Final Exam (GI, Dermatology, and Pediatrics) Flashcards

(312 cards)

1
Q

What is the main energy source for humans? What is the use?

A

Carbohydrates; generate many metabolic intermediates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are excess carbohydrates in the diet converted to?

A

glycogen and triacylglycerol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are examples of simple carbohydrates?

A

Sugars, fruits, vegetables, and milk, simple sugars (glucose, fructose, galactose), disaccharides (sucrose, lactose, maltose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are complex carbohydrates?

A

polysaccharides; glycogen (starch and fiber in plants)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is another name for glucose?

A

dextrose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the most important carbohydrate fuel for the body?

A

glucose/dextrose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is fructose found?

A

Fruits, vegetables, honey

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does fructose lead to increases of in the blood?

A

Does not cause a great rise in blood glucose compared to other sugars; causes an increase in blood lipids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What ingredient has been suggested to be related in the increased incidence of diabetes and obesity?

A

high-fructose corn syrup.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does a-amylase do?

A

Hydrolyzes starch and glycogen to maltose and maltotriose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where is a-amylase found?

A

in the saliva and pancreatic juice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What enzymes are found on the luminal surface of the small intestine and what is their function?

A
  • maltase: converts maltose and maltotriose to glucose
  • sucrase: converts sucrose to glucose and fructose
  • lactase: converts lactose to glucose and galactose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What carbohydrates can be absorbed into the body?

A

only monosaccharides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How are indigestible carbohydrates metabolized and what do they produce?

A

converted to monosaccharides by bacterial enzymes and metabolized anaerobically by bacteria.
produce short chain fatty acids, lactate, H2, CH4, and CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do indigestible carbohydrates cause and what is an example?

A

flatulence and abdominal discomfort; ex: raffinose; found in beans and peas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does the glycemic index measure?

A

How quickly individual foods will raise blood glucose level; ratio of the area of the blood glucose response curve to that of glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a food listed in lecture with the highest glycemic index?

A

white potato

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is a food listed in lecture with the lowest glycemic index?

A

Beans (kidney)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are examples of dietary fibers? Are they soluble or no?

A

Cellulose and hemicellulose – insoluble
Lignin – insoluble
Pectin – soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is an example of cellulose and hemicellulose and what is its function?

A
  • unrefined cereals, bran, and whole wheat
  • increase stool bulk and decrease intestinal transit time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is an example of lignin and what is its function?

A

Woody parts of vegetables; binds cholesterol and carcinogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is an example of pectin and what is its function?

A

Fruits; decreases rate of sugar uptake and decreases serum cholesterol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the purpose of lipids in the diet?

A
  • efficient source of energy
  • provides satiety
  • adds flavor and aroma to diet
  • carrier for fat-soluble vitamins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the main source for dietary fat?

A

triacylglycerol (glycerol + three fatty acids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are secondary sources of dietary fat?
phospholipids, cholesterol, cholesterol esters, fatty acids
26
What are the essential fatty acids? What are they used for?
Omega-3 and Omega-6 fatty acids; used to synthesize eicosanoids in the body
27
what are the omega-3 fatty acids and what are they found in?
a-linolenic acid -- in vegetable oils EPA and DHA in fish oils
28
what are the omega-6 fatty acids and what are they found in?
linoleic acid -- corn oil arachidonic acid -- in meat and fish
29
What are trans fatty acids?
produced by hydrogenation processes to convert unsaturated fatty acids to saturated fatty acids (a byproduct of this conversion) have higher melting points than the same fatty acid in the cis configuration; raise blood cholesterol levels and increase the risk of heart disease.
30
How are lipids digested?
dispersed into small droplets and solubilized by bile acids
31
What is the role of gastric and pancreatic lipases?
hydrolyze triacylglycerol to fatty acids and monoacylglycerol; produce fatty acids that act as surfactants.
32
What is the role of esterase?
hydrolyzes monoacylglycerol and cholesterol ester.
33
How are lipids delivered to the peripheral tissues?
directly delivered by chylomicron
34
How is fat used by the muscles?
As an energy source
35
Where is excess lipids stored?
stored as fat in adipose tissues
36
brain and lipids?
the brain does not use fat as an energy source
37
How are lipids utilized during starvation?
The liver converts fatty acid to ketone bodies through ketogenesis, which can be used as an energy source by the brain and muscle.
38
What is the role of dietary proteins?
structural component; used for enzymes, hormones, plasma proteins, and antibodies
39
What is excess protein in the diet used for?
source of energy, glucogenic amino acids used to make glucose, ketogenic amino acids used to make keto acids and fatty acids; eventually extra protein is used to make triacylglycerol in adipose tissue
40
What does a negative nitrogen balance indicate?
Inadequate dietary intake of protein; trauma or illness
41
What does a positive nitrogen balance indicate?
net increase in body protein stores; seen in growing children, pregnant women, and adults recovering from illness
42
how are proteins digested?
- low pH of gastric juice in the stomach (less than 2) denatures the proteins - broken down by pepsins, which are stable and active at acidic pH (ex: aspartic protease) - digested by peptidases at the luminal surface in the intestines (called the brush border) - digested by intracellular peptidases through an amino acid and peptide transport system. - di and tri-peptides are hydrolyzed intracellularly
43
What amino acids are released into the blood?
only free amino acids are released into the blood
44
What is celiac disease? traits and characteristics
gluten intolerance; an autoimmune disorder - caused by exposure to gluten which is in proteins in wheat, rye, and barley. - inflammation and damage of the lining of the small intestine upon exposure - characterized by diarrhea, weight loss, and malnutrition
45
what is the energy content of carbohydrates?
4 kcal/g
46
What is the energy content of fat?
9 kcal/g
47
What is the energy content of protein?
4 kcal/g
48
what is the energy content of alcohol
7 kcal/g
49
What are the 3 main forms of energy reserve?
- fat in adipose tissues - glycogen in the liver to maintain blood glucose levels - glycogen in muscle used for exercise
50
What are the characteristics of a well-fed state?
- insulin release - glycolysis - glycogen synthesis - catabolism of amino acids - fatty acid synthesis - no gluconeogenesis
51
What are the characteristics of the early fasting state?
- glucagon release - glycogen breakdown - gluconeogenesis (cori cycle and alanine cycle) - no catabolism of amino acids
52
What are the characteristics of a fasting state?
- glucagon release - gluconeogenesis - protein is used as a major carbon and nitrogen source - lipolysis in adipose tissue - fatty acid oxidation - ketogenesis - reduced thyroid hormones
53
What happens when blood glucose drops below 1.5 mM
hypoglycemia; coma and death shortly follow
54
What are complications of hyperglycemia?
dehydration, hyperglycemic coma, complications of diabetes
55
What fuels the brain/ how much is needed?
glucose; brain uses more than 20% total energy 100 to 120 g glucose per day 15 to 20% of total oxygen
56
Energy storage in the brain?
no energy storage; the brain does not use fat
57
How does the brain adapt to starvation?
through the ketone bodies made in the liver
58
What is marasmus?
inadequate intake of protein and energy; thin, wasted appearance
59
What is kwashiorkor?
inadequate protein intake with adequate energy intake - plump appearance due to edema
60
What are recommended dietary allowances?
original allowances published in 1968
61
What are the dietary reference intakes?
nutrition recommendations from the institute of medicine of the national academies. contains many different types of requirements
62
What is the estimated average requirement?
amount of nutrient estimated to meet the need of 50% of the healthy individuals in an age and gender group.
63
What is the recommended dietary allowance?
- two standard deviations above the EAR (estimated average requirement) - will meet the need of 97-98% of the healthy individuals in a group.
64
What is adequate intake?
Used when scientific evidence is inadequate to set an EAR approximations of the average nutrient intake by a healthy population
65
what is the tolerable upper intake level?
maximum level of daily intake of a nutrient without any health risk
66
What are the fat soluble vitamins?
vitamin A, vitamin D, Vitamin E, vitamin K
67
What are the water-soluble vitamins?
group of vitamin Bs and Vitamin C
68
What are macrominerals?
Ca2+ and Mg2+
69
what are trace minerals?
iron, iodine, zinc, copper, chromium, selenium, manganese, molybdenum, fluoride, and boron
70
What is the name for vitamin B6?
pyridoxine
71
What is the name for vitamin B12?
Cobalamin
72
How is vitamin A produced?
produced by carotenoids (organic pigments in plants)
73
What is a characteristic of vitamin A deficiency?
night blindness
74
What is retinoic acid and what is its function?
vitamin A; functions as steroid hormones and regulates cell growth and differentiation
75
Use and storage of carotenoids?
effective antioxidants that reduce the risk of cancers; stored in the liver as retinol palmitate
76
What are the dietary sources of carotenoids (vitamin A)?
dark green and yellow vegetables, liver, egg yolk, butter, and whole milk
77
Which vitamin is most commonly deficient?
Vitamin D
78
What is the function of vitamin D?
steroid hormones; maintain calcium homeostasis
79
How is vitamin D synthesized?
By an intermediate in cholesterol biosynthesis; can be produced photochemically in the skin
80
What is vitamin D deficiency caused by and what is this characterized by?
insufficient exposure to sunlight; rickets in young children and osteomalacia in adults
81
What are dietary sources of vitamin D?
milk, saltwater fish, liver, and egg yolk
82
How does vitamin E occur naturally in the diet?
tocopherols and tocotrienols
83
What is the function of vitamin E in the diet?
naturally occurring antioxidants protecting unsaturated fatty acids.
84
Where does vitamin E accumulate?
circulating lipoproteins, cellular membranes, and fat deposits
85
how does vitamin E reduce the risk of cardiovascular disease?
prevents oxidation of LDL; oxidized form of LDL increases cardiovascular risk.
86
what are the dietary sources of vitamin K?
vegetable oils rich in polyunsaturated fatty acids
87
What is vitamin K essential for?
- formation of carboxyglutamic acids (allow proteins to bind Ca2+) - essential for blood clotting - essential for bone mineralization
88
What is warfarin?
- an anticoagulant and vitamin K antagonist - reduces formation of carboxyglutamic acid - prevents thrombosis - inhibits vitamin K epoxide reductase
89
What are dietary sources of vitamin k?
- K1-- in green vegetables - K2 -- synthesized by intestinal bacteria
90
What is vitamin B1?
thiamin
91
what is the role of thiamin in the body?
- thiamin pyrophosphate functions as a cofactor in enzymatic catalysis - thiamin triphosphate functions in transmission of nerve impulse in peripheral nerve membranes
92
What is thiamin deficiency called and what is it characterized by?
beriberi-- muscular atrophy and weakness
93
What populations is thiamin (B1) deficiency seen in?
populations exclusively eating polished rice & alcoholics
94
What is riboflavin (b2) deficiency characterized by?
angular cheilitis, glossitis, and scaly dermatitis
95
What population is riboflavin deficiency seen in?
alcoholics
96
What foods is thiamin (b2) found in?
milk, meat, eggs, and cereal products
97
What is the role of Niacin (B3) in the body?
converted to cofactors NAD and NADP used in redox reactions and cellular respiration as electron acceptors/ hydrogen donors
98
What is niacin (B3) deficiency called? what are the symptoms/characteristics?
pellagra; dermatitis, diarrhea, and dementia
99
What populations is niacin (b3) deficiency seen in?
Rare; in alcoholics, patients with malabsorption, and elderly on restrictive diets
100
What foods is niacin (B3) found in?
meats, peanuts, and enriched cereals
101
What is the use of pyridoxine (B6) in the body?
- amino acid metabolism - synthesis of neurotransmitters - synthesis of sphingolipids
102
what are symptoms of pyridoxine (B6) deficiency?
mild: irritability, nervousness, and depression severe: peripheral neuropathy and convulsions
103
What foods in pyridoxine (B6) found in?
meat, vegetables, and whole grain cereals
104
What is the purpose of biotin (b7) in the body?
- cofactor for activation of carbon dioxide in carboxylase enzymes - covalently bound to lysine side chains in enzymes
105
What are risk factors for biotin deficiency?
- excessive consumption of raw egg whites - pregnancy
106
What is the use of folic acid (B9) in the body?
- used in synthesis of amino acids and nucleotides - essential for DNA synthesis and cellular proliferation
107
What are characteristics/ risk factors of folic acid (B9) deficiency?
- inhibition of DNA synthesis - results in anemia - increases risk of birth defects (neural tube defect) - common in alcoholics
108
What is vitamin B12 called?
cobalamin
109
What is vitamin B12 deficiency characterized by?
- accumulation of homocysteine and methylmalonic acid causing anemia and neurological damage.
110
Vitamin B12 deficiency risk factors
severe malabsorption diseases and long-term vegetarians
111
What is another name for vitamin c?
ascorbic acid
112
What is the role of vitamin C in the body?
- collagen stability essential for maintenance of normal connective tissue, wound healing, and bone formation - aids in absorption of iron - protects vitamin A, E, and some B vitamins from oxidation
113
What is mild vitamin C deficiency characterized by?
capillary fragility, easy bruising, and decreased immunocompetence
114
What is severe vitamin C deficiency called and characterized by?
Scurvy; decreased wound healing, osteoporosis, hemorrhaging, anemia
115
What are the roles of calcium in the body?
making bones, second messenger, used by enzymes, essential for blood coagulation and muscle contractility.
116
How is calcium serum levels regulated?
- elaborate homeostatic control system - bones serve as reservoir - dietary insufficiency results in loss of Ca2+ from bones - vitamin D required for calcium utilization
117
What is calcium deficiency characterized by?
- resembles vitamin D deficiency - may contribute to osteoporosis - muscle cramps
118
what are the dietary sources of calcium?
dairy products, nuts, beans, seeds, and seaweeds
119
What is a result of iron deficiency?
anemia; common in children and menstruating females
120
Why is iron homeostasis tightly regulated?
- toxic when by itself; generates free radicals - must always be bound in the blood/body
121
iodine use in the body
used for synthesis of thyroid hormones
122
best natural food source of iodine
seafood (fish and seaweeds)
123
Iodine deficiency
goiter- enlargement of thyroid gland cretinism- stunted physical and mental growth
124
zinc deficiency characteristics
- poor growth and impairment of sexual development in children - poor wound healing, dermatitis, impaired immune function
125
copper use in body
required for function of many enzymes
126
copper deficiency characteristics
anemia, bone demineralization, and blood vessel fragility
127
What is one of the first messengers involved in acid secretion?
gastrin
128
What cell activates the proton pump in the stomach to produce acid?
parietal cells
129
What are three second messengers used to activate parietal cells?
ACh, Histamine, and gastrin
130
What are three second messengers used to activate parietal cells?
ACh, Histamine, and gastrin
131
Which messenger provides negative feedback in acid secretion?
somatostatin
132
What are ulcers caused by?
depletion of mucus layer by inhibition of prostaglandins
133
what are adverse effects of sodium bicarbonate?
systemic alkalosis, fluid retention
134
What are adverse effects of calcium carbonate?
hypercalcemia, nephrolithiasis, milk-alkali syndrome
135
What are adverse effects of aluminum hydroxide?
constipation, hypophosphatemia,
136
What are the adverse effects of magnesium hydroxide?
diarrhea
137
What is the MOA of cimetidine?
competitive antagonist of H2 histamine receptor reduce gastric acid secretion in response to histamine, gastrin, acetylcholine
138
What are the second generation H2 blockers?
ranitidine, famotidine, nizatidine
139
What is the difference between cimetidine and famotidine?
1st gen vs 2nd gen H2 blockers - 2nd gen has: - longer half life - fewer effects on CYP 450 system - greater potency - absorbed quickly
140
what cell and second messenger are stimulated/released even when on a PPI?
G cell; Gastrin
141
What cell and second messenger are not stimulated/ released when on a PPI?
D cell; somatostatin (no negative feedback)
142
What is the difference between omeprazole and esomeprazole?
omeprazole- racemic mixture; less potent esomeprazole-- purified s enantiomer; more potent (more expensive)
143
MOA of PPIs?
- taken up by parietal cells in the stomach - prodrugs activated by acidic pH - irreversible inhibition of proton pump (forms a disulfide bond) - short plasma half life but long duration of action due to covalent inhibition and slow turnover of proton pumps
144
What is a risk of discontinuing PPIs?
rebound hypersecretion of gastric acid; hypergastrinemia
145
Which drug class is most effective in reducing acid in the stomach?
PPIs
146
Which drug class can tolerance be built to?
H2 antagonists
147
What are risks of PPI therapy?
vitamin B12 deficiency decreased Ca2+ absorption/ increased bone fractures
148
What is sucralfate?
a mucosal protective agent; forms protective barrier at ulcer site.
149
What is the use of misoprostol?
semi-synthetic prostaglandin; reduced acid secretion; enhance mucus and bicarbonate secretion can be used in combination with chronic NSAIDS
150
Why is bismuth subsalicyclate used for h pylori treatment?
coating agent in the stomach; anti inflammatory and antibacterial properties
151
What is bismuth subsalicylate used for?
nausea, heartburn, indigestion, upset stomach, diarrhea, h-pylori treatment
152
what antibiotics are commonly used to treat H. pylori?
metronidazole, tetracycline, amoxicillin, and clarithromycin
153
What controls the smooth muscles in the gut?
the enteric nervous system
154
how do bulk and osmotic laxatives work?
form hydrophilic mass and increase water in the intestinal lumen which stimulates stretch receptors and increases peristalsis
155
How do stool softeners work?
acts as a surfactant and lubricant; make passage easier and decrease water absorption
156
how do secretory/stimulant laxatives work?
irritation of mucosa affects fluid secretion/absorption balance and induces peristalsis
157
What is gastroparesis?
neuropathy during diabetes or Parkinson's disease
158
what is metoclopramide?
D2 dopamine receptor antagonist
159
How does metoclopramide work?
block of D2 receptors in myenteric plexus leads to increased acetylcholine release; also produces anti-emetic effects
160
What are the centrally acting opioid receptor antagonists
naloxone, naltrexone, nalmefene
161
What are the peripherally acting opioid receptor antagonists?
naloxegol, alvimopan, naldemedine
162
What is lubiprostone?
type II chloride channel activator
163
What are linaclotide (linzess) and plecanatide (trulance)?
peptide activators of guanylate cyclase C
164
What are opiates used as anti-diarrheals?
diphenoxylate + atropine (lomotil) -- active in CNS and loperamide (imodium) -- activates Mu opiod receptors in GI
165
What are 5-HT3 receptor antagonists used for?
block activity of afferent nerves from stomach and small intestine to prevent nausea and vomiting
166
What is ondansetron?
a 5-HT3 receptor antagonist
167
What are side effects of ondanstron
constipation
168
What are some antihistamines/ anticholinergics that can be used as antiemetics?
Diphenhydramine, meclizine, scopolamine
169
What are the D2 dopamine receptor antagonists that have anti-emetic and sedative properties?
metoclopramide, prochlorperazine, promethazine, droperidol
170
risk factors of GERD
obesity, tobacco smoking, pregnancy, delayed gastric emptying, genetic predisposition, nonalcoholic fatty liver disease, major depressive disorder, asthma
171
What is one medication that reduces the LES pressure?
tetracycline
172
What are medications that directly irritate esophageal mucosa?
aspirin, bisphosphonates, NSAIDS
173
What are the three main clinical presentations of GERD? (all 3 must be present for diagnosis)
heartburn, regurgitation/belching, and reflux chest pain
174
What are extraesophageal symptoms of GERD?
chronic cough, laryngitis, wheezing, asthma
175
What are the alarm symptoms for GERD?
dysphagia (difficulty swallowing), painful swallowing, bleeding, weight loss
176
what is barrett's esophagus?
thickening of the esophagus lining
177
first-line prevention and treatment of GERD
lifestyle modifications
178
first-line agent to neutralize acid
antacids
179
first-line agent to reduce gastric acid secretion
H2RAs and PPIs
180
Which GERD medications are PRN?
antacids and sometimes H2RAs
181
Which GERD medications are scheduled?
PPIs and sometimes H2RAs
182
What is always first line treatment for GERD?
lifestyle mods to address triggers
183
how long is the OTC trial for GERD before referring?
2 weeks
184
How long is a rx trial of PPI before switching?
8 weeks
185
What can be avoided to improve gerd symptoms?
fatty meals, carbonated beverages, excessive exercise
186
What are other recommendable lifestyle modifications for GERD?
eat smaller meals, lose weight, stop smoking, sleep with head elevated, sleep on left side
187
How do antacids work?
- maintain pH>4 and increase LES pressure; offer immediate symptomatic relief
188
Which antacids cause constipation?
Calcium and aluminum
189
Which antacid causes diarrhea?
magnesium
190
What are side effects all antacids can cause?
N/V
191
What are drugs that commonly interact with antacids?
antimicrobials, levothyroxine, iron, steroids, digoxin
192
When should interacting medications with antacids be taken?
2 hours before or 4-6 hours after antacids
193
What is the maximum frequency of all antacids
up to 4x/day
194
which antacid medications cannot be given to children?
Alka-seltzer and pepto-bismol
195
What is the MOA for H2RAs?
reversible inhibition of histamine receptors
196
Which H2RA has many drug-drug interactions and is not commonly used?
cimetidine
197
What are side effects of H2RAs?
headache, dizziness, fatigue, constipation or diarrhea, confusion/delerium, agitation, B12 deficiency with long-term use
198
What are the clinical pearls of H2RAs?
tachyphylaxis occurs with long-term use on beer's criteria not as efficacious as PPIs useful for nocturnal symptoms
199
MOA for PPIs
irriversible inhibition of proton/potassium ATPase
200
What is Dexilant
Dexlansoprazole; newer PPI; dual release formulation allows 2 different onsets; can be taken without regard to meals
201
How long is OTC treatment with PPIs?
2 weeks only; if needed for longer or if needed again before 4 months, refer
202
Omeprazole release
only immediate release PPI when combined with sodium bicarbonate
203
What is omeprazole/ esomeprazole metabolized by?
CYP 2C19
204
What drugs do PPIs increase the effect of?
methotrexate, phenytoin, warfarin
205
What drugs do PPIs decrease the effect of?
iron, bisphosphonates, HIV drugs, clopidogrel
206
What are potential long-term side effects of PPIs?
Hypomagnesemia, bone density decrease/fractures, vitamin B12 deficiency, chronic kidney disease (rare)
207
Which PPI interacts with clopidogrel?
omeprazole/ esomeprazole
208
When is sucralfate recommended for GERD?
in pregnancy
209
What are the options for combination therapy?
antacids and H2RAs PPIs and H2RAs
210
How should PPIs be discontinued?
taper to decrease hypergastrinemia
211
Which medications are on beers criteria?
both PPIs and H2RAs
212
In pregnancy, what is the desired order of treatment for reflux?
lifestyle modifications >> antacids/ sucralfate >> H2RAs >> PPIs (last line; any except omeprazole)
213
What is first line treatment in those lactating
antacids >> PPIs and H2RAs found in breast milk
214
alarm symptoms of GERD in children
weight loss, fever, seizure, persistent vomiting/diarrhea
215
non-pharm options for children
thickening formula/food, decreasing volume of intake, milk free diet, positioning therapy
216
What antacids should be avoided in those younger than 12?
aluminum or bismuth subsalicyclate
217
safe OTC options for children?
simethicone and probiotics
218
Where is the common site of damage for H. Pylori induced ulcer?
D>S
219
Where is the common site of damage for NSAID or stress-induced ulcers?
S>D
220
what type of ulcer presents with epigastic pain?
H. Pylori
221
Which type of ulcer is generally the most deep
NSAID-induced
222
What type of ulcers generally result in more bleeding?
NSAID and Stress
223
What are aggressive risk factors for PUD
pepsin, NSAIDS, H. Pylori, gastric acid
224
What are protective factors for PUD?
blood flow to mucosa, bicarbonate, prostaglandins and mucus
225
In what type of ulcer does food relieve the pain?
duodenum
226
in what type of ulcer does food worsen the pain?
stomach
227
what is the general treatment regimen for h.pylori
PPI plus 2-3 antibiotics
228
What is the preferred regimen for h. pylori?
quadruple therapy: PPI BID, bismuth subsalicyclate, metronidazole, tetracycline x10-14 days
229
What is helidac?
convenience packaging of the bismuth quadruple (14 day therapy)
230
What is pylera?
3 in 1 capsule of the bismuth quadruple (10 day therapy) PPI is separate
231
How long should PPIs be used for h. pylori therapy?
14 days; should not be continued indefinitely
232
bismuth salts MOA
topical bactericidal effect; improves ulcer healing by inhibiting aggressive factors and increasing protective factors
233
adverse reactions of metronidazole
avoid alcohol due to N/V
234
adverse effect of levofloxacin
tendon rupture, mental status change, QTC prolongation
235
What class is levofloxacin?
fluoroquinolone
236
adverse effect of amoxicillin
GI upset (N/V) diarrhea; take with food to help alleviate
237
adverse effect of tetracycline and doxycycline
photosensitivity
238
amoxicillin class
penicillin
239
tetracycline and doxycycline class
tetracyclines
240
clarithromycin class
macrolide
241
azithromycin class
macrolide
242
adverse effect of clarithromycin
QTC prolongation, photosensitivity, GI upset
243
what can probiotics be used for?
prophylaxis for h.pylori colonization; supplement to antibiotic therapy
244
What therapies are no longer recommended in the US due to resistance?
clarithromycin based therapies
245
How do NSAIDs increase the risk of PUD?
by reducing protective factors such as prostaglandins (impaired mucosal defense)
246
What is included in prophylaxis of NSAID induced PUD?
PPIs, H2RAs (duodenal ulcer only), misoprostol
247
What is included in treatment of NSAID induced PUD?
PPIs, H2RAs, sucralfate
248
When is misoprostol used?
As prophylaxis only (prostaglandin analogue)
249
When is sucralfate used?
For an NSAID induced ulcer; administer on an empty stomach 2 hours before or 4 hours after other meds
250
What is the preferred non-selective agent?
Naproxen
251
What is the preferred cox-2 specific agent?
celecoxib
252
Which agent is less likely to cause ulcers?
celecoxib
253
Which agent has the least cardiovascular risk?
naproxen
254
When are H2RAs used for NSAID induced ulcers?
for prophylaxis or treatment; duodenal ulcer prevention only
255
What is the result of an increase in intestinal motility?
diarrhea
256
what is the result of a decrease in intestinal motility?
constipation
257
what is acute diarrrhea?
less than 14 days
258
what is persistent diarrhea?
>14 days
259
What is chronic diarrhea?
>30 days
260
What is secretory diarrhea characterized by?
large stool volumes; caused by laxatives, not altered by fasting
261
What is an example of osmotic diarrhea
lactose intolerance
262
characteristics of osmotic diarrhea
improves with fasting state
263
what is exudative diarrhea characterized by?
inflammatory diseases of the bowel; large stool volumes
264
most common causes of diarrhea in the US
salmonella, norovirus
265
complications of diarrhea
inconvenience, social isolation, dehydration, electrolyte imbalance (may cause cardiac arrythmia)
266
diet management in diarrhea
most important for osmotic diarrhea; do not stop feedings in those with bacterial diarrhea; BRAT diet x24 hours
267
non-pharmacologic diarrhea treatment
diet, fluid/electrolyte replacement
268
pharmacologic diarrhea treatment
antimotility agents; loperamide; short term use only; do not use with bacterial diarrhea
269
absorbents
used in people with chronic diarrhea who have trouble forming solid stools; psyllium (metamucil) and fibercon
270
antisecretory agents
reduce secretions in the gut; bismuth subsalicyclate
271
Symptoms of constipation
cramping, bloating, lumpy and hard stools, straining, and sense of incomplete evacuation or blockage
272
acute constipation classification
less than 3 bowel movements per week
273
chronic constipation causes
medications, obstruction, metabolic, neurological, systemic, psychiatric, slow transit, evacuation disorder
274
long-term use of what medication(s) may cause constipation
analgesics/ NSAIDs (short term use of opioids can cause constipation), antacids, antihistamines, antimuscarinics, verapamil, clonidine, CA channel blockers, diuretics
275
When to refer for constipation
symptoms for greater than 2 weeks with appropriate interventions, bleeding (black/tarry stools), abdominal pain/discomfort, fever, severe N/V, family history of IBD or colon cancer, drastic change in symptoms
276
lifestyle modifications for constipation
6-8 glasses of water/day, add high fiber foods slowly (20-30g fiber/day), prunes (contains sorbitol), fresh kiwi
277
When are the best times to defecate?
first thing in the AM, within 30 minutes of meals
278
Bulk laxatives and examples
psyllium (metamucil), methylcellulose (citrucel), calcium polycarbophil (fibercon)
279
Bulk laxatives MOA
forms emollient gels which retain water, swell, and stimulates stretch receptors
280
bulk laxatives advantages/disadvantages
best for softening stools, well tolerated. need adequate fluid intake, not ideal for bedridden patients, gas formation, impact on drug absorption
281
Surfactants/ Emollients
Docusate
282
Docusate MOA
decrease fecal surface tension; stool softener
283
Saline laxatives examples and uses
MOM; Mg citrate; draws fluid into colon and stimulates motility. used for acute constipation; quick onset
284
Hyperosmotic agents examples
glycerin suppositiories, Miralax (PEG)
285
hyperosmotic agents use
chronic constipation; softens and stimulates BM
286
Stimulant laxatives MOA
locally stimulates enteric nerves which stimulates contractions and mobility; increase in fluid and Na secretion into the lumen
287
stimulant laxatives examples
senna, bisacodyl
288
stimulant laxatives use
in patients with motility disorders, in patient who use opiods
289
lubiprostone brand name and MOA
amitiza; chloride channel activator (increases fluid movement into intestinal lumen)
290
when to use lubiprostone
in patients who do not respond to /tolerate other laxatives
291
linaclotide brand name and MOA
linzess; increase chloride and bicarbonate secretions into the intestinal lumen; guanylate cyclase-c receptor activator
292
plecanitide brand name and MOA
trulance; guanylate cyclase-c receptor activator
293
how to relieve acute constipation
within 1 hour -- enema or bisacodyl or glycerin suppository within 3-6 hours-- citrate of magnesia, large doses of PEG within 24 hours -- bisacodyl or senna tablets within 48 hours-- milk of magnesia or PEG
294
chronic constipation steps
1) relieve acute symptoms 2) dietary mods 3) bulk forming laxatives and fluids 4) PEG or lactulose or sorbitol 5) short term use of stimulant then maintenance agent 6) new drugs (linzess)
295
what should be used for constipation in pregnancy?
diet, fiber, docusate (senna for severe cases)
296
what should be used in diabetes?
preokinetic agents and stimulants
297
what should be used in patients on opiods?
stimulants, docusate, lactulose, or PEG prn AVOID bulk forming laxatives opioid receptor antagonists
298
what two drugs can be used in patients who use opioids for constipation? (last line)
methylnaltrexone (relistor) (SC injection) and naloxegol (movantik) (oral tablet)
299
What types of laxatives are used for GI procedures?
hyperosmotics and saline laxatives
300
Which class of laxatives are most effective at softening the stool?
bulk laxatives
301
IBS syndrome definition/ characteristics
abdominal pain or cramping and changes in bowel function; chronic condition; ABDOMINAL PAIN ASSOCIATED WITH ABNORMAL BOWEL MOVEMENTS; can include predominantly constipation, diarrhea, or a mix of the two
302
alarming features/ referral necessary
- rectal bleeding - weight loss - iron deficient anemia - nocturnal symptoms - family history of colorectal cancer, IBD, or celiac disease
303
IBS non-pharmacologic treatment
- avoid foods that make symptoms worse - increase fiber, water, aerobic exercise, avoid postponing defecation
304
pharmacologic treatment
- add a bulk-forming laxative for routine use - may consider anti-spasmodic or anticholinergic agent for GI symptoms - may consider lubiprostone or linaclotide for constipation and abdominal pain
305
for treatment of IBS constipation:
soluble fiber psyllium (increase stool volume); polyethylene glycol (osmotic laxative)
306
second line for IBS constipation:
hyoscyamine (anticholinergic anti-spasmodic; on beers list); dicyclomine (improves abdominal pain)
307
IBS constipation last line:
SSRIs (citalopram, escitalopram, fluoxetine, paroxetine, sertraline) reduces visceral sensitivity
308
other medications that help with constipation (last line)
linaclotide and lubiprostone
309
treatment of IBS diarrhea predominant
manage stress plus lactose and caffeine free diet; avoid foods that increase symptoms
310
stepwise treatment of IBS-D
1) may add routine use of bulk laxatives 2) add loperamide or ani-spasmodic agent 3) replace with eluxadoline if pain persists 4) consider rifaximin 5) add serotonin-3 antagonist 6) antidepressants
311
viberzi (eluxadoline) use
reduce abdominal pain and diarrhea in IBS-D patients
312
TCAs
antidepressants used in IBD-D predominant (notriptyline and amitryptyline)