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z S1: Module > Endocrine-1 > Flashcards

Endocrine-1 Flashcards

1
Q

The coupling of the two outer rings of DIT
or of one outer ring of DIT with that of
MIT (each with the net loss of alanine)
leads to the formation of ___ and ___,
respectively.

A

T4 and T3

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2
Q

____________ (Tg) serves as the matrix for
the synthesis of T4 and T3 and as the
storage form of the hormones and iodide

A

Thyroglobulin

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3
Q

TRH is ____ amino acids long (_________) secreted by the hypothalamus. Its basic
sequence is pyro-glutamyl-histidine-proline amide

A

three (tripeptide)

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4
Q

The formation of thyroid hormones involve:
(1) active uptake of _______ by the follicular cells
(2) oxidation of iodide (I-) to hypoiodite (IO-) by H2O2 and ___________ (TPO) and formation of iodotyrosyl residues (MIT and DIT) of thyroglobulin (Tg) through aromatic iodination, (3) formation of iodothyronines from iodotyrosines through ________ reaction catalyzed by TPO and H2O2
(4) _______ of Tg & release of T4 & T3 into blood
(5) conversion of T4 to T3 by the action of _____

A

iodine
thyroperoxidase
coupling
proteolysis
5’-deiodinase

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5
Q

T4 is a prohormone and its peripheral
metabolism occurs in two ways:

A

outer ring deiodination -> T3
inner ring deiodination ->T4
conjugation of phenolic hydroxyl group and oxidative deamination of inner tyrosyl ring

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6
Q

Liotrix is a synthetically derived thyroid hormone replacement preparation. It consists of
Levothyroxine sodium and Liothyronine sodium in a __ to __ ratio by weight.

A

4 to 1

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7
Q

The phenyl-X-phenyl nucleus is essential for thyroid hormonal activities and should
have the following structural features:

A

Aliphatic Side Chain (R1)
Alanine-Bearing Ring (R3 and R5)
Phenolic Hydroxyl Group (R’4)
Bridging Atom (X)
Phenolic Ring (R’3 and R’5)

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8
Q

Antithyroid Drugs are potent inhibitors of ______________, which is responsible for the iodination of tyrosine residues of thyroglobulin (Tg) and the coupling of iodotyrosine residues to form iodothyronines

A

thyroperoxidase (TPO)

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9
Q

The most clinically useful thionamides are thioureylenes, which are five- or sixmembered heterocyclic derivatives of thiourea including what

A

Propylthiouracil (PTU)
1-methyl-2-mercaptoimidazole (Methymazole, MMI)

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10
Q

The grouping R-CS-N- has been referred to as _______, or if R is N, as it is in Thiouracil, PTU, and MMI, it is called a ________

A

thioamide
thioureylene tautomers (keto or enol)

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11
Q

SARs of the thiouracils and other related compounds as inhibitors of outer ring deiodinase states that the C-2 thioketo/thioenol group and an _________ N-1 position are essential for activity.

A

unsubstituted

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12
Q

Structural modifications leads to produce inactive ______ inhibitors N1-alkyl or aryl and Thiol alkylation or arylation

A

TPO

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13
Q

Thyroid Gland

A

neck surrounding trachea below the larynx

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14
Q

Thyroid Structure: follicles surround the colloid core storing __________, a substrate in thyroid hormone synthesis

A

thyroglobulin

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15
Q

What two things stimulate the release of T3 and T4 synthesis and release

A

TRH
TSH

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16
Q

____________ symporter (NIS) transports iodide into follicles

A

Sodium/Iodide

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17
Q

What is Organification

A

tyrosine residues are iodinated to form moniodotyrosine (MIT) and diiodotyrosine (DIT)

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18
Q

Thyroidal peroxidase:

A

inhibition by I-, thioamides
Inhibits T4→T3 conversion
* Methimazole (Tapazole)
* Propylthiouracil (PTU)

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19
Q

T3 not bound to T3 receptor dimer, suppresses what

A

thyroid hormone response element (TRE)

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20
Q

T3 bound to T3 receptor, activates thyroid
hormone response element promotes heterodimerization with

A

retinoid X receptor (RXR)

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21
Q

Primary Hypothyroidism:

A

Deficient thyroid hormone levels
TSH high; T4 low

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22
Q

Secondary (Central) Hypothyroidism:

A

Deficient TSH
TSH low; T4 low

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23
Q

Peripheral Hypothyroidism:

A

Deficient transport, metabolism or
action of thyroid hormones

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24
Q

Severe Hypothyroidism symptoms

A

myxedema (swelling of skin)
myxedema coma (water intox, shock, coma)

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25
Q

Congenital Hypothyroidism

A

-Initially asymptomatic from maternal T4
-Extended gestation, weight/length normal
-Wide posterior fontanelle
-Extended jaundice

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26
Q

Causes of Hypothyroidism in US

A
  • Hashimoto’s Thyroiditis (autoimmune)
  • Drug induced
  • Dyshormonogenesis: deficiency of synthetic hormones
  • Thyroid Damage: Radiation or surgery
  • Congenital: primarily genetic; autoimmune, dietary
  • Pituitary or hypothalamic disease (Secondary)
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27
Q

Risk factors for hypothyroidism

A

pregnancy
age
autoimmune disease
FH

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28
Q

Causes of hyperthyroidism

A

grave disease
toxic adenoma
plummer’s disease
thyroiditis

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29
Q

Graves disease

A

Autoimmune Disorder
* TSH receptor antibody stimulates the receptor
* AKA thyroid-stimulating immunoglobulins
tremor, exophthalmoses

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30
Q

Iodination is inhibited by what kind of mechanism

A

feedback inhibition

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31
Q

Primary disease of endocrine gland

A

problem is with the endocrine gland itself
(ex: primary hyperthyroidism, primary hypothyroidism, primary ovarian failure)

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32
Q

Secondary disease of endocrine gland

A

Problem usually in pituitary
(ex: secondary adrenal insufficiency, hypogonadotropic hypogonadism)

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33
Q

Tertiary disease of endocrine gland

A

something wrong with hypothalamus (very rare)

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34
Q

What are the three effects of TSH

A

-stimulate increase thyroid cell growth, increase cell size, and vascularity of gland
-TSH increase all step in synthesis of thyroid hormone
-TSH increase all step in release of thyroid hormone

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35
Q

What is thyroid autoregulation

A

adaption of thyroid activity based on iodine availability

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36
Q

Results of thyroid autoregulation

A

independent of TSH activity
sensitivity of thyroid gland to TSH can be altered
rate of synthesis and secretion of thyroid hormones can be altered

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37
Q

Examples with excessive intake of iodine

A

wolff-chaikoff effect
inhibition of thyroid peroxidase activity
decreased sensitivity of gland to the effects of TSH

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38
Q

Triiodothyronine (selected thyroid function test)

A

Serum T3 measures the total level of hormone
FT3 measures amount of free hormone

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39
Q

Thyroxine (selected thyroid function test)

A

Serum T4 measures the total level of hormone
FT4 measures amount of free hormone

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40
Q

Serum TSH (selected thyroid function test)

A

in patients with primary thyroid disease
-TSH is the most sensitive indicator of overall thyroid function
-primarily used for screening

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41
Q

Euthyroidism

A

normal thyroid function; TSH and fT4 are both in normal range

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42
Q

Primary hypothyroidism FT4 and TSH levels

A

FT4: below normal
TSH: above normal

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43
Q

Primary hyperthyroidism FT4 and TSH levels

A

FT4: above normal
TSH: below normal

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44
Q

Secondary hypothyroidism FT4 and TSH levels

A

FT4: below normal
TSH: below normal

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45
Q

Secondary hyperthyroidism FT4 and TSH levels

A

FT4: above normal
TSH: above normal

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46
Q

Subclinical hypothyroidism FT4 and TSH levels

A

FT4: normal
TSH: above normal

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47
Q

Subclinical hyperthyroidism FT4 and TSH levels

A

FT4: normal
TSH: below normal

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48
Q

Goiter

A

any enlargement of thyroid gland

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49
Q

What are the two types of goiters

A

diffuse: general overall enlargement of gland
nodular: irregular or lumpy enlargement
-single node
-multiple nodules

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50
Q

Endemic goiter

A

aka iodine deficiency goiter
most occur in developing countries

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51
Q

Examples of antibody testing for thyroid disease

A

TSH receptor antibodies (TRAb) -> graves
Anti-TPO antibodies (TPOAb) -> hashimotos, antibodies develop in response to inflammation indicating damage

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52
Q

Diagnostic radioactive iodine uptake (RAIU)

A

pt given I123
indicates how active thyroid gland is at taking up iodine
(high RAIU = graves, low RAIU = thyroiditis)

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53
Q

What is Hashimoto’s thyroiditis

A

autoimmune disease caused by hypothyroidism
thyroid follicles replaced by lymphocytes and fibrous tissue

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54
Q

What are the 4 etiologies of hypothyroidism

A

Hashimoto
iodine deficiency
congenital
iatrogenic (thyroidectomy, after RAI, drug-induced mainly amiodarone)

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55
Q

Levothyroxine treatment in hypothyroidism

A

synthetic T4
bind to plasma proteins
converted to T3 in periphery

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56
Q

ADR of levothyroxine treatment

A

only develop if a patient is overtreated (hyperthyroid symptoms)

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57
Q

Liothyronine therapy in hypothyroidism

A

synthetic T3
25 mcg of T3 approx equiv to 100 mcg of T4
not considered appropriate initial therapy

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58
Q

When to use liothyronine in patients

A

patients on levothyroxine whose thyroid labs are normal but they are still having symptoms despite having levels in normal range

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59
Q

What are the combination drugs of T4/T3

A

liotrix (thyrolar)
Desiccated thyroid gland (Armour® thyroid, USP, generics)

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60
Q

Levothyroxine replacement therapy what are the two factors that impact the choice of initial dose

A

age >60 yo
History of coronary heart disease (CHD)
use 25 or 50 mcg once daily

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61
Q

How to calculate healthy adults hypothyroidism dose

A

1.6 mcg/kg/day
use ideal body weight

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62
Q

What are the 3 weird doses of levothyroxine

A

88mcg
112 mcg
137 mcg

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63
Q

When to check TSH levels

A

6-8 weeks

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64
Q

Goals of TSH Initial monitoring & follow-up for primary hypothyroidism

A

feel better, relief of symptoms
want TSH in a normal range
free T4 in normal range

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65
Q

usual counseling of levothyroxine

A

Take in the morning with water
Take on an empty stomach…at least 30-60 minutes before eating anything

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66
Q

Drug / Food interactions of levothyroxine

A

Fiber supplements
Ferrous sulfate
Calcium / Aluminum
Soy

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67
Q

What to do in patients on levothyroxine who become pregnant

A

Dose increased 30%
-take 2 extra doses per week
-monitor every 4 weeks

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68
Q

Congenital Hypothyroidism babies testing

A

Mandatory testing in newborn babies in most developed nations to identify it

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69
Q

Goal of Congenital Hypothyroidism

A

start thyroid replacement by 14 days old

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70
Q

Causes of thyrotoxicosis (hyperthyroidism)

A

-Primary hyperthyroidism – the problem is with the thyroid gland
-Secondary hyperthyroidism – the problem is with the pituitary (rare)
-Exogenous / Iatrogenic / Drug induced

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71
Q

Goals of treating thyrotoxicosis

A

-To relieve symptoms IF they are present
-To stop thyrotoxicosis (and restore euthyroidism if possible)
-IF possible - cause a “remission” (remaining euthyroid for 1 year after stopping drug therapy)

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72
Q

Radioactive iodine I131 (drug in thyrotoxicosis) MOA

A

slow destruction from radiation

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73
Q

methimazole (Tapazole) and propylthiouracil (drugs in thyrotoxicosis) MOA

A

inhibition of thyroid hormone synthesis
-Inhibition of the enzyme thyroid peroxidase
-Inhibition of enzyme 5’deiodinase – ONLY propylthiouracil does this, decrease peripheral conversion of T4 to T3

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74
Q

methimazole ADR

A

are dose related; rare if dose is < 30mg/day

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75
Q

propylthiouracil ADR

A

idiosyncratic

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76
Q

Major side effects of concern of methimazole and propylthiouracil

A

Agranulocytosis
Vasculitis
Hepatotoxicity

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77
Q

What is the preferred hyperthyroidism drug in most patients

A

methimazole
(except for 1st trimester then you use propylthiouracil)

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78
Q

Monitoring for hyperthyroidism

A

TSH, fT4, & fT3 periodically
-Most patients will improve or normalize thyroid function in 4-12 weeks
-Decrease dose to lowest effective dose to avoid adverse effects

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79
Q

symptoms of methimazole and propylthiouracil

A

mainly fever and sore throat
(fatigue, joint pain, bruising, jaundice)

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80
Q

Clinical use of Beta Blockers in hyperthyroidism

A

For the symptomatic relief of tachycardia/palpitations, heat intolerance/sweating, and nervousness/anxiety/tremor that occur during thyrotoxicosis; target to a pulse <90

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81
Q

What is the special consideration of propranolol in thyroid use

A

stop conversion of T4 to T3

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82
Q

Iodide use in hyperthyroidism MOA

A

-induce the Wolff-Chaikoff block
Makes the gland firmer, decrease size and decrease vascularity of the thyroid gland

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83
Q

etiology of graves disease

A

-An autoimmune disorder
-Antibodies develop to the TSH receptors of the thyroid gland. (TSH-R-Ab)

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84
Q

Diagnosis of graves disease

A

Goiter
Thyrotoxic symptoms may be present
IF a RAIU with I123 is done, uptake is elevated; entire gland will be overactive

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85
Q

Unique features of Grave’s disease (Orbitopathy)

A

Immune reaction causes soft tissue swelling/edema behind the eyes
-Protrusion of the eyes
-may lead to double vision
-smoking is a risk factor for eye involvement

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86
Q

Unique features of Grave’s disease (Infiltrative dermopathy)

A

-Front of the shins
-Hard, non-pitting edema
-occasional raised hyperpigmented papules or “bark-like” appearance

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87
Q

Adult patients should receive the anti-thyroid drug therapy for ___ to ___ months in treatment of graves disease

A

12-18 months
(Patients whose TSH-R-Ab remained at higher levels are at > risk of relapse)

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88
Q

Follow-up / Monitoring of using I123 in graves disease

A

-Hypothyroidism
-function will normalize within 2-6 months
-Hypothyroidism generally occurs within 4-12 months

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89
Q

Thyroidectomy treatment for graves disease

A

Anti-thyroid drug
Might give Iodide to ↓ vascularity of the gland & make removal easier

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90
Q

Nodular thyroid disease

A

autonomously functioning nodules secrete thyroid hormone

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91
Q

Types of Nodular thyroid disease

A

Toxic multi-nodular goiter (at least 2 nodules present)
Solitary toxic thyroid nodule (1 unilateral nodule)

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92
Q

Clinical diagnosis of toxic nodular goiter

A

-hyrotoxic symptoms may be present
-Nodular goiter is present
-RAIU with I123 will reveal the presence of active nodules; uptake is elevated

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93
Q

Treatment options for Nodular thyroid disease

A

Beta-blocker
Radioactive iodide
Surgery

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94
Q

Nodular thyroid disease surgery antithyroid drugs

A

methimazole (dont use longterm therapy)

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95
Q

Nodular thyroid disease surgery iodide drugs

A

never use in toxic nodules

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96
Q

Thyroiditis

A

an inflammatory condition of the thyroid gland

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97
Q

Etiology of Thyroiditis

A

Autoimmune (i.e. Hashimoto’s)
Radiation
Drug induced
Infectious

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98
Q

Thyroiditis Inflammation → follicle cell damage → ________ of already formed thyroid hormone

A

leaking

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99
Q

Subacute thyroiditis

A

symptom is pain
often occurs after viral URI

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100
Q

Autoimmune lymphocytic inflammation

A

painless thyroiditis (variant of Hashimoto’s thyroiditis)
Postpartum thyroiditis (occurs after pregnancy)

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101
Q

Treatment of thyroiditis in subacute and painless

A

subacute treat pain (NSAIDs or prednisone)
painless thyroiditis (beta blocker, maybe low dose levothyroxine)

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102
Q

Levothyroxine suppressive therapy

A

TSH is a trophic hormone – it may influence some nodules to “grow”
Thyroid axis suppression – can be induced by giving excessive levothyroxine

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103
Q

Treatment of nodules

A

-High index of suspicion for carcinoma = surgical removal of the nodule
-Low index of suspicion = 6-12 month trial of suppressive levothyroxine therapy to see if the
nodule regresses

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104
Q

Epithelial cells

A

the cells that make thyroid hormones

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105
Q

Rationale for suppressive levothyroxine after surgery

A

To reduce the risk of future thyroid cell development that might be stimulated by TSH

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106
Q

Levothyroxine suppressive therapy (TSH suppression) goals

A

To intentionally “over treat” with levothyroxine
To intentionally suppress the TSH below normal
To cause an asymptomatic subclinical hyperthyroidism

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107
Q

Risks of Levothyroxine suppressive therapy

A

Development of overt clinical hyperthyroidism
Cardiac arrhythmias
Osteoporosis

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108
Q

Dosing / Monitoring of Levothyroxine suppressive therapy

A

Usually give 100-150mcg levothyroxine initially
Usually requires a dose > 2mcg/kg/day

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109
Q

Subclinical hypothyroidism what might happen

A

Progression to overt hypothyroidism
TSH will become normal within a year

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110
Q

Who should be treated for subclinical hypothyroidism

A

TSH >10mIU/L treat always
TSH <10 treat if pregnant or planning to become pregnant, symptoms consistent w/hypothyroidism

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111
Q

Iatrogenic subclinical hypothyroidism

A

adherence must be assessed
(labs indicate they might be “undertreated”)

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112
Q

Subclinical hyperthyroidism what might happen

A

Early multi-nodular goiter
Early Grave’s disease

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113
Q

What are the risks of NOT treating Subclinical hyperthyroidism

A

Increased risk of atrial fibrillation
Increased risk of bone loss / osteoporosis

114
Q

Iatrogenic subclinical hyperthyroidism

A

Patients receiving levothyroxine (labs indicate they might be “over-treated”)

115
Q

Patients receiving levothyroxine replacement therapy for hypothyroidism in Iatrogenic subclinical hyperthyroidism

A

being overtreated (need to decrease dose)

116
Q

Patients receiving levothyroxine suppressive therapy for thyroid nodules or cancer in Iatrogenic subclinical hyperthyroidism

A

leave dose where it is

117
Q

Assessment of “subclinical” lab values

A

screening
diagnose
monitoring therapy

118
Q

ACTH stimulates the release of what

A

cortisol

119
Q

ACTH synthesis: prohormone convertase 1

A

proteolytic cleavage enzyme for POMC hormones

120
Q

ACTH synthesis: Pro-opiomelanocortin (POMC)

A

precursor for ACTH (and other hormones)

121
Q

ACTH stimulates de novo cortisol synthesis via ____-Protein Kinase A pathway

A

MC2R

122
Q

Adrenocorticosteroids

A

steroid hormones secreted by the adrenal cortex

123
Q

Glucocorticoids

A

metabolic regulation

124
Q

Mineralocorticoids

A

electrolyte regulation

125
Q

Adrenal gland: Adrenal Cortex and Adrenal Medulla

A

Adrenal Cortex: outer portion
Adrenal Medulla: inner portion

126
Q

Zona Glomerulosa: angiotensin II (Ang II) and K+ stimulate _________________ release

A

mineralocorticoid

127
Q

Zona Fasciculata

A

ACTH stimulates cortisol release

128
Q

Zona Reticularis

A

ACTH stimulates dehydroepiadrosterone (DHEA) and DHEA-S - androgen precursors

129
Q

Where do you get endogenous cholesterol from

A

de novo biosynthesis

130
Q

Glucocorticoid Receptors: Expressed in almost every cell (cytosol) – ____ _________ of development, metabolism, and immune response.

A

gene regulation

131
Q

Cortisol (S) bound in plasma corticosteroid-binding globulin (CBG) interacts with intracellular _______________ __________ and binds to glucocorticoid response element

A

glucocorticoid receptor

132
Q

Certain cells (kidney, colon, salivary gland) contain 11β-hydroxysteroid dehydrogenase
Type II (11βHSD2), which metabolizes ___________ to an inactive form

A

glucocorticoids
(11β-HSD1 which does the opposite)

133
Q

Metabolic effect of cortisol in glucose, fat, and proteins

A

glucose: increase
fat: decrease
protein: decrease

134
Q

Synthetic Steroids

A

Cortisone, prednisone

135
Q

Tissues with low 11βHSD1 what steroids are preferred

A

hydrocortisone and prednisolone

136
Q

Treatment of hypercortisolism

A

Ketoconazole and Metyrapone

137
Q

Drugs that are used for Growth Hormone Excess

A

Octreotide: somatostatin agonist
Pegvisomant: GH receptor antagonist

138
Q

Hyperprolactinemia drugs

A

Bromocriptine: partially-selective dopamine receptor 2 (DRD2) agonist
Cabergoline: “more” selective and potent DRD2 agonist

139
Q

A ________________ (rings A, B, and C) is the completely saturated derivative of phenanthrene

A

perhydrophenanthrene

140
Q

The polycyclic hydrocarbon known as _________ refers to a steroid with 27 carbons that includes a side chain of eight carbons at position 17.

A

cholestane

141
Q

5a-cholestane is said to have a _____________________ backbone

A

trans-anti-trans-anti-trans
(5 beta is cis-anti-trans-anti-trans)

142
Q

Cholestane contains ___ carbon atoms
Pregnanes are steroids with __carbon atoms
Androstanes contain ___ carbon atoms
Estranes contain ___ carbon atoms, with the C19 angular methyl group at C10 replaced by hydrogen

A

27
21
19
18

143
Q

This C21 steroid is converted via enzymatic oxidations and isomerization of the double bond to a number of physiologically active C21 steroids, including the female sex hormone progesterone and the adrenocorticoids cortisol, corticosterone, and aldosterone

A

Pregnenolone

144
Q

_______ is metabolized by the liver and is mainly
excreted in the urine as inactive O-glucuronide
conjugates at 3 and 21 positions and minor O-sulfate conjugates of urocortisol, 5b-dihydrocortisol, and urocortisone

A

cortisol

145
Q

All of the biologically active __________ contain a ketone at the 3-position and a double bond in the 4,5-position

A

adrenocorticoids

146
Q

The conserved structural features of glucocorticoids like Hydrocortisone include: Δ4-keto, an a,b-unsaturated carbonyl system, which means the presence of double bond at position 4 and ____ group at position 3, _____ at position 20 and hydroxyl alcoholic group at position 21

A

keto
ketone

147
Q

The 17b-ketol side chain and the Δ4-3-ketone contribute to the _________ of adrenocorticoids

A

potency

148
Q

The ________ _______ donating 11b-OH group of Hydrocortisone (active) is essential for drug-receptor interaction

A

hydrogen bond

149
Q

Structural Modifications on Hydrocortisone purpose is to produce glucocorticoids with ________ potency enhancement and/or to _______ selectivity over MR

A

greater
increase

150
Q

Glucocorticoids: Insertion of a ______ _____ between positions 1 and 2 in Hydrocortisone increases binding affinity

A

double bond

151
Q

Glucocorticoids: Insertion of an a-CH3 group at position 6 provides ______ selectivity, prevents the metabolism at the 3-keto, and increases glucocorticoid activity

A

greater

152
Q

Glucocorticoids: Insertion of a-OH groups into positions (e.g., 6, 7, and 16) or reduction of the 20-ketone decreases
glucocorticoid activity due to increased __________

A

hydrophilicity

153
Q

Glucocorticoids: 16a-OH to the 16a-methyl increases GR binding affinity due to favorable _______ contacts of the 16a-methyl group within a hydrophobic pocket of GR that is not available in MR

A

hydrophobic

154
Q

Glucocorticoids: Replacement of the 21-OH group with _________ increases glucocorticoid and sodium-retaining activities

A

fluorine

155
Q

In C: Rigidity of A-ring is increased. Flattening of
A-ring enhances GR affinity binding, increases
potency and half-life and producing ______ active
agents.

A

orally

156
Q

lack of substituents on Aldosterone’s ______ face explains higher affinity for MR over GR.

A

alpha

157
Q

The 21-esters are __________. Hydrolysis provides the 21-OH active derivatives

A

prodrugs

158
Q

The extremely water-soluble 21-sodium succinate and 21-sodium phosphate _______ are used for IV or IM injection in the management of emergency conditions

A

esters

159
Q

Increased lipophilicity improves penetration through the ________ ________. accomplished by introducing 6a, 7a, and/ or 9a halogens, removing the 17a-hydroxy group, masking 16a-,17a-,or 21 hydroxy groups using cyclic ketals esters, or replacing the 21-hydroxy group with a halogen

A

stratum corneum

160
Q

The topical glucocorticoids can be classified based on their 16-position substitution into derivatives of

A

triamcinolone (16a-hydroxyl)
dexamethasone (16a-methyl
betamethasone (16b-methyl)
prednisolone (no 16-substituted).

161
Q

The new inhaled/ intranasal glucocorticoids are more lipophilic than those used in oral and systemic therapy and have greater affinity for the ______

A

GR

162
Q

_________ is a highly potent nonhalogenated
glucocorticoid composed of a 1: 1 mixture of epimers of the 16,17-butylacetal, which creates a chiral center. The 22Repimer binds to the GR with higher affinity than does the 22S-epimer

A

Budesonide

163
Q

__________ is a third-generation nonhalogenated Prednisolone analog. It is the 21-isobutyrate ester and the 16a, 17a-acetal of the cyclohexane carboxaldehyde analog of Prednisolone

A

ciclesonide

164
Q

__________ ____________ is a trifluorinated thiester
glucocorticoid with the 17a-propionoxy group

A

Fluticasone propionate

165
Q

The intact furoate side chain occupies a discrete
pocket, conferring ________ _______ with higher GR affinity and higher nasal and lung tissue affinity compared to Fluticasone propionate

A

Fluticasone furoate

166
Q

What are the two functions of prolactin

A

stress hormone (help regulate metabolism)
stimulates proliferation of breast tissue in preparation for lactation

167
Q

What are the two synthesis steps of prolactin

A

-prolactin is produced by the lactotroph cells of the anterior pituitary
-synthesis is under tonic inhibition by dopamine from the hypothalamus

168
Q

What are the normal serum prolactin levels for women and men

A

women: <20mcg/L
men: <15mcg/L

169
Q

What are the three things that can override the tonic inhibition by dopamine

A

certain types of nerve impulses
estrogen
TRH

170
Q

What is the prolactin mechanism when a baby suckles

A

prolactin continues to increase causing milk production
stimulates oxytocin release form the posterior pituitary which ejects milk from breast

171
Q

Pathologic hyperprolactinemia

A

abnormal state of continuously elevated prolactin levels

172
Q

High levels of TRH stimulate the anterior pituitary what occurs in the thyrotroph cells and lactotroph cells

A

thyrotroph cells: increase TSH production
lactotroph cells: increase prolactin production

173
Q

What are typical antipsychotics

A

potent D2 antagonists and disassociate slowly from the receptor
increase prolactin levels and may cause sustained hyperprolactinemia

174
Q

What are atypical antipsychotics

A

they have a variety of structures and receptor activity
most are prolactin-sparing
(exception: risperidone increase prolactin)

175
Q

What is prolactinoma

A

a pituitary adenoma that secretes prolactin

176
Q

Pathophysiology of prolactin: most are due to ________________ _______________

A

hypogonadotropic hypogonadism (secondary hypogonadism)

177
Q

Increase of prolactin causes a decrease in GnRH which decreases FSH/LH secretion causing a decrease in what

A

gonad hormones (causes disorders in reproductive function)

178
Q

treatment of prolactinomas

A

medical management of dopamine agonists
(drug therapy is preferred)

179
Q

MOA of prolactinomas

A

agonist drug binds to D2 receptors on lactotroph cells of the anterior pituitary restoring tonic inhibition of prolactin secretion

180
Q

What are the two prolactinoma drugs

A

bromocriptine
cabergoline
(monitor prolactin levels)

181
Q

Goals of prolactinoma drug treatment

A

reduce prolactin levels
improve symptoms
reduce adenoma size
restore fertility
decrease long-term risk of osteoporosis

182
Q

ADH MOA

A

When ADH is present, the renal collecting ducts become permeable to water (increase urine concentration)
When ADH is absent, the renal collecting ducts become almost impermeable to water

183
Q

What is ADHs relation to plasma osmolality

A

is the most important determinant of ADH secretion
Osmoreceptors in the hypothalamus monitor osmolality
thirst is backup mechanism

184
Q

Diabetes insipidus (DI)

A

A condition of abnormal water regulation/conservation.
Patients urinate a very large amount

185
Q

Diabetes insipidus (DI) symptoms

A

Polyuria
Polydipsia

186
Q

Central Diabetes insipidus (CDI) etiology

A

lack of ADH

187
Q

What are the 4 causes of ADH deficiency

A

Can be a total loss or a partial loss
Can be inherited genetically
Can be acquired… through trauma, surgery, tumors, and infections
Can be idiopathic

188
Q

Symptoms of Central Diabetes insipidus (CDI)

A

Occur when ~80% of ADH producing cells have been lost (are severe when >95% lost)
Severity is variable; it depends on the cause of loss and the speed of the loss

189
Q

Treatment of Central Diabetes Insipidus (CDI)

A

Desmopressin acetate (synthetic ADH agonist with V2 receptor specificity)

190
Q

goals of treatment for CDI

A

Improve the patient’s quality of life
(more tolerable water intake, prevent nocturia and sleep deprivation)
Maintain Safety
Educate Patients (must not drink water unless they are thirsty)

191
Q

Nephrogenic Diabetes Insipidus (NDI) etiology

A

V2 receptor resistance

192
Q

Syndrome of Inappropriate ADH (SIADH)

A

SIADH a condition of excessive ADH….which causes hyponatremia….without edema
(hyponatremia)

193
Q

Syndrome of Inappropriate ADH (SIADH) etiology

A

↑ADH from the posterior pituitary due to trauma, surgery, brain tumors
An “ectopic” source of ADH production exists somewhere
Iatrogenic / Drug induced – may ↑ the amount of ADH released or ↑sensitivity to ADH

194
Q

Symptoms of hyponatremia

A

Depend on the rate of sodium loss
Depend on how low the level of serum sodium is
(Na level < 120meq /L, Nausea /Vomiting / Headache)
(Na level < 110meq /L,seizures, coma, death)

195
Q

Treatment of SIADH

A

FLUID RESTRICTION

196
Q

Nocturnal enuresis / “Bedwetting” treatment

A

NON-DRUG therapy
(is have to use drugs use desmopressin)

197
Q

Nocturnal polyuria treatment

A

Nocdurna® (desmopressin) sublingual tablets

198
Q

GH secretion is under dual control what are they

A

Somatostatin – provides a tonic inhibition of GH secretion (it sets the basal rate)
GHRH – is released: in pulses – which stimulates GH release: in pulses.

199
Q

Direct and indirection physiologic action of growth hormone

A

Direct action – GH itself acts on certain tissue surface receptors (such as adipose tissue)
Indirect action – GH stimulates production of IGF-1 (insulin-like growth factor)
(majority growth due to IGF-1

200
Q

Major functions of GH: metabolism

A

Stimulates lipolysis
Promotes protein synthesis & retention of nitrogen
Increases gluconeogenesis in the liver
Promotes glycogen storage in the liver
Decreases glucose uptake by extrahepatic tissues

201
Q

Major functions of GH: growth

A

Bones and cartilage
Soft tissues, organs (mainly adults)

202
Q

Evaluation of Grown Hormone levels

A

Taking a random sample of GH is NOT a reliable way to determine GH status
GH levels decline with age; GH levels are also suppressed in obese patients

203
Q

Proactive testing of growth hormone levels

A

GH Stimulation Tests – may be used to confirm GH deficiency
-Insulin Tolerance Test
-Intravenous infusion of arginine

204
Q

GH Suppression Test of growth hormone levels

A

Oral Glucose Tolerance Test

205
Q

Growth Hormone deficiency etiology

A

Congenital disorders – GHRH deficiency, GH gene deletion, pituitary aplasia/hypoplasia…
Acquired disorders – due to hypothalamic or pituitary disease, surgery, radiation, trauma…

206
Q

Growth Hormone Deficiency in children

A

Delayed sexual development associated with normal mental function
Poorly developed muscles (decreased protein synthesis)
Tendency toward hypoglycemia (no GH to respond to low glucose levels)
↑subcutaneous fat (b/c no GH to promote lipolysis)

207
Q

Diagnostic parameters of growth hormone deficiency

A

↓ linear growth (growth charts)
decrease “Bone Age” (patient’s bone x-rays are compared to standardized bone x-rays)
decrease IGF-I levels

208
Q

Growth Hormone Deficiency in adults

A

Depression, reduced energy, ↓ QoL
↓ BMD (bone mineral density) – increases risk for osteoporosis and fractures
Change in body composition (↑abdominal obesity, ↓ muscle mass)
Hyperlipidemia; increased markers of atherosclerosis

209
Q

Examples of Non-Deficient indications to receive GH therapy

A

Certain genetic syndromes
Idiopathic Short Stature
Small for Gestational Age
Growth failure in children with Chronic Kidney Disease
HIV associated wasting/cachexia; HIV associated lipodystrophy

210
Q

Growth Hormone Therapy goals for children and adults

A

For children: ↑growth and height; ↑bone age, ↑muscle tone, etc…
For adults: to improve their QoL, decrease the risk of bone fractures

211
Q

Growth hormone therapy somatropin administration

A

injection
given in evening

212
Q

Dosing of somatropin

A

Children - is always Weight Based
Adults - 0.2mg/day (range 0.15 – 0.3mg)

213
Q

Monitoring of somatropin in children

A

growth measurements
x-rays to monitor bone age
IGF-1

214
Q

Growth Hormone Excess

A

A condition of excessive GH secretion that occurs after the closure of the epiphyses

215
Q

Cause of Growth Hormone Excess

A

A pituitary adenoma that secretes GH
Results in sustained high levels of GH…and therefore high levels of IGF-I

216
Q

signs and symptoms of growth hormone excess

A

Coarsening of facial features
Joints / Soft tissue enlargement
Cardiovascular effects
Excessive sweating
Hypertension
Sleep apnea
Glucose intolerance
Increase in colon polyps

217
Q

Diagnosis of growth hormone excess

A

Clinical suspicion
Biochemical confirmation
(random IGF-1 measurement)
(glucose suppressed GH measurement)

218
Q

Treatment options of growth hormone excess

A

Surgery to remove adenoma – is the treatment of choice
Medical Management (Drug Therapy)
Radiation – last line

219
Q

Drugs for growth hormone excess

A

Somatostatin analogs
-octreotide
GH receptor antagonist
-pegvisomant

220
Q

Gigantism

A

is due to GH excess in children before the closure of the epiphyses

221
Q

Gigantism cause

A

a pituitary adenoma that secretes GH

222
Q

Gigantism symptoms

A

Symmetric growth of stature, sometimes reaching 8-9 feet
Cardiac hypertrophy & mild HTN that may proceed to heart failure
Osteoporosis and muscle weakness in later stages (bone growth > Ca intake)
Symptoms of acromegaly may also occur if the excess growth stimulus continues
beyond the closure of the epiphyses

223
Q

Gigantism Diagnosis & Treatment

A

identical to acromegaly

224
Q

The circadian rhythm

A

ACTH release – is controlled by CRH, free cortisol levels, & the sleep cycle
ACTH is released in pulses – the largest pulse occurs in early morning

225
Q

The “stress” response of Neuroendocrine control

A

Stress increases the output of ACTH
Up to 10x of the normal cortisol may be released if necessary
Stress response can override the circadian rhythm

226
Q

Glucocorticoids: Metabolic homeostasis / supports ↑energy needs during stress, hypoglycemia

A

Permits lipolysis to happen
Inhibits protein synthesis
Stimulates the process of gluconeogenesis

227
Q

Short term and long term of glucocorticoids

A

Short term - excessive GC production or GC drug therapy ↑glucose levels
Long term - hyperglycemia …↑ insulin secretion …↑ fat storage/weight gain

228
Q

Glucocorticoids CNS deficiency

A

apathy, fatigue, depressed mood may occur

229
Q

Glucocorticoids CNS excess

A

Common - initial euphoria (feeling good, energy) ↑appetite
- INSOMNIA
Less common– irritability, confusion, mania, and overt psychosis

230
Q

Glucocorticoids Connective tissue

A

Excessive GC inhibits fibroblasts…↓ collagen synthesis & connective tissue
Thin skin, easy bruising, striae (stretch marks), and poor wound healing may occur

231
Q

Glucocorticoids bone

A

GC delays linear bone growth: growth may catch up if discontinued before puberty
GC inhibit bone formation by inhibiting osteoblasts
GC effects Ca/P processes which promote bone resorption

232
Q

Glucocorticoids eyes

A

↑ development of cataracts
↑ intraocular pressure…↑ risk for glaucoma

233
Q

Mineralocorticoids: Things that regulate aldosterone secretion

A

↓ intravascular blood volume or effective circulating volume
K+ levels
Na+ levels

234
Q

Physiologic actions of aldosterone

A

Aldosterone causes Na+ reabsorption and K+ excretion
water follows the sodium
H+ follows the potassium

235
Q

Aldosterone excess results in

A

Hypertension
Hypokalemia
Metabolic alkalosis

236
Q

Aldosterone deficiency results in

A

Hypotension
Hyperkalemia
Metabolic acidosis

237
Q

Adrenal androgens: primarily (DHEA)

A

Have little physiologic androgen activity themselves
They are precursors for peripheral conversion to testosterone & dihydrotestosterone

238
Q

Adrenal androgens: in adult females and adult males

A

In adult males: they account for ~5% of testosterone production
In adult females: DHEA / androstenedione significantly contributes to androgen production

239
Q

Primary Adrenal Insufficiency

A

Addison’s disease

240
Q

Etiology of Addison’s disease

A

Autoimmune disease (~90% cases)
Infectious
Other - adrenal hemorrhage, metastatic cancer, genetic disorders

241
Q

All 3 zones of the cortex are destroyed = deficiency of cortisol, aldosterone in what disease

A

addisons disease

242
Q

Signs/Symptoms of Addison’s disease

A

Muscle weakness
Hyperpigmentation
Weight loss
Hypotension
Lab abnormalities (hypoglycemia, hyponatremia, hyperkalemia)

243
Q

Diagnosis / Initial lab tests of addisons disease

A

Basal morning cortisol (should be high)
Cosyntropin stimulation test

244
Q

HC doses of ~50mg also have mineralocorticoid activity equivalent to ______ fludrocortisone

A

~0.1mg

245
Q

Dexamethasone does NOT interfere (cross react) with the measurement of _______ levels

A

cortisol

246
Q

Management of Addison’s disease goals

A

Improve symptoms / ↑ QoL / less fatigue
Avoid excessive GC replacement / do not over treat / minimize side effects
Prevent adrenal crisis

247
Q

Glucocorticoid replacement

A

hydrocortisone (drug of choice)
~2/3 in morning
~1/3 about 6-8 hours later

248
Q

Mineralocorticoid replacement

A

fludrocortisone

249
Q

Monitoring of fludrocortisone

A

BP
edema
K+/Na+

250
Q

With glucocorticoids does the patient need to receive an extra “stress dose” of fludrocortisone?

A

no, since you are giving a high dose already

251
Q

Androgen replacement

A

men do not need it
women its not required (improves libido)

252
Q

Symptoms of Adrenal crisis

A

Severe weakness/fatigue
Nausea/Vomiting
Hypoglycemia
Hypovolemia / dehydration leading to hypotension/shock

253
Q

Treatment of Adrenal Crisis

A

Identify and treat the underlying cause of the “stress”
Intravenous fluid replacement to maintain blood pressure & glucose
Intravenous hydrocortisone injection (high dose / stress dosing)

254
Q

Controversy in Critically Ill patients: If adrenal insufficiency is suspected and is not corrected…the patient may not recover

A

Option 1 – treat first and then assess the outcome
Option 2 – assess the HPA axis to decide if treatment might be needed

255
Q

What is the problem with secondary adrenal insufficiency

A

lack of ACTH

256
Q

What are the causes of secondary adrenal insufficiency

A

Any pituitary disease that results in a loss of ACTH production
HPA axis suppression – from glucocorticoid drug therapy

257
Q

Symptoms of secondary adrenal insufficiency

A

-Muscle weakness, fatigue, anorexia, weight loss, N/V/D, hypoglycemia
-Acute Adrenal Insufficiency
(NO Hyperpigmentation or low BP, Na+, K+)

258
Q

Management of SECONDARY adrenal insufficiency

A

-IF due to pituitary disease: pts need chronic GC replacement therapy + stress doses prn
-For patients with medical conditions receiving chronic GC therapy: Only stress doses need sick day plan

259
Q

Key point for secondary adrenal insufficiency management

A

MC replacement (fludrocortisone) is NOT needed – aldosterone secretion is normal

260
Q

What is “Cushing’s syndrome” (hypercortisolism)

A

The physiologic changes that occur from prolonged excessive levels of glucocorticoids

261
Q

General signs and symptoms of cushing’s syndrome (hypercortisolism)

A

central obesity
facial rounding
fat accummulation
hypertension
edema

262
Q

Metabolic signs and symptoms of cushing’s syndrome (hypercortisolism)

A

glucose intolerance
Type 2 DM

263
Q

Musculoskeletal signs and symptoms of cushing’s syndrome (hypercortisolism)

A

Muscle weakness
Osteoporosis

264
Q

Skin signs and symptoms of cushing’s syndrome (hypercortisolism)

A

striae (stretch marks)

265
Q

Causes of Cushing’s syndrome: A source of excessive ACTH exists somewhere

A

pituitary ACTH-secreting adenoma
Ectopic ACTH syndrome

266
Q

Causes of Cushing’s syndrome: A source of Cortisol or GC drug exists somewhere

A

Primary adrenal tumor/neoplasm
Iatrogenic / Drug induced: chronic administration of GC drugs

267
Q

Diagnosis of Cushing’s syndrome

A

Medical history
Physical exam
Laboratory tests

268
Q

Selected tests for the evaluation of patients with Cushing’s syndrome

A

Late-night serum cortisol (should be low)
24-hour urine free cortisol
Overnight LOW DOSE dexamethasone SUPPRESSION test

269
Q

Treatment of Cushing’s syndrome

A

-Evaluation for ANY possible source of exogenous glucocorticoid
-IF the cause is an adenoma or tumor – SURGERY to remove
-Pharmacologic therapy
May be used if the patient is not a surgical candidate or as an adjunct to surgery if needed

270
Q

Steroidogenic inhibitors –drugs that inhibit the synthesis of cortisol

A

ketoconazole (drug of choice - inhibits CYP450 enzymes)
mitotane
metrapone
aminoglutethimide

271
Q

Suppression of HPA axis with GC administration: Degree of adrenal suppression depends on what factors

A

dose
duration
route of administration
the patient

272
Q

In general: GC doses < prednisone 7.5mg/day (or equivalent) for ____ weeks is not expected to suppress HPA axis

A

<3 (want to taper doses)

273
Q

Definition of Conn’s syndrome aldosterone adenoma (primary aldosteronism)

A

describes a group of conditions of excess aldosterone production by the zona glomerulosa

274
Q

Primary Aldosteronism clinical manifestations

A

HTN
hypokalemia
metabolic alkalosis

275
Q

Treatment of primary aldosteronism

A

surgery
spironolactone
amiloride

276
Q

Pheochromocytoma

A

syndrome of catecholamine excess

277
Q

Etiology of Pheochromocytoma

A

catecholamine producing tumor of the adrenal medulla

278
Q

Dominant clinical feature of pheochromocytoma

A

hypertension

279
Q

Diagnosis of pheochromocytoma

A

S/S of pheochromocytoma
24h urine measurement of catecholamines and their metanephrine metabolites
MRI or CT to localize tumor

280
Q

Treatment of pheochromocytoma

A

SURGERY
Medical management - BP must be stabilized before surgery can occur
phenoxybenzamine

z S1: Module (8 decks)

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