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ERM > Endocrinology Part 1 > Flashcards

Endocrinology Part 1 Flashcards

1
Q

What are the sex steroids?

A

Progesterone, androgens, and estrogens

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2
Q

What is the main minaralocorticoid?

A

Aldosterone

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3
Q

What is the main glucocorticoid?

A

Cortisol

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4
Q

How are all steroid hormones made?

A

Cystolic cholesterol is converted to mitochondrial cholesterol by StAR which is then converted to pregnenolone by SCC.

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5
Q

How are steroids released from the cell?

A

Diffuse out of the cell (non-vesicular storage)

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6
Q

How are steroids transported? Metabolized/excreted?

A

Transport by binding proteins

Metabolized into an inactive form then excreted by either the liver or the kidney

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7
Q

What carrier protein does cortisol use?

A

Transcortin

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8
Q

What carrier protein do thyroid hormones use?

A

Thyroxine-binding Globulin (TBG)

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9
Q

What carrier protein do most steroid hormones use?

A

Albumin (it is non-specific)

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10
Q

What is the MOA of ketoconazole?

A

Inhibits SCC and CYP17

Decrease the synthesis of all steroids

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11
Q

What is ketoconazole used for?

A

Antifungal agent

Decrease tumor production of steroids

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12
Q

What is the MOA of finasteride?

A

Inhibits 5-alpha-reductase

Decrease the synthesis of dihyrdotestosterone (DHT)

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13
Q

What is finasteride used for?

A

Alopecia and BPH

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14
Q

What precautions should be taken with finasteride?

A

Do not touch if pregnant

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15
Q

What is the MOA of letrozole?

A

Inhibit aromatase

Decreases estrogens

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16
Q

What is letrozole used for?

A

Estrogen Receptor (+) Breast Cancer

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17
Q

What is the MOA of metyrapone?

A

Inhibit 11-beta-hyroxylase

Decrease cortisol

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18
Q

What is metyrapone used for?

A

Adrenal cortex excess production

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19
Q

How are hormones synthesized from peptides/proteins made?

A

Amino acids link to form a pre-prohormone –> prohormone –> hormone

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20
Q

How are peptide/protein hormones released?

A

Exocytosis from a vesicle

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21
Q

How are peptide/protein hormones transported? Metabolized/excreted?

A

Transported by some binding proteins but mostly water soluble and move in plasma

They are endocytosed and degraded by proteases

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22
Q

What are the major catecholamines?

A

Dopamine, norepinephrine, epinephrine

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23
Q

How are catecholamines synthesized?

A

Tyrosine –> L-DOPA –> dopamine –> norepinephrine –> PNMT converts it to epinephrine

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24
Q

How are catecholamines released? Transported? Metabolized/excreted?

A

Released by exocytosis from vesicles

Transported in plasma (water soluble) or bound to albumin

Uptake and breakdown by monamine oxidase (MAO) or catechol-o-methyltransferase (COMT)

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25
Q

What is the common metabolite from catecholamine metabolism?How is it used diagnostically?

A

Vanillylmandelic acid (VMA)

If the patient has a catecholamine secreting tumor VMA will be found in high amounts in urine

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26
Q

What are two hormones are amino acid derivatives?

A

Thyroid hormones and melatonin

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27
Q

What are thyroid hormones made up of?

A

2 tyrosines plus iodides

28
Q

What does melatonin come from?

A

Tryptophan

29
Q

What are the major eicosanoids?

A

Prostaglandins, thromboxanes, and leukotrienes

30
Q

How are eicosanoids made?

A

Pathway 1: PLA2 breaksdown phospholipids to arachidonic acid which is broken down by COX or LOX into eicosanoids

Pathway 2: DAG lipase breaksdown DAG to arachidonic acid which is broken down by COX and LOX into eicosanoids

31
Q

How are eicosanoids released? Where do the act? Metabolized/excreted?

A

Diffuse out of the cell (non-vesicular storage)

Act locally (no transport)

Metabolized by enzymatic breakdown

32
Q

What is the MOA of NSAIDs?

A

Inhibit COX

Decrease synthesis of PG and TX

May increase LT synthesis

33
Q

What are NSAIDs used for?

A

Anti-inflammatory/immune agents

Decrease clot formation

34
Q

What is the MOA of cortisol?

A

Inhibit COX and PLA2

Decrease PG synthesis

35
Q

What is cortisol used for?

A

Anti-inflammatory/immune agent

ex. athletes get cortisone shots when they have major inflammatory injuries

36
Q

What is the MOA of zilueton?

A

Inhibit LOX

Decrease LT synthesis

37
Q

What is zilueton used for?

A

Asthma, rhinitis, and nasal congestion

38
Q

What are two characteristics of negative feedback?

A
  1. Holds the system at the set point

2. Has an odd number of inversions

39
Q

What are two characteristics of positive feedback?

A
  1. Disrupts homeostasis

2. Has zero or an even number of inversions

40
Q

What hormones are released from the posterior pituitary?

A

Antidiuretic hormone (aka arginine vasopressin)

Oxytocin

41
Q

Hormones released from the posterior pituitary are made in the cell bodies of what neurons? Where are they stored?

A

Magnocellular neurons

Stored in vesicles at axon terminals

42
Q

What does ADH do and at what receptors?

A

V1 (Gq) = vasoconstriction

V2 (Gs) = renal water reabsorption, urea reabsorption

43
Q

What does the release of ADH trigger?

A

Thirst
Factor VIII release
von Willebrand factor release

44
Q

What stimulates the release of ADH?

A

Increase in Posm

Decrease in BP/blood volume

Ang II

Medications

Surgery/anesthesia

45
Q

What inhibits the release of ADH?

A

Ethanol

46
Q

What is central diabetes insipidus?

A

Low ADH due to synthesis or release problems

47
Q

What is nephrogenic diabetes insipidus?

A

Low ADH due to receptor problems (V2, Aq2)

Low ADH due to lithium or demclocycline

48
Q

What is seen clinically in diabetes insipidus?

A

Cell dehydration (hypernatremia, high Posm)
Low Uosm
Polyuria
Thirst

49
Q

How can both types of diabetes insipidus be treated?

A

Both types treat with water

50
Q

What is SIADH?

A

Syndrome of Inappropriate ADH (aka high ADH activity)

51
Q

What can cause SIADH?

A

ADH producing tumors (usually lung)

CNS damage

Pulmonary disease (TB, pneumonia)

Surgery

Medications

52
Q

What is seen clinically with SIADH?

A

Cerebral edema (hyponatremia, low Posm)

High Padh

High Uosm

53
Q

How is SIADH treated?

A

Treat the cause (aka tumor)

Hypertonic saline

Fluid restriction

Furosemide (decrease concentrated urine)

Demeclocycline (inhibit ADH pathway)

Tolvaptan (V2 receptor antagonist)

54
Q

What does oxytocin do and at what receptors?

A

OT receptor (Gq) = smooth muscle contraction of the milk ducts and uterus myometrium (during birth)

55
Q

What stimulates the release of oxytocin?

A

Nursing and cervical stretch

56
Q

What is the MOA of pitocin?

A

Synthetic oxytocin

57
Q

What is pitocin used for?

A

Induce/maintain labor

Post-partum hemorrhage

58
Q

What are tocolytics used for?

A

To decrease uterus contractions associated with premature labor

59
Q

What are the four main tocolytics and at what receptor to the act?

A

Ritodrine = Beta2 agonist

Nifedipine = LTCC blocker

Mg2+ Sulfate = LTCC blocker and decreases MLCK activity

Atosiban = OT receptor blocker

60
Q

What is the MOA of ergot alkaloids?

A

Increase smooth muscle contraction by stimulating the 5-HT1b/1d receptors

61
Q

What are ergot alkaloids used for?

A

Migraines

Post-partum hemorrhage

62
Q

What is a precaution taken with ergot alkaloids?

A

Don’t take during pregnancy because it will decrease blood flow to the fetus

63
Q

How can central diabetes insipidus be treated?

A

Central = give desmopressin (synthetic ADH)

64
Q

How can nephrogenic diabetes insipidus be treated?

A

give HCTZ (induces water reabsorption due to diuretic breaking)

65
Q

How can lithium induced nephrogenic diabetes insipidus be treated?

A

give amiloride (blocks Li2+ entry through ENaC)

66
Q

How can demeclocycline induced nephrogenic diabetes insipidus be treated?

A

change antibiotics

67
Q

What meds can cause SIADH

A

Antidepressants
Antipsychotics
Opiates
Vinca alkaloids

ERM (27 decks)

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