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Patho > Week 4: Endocrine > Flashcards

Week 4: Endocrine Flashcards

1
Q

Major role of the endocrine system

A

Regulation and integration of body functions

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2
Q

Structure of the endocrine system

A

Made up of several glands which communicate using chemical messengers: hypothalamus, pituitary, pineal, adrenal, pancreas and sex organs

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3
Q

Basic features of the endocrine system

A

hormones are released from endocrine glands, travel through the blood and interact with a target organ

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4
Q

What does the chemical nature of hormones determine? (4)

A

their synthesis, release, transport and receptor site on the target site

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5
Q

What kind of hormones are water-soluble?

A

peptides and catecholamines

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6
Q

What kind of hormones are lipid-soluble?

A

steroid and thyroid hormones

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7
Q

Water-soluble hormones: Identify the structural classes, synthesis and storage, release, transport, receptor & type of cellular response

A

structural classes: Peptide and catecholamines
synthesis & storage: in advance and stored in vesicles
release: exocytosis with calcium signal
transport: without a carrier to the target tissue
receptor: on target cell surface
cellular response: second messenger systems

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8
Q

Lipid-soluble hormones: Identify the structural classes, synthesis and storage, release, transport, receptor & type of cellular response

A

structural classes: Steroid and thyroid hormones
synthesis & storage: On demand, cannot be stored
release: diffusion once made
transport: requires protein carrier to target tissue
receptor: inside cell in cytoplasm or nucleus
cellular response: alter gene transcription

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9
Q

What are the 3 causes of gland hypofunction? Give an example

A
  1. Congenital defect resulting in loss of gland or key enzyme
    Example: congenital hypothyroidism
  2. Destruction of the gland due to ischemia, infection, inflammation, autoimmunity, neoplastic growth
    Example: Addison’s
  3. Aging or atrophy of a gland
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10
Q

What are the 3 causes of gland hyperfunction? Give an example

A
  1. Excessive endogenous hormone production
    Examples: Graves’, Cushing
  2. Excessive administration of exogenous hormones
  3. Autoimmune stimulation of the gland
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11
Q

What are the 2 causes of alteration in target tissue responsiveness? Give an example

A
  1. Loss of receptors on a target tissue
    Example: Diabetes Mellitus
  2. Production of antibodies that block the ability of a hormone to bind to a receptor
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12
Q

What are the 3 functional alterations of glands?

A
  1. hypofunction
  2. hyperfunction
  3. alteration in target tissue responsiveness
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13
Q

Define and give an example of a primary endocrine disorder

A

definition: originates in the gland responsible for producing the hormone
example: hyperparathyroidism

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14
Q

Define and give an example of a secondary endocrine disorder

A

definition: caused by decreased hormone production or release from the pituitary
example: pituitary adenoma

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15
Q

Define and give an example of a tertiary endocrine disorder

A

definition: due to dysfunction of the hypothalamus
example: tumors and mass lesions of the hypothalamus

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16
Q

What are the diagnostic approaches to endocrine disorders? (5)

A

Blood tests: measure hormone levels
Urine tests: measure hormone levels or metabolites
Stimulation and suppression tests: hypofunction testing (stimulation); determine if negative feedback regulation is intact (suppression)
Genetic tests: identify genetic changes, screening
Imaging: scan for anatomical changes, density changes, uptake

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17
Q

What are the normal functions of growth hormone? (2 categories)

A

Structural: promotes growth of skeletal muscle and stimulates extension of the long bones before puberty by acting on the epiphyseal plate

Metabolic: stimulation of protein anabolism and fat catabolism while sparing glucose to maintain homeostasis

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18
Q

What is the most common cause of growth hormone excess?

A

Excess commonly caused by secretory pituitary adenoma, may occur in acute illness, chronic renal failure, cirrhosis

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19
Q

What is gigantism and how does it occur?

A

What is it: Symmetric excessive linear growth

How does it occur: Excess of growth hormone prior to closure of epiphyseal plates during childhood

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20
Q

What is acromegaly and how does it occur?

A

What is it:
-Tissue thickening and growth on hands, feet, nose and mandible
- Arthritis due to growth of joint cartilage and increased bone absorption
- General systemic disorder of the lungs, liver, spleen and kidneys, enlargement of intestines
- Hypertension, coronary artery atherosclerosis, CHF
How does it occur: excess of GH during adulthood

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21
Q

What are the consequences of growth hormone deficit in adults (4) vs. children (5)?

A

adults: normal height, increased body fat, decreased lean body mass, decreased bone mineral density
children: short stature, obesity, immature appearance/voice, delay in skeletal maturation, hyperlipidemia

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22
Q

What are the clinical manifestations of congenital growth hormone deficit? (6)

A

Short stature, obesity, immature appearance/voice, delay in skeletal maturation, hyperlipidemia, normal intelligence

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23
Q

What is the cause and what are the clinical manifestations (4) of acquired growth hormone deficit?

A

cause: abnormalities of the hypothalamus and pituitary
CM: Obesity, delayed skeletal maturation, increased cardiovascular mortality, other syndromes

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24
Q

Which two hormones are involved in endocrine regulation of calcium balance?

A

Two hormones regulate calcium levels: calcitonin & parathyroid hormone

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25
Q

Where does calcitonin come from and what is it’s general action?

A

released from thyroid gland when calcium levels are high - stimulates uptake of calcium

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26
Q

Where does parathyroid hormone come from and what is it’s general action?

A

released from parathyroid gland when levels are low - promotes release of calcium and phosphate into the blood

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27
Q

What are the 3 specific actions of parathyroid hormone?

A
  1. Stimulates osteoclasts to promote release of calcium and phosphate
  2. Stimulates enzymes in liver and kidney to produce an active form of vitamin D which increases calcium absorption in the GI tract
  3. Stimulates renal tubules to promote calcium reabsorption and decrease phosphate reabsorption
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28
Q

What is hypoparathyroidism?

A

decreased secretion of PTH or decreased hormonal response to PTH in the tissues

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29
Q

What is the cause and major consequence of hypoparathyroidism?

A

cause: due to removal or autoimmune destruction of parathyroid gland
consequence: decreased calcium levels which leads to increased neuromuscular activity and tetany

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30
Q

What are the symptoms of hypoparathyroidism (5)?

A

tetany, chvostek sign, trousseau sign, parasthesias, prolonged QT interval

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31
Q

What is the definition of hyperparathyroidism?

A

enhanced activity of parathyroid gland

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32
Q

What are the causes of primary hyperparathyroidism? (3)

A

adenoma, hyperplasia, carcinoma of parathyroid glands

33
Q

What are the causes of secondary hyperparathyroidism? (2)

A

chronic renal failure, renal phosphate retention

34
Q

What are the symptoms of hyperparathyroidism? (5)

A

Fatigue, hypertension, constipation, renal stones, bone pain

35
Q

What is the normal function of thyroid hormone (5)?

A

major metabolic hormone, important for growth and development

  • Permissive for growth-promoting actions of GH
  • Essential for development of the nervous system
  • Increases protein synthesis of many types of cells
  • Regulates the rate of oxidative phosphorylation
  • Controls O2 consumption and the production of heat, which determines the BMR
36
Q

What are the two hormones produced by the thyroid?

A

thyroid hormone & calcitonin

37
Q

What is the normal function of calcitonin?

A

reduces plasma calcium levels by causing calcium to be deposited into the bone

38
Q

Which hormones comprise thyroid hormone? Which is the major form of TH? Which is the most potent form of TH?

A

Thyroid hormone includes thyroxine (T4) and triiodothyronine (T3)
Major/most potent form & active form = T3

39
Q

Normal feedback loop for thyroid hormone?

A
  1. Hypothalamus stimulated (by sleep, cold temperature, stress) releases thyrotropin-releasing hormone or TRH
  2. TRH stimulates the pituitary gland to produce TSH
  3. TSH stimulates the thyroid gland to secrete TH
  4. When level of hormones reaches a certain threshold, the hormones communicate with the hypothalamus to stop the hormone cascade
40
Q

What is a permissive hormone, and how does thyroid hormone function as one?

A

Permissive hormone = exert profound effects on the ability of cells to respond to other hormones

TH increases cellular responsiveness to catecholamines

41
Q

Define hypothyroidism. How is it diagnosed?

A

deficiency of thyroid hormone
In children = cretinism
Adults = myxedema
TSH & TH levels -TSH will be elevated & TH decreased in primary hypothyroidism; both decreased in secondary hypothyroidism

42
Q

Define hyperthyroidism

A

overproduction of TH

43
Q

Causes of hypothyroidism

A

congenital or acquired, almost always primary, may be secondary
Most common cause = Hashimoto’s disease

44
Q

S/S of hypothyroidism (child (2) vs. adult (8))

A

Child or infant - mental retardation, growth deficiencies

Adult - generalized and consistent with overall decrease in metabolism; weakness & fatigue, cold intolerance, dry skin, bradycardia, delayed deep tendon reflexes, anemia, hyponatremia and depression

45
Q

What is the common cause of hyperthyroidism? What is it’s etiology?

A

Graves’ disease
Etiology: Involves autoimmune production of an antibody against the TSH receptor that continually stimulates TSH action leads to excess TH and goiter

46
Q

What are the consequences of Graves’ disease (5)?

A
  • Hypermetabolism: weight loss, muscle weakness, increased ventilation to meet O2 demand, increased heat production
  • Increase in SNS activity
47
Q

Treatment of Graves’ disease

A

surgery or radioactive iodine to ablate part of the thyroid; thiouracil to block TH synthesis, lithium to block TSH secretion and iodine to block the additional production of TH

48
Q
  1. What is thyrotoxicosis? 2. If left untreated, what can it give rise to?
A
  1. Characterized by increased synthesis and secretion of T3 and T4 which gives rise to increased metabolic rate
  2. Thyroid storm
49
Q

What is goiter?

A

enlargement of thyroid gland

50
Q

How can goiter occur in hypothyroidism?

A

thyroid gland enlarges in an attempt to produce more thyroid hormones

51
Q

How can goiter occur in hyperthyroidism?

A

thyroid enlarges due to overstimulation

52
Q

Is Hashimoto’s Thyroiditis hypothyroidism or hyperthyroidism? What is it?

A

Primary hypothyroidism

autoimmune destruction of the thyroid gland at the thyroid peroxidase, thyroglobulin and TSH receptors

53
Q

Tx of Hashimoto’s

A

replacement of thyroid hormone

54
Q

What is myxedema?

A

presence of non-pitting mucus type edema caused by an accumulation of hydrophilic mucopolysaccharide substance in the connective tissues

55
Q

What is congenital iodine deficiency syndrome (cretinism)?

A

hypothyroidism due to decrease in iodine after birth

56
Q

Structure of the adrenal gland

A

two bean-shaped glands on the top of the kidneys

two regions: medulla (inner portion) & cortex (outer portion)

57
Q

Normal function of the two regions of the adrenal gland

A

Adrenal Medulla: produces catecholamines released after sympathetic stimulation: epinephrine & norepinephrine
Adrenal Cortex: produces three steroid hormone types: mineralocorticoids, glucocorticoids, sex hormones

58
Q

What are the general functions of the hormones released by the adrenal medulla?

A

Released in response to sympathetic stimulation - occurs in response to short-term stress

59
Q

What are the general functions of the hormones released by the adrenal cortex?

A

Mineralcorticoids: regulation of minerals - sodium and potassium (eg. Aldosterone)
- Stimulate sodium and water retention to maintain fluid and electrolyte homeostasis

Glucocorticoids: promotion of cellular metabolism and response to long-term stress by regulating glucose levels (eg. Cortisol)
- Protect against hypoglycemia by promoting gluconeogenesis & glycogenolysis

Sex hormones: androgens and some estrogens

60
Q

What is the normal feedback loop for cortisol?

A
  1. Stress stimuli
  2. Hypothalamus stimulates pituitary gland by releasing CRH
  3. Pituitary gland secretes ACTH
  4. Adrenal glands release cortisol
61
Q

Define adrenal insufficiency

A

reduction of one or more hormones secreted from the adrenal complex

62
Q

Define primary adrenal insufficiency and give an example. Why does hyperpigmentation occur?

A

Primary adrenal insufficiency: damage to adrenal cortex
Example: autoimmune diseases and TB
Hyperpigmentation: increased ACTH stimulates melanocytes (this does not occur in a diminished level of ACTH)

63
Q

Define secondary adrenal insufficiency and give an example.

A

occurs when there is a lack of ACTH from anterior pituitary

Example: exogenous glucocorticoid therapy or pituitary or hypothalamic tumor

64
Q

What causes adrenal crisis and what are the s/s (7)?

A

Cause: Occurs due to insufficient glucocorticoids (rapid withdrawal of exogenous glucocorticoids or Addison’s)
S/S: confusion, headache, N/V, muscular weakness, hypotension, dehydration, vascular collapse

65
Q

What is Addison’s disease?

A

Primary adrenal insufficiency - atrophy of adrenal glands due to autoimmune response

66
Q

What are the consequences of Addison’s on adrenal function?

A
  • Loss of 90% of adrenal cortices resulting in an insufficiency of tissue required to produce hormones
  • Decrease in adrenal secretion of cortisol and increase in ACTH release
67
Q

S/S of Addison’s (13)

A
  • Hyperpigmentation: increased ACTH stimulates melanocytes
  • Hypoglycemia
  • Hypotension
  • Decrease in cardiac size
  • Decreased mineralcorticoid activity - fluid and electrolyte imbalances, changes in WBC
  • Weakness, fatigue, anemia, anorexia, vomiting, diarrhea, muscle and joint pain
68
Q

Treatment of Addison’s

A

replacement of missing hormones

Hydrocortisone to counter the loss of mineral and glucocorticoids

69
Q

What is Cushing’s syndrome?

A

physical and physiologic manifestation of overproduction of cortisol

70
Q

What is the cause of Cushing’s?

A

excess production of ACTH from pituitary tumor

71
Q

S/S of Cushing’s (9)

A
  • Fat redistribution: moon face or buffalo hump
  • Altered protein metabolism: muscle wasting particularly in extremities
  • Accelerated bone metabolism - osteoporosis, renal calculi
  • Altered glucose metabolism - presents like DM
  • Loss of immune cell activity - increased risk of infection
  • Increased androgens - hirsutism, acne, irregular menstruation
72
Q

Treatment of Cushing’s

A

depends on underlying cause: surgery, radiation or medicine

73
Q

Insulin: where is it released from, when is it released, consequences of release on blood glucose levels

A

Where is it released: Beta-islet in pancreas
When is it released
- in response to high BG levels
- in response to parasympathetic stimulation (eating)
- In response to hormones produced by GI tract when food is being metabolized
Consequences of release on BG levels
- Causes recruitment of glucose transporters to the cell surface
- Insulin takes glucose into cells, lowering BG levels
- Glucose used for energy metabolism, converted to glycogen or fats for storage or used to synthesize proteins

74
Q

Glucagon: where is it released from, when is it released, consequences of release on blood glucose levels

A

Where is it released: Alpha-islet in pancreas
When is it released
- in response to low BG levels
- Strenuous exercise when fuel requirements are increased
Consequences of release on BG levels
- Raises BG levels by converting glycogen into glucose
- Stimulation of glycogenolysis, lipolysis and gluconeogenesis

75
Q

Define: glycolysis; glycogenesis; glycogenolysis; gluconeogenesis

A

glycolysis: breakdown of glucose, occurs in response to increased glucose levels
glycogenesis: glycogen synthesis, occurs during rest periods and in response to high glucose levels
glycogenolysis: catabolism of stored glycogen in liver to raise BG levels - occurs when BG levels decrease
gluconeogenesis: formation of glucose from sources other than carbohydrates when carbohydrates are unavailable

76
Q

Type I DM: cause, underlying impact on insulin release, consequences and treatment

A

Cause: autoimmune, viral or genetic destruction of B-islet cells coupled with an environmental trigger
Underlying impact on insulin release or action: complete or near absence of insulin
Consequences: high plasma glucose levels, DKA (fats used in the absence of insulin, results in formation of ketones)
Treatment: exogenous insulin

77
Q

Type II DM: cause, underlying impact on insulin release and treatment

A

Cause: genetic component but obesity
Underlying impact on insulin release or action: decreased responsiveness to insulin due to decreased receptor number or sensitivity, high BG levels
Treatment: dietary changes and exercise, may need exogenous insulin, medication therapy

78
Q

Which type of diabetes is more common? (1)

Which type is more likely to experience DKA? (2)

A
  1. Type II

2. Type I

79
Q

Long-term consequences of diabetes (4)

A

Microvascular disease - thickening of arterioles and capillaries; ischemia can damage vulnerable tissues such as in the eye
Atherosclerosis: increased r/f plaque formation which can lead to coronary artery disease and stroke
Neuropathies: often seen with changes in Schwann cells
Infection: loss of sensation, decreased perfusion and increased glucose fosters microbial growth + impaired WBC

Patho (14 decks)

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