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Spring 2023 > PHCL Exam 2 > Flashcards

PHCL Exam 2 Flashcards

1
Q

Hypothalamic-Pituitary-Adrenal (HPA) Axis

A

stress -> hippocampus -> hypothalamus ->(release of CRH)-> anterior pituitary -> (release of ACTH) -> adrenal cortrex -> (release of cortisol)

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2
Q

zone of fasciculata

A

cortisol and androgens
enzyme = CYP11B1 & CYP17

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3
Q

zone of glomerulosa

A

enzyme = CYP11B2 -> aldosterone

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4
Q

zone of reticularis

A

cortisol and androgens
enzyme = CYP11B1 & CYP17

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5
Q

adrenal medulla

A

epinephrine and norepinephrine
enzyme = CYP17 -> DHEA

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6
Q

glucocorticoids

A

cortisol = affects metabolism and immune function
in blood binds to corticosteroid - binding globulin

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7
Q

mineralocorticoids

A

aldosterone - salt retaining
causes sodium resorption in distal renal tubule, sweat glands, salivary glands, GI

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8
Q

Deoxycorticosterone

A

secreted precursor to Aldosterone

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9
Q

glucocorticoids effect on the body

A

increase glucose production
increase muscle atrophy
increase bone loss
increase lipolysis
increase anti-inflammatory genes
decrease proinflammatory

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10
Q

Adrenergic or Estrogenic hormones

A

Sexual maturity and characteristics

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11
Q

Cortisol can feed back to the pituitary and hypothalamus to

A

reduce further stimulation of the system (feedback inhibition)

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12
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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13
Q

Corticosteroids

A

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

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14
Q

Repeated stress can lead to

A

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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15
Q

Addison’s disease

A

Corticosteroid deficiency
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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16
Q

Cushing’s Syndrome

A

Corticosteroid overload
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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17
Q

Cortisone

A

was 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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18
Q

therapeutic vs adverse effects of glucocorticoid

A

therapeutic= anti-allergic, decrease pain swelling stiffness physical disability
adverse = cataract glaucoma, increased cardiac risk, osteonecrosis and osteoporosis, infections

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19
Q

clinical causes for both Addison’s disease

A

adrenal glands not function
-autoimmune disease

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20
Q

clinical causes for both Cushing’s syndrome.

A

-too much HPA activation
-tumor maybe
-can be born or develop when older

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21
Q

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

A

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

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22
Q

Glucocorticoids bind with great affinity

A

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

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23
Q

in the cell, glucocorticoids bind to their receptor, cause

A

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

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24
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

25
Cortisone
was isolated from cows in the 1940s and used for rheumatoid arthritis for the first time in 1948 – quickly became a widely used drug.
26
Biological Activities of Corticosteroids
-energy metabolism -stimulate gluconeogenesis -inhibit glucose uptake by muscle or adipose tissue (because brain needs the glucose) -increase serum glucose levels -increase short term memory
27
alpha cells
release glucagon. Stimulates breakdown of glycogen to produce glucose (liver, muscle)
28
beta cells
release insulin, C-peptide, amylin. Insulin stimulates glucose uptake into cells
29
delta cells
release somatostatin
30
G cells
release gastrin
31
F cells
release pancreatic peptide release
32
Therapeutic insulin
Different half lives. Drives glucose uptake
33
Exenatide
LP-1 receptor agonist, blocks glucagon release
34
Pramlintide
binds amylin receptors to decrease appetite)
35
Octreotide
(mimics somatostatin, blocks growth hormones, glucagon and insulin)
36
Cleavage of pro-insulin by proprotein convertases
create functional insulin and its by-product, C-peptide
37
DPP-4 inhibitors
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
38
GLP-1 receptor agonists
GLP-1 stands for glucagon-like peptide-1. Receptor is found on beta cells. GLP-1 receptor agonists decrease glucagon and increase insulin.
39
Sulfonylureas
diabetes drug (close K+ channels)
40
Metformin
diabetes drug that target AMPK or AMPkinase which inhibits glucose production in the liver in the Biguanides class of drug
41
A1C
a measure of glycation of blood hemoglobin
42
insulin
A peptide hormone produced by beta cells of the pancreas, and is central for regulating carbohydrate and fat metabolism
43
glycogen
polysacchairde
44
glucagon
peptide hormone produced by alpha cells of the pancreas
45
glucose
small molecule
46
understand the role of the pancreas in glucose metabolism and which types of pancreatic cells are involved
the pancreas has the islets of langerhans which are the alpha cells, beta cells, and delta cells the alphas cells secrete glucagon which increase blood glucose the beta cells secrete insulin, C-peptide, amylin that lower blood glucose the delta cells secrete somatostatin the g cells secrete gastrin the f cells secrete pancreatic polypeptide
47
Function of Secreted Products of Pancreatic Cells
glucagon = hypoglycemic factor that mobilizes glycogen stores Insulin = the storage and anabolic hormone Amylin = modulate appetite, gastric emptying, glucagon and insulin secretion Somatostatin = inhibitor of secretory cells, growth hormone inhibitor Gastrin = stimulate gastric acid secretion
48
what it means to be insulin resistant
Two major variants of insulin receptor abnormalities associated with acanthosis nigricans have been described—the classic type A insulin resistance syndrome, which is due to an absent or dysfunctional receptor, and type B insulin resistance syndrome, which results from autoantibodies to the insulin receptor (very rare)
49
Understand the effects of insulin on muscle, liver and adipose tissue
insulin effect on muscle : increase protein synthesis increase amino acid transport increase ribosomal protein synthesis increase glycogen synthesis increase glucose transport INDUCES glycogen synthase and inhibits phosphorylase insulin effect on liver : reversal of catabolic features on insulin deficiency inhibits glycogenolysis inhibits conversion of fatty acids to keto acid inhibits conversion of amino acids to glucose anabolic action = promotes glucose stage as glycogen increase triglyceride synthesis and VLVL insulin effect on adipose tissue: increase triglyceride storage
50
Define diabetes mellitus, know the four different types
elevated blood glucose associated with absent or inadequate pancreatic insulin secretion, with or without impairment of insulin action Type 1: insulin-dependent diabetes, selective beta cell destruction, insulin deficiency Type 2: non-insulin dependent, tissue resistance to insulin, relative deficiency of insulin Type 3: other, such as pancreatectomy, pancreatitis, drug therapy Type 4: gestational diabetes mellitus, placental hormones cause insulin resistance
51
understand the root causes and symptoms of type 2 diabetes.
over time you have insulin resistance -age -inactivity -high lipid levels -over wight -family history
52
Cleavage of pro-insulin by proprotein convertases (enzymes
create functional insulin and its by-product, C-peptide
53
GLUT 2 transporter on beta cells
glucose goes into GLUT 2 transporter on beta cells leads to ATP least to blockage of potassium channel leads to opening of calcium channel leads to vesicles release insulin
54
GLUT 4 transporter
insulin leads to insulin receptor on muscle / fat leads to signaling lead to translocation on GLUT 4 vesicles membrane
55
all increase blood glucose levels
Food, glucagon and glucocorticoids
56
fasting versus prandial state
fasting blood sugar is taken before eating a meal and your postprandial blood sugar is taken after the meal
57
GLP-1 receptor agonists
GLP-1 stands for glucagon-like peptide-1. Receptor is found on beta cells. GLP-1 receptor agonists decrease glucagon and increase insulin
58
DPP-4 inhibitors
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.
59
Sulfonylureas
(close K+ channels), GLP-1 Receptor Agonists, DPP-4 inhibitors

Spring 2023 (7 decks)

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