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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
Q

Cortisone

A

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
Q

Biological Activities of Corticosteroids

A

-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
Q

alpha cells

A

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

28
Q

beta cells

A

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

29
Q

delta cells

A

release somatostatin

30
Q

G cells

A

release gastrin

31
Q

F cells

A

release pancreatic peptide release

32
Q

Therapeutic insulin

A

Different half lives. Drives glucose uptake

33
Q

Exenatide

A

LP-1 receptor agonist, blocks glucagon release

34
Q

Pramlintide

A

binds amylin receptors to decrease appetite)

35
Q

Octreotide

A

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

36
Q

Cleavage of pro-insulin by proprotein convertases

A

create functional insulin and its by-product, C-peptide

37
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

38
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.

39
Q

Sulfonylureas

A

diabetes drug (close K+ channels)

40
Q

Metformin

A

diabetes drug that target AMPK or AMPkinase which inhibits glucose production in the liver
in the Biguanides class of drug

41
Q

A1C

A

a measure of glycation of blood hemoglobin

42
Q

insulin

A

A peptide hormone produced by beta cells of the pancreas, and is central for regulating carbohydrate and fat metabolism

43
Q

glycogen

A

polysacchairde

44
Q

glucagon

A

peptide hormone produced by alpha cells of the pancreas

45
Q

glucose

A

small molecule

46
Q

understand the role of the pancreas in glucose metabolism and which types of pancreatic cells are involved

A

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
Q

Function of Secreted Products of Pancreatic Cells

A

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
Q

what it means to be insulin resistant

A

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
Q

Understand the effects of insulin on muscle, liver and adipose tissue

A

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
Q

Define diabetes mellitus, know the four different types

A

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
Q

understand the root causes and symptoms of type 2 diabetes.

A

over time you have insulin resistance
-age
-inactivity
-high lipid levels
-over wight
-family history

52
Q

Cleavage of pro-insulin by proprotein convertases (enzymes

A

create functional insulin and its by-product, C-peptide

53
Q

GLUT 2 transporter on beta cells

A

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
Q

GLUT 4 transporter

A

insulin leads to insulin receptor on muscle / fat leads to signaling lead to translocation on GLUT 4 vesicles membrane

55
Q

all increase blood glucose levels

A

Food, glucagon and glucocorticoids

56
Q

fasting versus prandial state

A

fasting blood sugar is taken before eating a meal and your postprandial blood sugar is taken after the meal

57
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

58
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.

59
Q

Sulfonylureas

A

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

Spring 2023 (7 decks)

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