Team Block 2 Endo

Front 1

What are adrenal cortex and medulla derived from?

Back 1

cortex -> neural crest
medulla -> mesoderm

Front 2

What are the layers of the adrenal medulla?

Back 2

capsule, zona fasiculata, zona glomerulosa and zona reticularis.

Front 3

chemicals secreted by adrenal medulla

Back 3

catecholamines (epinephrine and norepinephrine) by chromaffin cells

Front 4

chemicals secreted by adrenal cortex

Back 4

fasiculata - salt - aldosterone
glomerulosa - stress/sugar - Cortisol (glucocorticoids)
reticularis - sex - androgens
"it gets sweeter as you go deeper"

Front 5

alternate names for anterior and posterior pituitary

Back 5

pars nervosa or neurohypophysis (posterior)
and
pars distalis or adenohypophysis (anterior)

Front 6

Chemicals secreted by anterior pituitary?

Back 6

GPA - Acidophils --> prolactin, growth hormone

B-FLAT - basophils --> FSH, LH, ACTH, TSH

Chromophobes --> secretions unknown

Also secretes melanotropin (MSH), important in skin darkening symptoms in endocrine disorders (acanthosis nigricans)

Front 7

anterior pituitary embryo derivative

Back 7

oral ectoderm

Front 8

posterior pituitary embryo derivative

Back 8

neuroectoderm --> diencephalon

Front 9

islets of langerhanns cell types and their chemical products

Back 9

INSulin INSide:
Beta cells (central core of islets) - insulin
-----
Alpha cells (peripheral) - glucagon
Delta cells (interspersed) - somatostatin

Front 10

glucose transporter found in skeletal muscle and adipose tissue

Back 10

GLUT-4

Front 11

glucose transporter found in brain and RBCs

Back 11

GLUT-1

Front 12

prolactin inhibition chemical

Back 12

dopamine

Front 13

results of prolactinomas

Back 13

high dopamine to counteract high prolactin.

Leads to inhibition of GnRH, inhibition of ovulation, and Amenorrhea in women. Can cause hypogonadism in men by GnRH inhibition.

Front 14

chemicals released by hypothalamus

Back 14

GnRH, GHRH, TRH, CRH, Dopamine

Front 15

hypothalamic-pituitary regulation

Back 15

TRH --> + --> TSH, prolactin
Dopamine --> - --> prolactin
CRH --> + --> ACTH
GHRH --> + --> GH
Somatostatin --> - --> TSH, GH
GnRH --> + --> FSH, LH
Prolactin --> - --> GnRH

Front 16

transport system for endocrine glands

Back 16

blood

Front 17

transport system for exocrine glands

Back 17

ducts

Front 18

Parathyroid Glands secretion

Back 18

parathyroid hormone (PTH)

Front 19

thyroid secretions

Back 19

Follicular Cells: T3 and T4 parafollicular cells: Calcitonin

Front 20

ovaries and testes secretions

Back 20

ovaries --> estrogen
testes --> testosterone

Front 21

Actions of Insulin

Back 21

Stimulates Glucose Uptake By Cells
Inhibits Breakdown Of Fat And Protein
Inhibits Hepatic Glucose Production
Inhibits Glycogen Breakdown and Stimulates Glycogen Synthesis
Inhibits Gluconeogenesis
Inhibits Hepatic Ketoacid Production

Front 22

What are ketoacids

Back 22

high energy molecules dewrived from breakdown of fat during starvation
regulated by insulin
synthesis upregulated during times of insulin deficiency (type 1 DM)
high concentrations are dangerous to body;

Front 23

glucagon actions

Back 23

Stimulates Hepatic Glucose Production
Stimulates Gluconeogenesis
Stimulates Glycogen Breakdown
Stimulates Ketoacid Production
Stimulates Fat Breakdown

Front 24

alternate name for type 1 DM

Back 24

diabetic ketoacidosis

Front 25

alternate name for type 2 DM

Back 25

Nonketotic hyperosmolar Coma

Front 26

parathyroid histology

Back 26

fat cells interspercing islands of chief or principle cells, which secrete PTH

Front 27

actions of PTH

Back 27

Increased Bone Resorption With Release Of Calcium From Bone Into
Blood
Increased Retention Of Calcium In The Kidneys
Increased Absorption Of Calcium From Gut (Indirectly – By
Stimulating Increased Synthesis Of The Activated Form Of Vitamin D)

Front 28

hypercalcemia labs findings

Back 28

↑ Parathyroid Hormone
Secretion
↑ 1,25 Dihydroxy Vitamin D

Front 29

hypocalcemia lab findings (see IQ 10)

Back 29

↓ Parathyroid Hormone
Action
↓1,25 Dihydroxy Vitamin D Action

Front 30

which is more potent, T3 or T4

Back 30

T3

Front 31

Which is more prevalent in vivo, T3 or T4?

Back 31

T4

Front 32

Action of thyroid hormone

Back 32

increase basal metabolic rate

Front 33

goiter definition

Back 33

enlarged thyroid (not necessarily nodular)

Front 34

Actions of cortisol

Back 34

Comes from Zona Fasciculata
Helps The Body Fight
Stress
Increases Blood
Levels of Glucose, Amino Acids, and Fatty Acids
Reduces Inflammation

Front 35

chemicals secreted by posterior pituitary and their actions

Back 35

ADH (Vasopressin) --> stimulates reabsoption of water from tubular fluid in kidneys
Oxytocin --> stimulates uterine contractions and milk let down

Front 36

action of ACTH

Back 36

stimulates cortisol secretion from adrenal cortex

Front 37

action of prolactin

Back 37

stimulates breast development and milk synthesis in women

Front 38

action of growth hormone (GH)

Back 38

stimulates growth of bones, soft tissues and organs

Front 39

action of TSH

Back 39

stimulates thyroid hormone secretion from thyroid gland

Front 40

actions of LH and FSH

Back 40

regulate ovarian and testicular function

Front 41

thyroid gland histology

Back 41

spherical follicles surrounding a lumen filled with colloid

Front 42

another name for parafolicular cells and what do they secrete

Back 42

C cells; calcitonin

Front 43

is reverse T3 (rT3) biologically active?

Back 43

nope

Front 44

iodine is obtained exogenously or endogenously

Back 44

get iodine exogenously from food. naturally present in soil and sea water.

Front 45

symptoms of iodine deficiency

Back 45

—Maternal and fetal hypothyroidism
—Increased risk of miscarriage
—Preterm delivery
—Intellectual impairment of the
offspring.
Abnormal fetal development  “changes are not reversible with postnatal thyroid hormone therapy”.

Front 46

Iodine ingestion

Back 46

Ingested as iodide, distributed in extra cellular fluid.
Leaves pool by transport into thyroid and exretion into urine
Iodine concentrated in thyroid gland by action of sodiumiodide symporter (NIS)

Front 47

Protein that imports iodine into thyroid

Back 47

sodium/iodide symporter (NIS): ion pump that actively transports iodide (I-) across basolateral membrane in thyroid epithelial cells

Front 48

agents that block NIS

Back 48

perchlorate and thiocyanate; can lead to impaired thyroid hormone synthesis and development of goiter

Front 49

function of Pendrin

Back 49

membrane iodide-chloride transporter that transports iodide to exocytotic vesicles fused with apical cell membrane.
iodide oxidized and bound to tyrosyl residues of thyroglobulin

Front 50

function of thyroglobulin

Back 50

glycoprotein found in lumen of thyroid follicles
synthesized in the rough endoplasmicreticulum and secreted into lumen
helps with iodinization of tyrosine

Front 51

function of thyroid peroxidase

Back 51

couples DIT and MIT, forming T3 or T4 depending on the combination
DIT + DIT = T4
DIT + MIT = T3

Coupling process is not random; thyroglobulin has regions of unique amino acid sequences

Front 52

what happens after formation of T3 and T4 in the thyroid hormone synthesis pathway?

Back 52

thyroglobulin is resorbed into follicular cells in form of colloid droplets.
Droplets fuse with lysosomes forming phagolysosomes which hydrolze thyroglobulin to T3 and T4
some T4 is converted to T3
hormones are secreted into extraceullar fluid and enter circulation

Front 53

function of iodotyrosine deiodinase

Back 53

Strips iodide from iodotyrosine residues, most iodine atoms are recycled in the cell and tyrosine residues exit

Front 54

Extrathyroidal T3 production - how?

Back 54

5' deiodination of T4, catalyzed by two T4-5'-deiodinase (type I and II)
enzymes found in liver and kidney (major sources of serum T3)

Reverse T3 is formed by T4-5'-deiodinase type III

Front 55

radioactive iodine scan - describe

Back 55

„Iodine Scan used in the diagnosis
of some thyroid problems, particularly hyperthyroidism. The patient is given a
small dose of I123 after which  images are taken.

„The normal uptake is between 15 and
25 percent.

„High uptake suggests
hyperthyroidism

„Low uptake suggests thyroiditis.

Front 56

transport of T4 and T3 in blood

Back 56

>99% of both T3 and T4 are bound to serum binding proteins.
mostly thyroxin-binding globulin (TBG)
also bound to transthyretin, albumin and lipoproteins

Front 57

effect of changes in serum concentrations of TBG

Back 57

large effect on serum total T4 and T3, but doesnt affect free hormone concentration

Front 58

T3 nuclear receptors

Back 58

„Nuclear receptors mediate most if not all of the physiologic actions of thyroid hormone.

„Cytosolic T3 diffuses or is transported into nuclei, and then binds to the chromatin-localized receptors.
„
The nuclear receptors bind T3 much more avidly than T4
„
There are two T3-nuclear receptors, alpha and beta with different tissue distribution and
binding characteristics.

Front 59

action of thyrotropin (TSH)

Back 59

Thyrotropin — TSH
is synthesized and secreted by the thyrotrophs of
the anterior pituitary.

—It is composed of noncovalently
bound alpha and beta subunits, and contains about 15 percent carbohydrate .

Front 60

thyroid hormone regulation of TSH secretion

Back 60

TSH secretion inhibited by small increases in serum T4 and T3 concentrations

T4 and T3 inhibit the synthesis and release of TSH and TRH.

Front 61

name all steps of thyroid hormone synthesis and release (there are 9 of them)

Back 61

(1)Iodide (I-) Trapping, NIS
(2)Diffusion of Iodide
(3)Transport of iodide into the colloid
(4)Oxidation of inorganic iodide to iodine and incorporation of iodine into tyrosine residues within thyroglobulin molecules in the colloid
(5)Combination of two diiodotyrosine (DIT) or of monoiodotyrosine (MIT) with DIT.
(6)Uptake of thyroglobulin from the colloid into the follicular cell by endocytosis,
(7)Fusion of the thyroglobulin with a lysosome, and proteolysis and release of T4, T3,
DIT, and MIT
(8) Release of T4 and T3 into circulation

Front 62

Name the different kinds of insulin and their relative half lifes

Back 62

Fast-acting:
lispro and aspart (4-6 hrs)
regular (6-10 hours)

Long acting:
NPH (12-20 hours)
Ultralente (18-24 hours)
Glargine and Detemir (20-26 hours)

Front 63

half life of GnRH

Back 63

short - 2-4 mins

Front 64

where are GnRH secreting cell bodies located

Back 64

arcuate nucleus of hypothalamus

Front 65

Kallman syndrome presentations

Back 65

anosmia and hypogonadism.
deficiency in GnRH production because of defect in migration of neural crest cells
lacking GnRH cell bodies and also olfactory neurons
a form of primary pituitary insufficiency

Front 66

How a single hormone (GnRH) is capable of generating different responses in 2 different hormones

Back 66

Lower GnRH
pulse frequencies favor FSH secretion -- pulse
frequencies greater than 120 min

Higher GnRH
pulse frequencies favor LH secretion -- Pulse
frequencies greater than 90 minutes

Memonic: LOW Flyer Pulse or HIGH Leap Pulse

pulse frequencies increase at ovulation in female

Front 67

definition of down regulation

Back 67

Decrease in response in the presence of continuous stimulation of the receptor

Front 68

function of 5alpha reductase

Back 68

converts testosterone to DHT (irreversible)
DHT is more potent than testosterone

Front 69

function of aromatase

Back 69

conversion of testosterone to estradiol

Front 70

effects of estradiol, progesterone, and testosterone on GnRH release

Back 70

Estradiol reduces GnRH pulse amplitude

Progesterone slows GnRH pulse frequency

Testosterone slows frequency AND decreases amplitude

Front 71

where is inhibin made, what is its action and and what gland does it inhibit

Back 71

made by granulosa cells in female.
inhibits pituitary release of FSH and LH

Front 72

regulation of gonadotropins during follicular phase, starting with theca cell secretions

Back 72

androsteindione or testosterone in response to LH
androsteindione is converted to estrogen by granulosa cells
estradiol inhibits hypothalamic release of GnRH
Inhibin A predominantly made during follicular phase

Front 73

what receptors do theca cells have

Back 73

LH receptors only

Front 74

theca cell function

Back 74

convert cholesterol to androstenedione

Front 75

granulosa cell receptors and function

Back 75

has both FSH and LH receptors
production of Inhibin A
conversion of testosterone to estrogen
responds only to FSH during follicular phase.
starts expressing LH receptors during onset of luteal phase

Front 76

luteal phase regulation of gonadotropins

Back 76

LH stimulates both theca and leutinized granulosa cells
granulosa cells make more progesterone, which also inhibits hypothalamus

Front 77

how many estrogen withdrawals are there during menstrual cycle

Back 77

two.
one before luteal surge (ovulation) and one before menstruation

Front 78

When is inhibin A and B made during female menstrual cycle

Back 78

Inhibin A mostly made during luteal phase, inhibin B mostly made during follicular phase

Front 79

gonadotropin regulation in male

Back 79

leydig cells secrete testosterone
sertoli cells stimulated by FSH, secrete androgen binding protein which captures testosterone used for sperm maturation
some testosterone converted to estrogen, both of which inhibit pituitary and hypothalamus
sertoli cells make inhibin B, which inhibits only pituitary

memonic to remember this:
Sertoli Fishes for Testosterone B --> sertoli stimulated by FSH, grabs testosterone, makes inhibin B
Leydig loses testosterone --> leydig stimulated by LH, produces testosterone

Front 80

transport of sex hormones in blood

Back 80

bound to sex hormone binding protein (SHBG)
in order of affinity:
DHT>T>E

albumin has one low affinity binding site
Cortisol Binding Globulin (CBG) - binds only cortisol and progesterone

68% are carried by albumin
2% are free
active fractoin includes free + albumin-bound fraction

Front 81

affects of androgens (general physiologic changes)

Back 81

Increased Spermatogenesis

Increased Bone Growth - Increased bone matrix, calcium deposition and promotes growth spurt and epiphyseal
closure

Increased Nitrogen Balance - Increased muscle mass, larynx size

Increased atheletic performance - Increased basal metabolic rate, red blood cell density oxygen utilization

Altered Skin Function - Increased thickness, melanin deposition sebaceous gland secretion, male body odor, increased terminal hair growth

Front 82

Name twe two main androgen receptors and their interactions (this is a whole slide full of information)

Back 82

Both testosterone (T) and dihydrotestosterone
(DHT) interact with same androgen receptor

DHT has a higher affinity for the androgen receptor than T

T-Androgen Receptor Interaction
Feedback regulation of gonadotropin secretion
Differentiation of Wolffian duct in utero

DHT-Androgen Receptor Interaction
External genitalia differentiation in utero
Virilization during puberty 

Testosterone --> internal genetalia
DHT --> external genetalia

Front 83

Sertoli Cell Functions

Back 83

Nourish healthy cells & phagocytize damaged germ cells
Synthesize luminal proteins
Maintain tubular fluid
Convert androgens to estrogens
Are site for hormonal modulation of tubular function

Front 84

regulation of spermatogenesis

Back 84

GnRH --> LH --> Leydig cells --> testosterone --> secondary sex characteristics
GnRH --> FSH --> Sertoli cells --> spermatoctye maturation
Inhibin B feedback – FSH, testosterone – short & long loops

Front 85

name three products from sertoli cells and what other cells they modulate

Back 85

Sertoli cell products estradiol, inhibin, activin and other proteins modulate leydig cell activity
Sertoli cell products modulate germ cell function

Front 86

name main product of leydig cells and what it modulates

Back 86

Leydig cell testosterone modulate peritubular & Sertoli cell function
Peritubular cell products influence Sertoli cell activity

Front 87

what are the three steps to ovulating an egg

Back 87

recruitment, selection, dominance.

during selection, the follicle with the most FSH receptors wins
selected follicle produces more estrogen to decrease FSH, inhibiting growth of other follicles while it maintains sensitivity because of upregulation of FSH receptors

Front 88

what are the chemical products of the post menopausal ovary

Back 88

androsteinedione and testotserone

any estrogen is due to extra-glandular aromatization of androstenedione
estrone derives predominantly from the periveral aromization of adrenal and ovarian androstenedione

Front 89

are fsh levels higher in menopause or lower

Back 89

higher. The ovary stops producing as much estrogen and progesterone, which inhibit fsh, so the body compensates by upping the FSH

Front 90

what receptors do leydig cells have

Back 90

LH, analogous to theca cells in females

Front 91

what receptors do sertoli cells have

Back 91

FSH, analogous to granulosa cells in females

Front 92

what hormone do both sertoli and granlosa cells secrete

Back 92

inhibin B

Front 93

what two hormones determine internal genetalia

Back 93

anti-mullerian hormone and testosterone

Front 94

alternate names for wolfian and mullerian ducts and how long they coexist in embryo

Back 94

coexist for 8 weeks
woffian --> mesonephric
mullerian --> paramesonephric

remember: Wolfs make messes.

Front 95

what critical step in development is required for formation of mullerian ducts

Back 95

development of mesonephric tubes (renal)

Front 96

what does DHT do during development

Back 96

virilizes urogenital sinus and develops external genetalia

Front 97

describe androgen insensitivity syndrome. what will internal and external genetalia look like. what is karyotype

Back 97

Female phenotype despite normal male 46XY
Maternal X-linked recessive
Normal breast development with primary amenorrhea, absent pubic and axillary hair, a short, blind vaginal pouch and no uterus or cervix
Normal to slightly increased testosterone
Gonadectomy performed at age 16-18.

Front 98

what happens with 5alpha-reductase deficiency. what is inheritance mode. what will internal and external genetalia look like. what is karyotype

Back 98

Familial incomplete male (46XY) pseudohermaphroditism
Autosomal recessive
Severe perineal hypospadias and underdevelopment of the vagina
Masculinization occurs at puberty and breasts remain male. Will need gonadectomy.
Reared as females with an enlarged clitoris if phallus is inadequate.
Early correction of cryptorchidism and hypospadias can preserve fertility and allow male life.
Familial incomplete male (46XY) pseudohermaphroditism
Autosomal recessive
Severe perineal hypospadias and underdevelopment of the vagina
Masculinization occurs at puberty and breasts remain male. Will need gonadectomy.
Reared as females with an enlarged clitoris if phallus is inadequate.
Early correction of cryptorchidism and hypospadias can preserve fertility and allow male life.

Front 99

name two disorders that lead to a 46 XY female or incomplete male karyotype?

Back 99

5alpha-reductase deficiency
androgen insensitivity syndrome (AIS)

Front 100

describe longitudinal vaginal septa

Back 100

Error in lateral fusion, canalization or septum resorption.
May be associated with uterine fusion defects (didelphic uterus) and renal anomalies.
Virtually all patients with hemi-obstruction have renal agenesis ipsilateral to side of obstruction.
Less than 10% of non-obstructed patients will have renal agenesis.
All obstructed septa must be excised.

Front 101

what three hormones are withdrawn with demise of corpus luteum?

Back 101

estrogen, progesterone, inhibin A

Front 102

what two hormones increase during follicular phase

Back 102

progressive
increases in estradiol and inhibin
B associated with follicle selection

Front 103

what is the switch that drives the ovulatory phase

Back 103

LH surge
preceded by rapid rise in estradiol, initiation of progesterone secretion as LH receptors appear in the graunlosa cells

Front 104

how long does the LH surge occur?

Back 104

~48hrs

Front 105

when does ovulation occur relative to the onset of LH surge (give answer in hours)

Back 105

35-44hr

Front 106

in the Luteal phase: what hormone becomes dominant. what happens to theca-granulosa cells. what are inhibin A levels. what is GnRH pulsatility (frequency)

Back 106

Shift to a progesterone dominated phase
Luteinization of the theca-granulosa cells
Inhibin A levels increase in the luteal phase
The demise of the corpus luteum leads to rapid endometrial changes and menses; with hCG the opposite is true
Poor LH support / GnRH pulsatility leads menses

Front 107

what is GnRH pulsatility shift (frequency and amplitude) going from luteal to follicular phase (menstruation)

Back 107

Luteal-follicular transition there is a shift from low-frequency and high amplitude LH pulses to high frequency low amplitude pulses with subsequent rise in FSH

Front 108

what are the effects of estrogen on the endometrium

Back 108

promotes endometrial cell mitosis, stimulates proliferative development

Front 109

what are the effects of progesterone on the endometrium

Back 109

opposes mitosis, stimulates secretory changes

Front 110

what are four ways of getting menstruation

Back 110

Estrogen Breakthrough Bleeding
Estrogen Withdrawal Bleeding
Progestin Breakthrough Bleeding
Progesterone Withdrawal

Front 111

give an example of progesterone withdrawal bleeding

Back 111

normal menstruation. also oral contraceptives

Front 112

give an example of progesterong breakthrough bleeding

Back 112

oral contraceptives

Front 113

give an example of estrogen withdrawal bleeding

Back 113

oophorectomy

Front 114

give an example of estrogen breakthrough bleeding

Back 114

anovulation and poly cystic ovary syndrome.

Front 115

what two hormones does somatostatin inhibit the release of

Back 115

TSH and GH

Front 116

what hormone from hypothalamus stimulates ACTH release from pituitary?

Back 116

CRH

Front 117

what time of day is cortisol secretion natrually the highest

Back 117

morning around 8am

Front 118

how can you test for a patients cortisol response

Back 118

insulin induced hypoglycemia. The body will natrually increase ACTH and thus cortisol to promote gluconeogenesis

can also do a CRH stimulation test, Cortrosyn stimulation test

Front 119

what is the effect of taking exogenous glucocorticoids

Back 119

release of ACTH and CRH is inhibited, so adrenal glands will stop secreting their own glucocorticoids and thus atrophy of adrenal glands will occur

Front 120

what is addisons disease

Back 120

loss of cortisol secretion due to an adrenal disease (autoimmune)

Front 121

describe GH regulation

Back 121

GH acts on all tissues, causing them to release IGF1. 90% of IGF1 comes from the liver. IGF1 inhibits GH release

Front 122

what are IGF1 independent actions of GH

Back 122

Anti-insulin
lipolysis
Ketogenesis
Na/ fluid retention

Front 123

what are IGF1 dependent actions of GH

Back 123

Growth-promoting action
Increased protein synthesis
AA transport
muscle mass
cartilage growth
cell proliferation

Front 124

name three things that decrease GH secretion (non-pathological)

Back 124

age (14%/ decade decline in IGF1 levels)
obesity
meal intake

Front 125

name two things that stimulate GH release (normal activities, not pathology or physiology)

Back 125

sleep and exercise

Front 126

what is the best marker for GH secretion

Back 126

IGF1

Front 127

name some ways you can stimulate GH levels in a clinical setting

Back 127

sleep, exercise, hypoglycemia, arginine

Front 128

name one way you can suppress GH levels in a clinical setting

Back 128

glucose suppreses GH levels

Front 129

what is normal GH secretion profile. Contrast with GH secretion profile of patient with acromegaly

Back 129

normal: GH has high pulses only during sleep
acromegaly: GH is pulsatile at a similar level all the time (pituitary GH secreting tumor)

Front 130

what are some signs of a hyperprolactinemia (clinical presentations, no lab values)

Back 130

hypogonadism
amenorrhea and galactorrhea
infertility

these are caused by inhibited GnRH secretion due to overproduction of dopamine to inhibit high prolactin levels

Front 131

what class of drugs is effective in treating excess prolactin levels

Back 131

dopamine agonists: bromocriptine; pergolide; cabergoline (most effective)

Front 132

what is metyrapone test

Back 132

metyrapone is drug that inhibits enzyme that makes cortisol (11Betahydroxylase). its less common test to stimulate ACTH release

Front 133

what effect does an ACE inhibitor have on aldosterone secretion

Back 133

low aldosterone, high renin

Front 134

what does ACE do

Back 134

converts angiotensin I to angiotensin II

Front 135

what enzyme converts angiotensinogen to angiotensin I

Back 135

renin

Front 136

how does increased ACTH lead to hyperpigmentation

Back 136

increased ACTH means increased ACTH precursors, one of which is involved in hyperpigmentation (MSH)

Front 137

Describe congenital adrenal hyperplasia

Back 137

loss of enzyme function, usually 21hydroxylase function which is involved in cortisol production
neonates cant make aldosterone or cortisol.
in utero they survive on mothers cortisol, but die within a day or two. Body gets rid of stacked up intermediates by converting them to other things (androgens)
as a result, females have ambiguous genetalia and males have large penises

Front 138

describe klienfelters disease

Back 138

genetic disease where a male has an extra X. testes will be scarred and atropic
feeback will go up with respect to gonadotropins

Front 139

what is the usual karyotype for turners syndrome

Back 139

45, X female

Front 140

what is sheehans syndrome

Back 140

ischemic necrosis of pituitary.
FSH and LH are low

Front 141

what are effects of growth hormone deficiency

Back 141

short stature, chubby appearance (since GH promotes lypolysis

short stature would not occur if GH deficiency was encountered AFTER puberty

Front 142

what are lab findings of patients with GH resistance

Back 142

increased GH levels, low IGF1 levels

Front 143

name two ways to treat excessive GH secretion

Back 143

somatostatin administreation to inhibit GH secretion or GH receptor antagonist

Front 144

when is prolactin secretion highest (time of day)

Back 144

at night

Front 145

what cells make prolactin

Back 145

lactotrophs. They get bigger during pregnancy

Front 146

what effect does hypothyroidism have on prolactin secretion

Back 146

prolactin will go up since TRH will elevate (assuming no problem with hypothalamus)

Front 147

what effect might a pituitary tumor have on vision

Back 147

loss of peripheral vision aka bitemporal dypenopsia

Front 148

how do you treat hypogonadism as brought about by hyper prolactinemia

Back 148

GnRH administration will cause body to return to normal state of gonadotropin secretion

Front 149

what would happen to hormone release from pituitary if you cut the pituitary stalk?

Back 149

all hormones would cease to be released except prolactin since the cells want to produce those by themself. when you cut the stalk, you are cutting dopamine, which is negative inhibition for prolactin release

Front 150

what are cellular actions of cortisol

Back 150

Intermediary metabolism: gluconeogenesis
Anti-inflammatory effects
Vascular effects
Maintaining vascular tone
Endothelial integrity
Increased sensitivity to pressors
Reduction of nitric oxide-mediated vasodilatation,
Modulation of angiotensinogen synthesis

Front 151

what are two effects of excess cortisol

Back 151

hyperglycemia and insulin resistaince

Front 152

what two proteins does cortisol bind to in blood

Back 152

transcortin and albumin

Front 153

how can a person be hyperthyroid yet have normal free thyroid hormone

Back 153

they may have upregulation of serum binding proteins. The body adjusts thyroid hormone levels based on free thyroid hormone. If more binding proteins are produced, the body will sense a decrease in free T3 and T4 and produce more to bring free level up to normal

normal free T3 and T4 does not rule out hyperthyroid, in other words

Front 154

what are effects of aldosterone

Back 154

primary: increase sodium levels and decrease potassium levels
secondary: decrease metabolic buffers and increase ammonium secretion

Front 155

what kind of chemicals go from the angiotensin II step to aldosterone secretion

Back 155

non-renin stimulants

Front 156

what enzyme converts cortisol into cortisone. why does it do this?

Back 156

11beta HSD2

this conversion takes place to "pre-receptor inactivate" cortisol so that glucocorticoids dont bind mineralocorticoid receptors in vivo

in vitro, glucocorticoids have some mineralocorticoid activity

Front 157

what is DHEA

Back 157

ACTH-dependant steroid secreted by zona reticularis
DHEA-S: Derived from the sulfation of DHEA
Variable levels (steroid use, age, gender, stress,)
Half-life: 10-20 hrs
Strongly bound to albumin
Does not follow circadian
rhythm
Levels are low in patients with ACTH deficiency or primary adrenal insuffiiency

Front 158

what are 4 short term adaptations to stress and cortisol secretion

Back 158

changes in circulation
increased heart and respiratory rates
mobilization of glucose reserves
increased energy use by all cells

Front 159

What are the two kinds of adrenal insufficiencies and define them

Back 159

Practical/ Traditional definition: Condition whereby there is a partial or complete loss of GC secretion as a result of:

1) Primary adrenal insufficiency (addison's disease): Loss of all 3 adreno-cortical steroids

2) Central adrenal insufficiency: Loss of/ decrease in ACTH secretion: Loss of GC and adrenal androgens

Front 160

what steroids are lost during central adrenal insufficiency

Back 160

ACTH-dependent steroids: glucocorticoids, adrenal androgens

Front 161

what are main causes of central adrenal insufficiency

Back 161

exogenous glucocoricoid and hypothalamic/pituitary disease

Front 162

what are lab findings for central adrenal insufficiency

Back 162

low cortisol, low ACTH, low DHEA, normal aldosterone

can treat dz with hormone replacement therapy

Front 163

what steroids are lost in addisons disease (primary adrenal insufficiency)

Back 163

Insufficient production of ALL steroids by the adrenal cortex:
Glomerulosa: Loss of mineralocorticoids
Fasciculata: Loss of glucocorticoids
Reticularis: Loss of adrenal androgen

often caused by autoimmune disease (80%). Sometimes caused by non-autoimmune infections or other non-autoimmune causes (20%)

Front 164

what are lab findings of person with addisons

Back 164

increased ACTH and PRA, low sodium, high potassium (because of no aldosterone)
anemia, change in WBC differential

Front 165

what are symptoms of addisons

Back 165

postural dizziness, salt craving, low energy level, diurnal variation, nausea, fatigue
low BP, hyperpigmentation, diminished axillary and pubic hair (women)

Front 166

describe cushings syndrome

Back 166

too much cortisol (opposite of addisons, in a way); sustained exposure to glucocorticoids (endogenous vs exogenous)

EXOGENOUS CAUSES:
Taking exogenous glucocorticoids. Iatrogenic cause is doctor giving too much ACTH to treat an ACTH insufficiency

ENDOGENOUS CAUSES:
ACTH-dependent (80-85%): tumor in pituitary (most common) or ectopic ACTH secretion
ACTH-independent (15-20%): adrenal tumors (ademona 65% / carinoma 35%)

Front 167

what are lab findings of cushings syndrome

Back 167

increased Glucocorticoid secretion and serum cortisol

loss of diurnal rhythm

Front 168

what are findings in primary hyperaldosteronism

Back 168

increased aldosterone, not in response to physiologic stimuli

Front 169

what are findings in seconday hyperaldosteroneism

Back 169

high aldosterone in response to physiologic stimuli: increased sodium retention, increased potassium excretion

Front 170

what are some causes of primary hyperaldosteronism

Back 170

adrenal adenoma (conns syndrome)
adrenal hyperplasia
adrenal cortical carcinoma

Front 171

what are lab findings for isolated minaralocorticoid defficiency

Back 171

hyperkalemia (because of low aldosterone)
type IV renal tubular acidosis

usually occurs in setting of mild renal insufficiency especially diabetic nephropathy and gout

Front 172

what is the dexamethasone suppression test

Back 172

administration of dexamethasone (23 times more potent than cortisol) to see if negative feedback is achieved and ACTH and/or cortisol levels are decreased. Used to diagnose and differentiate between forms of cushings syndrome

Front 173

what are main uses of calcium in vivo

Back 173

maintain nerve and muscle function and control cellular activities in virtually all cells
major structural component of body in both bone and extracellular compartments

Front 174

what two hormones regulate (increase) serum calcium

Back 174

parathyroid hormone and 1,25-dihydroxy vitamin D

Front 175

what are sources of vitamin D

Back 175

sunlight (>90%)
dietary intake (<10%)

Front 176

where is vitamin D converted to 25 hydroxy vitamin D and what enzyme is used

Back 176

liver; 25 alpha hydroxylase

Front 177

where is 25 hydroxy vitamin D converted to active 1,25 dihydroxy vitamin D and what enzyme is used

Back 177

kidney; 1 alpha hydroxylase

Front 178

what are two main places where PTH exerts its effects

Back 178

bone and kidneys

Front 179

what are functions of osteoclasts and osteoblasts

Back 179

osteoclasts: break down bown, increase plasma calcium levels
osteoblasts: form bone, decrease plasma calcium levels

Front 180

what is action of PTH on bone

Back 180

mobilizes calcium from skeletal stores
stimulates release of calcium by activation of bone resorption

Front 181

what is action of PTH on kidney

Back 181

increases reabsoprtion of calcium from tubular fluid
increased LOSS of phosphate
stimulates synthesis of active form of vitamin D

Front 182

what is function of 1,25-dihydroxy vitamin D and what are target tissues

Back 182

increases calcium and phosphate absorption in small intestine
increases Ca and P in blood (latter opposes action of PTH on kidney)

Front 183

what is main hormonal regulator of PTH secretion

Back 183

calcium - binds to cell surface receptors and inhibits PTH synthesis

1,25dihydroxy vitamin D also has some inhibition powers on parathyroid

Front 184

where are calcium sensing receptors (CaSR) located

Back 184

surface of parathyroid glands cells
basolateral membrane on cells of thick ascending limb of loop of Henle
in condrocytes, osteoblasts, osteoclast precursors and some osteoclasts

Front 185

what are causes of HYPOcalcemia?

Back 185

increased urinary exretion and bone mineralization.
decreased GI absorption of Ca and bone resorption

Front 186

what are causes of HYPERcalcemia

Back 186

decreased urinary exretion and bone mineralization.
increased GI absorption of Ca and bone resorption

Front 187

what is corrected Calcium level?

Back 187

correct serum calcium measurement taking into account patients serum albumin levels. similar issue as with measuring free vs bound thyroid hormone

Front 188

what are CNS manifestations of hypercalcemia

Back 188

lethargy, depression, slow mentation, confusion, poor memory
sometimes coma and death

Front 189

what are GI manifestations of hypercalcemia

Back 189

Poor Appetite, Nausea, Vomiting
Constipation
Abdominal Pain
Peptic Ulcer Disease
Pancreatitis

Front 190

what are renal manifestations of hypercalcemia

Back 190

Excessive urination, dehydration, thirst
Decreased ability to reabsorb water from tubular fluid
Due to decreased renal response to antidiuretic hormone
Kidney stones
Nephrocalcinosis with renal failure

Front 191

what are musculoskeletal manifestations of hypercalcemia

Back 191

generalized weakness and aching in muscles and joints

Front 192

what happens to EKG of patient with hypercalcemia

Back 192

shortened QT interval

patient will also have diminished reflexes

Front 193

what are two pathological causes of hypercalcemia

Back 193

primary hyperparathyroidism
hypercalcemia due to malignancy

Front 194

what are symptoms of primary hyperparathyroidism

Back 194

Bones, Moans, and Stones:

increased bone resorption, lots of pain and aching, kidney stones and other calcifications form

Front 195

what are two ways malignancies can cause hypercalcemia

Back 195

local osteolytic hypercalcemia: cancer cells metastasize to bone, secrete cytokines that stimulate bone resorption
humoral hypercalcemia of malignancy: cancer cells nowhere near bone can secrete hormone-like substances that stimulate bone resorption. most common is parathyroid hormone related peptide (PTH-rP)

Front 196

what is familial benign hypocalciuric hypercalcemia

Back 196

autosomal dominant disorder where there is mutation of CaSR on renal tubular cells and parathyroid cells

mutation causes increased urinary calcium reabsoprtion (on renal CaSR) and increased PTH secretion on (Parathyroid CaSR)

Front 197

what pathologies cause increased gut absorption of calcium

Back 197

ingestion of excess vitamin D (need to take ALOT to get an excess)
granulomatous disease (TB, fungal infections, sarcoidosis)
lymphomas and leukemias which contain 1alpha hydroxylase, which causes overproduction of 1,25,dihydroxy vitamin D and thus too much calcium absorption in gut

Front 198

what are acute and chronic symptoms of hypocalcemia

Back 198

Acute
Neuromuscular
Cardiac
Psychiatric

Chronic
Dental
Basal ganglia calcification
Cataract

Front 199

what are EKG findings in patient with hypocalcemia

Back 199

lengthened QT interval and increased reflexes.

just remember QT interval is shortened and decreased reflexes with hypercalcemia and that hypocalcemia is opposite

Front 200

what is chvostek sign

Back 200

tapping of facial nerve induces contractoins of facial muscles. Is a sign of hypocalcemia

Front 201

what is trousseaus sign

Back 201

inflation of blood pressure cuff induces carpal spasm. sign of hypocalcemia

Front 202

what are two PTH related causes of hypocalcemia

Back 202

Parathyroid hormone Deficiency --> Hypoparathyroidism
Parathyroid hormone Resistance --> Pseudo-hypoparathyroidism

Front 203

what are two vitamin D related causes of hypocalcemia

Back 203

vitamin D deficiency or resistance

Front 204

what are lab findings in primary hyperparathyroidism

Back 204

high calcium and PTH, low phosphate

Front 205

what are lab findings in vitamin D deficiency

Back 205

low vitamin D, low calcium, high PTH, low phosphate

Front 206

what are lab findings in hypoparathyroidism or renal failure

Back 206

low to high pth, low calcium, high phosphate

Front 207

what are lab findings in hypercalcemia of malignancy

Back 207

low pth, high calcium, high phosphate

remember that if pth is low, phosphate would be expected to be high

Front 208

what is tertiary adrenal insufficiency

Back 208

loss of CRH signal

Front 209

what happens after T3 binds its receptor

Back 209

the dimer (thyroid hormone receptor and retinoid x receptor) binds the thyroid response element (TRE) in the DNA, triggering transcription that ultimately influences the Na-K pump, beta-andregenic receptor tone, gluconeogenic enzymes, respiratory enzymes, myosin heavy chain, and many others.

Front 210

what does thyroid hormone do in general

Back 210

increase basal metabolic rate

Front 211

what does thyroid hormone do in the liver

Back 211

increase hepatic gluconeogenesis and glycogenolysis
increased consumption of oxygen (in part by stimulating Na+-K+ ATPase)
increased turnover of protein and lipids
If pathogenic: increase futile catabolism (building and degrading proteins and lipids, expanding energy but not doing any useful work)

Front 212

what does thyroid hormone do in muscle

Back 212

Increase speed of muscle contraction and
relaxation (increase expression of contractile isoforms of myosin heavy chain). Leads to increased bowel movement and respiration rate
Increases heart rate through following
mechanisms:

1. increase
expression of contractile isoforms of myosin heavy chain = contributes to
enhanced systolic function

2. increase rate of
depolarization and repolarization of sinoatrial node

3. stimulate
transcription of sarcoplasmic reticulum Ca2+ ATPase = increase rate of
myocardial diastolic relaxation

Front 213

what is thyrotoxicosis and how does it happen

Back 213

occurs when there is too much T3/T4 in serum. Leads to high metabolism (loss of weight and muscle wasting) and increased sensitivity of brown fat to catecholamines.

Front 214

what are disorders that cause thyrotoxicosis

Back 214

graves disease (most common) and thyroiditis.
graves disease is autoimmune where an antibody pushes on the TSH receptor in follicular cells causing them to release too much T3/T4
thyroiditis is inflammation that causes transient hyperthyroidism due to release of pre-formed hormone from colloid space.

radioactive scans can be normal but the patient can still be hyperthyroid --> Scans only show what the production rate of T3/T4 is and not the rate of release into blood stream.

in addition, it can be caused by taking exogenous T3/T4

Front 215

what is the frontline therapy for graves disease

Back 215

radioactive iodine to kill parts if not all of the thyroid. Sometimes the dosage is right and patient goes into remission with euthyroid. Often times patients thyroid is completely destroyed and becomes hypothyroid, requiring levothyroxine as hormone replacement therapy

Front 216

what are actions of methimazole and propylthiouracil (PTU)

Back 216

both lower thyroid activity by inhibiting thyroperoxidase, which converts iodide anions to iodine (without this step, iodine can't be added to tyrosine residues) and tetaiodothyronine 5' deiodinase, which converts T4 to T3 (peripheral action of drugs. PTU is usually used in pregnant women. If taken for too long, these drugs can have negative effects on stem cells in bone marrow.

Front 217

what is mechanism of action of levothyroxine

Back 217

Binds to expected serum proteins (thyroxine-binding globulin (TBG), thyroxine-binding prealbumin (TBPA), and albumin (TBA)) for transport
Binds at approx. 99% capacity (strong affinity)
Levothyroxine is broken down into T3 in target tissues just like natural T4

Front 218

what is mechanism of absoption and metabolism of levothyroxin

Back 218

Oral pill taken in prescribed dosage based on patient deficiency
Mainly absorbed through small intestine (jejunum and ileum)
Bioavailability is high (48%-80%)
Compound is cleared the same way as natural T4 (recycled with normal mechanisms through blood circulation)

Front 219

list and describe two laboratory tests for hypothyroidism

Back 219

radioactive iodine uptake: radioactively labeled iodine is ingested. Low levels of iodine uptake is sign of hypothyroidism whereas high levels of uptake suggest hyperthyroidism

TSH levels: high levels of TSH (with symptoms of hypothyroidism) are indicative of a primary thyroid problem...the feedback loop is still functional because the pituitary is trying to activate T3/T4 production by increasing TSH levels. low levels of TSH are indicative of a secondary thyroid problem....the feedback loop is not functional and the reason for low levels of T3/T4 is incorrect stimulation from the pituitary

Front 220

what is anti-TPO?

Back 220

autoimmune antibodies for thyroid peroxidase, which, if found, could lead to diagnosis of hypothyroidism as loss of TPO activity would result in decreased production of thyroid hormone

Front 221

name some (at least 5) signs/symptoms of hypothyroidism

Back 221

listlessness
- slowed movement
- somnolence (drowsiness)/lethargy
- impaired memory
- decreased mental capacity
- decreased metabolic rate and weight gain without increased food intake
- decreased heat production and cold intolerance
- decreased heart rate
- slurred speech
- periorbital puffiness
- constipation → slowed peristalsis
- hair loss
- menstrual dysfunction
- myxedema

Front 222

describe normal pubertal development in male

Back 222

from age 10 to 17 or 18, normal male undergoes these changes:

growth of scrotum & testes
change in voice
lengthening of the penis (Beep. Bob Kelso. 10 Inches.)
growth of pubic hair
growth spurt (lasts from age 11 to 17 according to merck manual; peaks between ages 13 and 15)
change in body shape
growth of facial and underarm hair (usually starts at age 13)

Front 223

what are the actions and target tissues of testosterone (from IQ Case 4 LO 8)

Back 223

androgens affect nearly every tissue in the body:
1.) help determine internal and external genitalia during development
2.) stimulate maturation of external genitalia and accessory organs (penis, scrotum, prostate, and seminal vesicles)
3.) larynx size and length/thickness of vocal cord→ voice changes
4.) facial, axillary and pubic hair growth
5.) temporal hair recession
6.) stimulation of linear body growth and closure of the epiphyseal plates
7.) muscle development

Front 224

identify hormonal interactions which stimulate ovary to synthesize estrogen (from IQ Case 5 LO 7)

Back 224

LH stimulates the theca cells of the ovary to produce androstenedione
FSH stimulates the granulosa cells of the ovary to convert androstenedione into estradiol

Front 225

how does estrogen interact with its target tissues

Back 225

The receptor for estradiol resides in the cell nucleus. The estrogen receptor (ER) functions as a homodimer. The estrogen–estrogen receptor complex interacts with steroid response elements on chromatin and rapidly induces the transcription of specific genes to produce mRNA. The RNA enters the cytoplasm and increases protein synthesis, which modulates numerous cellular functions. Over the next several hours, DNA synthesis increases, and the mitogenic action of estrogens becomes apparent. Estrogens almost exclusively affect particular target sex organs that have the estrogen receptor. These organs include the uterus and the breasts.

Front 226

what are estrogens target tissues and how does it lead to development of secondary sex characteristics in the female (IQ Case 5 LO 5)

Back 226

Breast—Estrogen stimulates growth and differentiation of the ductal epithelium, induces mitotic activity of ductal cylindric cells, and stimulates the growth of connective tissue. The density of estrogen receptors in breast tissue is highest in the follicular phase of the menstrual cycle and falls after ovulation. Estrogen can also indirectly affect mammary gland development by elevating prolactin and progesterone levels and inducing progesterone receptors in mammary epithelium. The growth-promoting effects of estrogen have been implicated in breast and endometrial cancer

Uterus—Estrogen promotes proliferation of the endometrium by stimulating mitosis of the stratum basale and angiogenesis of the stratum functionale. Estrogen sensitizes uterine smooth muscle to the effects of oxytocin by increasing the expression of oxytocin receptors and contractile proteins. Estrogen increases watery cervical mucus production.

Bone— Estrogen promotes bone maturation and closure of epiphysial plates in long bones. During puberty, estrogen is essential for initiation of pubertal growth, closure of the growth plate, and augmentation accrual of bone.

Central nervous system—Estrogen has neuroprotective actions, and its age-associated decline is associated with a decline in cognitive function.