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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
Thyroglossal duct cyst
- cystic midline mass - near hyoid bone - Treatment: surgery (remove hyoid or prox duct)
26
Acute thyroiditis
****BACTERIAL (usually staph aureus clin: fever, tender, cervical adenopathy, initial thyrotoxicosis, dec 123-I uptake Treat: penicillin or ampicillin
27
Sub-acute granulomatous thyroiditis
****VIRAL (mumps, coxsackievirus) clin: - PAINFUL* thyroid gland - most common cause is preceding URI -Self-limiting
28
Hashimoto thyroiditis
- autoimmune - ***most common cause of hypothyroidism -pathogenesis: cytotoxic T cells destroy gland, dec THS, macrophages destroy tissue
29
Cretinism
-hypothyroidism in infancy Cause: maternal hypothyroidism, iodine deficiency clin: mental retardation, inc wt, short stature
30
Myxedema coma
- extreme hypothyroidism | - mortality 20-50%
31
Thyrotoxicosis (what is it)
- thyroid hormone excess regardless of cause | - could be due to graves, thyroiditis, inc exogenous hormone intake, plummer disease, thyroid storm
32
Thyrotoxicosis (constitutional signs and cardiac findings)
constitutional: -wt loss, anxiety, tremor, lid stare cardiac: -sinus tachycardia, inc risk for a-fib, systolic hypertension
33
Thyrotoxicosis lab findings
- dec TSH - inc T4* - 123-I depends on disease (inc or dec) - hyperglycemia, hyper calcemia, hypocholesterolemia, lymphocytosis
34
Hyperthryoidism (gen)
-hormone excess due to inc synthesis - graves - plummer disease
35
Graves disease
- most common cause of hyperthyroidism and thyrotoxicosis - autoimmune - production of antibodies that compete with TSH - Thyromegaly (symmetrical, nontender)
36
Graves: clinical findings
- *Exophthalmos, proptosis (eye bulge) - antibodies to TSH receptor can cross placenta - pretibial myxedema - thyroid acropachy (digital swelling/clubbing, nails lifted)
37
Apathetic hyperthyroidism
-Graves disease inelderly
38
Graves disease: treatment
- beta blockers (dec adrenergic affects) - thioamides (dec hormone synthesis) - radioactive ablation of thyroid with 131-I (if other treatments fail)
39
Plummer disease
- aka toxic multinodular goiter - 1+ nodules become TSH-indep * no exophthalmos * no pretibial myxedema Treatment: surgery
40
Thyroid storm
- too much hormone - cause: anything that causes too much hormone - treat: stuff to dec hormone levels
41
Euthyroid sick syndrome
- 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
Nontoxic goiter (types and general what is it)
=thyroid enlargement from excess colloid types -Endemic (****iodide deficiency = most common) -Sporadic (Goitrogens, enzyme deficiceny, puberty, pregnancy)
43
Nontoxic goiter: pathology and treatment
- deficiency of thyroid hormone - hyperplasia and hypertrophy - gland involution due to failure to sustain systhesis - diffuse thryomegaly -> multinodular goiter Treatment: levothyroxine or surgery
44
Nontoxic goiter: complications
- hemorrhage into cysts - jugular vein compression (pemberton sign) - could become toxic - hoarseness - dyspnea
45
Solitary thyroid nodule
- usually cold - risk of malignancy inc with hx of radiation - diag: FNA and labs - Treat: benign = watch it, malignant = removal
46
Follicular adenoma
- most common benign tumor - complete capsule - solitary cold nodule - 10% malignant transformation
47
Papillary adenocarcinoma (general)
- most common endocrine cancer - most common thyroid cancer - F > M - 2nd and 3rd decades - radiation exposure association
48
Papillary adenocarcinoma: Pathology
- multifocal - papillary fronds in follicles - *psammoma bodies - *orphan annie nuclei - appear empty - invade lymph tissue - metastasis to lungs and nodes
49
Papillary adenocarcinoma: diag, treat, prog
diag: FNA treat: thyroidectomy, 123-I radiotherapy, thyroid hormone replacement prog: >95% 5 year survival
50
Follicular carcinoma
- 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
Medullary carcinoma
- 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
MEN IIa
- medullary carcinoma - primary hyperparathyroidism - pheochromocytoma
53
MEN IIb
- medullary carcinoma - mucosal neuromas - pheochromocytoma - marfin-like habitus
54
Primary B-cell malignant lymphoma
-mostly due to Hashimoto's
55
Anaplastic thyroid cancer
- elderly women - risk: multinodular goiter, hx of follicular CA - rapid progression, fatal - Treat: palliation (decompress trachea), radiation/chemo
56
Adrenal cortex hormones: layers superficial to deep***
- zona glomerulosa: "salty" - zona fasciculta: "sweet" - zona raticularis: "sex" superficial to deep
57
Adrenal medulla hormones: origin and produces
Origin: *** neural crest Produces: ***EPI and NE Produces metabolic end produces of catecholamines also? metanephrine, vanillylmandelic acid
58
Causes of Acute adrenocortical insufficiency
- ***adrupt withdrawal of steroids - Waterhouse-Friderichsen syndrome - anticoagulation therapy
59
Waterhouse-Friderichsen syndrome
- Associated with ***Neisseria meningitidis sepsis - Endotoxic shock - ***bilateral adrenal hemorrhage
60
Addison disease
- **Chronic adrenal insufficiency. (mineral and glucocorticoid deficiency) - **low cortisol Causes: ***autoimmune most common Clin findings: sodium loss, ACTH stimulated melanocytes =hyperpigmentation)
61
Addison disease: labs
- short and prolonged ACTH stim test - Metyrapone test: **inc ACTH - **inc plasma ACTH
62
Congenital adrenal hyperplasia
-aka adrenogenital syndrome -genetic disorder -Patho: **** hypocortisolism *** increase ACTH clinical findings: ambiguous genital, quicker puberty -screen for 17-OH progesterone****
63
Disease differentiation: cortisol levels (high vs low)
too low = addison | too high = cushing
64
Cushing syndrome: causes
- ***prolonged corticosteroid therapy (most common!) - pituitary adenoma - adrenal stuff - ectopic cushing
65
Cushing syndrome: clinical findings
- 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
Cushing syndrome: Labs
- urine: inc free cortisol - ***dexamethasone suppression test (low and high dose. differentiate between types) - hyperglycemia - metabolic alkalosis - hypokalemia
67
Neuroblastoma
- Malignant tumor * **postganglionic sympathetic neurons * ** most common in the adrenal medulla -kids under 5yrs. 3rd most common cancer in kids
68
Neuroblastoma Pathology
- malig neuroblasts - small cell tuor - Homer-Wright rosettes - Neurosecretory granules
69
Neuroblastoma clinical findings
opsoclonus-myoclonus syndrome palpable ab mass diastolic HTN inc urine VMA and HVA
70
Neuroblastoma: diag, treat, prog, metastasis
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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