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Pharmacology > Module 7 Diabetes > Flashcards

Module 7 Diabetes Flashcards

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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
what happens in GERD
there is a reflux of the acidic gastric contents back into the esophagus chronic reflux can lead to errosive esophagitis and other complicatons
26
what is the regimen for eradication fo h pylori
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
27
what are the side effects and considerastions for h2 blocker/antagonist
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
28
what are the proton pump inhibitors
omeprazole (prilosec) esomeprazole (nexium) lansoprazole (prevacid)
29
what is the pharmacology of proton pump inhibitors
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
30
what are clinical uses in proton pump inhibitor
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
31
what are side effects of proton pump inhibitors
some otc short term well toelrated long term vitamin b12 deficincy
32
what is the mechanism of teh h pylori infection decreases in d cells
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
33
what is used in h pylori infection treatment
amoxicillin or metronidazole proton pump inhibitor clarithromycin the abx act through 2 different mechanisms
34
what is difference between amoxicilling nad clarithromyclin
amoxicillin is a bacterial wall synthesis inhibitor while clarithromycin is a proton synthesis inhibior
35
what are 2 beneits fo using proton pump inhibior in pt with h pylori induced peptic ulcers
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
why is pepto bismol also added in h pylori regimen
pepto bismol provides a protective layer over the ucler sheilding it from stomach acid also has some antimicrobial activity against h pylori
37
what are benefits of proton pump inhibitor
inhibits gastric acid secretion increases gastric ph increasig antibotic efficacy
38
what are the treatments for type 1 diabetes
subcutaneous insulin
39
what are the treatments for type 2 diabetes
sulfonylureas biguanides glitazones glp 1 agonist flozins
40
what are characteristics of type I diabetes
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
what are characteristics of type II diabetes
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
what are the short acting insulins
regular, lispro, aspart
43
what are trade names of regular insulin
humulin r and novolin r 2-4 hours peak action
44
what are trade names of lispro insulin
humalog 0.5-1.5 hours peak action
45
what are trade names of aspart insulin
novolog 0.5-1.5 peak hours
46
what are the intermediate acting insulins
nph known as humulin n and novolin n 6-12 peak hours
47
what are the long acting insulins
glargine ( lantus) detemir (levemir) no peak
48
what are the insulin mixutres
regular/nph (humulin 50/50 70/30) peak varies lispro protamine/ lispro (humalog mix (75/25) peak varies
49
how is insulin usually administered
sub cutaneous iv an im
50
what is the action of short acting insulin
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
what are insulin analongs
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
what is the action of intermediate acting insulin
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
what is the action of long acting insulin
glargine and detemir insulins onet occurs wihtin 1-2 hours provide 20-24 hours of basal insuulin activity
54
what is the goal of insulin therapy
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
what do oral hypoglyceic agents do
lower blood glucose levels in type II patient not used in type i patient who require insulin injections
56
what are the oral hypoglycemic agents
sulfonylureas glp1 metofmrin flozins glitazones
57
what do sulfonylureas do
stimualte insulin release from the pancreas
58
what do glp1 do
endogenous hormone produced by gi tract that stimuates insulin release in a glucose dependent manner
59
what does metformin do
most commonly prescribed dug for treating diabetes acts to reduced glucose synthesis and release in the liver
60
what does floxins such as enagloflozin do
decrease glucose reabsoprtion in the kidney thus reducing blood glucose
61
what does glitazones do
enhance the effects of insulin in peripheral tissue such as fat
62
what is the principle secretatory involed in the release of insulin from the beta pancreatic cells
glucose
63
what membrane proteins are inn the beta cells
glucose transporter receptor for sulfonylurea drugs and glp 1 agonists potassium channel (ATP senstive K channel)
64
what does gluocse transporter do
transports glucose into the cell
65
what do ATP sensitive pootassium channels do
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
when plasma glucose levels rise what happens
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
what do sulfonylureas do
increase insulin release by inhibing the atp sensitive channels this causes cell depolarization and insulin release
68
what do glp1 agonists do
increase cyclic amp in the cells and stimulate protien kinase a this enhances insulin release pratly bby increasing cellualr calcium
69
what are examples of sulfonylurea
glyburide and glipizide
70
what is the pharmacology of sulfonylureas
inhibit atp sensitive k+ channel in beta pancreatic cells - potentiation of insulin release (ehnahce/incrase insulin releas) used in t2d
71
what are side effects of sulfonylureas
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
what is an example of biguanides
metformin
73
what is the pharmacology of biguanides/metformin
decreases hepatic glucose synthesis and release does not stimulate insulin release so no hypoglycemia most commonly prescibed in t2d
74
what are side effects of metformin
gi upset (anorexia) lactic acidosis (phenfomin - not used anymore) especially in kidney disease can be used with sulfonylurea drugs
75
what are the glitazones
rosiglitazone
76
what is the pharmacology of glitazone/rosiglitazone
binds to peroxisome proliferator activated receptors (PPARS) reduces insulin resistance increase glucose uptake into adipose tissue lower blood glucose
77
what are side effects and considerations of glitazones/rosiglitazone
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
what are examples of glp1 agnoists
exenatide, dulaglutide and liraglutide
79
what is the pharmacology of glp1 agonists
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
where was exenatide was isolated from where
gila monster
81
what are side effects of glp 1 agonists
gi disturbances risk fo pancreatitis and gastroparesis
82
what are the formulations for glp 1 agonists
subcutaneous and oral dosing intervals semaglutide (wegovy) and liraglutide (saxenda) are fda approved for weight loss daily or weekly bc long half life
83
what are examples of flozins
canagliflozin and empagliflozin
84
what is the pharmacology of flozins
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
what are the side effects of flozins
urinary tract infections concerns about acute kidney failure and incraesed risk fo amputations
86
how is glp1 agonist half life logner
modited to reversibly bind albumin in serum to increase half life

Pharmacology (6 decks)

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