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PTH560 Pathology > Exam 2 - other endocrine diseases > Flashcards

Exam 2 - other endocrine diseases Flashcards

1
Q

anatomically (parathyroid?) derived from

A

3rd and 4th pharyngeal pouches

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2
Q

Parathyroid hormone function

A

*** maintains ionized serum calcium levels

  • inc renal calcium reabsorb
  • dec renal phosphorus reabsorb
  • inc intestinal calcium and phosphorus reabsorb
  • dec bicarbonate reabsorb

-inc 1-alpha hydroxylase synthesis in kidney (increases calcitriol synthesis)

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3
Q

Parathyoid hormone (stim and suppressed by)

A

stim:

  • hypocalcemia
  • hyperphosphatemia

suppressed by:

  • hypercalcemia
  • hypophosphatemia
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4
Q

Calcium (total serum vs free-ionized)

A
  • total serum bound to albumin

- free-ionized is metabolically active and is a negative feedback on PTH

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5
Q

What happens if calcium is decreased?

A

tetany:
- partial depolarization of nerves and muscles
- carpopedal spasm
- Chvostek sign: facial twitch with facial nerve tap

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6
Q

Hypoalbuminemia is what?

A
  • decreased total calcium

- normally free, ionized calcium

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7
Q

What is hypoparathyroidism?

A

-a hypofunction of the parathyroid glands resulting in hypocalcemia

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8
Q

What are the causes of hypoparathyroidism?

A
  • Autoimmune (most common)
  • previous thyroid surgery
  • DiGeorge syndrome (failure of 3rd and 4th pharyngeal pouches to develop)
  • hypomagnesemia (Mg needed for cAMP, which is required for PTH use)
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9
Q

Hypoparathyroidism: clinical findings

A
  • tetany
  • basal ganglia calcification (inc phosphorus drives calcium into brain)
  • cataracts
  • Candida assocation
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10
Q

Hypoparathyroidism: labs and treatment

A

labs:

  • dec calcium and PTH (parathyroid hormone)
  • inc phosphorus

Treatment:
-calcium, vid D3, teriparatide

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11
Q

Primary hyperparathyroidism

A

-***most common nonmalignant cause of hypercalcemia

  • postmenopausal women
  • asymptomatic in 50%
  • MEN I and IIa association
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12
Q

Primary hyperparathyroidism: Adenoma

A
  • ***single adenoma
  • usually right inferior gland
  • sheets of chief cells (no intervening adipose)
  • atrophy in rest of gland
  • hypercalcemia decrease PTH secretion from tissue
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13
Q

Primary hyperparathyroidism: Primary hyperplasia

A
  • *** all four glands

- chief cell hyperplasia

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14
Q

Primary hyperparathyroidism: clinical findings

A

*-“Stones, bones, groans, and psychic overtones”

due to hypercalcemia

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15
Q

Primary hyperparathyroidism: LABS and treatment

A

Labs:

  • **- inc PTH
  • **- inc calcium
  • **- dec phosphorus

treatment: surgery to remove, treat the hypercalcemia

***Hypercalcemia from malignancy normally has a dec PTH!

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16
Q

What is Secondary Hyperparathyroidism?

A
  • hyperplasia of all four glands

* **physiological compensation for hypocalcemia

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17
Q

Secondary Hyperparathyroidism: Labs

A

Labs:

  • dec calcium
  • inc PTH

-may eventually normalize labs (tertiary hyperparathyroidism, autonomous glands)

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18
Q

Normal thyroid A&P

A

-contains largest store of hormones out of all endocrine glands

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19
Q

Thyroid hormone function

A
  • ***controls BMR
  • turnover of hormones
  • cell regen
  • growth and maturation of tissue
  • receptor synthesis
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20
Q

Thyroid labs look at

A
  • total serum T4
  • TSH
  • (a specific) Iodine uptake
  • thyroglobulin
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21
Q

Total serum T4 and TBG

A

-total serum t4 is free t4 and TBG-bound T4

TBG (thyroid binding globulin)

  • produced in liver
  • production inc by estrogen
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22
Q

Thyroid stimulating hormone (TSH)

A
  • screen for dysfunction
  • ***produced in anterior pituitary
  • increased with inc TRH
  • inc with low T3 and T4
  • dec with high T3 and T4
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23
Q

123Iodine uptake

A
  • measures synthetic activity in thyroid
  • iodide needed in thyroid hormone synthesis
  • inc uptake = inc T4 synthesis
  • dec uptake = gland inactivity/inflammation
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24
Q

Lingual thyroid

A
  • failed decent of thyroid (remains at base of tongue)
  • clinical find: dysphagia, mass lesion
  • Diag: 123-I uptake
  • Treat: thyroxine suppression, ablation, surgery
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25
Q

Thyroglossal duct cyst

A
  • cystic midline mass
  • near hyoid bone
  • Treatment: surgery (remove hyoid or prox duct)
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26
Q

Acute thyroiditis

A

**BACTERIAL (usually staph aureus

clin: fever, tender, cervical adenopathy, initial thyrotoxicosis, dec 123-I uptake

Treat: penicillin or ampicillin

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27
Q

Sub-acute granulomatous thyroiditis

A

**VIRAL (mumps, coxsackievirus)

clin:
- PAINFUL* thyroid gland
- most common cause is preceding URI

-Self-limiting

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28
Q

Hashimoto thyroiditis

A
  • autoimmune
  • ***most common cause of hypothyroidism

-pathogenesis: cytotoxic T cells destroy gland, dec THS, macrophages destroy tissue

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29
Q

Cretinism

A

-hypothyroidism in infancy

Cause: maternal hypothyroidism, iodine deficiency

clin: mental retardation, inc wt, short stature

30
Q

Myxedema coma

A
  • extreme hypothyroidism

- mortality 20-50%

31
Q

Thyrotoxicosis (what is it)

A
  • thyroid hormone excess regardless of cause

- could be due to graves, thyroiditis, inc exogenous hormone intake, plummer disease, thyroid storm

32
Q

Thyrotoxicosis (constitutional signs and cardiac findings)

A

constitutional:
-wt loss, anxiety, tremor, lid stare

cardiac:
-sinus tachycardia, inc risk for a-fib, systolic hypertension

33
Q

Thyrotoxicosis lab findings

A
  • dec TSH
  • inc T4*
  • 123-I depends on disease (inc or dec)
  • hyperglycemia, hyper calcemia, hypocholesterolemia, lymphocytosis
34
Q

Hyperthryoidism (gen)

A

-hormone excess due to inc synthesis

  • graves
  • plummer disease
35
Q

Graves disease

A
  • most common cause of hyperthyroidism and thyrotoxicosis
  • autoimmune
  • production of antibodies that compete with TSH
  • Thyromegaly (symmetrical, nontender)
36
Q

Graves: clinical findings

A
  • *Exophthalmos, proptosis (eye bulge)
  • antibodies to TSH receptor can cross placenta
  • pretibial myxedema
  • thyroid acropachy (digital swelling/clubbing, nails lifted)
37
Q

Apathetic hyperthyroidism

A

-Graves disease inelderly

38
Q

Graves disease: treatment

A
  • beta blockers (dec adrenergic affects)
  • thioamides (dec hormone synthesis)
  • radioactive ablation of thyroid with 131-I (if other treatments fail)
39
Q

Plummer disease

A
  • aka toxic multinodular goiter
  • 1+ nodules become TSH-indep
  • no exophthalmos
  • no pretibial myxedema

Treatment: surgery

40
Q

Thyroid storm

A
  • too much hormone
  • cause: anything that causes too much hormone
  • treat: stuff to dec hormone levels
41
Q

Euthyroid sick syndrome

A
  • abnormal T3 and T4 but gland appears to be functioning normally
  • pathophysiology: conversion of T3/T4 is messed up so stuff is messed up
42
Q

Nontoxic goiter (types and general what is it)

A

=thyroid enlargement from excess colloid

types
-Endemic (**iodide deficiency = most common)

-Sporadic (Goitrogens, enzyme deficiceny, puberty, pregnancy)

43
Q

Nontoxic goiter: pathology and treatment

A
  • deficiency of thyroid hormone
  • hyperplasia and hypertrophy
  • gland involution due to failure to sustain systhesis
  • diffuse thryomegaly -> multinodular goiter

Treatment: levothyroxine or surgery

44
Q

Nontoxic goiter: complications

A
  • hemorrhage into cysts
  • jugular vein compression (pemberton sign)
  • could become toxic
  • hoarseness
  • dyspnea
45
Q

Solitary thyroid nodule

A
  • usually cold
  • risk of malignancy inc with hx of radiation
  • diag: FNA and labs
  • Treat: benign = watch it, malignant = removal
46
Q

Follicular adenoma

A
  • most common benign tumor
  • complete capsule
  • solitary cold nodule
  • 10% malignant transformation
47
Q

Papillary adenocarcinoma (general)

A
  • most common endocrine cancer
  • most common thyroid cancer
  • F > M
  • 2nd and 3rd decades
  • radiation exposure association
48
Q

Papillary adenocarcinoma: Pathology

A
  • multifocal
  • papillary fronds in follicles
  • *psammoma bodies
  • *orphan annie nuclei
  • appear empty
  • invade lymph tissue
  • metastasis to lungs and nodes
49
Q

Papillary adenocarcinoma: diag, treat, prog

A

diag: FNA
treat: thyroidectomy, 123-I radiotherapy, thyroid hormone replacement
prog: >95% 5 year survival

50
Q

Follicular carcinoma

A
  • most common solid cold nodule thyroid cancer (F>M)
  • pathology: encapsulated or invasive. Vessels invaded by neoplastic follicles
  • lung and bone metastasis (lymph node uncommon)
  • Treatment (same as others: remove, radio, replacement)
51
Q

Medullary carcinoma

A
  • Produces ACTH
  • types (80% sporadic, 20% familiar - MEN IIa/IIb)

patho: C-cell hyperplasia, tumors from parafollicular C cells
diag: FNA, serum calcitonin (converted to amyloid)

Treat: thyroidectomy, genetic screening

52
Q

MEN IIa

A
  • medullary carcinoma
  • primary hyperparathyroidism
  • pheochromocytoma
53
Q

MEN IIb

A
  • medullary carcinoma
  • mucosal neuromas
  • pheochromocytoma
  • marfin-like habitus
54
Q

Primary B-cell malignant lymphoma

A

-mostly due to Hashimoto’s

55
Q

Anaplastic thyroid cancer

A
  • elderly women
  • risk: multinodular goiter, hx of follicular CA
  • rapid progression, fatal
  • Treat: palliation (decompress trachea), radiation/chemo
56
Q

Adrenal cortex hormones: layers superficial to deep***

A
  • zona glomerulosa: “salty”
  • zona fasciculta: “sweet”
  • zona raticularis: “sex”

superficial to deep

57
Q

Adrenal medulla hormones: origin and produces

A

Origin: ** neural crest
Produces: **EPI and NE
Produces metabolic end produces of catecholamines also? metanephrine, vanillylmandelic acid

58
Q

Causes of Acute adrenocortical insufficiency

A
  • ***adrupt withdrawal of steroids
  • Waterhouse-Friderichsen syndrome
  • anticoagulation therapy
59
Q

Waterhouse-Friderichsen syndrome

A
  • Associated with ***Neisseria meningitidis sepsis
  • Endotoxic shock
  • ***bilateral adrenal hemorrhage
60
Q

Addison disease

A
  • **Chronic adrenal insufficiency. (mineral and glucocorticoid deficiency)
  • **low cortisol

Causes: ***autoimmune most common

Clin findings: sodium loss, ACTH stimulated melanocytes =hyperpigmentation)

61
Q

Addison disease: labs

A
  • short and prolonged ACTH stim test
  • Metyrapone test: **inc ACTH
  • **inc plasma ACTH
62
Q

Congenital adrenal hyperplasia

A

-aka adrenogenital syndrome
-genetic disorder
-Patho:
** hypocortisolism
*** increase ACTH
clinical findings: ambiguous genital, quicker puberty

-screen for 17-OH progesterone**

63
Q

Disease differentiation: cortisol levels (high vs low)

A

too low = addison

too high = cushing

64
Q

Cushing syndrome: causes

A
  • ***prolonged corticosteroid therapy (most common!)
  • pituitary adenoma
  • adrenal stuff
  • ectopic cushing
65
Q

Cushing syndrome: clinical findings

A
  • weight gain. moon facies, buffalo hump
  • muscle weakness. cortisol breaks down muscle
  • diastolic hypertension
  • osteoporosis
  • Hirsutism (hair from increased androgens)
  • purple striae (skin thing cuz cortisol weakens collagen)
66
Q

Cushing syndrome: Labs

A
  • urine: inc free cortisol
  • ***dexamethasone suppression test (low and high dose. differentiate between types)
  • hyperglycemia
  • metabolic alkalosis
  • hypokalemia
67
Q

Neuroblastoma

A
  • Malignant tumor
    • **postganglionic sympathetic neurons
    • ** most common in the adrenal medulla

-kids under 5yrs. 3rd most common cancer in kids

68
Q

Neuroblastoma Pathology

A
  • malig neuroblasts
  • small cell tuor
  • Homer-Wright rosettes
  • Neurosecretory granules
69
Q

Neuroblastoma clinical findings

A

opsoclonus-myoclonus syndrome

palpable ab mass
diastolic HTN
inc urine VMA and HVA

70
Q

Neuroblastoma: diag, treat, prog, metastasis

A

diag: urine, imaging
treat: surgery, radiation/chemo
prog: younger when dx the better
metastasis: skin and bones

PTH560 Pathology (15 decks)

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