1
Q
what is the pH of the stomach
A
2-3
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
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
4
Q
what is intrinsic factor important for
A
the absorption of B 12
5
Q
what is peptic ulcer disease
A
a lesion or erosion in the stomach or duodenum
the hyper secretion of HCL
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
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
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.
9
Q
a patient who is on long term corticosteroids should also be taking what
A
PPI’s
10
Q
how does alcohol cause peptic ulcer disease
A
promotes HCL secretion and reduces bicarb production.
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)
12
Q
what is H. Pylori
A
a corkscrew shaped bacteria that screw themselves in to the lining of the stomach.
13
Q
how is H pylori transmitted
A
through contaminated water (sewage), stool or mouth fluids-
it then triggers ulcers
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
15
Q
what does an H pylori infection cause
A
triggers ulcers
-chronic inflammation of the gastric or duodenal lining.
16
Q
what is the most accurate way to diagnose an H pylori infection
A
-via endoscopy and take a bx of the lining
17
Q
what is the treatment for an H Pylori infection
A
antibiotics ( usually 2-3) in conjunction with PPIs or histamine blockers.
18
Q
what is GERD
A
stomach acid that enters the esophagus
risk of esophageal lining
19
Q
what are symptoms of GERD
A
"heartburn" dysphagia dyspepsia heartburn belching nausea (some pts feel chest pain)
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
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
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
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
24
Q
what drug classes can help with GERD and peptic ulcer disease
A
- proton pump inhibitors
- H2 receptor antagonists
- antacids
25
what is a consequence of taking meds for GERD
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
26
what is a PPI drug and what is it used for
Pantoprozole
used for management of PUD and treatment of GERD
27
how do PPIs work
they blocky eh H+ K+ ATPase pump(enzyme that is repsonsible for secretion of HCL)
blocking this pump will decrease HCL
28
why are PPIs more beneficial that H2 blockers
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
29
what are implementations of PPIs
- 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
30
what are side effects of PPIs
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
31
what is the H2 blocker and its indication
Ranitidine
short term treatment of duodenal and gastric ulcers (promotes healing & prevent recurrence)
- maintenance therapy AFTER healing
- Gerd and dyspepsia
32
how do H2 blockers work
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
33
how long do ulcers take to heal
gastric-up to 12 weeks
| duodenal-6-8 weeks because the duodenum secretes alkaline in the chyme thus reducing acidity
34
what is contraindicated with H2 blockers
not given with antacids because the antacids decrease the absorption of H2 blockers
35
when should h3 blockers be administered
with or immediately after meals and at HS
36
what do antacids do
- neutralize stomach acid and cause temporary relief from heartburn
- they stimulate prostaglandin production (producing bicarb and mucus)
alkaline substance
37
why should antacids not be taken long term
can cause metabolic alkalosis because there is too much intake of an alkaline substance
38
what are different antacids
- MOM- magnesium containing
- Amphogel- aluminum containing
- Maalox/mylanta-aluminum containing w/ mg
- Tum- calcium containing
39
```
what is the adverse effect of
MOM
Amphogel
Maalox/mylanta
tums
```
```
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
```
40
what is simethicone
an antiflatulent
| -has ability to reduce gas bubbles in gi tract that can be caused by indigestion or PUD
41
how does simethione work
brings the gas bubbles together into one big gas bubble and allows belching or passing of gas
42
what is sucralfate
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
43
what are the indications for sucralfate
short term therapy for ulcers
44
what is an adverse side effect of sucralfate
constipation
45
what is the implementation for sucralfate
- 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
what are the anti emetic meds
promethazine
prochlorperazine
metoclopramide
ondansetron
47
what does promethazine do
blocks effects of Histamine receptors and CTZ
48
what does prochlorperazine
alters the effects of dopamine receptors and depresses CTZ
49
what does metoclopramide
blocks dopamine receptors in CTZ
| accelerates gastric emptying
50
what does ondansetron do
blocks the effects of serotonin receptors in CTZ
51
what are the side effects of anti emetics.
```
extrapyramidal reactions (tremors, pill rolling, involuntary movements)
constipation
dry mouth
sedation
drowsy
HA
diarrhea
```
52
what causes angina
```
CAD
narrowing of vessels
atherosclerosis
-ischemia of myocardium
-percipitated by exertion or stress and relieved with rest and decreased cardiac demand
```
53
what is the goal for tx of angina
- increase blood flow
- decrease myocardial oxygen demand
- minimize frequency of attacks
- decreased duration and intensity
- prevent MI
54
what may a pt feel when experiencing angina
-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
what forms does nitroglycerin come in
PO, transdermal, patch, spray and sublingual
spray and sublingual are rapid acting-used to terminate acute anginal episode
56
how does nitroglycerin work
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
what are adverse effects of nitroglycerin
- dizzy
- HA (vasodilates in head)
- tachy (d/t drop in bp)
- hypotension
58
what are the drug drug interactions with nitroglycerin
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
what are the outcomes of nitroglycerin
- decrease frequency and severity of angina attacks
| - increased activity tolerance
60
what is special about sublingual nitroglycerin
- 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
what is special about nitro-bid
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
what is used for long term management of angina
isosorbide
63
what is special about transdermal nitroglycerin
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
what does the alpha 1 receptor do and where is it
located on vascular smooth muscle and causes vasoconstriction
65
what does the beta 1 receptor do and where is it
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
what does the beta 2 receptor do and where is it
located on the smooth muscles -pulmonary and coronary artery
causes bronchodilation
67
what do beta1 blockers do
"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
what are the beta 1 blockers
metoprolol
| atenolol
69
what is atenolol used for
HTN
angina
prevention of MI
70
what are adverse effects of atenolol
- bradycardia
- hypotension
- sexual dysfunction
- hypo/hyperglycemia
71
what is a NEED TO KNOW with atenolol
hold if the apical pulse is <50
or if arrhythmia occurs.
standard to hold if sap <100
72
what can abrupt d/c of atenolol do
cause rebound HTN
angina
life threatening arrhythmias
73
what drugs interact with atenolol
- digoxin- bradycardia
- CCB- bradycardia
- other anti HTN- cause hypotension
- nitrates= hypotension
- alterations with hypoglycemics
74
what is the outcome for atenolol
- decreased BP
- decreased HR
- decreased frequency of angina
- prevent MI
75
what is metoprolol and what is it for
a beta 1 blocker
- its is used for HTN
- angina
- prevent MI
- decrease mortality with MI
- manage STABLE HF
76
adverse effects of metoprolol
- bradycardia
- hypotension
- sexual dysfunction
- hypo/hyperglycemia
77
drug interactions with metoprolol
- digoxin- bradycardia
- CCB- bradycardia
- other anti HTN- cause hypotension
- nitrates= hypotension
- alterations with hypoglycemics
78
what needs to be done prior to administration of metoprolol
-assess apical pulse
hold <50
SBP <100
check orders
79
what its the outcome of metoprolol
- decrease BP
- decrease HR
- decrease frequency of anginal attacks
- prevent MI
help improve activity tolerance by decreasing O2 demand and increasing O2 supply
80
what is the non selective beta blocker and the indications
Carvedilol- acts on alpha and both beta receptors
- HTN
- management of HF
- LV dysfunction after MI
81
what are the adverse effects of carvedilol
- bradycardia
- hypotension
- sexual dysfunction
- hypo/hyperglycemia
82
what is the action of carvedilol
- 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
what is an implementation for carvedilol
-assess apical pulse
hold <50
check BP
dont abruptly d/c med d/t rebound HTN, arrhythmias, angina
84
what is the outcome for carvedilol
decreased BP HR
decreased severity of HF
well managed LV dysfunction
85
what is a calcium channel blocker
-Diltiazem
- causes vasodilation
- coronary artery vasodilation (increases O2 supply)
- slows cardiac conduction (decrease HR, anti arrhythmias)
86
what is calcium needed for
cardiac and vascular smooth muscle contraction
87
what is diltiazem used for
- HTN
- angina
- SVT(supra ventricular tachyarrhythmias)
- A-fib with RVR (rapid ventricular rates)
88
what are adverse effects of diltiazem
- peripheral vasodilation
- peripheral edema
- sexual dysfunction
89
what drugs does diltiazem interact with
- antihypertensives/nitrates-hypotension
| - beta blockers/digoxin-bradycardia
90
what is the implementation for diltiazem
assess HR and BP
| hold if HR <50 or SBP <90
91
what are the expected outcomes for diltiazem
- decrease in BP
- decrease severity and frequency of angina
- prevent tachyarrhythmias
92
what is digoxin
a cardiac glycoside
it is to increase force of myocardial contraction so pump is more effective
also slows conduction which slows HR
93
who is digoxin indicated for
HF
to improve the strength and force of Left ventricle
A-fib
its an anti arrhythmic
94
what are adverse effects of digoxin
fatigue
bradycardia
loss of appetite
N&V
95
what is a need to know about digoxin
**hypokalemia and hypomagnasemia can increase risk of digoxin toxicity
96
what needs to be monitored while a pt is on digoxin
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
what drugs interact with digoxin
-beta blockers/anti arrhythmias- bradycardia
98
what yo assess for digoxin
-assess apical pulse
hold if <60
-need to monitor digoxin levels
99
how is digoxin excreted
mainly in the kidneys
100
what is the digoxin level
0.5-2ng/mL
101
what are s/s of digoxin toxicity
abd pain, anorexia, N/V
visual disturbances (yellow halos)
bradycardia
102
what food interactions occur with digoxin
high fiber
| -may decrease digoxin absorption
103
what is implentation for digoxin
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
what is the antidote for digoxin toxicity
digoxin immune Fab
(digibind)
IV form
105
how does Digibind work
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
when should you see improvement of the antidote of digoxin toxicity
-within 30 minutes
will be able to tell if it is working by resolution of symptoms
107
what is the adverse effect of digoxin immune fab
-hypokalemia
108
when should digoxin levels be assessed after admin of digoxin immune fab
-5-7 days after admin because the levels don't show the bound digoxin- they just show the total digoxin levels
202D
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