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Pharmacology II > Diabetes (exam ?) > Flashcards

Diabetes (exam ?) Flashcards

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1
Q

apple shape

A

more visceral fat
higher risk of weight related health problems

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2
Q

pear shape

A

less visceral shape
lower risk of weight related health problems

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3
Q

BMI that classifies overweight

A

over 25

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4
Q

BMI that classifies obesity

A

over 30

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5
Q

obesity reduces life expectancy around ___________ and morbid obesity reduces life expectancy around __________

A

3 years

10 years

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6
Q

abdominal obesity is a major risk factor for

A

metabolic syndrome

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7
Q

in obesity, there is an accumulation in adipocytes leads to

A

pro inflammatory factors, adiopocytokines, and lipotoxicity

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8
Q

obesity can lead to

A

T2DM
HTN
CV diseases
non alcoholic fatty liver disease
cancers

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9
Q

in obesity energy intake _________ energy expenditure

A

exceeds

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10
Q

key players in control of energy intake

A

ghrelin (hunger hormone)
leptin (feeling of fullness)

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11
Q

in obesity there is a ________ sensitivity of leptin receptors

A

decreased

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12
Q

control of energy expenditure is controlled by

A

basal metabolic rate being lowered/increased

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13
Q

substances that promote weight gain

A

cannabinoids
orexin
ghrelin
insulin

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14
Q

substances that promote weight loss

A

histamine
NE
DA
thyroid hormone
leptin
GLP-1

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15
Q

adipose tissue secretes ________________ which can promote ____________________

A

hormones, inflammatory cytokines, and other substances

inflammation and alter body homeostasis

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16
Q

obesity increases

A

clotting
insulin resistance
atherosclerosis
blood pressure
cancer risk

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17
Q

insulin binding activates downstream ______________ resulting in the ___________________ to the cell surface

A

Akt kinase

translocation and exocytosis of intracellular GLUT4 vesicles

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18
Q

what happens during insulin resistance when there is chronic high FA levels?

A

decreased secretion of insulin from the pancreas
activation of PKC0 which does not form active Akt kinase
GLUT4 vesicles cannot go to the surface

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19
Q

weight loss in indicated in patients with a BMI of

A

25 to 30 with 1 or more indications of increased CVD risk
or
any patients with a BMI over 30

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20
Q

initial goal of weight loss is _____________ which can significantly improve ______________

A

5-10%

blood pressure, lipid levels and glucose tolerance

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21
Q

non pharmacological therapy for weight loss

A

dietary changes
increased physical activity
behavioral modification

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22
Q

when can bariatric surgery be considered?

A

BMI over 40
BMI over 35 with significant comorbidites

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23
Q

general approach to treatment of obesity

A

suppress appetite
reduce fat absorption
increase WAT lipolysis and oxidation

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24
Q

pharmacological therapy can be considered as adjunctive treatment for

A

BMI over 30
BMI 27-29 with at least one weight related comorbidity

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25
use of medication leads to about an ____________ weight loss in the average patient
8-20lb
26
if ____________ weight loss is not achieved after ______ weeks then the drug should be discontinued
4-5% 12
27
stimulants/sympathomimetics examples
phentermine (adipex P) diethylpropion (tenuate) phendimetrazine (bontril)
28
stimulant and anticonvulsant examples
phentermine/topiramate ER (qsymia)
29
NDRI and opioid antagonist example
Bupropion/Naltrexone (contrave)
30
GLP1 antagonists examples
liraglutide (saxenda) semaglutide (wegovy)
31
lipase inhibitor example
orlistat (Xenical - RX or Alli - OTC)
32
superabsorbent hydrogel example
cellulose/citric acid complex (plenity)
33
stimulants/sympathomimetics MOA
increase presynaptic release of NE in the brain via reverse transport of NE transporter increases NE levels and reduces appetite
34
stimulants/sympathomimetics shouldn't be taken at night due to
insomnia
35
stimulants/sympathomimetics are limited to short term treatment due to
CV risk and abuse potential
36
Phentermine increases ______________ because it blocks ________________
DA and NE in the hypothalamus NE and DA reuptake transporters
37
which pathway does stimulants/sympathomimetics affect? what hormone increases to suppresses appetite partially?
appetite suppressing pathway alpha-melanocyte stimulating hormone
38
stimulants/sympathomimetics hepatic metabolism including
3A4
39
ADRs of stimulants/sympathomimetics
adrenergic effects decrease the seizure threshold
40
avoid stimulants/sympathomimetics in patients with
history of seizures CV disease hyperthyroidism history of substance abuse
41
ADRs of stimulant and anticonvulsant
adrenergic effects decrease seizure threshold paresthesia, dizziness, cognitive impairment, kidney stones, alkaline urine
42
stimulant and anticonvulsant should be
tapered during discontinuation to reduce seizure risk
43
topiramate is a
teratogen (harmful in pregnancy)
44
topiramate __________ the actions of phentermine by ________________
potentiates inhibiting the appetite stimulating pathway
45
how does topiramate inhibits the appetite stimulating pathway?
reduces excitatory glutamaterigc input by increasing inhibitory GABAergic input
46
MOA of bupropion in NDRI and opioid antagonist
inhibits presynaptic reuptake of NET and DAT leading to increased NE and DA levels suppresses appetite
47
MOA of naltrexone in NDRI and opioid antagonist
reduces food cravings reduces activation of reward pathways associated with food
48
naltrexone ______________ the actions of bupropion by __________________
potentiates blocking the endorphin/endogenous-opioid-mediated negative feedback loop
49
naltrexone acts on the
appetite suppressing pathway
50
Bupropion is a ___________ inhibitor
CYP2D6
51
ADRs of NDRI and opioid antagonist
lowering seizure threshold, insomnia adrenergic effects nausea, headache
52
NDRI and opioid antagonist should not be used in
uncontrolled HTN seizure disorders eating disorders opioid users
53
GLP1 agonist MOA
peptide agonist at GLP1 receptors which reduces appetite and delays gastric emptying increases satiety
54
GLP1 also stimulates _______________ secretion and reduces ________________
glucose dependent insulin secretion glucagon secretion
55
mechanisms of potent GLP1 agonists
delayed gastric emptying increased glucose dependent insulin secretion reduced glucagon levels reduced food intake by CNS effects
56
short acting GLP1 agent exert their effect mostly by
slowing gastric empyting
57
long acting GLP1 agents exert their effect mostly by
reducing fating glucose levels mediated by their effect on insulin and glucagon release
58
GLP1 agonists are metabolized by
protease enzymes
59
half life of liraglutide is half life of semaglutide is
12 hrs 1 week
60
ADRs of GLP1 agonsts
nausea abdominal pain vomiting diarrhea increased HR hypoglycemia
61
rare ADR of GLP1 agonists
acute pancreatitis
62
GLP1 agonists have a black box warning for
risk of thyroid tumors
63
GLP1 agonists are not recommended for
patients with gastroparesis
64
Zepbound (tirzepatide) is a
dual GIP and GLP1 receptor agonist
65
half life of zepbound
5 days
66
MOA of lipase inhibitor
reversible inhibition of gastric and pancreatic lipases reduction of fat absorption by GI tract
67
lipase inhibitors are excreted
through the feces as unchanged drug
68
ADRs of lipase inhibitors
abdominal cramping flatulence fecal incontinence diarrhea
69
rare ADRs of lipase inhibitors
liver toxicity oxalate-induced kidney stones
70
lipase inhibitors interfere with the absorption of
some medications and fat soluble vitamins (A,D,K,E)
71
super absorbent hydrogel MOA
small cellulose and citric acid particles released into the stomach and hydrate up to 100x their weight promotes fullness
72
hydrogel particles are broken down in the
colon releasing water for reabsorption
73
super absorbent hydrogel is approved as a ________ by the FDA
device
74
ADRs of super absorbent hydrogel
abdominal pain diarrhea flatulence abdominal distension nausea
75
super absorbent hydrogel is approved for
BMI over 25
76
super absorbent hydrogel is not recommended in patients with
GI abnormalities or conditions
77
PK of super absorbent hydrogel
no absorption, distribution and metabolism excreted through feces

Pharmacology II (18 decks)

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