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202D > final 2 lectures > Flashcards

final 2 lectures Flashcards

1
Q

what is the pH of the stomach

A

2-3

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2
Q

what are the functions of the stomach

A

mechanical- squeezes the stomach that churns and mixes the food
-chemcial function: ability to secrete substances from gastric glands critical for digestion

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3
Q

what are the cells of the stomach and what do they secrete

A
  • chief cells- pepsinogen
  • parietal cells- secrete HCL and activate pepsinogen and intrinsic factor
  • mucus neck cells- secrete mucus and bicarb
  • prostaglandins- stimulate mucus and bicarb secretion (a protective hormone) promotes repair of damage cells and dilates blood vessels
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4
Q

what is intrinsic factor important for

A

the absorption of B 12

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5
Q

what is peptic ulcer disease

A

a lesion or erosion in the stomach or duodenum

the hyper secretion of HCL

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6
Q

what are risk factors for developing peptic ulcer disease

A
  • family hx
  • use of corticosteroids, NSAIDS and platelet inhibitors
  • smoking
  • alcohol
  • caffeine
  • H Pylori
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7
Q

why does NSAIDS and aspirin lead to peptic ulcers

A

because they irritate the gastric lining

there is cox 1 enzyme in the mucosal lining that helps protect the stomach.
there is cox 2 which is the enzyme that promotes prostaglandin release

aspirin and NSAIDS are non selective meaning they block both cox 1 and 2 which reduces the ability to protect the gastric mucosa

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8
Q

what can long term use of steroids do r/t peptic ulcer disease

A

they reduce the prostaglandin synthesis b/c they suppress the immune system.
They block prostaglandins- the stomachs ability to protect itself by secreting bicarb and increase mucus.

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9
Q

a patient who is on long term corticosteroids should also be taking what

A

PPI’s

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10
Q

how does alcohol cause peptic ulcer disease

A

promotes HCL secretion and reduces bicarb production.

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11
Q

what are symptoms of peptic ulcer disease

A
  • burning pain
  • discomfort 1-3 hours after a meal
  • worsened discomfort on empty stomach(gets better when eat)
  • risk of bleeding (the constant hypersectreion of acid can increase risk for bleeding b/c the erosion progresses until it starts to bleed)
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12
Q

what is H. Pylori

A

a corkscrew shaped bacteria that screw themselves in to the lining of the stomach.

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13
Q

how is H pylori transmitted

A

through contaminated water (sewage), stool or mouth fluids-

it then triggers ulcers

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14
Q

what are characteristics of H Pylori

A
  • it can survive low acidity

- has ability to generate ammonia (acts as a buffer to HCL) which gives it the chance to proliferate and create a colony

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15
Q

what does an H pylori infection cause

A

triggers ulcers

-chronic inflammation of the gastric or duodenal lining.

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16
Q

what is the most accurate way to diagnose an H pylori infection

A

-via endoscopy and take a bx of the lining

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17
Q

what is the treatment for an H Pylori infection

A

antibiotics ( usually 2-3) in conjunction with PPIs or histamine blockers.

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18
Q

what is GERD

A

stomach acid that enters the esophagus

risk of esophageal lining

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19
Q

what are symptoms of GERD

A 
"heartburn"
dysphagia
dyspepsia 
heartburn
belching
nausea
(some pts feel chest pain)
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20
Q

what factors worsen GERD

A 
acidic foods/drinks
spicy foods
smoking
alcohol
obesity (increased weight on stomach creates increased intraabdominal pressure placing pressure on the LES)
NSAIDS, Corticosteroids
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21
Q

why would a pt be on a PPI when they have cardiac conditions

A

to r/o the cause of chest pain by GERD.

if pts chest pain is relieved while on PPIs their chest pain is most likely not r/t cardiac condition

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22
Q

what are lifestyle changes to help with GERD

A
  • HOB elevated so acid doesn’t reflux back
  • smaller meals more frequently
  • losing weight to reduce pressure
  • acetaminophen for pain (no aspirin/nsaids d/t the increased risk for peptic ulcer disease)
  • stay upright 2-3 hrs after meals
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23
Q

what can be a possibility if a pt has a hx of gerd and now has a chronic cough

A

possibly d/t aspiration of stomach acid

acid came as far up to the mouth and swallows and the acid went to the lungs

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24
Q

what drug classes can help with GERD and peptic ulcer disease

A
  • proton pump inhibitors
  • H2 receptor antagonists
  • antacids
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25
Q

what is a consequence of taking meds for GERD

A

reduced absorption of vitamins and minerals d/t the decreased stomach acid

B12 decreased because intrinsic factor is not being secreted thus b12 can’t bind to it and thus can’t be absorbed.

vitamin B1, C, iron, folic acid- all need an acidic environment

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26
Q

what is a PPI drug and what is it used for

A

Pantoprozole

used for management of PUD and treatment of GERD

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27
Q

how do PPIs work

A

they blocky eh H+ K+ ATPase pump(enzyme that is repsonsible for secretion of HCL)

blocking this pump will decrease HCL

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28
Q

why are PPIs more beneficial that H2 blockers

A

they have a longer duration of action and can still have an effect 3-5 days after med is stopped.

they are very effective in healing ulcers within 4-8 weeks

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29
Q

what are implementations of PPIs

A
  • needs to be given 20-30 minutes before a meal (b.c the pump is activated by food- want to give when there is not as much acidity in stomach)
  • preferrably given in the morning
  • capsule can be opened and sprinkled in applesauce or pudding
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30
Q

what are side effects of PPIs

A

C-diff and respiratory infections because the decrease in stomach acidity allows opportunistic bacteria to grow.
infection in the lungs caused from these overgrowing bacteria in the stomach is aspirated and enters the lung

long term therapy can lead to osteoporosis

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31
Q

what is the H2 blocker and its indication

A

Ranitidine

short term treatment of duodenal and gastric ulcers (promotes healing & prevent recurrence)

  • maintenance therapy AFTER healing
  • Gerd and dyspepsia
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32
Q

how do H2 blockers work

A

interferes with acid production by blocking the H2 receptors causing a decrease in volume and secretion of gastric acid.

we have H1 receptors (activation of these cause allergic reactions -itchy watery eyes)
and
H2 receptors- located at the parietal cell area that promotes gastric acid secretion in the stomach

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33
Q

how long do ulcers take to heal

A

gastric-up to 12 weeks

duodenal-6-8 weeks because the duodenum secretes alkaline in the chyme thus reducing acidity

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34
Q

what is contraindicated with H2 blockers

A

not given with antacids because the antacids decrease the absorption of H2 blockers

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35
Q

when should h3 blockers be administered

A

with or immediately after meals and at HS

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36
Q

what do antacids do

A
  • neutralize stomach acid and cause temporary relief from heartburn
  • they stimulate prostaglandin production (producing bicarb and mucus)

alkaline substance

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37
Q

why should antacids not be taken long term

A

can cause metabolic alkalosis because there is too much intake of an alkaline substance

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38
Q

what are different antacids

A
  • MOM- magnesium containing
  • Amphogel- aluminum containing
  • Maalox/mylanta-aluminum containing w/ mg
  • Tum- calcium containing
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39
Q 
what is the adverse effect of 
MOM
Amphogel
Maalox/mylanta
tums
A 
MOM- diarrhea (also used as a laxative)
Amphogel- constipation- possible inhibition of iron absorption
-maalox/mylanta- constipation/diarrhea
increased risk for ca+ loss
-tums-
constipation and kidney stones
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40
Q

what is simethicone

A

an antiflatulent

-has ability to reduce gas bubbles in gi tract that can be caused by indigestion or PUD

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41
Q

how does simethione work

A

brings the gas bubbles together into one big gas bubble and allows belching or passing of gas

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42
Q

what is sucralfate

A

a mucosal protectant
contains aluminum salt and when it mixes with gastric acid- it adheres to the eroded spot and acts as a band aid

it does not effect the secretion of gastric acid
it protects the eroded spot from further damage and allows it to heal

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43
Q

what are the indications for sucralfate

A

short term therapy for ulcers

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44
Q

what is an adverse side effect of sucralfate

A

constipation

45
Q

what is the implementation for sucralfate

A
  • it needs to be given 1 hr before a meal and at bed time (3-4 times /day)
  • not to be given with antacids, h2 blocks or PPIs because it needs the gastric acid to create that liquid band aid
46
Q

what are the anti emetic meds

A

promethazine
prochlorperazine
metoclopramide
ondansetron

47
Q

what does promethazine do

A

blocks effects of Histamine receptors and CTZ

48
Q

what does prochlorperazine

A

alters the effects of dopamine receptors and depresses CTZ

49
Q

what does metoclopramide

A

blocks dopamine receptors in CTZ

accelerates gastric emptying

50
Q

what does ondansetron do

A

blocks the effects of serotonin receptors in CTZ

51
Q

what are the side effects of anti emetics.

A 
extrapyramidal reactions (tremors, pill rolling, involuntary movements)
constipation
dry mouth
sedation
drowsy
HA 
diarrhea
52
Q

what causes angina

A 
CAD
narrowing of vessels
atherosclerosis 
-ischemia of myocardium
-percipitated by exertion or stress and relieved with rest and decreased cardiac demand
53
Q

what is the goal for tx of angina

A
  • increase blood flow
  • decrease myocardial oxygen demand
  • minimize frequency of attacks
  • decreased duration and intensity
  • prevent MI
54
Q

what may a pt feel when experiencing angina

A

-pain feeling like squeeizing, crushing, heaviness,
radiates to left or right side
can go to the jaw as well as epigastric pain

may feel dyspneic, diaphoretic, or tachycardia

55
Q

what forms does nitroglycerin come in

A

PO, transdermal, patch, spray and sublingual

spray and sublingual are rapid acting-used to terminate acute anginal episode

56
Q

how does nitroglycerin work

A

helps relax the arterial and venous smooth muscle = vasodilation
decreases the amount of blood returning to the heart = less blood for ventricles to pump = reduced cardiac output = reduced work load and reduced oxygen demands

-increases blood flow to coronary arteries by vasodilation of coronary arteries = increased o2 supply to the heart

57
Q

what are adverse effects of nitroglycerin

A
  • dizzy
  • HA (vasodilates in head)
  • tachy (d/t drop in bp)
  • hypotension
58
Q

what are the drug drug interactions with nitroglycerin

A

erectile dysfunction meds

  • sildenafil
  • tadalafil
  • this increases the risk of life threatening hypotension
  • nitroglycerin should not be given within 24 hours of these meds
59
Q

what are the outcomes of nitroglycerin

A
  • decrease frequency and severity of angina attacks

- increased activity tolerance

60
Q

what is special about sublingual nitroglycerin

A
  • they need to be stored in a dark container so they remain effective
  • needs to be taken at the first sign of chest pain

-may repeat 2 more times q5 min if pain is unrelieved.
if pain persists after call EMS

61
Q

what is special about nitro-bid

A

it is nitroglycerin ointment

  • dosage measured out on dosing paper.
  • WEAR GLOVES if chance of coming in contact
  • sites need to be rotated
  • area needs to be cleaned thoroughly prior to applying another dose.

-excess goes in black container

62
Q

what is used for long term management of angina

A

isosorbide

63
Q

what is special about transdermal nitroglycerin

A

patch is on for 12-14 hours then removed.
there should be 10-12 hrs over night WITHOUT nitroglycerin
d/t risk of tolerance

64
Q

what does the alpha 1 receptor do and where is it

A

located on vascular smooth muscle and causes vasoconstriction

65
Q

what does the beta 1 receptor do and where is it

A

it is in the heart(primarily)
it increases contractility, HR and conduction (electrical activity)

also located in the juxtaglomerular cells in the kidneys
-increases renin secretion

66
Q

what does the beta 2 receptor do and where is it

A

located on the smooth muscles -pulmonary and coronary artery

causes bronchodilation

67
Q

what do beta1 blockers do

A

“cardioselective”

decrease HR, contractility (=decreased cardiac output and O2 demand) , prevents renin release = decreased bp = less work = less O2 demand, and conduction (helpful for dysrhythmias)

68
Q

what are the beta 1 blockers

A

metoprolol

atenolol

69
Q

what is atenolol used for

A

HTN
angina
prevention of MI

70
Q

what are adverse effects of atenolol

A
  • bradycardia
  • hypotension
  • sexual dysfunction
  • hypo/hyperglycemia
71
Q

what is a NEED TO KNOW with atenolol

A

hold if the apical pulse is <50
or if arrhythmia occurs.
standard to hold if sap <100

72
Q

what can abrupt d/c of atenolol do

A

cause rebound HTN
angina
life threatening arrhythmias

73
Q

what drugs interact with atenolol

A
  • digoxin- bradycardia
  • CCB- bradycardia
  • other anti HTN- cause hypotension
  • nitrates= hypotension
  • alterations with hypoglycemics
74
Q

what is the outcome for atenolol

A
  • decreased BP
  • decreased HR
  • decreased frequency of angina
  • prevent MI
75
Q

what is metoprolol and what is it for

A

a beta 1 blocker

  • its is used for HTN
  • angina
  • prevent MI
  • decrease mortality with MI
  • manage STABLE HF
76
Q

adverse effects of metoprolol

A
  • bradycardia
  • hypotension
  • sexual dysfunction
  • hypo/hyperglycemia
77
Q

drug interactions with metoprolol

A
  • digoxin- bradycardia
  • CCB- bradycardia
  • other anti HTN- cause hypotension
  • nitrates= hypotension
  • alterations with hypoglycemics
78
Q

what needs to be done prior to administration of metoprolol

A

-assess apical pulse
hold <50
SBP <100
check orders

79
Q

what its the outcome of metoprolol

A
  • decrease BP
  • decrease HR
  • decrease frequency of anginal attacks
  • prevent MI

help improve activity tolerance by decreasing O2 demand and increasing O2 supply

80
Q

what is the non selective beta blocker and the indications

A

Carvedilol- acts on alpha and both beta receptors

  • HTN
  • management of HF
  • LV dysfunction after MI
81
Q

what are the adverse effects of carvedilol

A
  • bradycardia
  • hypotension
  • sexual dysfunction
  • hypo/hyperglycemia
82
Q

what is the action of carvedilol

A
  • vasodilation by blocking alpha 1 = low BP
  • decrease contractility by blocking alpha 1

-decreased contractility, HR and conduction by blocking beta 1
decreased renin secretion by blocking beta 1 causing vasodilation = low bp
-broncho constriction by blocking beta 2

83
Q

what is an implementation for carvedilol

A

-assess apical pulse
hold <50
check BP

dont abruptly d/c med d/t rebound HTN, arrhythmias, angina

84
Q

what is the outcome for carvedilol

A

decreased BP HR
decreased severity of HF
well managed LV dysfunction

85
Q

what is a calcium channel blocker

A

-Diltiazem

  • causes vasodilation
  • coronary artery vasodilation (increases O2 supply)
  • slows cardiac conduction (decrease HR, anti arrhythmias)
86
Q

what is calcium needed for

A

cardiac and vascular smooth muscle contraction

87
Q

what is diltiazem used for

A
  • HTN
  • angina
  • SVT(supra ventricular tachyarrhythmias)
  • A-fib with RVR (rapid ventricular rates)
88
Q

what are adverse effects of diltiazem

A
  • peripheral vasodilation
  • peripheral edema
  • sexual dysfunction
89
Q

what drugs does diltiazem interact with

A
  • antihypertensives/nitrates-hypotension

- beta blockers/digoxin-bradycardia

90
Q

what is the implementation for diltiazem

A

assess HR and BP

hold if HR <50 or SBP <90

91
Q

what are the expected outcomes for diltiazem

A
  • decrease in BP
  • decrease severity and frequency of angina
  • prevent tachyarrhythmias
92
Q

what is digoxin

A

a cardiac glycoside

it is to increase force of myocardial contraction so pump is more effective

also slows conduction which slows HR

93
Q

who is digoxin indicated for

A

HF
to improve the strength and force of Left ventricle

A-fib
its an anti arrhythmic

94
Q

what are adverse effects of digoxin

A

fatigue
bradycardia
loss of appetite
N&V

95
Q

what is a need to know about digoxin

A

**hypokalemia and hypomagnasemia can increase risk of digoxin toxicity

96
Q

what needs to be monitored while a pt is on digoxin

A

the lab levels.
K+ and Mg+

if these are low the med needs to be held and MD notified.
need to obtain K+ supplement to counteract so we can give digoxin
we don’t want to not give digoxin d/t abrupt d/c can cause problems

97
Q

what drugs interact with digoxin

A

-beta blockers/anti arrhythmias- bradycardia

98
Q

what yo assess for digoxin

A

-assess apical pulse
hold if <60
-need to monitor digoxin levels

99
Q

how is digoxin excreted

A

mainly in the kidneys

100
Q

what is the digoxin level

A

0.5-2ng/mL

101
Q

what are s/s of digoxin toxicity

A

abd pain, anorexia, N/V
visual disturbances (yellow halos)
bradycardia

102
Q

what food interactions occur with digoxin

A

high fiber

-may decrease digoxin absorption

103
Q

what is implentation for digoxin

A

needs to be administered 1 hour BEFORE or 2 hours after reading a high fiber meal

pts with cardiac hx need a cardiac diet which is high fiber diet.
this med is given for pts w/ cardiac hx
(thats why this is important)

104
Q

what is the antidote for digoxin toxicity

A

digoxin immune Fab
(digibind)
IV form

105
Q

how does Digibind work

A

has digoxin specific antibodies- has ability to bind and form complex which prevents the med from binding to the cardiac muscle.

it is then excreted through the kidneys

106
Q

when should you see improvement of the antidote of digoxin toxicity

A

-within 30 minutes

will be able to tell if it is working by resolution of symptoms

107
Q

what is the adverse effect of digoxin immune fab

A

-hypokalemia

108
Q

when should digoxin levels be assessed after admin of digoxin immune fab

A

-5-7 days after admin because the levels don’t show the bound digoxin- they just show the total digoxin levels

202D (6 decks)

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