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Endo / Repro > Endo Phys (FA) > Flashcards

Endo Phys (FA) Flashcards

1
Q

What are the steps of insulin synth?

A

Preproinsulin (RER) –> cleavage of presignal –> Proinsulin stored in sectretory granules –> cleavage of proinsulin –> exocytosis of insulin and C-peptide

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2
Q

What is the use of C-peptide count?

A

Only indigenous insulin production results in C-peptide production.

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3
Q

What type of cell signaling takes place due to insulin?

A

Cell surface receptor –> tyrosine kinase activity –> inducing glucose uptake and gene transcription

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4
Q

What are the anabolic effects of insulin and in what tissues does it act?

A

Incr. gluc transport into sk. muscle and adipose tissue

incr. glycogen synth and storage
incr. triglyceride synth
incr. Na retention in kidneys
incr. protein synth
incr. cellular uptake of K+ and a.a.
decr. glucagon release

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5
Q

Does insulin cross the placenta? Does glucose?

A

No, Yes

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6
Q

What is the primary insulin-dependent glucose transporter and on what tissues is it found?

A

GLUT-4: adipose, sk. muscle

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7
Q

What are the insulin-independent glucose transporters and on what tissues are they found?

A

GLUT-1: RBC, Brain, Cornea
GLUT-2: B-islet cells, liver, kidney, sm. intestine
GLUT-5: spermatocytes, GI tract

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8
Q

What is the source of metabolism of the brain during the fed and fasting states?

A

Glucose, keytone bodies

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9
Q

What cell type always uses glucose as its only source of energy and why?

A

RBCs, they lack mitochondria

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10
Q

What is the acronym for insulin-independent glucose uptake tissues?

A

BRICK-L

Brain, RBC, Intestine, Cornea, Kidney, Liver

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11
Q

What is the major regulator of insulin release?

A

Glucose

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12
Q

How do GH and B-2 agonists influence insulin levels?

A

Both increase it. GH –> increase insulin resistance –> incr. insulin release)

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13
Q

What is the pathway by which glucose increases insulin release from a cell?

A

Gluc enters B cell –> increase in ATP generation –> Close of K+ channels –> open Ca++ channels (Ca++ enters cell) –> insulin exocytosis

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14
Q

What cells produce glucagon?

A

a-cells in pancreas

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15
Q

What are the metabolic effects of glucagon?

A

Glycogenolysis, Gluconeogenesis, Lipolysis, Ketone Production

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16
Q

What are the + and - regulation of glucagon?

A

+ : Hypoglycemia

- : insulin, hyperglycemia, and somatostatin

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17
Q

What hormones are influenced by corticotropin releasing hormone?

A

Incr. ACTH, MSH, and B-endorphin

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18
Q

What is the effect chronic exogenous steroid use has on CRH?

A

Decreased

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19
Q

What is the primary inhibitor of prolactin?

A

Dopamine

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20
Q

What is the function of gonadotropin releasing hormone?

A

Incr. FSH and LH

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21
Q

What is the regulatory hormone of GnRH?

A

Prolactin and androgens

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22
Q

What is the primary hypothalamic hormone responsible for puberty and fertility?

A

GnRH

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23
Q

What is the primary inhibitory hormone of GnRH?

A

Prolactin

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24
Q

By what pathway does Prolactinoma cause amenorrhea and osteoporosis?

A

Incr. prolactin –> decr GnRH –> amenorrhea and osteoporosis

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25
Q

How is acromegaly treated (class) and the MoA?

A

Somatostatin analogues –> decr. in GH and TSH

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26
Q

What are the effects of TRH?

A

incr. TSH and prolactin

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27
Q

What is the source of prolactin?

A

Anterior Pituitary

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28
Q

What is the function of prolactin?

A

Milk production, inhibit ovulation and spermatogenesis by inhibiting GnRH

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29
Q

How does hypoprolactinemia influence libido?

A

Decrease

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30
Q

What is the primary inhibitory substance of prolactin?

A

Dopamine

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31
Q

What stimulates prolactin release?

A

TRH

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32
Q

What is the primary pharmacologic used for inhibiting prolactin secretion?

A

Bromochriptine (dopamine agonist)

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33
Q

What classification of drugs stimulate dopamine secretion?

A

antipsychotics

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34
Q

How does estrogen influence prolactin release and in what context is it typically presented?

A

Increase, OCP and pregnancy

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35
Q

What is another name for GH?

A

Somatotropin

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36
Q

From what area is GH secreted?

A

Anterior pituitary

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37
Q

What is the mechanism by which GH stimulates growth?

A

IGF-1

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38
Q

How does GH influence insulin sensitivity?

A

Increase resistance

39
Q

What are the regulatory factors of GH?

A

GHRH, increased during exercise and sleep.

Inhibited by glucose and somatostatin

40
Q

What results from excessive GH secretion?

A

Acromegaly in adults

Gigantism in kids

41
Q

Where, specifically, is ADH synthesized and released?

A

Supraoptic nuclei of the hypothalamus

Posterior Pituitary

42
Q

What is the main action of ADH and the mechanism by which it acts?

A

Increase Ser. Osmolality via V2-R in the kidney, increasing aquaporin transcription in the principal cells of the collecting ducts and BP via V1-R in vessels.

43
Q

What are the ADH levels in central DI, nephrogenic DI, and primary polydipsia?

A

Decreased, Increased, Varies

44
Q

What is the most common cause of nephrogenic DI?

A

V2-R mutation

45
Q

What is the DoC for central DI?

A

Desmopressin

46
Q

Where are the physiologic regulators of ADH?

A

Osmoreceptors in the hypothalamus and hypovolemia in the carotids

47
Q

What enzyme is responsible for the committed (and rate limiting) step in steroid hormone synthesis?

A

Cholesterol Desmolase

48
Q

How are the kidneys grossly affected in congenital adrenal hyperplasia and what is the mechanism?

A

Bilateral renal enlargement due to increase ACTH (from decreased cortisol)

49
Q

What lab values are present in 17a-hydroxylase deficiency?

A

Incr. mineralocorticoids, decreased cortisol, decreased sex hormones, Hypertension, Hypokalemia, decr. DHT

50
Q

What is the underlying reason for XY pseudohermaphroditism and XX lack of secondary sexual development?

A

17a-hydroxylase def.

51
Q

What lab values are present in 21-hydroxylase deficiency?

A

decr. mineralocorticoids, decr cortisol, increased sex hormones, hypotension, hyperkalemia, incr. renin activity, incr. 17-hydroxyprogesterone

52
Q

What are the most common presentations in 21-hydroxylase deficiency?

A

infant salt washing, precocious puberty, virilization (deep voice)

53
Q

What are the lab values in 11B-hydroxylase deficiency?

A

decr aldosterone, incr 11-deoxycorticosterone (inc. BP), decr cortisol, incr. sex hormones, hypertension (low renin)

54
Q

What is the most common presentation with 11B-hydroxylase deficiency?

A

virilization

55
Q

Where is cortisol synthesized?

A

Adrenal zona fasciculata

56
Q

What is the effect of cortisol on BP and the mechanism?

A

Incr by up regulating a1 receptors on arterioles, resulting in increased sensitivity to Epi / NE

57
Q

How is cortisol diabetogenic?

A

Increases insulin resistance

58
Q

What is cortisol’s effect on GNG, lipolysis, and proteolysis?

A

Increases all

59
Q

How does cortisol cause striae?

A

Decrease in fibroblast activity

60
Q

What is cortisol’s effect on immunity?

A

Decreases both immunity and inflammation

61
Q

What is cortisol’s effect on bone formation and the mechanism?

A

Decrease via decreased osteoblast activity

62
Q

How is cortisol regulated?

A

CRH from the hypothalamus stimulates ACTH release in the pituitary, stimulating cortisol synth in the fasciculata

63
Q

What is the acronym for the effects of cortisol?

A

Big Fib
Incr BP, insulin, and GNG
Decr. Fibroblast, inflammation, and Bone

64
Q

What is the source of PTH?

A

Chief cells of parathyroid

65
Q

What are the effects of PTH?

A

Incr. bone resorption (Ca++ and PO4)
Incr. kidney reabsorption of Ca++ in DT
Decr. PO4 reabsorption in PT
Incr. 1,25-(OH)2D3 (calcitriol) production in kidney via 1a-hydroxylase stimulation

66
Q

How does PTH stimulate bone resorption?

A

Incr. RANK-L –> stimulate osteoblasts –> stimulate osteoclasts –> increase resorption

67
Q

How do low Ca++, low Mg, and very low Mg influence PTH?

A

Stimulate, Stimulate, Inhibit

68
Q

What are the three forms of serum Ca++ and there relative percentages?

A

Ionized (45%), Albumin (40%), Bound to anions (15%)

69
Q

How does and increase in pH influence serum Ca++ levels?

A

Favors albumin binding, resulting in hypocalcemia effect.

70
Q

What are some common manifestations of hypocalcemia?

A

cramps, pain, paresthesias, caporal spam (trosseau and chvostek signs)

71
Q

What are the sources of Vitamin D?

A

D3 from sun, D2 from plants

72
Q

What is the pathway for Vitamin D activation?

A

D2/D3 –> 25-OH in liver –> 1, 25-(OH)2 in kidney

73
Q

What is the function of Vitamin D?

A

increase Ca++ and PO4 dietary absorption and increase bone resorption

74
Q

What are the regulating factors of Vit D synth?

A

High PTH, low Ca++, Low PO4 increase

Negative feedback by 1,25-(OH)2

75
Q

What are the disease states caused by Vit D deficiency?

A

Rickets in kids, osteomalacia in adults

76
Q

How do PTH and Vit D differ in their physiological roles?

A

PTH: incr. Ca++ and decr. PO4 reabsorption in kidney

Vit D: Incr both Ca++ and PO4 absorption in gut

77
Q

What is the source of calcitonin, its function and regulation?

A

Parafollicular cells (C cells) of the thyroid, decease bone resorption (Ca++), incr serum Ca++ –> incr. calcitonin

78
Q

What is the acronym used to signify the hormones that use cAMP?

A

FLAT ChAMP
FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2-R), MSH, PTH,
calcitonin, GHRH, glucagon

79
Q

What hormones use cGMP?

A

ANP, NO

80
Q

What hormones use IP3?

A

GOAT HAG

GnRH, Oxytocin, ADH (V1-R), TRH, Histamine (H1-R), Angiotensin II, Gastrin

81
Q

What hormones use steroid receptors?

A

VETTT CAP

Vit D, Estrogen, Testosterone, T3/T4, Cortisol, Aldosterone, Progesterone

82
Q

What hormones use intrinsic tyrosine kinase?

A

Growth factors

Insulin, IGF-1, FGF, PDGF, EGF

83
Q

What hormones use receptor-associated tyrosine kinase?

A

PIG: Think acidophils and cytokine

Prolactin, Immunomodulators, GH

84
Q

What is the generic pathway of steroid hormones?

A

Circulate bound to globulin –> enter cell (lipophilic) –> Bind to cytoplasmic or nuclear receptor –> transformation of receptor and expose DNA binding site –> increase transcription –> increase protein translation

85
Q

How does the concept of transport protein mediation influence pathology related to steroid hormones in males and females?

A

Incr in transport protein –> decrease in free hormone and vice versa
Increase in sex hormone binding globulin in male –> decrease in available testosterone –> gynecomastia
In females decrease in SHBG –> increase in testosterone –> hirsutism

86
Q

What is the main effect of T3/T4 on the body?

A

Basal Metabolic rate regulation

87
Q

What is the source of T4 and T3?

A

T4: Follicles of the thyroid
T3: peripheral tissues convert T4 –> T3

88
Q

How does T4 affect Bone growth, the CNS, CV system, Basal metabolic rate, and glucose stores?

A

It increases all via synergistic effect with GH, increasing B1 receptors, Na/K ATPase activity, and inc. GNG (etc.)

89
Q

How are T3/T4 levels regulated?

A

TRH (hypothalamus) –> incr. TSH (pituitary) –> stimulate follicular cells
Negative feedback by free T3/T4, decr. sensitivity to TRH in the ant. pituitary

90
Q

What is the Wolff-Chaikoff effect (excess iodine)?

A

Excess iodine temporarily inhibits thyroid peroxidase

91
Q

Under what conditions are Thyroxine-binding globulin levels affected?

A

Decr in hepatic failure

Incr. in pregnancy and OCP use (estrogen incr. TBG)

92
Q

What enzyme is responsible for T4 –> T3 in the periphery?

A

5’-deiodinase

93
Q

What are the MoA of propylthiouracil and methimazole?

A

PTU inhibits both peroxidase and 5’-deiodinase

Methimazole inhibits peroxidase only

Endo / Repro (15 decks)

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