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Path4 My Cards > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

Hyperpituitarism causes and common symptom

A

Caused by adenomas (too many cells, too many hormones)

  • The pituitary is right above a set of optic nerves. So a larger pituitary will “stomp out” the optic nerves beneath it.
  • This reduces outer peripheral eyesight In general for the endocrine system: if know hormone, can guess the symptoms
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2
Q

Hyperpituitarism caused by three types of adenomas

A

Prolactinoma

Somatotroph Adenoma

ACTH-producing adenoma

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3
Q

Hyperpituitarism

-histopathology

A
  • usually pituitary has diverse cells
  • can tell if an adenoma cuz things will look uniform
  • CANT tell what type of adenoma by looking at the cells
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4
Q

Prolactinoma

A

“prolactin, milk, breasts, sex characteristics”

with too much prolactin:

  • Amenorrhea and spontaneous release of milk (galactorrhea) in women
  • Loss of libido/impotency in males
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5
Q

Somatotroph Adenoma produce what?

A

“somatic, body, body builders, Growth Hormone”

  • Growth Hormone producing adenomas
  • GH stimulates insulin-like growth factor 1 (ILGF-1)
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6
Q

Somatotroph Adenoma clinical

A

GH symptoms:

-Gigantism (if adenoma happens before epiphyses close) -Acromegaly (if after epiphyses close)

Insulin like growth factor 1 symptoms:

-Can cause diabetes mellitus/abnormal glucose tolerance

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7
Q

ACTH-producing Adenoma produce what?

A

Too much ACTH which activates adrenocorticoid production

This will make the adrenal produce too much cortisol

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8
Q

ACTH-producing Adenoma manifestations clinical

A

manifestations:

-hypercortisolism manifests itself as cushing disease

clinical:

  • cortisol has a feedback loop to turn off ACTH production. So if take out adrenal to Tx Cushings feedback lost and cells will make more ACTH, causing adenoma to grow faster and become more aggressive
  • Hyperpigmentation may also occur, as ACTH is derived from a melanin regulator precursor
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9
Q

Hypopituitarism Causes

A

Not enough hormones

-why?

Usually something is cramping the pituitary’s space causes:

  • Tumors (Pit. tumors, craniopharyngiomas, gliomas)
  • Ischemic pituitary necrosis (hypotension from post partum hemorrhage)
  • or, if not a ceiling over pituitary, brain will crush it (called Empty Sella Syndrome)
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10
Q

hypopituitarism -clinical

A

clinical:

  • pallor (no melanin production)
  • hypothyroidism (no TSH)
  • Failure of lactation (no prolactin)
  • Adrenal insufficiency (no ACTH)
  • ovarian failure w/amenorrhea (no LH)
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11
Q

Posterior Pituitary Syndrome

A

Diabetes Insipidus

post. pituitary makes ADH (which acts to retain water)

Too little ADH = lack of water retention Na still retained and this coupled with water loss leads to an increased sodium concentration

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12
Q

posterior pituitary syndrome clinical

A

clinical:

  • polyuria (urinating often)
  • Thirst
  • Polydipsia (excessive thirst)
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13
Q

Hyperthyroidism

A

Too much metabolism

  • bulging eyes, sweaty, hot, bad tempered etc
  • Graves disease:

Ab-mediated hyperthyroidism

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14
Q

Hypothyroidism -two causes

A
  1. can be caused by dietary iodine deficiency
  2. Or can be autoimmune (Hashimoto’s)

symptoms opposite to hyperthyroidism (tend to be overweight, cold etc)

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15
Q

Hashimoto’s Thyroiditis -mechanism -at risk for

A

Mechanism:

-humoral and cellular immunity

At risk for:

  1. Thyroid follicles being destroyed which lets thyroid hormone precursor spew out everywhere, putting patient at risk for thyrotoxicosis
  2. B cells overproliferating creates risk for B-cell non-Hodgkin Lymphoma
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16
Q

Goiter

A
  • Reflects inadequate synthesis of thyroid hormone
  • may seem contradictory
  • the idea is that the thyroid is storing a lot of thyroid precursor which builds up, causing the goiter
17
Q

Hyperparathyroidism -Three Types

A
  1. Primary
    - spontaneous hypersecretion of PTH -mainly due to parathyroid adenomas
  2. Secondary
    - Enlargement/hypersecretion in response to hypocalcemia
  3. Tertiary
    - Enlargement from secondary remains after the cause is gone
18
Q

Hyperparathyroidism -clinical manifestations (same for all three types)

A

Clinical

  • PTH normally demineralizes bone to increase blood calcium levels
  • so blood calcium will be raised, patient will make more stones and this will mess with conduction in the heart
19
Q

Papillary Carcinoma

-What is it?

A

The most common form of Thyroid Cancer

20
Q

Papillary Carcinnoma

  • Pathogenesis
  • Histopathology
A

Pathogenesis:

-activation of MAP Kinase pathway involved in most cases

Histopathology:

  1. Psamomma bodies -concentric calcified structures which look like onions
  2. “Orphan Annie Eye” Nuclei -Nuclei look empty due to finely dispersed chromatin
21
Q

Adrenals:

  • Adrenal Cortex:
  • Adrenal Medulla:
A

Adrenal cortex:

  • makes Glucocorticoids which control carb, fat and protein metabolism
  • Makes mineralcorticoids which control the amount of water and electrolytes present in the body

Adrenal medulla:

-makes catecholamines

22
Q

Cushing Syndrome

  • Where is it?
  • How to remember?
A

Cushing Syndrome

-In the adrenal cortex

“c for cushing, c for corticosteroid”

23
Q

Cushing Syndrome

-Causes

A
  • Administration of exogenous steroids
  • Pituitary Adenoma (Increased ACTH)
24
Q

Cushing Syndrome

-Clinical

A

Corticosteroids increase blood sugar in any way possible. This sugar will inevitably be stored as fat

Signs:

  • Obesity (extremities unaffected)
  • Moon Face (obesity of the face)
  • Buffalo Hump (obesity of the neck)
25
Q

Addison Syndrome

  • Where is it?
  • How to remember?
A
  • Adrenal Cortex
  • If Cushing is too much corticosteroid, addison is too little (its the opposite of Cushings)
26
Q

Addison syndrome

-Causes

A
  • Autoimmune Adrenalitis
  • TB
  • AIDS
  • Metastatic Cancers
  • Withdrawal of long term corticosteroid Tx
27
Q

Addison syndrome

-Clinical

A

Things associated with not enough corticosteroids:

  • weakness
  • weight loss
  • GI symptoms
  • HYPERPIGMENTATION*

*Adrenal insufficiency will lead pituitary to produce more ACTH and, consequently, more POMC (melanin precursor)

28
Q

Pheochromocytoma

  • Where is it
  • How to remember?
  • Are most cases unilateral or bilateral?
A
  • In the Adrenal Medulla
  • Pheochromocytoma looks like it can be abbreviated as PCC with CC corresponding to CateCholamines
  • It is a neoplastic condition springing from a single cell so most cases are unilateral
29
Q

Pheochromocytoma

  • Histopathology
  • Dx
  • Clinical
A

Histopathology:

-“Cell Ballin”–> forms Zell Ballen, or circumscribed nests of neoplastic cells

Dx:

-Increased levels of catecholamine metabolites, particularly vanillylmandelic acid (VM acid)*

*mandelic looks like medulla

Clinical:

  • Catecholamines cause hypertension and the antsy behavior associated with nervousness
  • Hypertension -Tachycardia -nervousness

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