Endocrine Flashcards

1
Q

Thyroid Stimulating Hormone

A

Tyrotrope cell

Stimalation of Thyroid hormones and growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Follicle Stimulating Hormone

A

Gonadotrope cell
ovarian follicle growth in female
Spermatogenesis in male

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Luitenizing Hormone

A

Ovulation in female
Testosterone in male
Gonadotrope cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Human Grown Hormone (HGH, Somatotropin

A

Somatotrope cell
Body growth
Inhibit insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Prolactin

A

Lactotrope
Milk secretion
Maternal behavior
Inhibition of ovulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Adrenocorticotrophic hormone ( ACTH)

A

Cortiocotrope
Adrenal cortex secretion
Growth
Steroid production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Beta Lipotropin

A

Corticotrope

Precursor of endorphin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Oxytocin - Posterior

A

Paraventricular nuclei
Ejection of milk
Uterine contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Arginine Vassopressin-posterior

A

Supraoptic Nuclei
Water retention
Plasma Osmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Most abundant anterior pituitary hormone

A

Growth Hormone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HGH specific effect is

A

Stimulation of Linear bone growth through the epiphyseal cartilage plate of long bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acromegaly vs Gigantism

A

Acromegaly: Excess GH after epiphyseal closes— bone thicker not longer
Gigantism : Excess GH before epiphyseal plate closes . Long bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Growth Hormone Metabolic effects

A

Anabolic: Increase synthesis of protein
Ketogenic: increased mobilization of fatty acid
Diabetogenic: inhibits insulin secretion
Na+ and H2O retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What stimulates GH?

A
Hypoglycemia
Fasting
Estrogen 
GH- releasing Hormone 
Sleep
Decreased Free Fatty Acid 
Increased Amino Acid
Stress 
Alpha - adrenergic 
Dopamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What inhibits growth hormone

A

Insulin like growth factor 1
Cortisol- large doses of corticosteroids
Obesity
Pregnancy
Hyperglycemia
Free Fatty acid increase
Growth- Hormone inhibiting hormone ( Somatostatin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What inhibits release of prolactin

A

Dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What increases prolactin

A

Preop anxiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

2 things decrease the secretion of TSH

A

Corticosteroid

SNS stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is TSH released?

A

Proteolysis of thyroglobulin in follicles of thyroid cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is T3 produced? Triiodothyronine.

A

Direct metabolism of tyrosine yields T3 ( it is 5 times more active than T4)
Conversion of T4 in the peripheral tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is T4 produced ? Thyroxine

A

Prohormone synthesized by Thyroxine , is 80% of the thyroid hormone in circulation . It serves as prohormone to T3

22
Q

1/2 life T3- T4

A

T3: 1.5 days
T4: 7 days

23
Q

Thyroid and O2 consumption

A

Thyroid hormone increased O2 requirement in all tissue except brain = Minimal changes in MAC requirement for patient with hyper or hypothyroidism
Excess= tissue O2 consumption increased by 100%
Absent= tissue O2 consumption decrease by 40%

24
Q

Thyroid secretes

A

T3
T4
Calcitonin

25
Q

Earliest sign of thyroid hormone abnormality

A

Cardiac changes

26
Q

Thyroid hormone most effect through

A

Control of protein synthesis.activated DNA transcription in the cell nuclei = new proteins and enzymes

27
Q

Cardiac cholinergic receptor numbers and thyroid

A

They are decreased = not enough inhibitory cholinergics in heart = high HR compared to increase in CO

28
Q

Thyroid hormone modulates what adrenergic receptors

A

Al;pha and Beta

29
Q

How does thyroid increase CO?

A

Accelaration of metabolism = tissues (not veins) vasodilate= more blood available in the vessels = increased CO but : SBP does not go up bc peripheral vasodilation offset that ( less SVR)

30
Q

PTH inversely related to

A

ionized calcium concentration

31
Q

PTH and calcium

A

Stimulates release of calcium from bone ( Osteoclasts) ( Bone )
Converts Vit D to active 1,25,Dihydroxicholecalciferol to increase absorb of ca in GI (GI)
Prevents reabsorption of phosphate in renal to increase ca and decrease Phosphate( renal tubule)

32
Q

Cholesterol is precursor of …

A

Corticosteroids

33
Q

What can cause Diabetes . Table 38-2

A

Type 1+ absolute deficiency destroyed pancreatic B cells
Type2- Insulin resistance and deficiency
Exogenous pancreas disease: hemochromatosis, cystic fibrosis, pancreatitis, pancreatectomy
Gestational
Drug induced: Thiazides, glucocorticoid, thyroid hormone, Beta adrenergic
Endocrinopathy: acromegaly, Cushing syndrome
Defect of pancreatic B cells
Defect of insulin action- resistance
Infection : congenital rubella, CMV
Uncommon immune mediated diabetes : Stiff man syndrome , anti-insulin receptor antibody

34
Q

Hyperglycemia cause

A

Impaired vasodilation

Chronic pro inflammatory, prothrombogenic, proartherogenic , = vascular

35
Q

IV insulin 1/2 time

A

5- 10 minutes

36
Q

Insulin metabolized by

A

Kidney and Liver by proteolytic enzyme

37
Q

Insulin goes to liver how?

A

50% goes to liver via the portal vein

38
Q

Which affects insulin clearance rate more ?

A

Renal more than liver

39
Q

Type 2 Diabetes

A

Oral before Insulin

Pancreatic beta cell dysfunction or auto antibody have developed

40
Q

Primary Failure of Sulfonylurea

A

20% of patients started on it do not have adequate hypoglycemic to max dose .,

41
Q

Secondary Failure of Sufonulurea

A

Initially responded but then failed to respond

42
Q

Effects of ETOH and salicylates on BG

A

Decreases = with sulfonylureas hypoglycemia worse !!!

43
Q

What meds patient sulfonylureas

A

Warfarin and Sulfonamide

44
Q

Risk factors for sulfonylurea hypoglycemia

A

Poor nutrition
>60 y.o.
Warfarin and sulfa abx- potentiate sulfonylurea
Salicylate and ETOH - decrease BG
Impaired renal function - can’t eliminate

45
Q

Excretion of Glyburide

A

50% in feces

46
Q

The 2 sulfonylurea most likely to cause low BG

A

Glyburide - long 1/2 time 4.6- 12 hrs- 18/24hrs duration

Chlorpropamide - longest 1/2 time- 30/36 hrs - 36 hrs duration

47
Q

Which sulfonylurea favorable for renal pts?

A

Glypizide - feces and only small unchanged in kidney

Torbutamide- only small unchanged in kidney

48
Q

How does sulfonylurea affect ischemic preconditioning ?

A

By closing K-ATP channels. Increase CV mortality with sulfonylurea

49
Q

Sulfonylurea and placenta

A

Crosses= fetal hypoglycemia

50
Q

Sulfonylurea with lowest elimination 1/2 life

A

Acetoheximibe : 1.3 to 6 hrs

51
Q

Which sulfonylurea can you give with liver dysfunction

A

Acetoheximibe, bs lower 1/2 life, less prolonged elimination in liver patients = less chances of hypoglycemia