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Patho Exam 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Functions of endocrine system

A
  • growth and development
  • sex differentiation
  • metabolism
  • adaption
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2
Q

4 hormones of hypothalamus

A
  • TRH
  • CRH
  • growth hormone
  • GnRh
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3
Q

Hormones of anterior pituitary

A
  • TSH
  • LH
  • FSH
  • ACTH
  • GH
  • Prolactin
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4
Q

Hormones of posterior pituitary

A
  • Oxytocin

- ADH

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5
Q

Primary disorder

A

Malfunction of the actual target organ

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6
Q

Secondary disorder

A

Target gland is normal, however altered function of the stimulating hormones - it is a pituitary problem

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7
Q

Tertiary

A

Both pituitary and target problem

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8
Q

Low TSH

High T3 and T4

A

Primary hyperthyroidism

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9
Q

High TSH

Hight T3 and T4

A

Secondary hyperthyroidism

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10
Q

High TSH

Low T3 and T4

A

Primary hypothyroidism

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11
Q

Low TSH

Low T3 and T4

A

Secondary hypothyroidism

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12
Q

What are the basics of the hypothalamus-pituitary axis-thyroid gland axis?

A

Hypothalamus (TRH) –> Pituitary (TSH) –> Thyroid (T3 and T4)

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13
Q

What mineral deficiency can lead to hypothyroidism?

A

Iodine deficiency

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14
Q

How does hypothyroidism affect metabolism?

A

Metabolism decreases

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15
Q

What happens in long-standing hypothyroidism?

A

Myxedema

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16
Q

What are the clinical manifestations of hypothyroidism

A
  • Bradypnea
  • Constipation
  • Cold intolerance
  • Fatigue
  • Weakness
  • Dry skin
  • Coarse hair
  • Impaired memory and reproduction
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17
Q

What are the clinical manifestations of Myxedema

A
  • Swollen face
  • Puffiness around the eyes
  • Swelling of tongue
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18
Q

Another term for Myxedema

A

Cardiomegaly

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19
Q

What kind of patients would you see Myxedema in?

A
  • Patients who haven’t been compliant with the hormone treatment
  • Get sick
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20
Q

What differs in Myxedema Coma from Myxedema

A

More diffuse edema, precipitated by an acute event, weakness, confusion

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21
Q

What do you look for in lab diagnostics of hypothyroidism?

A

TSH levels
T3 and T4 levels
Thryoid autoantibodies - to see if an autoimmune disease attacked the thyroid
Antithyroglobulin

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22
Q

How do you treat primary hypothyroidism?

A

Thyroid hormone replacement therapy

i. e. levothyroxine and syntheroid
- slowly raise the levels

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23
Q

How do you treat secondary hypothyroidism?

A

Removal of the pituitary tumor

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24
Q

What happens to the metabolism in hyperthyroidism?

A

Metabolism increases

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25
Q

What condition is a form of secondary hyperthyroidism?

A

Grave’s disease (autoimmune disease)

-IgG binds to TSH receptors on the thyroid

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26
Q

What clinical manifestation is present in both hypo and hyperthyroidism?

A

Goiter

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27
Q

What are clinical manifestations of hyperthyroidism?

A
  • Diarrhea
  • Weight loss
  • Oily skin
  • Fine hair
  • Exopthalmus
  • Heat intolerance
  • Tachycardia, agitation
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28
Q

What is Thyroid Storm ?

A

Worsening of hyperthyroidism symptoms due to stress, infection, pulmonary or cardiovascular disorders
-extreme vitals

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29
Q

What can occur after thyroidectomy?

A

Thyroid crisis = exaggeration of the effects of hyperthyroidism

30
Q

Describe the effect of immobility on serum Ca and PTH

A

Immobile –> bone release Ca –> hypercalcemia –> inhibit PTH

31
Q

Describe the effect of renal disease on serum Ca and PTH

A

Renal disease –> inability reabsorb Ca –> hypocalcemia –> stimulation of parathyroid –> releases PTH –> bone release Ca –> bone loss

32
Q

What are the calcium levels in hypoparathyroidism?

A

Low serum calcium (hypocalcemia)

33
Q

What state of serum magnesium causes hypothyroidism?

A

Hypomagnesemia

34
Q

How does magnesium affect PTH

A

Magnesium is needed for adequate production of PTH

35
Q

What is the relationship between calcium and phosphate?

A

They are inverse

Hypocalcemia = hyperphophatemia

36
Q

Describe the relationship between hyperphosphatemia and hypocalcemia?

A

High phosphate levels interfere with vitamin D activation –> cannot absorb calcium –> hypocalcemia

37
Q

How does vitamin D affect calcium absorption

A

Vitamin D activation is needed for calcium absorption in the GI

38
Q

What is the relationship between calcium and neuromuscular excitability?

A

They are inverse

-Calcium is necessary for resting membrane potential, thus lack of calcium = increased neuromuscular excitability

39
Q

Clinical Manifestations of Hypothyroidism?

A
  • Tetany
  • Muscle spasm
  • dry skin
  • loss of body hair
  • diarrhea
  • increased peristalsis
40
Q

What are unique diagnostic findings in hypothyroidism?

A

Chvostek and Trousseau signs

  • low Ca
  • low PTH
41
Q

What causes primary hyperparathyroidism?

A

Error in the negative feedback loop
-High Ca levels normally inhibit PTH release –> but neg feedback loop is malfunctioning –> so PTH continues to be released

42
Q

What causes secondary hyperparathyroidism

A

Increase PTH due to issues not related to the feedback loop (hypocalcemia)

43
Q

How does chronic renal failure affect PTH levels?

A

Chronic renal failure –> lack of Ca reabsorption –> hypocalcemia –> high PTH

44
Q

How does lack of vitamin D activation affect PTH levels?

A

Vitamin D is necessary to absorb Ca through GI –> lack of vitamin D = lack of Ca absorption –> hypocalcemia –> high PTH

45
Q

Clinical manifestations of Hyperparathyroidism

A
  • Decreased neuromuscular excitability
  • Bone disease
  • Calcium stones
  • Polyuria (b/c kidneys are trying to flush calcium out)
  • Constipation
  • Abdominal pain
  • Anorexia
46
Q

In chronic kidney disease, are the phosphate levels increased or decreased?

A

In CKD, hyperphosphatemia due to decreased phosphorus secretion.

47
Q

How does the kidney response to the hyperphoshatemia lead to hypocalcemia?

A

Kidneys excrete calcium as a precept with the phosphorus –> excretion of Ca –> hypocalcemia

48
Q

Why are patients with CKD stay in hypocalcemia states despite hyperparathyroidism?

A

PTH causes release of calcium from the bone but their inability to activate vitamin D decreases calcium absorption

49
Q

What is another term for ADH?

A

Vasopressin

50
Q

What is the most common cause of SIADH?

A

Ectopic secretion

51
Q

What kind of sodium imbalance occurs with SIADH?

A

Hypotonic hyponatremia

52
Q

Clinical Manifestations of SIADH

A
  • decreased urine output
  • concentrated urine
  • hyponatermia –> irritability, weakness, nausea and vomiting, coma
  • edema / third spacing
53
Q

How does water intoxication mimic DI?

A

Water intoxication –> body has sufficient water –> body thinks we no longer need ADH –> less ADH production –> mimics DI

54
Q

Clinical Manifestations of DI?

A
  • polyuria
  • dilute urine
  • hypernatremia –> CNS manifestations (seizures and coma)
  • hypovolemic shock
55
Q

What is the serum osmolality in DI?

A

High serum osmolality due to the hypernatremia

56
Q

Will the specific urine gravity be high or low in DI?

A

Low (because of low electrolyte content)

57
Q

When is the adrenal gland axis triggered?

A

When the body is under stress

58
Q

What is the pathway of the adrenal gland axis?

A

Hypothalamus –> secretes CRH –> anterior pituitary releases ACTH –> triggers adrenal gland –> production and release of steroids, glucoroticoids, and corticoids

59
Q

What are the two different causes of Cushing’s?

A
  • Long term administration of glucocorticoids (i.e. prednisone) –> cushing’s syndrome
  • Ectopic secretion –> cushing’s disease
60
Q

Clinical manifestations of Cushing’s

A
  • Moon face
  • Buffalo hump
  • Fat pad
  • Obesity of trunk
  • Weakness
  • Osteoporosis
  • Kidney Stones
  • Hyperglycemia (due to cortisol inhibiting insulin production)
  • Suppression of immunity
  • Hypokalemia
61
Q

In Cushing’s is cortisol high or low?

A

High cortisol

62
Q

Is ACTH high or low in Cushing’s

A

High ACTH

63
Q

Is ACTH high or low in Addison’s

A

Low ACTH

64
Q

What does PTH respond to?

A

Low levels of calcium

65
Q

Describe primary Addisons’s

A

Problem with the adrenal gland –> low glucocorticoid, mineralcorticoid, and androgen production

  • Low levels trigger ACTH b/c of negative feedback
  • Increased level of ACTH
66
Q

Is glucocorticoid/mineralcorticoid/androgen level high or low in Cushing’s?

A

High

67
Q

Is glucocorticoid/mineralcorticoid/androgen level high or low in Addison’s?

A

Low

68
Q

What is secondary Addison’s?

A

Low ACTH (and low production by adrenal gland)

69
Q

Clinical manifestations of Addison’s

A

If primary (high ACTH) –> hyper pigmentation

  • Hypoglycemia
  • Lack of aldosterone –> salt cravings
  • Dehydration
  • Hyperkalemia –> arrhythmia
70
Q

What is the adrenal stimulation test?

A

ACTH is given, and serum cortisol levels are monitored over time to see if adrenals are responding to the ACTH.

71
Q

What type of Addison’s does the adrenal stimulation test test for? (Primary or secondary)

A

Primary Addison’s

72
Q

In treating a patient with Addison’s what should you educate them on?

A

Signs and symptoms of addison/adrenal crisis

Patho Exam 2 (4 decks)

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