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DMD 5248 > Bikman: Endocrine Path > Flashcards

Bikman: Endocrine Path Flashcards

1
Q

Anterior Pituitary hormones

A

ACTH

LH

FSH

GH

PRL

TSH

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2
Q

Which glands are affected with primary, secondary, tertiary deficiencies?

A

Primary - Target gland

Secondary - Pituitary

Tertiary - Hypothalamus

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3
Q

Where do most problems occur in the hypothalamus-pituitary axis?

A

Hypothalamus and Pituitary

(Tertiary and Secondary)

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4
Q

Posterior pituitary

A
  • Consists of neurons with a cell body in the hypothalamus and the axon ending in the posterior pituitary
    • Neurons release the small peptides oxytocin and ADH directly into the blood
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5
Q

Posterior Pituitary Disorders

A

Hypersecretion of ADH - SIADH

Hyposecretion of ADH - Diabetes Insipidus

Hypersecretion of oxytocin - Galactorrhea

Hyposecretion of oxytocin - lack of milk ejection, prolonged labor, lack of compassion/bonding

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6
Q

What are the causes of SIADH?

A
  • Ectopic production of ADH (by cancer cells)
  • Surgery (surgery related stress)
  • Some drugs
  • Cranial abnormalities (trauma, tumor, etc)
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7
Q

What are the clinical manifestations of SIADH?

A
  • ↑water retention
  • ↑Na+ loss due to ↑BV
  • Hyponatremia - blood is becoming more dilute while urine is becoming more concentrated
  • Hypoosmolarity - ↓serum osmolarity

The body is slowlyl becoming hypOtonic; the urine, hypERtonic

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8
Q

What are actions of SIADH?

A
  • ↑permeability of renal collecting duct to water
    • ADH inserts aquaporins into the wall of the collecting duct
  • Constriction of arterial SM @ high concentrations
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9
Q

What are treatments for SIADH?

A
  • Restrict H2O
  • Remove tumor (if present)
  • ADH receptor blocker
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10
Q

What are the clinical manifestations of diabetes insipidus?

A
  • Manifests with polyuria (high urine flow)
  • Polydipsia - drinking lots of H2O
  • Dilute urine - cannot concentrate it
  • Dehydration
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11
Q

What are the different types of diabetes insipidus?

A
  • Neurogenic
  • Nephrogenic
  • Psychogenic
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12
Q

Neurogenic Diabetes Insipidus

A

Insufficient ADH

Damage to the brain or posterior pituitary from head trauma, cranial surgery or tumor; idiopathic

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13
Q

Nephrogenic Diabetes Insipidus

A

Insufficient ADH response

  • Lack of ADH receptors in kidney or failure of receptors to modify permeability of the collecting duct
  • Genetic
  • Temporary nephro DI can be caused by some drugs, pregnancy, electrolyte imbalance, kidney trauma
  • Permanent nephro DI from kidney failure
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14
Q

Psychogenic Diabetes Insipidus

A

Drinking too much H2O

From trying to get rid of toxins, demons?!, etc

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15
Q

Tx for Neurogenic DI?

A

ADH replacement

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16
Q

Tx for nephrogenic DI?

A

Drink lots of H2O and eat a lot of NaCl

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17
Q

Tx for psychogenic DI?

A

Restrict H2O intake

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18
Q

What is oxytocin release stimulated by?

A
  • Cervix stretching during birth
  • Breast stimulation (nursing)
  • Psychological: Hearing the baby cry, thinking about the baby, stress
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19
Q

What are the effects of oxytocin?

A
  • Role in intimacy (bonding, orgasm)
  • May cause a degree of amnesia
  • Endorphins might also play a role
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20
Q

What are the hormones that are released by the anterior pituitary?

A
  • FSH - Follicle Stimulating hormone
  • LH - Lutenizing hormone
  • ACTH - Adrenocorticotrophic hormone
  • TSH - Thyroid Stimulating hormone
  • PRL - Prolactin
  • GH - Growth hormone
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21
Q

Hormone pairs in the hypothalamic-pituitary axis

A
  • GnRH –> FSH, LH
  • TRH –> TSH
  • CRH –> ACTH
  • PIF –> PRL
  • GHRH –> GH
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22
Q

Hypothalamic Factor Stimulation Tests

A

Determining if problem originates in hypothalamus or anterior pituitary

  1. Take blood from patient under resting conditions
  2. Inject one or more hypothalamic releasing factors
  3. Wait a few minutes and then take another sample
  4. Compare the amount of various anterior pituitary hormones before and after injection of hypothalamic factors

If pituitary hormone increases - Hypothalamus

If pituitary hormone does NOT increase - Pituitary

Hypothalamic hormone is high, pituitary hormone is low - Target gland

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23
Q

Anterior pituitary disorders

A

Hypopituitarism - Pituitary infarction, Empty sella syndrome

Hyperpituitarism - Pituitary adenoma, end organ destruction, hypothalamic disorder, carcinoma (not as common as adenoma)

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24
Q

Tx of pituitary adenoma

A
  • Hormone therapies (depending on the problem)
  • Surgery (may return)
  • Radiation
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25
Q

Symptoms of pituitary adenoma

A
  • Visual defect (if tumor is large)
  • Headache (if tumor is large)
  • Oculomotor palsies may result
    • Manifestation: can’t properly dilate or constrict the pupil in one or both eyes
    • No eye tracking
    • Can’t open eyelids properly
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26
Q

Regulation of PRL Release

A
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27
Q

Actions of PRL

A
  • Proliferation of glandular tissue of mammary glands
  • Synthesis of milk proteins by mammary glands
    • ↑calcium mobilization from bone and secretion of calcium into milk
  • Stimulates immune system
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28
Q

Sex Effects of Hypersecretion of PRL

A
  • Females
    • Amenorrhea
    • Galactorrhea
    • Hirsutism
    • Osteopenia - weakening of the bones due to ↑Ca2+ mobilization
  • Males
    • Hypogonadism
    • Impaired libido
    • Infertility
    • Gynecomastia
    • Galactorrhea
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29
Q

Tx for Hypersecretion of PRL

A
  • DA agonists i.e. bromocryptin
  • Somatostatin analogs i.e. octreotide
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30
Q

Manifestation of Hyposecretion of PRL

A
  • Poor milk production
  • Poor immune system function
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31
Q

Tx for Hyposecretion of PRL

A
  • ↓plasma concentrations of PRL
  • TRH-stimulation test utilized to determine if the problem is at pituitary or hypothalamus
    • ↓PRL after TRH injection: problem at pituitary
    • ↑PRL release after TRH injection: problem at hypothalamus
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32
Q

Hypersecretion of GH disorders

A
  • Gigantism (pre-pubertal adenoma)
    • Tall & long limbs
  • Acromegaly (post-pubertal adenoma)
    • May be tall
    • Enlarged bones of face, hands
    • Enlarged soft tissues (tongue, heart)
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33
Q

Why can GH hypersecretion be lethal?

A

Increased risk of hypertrophic cardiomyopathy

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34
Q

What are clinical manifestations of GH hypersecretion?

A
  • Large tongue, lips, fingers, toes, jaw bone, ears, skull bones
  • ↑blood glucose
  • Headaches if tumor is large
  • Vision problems if tumor is large
  • Joint pain
  • Barrel chest
  • CV diseases - HTN, cardiac hypertrophy, etc. = early death
  • Malignancies may become more aggressive (GH and IGF are growth factors)
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35
Q

Tx for hypersecretion of GH

A

Somatostatin analog - inhibits GH, glucagon, insulin

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36
Q

Hyposecretion of GH

A
  • Growth failure
  • ↑% of fat and reduced lean mass
  • Poor strength and development of bones (bones are thin and fragile)
  • Poor immune function
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37
Q

Hyposecretion of GH: young adult onset

A
  • Poor lactation
  • Poor immune function
  • ↓blood glucose
  • Depression
  • ↓mass of bone
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38
Q

Hyposecretion of GH: GH and aging

A
  • GH falls at about age 60-65
    • May cause ↓function of immune system, ↑fat mass, ↓protein mass, ↓bone density associated with aging
  • IGF ↑tumor aggressiveness
39
Q

What is the normal regulatory pathway for thyroid hormone?

A

Hypothalamic TRH > Pituitary TSH > T3/T4

46
Q

What are the actions of T3?

A
  • Regulates basal activity of most cells - “Metabolic choke valve”
  • Affects cellular activity by binding to an IC receptor and interacting with DNA to ↑mRNA synthesis
  • Functions of most cells require thyroid hormones (muscles, nerves, glands, etc)
    • ↓thyroid hormones = ↓cell growth, poor protein synthesis, poor conduction of nerve impluses
47
Q

Clinical manifestations of hyerthyroidism AKA thryotoxicosis

A
  • General: weight loss, heat intolerance
  • Cardiac: rapid pulse, arrhythmias, clots
  • Neuromuscular: tremor
  • Skin: warm, moist
  • GI: diarrhea
  • Eye: exophthalmos, lid lag
  • Thyroid storm: extreme, dangerous symptoms
48
Q

What are common causes of hyperthyroidism AKA thyrotoxicosis?

A
  • Graves disease
  • Multinodular goiter
  • Thyroid adenoma
49
Q

What are uncommon causes of hyperthyroidism AKA thyrotoxicsis?

A
  • Thyroiditis
  • Thyroid carcinoma
  • Pituitary adenoma
  • Struma ovarii
  • Factitious
50
Q

Clinical manifestations of hypothyroidsm AKA myxedema?

A
  • General: fatigue, weight gain, cold intolerance, edema
  • Cardiac: slow pulse
  • Nervous: delayed reflexes, lethargy
  • Skin: rough, dry; hair loss
  • Oral: macroglossia
  • Myxedema: deepened voice
  • Myxedema coma: deteriorating mental status
51
Q

What are common causes of hypothyroidism?

A
  • Hashimoto
  • Iatrogenic
52
Q

What are uncommon causes of hypothyroidism?

A
  • Too little iodine
  • 2° hypothyroidism
  • 3° hypothyroidism
  • Other thyroiditis
53
Q

What are some non-neoplastic thyroid disease?

A
  • Thyroiditis
  • Graves Disease
  • Goiter
54
Q

What diseases fall under thyroiditis?

A
  • Hashimoto
  • DeQuervain
  • Silent
  • Reidel
55
Q

What is Hashimoto?

A

Hashimoto - Autoimmune destruction of thyroid

  • Most common cause of hypothyroidism in US
  • Females (more susceptible to autoimmune disorders in general)
  • Histological markers: Hurthle cells
56
Q

What is DeQuervain?

A

DeQuervain - Immune cross-reaction with thyroid follicles

  • Enlarged, sore thyroid
  • Follows URI
  • Self-limiting
  • Histological markers: Multinucleated giant cell
57
Q

What is Silent Thyroiditis?

A

Silent - Cycles of hyper- and hypo-

  • Post-partum or middle age
  • Painless, slightly enlarged thyroid
  • Histological markers: Lymphoid infiltrate
58
Q

What is Reidel?

A

Reidel - Hard, inflamed mass

  • Hypothyroidism
  • Rare
  • If large enough, may compress the trachea
  • Histological markers: Extensive fibrosis
59
Q

Graves Disease

A

Graves Disease

  • Most common cause of hyperthyroidism in the US
  • Type II hypersensitivity - Ab-Ag complex mediated
  • Autoimmune: Anti-TSH receptor antibodies stimulate TSH receptors
    • TSI activates hormone production and thyroid gland growth so TSH and TRH would be low because they’re trying to make them stop producing the thyroid hormone
  • Triad of symptoms
  • Histological markers: Hyperplasia of epithelium; scalloped colloid
60
Q

What is the Triad of Symptoms for Graves Disease?

A

Triad of symptoms:

  • General Hyperthyroidism Symptoms
  • Exophthalmos
  • Dermopathy - abnormal edema (like a unique form of edema); skin texture looks like an orange peel
61
Q

Tx for Graves Disease?

A

Treatment - controlling symptoms

  • Beta blockers (to control symptoms)
  • Iodine blockers (thiouracil)
  • Hot iodine (radioactive)
  • Surgery
62
Q

Goiter

A

The presence of a goiter only provides evidence that there is some problem with the thyroid axis

Two origins

  1. Inflammatory
  2. Non-inflammatory (hyperstimulation)

Can be present with:

  • ↓thyroid hormones
  • ↑thyroid hormones
  • Normal thyroid hormones

As TSH levels are high to make more thyroid hormone, but also stimulates growth

–> Goiter

63
Q

What is T3 and T4?

A

T3 = Thyroxine

T4 = Triiodothyronine

64
Q

What are neoplastic thyroid diseases?

A

Adenoma

Carcinoma

65
Q

Thyroid Adenoma & Carcinoma - Which is common? Uncommon?

A

Adenoma - Common

Carcinoma - Uncommon

66
Q

What are the different types of thyroid carcinomas? Rank in order from most common to rarest..

A

Most Common

  1. Papillary thyroid carcinoma
  2. Follicular thyroid carcinoma
  3. Medullary thyroid carcinoma
  4. Anaplastic thyroid carcinoma

Rarest

67
Q

Papillary Thyroid Carcinoma

A

Papillary thyroid carcinoma - MOST COMMON

  • >95% 10yr survival
  • Orphan Annie tumor
  • Younger women
  • Mild
  • Nuclei
  • Histological features: Psamomma body (Ca2+ rich deposits)
68
Q

Follicular Thyroid Carcinoma

A

Follicular thyroid carcinoma - SECOND MOST COMMON

  • 95% 10yr survival in young patients with small, minimally invasive tumor
  • Prognosis gets worse with ↑age, size, invasiveness
  • Histological features: Vascular invasion
69
Q

Medullary Thyroid Carcinoma

A

Medullary thyroid carcinoma - RARE

  • Endocrine tumor (or parafollicular cells)
    • Parafollicular cells release calcitonin (regulates Ca2+ cells)
  • 90% 10yr survival if confined to thyroid
  • 20% 10 yr survival if metastasized
70
Q

Anaplastic Thyroid Carcinoma

A

Anaplastic thyroid carcinoma - RAREST TYPE

  • Bulky, fast-growing, invasive neck mass
    • Pure chaos in the thyroid gland
  • Usually metastatic at dx
  • BAD PROGNOSIS - <10% 5yr survival
71
Q

Parathyroid Glands

A
  • Small glands located behind the upper and lower poles of the thyroid gland
  • Produce parathyroid hormone
    • Regulate serum Ca2+
    • Calcitonin antagonist
72
Q

Alterations of parathyroid function

A

Hyperparathyroidism

Hypoparathyroidism

73
Q

Types of hyperparathyroidism

A
  • Primary hyperparathyroidism
    • Excess secretion of PTH from one or more parathyroid glands
  • Secondary hyperparathyroidism
    • ↑PTH secondary to a chronic disease causing hypocalcemia (i.e. renal failure)
74
Q

What usually causes hypoparathyroidism?

A

Parathyroid damage during thyroid sugery

75
Q

What are the different layers of the adrenal glands? What hormones are produced by each layer?

A
  • Cortex
    • Glomerulosa
      • Mineralocorticoids - Aldosterone
        • Retain SALT
    • Fasciculata
      • Glucocorticoids - Cortisol
        • Release SUGAR
    • Reticularis
      • Sex hormones - Androgens, Estrogens
        • SEX
  • Medulla
    • Epi
    • NE
76
Q

Cushing Syndrome vs. Cushing Disease

A
  • Cortisol Hypersecretion
  • Cushing Syndrome - Elevated plasma cortisol
    • Iatrogenic (taking too much cortisol) - most common
    • Adrenal tumor
  • Cushing Disease - Elevated ACTH production b/c of pituitary tumor
    • W/ subsequent elevated cortisol
77
Q

Tx for cortisol hypersecretion

A

Tx: Remove or destroy the tumor; ↓cortisol injections

78
Q

Clinical manifestations of cortisol hypersecretion

A

Clinical manifestations

  • Insulin resistance
  • Weight gain (trunk and moon face)
  • ↑blood glucose
  • Muscle wasting, weakness b/c of muscle breakdown
    • AA supporting gluconeogenesis
  • Osteoporosis
  • ↓inflammatory activity
    • Poor wound healing and immune system function
  • Thin skin
  • ↑sensitivity to catecholamines b/c of ↑adrenergic receptors
    • ↑BP, HR
  • Altered mental status (depression, psychosis, irritability)
79
Q

Sex steroid hypersecretion

A
  • Feminization - estrogens
  • Virilzation - androgens

Problem @ reticularis layer?

80
Q

Catecholamine Hypersecretion

A

Adrenal Medulla Hyperfunction

Caused by tumors derived from chromaffin cells of the ADRENAL MEDULLA

Pheochromocytoma

81
Q

Symptoms of catecholamine hypersecretion

A
  • ↑HR, BP
  • Diaphoresis (sweating)
  • Weight loss
  • Hyperglycemia/hyperlipidemia
82
Q

What are some adrenal hypotension syndromes?

A

Addison Disease (primary adrenal insufficiency)

Waterhouse-Friderichsen Syndrome

83
Q

What is Addision Disease

A

Primary adrenal insufficiency

  • ↓↓cortisol and mineralocorticoids
  • Usually autoimmune at origin
84
Q

What are symptoms of Addison Disease?

A
  • Slow onset
  • Weakness
  • Hypotension
  • Skin hyperpigmentation: oral manifestation - making too much ACTH because there’s no feedback that cortisol levels are low due to adrenal gland deficiency and when you have a lot of ACTH, you also have a lot of MSH
85
Q

What is Waterhouse-Friderichsen Syndrome?

A

Hemorrhaging at the adrenal gland caused by

  • Bacterial infection (N. meningitidis)
  • Massive, bilateral adrenal hemorrhage
  • Hypotension, shock
  • DIC - disseminated intravascular coagulation
86
Q

What is MEN syndrom and what are the two classifications?

A

Multiple Endocrine Neoplasia

  • Genetic disorder
  • Endocrine disorder
  • Two classifications:
    • MEN-1
    • MEN-2
87
Q

What are the features of MEN syndrome?

A
  • Younger people
  • Multifocal
  • Aggressive
88
Q

What are the features of MEN-1?

A
  • Parathyroid hyperplasia
  • Pancreatic hormone tumors
  • Pituitary adenoma
  • Duodenal gastrinoma
  • Carcinoid (neuroendocrine tumor AKA gut tumor producing 5HT)
  • Thyroid/adrenal adenomas
  • Lipomas
89
Q

What are the genetics of MEN-1?

A

MEN1 gene mutation

  • Encodes menin
  • Tumor suppressor gene
  • Mutation turns gene off
90
Q

What are the features of MEN-2A & -2B?

A
  • *Medullary thyroid carcinoma
  • Pheochromocytoma - produces catecholamines
  • Parathyroid hyperplasia
91
Q

What are the genetics of MEN-2A & -2B?

A

RET gene mutation

  • Proto-oncogene
  • Encodes tyrosine kinase receptor
  • Mutation turns gene on
92
Q

What is the only difference between MEN-2A and -2B?

A

MEN-2B has a collagen mutation!!!!!

  • Marfanoid habitus

DMD 5248 (6 decks)

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