551 Endocrine Exam 1

Front 1

Cushing syndrome endogenous etiology

Back 1

abnormal adrenal gland (abnormal cortical tissues)
pituitary adenomas
ectopic tumors
corticotropin hypersecretion

Front 2

Cushing syndrome metabolic presentation

Back 2

fat redistribution --> buffalo hump, moon face
increase in blood glucose

Front 3

Cushing syndrome cardiovascular presentation

Back 3

increase in Na+/H2O retention --> increase in BP --> increased risk for HF
increase in thrombotic events

Front 4

Cushing syndrome integument changes

Back 4

hirsutism
hyperpigmentation
decreased wound healing
increased risk of infection
thinned skin --> striae

Front 5

Cushing syndrome muskuloskeletal presentation

Back 5

osteoporosis
muscle wasting and weakness

Front 6

Cushing syndrome reproductive presentation

Back 6

acne, hair thinning on scalp, hirsutism elsewhere, decreased libido
impotence

Front 7

Cushing syndrome mental presentation

Back 7

steroid psychosis

Front 8

Cushing syndrome ocular presentation

Back 8

reversible (to a point) increased intraocular pressure
cataracts

Front 9

Cushing syndrome 1st-line treatment

Back 9

surgery

Front 10

Cushing syndrome pharmacologic treatment (general drug classes)

Back 10

steroidogenic inhibitors
adrenolytic agents
neuromodulators of ACTH release
glucocorticoid-receptor blockers
these are rarely used

Front 11

Addison's disease

Back 11

chronic adrenal insufficiency
etiology: autoimmune, infection, or tumor
treatment: steroid replacement therapy

Front 12

Adrenal crisis

Back 12

Acute adrenal insufficiency
--> medical emergency

Front 13

Adrenal crisis cardiovascular presentation

Back 13

decreased Na+/H2O --> decreased BP --> increased risk of shock

Front 14

Adrenal crisis gastrointestinal presentation

Back 14

N/V
abdominal pain (e.g. cramping)

Front 15

Adrenal crisis metabolic presentation

Back 15

decreased blood glucose
decreased K+
fever

Front 16

Adrenal crisis integument changes

Back 16

vitiligo

Front 17

Adrenal crisis treatment

Back 17

hydrocortisone 100mg IV q8h --> then convert to oral prednisone as tolerated
supportive therapy: fluids, K+, glucose

Front 18

Endogenous cortisol secretion, T1/2

Back 18

8-15mg/day
T1/2 = 30 - 90 min
T1/2-biological = 8-12 hours

Front 19

Homeostatic steroid action: carbohydrate metabolism

Back 19

stimulates gluconeogenesis
decreases peripheral utilization of glucose
stimulates glycogen storage

Front 20

Homeostatic steroid action: lipid metabolism

Back 20

stimulates lypolysis
changes fat distribution

Front 21

Homeostatic steroid action: electrolyte and water balance

Back 21

increase absorption of Na+ and water
increase excretion of K+, H+, and Ca++
decrease GI absorption of Ca++

Front 22

Homeostatic steroid action: bone and growth

Back 22

inhibits osteoblast formation
decreases cartilagenous matric and epiphyseal proliferation
stimulates closing of epiphyseal plate
decreases GI absorption of Ca++ (via vit D inhibition)
decreases growth hormone release

Front 23

Homeostatic steroid action: CNS

Back 23

may interrupt circadian rhythm

Front 24

Homeostatic steroid action: immune system

Back 24

increases neutrophils
decreases lymphocytes, monocytes, eosinophils, basophils
inhibits macrophage phagocytosis

Front 25

corticosteroid with PK/PD profile most similar to cortisone

Back 25

hydrocortisone

Front 26

corticosteroid with PK/PD profile most similar to prednisone

Back 26

prednisolone

Front 27

corticosteroid with PK/PD profile most similar to triamcinolone

Back 27

methylprednisolone

Front 28

corticosteroid with PK/PD profile most similar to betamethasone

Back 28

dexamethasone

Front 29

four corticosteroid drugs with 0 relative mineralocorticoid potency

Back 29

triamcinolone
methylprednisolone
dexamethasone
betamethasone

Front 30

morning cortisol level required for everyday activities

Back 30

>15μg/dL

Front 31

When, why, and how to perform ACTH test

Back 31

when: morning cortisol is <15μg/dL
why: to see if HPA can be stimulated
how: cosyntropin 250μg IV/IM

Front 32

general corticosteroid tapering rules

Back 32

1. for doses > 5mg-7.5mg / day prednisone, half dose every ~week
2. when at 5mg-7.5mg / day, decrease by 1mg prednisone per week
3. monitor underlying disease for flare-ups
4. ACTH stress test for conservative tapering

Front 33

Range: Thyroid-stimulating hormone (TSH)

Back 33

Normal: 0.4-6 µU/mL

Front 34

Range: Thyroxin (T4) total

Back 34

Normal: 5.0-11.0 µg/dL

Front 35

Range: Triodothyronine (T3)

Back 35

Normal: 95-190 ng/dL

Front 36

3 types of hormones

Back 36

1. Proteins/Polypeptides
2. Steroids
3. Tyrosine derivatives

Front 37

What dictates half-life of hormones?

Back 37

Structure

Thyroid > Steroids/Proteins > Polypeptides > Amines

Front 38

Largest class of hormones

Back 38

Polypeptides/Proteins

Front 39

Supraoptic nuclei in neurohypophysis makes

Back 39

Vasopressin (ADH)

Front 40

Magnocellular cells of Paraventricular nuclei (PVN) of posterior pituitary makes

Back 40

Oxytocin & Vassopressin (ADH)

Front 41

Parvocellular cells of PVN of posterior pituitary releases

Back 41

Anterior pituitary controlling hormones into median eminance

(CRF, TRH, GHRH, GHIH, GnRH, PIH)

Front 42

Composition of anterior pituitary

Back 42

30-40% Somatotropes

20% Corticotropes

3-5% Thyrotropes, Gonadotropes, Lactotropes

Front 43

Somatotropes makes

Back 43

Human growth hormone (hGH)

In response to GHRH

Front 44

Corticotropes make

Back 44

Adrenocorticotropin (ACTH)

In response to CRF

Front 45

Thyrotropes make

Back 45

Thyroid stimulating hormone (TSH)

In response to THR

Front 46

Gonadotropes make

Back 46

Follicle stimulating hormone (FSH)
& Leutenizing hormone (LH)

In response to GnRH

Front 47

Lactotropes make

Back 47

Prolactin (PRL)

Dopamine (PIH) inhibits release

Front 48

Acromegaly caused by

Back 48

Over secretion of growth hormone (GH)

Basically gigantism

Front 49

Symptom of Inappropriate ADH release (SIADH)

Back 49

Over secretion of ADH from post. pituitary

Causes hyponatremia, fluid overload

Front 50

Grave's Disease

Back 50

hyperthyroidism
s/s: sweating, eye bulging, anxiety

Front 51

Dwarfism

Back 51

Undersecretion/production Growth hormone (GH)

Front 52

Diabetes Insipidus

Back 52

Undersecretion/production of vasopressin (ADH)

Front 53

Layers of the Adrenal gland

Back 53

1. Capsule
2. Glomerulosa
3. Fasciculata
4. Reticularis
5. Medulla

Front 54

Zona glomerulosa physiology

Back 54

~15% of mass

Only region to express Aldosterone Synthase

Makes Mineralocorticoids

Under Ang II and K+ control

Front 55

Zona Fasciculata physiology

Back 55

Makes glucocorticoids

Expresses 11β hydroxylase

Controlled by ACTH

Front 56

Zona Reticularis physiology

Back 56

Makes Androgens

Expresses 17α hydroxylase and
a lyase

Front 57

P450SCC

Back 57

Side chain cleavage enzyme

takes cholesterol ➝ pregnenolone

Front 58

Precursors for mineralocorticoids

Back 58

Cholesterol ➝ Pregnenolone ➝ Progesterone ➝ Mineralocorticoids

Front 59

Precursors for glucocorticoids

Back 59

Cholesterol ➝ Pregnenolone ➝ 17OH Pregnenolone ➝ 17OH Progesterone ➝ Glucocorticoids

Front 60

Precursors for Androgens/Estrogens

Back 60

Cholesterol ➝ Pregnenolone ➝ DHEA ➝ Androstenedione ➝ Androgens/Estrogens

Front 61

Corticosterone is a precursor for

Back 61

Aldosterone in glomerulosa

Cortisol in Fasciculata

Front 62

Androstenedione is the precursor for

Back 62

Androgens or Estrogens

Front 63

This is the most abundant steroid in the human body

Back 63

DHEA (dihydroepiandosterone)

Made in the reticularis

Front 64

17α-Hydroxylase makes

Back 64

Progesterone ➝ 17 Hydroxy progesterone

Leads to cortisol production in smooth ER of Fasciculata

Front 65

11β-Hydroxylase makes

Back 65

11β-deoxycortisol ➝ Cortisol

In mitochondria of fasciculata

Front 66

5α-Reductase makes

Back 66

Testosterone ➝ Dihydrotestosterone (DHT)

in Smooth ER of Reticularis

Front 67

Aldosterone Synthase makes

Back 67

Corticosterone ➝ Aldosterone

In mitochondria of Glomerulosa

Front 68

Lysodren

Back 68

Mitotane

Inhibits P450SCC & 11β-Hydroxylase in mitochondria of adrenal cortex

Front 69

11-deoxycorticosterone

Back 69

made from progesterone
converted to Corticosterone

Has weak MR affinity

Front 70

Mitotane inhibits formation of

Back 70

Pregnenolone and Corticosterone

in mitochondria of Adrenal cortex

Front 71

Mitotane is toxic at doses of

Back 71

>4g/day

Only in fasciculata and reticularis
(specific mitochondrial metabolism occurs here)

Front 72

Metopirone

Back 72

Metyrapone

Inhibits 11β-Hydroxylase in adrenal cortex
MR effects < Mitotane

Used to test HPA function

Front 73

High dose Ketoconazole inhibits

Back 73

CYP17 aka 17α-Hydroxylase

at even higher doses it inhibits P450SCC

Front 74

Periactin

Back 74

Cyproheptadine

5-HT and H1 antagonist

Inhibits CRF at hypothalamus and ACTH secretion at ant. pituitary

Front 75

Major component of colloid is

Back 75

Thyroglobulin

Front 76

Parafollicular cells secrete

Back 76

Calcitonin

Front 77

Cold will do what to HPT axis?

Back 77

Directly stimulates hypothalamus to ↑ release of TRH

End result is ↑ Thyroid levels
↑ BMR and ↑ body heat

Front 78

How do heat, stress, anxiety, SNS outflow affect TRH?

Back 78

These variables serve to decrease TRH release

Front 79

Amount of Iodide necessary for thyroid synthesis

Back 79

~1mg/week

Front 80

Three functions of TSH

Back 80

1. increases sodium-iodide symporter activity

2. increases TPO activity

3. increases release of T3 and T4

Front 81

Pendrin

Back 81

Iodide channel connecting the follicular cells and colloid

Front 82

Thyroperoxidase (TPO)

Back 82

Located in colloid
Converts Iodide to nacent Iodine (I-zero)
Iodinates Thyroglobulin
Couples DITs/MITs

Front 83

Thyroglobulin is made where?

Back 83

Follicular cells

Consists of about 70-120 Tyrosine residues

Exocytosed into colloid

Front 84

TPO requires this to function

Back 84

Hydrogen peroxide (H2O2)

Front 85

Organification

Back 85

Iodination of Thyroglobulin by TPO

Front 86

Iodinase

Back 86

Involved to a lesser extent than TPO in iodination of tyrosine residues

Front 87

How is thyroglobulin moved back to follicular cells?

Back 87

Pinocytosis

Front 88

How is thyroid hormone cleaved from thyroglobulin?

Back 88

Lysosomal degradation leaving free T4 and T3

Front 89

Deiodinase

Back 89

Salvages Iodide from T3 and T4 synthesis from the leftover MIT, DIT and thyroglobulin

Front 90

A deiodinase deficiency would lead to what?

Back 90

Iodine deficiency

Front 91

Grave's disease

Back 91

Auto-Abs stimulation of TSH receptor

Causes goiter

Front 92

High levels of circulating iodine will cause

Back 92

Decrease T3
and
Increase TSH as a result

Front 93

Increased Deiodinase activity will result in

Back 93

T2 formation

Front 94

another name for TSH

Back 94

Thyrotropin

Front 95

Plasma T3 and T4 levels increase in pregnancy due to

Back 95

Increase in Thyroid binding globulin (TBG)

Increases total thyroid levels (bound)

Front 96

Ultimate treatment for hyperthyroidism is?

Back 96

radioactive Iodine, then surgery if that doesn't work

Front 97

17α-Hydroxylase is absolutely required for synthesis of these two steroid classes

Back 97

Cortisol and sex steroids

Front 98

The majority of hormones are

Back 98

Peptides

Front 99

Epinephrine is made in only one place, where?

Back 99

Cytosol of Adrenal Medulla

b/c it's only place the PNMT is expressed

Front 100

Where and what kind of receptor is the TSH receptor?

Back 100

Located on follicular cells of thyroid gland

Gs GPCR

Front 101

T4 is converted to T3 primarily in?

Back 101

The liver

Front 102

Thick skin and nails is indicative of which thyroid disorder?

Back 102

Hypothyroid

Front 103

Thin skin, hair, and nails is indicative of which thyroid disorder?

Back 103

Hyper

Front 104

Goiters are typically larger in which thyroid disorder?

Back 104

Hypo

The higher levels of TSH b/c no thyroid is inhibiting its release

Front 105

T4 half-life = ?

Back 105

6-8 days

Front 106

T3 half-life = ?

Back 106

~24 hours

Front 107

The thyroid hormone receptor is of what type?

Back 107

Intracellular

Dimerized to RXR

Front 108

propylthiouracil

Back 108

PTU
TPO inhibitor
deiodinase inhibitor (stops T4 --> T3)