thyroid carcinoma | -->prognosis
10 yr survival rate is >95% | indolent lesions
67
follicular carcinoma | -who does it affect
older age than papillary thyroid carcinoma | areas with dietary iodine deficiency
68
follicular carcinoma | -presentation
resemebles an adenoma w/ capsule | must see invasion through capsule or into blood vessels
69
anaplastic thyroid carcinoma - what is it? - common? - prognosis - etiology
rapid enlargement in a long standing goiter rare may be sporadic or familial extremely poor prognosis
70
medullary thyroid carcinoma - common? - derived from which cells? - etiology - alter hormones?
uncommon derived from parafollicular (C) cells may be sporadic or familial mutation in RET proto-oncogene increase serum calcitonin
71
parathyroid developed embryologically from where?
third and fourth pharyngeal pouches
72
what cells are in the parathyroid
most chief cells | also oxyphil cells
73
function of chief cells in parathyroid
regulate free Ca2+ levels in the blood secretes PTH
74
function of oxyphil cells in the parathyroid
no known fxn
75
what is parathyroid hormone
secreted from the chief cells in the parathyroid to regulate free Ca2+ levels in the blood stream
76
what happens when the parathyroid detects there is a decrease in free Ca2+ levels in the blood
stimulates synthesis and secretion of PTH
77
what are the physiologic effects of the body when PTH is secreted (4) what is the net effect?
1. increase renal reabsorption of Ca2+ 2. increase urinary excretion of phosphate 3. increase osteoclastic activity which releases Ca2+ from bone 4. increase conversion of Vit D into active form to increase GI absorption of Ca2+ NET EFFECT: increase in free level of Ca2+ in the blood which will inhibit further PTH secretion
78
what is a main complication of hyperparathyroidism
hypercalcemia | -->excessive secretion of PTH
79
two types of hyperparathyroidism
primary: spontaneous overproduction of PTH secondary: results from pts primary disease of chronic renal failure
80
primary hyperparathyroidism - ->who does it effect most? - ->what is usually the cause? - ->clincial features
WHO: adults, females 4:1 Cause: parathyroid adenoma, hyperplasia CLINICAL FEATURES: -->"painful bones, stones, abdominal groans, psychic moans" - ->fractures due to osteoporosis - ->kidney stones - ->constipation, peptic ulcers, gallstones - ->depression, lethargy, seizures
81
what are some presentations found in primary hyperparathyroidism that you can notice on a radiograph or during your clinical exam?
radiograph: ground glass appearance brown tumor in the jaws
82
what complication might you see in primary hyperparathyroidism that poses problems with blood vessels?
metastatic calcifications calcium deposits throughout the body, including blood vessels
83
what is the most common cause of secondary hyperparathyroidism?
renal failure
84
what role does renal failure play in secondary hyperparathyroidsim?
causes phosphatemia because of inefficient phosphate excretion this depresses serum free Ca2+ levels which stimulates PTH-->causes hyperplastic parathyroid glands
85
besides causing phosphatemia, why else is kidney dysfunction a problem that exacerbates an already hyperplastic parathyroid gland?
kidney normal converts vitamin D into active from which allows Ca2+ to be absorbed in the gut because there is kidney failure there is decreased vitamin D synthesis so there is decreased intestinal absorption of Ca2+-->does not help the already bad situation
86
secondary hyperparathyroidism symptoms
dominated by renal failure symptoms same symptoms as primary parathyroidism but less severe
87
secondary hyperparathyroidism clincial manifestation
bone changes--renal osteodystrophy
88
what happens to serum Ca2+ levels with secondary hyperparathyroidism
stays near normal because PTH increase raises Ca2+ levels although they are being depleted due to kidney failure
89
hypoparathyroidism - ->prevalence - ->etiology - ->clinical manifestations
prevalence: uncommon etiology - ->surgical removal of parathyroid gland by accident during thyroidectomy - ->congenital absence (DiGeorge's Syndrome) - ->auto-immune disease clinical manifestations: - ->hypocalcemia - ->increase neuromuscular activity - ->cardiac arrhythmias - ->increase intracranial pressure and seizures
90
what is the connection between DiGeorge's Syndrome and the parathyroid gland
causes congenital absence of the gland | Causing hypothyroidism
91
tx of hyperparathyroidism | -->prognosis
surgical removal of hyperplastic parathyroid glands kidney transplant PROGNOSIS-->good
92
where does the pancreas arise embryologically
from the endoderm of the foregut
93
what is the name for the clusters of cells in the pancreas (endocrine)
islets of langerhans
94
what are cell types that make up the islets of langerhans
beta-->insulin alpha-->glucagon delta-->somatostatin PP-->pancreatic polypeptide
95
what is the leading cause of end stage renal disease (ESRD), blindness, and amputation
diabetes mellitus
96
what is the result of diabetes and the defective insulin secretion or action
hyperglycemia
97
what are the two types of diabetes - ->onset - ->symptoms - ->what is wrong with the insulin
TYPE 1: onset by age 20 - ->juvenile - ->insulin dependent - ->insulin deficiency because B cells are destroyed - ->polyuria, polyphagia, polydipsia - ->ketoacidosis: fat is primary energy source so build up of ketones in the blood which decreases the blood pH and leads to diabetic coma TYPE 2: onset after age 40 - ->polyuria and polydipsia - ->insulin is there but body does not respond to it, peripheral resistance to insulin
98
what is normal blood glucose level what is considered diabetic
70-120 mg/dL diabetic if over 200 mg/dL; or fasting glucose is greater than 126 mg/dL
99
disposing factors for type 2 diabetes
- ->obesity - ->pregnancy - ->stress
100
what happen in pancreas w/ diabetes
reduces size and number of islets heavy inflammatory infiltrate amyloid deposition
101
what happen in vessel due to diabetes
atherosclerosis MI and stroke gangrene
102
what happens in the kidney due to diabetes
2nd leading cause of death behind vascular diseases glomerularsclerosis, proteinuria, ESRD nodular glomerularsclerosis renal atherosclerosis pyelonephritis
103
how does diabetes affect the eye
4th leading cause of blindness retinal detachment
104
can diabetes affect the nerves
YES diabetic neuropathy
105
islet cell tumors
insulinoma gastrinoma zollinger-ellison syndrome
106
insulinoma - ->cell and affect on insulin - ->symptoms - ->tx
beta cell tumor causes hyperinsulinism most are asymptomatic surgical excision
107
gastrinoma - -where? - - secrete what?
duodenum, peripancreatic tissue, pancreas gastric acid hypersecretion
108
Zollinger-Ellison Syndrome - -what? - -secretion? - -benign or malignant? - -Tx?
pancreatic islet tumor gastric acid hypersecretion most are malignant surgical resection

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