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Endocrine Pathology Flashcards

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1
Q

Anterior Pituitary

A

glandular organ –> arises from Rathke’s pouch

  • secretes GH, PRL, FSH, LH, ACTH, TSH
  • all hormones are controlled by hypothalamus (stimulatory except PRL which is inhibited by dopamine)
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2
Q

Posterior Pituitary

A

Neural ectoderm -> from diencephalon

  • doesn’t make hormones, it stores hormones (oxytocin and ADH)
  • extension of hypothalamus
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3
Q

Acidophils

A

secretes GH and PRL

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4
Q

Basophils

A

secretes FSH, LH, ACTH, TSH

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5
Q

Oxytocin

A 
Labor induction
Milk let down
Cuddle hormone
Monogamy
Trust
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6
Q

Hyperpituitarism

A

too much of one or more anterior pituitary hormones

  • most common cause = pituitary adenoma
  • endocrine abnormalities occur when adenomas secrete hormones, otherwise it can be latent until growth becomes big enough to cause mass effect
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7
Q

Mass Effect

A

Visual field abnormalities - bitemporal hemianopsia (optic chiasm)
Symptoms of increased cranial pressure
Compression of pituitary -> HYPOpituitarism

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8
Q

Functional vs. Nonfunctional pituitary adenomas

A 
functional = produces pituitary hormone
non-functional = doesn't produce hormone -> becomes really big (mass effect)
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9
Q

Epidemiology of pituitary adenomas

A

occurs most common in adults
3% arise from multiple endocrine neoplasia
- can cause “pituitary apoplexy” –> sudden bleeding that is BAD

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10
Q

Microscopic appearance of pituitary adenoma

A

can’t tell type of hormone from histology –> need special stains
- most commonly involve one cell type, can be pleomorphic
MOST COMMON - prolactin-producing
LEAST COMMON - thyroid-stimulating hormone producing

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11
Q

Molecular mutations in pituitary adenomas

A

mutated G-proteins -> GNAS1 gene

  • alpha subunit doesn’t turn off -> GTP constantly causing cAMP and PKA pathways
  • some can cause activating mutation of RAS oncogene or overexpression of c-MYC oncogene
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12
Q

Prolactin-producing adenoma

A

MOST COMMON type of pituitary adenoma
- secretes prolactin efficiently -> causes symptoms (amenorrhea, galactorrhea, infertility, loss of libido)
- drugs that interfere with dopamine action can also cause increased prolactin
Tx = bromocriptine (D2 receptor agonist)

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13
Q

Growth hormone producing adenoma

A

Gigantism = GH adenoma BEFORE puberty
Acromegaly = GH adenoma AFTER puberty (changes can happen subtly so that patient doesn’t realize)
Lab - GH unreliable because of pulsatile secretion, check IGF-1
- can also perform glucose test (administer glucose should decrease GH but it won’t)
Tx = get GH back to normal (surgery/radiation)

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14
Q

ACTH producing adenoma

A

makes ACTH –> revs up adrenal glands which make cortisol
Cushing Syndrome -> too much cortisol
Cushing Disease -> ACTH producing adenoma that causes cushing syndrome
Nelson Syndrome -> removal of adrenals with cushing syndrome -> BAD (no inhibition of pituitary)

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15
Q

FSH and LH producing adenomas

A

secrete FSH and LH very inefficiently

- mass effect brings it to attention rather than endocrine abnormalities

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16
Q

TSH-producing adenomas

A

RARE!!!!!

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17
Q

Non-functioning adenoma

A

secretes no hormones –> gets BIG and causes mass effect

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18
Q

Hypopituitarism

A

decreased secretion of pituitary hormones
Causes:
1. Pituitary destruction –> more than 75% (surgery, radiation, tumor compressing it)
2. Ischemic Necrosis -> Sheehan syndrome (pregnancy), pituitary increases in size but not blood supply, hemorrhage of shock during delivery infarcts the pituitary
3. Empty Sella syndrome -> arachnoid membrane and CSF herniate down into sella turcica (more than 75%)
4. Pituitary Apoplexy -> sudden, spontaneous infarct of pituitary (symptoms of severe headache, stiff neck, N/V) -> bad bleeding

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19
Q

Clinical finding of hypopituitarism

A

insidious, chronic onset (need 75% or more of pituitary affected)
Order of Loss of Hormones = GH, FSH/LH, TSH, ACTH
GH -> dwarfism (childhood), muscle atrophy and weakness (adulthood)
FSH/LH -> menstrual abnormalities
PRL -> prevents lactation
TRH -> secondary hypothyroidism
ACTH -> adrenal insufficiency

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20
Q

Posterior Pituitary Syndromes

A

Diabetes Insipidus and Syndrome of Inappropriate ADH Secretion

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21
Q

Diabetes Insipidus

A

central or nephrogenic decrease in ADH secretion
- ADH deficiency leads to dilute, massive amounts of urine
- increase in serum osmolality
- head trauma, tumors, or ethanol
Tx = increase water intake and give ADH (vasopressin)

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22
Q

SIADH

A

ADH excess causes kidneys to excrete SUPER concentrated urine –> lots of water retention (decrease serum osmolality)
Most common cause -> ectopic ADH producing tumor (small-cell lung cancer)
Tx = restrict water intake

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23
Q

Thyroid Embryology

A

thyroid develops from pharyngeal epithelium from back of tongue -> descends anterior portion of neck

  • remnants = thyroglossal duct cyst
  • bilobed structure with isthmus, follicles contain colloid
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24
Q

Thyroid Physiology

A

hypothalamus secretes TRH –> anterior pituitary secretes TSH –> thyroid synthesizes and releases T3 and T4, grows, uptakes iodine

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25
Thyroid Hormone Function
increase fat breakdown, decrease carb utilization, stimluate protein synthesis, increased BMR
26
Thyroid Lab Testing
TSH -> amount of TSH in blood, VERY sensitive (even a small fluctuation in T4 causes a rapid, inverse change in TSH) Free T4 -> tells how much active, free T4 patient has (don't confuse with total T4 which is bound, inactive) Free or total T3 -> how much free or total T3 patient is making TBG - measures thyroglobulin (carrier for thyroid hormone) Anti-thyroid antibody test - Graves'
27
Radioiodine thyroid screening
123-I radiolabeled is taken up by thyroid - evaluate thyroid nodules or determine appropriate dosing Hot -> almost always benign because cancer doesn't make hormones Cold -> occasionally malignant because cancer doesn't make hormone
28
Hyperthyroidism
HYPERMETABOLIC state caused by increased thyroid hormone levels Primary -> thyroid over-functioning because of intrinsic problem Secondary -> thyroid over-functioning because too much TSH (pituitary problem)
29
Signs and Symptoms of hyperthyroidism
Cardiac -> rapid pulse, cardiomegaly, arrhythmias Neuro -> nervous, tremor, emotional Eye -> lid lag, wide-staring gaze Skin -> warm, moist, flushed skin GI -> diarrhea, weight loss Skeletal -> osteoporosis Thyroid Storm --> BAD SHIT -> coma and death
30
Causes of hyperthyroidism
Graves' disease --> MOST COMMON CAUSE | - goiter, thyroid adenoma, thyroiditis, ingestion of thyroid hormones, pituitary adenoma, struma ovarii, factitious
31
Diagnosis of hyperthyroidism
TSH and free T4 Primary -> high T4 and low TSH Secondary -> high T4 and high TSH
32
Hypothyroidism
HYPOMETABOLIC state by decreased levels of thyroid homrones Primary -> under-functioning because of intrinsic problem Secondary -> under-functioning because of low TSH (pituitary problem)
33
Signs and Symptoms of Hypothyroidism
Slowing of mind and body -> fatigue, mental slowness, irritability, loss of interest Myxedema -> accumulation of ground substance in tissues -> not fluid Cardiac -> slow pulse, diminished contractility GI - > constipation Skin -> dry, cool, pale Cold Intolerance Delayed deep tendon reflexes Myxedema Coma -> opposite of thyroid storm
34
Causes of Hypothyroidism
Congenital (Cretinism) -> iodine deficiency, developmental or genetic - symptoms reflect impaired development = short, mental retardation (range of severities) Acquired (adulthood) -> Hashimoto thyroidits (autoimmune), iatrogenic (surgery or radiation), goiter, amyloidosis, sarcoidosis, thyroiditis
35
Diagnosis of Hypothyroidism
TSH and free T4 Primary -> low T4 and high TSH Secondary -> low T4 and low TSH
36
Thyroiditis
inflammation of thyroid gland - Hashimoto is most common - may be euthyroid, hypothyroid, or hyperthyroid (colloid spilling out) - radioactive uptake is decreased ("cold" thyroid tissue)
37
Hashimoto thyroiditis
MOST COMMON thyroiditis (F>M) - Primary Hypothyroidism (T4 low, TSH high) - enlarged, non-tender thyroid (gradually hypothyroid) Lab Testing = thyroid tests reflect thyroid status - anti-peroxidase antibodies (detected by immunofluorescence) Patho = autoimmune destruction of thyroid gland (T-cells attack thyroid AND stimulate B-cells) --> anti-TSH receptor antibody
38
DeQuervian thyroiditis
occurs after upper respiratory infection (viral infection) - many patients have HLA-B35 antigen - painful, enlarged thyroid (abrupt) - self-limiting disease - damaged, disrupted follicles and multinucleate giant cells
39
Silent thyroiditis
painless, slightly enlarged thyroid (asymptomatic) - middle age or after pregnancy - transient and self-limiting - abundant lymphocytes (like Hashimoto but none of the features of Hashimoto)
40
Reidel's thyroiditis
Rock-hard, woody neck mass --> fibrosis | - fibrosis may progress and put pressure on trachea
41
Graves' Disease
MOST COMMON cause of hyperthyroidism (F>M) - Classic Triad = hyperthyroidism, ophthalmopathy, dermopathy Labs = high T4, low TSH, high uptake of iodine - Autoimmune disease with anti-TSH receptor antibodies (opposite effect of Hashimoto) - eye muscles and skin has TSH receptors --> that's how those symptoms occur
42
Treatment of Graves'
decrease symptoms of hyperthyroidism (beta-blocker) | decrease synthesis of thyroid hormones = PTU, radioiodine ablation
43
Goiters
big thyroid gland low T4 --> high TSH --> BIG THYROID Simple --> first stage (smooth) Multinodular --> second stage (bumpy and big) Labs = euthyroid Histo --> hyperplastic cells, then cells become exhausted and involute (oversized colloid)
44
Cause and Treatment of Goiters
Lack of iodine, diet rich in goitrogen Tx = levothyroxine --> suppress TSH and shrink goiter - be careful of Jod-Basedow phenomena --> giving iodine to patient --> acute hyperthyroidism
45
Neoplastic thyroid disease
most thyroid bumps are non-neoplastic --> but need to aspirate/biopsy to make sure
46
Thyroid Adenoma
euthyroid patients, commoner in adults - Labs = normal T4 and TSH, cold thyroids Solitary nodules, encapsulated, and generally not invasive Tx = surgical removal - need to look at capsule to see if there is tumor cells --> that means it's invasive
47
Papillary Adenocarcinoma
most common cause of thyroid carcinoma (best prognosis too) - papillary growth pattern - nuclei look empty (Orphan Annie's eyes), nucelar pseudoinclusions, psammoma body
48
Follicular Adenocarcinoma
follicular growth pattern, well-differentiated Hard to identify from thyroid adenoma - look for vascular invasion and tumor cells extending into thyroid capsule Tx = surgical excision, look for metastasis
49
Medullary Carcinoma
endocrine tumor - thyroid C-cells --> makes calcitonin -> creates amyloid deposits (congo red stain) - vague nests Tx = anyone suspected of MEN II or familial thyroid
50
Anaplastic thyroid carcinoma
rapidly-enlarging bulky neck mass --> often metastasized already upon presentation Anaplastic cells --> VERY undifferentiated = bad prognosis
51
Parathyroid Gland
``` 4 glands in 2 pairs Upper lobes -> 4th pharyngeal pouch Lower lobes -> 3rd pharyngeal pouch - chief cells -> PTH - oxyphil cells -> unknown function ```
52
Parathyroid Physiology
Chief cells secrete proparathyroid -> cleaved to PTH -> binds to PTH receptors -> stimulate AC -> PLC -> IP3 and DAG
53
PTH Actions
1. Stimulate osteoblasts -> stimulate osteoclasts -> increase blood calcium 2. Increase renal absorption of calcium 3. Increase renal conversion of Vit D to active form 4. Increase urinary excretion of phosphate 5. Absorb gut calcium
54
What controls PTH release?
serum calcium --> NOT pituitary serum calcium increases -> PTH decreases serum calcium decreases -> PTH increases
55
Hypercalcemia
``` Lots of things can cause it: M alignancy D iuretics P arathyroid I diopathic M egadose of Vit D P aget's disease S arcoidosis M ilk-alkali syndrome E ndocrine ```
56
Hyperparathyhroidism
Primary -> over-functioning because of intrinsic problem Secondary -> over-functioning because of something else causing chronic hypocalcemia Pseudohyperparathyroidism -> hypercalcemia caused by production of PTH related protein by cancers (squamous cell lung carcinoma)
57
Primary Hyperparathyroidism
Stone -> kidney stones (hypercalcemia) Bone -> bone pain (osteoclasts erode bone) - brown tumors -> microfractures and hemorrhage Groan -> GI problems (constipation, ulcers, nausea) Moan -> mental changes (depression, lethargy) Labs = increased PTH, increased Ca, decreased PO4, increased 24-hr urine Ca, increased urine cAMP
58
Causes of primary hyperparathyroidism
1. Parathyroid Adenoma -> most common - composed mostly of chief cells PRAD1 -> genetic alterations in sporadic cases MEN1 or RET -> genetic alterations in familial cases 2. Parathyroid Hyperplasia -> normal looking cells, just a lot of them, some MEN1 syndromes 3. Parathyroid Carcinoma -> abrupt onset of pain bain, usually just one gland affecteed, tumors are well-differentiated
59
Secondary Hyperparathyroidism
Due to chronic hypocalcemia -> renal failure, poor calcium, Vit D deficiency Pathophysiology = chronic renal failure -> phosphate not excreted -> Ca goes down -> stimulates PTH to be secreted Symptoms overshadowed by chronic renal failure
60
Hypoparathyroidism
Iatrogenic, congenital (DiGeorge's -> thymic aplasia, absence of parathyroids), familial
61
Signs and Symptoms of Hypoparathyroidism
TETANY -> tingling around mouth/extremities - Chvostek's sign -> stroking/tapping cheeck induces eye, mouth, and nose contraction - Trousseau's sign -> occluding forearm circulation induces carpal contraction Mental Status changes CV disease Dental Abnormalities
62
Adrenal Anatomy and Histology
paired gland at top of kidneys, cortex has 3 zones, medulla has chromaffin cells
63
Adrenal Cortex and Medulla and hormones
Zona glomerulosa -> mineralocorticoids Zona fasciculata -> glucocorticoids Zona reticularis -> sex steroids Medulla -> Catecholamines
64
Cushing Syndrome
``` increased glucocorticoids (cortisol) in blood - stable BP, decreased Bone, decreased inflammation, decreased immunity, increased gluconeogenesis ```
65
Signs of Cushings
``` HTN and weight gain adipose tissue distributed truncally, moon facies, buffalo hump - weakness - glucose intolerance - thin fragile skin - infections ```
66
Labs for Cushing
24 hr urine free cortisol --> diagnosis | ACTH level, dexamethasone test --> cause
67
Causes of Cushing
Iatrogenic -> drug ingestion (low ACTH, dex doesn't suppress cortisol) Pituitary adenoma -> ACTH high, dex suppresses cortisol Adrenal lesion -> ACTH low, dex doesn't suppress cortisol Ectopic ACTH production -> ACTH high, dex doesn't suppress cortisol
68
Hyperaldosteronism
High Aldosterone, high Na/low K Primary - high aldosterone -> low renin - HTN, weakness, fatigue - Labs = high aldosterone, low renin, high Na/low K, metabolic alkalosis Secondary - high renin -> high aldosterone - symptoms same - Labs = high aldosterone, high renin, high Na/low K, metabolic alkalosis
69
Adrenogenital syndromes
VIRILIZATION | Primary gonadal disorders, primary adrenal disorders
70
Congenital Adrenal Hyperplasia
enzyme block in cortisol pathway (21-hydroxylase MOST COMMON) - precursors are shunted to other pathways --> mostly to sex steroids (testosterone) --> turns females to have male features
71
Addison disease
Primary CHRONIC adrenal insufficiency -> intrinsic adrenal cortex problem leading to decreased cortisol and mineralocorticoids Causes -> autoimmune, infections, metastatic carcinoma Features -> chronic (takes a while for symptoms to appear), hypoglycemia, metabolic acidosis, skin hyperpigmentation from POMC -> makes both ACTH and MSH
72
Primary Acute adrenal insufficiency
adrenal SUDDENLY aren't releasing their stuff | *Addisonian crisis*, steroid withdrawal, massive adrenal hemorrhage
73
Massive Adrenal Hemorrhage
newborns following difficult delivery anticoagulated patients DIC following bacterial infection (WFS)
74
Waterhouse-Friderichsen syndrome
overwhelming bacterial infection (N. meningitidis) hypotension and shock DIC rapidly progressive massive adrenal hemorrhage
75
Secondary Adrenal Insufficiency
low ACTH -> low adrenal products Causes = pituitary insufficiency, hypothalamic insufficiency Features = symptoms of low cortisol and low sex steroids
76
Pheochromocytoma
Neoplasm of catecholamine producing cells derived from neural crest Pressure (BP), Pain, perspiration, palpitations, pallor 10% tumor = extra-adrenal, bilateral, familial, malignant, don't have HTN
77
Neuroblastoma
neoplasm derived from neural crest cells -> common childhood tumor - round, blue rosette cells - N-myc amplification associated with bad prognosis

Endo/Repro (34 decks)

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