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Pharmacology > Module 7 Diabetes > Flashcards

Module 7 Diabetes Flashcards

1
Q

what is the physiology of gastric acid secretion

A

enterchromaphin like cells ECL cells that are found in the fundus of the stomach store histamine in vesicles
the release of histamin fro, the ECL cells is regulated in several different ways
enteric nervous system,. g cels in antrium that release gastrin, horone somatostatin

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2
Q

how is histamine released from enteric nervous system

A

acetyl choline is released from these neurons which binds to muscarinic receptors on the ECL cells and stimualtes the release of histamine

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3
Q

what do G cells do in the release of histamine

A

g cells found in the antrium that release gastin
gastrin binds to gastrin receptors also called choleysysteinen receptors taht cayse histamine release

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4
Q

what does somatostatin do

A

produces a chronic inhibitory tone over the histamine release
somatostatin produced by gastric d cells

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5
Q

acetylcholien and gastrin do what

A

stimulate histamine release

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6
Q

what does somatostain do

A

produces chronic inhibition of histamine release

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7
Q

what is directly involved in the pathophysiology of peptic ulcer diease

A

disruption of this regulatory system is directly involved in pathophysiology of peptic ulcer diease

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8
Q

under normal physiological conditions what does gastric acid secretion look like

A

histamine is released from ECL cells and binds to histamine h2 receptors expressed in the parietal cells
this leads to a stimulation of the proton pump that trans[orts hydrogen ions into the gastric lumen
acetylcholine from the enteric nervous system and gastrin from the g cells can also activiate the proton pump
have an increase in h+ ions gastic acid section

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9
Q

what is the etiology of peptic ulcers

A

h pylori is the major cause of peptic ulcer disease about 70% of peptic ulcers are caused by this bacterium
nsaids
zollinger ellison syndrome

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10
Q

how does h pylori cause peptic ulcers

A

it is believed that h pylori infection decreases the number of d cells in teh stomach
a decrease in d cells means a decreaes in synthesis and release of somatostatin
the inhibitory tone produced by somatostatin si removal and there is now excessive release of histamine from the ECL cells

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11
Q

how do NSAIDS cause peptic uclers

A

inhibit cox1 inhibiting synthesis of prostaglandin E2
decrease mucus in lumen

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12
Q

what is zollinger ellison syndrome

A

gastrinoma
excessive amounts of gastrin
results in activation of gastric receptors both on ECL cells and parietal cells this will enhance gastric secretion

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13
Q

what is an ulcer

A

lesion through the mucus membrane in the gi tract

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14
Q

stomach ulcer is what

A

gastric ulcer

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15
Q

upper small intestine ulcer is what

A

duodenal ulcers

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16
Q

the factors in peptic ucler formation result in what

A

results in an excessive release of gastin increasing gastric acid secretion

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17
Q

how does smoking directly increases what

A

secretion
indirectly disrupts the cytoprotecitve barrier

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18
Q

alcohol alone is not a causive of peptic ulcer diease however alcohol can what

A

exacerbate teh diease by weaking the cytoproteive barrier

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19
Q

what are symptoms of peptic ulcer

A

dyspepsia - gnawing, buring, dull pain relieved by antacids
weight loss
anemia - from blood loss
perforation - elderly taking nsaids

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20
Q

what are the treatments of peptic ulcers

A

lifestyle changes such as discontinueing smoking and alcohol use
histamiine H2 receptor antagonist
proton pump inhibitors

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21
Q

what are the histamine H2 receptor antagonists

A

h2 receptor blockers\
cimetidine, ranitidine, famotidine

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22
Q

what is the action of h2 receptor blockers

A

these are drugs that bind to the histamine H2 receptor and prevent histamine from binding to the receptor
competitive antagonists at histamine h2 receptor
suppress basal acid secretions -> food stimulated secretions

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23
Q

what is no longer on the market

A

ranitidine

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24
Q

what are the clinical uses of h2 blcokers (antagonist)

A

h2 blockers are used in the treatment of gastric and duodenal uclers
also used in treatment of gastroesopahgeal reflux disease
zollinger ellison syndrome (gastrin stimulates histamine relase from ECL cells)
regimens for eradication of h pylori

they are more efficaous in hibiting basal acid secretion when compared with food stimulated secretion

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25
Q

what happens in GERD

A

there is a reflux of the acidic gastric contents back into the esophagus
chronic reflux can lead to errosive esophagitis and other complicatons

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26
Q

what is the regimen for eradication fo h pylori

A

in combination therapy with antibiotics (amoxicillin, clarithromycin, etc) and bismuth subsilicate
usually include proton pump inhibtior but the h2 antagonist can be used as alternative bc they are tolerated well

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27
Q

what are the side effects and considerastions for h2 blocker/antagonist

A

available OTC
side effect of cimetidine
inhibition of cyp450 enzymes so drug interactions with warfarin and phenytoin
anti androgenic effects reversible such as galactia and gynecomastia

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28
Q

what are the proton pump inhibitors

A

omeprazole (prilosec)
esomeprazole (nexium)
lansoprazole (prevacid)

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29
Q

what is the pharmacology of proton pump inhibitors

A

these drugs inhibit hydrogen potasssium atpase in the parietal cells that transport hysrogen ions into gastric lumen also called the proton pump
the inhibition caused by proton pump inhibitors is irreversible
new proton pumps need to be synthesized by the parietal cell for acid secretion
it takes several days for proton pump to be effective
suppress acid secretion caused by all stimuli

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30
Q

what are clinical uses in proton pump inhibitor

A

peptic ucler diease
gerd
zollinger ellison syndrome
regimens for eradiacation of h pylori preferred over h2 receptor antagonsits
prevention and treatment of nsaid induced ulcers

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31
Q

what are side effects of proton pump inhibitors

A

some otc
short term well toelrated
long term vitamin b12 deficincy

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32
Q

what is the mechanism of teh h pylori infection decreases in d cells

A

inhibitory effect of somatostatin on acid secretion is removed
use combo pf proton pump inhibitor and antibiotics 321 regimen
3 drugs used 2 times daily for 1 week
therapy may be extended for 2 weeks

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33
Q

what is used in h pylori infection treatment

A

amoxicillin or metronidazole
proton pump inhibitor
clarithromycin
the abx act through 2 different mechanisms

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34
Q

what is difference between amoxicilling nad clarithromyclin

A

amoxicillin is a bacterial wall synthesis inhibitor while clarithromycin is a proton synthesis inhibior

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35
Q

what are 2 beneits fo using proton pump inhibior in pt with h pylori induced peptic ulcers

A

by inhibiting gastric acid secretion proton pump inhibitos heal the ulcer
they raise the ph of the gastric surface which makes the antibotics more effective in eradicating h pylori
the bacteria grow at higher ph and are only sensitive to the antibootics when they are actively growing

36
Q

why is pepto bismol also added in h pylori regimen

A

pepto bismol provides a protective layer over the ucler sheilding it from stomach acid
also has some antimicrobial activity against h pylori

37
Q

what are benefits of proton pump inhibitor

A

inhibits gastric acid secretion
increases gastric ph increasig antibotic efficacy

38
Q

what are the treatments for type 1 diabetes

A

subcutaneous insulin

39
Q

what are the treatments for type 2 diabetes

A

sulfonylureas
biguanides
glitazones
glp 1 agonist
flozins

40
Q

what are characteristics of type I diabetes

A

severe form associated with complete absence of circulating insulin
usually diagnosed in young adults and it is the less common dorm of diabetes
autoimmune disease resulting in the destructin of the beta pancreatic cells
these pt require exogenous source of insulin to prevent hypoglycemia and ketoacidosis that is life threatening

5-10% of diabetes
less tahn 30 years old at onset
usually no pancreatic function
generally not strong family history
obesity not uncommon
preferred treatment
insulin, diet, exercise

41
Q

what are characteristics of type II diabetes

A

milder form of disease
these pt usually have low levels of insulin in their pancreas
more common in asults especially those who are obese
incrases in adipose tissue reduce insulin sensitivity
pt develop insulin resistance
can often be treated through diet and exercise
many pt require oral hypoglycemic agents and some need insulin

90% of diabetes
usually over 40 mins
lnsulin present in low to normal amounts
strong family history
obesity common 60-90%
treatment is diet, exercise, oral hopoglycemic agents/insulin

42
Q

what are the short acting insulins

A

regular, lispro, aspart

43
Q

what are trade names of regular insulin

A

humulin r and novolin r
2-4 hours peak action

44
Q

what are trade names of lispro insulin

A

humalog
0.5-1.5 hours peak action

45
Q

what are trade names of aspart insulin

A

novolog
0.5-1.5 peak hours

46
Q

what are the intermediate acting insulins

A

nph
known as humulin n and novolin n
6-12 peak hours

47
Q

what are the long acting insulins

A

glargine ( lantus)
detemir (levemir)
no peak

48
Q

what are the insulin mixutres

A

regular/nph (humulin 50/50 70/30) peak varies
lispro protamine/ lispro (humalog mix (75/25) peak varies

49
Q

how is insulin usually administered

A

sub cutaneous
iv an im

50
Q

what is the action of short acting insulin

A

regular insulin - soluble insulin with effects in 30 misn
onset occurs within 30 mints
peak activity between 2-4 hours
often injected with NPH insulin
lispro and aspart - insulin analogs with rapid onset (<15 mins)

51
Q

what are insulin analongs

A

structure of insulin modified to change the properties of insulin
change resutls in insulin with rapid onset of action
often used in insulin pumps

52
Q

what is the action of intermediate acting insulin

A

neutral protamien hagedorn (NPH)
onset occurs with 1 to 3 horus
peak activity occurs between 6 and 12 hours

mixture of insulin with protamine, argingine rich peptides
after subq injection protiolyic enzymes degrade the protamine to permit absorption of the insulin

53
Q

what is the action of long acting insulin

A

glargine and detemir insulins
onet occurs wihtin 1-2 hours
provide 20-24 hours of basal insuulin activity

54
Q

what is the goal of insulin therapy

A

intensive regimens with home glucose monitoring to prevent long term complications like neuropathy
lispro or aspart before meals/once a day glargine or detemir insulins
nph:regular insulin combination is commonly used

55
Q

what do oral hypoglyceic agents do

A

lower blood glucose levels in type II patient
not used in type i patient who require insulin injections

56
Q

what are the oral hypoglycemic agents

A

sulfonylureas
glp1
metofmrin
flozins
glitazones

57
Q

what do sulfonylureas do

A

stimualte insulin release from the pancreas

58
Q

what do glp1 do

A

endogenous hormone produced by gi tract that stimuates insulin release in a glucose dependent manner

59
Q

what does metformin do

A

most commonly prescribed dug for treating diabetes
acts to reduced glucose synthesis and release in the liver

60
Q

what does floxins such as enagloflozin do

A

decrease glucose reabsoprtion in the kidney thus reducing blood glucose

61
Q

what does glitazones do

A

enhance the effects of insulin in peripheral tissue such as fat

62
Q

what is the principle secretatory involed in the release of insulin from the beta pancreatic cells

A

glucose

63
Q

what membrane proteins are inn the beta cells

A

glucose transporter
receptor for sulfonylurea drugs and glp 1 agonists
potassium channel (ATP senstive K channel)

64
Q

what does gluocse transporter do

A

transports glucose into the cell

65
Q

what do ATP sensitive pootassium channels do

A

these channels are unique in that they are inhibited by intracellular atp
normally these channels are active and mainaint the cell resting potential at a relatively negative potenial

66
Q

when plasma glucose levels rise what happens

A

glucose is actively taken up into the beta cell and enters glycolysis producing atp
atp then inhibits the atp sensitive channel leading to depolarization of teh cell
this depolarization causes calcium channels to open allowing calcium to enter the beta cell
the rise incelluar calcium cause the secretory granules to release insulin
this calcium mediates relase of insulin similar to release of neurotransmitters

67
Q

what do sulfonylureas do

A

increase insulin release by inhibing the atp sensitive channels this causes cell depolarization and insulin release

68
Q

what do glp1 agonists do

A

increase cyclic amp in the cells and stimulate protien kinase a
this enhances insulin release pratly bby increasing cellualr calcium

69
Q

what are examples of sulfonylurea

A

glyburide and glipizide

70
Q

what is the pharmacology of sulfonylureas

A

inhibit atp sensitive k+ channel in beta pancreatic cells - potentiation of insulin release (ehnahce/incrase insulin releas)
used in t2d

71
Q

what are side effects of sulfonylureas

A

hypoglycemia/weight gain because of increased appetie
gi disturbances nasuea and vomting
undergo hepatic and renal metabolism risk of hypoglycemia in patients with liver or kidney impairment

72
Q

what is an example of biguanides

A

metformin

73
Q

what is the pharmacology of biguanides/metformin

A

decreases hepatic glucose synthesis and release
does not stimulate insulin release so no hypoglycemia
most commonly prescibed in t2d

74
Q

what are side effects of metformin

A

gi upset (anorexia)
lactic acidosis (phenfomin - not used anymore) especially in kidney disease
can be used with sulfonylurea drugs

75
Q

what are the glitazones

A

rosiglitazone

76
Q

what is the pharmacology of glitazone/rosiglitazone

A

binds to peroxisome proliferator activated receptors (PPARS)
reduces insulin resistance
increase glucose uptake into adipose tissue lower blood glucose

77
Q

what are side effects and considerations of glitazones/rosiglitazone

A

reduces insulin requiremnts for type ii bc of insulin senstivity
hepatoxicity risk (monitor liver enzymes)
cv concern incrase heart failure
now less commonly used

78
Q

what are examples of glp1 agnoists

A

exenatide, dulaglutide and liraglutide

79
Q

what is the pharmacology of glp1 agonists

A

glucagon like peptide 1 agonists similar to endogenous glp1
stimulate insulin release in a glucose dependent manner in pancreas
slow gastric emptying
cns effects on satiety

80
Q

where was exenatide was isolated from where

A

gila monster

81
Q

what are side effects of glp 1 agonists

A

gi disturbances
risk fo pancreatitis and gastroparesis

82
Q

what are the formulations for glp 1 agonists

A

subcutaneous and oral
dosing intervals
semaglutide (wegovy) and liraglutide (saxenda) are fda approved for weight loss

daily or weekly bc long half life

83
Q

what are examples of flozins

A

canagliflozin and empagliflozin

84
Q

what is the pharmacology of flozins

A

inhibit sodium glucose cotransporter 2 (SFLGT2)
inhibit glucose reabsoprtion in the kidney by inhibiting na/glucose transporter in the proximal tuble
reduces renal glucose reabsoption
weight loss adn natrietic action

85
Q

what are the side effects of flozins

A

urinary tract infections
concerns about acute kidney failure and incraesed risk fo amputations

86
Q

how is glp1 agonist half life logner

A

modited to reversibly bind albumin in serum to increase half life

Pharmacology (6 decks)

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