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Post Midterm Patho > Thyroid/ Adrenal Gland > Flashcards

Thyroid/ Adrenal Gland Flashcards

1
Q

What is the 2nd most common endocrine disorder?

A

Thyroid gland

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2
Q

What hormones are produced in the thyroid gland?

A

Thyroxine and Triiodothyrorine and Calcitonin

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3
Q

What is the function of T3/T4?

A

Involved in metabolism and growth / development of cells

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4
Q

What stimulates T3 / T4 to be secreated?

A

TSH

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5
Q

What causes TSH to be secreated by the anterior pituitary gland?

A

Hypothalmus signals the anterior pituitary gland in response to low levels of t3/t4 to produce/secrete TSH

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6
Q

Normal: the thyroid gland involves what type of feedback?

A

Negative feedback

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7
Q

Thyorid Gland disorder involes what thing that rhyms with boiter?

A

Goiter

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8
Q

Define Goiter:

A

structural enlargement of the thyroid gland

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9
Q

does a goiter mean a change in the thyroids function?

A

Not necessiarly. can be hypo or hyperfunction (hyper / hypothroidism)

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10
Q

What are the 2 types of Goiters?

A
  1. Endemic Goiter

2. Toxic Goiter

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11
Q

Explain an Endemic Goiter:

A

Idodine defeciency, leads to decreaesd t3/t4, compensatory mechanism increaes production / secreation of TSH , this causes hyperplasia / hypertrophy of the thyroid gland

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12
Q

Explain Toxic Goiter:

A
  • large, nodular gland

- d/t hyperactivity (excessive stimulation of the gland)

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13
Q

What is the most common disease caused by Hyperthyroidism?

A

Graves disease ( 80-90%)

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14
Q

What population does Graeves disease usually affect?

A

Young women

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15
Q

What causes hyperthyroidsm?

A

Mostly autoimmunity

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16
Q

Autoimmunity is usally causes destruction of self antigens.. in the case of hyperthyroidsm, are the cells being destroyed?

A

No. The function is being altered

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17
Q

What are the hallmarks of Graeves diesase? 3 things

A
  1. Goiter
  2. Hyperthyroidism
  3. Exopthalmus
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18
Q

What is the pathophysiology of Graves disease?

A

Autoimmunity targets TSH receptors on the thyroid gland –> TSabs (aka TSI) mimic TSH and bind to TSH receptors –> increases TH secreation (t3/t4), the increase of TH hormone inhibits TSH secreation –> low TSH – Thyroid gland STILL stimulated d/t the TSabs avoid enzyme degradation –> active longer / no negative feedback / more t3/t4

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19
Q

What is thyrotoxicosis?

A

A clinical presentation of hyperthyroidism (thyroid storm)

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20
Q

What are the clinical manifestations of thyrotoxicosis? 3 things

A
  1. Increased Metabolism (altered pathways)
  2. Hyperventilation (expel C02)
  3. excitable, irritable, insomnia, anxiety
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21
Q

Explain the increased metabolism.

  1. What is being increased?
  2. the increase of metabolism causes an increase of what?
  3. What compensates for this increased heat?
  4. Does this individual have a sensitivity to heat?
  5. What to HR and C0 do to meet increased demand for 02 / waste removal?
A
  1. protein and lipid catabolism (wt loss)
  2. metb heat
  3. heat loss mechanisms (flushed skin, perspiration)
  4. intolerance to heat
  5. Increase
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22
Q

What would happen if a person with hyperthyroidism did not compensate by hyperventiliating?

A

Acidosis could occur

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23
Q

What are the 3 treatment options for Hyperthyroidism?

A
  1. Antithyroid drugs
  2. Radioiodine Therapy
  3. Sx for large goiters
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24
Q

How do the antithyroid drugs work?

A

Suppress production of TH (t3/t4)

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25
Q

What is involved in radioiodine therapy?

A

Administartion of radioactive iodine –> bind to the proteins in the thyroid –> the iodine then admits radiation to everything around there

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26
Q

What can be a negative affect caused by Sx removal of large goiters?

A

Beware hypothyroidism could occur if too much removed

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27
Q

Hypothyroidism involves 3 different levels. What are they? Each level affects one system, what is it?

A
  1. Primary = thyroid gland
  2. Secondary = anterior pituitary gland
  3. tertiary = hypothalmus
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28
Q

Does hypothyroidism involve 3 stages?

A

NO! they are 3 different levels

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29
Q

Out of the 3 levels of hypothyroidism, which is the most common?

A

95% primary (thyroid gland)

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30
Q

What is the Et of hypothyroidism?

A

D/T radiation and or surgery for hyperfunction

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31
Q

The radiation and Sx for hyperfunction, if hypothyroidsm then occurrs, what is the etioloy define as?

A

Iatrogenic

32
Q

In hypothyroidism, is there an increase or decreased BMR?

A

Decreased

33
Q

What are the problems that occur with hypothyroidism? (4)

A
  1. Decreased body temp
  2. Decreased CO, impacts perfusion throughout the body
  3. Decrease CNS function
  4. Weak muscle action (d/t less ATP)
  5. Increased weight gain
34
Q
  1. Why the decreased body temp?
  2. Why the decreased CO?
  3. Why the weight gain?
A
  1. Lower BMR = less heat being produced d/t the decreased metabolism
  2. Directly related to the myocardial requirement of ATP
  3. Decreased metabolism, then when you intake food, the food will become stored if it is not being metabolized.
35
Q

What is Hashimoto’s Thyroiditis?

A

Hypothyroidism, inflammation of the thyroid

* Most common hypothyroid state

36
Q

Who does Hashimotos Thyroiditis mostly affect?

A

Middle aged women

37
Q

In Hashimotos Thyroiditis, what is causing the destrcution of the gland?

A

Autoimmune - Antithyroid abs

38
Q

What do the antithyroid ABs do?

A

Block the TSH binding receptors on the thyroid gland, therefore the thyroid is not stimulated to secrete T3/T4

39
Q

In Hashimotos Thyroiditis, what is happening with lymphocytes?

A

They are infiltrating the thyroid gland

40
Q

What is the treatment for Hashimotos thyroiditis?

  1. If an endemic goiter?
  2. If no endemic goiter
A
  1. Increase dietary iodine

2. T4 on daily basis

41
Q

Why is T4 given and not T3? (thyroid hormones)

A

Most T3 used to be T4, then becomes T3 when it comes in contact with other cells in the blood stream they give up an iodine, making it T3

42
Q

The Adrenal Glands have 2 Parts to them. What are they? (2)

A
  1. Adrenal Medulla (on the inside)

2. Adrenal cortex (on the outside)

43
Q

The adrenal medulla is involved in the secretion of what 2 hormones?
What mediates this?

A
  1. Epinephrine
  2. Norepenephrine
    SNS
44
Q

The Adrenal Cortex classes of the Hormones?

What are they? (3) What is the dominant hormone produced?

A
  1. Glucocortisoids: Cortisol
  2. Mineralcorticoids: Aldosterone
  3. Androgens: Tesosterone
45
Q

What is the function of Cortisol? (3)

A
  1. Aid in metabolism of protein/fat/carbs
  2. Involved in the stress response
  3. Antiinflammatory properties (so supresses the immune response)
46
Q

The hypothalmus chats with the anterior pituitary, that secretes what to work on the adrenal gland?

A

ACTH (Adrenocorticotropic hormone)

47
Q

Most disorders of the adrenal gland include the cortex? or the medulla?

A

The cortex

48
Q

What is 3 Etiologys of Hyperfunction of the adrenal cortex?

A
  1. Cortical tumor or hyperplasia —> ^^^cortisol, decreased ACTH
  2. Tumor or hyperplasia of Anterior pituitary —> ^^ ACTH
  3. Ectopic Secratory Tumor (secretes ACTH like substance)
49
Q

What is Cushings Syndrome? What is increased?

A

Glucogorticoid hypersecreation… therefore increase of cortisol

50
Q

What occurs to the muscles in cushings syndrome? D/t what?

A

They become weak. Protein catabolism

51
Q

Why do lipids become deposited to the neck, face, and abdomen in Cushings Syndrome?

A

Lipids are mobilized and deposited

52
Q

Explain what happens to lipids and proteins in Cushings Syndrome:

A

Gluconeogensis occurs: formation of new glucose from the lipids and proteins

53
Q

What does the gluconeogensis in Cushings syndrome lead to? which leads to what 2 problems?

A

Prolonged Hyperglycemia.
Leads to
1. Insulin Resistance
2. IGT

54
Q

In Cushings Syndrome, Na+ and h20 are reabsorbed. Why?

A

Excessive elevated levels of cortisol take on the function of aldosterone (cause Na+ and H20 to be retained, and K+ to be excreted)

55
Q

Is hypokolemia involved in Cushings syndrome? Why or why not?

A

Yes. D/t the excessive amounts of coritsol, acts like aldosterone, therefore Na+ + H20 reabsorbed, and H+ excreted

56
Q

Why would a person with Cushings syndrome have alterd shape to their face? What is the shape classified as? What about their shoulders?

A

D/t deposition of fats. “rounded moon face” “buffalo shoulders”

57
Q

Why would a patient with Cushings Syndrome be more susceptible to infection?

A

Cortisol steroid has antiinflammatory properties, therefore less defence to infections.
High levels of cortisol suppress the immune response

58
Q

Sometimes in cushings syndrome there is a hypersecreation of androgen hormones. Is this more common in a male or female? Why?

A

More common in a female (womens testosterone is produced in the adrenal cortex)

59
Q

What is the treatment for Cushings syndrome? (4)

A
  1. Excise tumor
  2. Radiation on the anterior pituitary
  3. Drugs for ectopic tumors
  4. Adrealectomy (removal of adrenal glands)
60
Q

What is Conn Syndrome? Hypersecreation of what?

A

Hypersecreation of mineral corticoids (aldosterone)

61
Q

is Conn syndrome common?

A

No sir.

62
Q

What is the etiology of Conn syndrome? (3)

A
  1. usually corticol adenoma (benign tumor)
  2. Idiopathic cortical hyperplasia
  3. renin secreting renal tumor
63
Q

What would the renin secreting renal tumor play a role in aldosterone hypersecretion?

A

It secretes renin, activates the RAAS system, d/t this, the adrenal cortex is stimulated to secrete Aldosterone, causing a reabsorption of Na+ and H20

64
Q

What are the Manifestations of Conn Syndrome? (3)

A
  1. HTN
  2. Hypokolemia
  3. Alkalosis
65
Q

Why does Conn syndrome have hypokolemia is a manifestation?

A

Aldosterone increase Na+ water reabsorption, and increases K+ excreation

66
Q

Why would alkalosis be an manifestation of Conn Syndrome?

A

Increased excretion of H+

67
Q

Why would HTN be a manifestation of Conn syndrome?

A

Increase Na+ and H20 reabsorption

68
Q

What is the treatment for Conn syndrome? (3)

A
  1. Adrenalectomy for adenoma
  2. Drugs for hyperplasia (can block receptors, even though there is more cells they wouldn’t then all be secreting)
  3. Na+ restriction
69
Q

What is the disease that we look at for hyposecretion?

A

Addison’s Disease

70
Q

What hormone classifications does Addison’s Disease affect? (3)

A
  1. Glucocoritocoids
  2. Mineralcorticoids
  3. Androgens
71
Q
  1. Addison’s Disease is primary or secondary deficiency? This means it affects what?
  2. Is Addison’s Disease common?
A
  1. Primary, affects the cortex

2. No, not common

72
Q

What is the Et of Addison’s Disease? (2)

A
  1. Autoimmunity (d/t tumor or infection)

2. High dose of glucocorticoid Tx

73
Q

What are the 3 Manifestations of Addison’s Disease?

A
  1. Hypotension
  2. Wt Loss
  3. Decrease GAS (General Adaptive Syndrome)
74
Q

Explain how Hypotension is a manifestation of Addison’s Disease?

A

Na+ and H20 loss –> hypovolemia –> Decreased CO –> Hypotension –> Weakness and fatigue

75
Q

When would Addisonian Crisis occur? Can this be fatal?

A

Acute insufficiency d/t stress. Yes.

76
Q

What is the Tx for Adissons Disease

  1. Acute
  2. Chronic
A
  1. IV Fluids, Glucocorticoids

2. Mineralcorticoids, glucocorticoids

Post Midterm Patho (16 decks)

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