Barker's Lectures For Final Exam

Front 1

What organs does the Thyroid axis consist of?

Back 1

Hypothalamus
Anterior Pituitary
Thyroid gland

Front 2

Thyroid Releasing Hormone target

Back 2

anterior pituitary

Front 3

Thyroxine

Back 3

storage form of T3 and T4

Front 4

T4 conversion to T3

Back 4

In liver and target cells, it is deiodinated

Front 5

TRH is synthesized from where?

Back 5

paraventricular nuclei of the hypothalamus

Front 6

What does the TRH do?

Back 6

induces quick release of TSH from anterior pituitary thyrotrophs

Front 7

Hypothalamic hypothyroidism

Back 7

lack of TRH

Front 8

What thyroidtrophs affect the anterior pituitary?

Back 8

TRH: MOST EFFECTIVE
somatostatin (inhibitory growth hormone)
Dopamine: inhibitory
Cortisol: inhibitory
estrogen: stimulatory

Front 9

TSH secretion

Back 9

episodic and pulsatile, onset of sleep induces secretion

Front 10

TSH structure

Back 10

A glycoprotien: alpha and beta chain
beta chains are what convey specificity of activity of hormone (alphas are somewhat the same)

Front 11

Target of TSH

Back 11

Thyroid glad cells

Front 12

Actions of TSH

Back 12

increases vascular flow
increased the active transport uptake of iodide
increases thyroid cell production of hormones
release t3 and t4

Front 13

Thiocyanates

Back 13

pharmaceutical that slows the iodide pump...incapacitating the formation of T3 and T4

Front 14

Perchlorates

Back 14

drug that competitively inhibits iodide up

Front 15

thyroid peroxidase

Back 15

oxidizes iodide and slows the system

Front 16

What does oxidation of iodide permit?

Back 16

iodination of tyrosine residues of thyroglobulin, a key step in some diseases.

Front 17

Thiouricil

Back 17

prevents binding of iodine to tyrosine residues of thyroglobulin

Front 18

what is important in the activities of tri-iodothyronine (T3) and tetraiodothyronine (T4)

Back 18

The placement of the I groups
rT3= reversed, I in wrong place, biologically inactive T3

Front 19

Where does thyroglobulin move to?

Back 19

follicular lumen

Front 20

what is the majority of the hormone that is secreted by the thyroid?

Back 20

T4 (T3 is secreted in very small amounts)

Front 21

What protien is T3 bound to?

Back 21

T3TBG (thyroid binding globulin)

Front 22

What proteins do T4 bind to?

Back 22

60% T4TBG
30% T4TBPA (precursor to TBG)
10% lossely to albumin

Front 23

What can cause a thyroid imbalance due to T4's protien binding

Back 23

albuminuria

Front 24

where is there the formation of monoiodo and diiodothyronines?

Back 24

follicular lumen

Front 25

What are the effects of T3 and T4 release?

Back 25

Calorigenesis
alertness, anxiousness
increases catecholamine receptors on heart- increases HR and force of contractibility
increases vigor of respiration
increases hematopoeisis

Front 26

What is the connection between T3 and vitamine A

Back 26

T3 is necessary to convert carotine to vitamine A to retinene

Front 27

Why is there yellow skin in hypothyroidism

Back 27

because serum carotene increases since it's not converted to Vitamin A
The Sclera stays white!

Front 28

What hormones does T3 and T4 potentate (support) ?

Back 28

insulin- increase in anabolic activity
catecholamines: increase in glycogenolysis with resultant hyperglycemia

Front 29

What happens when there is no T3 to the retina?

Back 29

There is no retinal pigment due to no retinene

Front 30

Thyrotoxicosis

Back 30

structural and functional alterations in tissues due to extensive hyerthyroidism

Front 31

Graves Disease

Back 31

most common type of hyperthyroidism
thyroid gland is uniformly enlarged
exophthalmus ocurs in about 50% of patients

Front 32

Thyroid storm

Back 32

accelerated hyperthyroidism due to surgery, myocardial infarction, or drugs

Front 33

Difference between thyroid storm and pheochromocytoma?

Back 33

symptoms of thyroid storm lasts for days

Front 34

Signs and Symptoms of Hypothyroidism

Back 34

slow growth, mental retardation in children
slowing down of metabolic activities, coarse features due to deposition of GAGs, edema in face and tongue.

Front 35

Treatment of Hypothyroidism

Back 35

Synthroid

Front 36

Activities of ionized calcium

Back 36

proper coagulation
stabilization of membranes
intercellular adhesion
muscle contraction
neurotransmitter transmitter
maintenance of teeth and bones

Front 37

Two pools in skeletal storage?

Back 37

Stable pool
Labile pool

Front 38

Stable pool

Back 38

where most of the calcium in the skeletal storage is found
Mature bone storage

Front 39

Labile Pool

Back 39

young, newly formed bone, about 1% of skeletal storage
constantly being remodled
readily exchangeable to supplement ECT Ca++

Front 40

Calcium concentration in ECF norms

Back 40

8.5-10.5 mg/dL

Front 41

Three dietary Ca++ intake forms- circulating ECF Ca++ (about 1% of total Ca)

Back 41

1. Ionized fraction (46%)
2. Protein bound fraction (46%)
3. Complexed Fraction (8%)

Front 42

Ionized fraction of Ca++

Back 42

only biologically active form of Ca
46% of the 1% (ECF) of Ca++ in body

Front 43

Protein Bound Fraction of Ca++

Back 43

biologically inert but readily available
bound to albumin and to some extent globulin
46% of the 1%

Front 44

If albumin is low, how does this affect Ca?

Back 44

The protein bound fraction of Ca++ will be decreased thus if there is hypokalcemia, must look at albumin levels.

Front 45

Complexed fraction of Ca++

Back 45

finite reserve
complexed to organic and inorganic acids
about 8% of ECF Ca
insignificant except for in disease

Front 46

Diffusible Fraction

Back 46

sum of ionized and complexed fractions of Ca++
This Ca can get into the cell

Front 47

Non Diffusible Fraction

Back 47

the protein bound fraction that cannot get into the cell and stays in bloodstream.

Front 48

Three Calcitropic Hormones

Back 48

1. Vitamin D3
2. Parathyroid Hormone (PTH)
3. Calcitonin

Front 49

Vitamin D2

Back 49

ingested in milk
not biological active form
precursor in skin to Vitamin D3

Front 50

Vitamin D3

Back 50

Activated by sun from D2.

Front 51

First step in Activation of Vitamin D

Back 51

Liver: hydroxylation of D3 to 25-OH vit D (CALCIDIOL)

Front 52

Second step in activation of Vitamin D

Back 52

Kidney: hydroxylation of calcidiol to 1,25-dihydroxy vit D or CALCITROL

Front 53

What stimulates the hydroxylation of calcidiol in the kidney?

Back 53

Parathyroid Hormone (PTH)
Insulin Growth Factor 1

Front 54

What inhibits the hydroxylation of calcidiol in the kidney?

Back 54

fibroblast derived growth factor 23
high blood levels of calcium and phosphate

Front 55

What are the target cells that absorb Ca?

Back 55

small intestines

Front 56

Actions of active Vitamin D3

Back 56

increases uptake of calcium in gut
alters bone reabsorption rate

Front 57

Source of PTH?

Back 57

Chief cells of the parathyroid gland

Front 58

Stimulus for the release of PTH?

Back 58

decreased plasma calcium levels

Front 59

What are the two receptors for PTH?

Back 59

1. PTH1
2. PTH2

Front 60

What does PTH1 receptor recognize?

Back 60

PTH and PTHrP (PTH related protien)

Front 61

Which receptor ONLY recognizes PTH?

Back 61

PTH2 receptor

Front 62

PTHrP

Back 62

PTH related protein
needed for mineralization of chondrocytes and development of mammary glands, skin and hair follicles

Front 63

What is produced in abundance in malignant tumors? (particularly alarming in mammograms)

Back 63

PRHrP: if there are Ca deposits seen in mammograms, signifies malignancy

Front 64

Actions of PTH

Back 64

Increase ECF Ca++ by:
1. Increases bone reabsorption
2. increases reabsorption of Ca out of the kidney (instead of eliminating it in urine)
3. facilitates kidney hydroxylation of Vitamin D

Front 65

Calcitonin

Back 65

Opposes PTH:
1.Decreases osteoclastic activity
2. increases the laying down of bony matrix

Front 66

Osteoclasts

Back 66

a type of bone cell that removes bone tissue by removing its mineralized matrix and breaking up the organic bone

Front 67

Hyperparathyroidism: major two characterizations

Back 67

hypercalcemia and hypophosphatemia

Front 68

Etiologies of Primary Hyperthyroidism

Back 68

1. unresolved
2. genetic link: MEN1 and MEN2
3. Adenomas
4.hyperplasia
5. Carcinomas

Front 69

Does the severity of hypercalcemia parallel the degree of parathyroid tissue involvement?

Back 69

yes

Front 70

Kidney manifestation from Hyperparathyroidism

Back 70

1. Nephrolithiasis: tendancy towards kidney stones
2. Pyelonephritis: inflammation of renal tubules. Leads to water loss and dehydration (polydipsia and polyuria)

Front 71

Skeletal manifestations of Hyperparathyroidism

Back 71

gross demineralizatin
atraumatic fractures
deep bone pain
joint pain

Front 72

Neuropyschiatric manifestations of hyperparathyroidism

Back 72

mental fatigability
emotional lability
irritability

Front 73

GI manifestations of hyperparathyroidism

Back 73

anorexia
nausea
vomiting
weight loss

Front 74

Cardiovascular manifestations of Hyperparathyroidism

Back 74

severe hypertension: laying down of Ca++ in blood vessels

Front 75

Ocular Manifestations of Hyperparathyroidism

Back 75

Distiguishes disease from others:
1. Band/Limbus keratopathy: Ca deposits around cornea

Front 76

What must you rule out to get Hyperparathyroidism?

Back 76

Vit D intoxication
Sarcoidosis
Multiple Myeloma
Metastatic or Primary Carcinomas
Thyrotoxicosis

All of these present increased serum Ca

Front 77

Differential Diagnosis of Hyperparathyroidism:
POLYDIPSIA and POLYURIA

Back 77

Diabetes

Front 78

Differential Diagnosis of Hyperparathyroidism:
Demineralization, emotional lability, elevated blood pressure

Back 78

Cushings Disease (hyper-corticolism)

Front 79

Differential Diagnosis of Hyperparathyroidism:
Anorexia, nausea, vomiting, weight loss

Back 79

Addisons (hypocorticolism, decrease in cortisol)

Front 80

Differential Diagnosis of Hyperparathyroidism:
long standing hypercalcemia

Back 80

Graves disease due to long term thyrotoxicosis

Front 81

Calcium levels in serum in Hypoparathyroidism

Back 81

less than 7mg/dL

Front 82

What does Hypoparathyroidism sometimes coexist with?

Back 82

Addison's disease

Front 83

Systemic signs of Hypoparathyroidism

Back 83

Tetany
Trousseaus sign
Chovstek's sign
Hyperreflexia
prolonged QT interval

Front 84

Ocular manifestation of Hypoparathyroidism

Back 84

PSC

Front 85

Vitamin D deficiency

Back 85

Rickets in children, osteomalacia in adults.
Decreased absorption of Calcium due to decreased Vitamin D

Front 86

Osteoporosis- signs

Back 86

rounding of the back and difficulty moving

Front 87

Causes of osteoporosis

Back 87

Decreased estrogen in females, not enough calcium ingested early in life
usually runs in families

Front 88

Somatomedins

Back 88

Growth factors
promote or facilitate growth and repair
IGF-1 and IGF-2

Front 89

Growth Hormones

Back 89

hormone that promotes linear growth

Front 90

IGF-1

Back 90

Somatomedin
mediates effects of growth hormones

Front 91

What is IGF-1 structurally similar to?

Back 91

Proinsulin/insulin (tertiary structure)
receptor characteristics similar to insulin receptor
considerable overlap in cellular reactions to both ligands

Front 92

How does IGF-1 circulate in plasma?

Back 92

As a complex with IGFBP-3 (binding protien) that extend the 1/2 life of IGF-1 and modulates action

Front 93

What is the first step in diagnosing a growth failure, test-wise?

Back 93

Measuring IGPFB-3 and IGF-1 since GH testing is expensive.

Front 94

What is a critical determinant of growth?

Back 94

locally produced IGF-1

Front 95

How are IGF-1 Receptor and the insulin receptor correlated?

Back 95

both are stimulated by the same stimulus for up and down regulation. (If there is a deficiency in one, there will be a deficiency in the other).

Front 96

What receptor is IGF-II similar to?

Back 96

mannose 6 phosphate receptor

Front 97

Which receptors can IGF-II bind to?

Back 97

IGF-II receptor, IGF-1 receptor, insulin receptor

Front 98

Where is IGF-1 and IGF-II synthesized primarily?

Back 98

Liver, but also in other tissues where it has paracrine function

Front 99

What controls IGF-1 synthesis?

Back 99

Growth Hormone
Insulin
Progesterone

Front 100

is IGF-II synthesis dependent on growth hormone?

Back 100

no, regulation unknown

Front 101

Effects of IGF-I:
Muscle and metabolism

Back 101

stimulates RNA/DNA synthesis for production of cartilage and preteoglycans
in muscle, equivalent to insulin to promote protien synthesis

Front 102

Effects of IGF-I:
adipose tissue

Back 102

acts like insulin to increase triglyceride and glucose uptake

Front 103

Effects of IGF-I:
cells

Back 103

inhibits cell death
induces differentiation
facilitate immune cell regulation
mitogenic responses

Front 104

Effects of IGF-I:
Systemic/Organismal effects

Back 104

Human longevity
wide distribution of IGF-I receptors throughout body

Front 105

Effects of IGF-I:
Brain aging

Back 105

sustains neuron health
contributes to B-amyloid clearance

Front 106

Effects of IGF-II

Back 106

Key regulatory of pluripotent human embryonic stem cells
important in early gestation

Front 107

What is secreted by the hypothalamus in the somatotropin axis?

Back 107

GHRH: Somatoliberin
GHIF: Somatostatin

Front 108

Somatoliberin, where is it secreted from?

Back 108

GHRH
Growth Hormon Releasing hormone secreted from the arcuate nucleus of hypothalamus

Front 109

What is the half life of somatoliberin?

Back 109

50 minutes

Front 110

Somatostatin, where is it secreted from?

Back 110

GHIF
Growth Homrone Inhibitory Factor
secreted from the paraventricular area of hypothalamus
also from various areas of the brain and pancreas and areas of GI tract

Front 111

Target of somatotrophs?

Back 111

Anterior Pituitary

Front 112

What does the anterior pituitary secrete in the somatotrophin axis?

Back 112

Growth Hormone

Front 113

What is the secretion of GH like?

Back 113

Pulsatile and episodic
Peak is 1-4 hours after onset of sleep
circulates 20-50 minutes

Front 114

What are the insulin-like features of GH?

Back 114

Increases chondrogenesis
increases skeletal growth
increases cell proliferation

Front 115

What are anti-insulin features of GH?

Back 115

Increases lipolysis in adipose tissue
increase beta oxidation which is ketogenic

Front 116

Influence of GH on carbohydrates

Back 116

increases gylcogenolysis
increases plasma glucose
increases receptor resistance to glucose entry (hyperglycemia)

Front 117

Why is it most difficult to manage diabetics at adolescence?

Back 117

They have twice as much growth hormone which increases the chances of ketoacidosis
both insulin deprived and has an increase in growth factor

Front 118

What hormone causes the close of epipheseal plates?

Back 118

Estrogen

Front 119

Facilitory homrones for Linear Growth

Back 119

GH
IGF-1
Insulin
T3 and T4
Androgens

Front 120

Inhibitory hormones for Linear Growth

Back 120

Estrogens
Glucocorticoids

Front 121

Alcohol's effect on IGF-1

Back 121

long term use: inhibits production in liver
short term use: alters the function in brain, suppressing release of hormones involved in onset of puberty

Front 122

Dwarfism

Back 122

height that is less than 2 standard deviations from the mean

Front 123

Gigantism

Back 123

height greater than 2 SD from the mean that occurs before the closing of epiphyses of long bones

Front 124

Acromegaly

Back 124

growth that occurs after the closure of epiphyses so girth increases
Elevated IGF-I levels and excess GH levels
occurs secondary to PITUITARY ADENOMA or HYPERPLASIA

Front 125

signs of Acromegaly

Back 125

enlarged hands, feet, coarsening of facial features, sweating, oily skin, fatigue, weight gain
Diabetics 25% of the time
Hyperinsulemia
Goiters
HTN, cariomegaly

Front 126

With any visual field defect, what must you rule out?

Back 126

Pituitary adenoma!!!! *****

Front 127

What is the most common type of pituitary adenoma?

Back 127

Prolactinoma (60%)
milky secretion from the nipples of both males and females

Front 128

Differential diagnosis for pituitary adenoma?

Back 128

Cushings Disease- there may be an excess of corticotrophs and ACTH

Front 129

Ocular signs and symptoms of Pituitary adenoma

Back 129

Headache
Bilateral Hemianopsia
Papilledema
chromatopsias (some loss of color vision)

Front 130

Cushings Syndrome

Back 130

excess Cortisol due to Pituitary tumor, adrenal tumor, or non-axial carcinoma

Front 131

Clinical manifestations of Cushings Syndrome

Back 131

hyperglycemia (cortisol excess)
moon face, buffalo hump
thin limbs
HTN with L ventrical hypertrophy
hyperpigmentation

Front 132

Increase Cortisol WITH increase ACTH

Back 132

Cushings Syndrome due to Pituitary tumor

Front 133

Increased Cortisol WITH OUT increase of ACTH

Back 133

Cushings due to adrenal tumor

Front 134

20-hydroxylase deficiency

Back 134

all corticosteroid production is affected due to deficiency in mobilization of cholesterol

Front 135

3-beta-hydroxysteroid deficiency

Back 135

decreases in cortisol, aldosterone, androgens due to no conversion of pregnenolone to progesterone

Front 136

17-alpha-hydroxylase deficiency

Back 136

increase of corticosterone (HTN), decrease in aldosterone and cortisol and androgens. Children remain infantile

Front 137

21-hydroxylase deficiency

Back 137

MOST COMMON CAUSE
decrease cortisol and aldosterone, increase of 18-OH corticosterone and androgens

Front 138

11-beta-hydroxylase deficiency

Back 138

decrease in cortisol, increase in HTN, Virilization, 11-deoxycorticosterone

Front 139

Addisons Disease

Back 139

Hypocorticolism due to adrenal failure
Decrease in cortisol, aldosterone

Front 140

Presentation of Addison's Disease

Back 140

urninary loss of Na: hypovolemia, hypotension
vomiting and diarrhea
increase BUN
Abdominal pain
weakness and weight loss
skin pigmentation: VITILIGO
hypoglycemia

Front 141

Hyperpigmentation due to Primary Addison's disease

Back 141

melanocyte-stimulating hormone (MSH) and adrenocorticotropic hormone (ACTH) share the same precursor molecule, Pro-opiomelanocortin (POMC). After production in anterior pituitary gland, POMC gets cleaved into Gamma-MSH, ACTH and Beta-lipotropin. The subunit ACTH undergoes further cleavage to produce Alpha-MSH, the most important MSH for skin pigmentation. In secondary and tertiary forms of Addison's, skin darkening does not occur.

Front 142

Primary Aldosteronism

Back 142

excessive production of aldosterone due to adrenal hyperplasia, adenoma or carcinoma

Front 143

Major signs of Aldosteronism

Back 143

Hypertension
Hypokalemia
Metabolic Alkalosis

Front 144

other signs of Aldosteronism

Back 144

Chovsteks sign
Trousseaus sign
frontal headache
muscle weakness
nocturia
polydipsia and polyuria

Front 145

Pathogenesis for Metabolic Alkalosis in primary aldosteronism

Back 145

1. excessive K secretion in exchange for Na+ reabsorption, K seen in urine
2. H moves intracellularly to comensate loss of K

Front 146

Secondary aldosteronism

Back 146

due to reduced renal flow, excessive renin production, or estrogen therapy

Front 147

Signs of Secondary Aldosteronism

Back 147

essential and malignant HTN, retinopathy

Front 148

Pheochromocytoma

Back 148

Adenomic tumor in which the size DOES NOT correlate with the severity.

Front 149

Characterizations of Pheochromocytoma

Back 149

HTN in paroxysms, postural fall
flushing of face
pounding headaches
lasts about 15 minutes
intermittent hyperglycemia (200-325)

Front 150

Normal Fasting Blood Glucose

Back 150

less than 100 mg/dL

Front 151

Impaired glucose tolerance

Back 151

100-126 mg/dL

Front 152

Hyperglycemia

Back 152

>126 mg/dL
need further testing

Front 153

Normal Hemoglobin A1C results

Back 153

3.5-5.6%

Front 154

Characteristics of Type I Diabetes Melitus

Back 154

severe hyperglycemia
tendancy towards ketoacidosis
renal involvement
neovascularization of retina

Front 155

Genetics of Diabetes Melitus

Back 155

HLA antigens: HLA-DQw2/8
highest incidence in Scandonavia and sardinia

Front 156

Markers for distruction of Pancreas in DM

Back 156

T cells mediate the destruction of beta cells in pancreas, antibodies are markers

Front 157

hyperglycemia
moon face
buffalo hump
HTN
Skin hyperpigmentation

Back 157

Cushings Syndrome (hypercortisolism)

Front 158

thin with muscle weakness
hyponatremia (loss of salt)
hypotension
increased BUN
vomitting and diarrhea dehydration
hypoglycemia

Back 158

Addison's Disease (hypocortisolism)

Front 159

severe frontal headache
muscle weakness
nocturia and polydipsia and polyurea
HTN
hypokalemia
metabolic acidosis
Chovstek's sign
Trousseau's sign

Back 159

Primary Aldosteronism (ecess aldosterone)

Front 160

HTN
Retinopathy
malignant HTN

Back 160

Secondary Aldosteronism (could be due to oral contraceptives)

Front 161

Paroxysms of HTN
Overwhelming feeling of foom
Palpitations
flushing
hyperglycemia (can be intermittent)
all episodes last about 15 minutes

Back 161

Pheochromocytoma

Front 162

o Background retinopathy – dot hemorrhage in middle layer of retina
o Proliferative retinopathy
o Vitreous hemorrhage
o Retinal detachments

Back 162

Type 1 DM

Front 163

• cardiovascular disease
• hypertension
• adult onset diabetes
• obesity
• stroke

Back 163

CHOAS

Front 164

• Hyperglycemia
• Hyperinsulinemia
• Dyslipidemia
• hypertension

Back 164

Syndrome X

Front 165

o goiter
o eye problems – dryness, difficulty in blinking
o exophthalmus – eye protrudes out of orbit
o dermatological problems – dry, scaly, red skin in lower leg area – called myxedema – a characteristic sign
o tend to tremor and feel tired

Back 165

Grave's Disease- diffuse toxic goiter due to hyperthyroidism

Front 166

Levothyroxine

Back 166

Pure synthetic T4 that is converted to T3 in the body
Drug of choice for long term
Oral

Front 167

Liothyronine

Back 167

Pure synthetic T3
Short half life so drug of choice for HYPOTHYROID CRISIS

Front 168

Thyroglobulin

Back 168

Peripheral extract of pig thyroid...allergy issues

Front 169

Thyroid

Back 169

natural preparation of pig or cow thyroid glands for T3 and T4
not drug of choice

Front 170

Loitrix

Back 170

Combo of T3 and T4, not drug of choice

Front 171

Propylthiouracil

Back 171

inhibits conversion of T4 to T3, antioxidant drug that interferes with the organification of Iodine salts

Front 172

Methimazole

Back 172

antioxidant drug that interferes with the organification of iodine salts
antithyroid

Front 173

Adverse effects of anti-thyroid drugs

Back 173

Agranulocytosis: failure of the bone marrow to make enough
white blood cells (neutrophils).

Front 174

Lugol's solution

Back 174

Iodine solution given in large doses to treat hyperthyroidism
Inhibits release of thyroid hormone

Front 175

Paresthesias of the extremities
tetany
laryngospasms
increased neuromuscular excitibility
convulsions
hypocalcemia

Back 175

Hypoparathyroidism

Front 176

Muscle weakness
life threatening cardiac arrhythmia
soft tissue calcification
constipation
nausea
hypercalciuria (renal)

Back 176

hyperparathyroidism

Front 177

Calcintonin used for treatment

Back 177

Hyperparathyroidism
idopathic hypercalcium
vit D intoxity
osteoclastic bone metastases

Front 178

Paget's disease

Back 178

bones become vascularized and weakened- can use calcitonin as treatment

Front 179

Fosamax

Back 179

oral bisphosphonate used in prevention of osteoporosis

Front 180

Aredia

Back 180

IV administered bisphosphonate used for hypercalcemia of malignancy

Front 181

Bisphosphonates

Back 181

Drug that inhibit the digestion of bone by osteoclasts

Front 182

Why do Androgenic Drugs need to be modified?

Back 182

Testosterone given by injection is too quickly absorbed, metabolized and excreted and given orally is ineffective due to first pass metabolism in liver

Front 183

What chemical modification is made to testosterone?

Back 183

Esterification of 17-beta-hydroxyl group with carboxylic acids

Alkylation at 17-alpha position for oral administration

Front 184

What type androgenic drug is given intramuscilarly and what does the lipid solubility correlate with?

Back 184

Testosterone Esters

the length of the carbon chain

Front 185

Methenolone Acetate

Back 185

C-1 methyl group oral testosterone ester

Front 186

Testosterone undecanoate

Back 186

abosrbed via the lymphatic circulation
oral testosterone ester

Front 187

C17 Alkylated Testosterone Derivatives

Back 187

All orally active

Front 188

Testosterone Cypionate
Testosterone Enanthate
Testosterone Propionate
Methyltestosterone

Back 188

1:1 Androgenic:anabolic activity

Front 189

Fluoxymestrone
Oxymetholone
Ethylesternol
Oxyandrolone*
Nandrolone
stanozolol

Back 189

more than 1:1 androgenic: anabolic activity

Front 190

Dihydrotestosterone

Back 190

what testosterone can be converted to in some tissues
binds to androgen receptor protein 10x more tightly than testosterone

Front 191

Endogenous Anti-androgens

Back 191

Estrogen
progesterone
norprogesterone

Front 192

GnRH Antagonists

Back 192

Androgen synthesis inhibitors
inhibits LH release (luteinizing hormone that causes making of testosterone)

Front 193

GnRH agonist

Back 193

androgen synthesis inhibitor
inhibits LH release due to receptor downregulation

Front 194

Spironolactone
Ketoconazole
Liarozole

Back 194

Inhibits cytochrome P450 enzymes involved in steroid biosynthesis (Androgen synthesis inhibitor)