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FALL 2022 > PHCL Exam 2 > Flashcards

PHCL Exam 2 Flashcards

1
Q

The Hypothalamic-Pituitary-Adrenal (HPA) Axis

A

is one mechanism our body uses to respond to stress (fight or flight response).
Stress -> Hippocampus-> Hypothalamus-> (Vasopressin, CRF)-> Pituitary-> to the blood-> (ACTH) Adrenal Cortex-> Cortisol

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2
Q

Cortisol can feed back to the

A

pituitary and hypothalamus to reduce further stimulation of the system (feedback inhibition)

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3
Q

Where is aldosterone made

A

in the zona glomerulosa

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4
Q

where are cortisol and androgens made?

A

zona fasciculata/zona reticularis`

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5
Q

where is epinephrine and norepinephrine made ?

A

in the adrenal medulla

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6
Q

Maastricht acute stress test

A

(hand in cold water and mental arithmetic)
men tended to release cortisol
faster and with a higher peak than women during this test.

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7
Q

Where are CYP11B1 and CYP17 expressed in the adrenal gland?

A

since they are enzymes for Cortisol in the ZF/ZR

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8
Q

diurnal cycle of serum glucocorticoids

A

: lowest in the middle of the night, but peaks in the morning – probably helps with waking.
No average difference between girls and boys, age, puberty, etc., but a lot of variance in the individual levels of glucocorticoids

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9
Q

Stress increases glucocorticoid release into blood

A

which typically is quickly resolved. But inappropriate
stress responses can result in too much/too long, or weak HPA axis response.

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10
Q

Corticosteroids

A

regulate energy metabolism, increase short-term memory (good for learning/tests!), maintain bp, inhibit inflammation, help with fetal lung development

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11
Q

Corticosteroid deficiency

A

Addison’s disease. Causes low blood sugar, low bp, weakness, muscle/joint pain, skin darkening or vitiligo,
salt craving (reduced salt, increased potassium) nausea/diarrhea, depression. These can be very dangerous if not controlled.

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12
Q

Corticosteroid overload

A

Cushing’s Syndrome. Skin thinning, depression/mood swings, memory loss/learning disability,
muscle wasting, poor wound healing/suppressed immune system, hypertension, diabetes, osteoporosis, anovulation

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13
Q

clinical causes for Addison’s disease

A

autoimmunity
Darkening of skin
Low blood sugar
Salt craving

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14
Q

clinical causes for Cushing’s syndrome.

A

Skin thinning
Diabetes
Delayed wound healing
Suppressed immune
response
Hypertension

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15
Q

Cortisone

A

isolated in the 1940s and used for rheumatoid arthritis for the first time in 1948 – quickly became a widely used drug.

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16
Q

Discussed multiple therapeutic uses of corticosteroids

A
  • Energy metabolism
  • stimulate gluconeogenesis (making glucose from non-
    carbohydrate sources)
  • inhibit glucose uptake by muscle or adipose tissue
  • increase protein and lipid catabolism
  • increase serum glucose levels
  • Increase short term memory
  • Maintaining vascular tone
  • Inhibit pro-inflammatory cytokines
  • Fetal and neonatal lung development
  • Inhibition of ACTH release by the anterior pituitary
    (feedback regulation)
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17
Q

Discussed therapeutic vs adverse effects of glucocorticoid use. Dose and length of treatment are important.

A

therapeutic:
anti-inflammatory and immunosuppressive
decrease pain
decrease swelling
decreased stiffness
decrease physical disability

adverse:
increased cardio risk
infections
myopathy
glaucoma
hirsutism
skin thinning
gastric ulcer

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18
Q

Glucocorticoids regulate 10-20% of genes in your body.

A

Bind to glucocorticoid receptor (GR) inside cells – can be alpha (active) or beta (blocks alpha)

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19
Q

Glucocorticoids bind with great affinity

A

to corticosteroid binding globulin (CBG) in plasma – not very well to albumin.

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20
Q

glucocorticoids bind to their receptor,

A

cause dimerization, translocate to the nucleus and bind to DNA to regulate transcription
of target genes.

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21
Q

Regulation of genes by the GR can either involve

A

transactivation of target genes, or transrepression (messing up other transcription
factors). Net result is increase in anti-inflammatory gene expression, decrease in pro-inflammatory gene expression

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22
Q

what can stressors lead to?

A

Repeated stress can lead to habituation, but some forms of chronic stressors (e.g., severe pain, blood loss, hypoglycemia)
can lead to no habituation. In both cases a novel stress can cause a hyper-response of the HPA axis

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23
Q

understand where estrogen is made and primary function

A

made from: theca cells from the follicle take LH and cholesterol and turn it into androstenedione and androstenedione goes to granulosa cells where FSH and androstenedione and aromatase make estradiol
primary function:

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24
Q

understand interplay and origins of GnRH in normal ovarian function

A

interplay:
origins: produced by hypothalamus

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25
Q

understand interplay and origins of LH in normal ovarian function

A

interplay:
origins:

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26
Q

understand interplay and origins of FSH in normal ovarian function

A

interplay:
origins:

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27
Q

understand interplay and origins of estrogen in normal ovarian function

A

interplay:
origins:produced by growing follicle

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28
Q

understand interplay and origins of progesterone in normal ovarian function

A

interplay:
origins:

29
Q

how does the pituitary and gonadal hormones regulate each other

A
30
Q

how does tamoxifen work

A
31
Q

Define Sertoli cells and their function

A
32
Q

understand interplay and origins of GnRH in normal testicular function

A

interplay:
origins:

33
Q

understand interplay and origins of FSH in normal testicular function

A

interplay:
origins:

34
Q

understand interplay and origins of estrogen in normal testicular function

A

interplay:
origins:

35
Q

understand interplay and origins of LH in normal testicular function

A

interplay:
origins:

36
Q

understand interplay and origins of testosterone in normal testicular function

A

interplay:
origins:

37
Q

Define Leydig cells and their function

A
38
Q

how does mifepristone work

A
39
Q

where is insulin produced

A
40
Q

where is glycogen produced

A
41
Q

where is glucagon produced

A
42
Q

where is glucose produced

A
43
Q

Islet of Langerhans in the pancreas is responsible for

A

insulin and glucagon release

44
Q

alpha cells release

A

glucagon. Stimulates breakdown of glycogen to produce glucose (liver, muscle

45
Q

beta cells release

A

insulin, C-peptide, amylin. Insulin stimulates glucose uptake into cells

46
Q

delta cells release

A

somatostatin

47
Q

G cells release

A

gastrin

48
Q

F cells release

A

pancreatic peptide release

49
Q

Therapeutic insulin,

A
50
Q

Exenatide

A

(GLP-1 receptor agonist, blocks glucagon release)

51
Q

Pramlintide

A

(binds amylin receptors to decrease appetite)

52
Q

Octreotide

A

(mimics somatostatin, blocks growth hormones,
glucagon and insulin)

53
Q

Cleavage of pro-insulin by proprotein convertases (enzymes) create

A

functional insulin and its by-product, C-peptide

54
Q

Discussed symptoms and definitions of diabetes

A
55
Q

Discussed causes of Type 2 Diabetes

A
56
Q

Discussed some basic metabolic differences between non-diabetic and diabetic people

A
57
Q

Discussed cellular causes of insulin resistance:

A

insufficient insulin receptors or improper signaling downstream of
the receptors

58
Q

Discussed complications and basic management of diabetes

A
59
Q

Discussed A1C

A

: a measure of glycation of blood hemoglobin

60
Q

Metformin

A

Metformin. Targets AMPK (or AMPKinase), which inhibits glucose
production in the liver. Class of drugs called Biguanides

61
Q

Sulfonylureas

A

(close K+ channels), GLP-1 Receptor Agonists, DPP-4 inhibitors

62
Q

GLP-1 receptor agonists

A

GLP-1 stands for glucagon-like peptide-1. Receptor is found on beta cells. GLP-1 receptor agonists = decrease glucagon and increase insulin.

63
Q

DPP-4 inhibitors

A

DPP-4 is an enzyme that breaks down GLP-1 in the body. Inhibiting this enzyme allows for more
GLP-1, so more insulin release

64
Q

Discussed basic organ system signaling during fasting versus prandial state

A
65
Q

Food, glucagon and glucocorticoids can all

A

increase blood glucose levels

66
Q

Glucose  Glut2 transporter on beta cells  ATP  block potassium channel  causes opening of Calcium channel 
vesicles release insulin

A
67
Q

insulin  Insulin receptor on muscle/fat  signaling  translocation of Glut4 vesicles to membrane

A
68
Q

understand interplay and origins of estrogen in normal testicular function

A

interplay:
origins:

69
Q

Understand the therapeutic uses of testosterone/anabolic steroids and
antiandrogens and side effects

A

FALL 2022 (5 decks)

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