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Therapeutics > Final Exam (GI, Dermatology, and Pediatrics) > Flashcards

Final Exam (GI, Dermatology, and Pediatrics) Flashcards

1
Q

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

A

Carbohydrates; generate many metabolic intermediates

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2
Q

What are excess carbohydrates in the diet converted to?

A

glycogen and triacylglycerol

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3
Q

What are examples of simple carbohydrates?

A

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

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4
Q

What are complex carbohydrates?

A

polysaccharides; glycogen (starch and fiber in plants)

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5
Q

What is another name for glucose?

A

dextrose

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6
Q

What is the most important carbohydrate fuel for the body?

A

glucose/dextrose

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7
Q

Where is fructose found?

A

Fruits, vegetables, honey

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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.

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9
Q

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

A

high-fructose corn syrup.

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10
Q

What does a-amylase do?

A

Hydrolyzes starch and glycogen to maltose and maltotriose

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11
Q

Where is a-amylase found?

A

in the saliva and pancreatic juice

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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
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13
Q

What carbohydrates can be absorbed into the body?

A

only monosaccharides

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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

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15
Q

What do indigestible carbohydrates cause and what is an example?

A

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

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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

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17
Q

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

A

white potato

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18
Q

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

A

Beans (kidney)

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19
Q

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

A

Cellulose and hemicellulose – insoluble
Lignin – insoluble
Pectin – soluble

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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
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21
Q

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

A

Woody parts of vegetables; binds cholesterol and carcinogens

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22
Q

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

A

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

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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
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24
Q

What is the main source for dietary fat?

A

triacylglycerol (glycerol + three fatty acids)

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25
Q

What are secondary sources of dietary fat?

A

phospholipids, cholesterol, cholesterol esters, fatty acids

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26
Q

What are the essential fatty acids? What are they used for?

A

Omega-3 and Omega-6 fatty acids; used to synthesize eicosanoids in the body

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27
Q

what are the omega-3 fatty acids and what are they found in?

A

a-linolenic acid – in vegetable oils
EPA and DHA in fish oils

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28
Q

what are the omega-6 fatty acids and what are they found in?

A

linoleic acid – corn oil
arachidonic acid – in meat and fish

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29
Q

What are trans fatty acids?

A

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.

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30
Q

How are lipids digested?

A

dispersed into small droplets and solubilized by bile acids

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31
Q

What is the role of gastric and pancreatic lipases?

A

hydrolyze triacylglycerol to fatty acids and monoacylglycerol; produce fatty acids that act as surfactants.

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32
Q

What is the role of esterase?

A

hydrolyzes monoacylglycerol and cholesterol ester.

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33
Q

How are lipids delivered to the peripheral tissues?

A

directly delivered by chylomicron

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34
Q

How is fat used by the muscles?

A

As an energy source

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35
Q

Where is excess lipids stored?

A

stored as fat in adipose tissues

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36
Q

brain and lipids?

A

the brain does not use fat as an energy source

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37
Q

How are lipids utilized during starvation?

A

The liver converts fatty acid to ketone bodies through ketogenesis, which can be used as an energy source by the brain and muscle.

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38
Q

What is the role of dietary proteins?

A

structural component; used for enzymes, hormones, plasma proteins, and antibodies

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39
Q

What is excess protein in the diet used for?

A

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

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40
Q

What does a negative nitrogen balance indicate?

A

Inadequate dietary intake of protein; trauma or illness

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41
Q

What does a positive nitrogen balance indicate?

A

net increase in body protein stores; seen in growing children, pregnant women, and adults recovering from illness

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42
Q

how are proteins digested?

A
  • 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
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43
Q

What amino acids are released into the blood?

A

only free amino acids are released into the blood

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44
Q

What is celiac disease? traits and characteristics

A

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

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45
Q

what is the energy content of carbohydrates?

A

4 kcal/g

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46
Q

What is the energy content of fat?

A

9 kcal/g

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47
Q

What is the energy content of protein?

A

4 kcal/g

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48
Q

what is the energy content of alcohol

A

7 kcal/g

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49
Q

What are the 3 main forms of energy reserve?

A
  • fat in adipose tissues
  • glycogen in the liver to maintain blood glucose levels
  • glycogen in muscle used for exercise
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50
Q

What are the characteristics of a well-fed state?

A
  • insulin release
  • glycolysis
  • glycogen synthesis
  • catabolism of amino acids
  • fatty acid synthesis
  • no gluconeogenesis
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51
Q

What are the characteristics of the early fasting state?

A
  • glucagon release
  • glycogen breakdown
  • gluconeogenesis (cori cycle and alanine cycle)
  • no catabolism of amino acids
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52
Q

What are the characteristics of a fasting state?

A
  • glucagon release
  • gluconeogenesis
  • protein is used as a major carbon and nitrogen source
  • lipolysis in adipose tissue
  • fatty acid oxidation
  • ketogenesis
  • reduced thyroid hormones
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53
Q

What happens when blood glucose drops below 1.5 mM

A

hypoglycemia; coma and death shortly follow

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54
Q

What are complications of hyperglycemia?

A

dehydration, hyperglycemic coma, complications of diabetes

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55
Q

What fuels the brain/ how much is needed?

A

glucose; brain uses more than 20% total energy
100 to 120 g glucose per day
15 to 20% of total oxygen

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56
Q

Energy storage in the brain?

A

no energy storage; the brain does not use fat

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57
Q

How does the brain adapt to starvation?

A

through the ketone bodies made in the liver

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58
Q

What is marasmus?

A

inadequate intake of protein and energy; thin, wasted appearance

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59
Q

What is kwashiorkor?

A

inadequate protein intake with adequate energy intake
- plump appearance due to edema

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60
Q

What are recommended dietary allowances?

A

original allowances published in 1968

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61
Q

What are the dietary reference intakes?

A

nutrition recommendations from the institute of medicine of the national academies. contains many different types of requirements

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62
Q

What is the estimated average requirement?

A

amount of nutrient estimated to meet the need of 50% of the healthy individuals in an age and gender group.

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63
Q

What is the recommended dietary allowance?

A
  • two standard deviations above the EAR (estimated average requirement)
  • will meet the need of 97-98% of the healthy individuals in a group.
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64
Q

What is adequate intake?

A

Used when scientific evidence is inadequate to set an EAR
approximations of the average nutrient intake by a healthy population

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65
Q

what is the tolerable upper intake level?

A

maximum level of daily intake of a nutrient without any health risk

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66
Q

What are the fat soluble vitamins?

A

vitamin A, vitamin D, Vitamin E, vitamin K

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67
Q

What are the water-soluble vitamins?

A

group of vitamin Bs and Vitamin C

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68
Q

What are macrominerals?

A

Ca2+ and Mg2+

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69
Q

what are trace minerals?

A

iron, iodine, zinc, copper, chromium, selenium, manganese, molybdenum, fluoride, and boron

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70
Q

What is the name for vitamin B6?

A

pyridoxine

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71
Q

What is the name for vitamin B12?

A

Cobalamin

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72
Q

How is vitamin A produced?

A

produced by carotenoids (organic pigments in plants)

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73
Q

What is a characteristic of vitamin A deficiency?

A

night blindness

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74
Q

What is retinoic acid and what is its function?

A

vitamin A; functions as steroid hormones and regulates cell growth and differentiation

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75
Q

Use and storage of carotenoids?

A

effective antioxidants that reduce the risk of cancers; stored in the liver as retinol palmitate

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76
Q

What are the dietary sources of carotenoids (vitamin A)?

A

dark green and yellow vegetables, liver, egg yolk, butter, and whole milk

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77
Q

Which vitamin is most commonly deficient?

A

Vitamin D

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78
Q

What is the function of vitamin D?

A

steroid hormones; maintain calcium homeostasis

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79
Q

How is vitamin D synthesized?

A

By an intermediate in cholesterol biosynthesis; can be produced photochemically in the skin

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80
Q

What is vitamin D deficiency caused by and what is this characterized by?

A

insufficient exposure to sunlight; rickets in young children and osteomalacia in adults

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81
Q

What are dietary sources of vitamin D?

A

milk, saltwater fish, liver, and egg yolk

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82
Q

How does vitamin E occur naturally in the diet?

A

tocopherols and tocotrienols

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83
Q

What is the function of vitamin E in the diet?

A

naturally occurring antioxidants protecting unsaturated fatty acids.

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84
Q

Where does vitamin E accumulate?

A

circulating lipoproteins, cellular membranes, and fat deposits

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85
Q

how does vitamin E reduce the risk of cardiovascular disease?

A

prevents oxidation of LDL; oxidized form of LDL increases cardiovascular risk.

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86
Q

what are the dietary sources of vitamin K?

A

vegetable oils rich in polyunsaturated fatty acids

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87
Q

What is vitamin K essential for?

A
  • formation of carboxyglutamic acids (allow proteins to bind Ca2+)
  • essential for blood clotting
  • essential for bone mineralization
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88
Q

What is warfarin?

A
  • an anticoagulant and vitamin K antagonist
  • reduces formation of carboxyglutamic acid
  • prevents thrombosis
  • inhibits vitamin K epoxide reductase
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89
Q

What are dietary sources of vitamin k?

A
  • K1– in green vegetables
  • K2 – synthesized by intestinal bacteria
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90
Q

What is vitamin B1?

A

thiamin

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91
Q

what is the role of thiamin in the body?

A
  • thiamin pyrophosphate functions as a cofactor in enzymatic catalysis
  • thiamin triphosphate functions in transmission of nerve impulse in peripheral nerve membranes
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92
Q

What is thiamin deficiency called and what is it characterized by?

A

beriberi– muscular atrophy and weakness

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93
Q

What populations is thiamin (B1) deficiency seen in?

A

populations exclusively eating polished rice & alcoholics

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94
Q

What is riboflavin (b2) deficiency characterized by?

A

angular cheilitis, glossitis, and scaly dermatitis

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95
Q

What population is riboflavin deficiency seen in?

A

alcoholics

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96
Q

What foods is thiamin (b2) found in?

A

milk, meat, eggs, and cereal products

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97
Q

What is the role of Niacin (B3) in the body?

A

converted to cofactors NAD and NADP
used in redox reactions and cellular respiration as electron acceptors/ hydrogen donors

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98
Q

What is niacin (B3) deficiency called? what are the symptoms/characteristics?

A

pellagra; dermatitis, diarrhea, and dementia

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99
Q

What populations is niacin (b3) deficiency seen in?

A

Rare; in alcoholics, patients with malabsorption, and elderly on restrictive diets

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100
Q

What foods is niacin (B3) found in?

A

meats, peanuts, and enriched cereals

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101
Q

What is the use of pyridoxine (B6) in the body?

A
  • amino acid metabolism
  • synthesis of neurotransmitters
  • synthesis of sphingolipids
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102
Q

what are symptoms of pyridoxine (B6) deficiency?

A

mild: irritability, nervousness, and depression
severe: peripheral neuropathy and convulsions

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103
Q

What foods in pyridoxine (B6) found in?

A

meat, vegetables, and whole grain cereals

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104
Q

What is the purpose of biotin (b7) in the body?

A
  • cofactor for activation of carbon dioxide in carboxylase enzymes
  • covalently bound to lysine side chains in enzymes
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105
Q

What are risk factors for biotin deficiency?

A
  • excessive consumption of raw egg whites
  • pregnancy
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106
Q

What is the use of folic acid (B9) in the body?

A
  • used in synthesis of amino acids and nucleotides
  • essential for DNA synthesis and cellular proliferation
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107
Q

What are characteristics/ risk factors of folic acid (B9) deficiency?

A
  • inhibition of DNA synthesis
  • results in anemia
  • increases risk of birth defects (neural tube defect)
  • common in alcoholics
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108
Q

What is vitamin B12 called?

A

cobalamin

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109
Q

What is vitamin B12 deficiency characterized by?

A
  • accumulation of homocysteine and methylmalonic acid causing anemia and neurological damage.
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110
Q

Vitamin B12 deficiency risk factors

A

severe malabsorption diseases and long-term vegetarians

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111
Q

What is another name for vitamin c?

A

ascorbic acid

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112
Q

What is the role of vitamin C in the body?

A
  • 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
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113
Q

What is mild vitamin C deficiency characterized by?

A

capillary fragility, easy bruising, and decreased immunocompetence

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114
Q

What is severe vitamin C deficiency called and characterized by?

A

Scurvy; decreased wound healing, osteoporosis, hemorrhaging, anemia

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115
Q

What are the roles of calcium in the body?

A

making bones, second messenger, used by enzymes, essential for blood coagulation and muscle contractility.

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116
Q

How is calcium serum levels regulated?

A
  • elaborate homeostatic control system
  • bones serve as reservoir
  • dietary insufficiency results in loss of Ca2+ from bones
  • vitamin D required for calcium utilization
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117
Q

What is calcium deficiency characterized by?

A
  • resembles vitamin D deficiency
  • may contribute to osteoporosis
  • muscle cramps
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118
Q

what are the dietary sources of calcium?

A

dairy products, nuts, beans, seeds, and seaweeds

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119
Q

What is a result of iron deficiency?

A

anemia; common in children and menstruating females

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120
Q

Why is iron homeostasis tightly regulated?

A
  • toxic when by itself; generates free radicals
  • must always be bound in the blood/body
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121
Q

iodine use in the body

A

used for synthesis of thyroid hormones

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122
Q

best natural food source of iodine

A

seafood (fish and seaweeds)

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123
Q

Iodine deficiency

A

goiter- enlargement of thyroid gland
cretinism- stunted physical and mental growth

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124
Q

zinc deficiency characteristics

A
  • poor growth and impairment of sexual development in children
  • poor wound healing, dermatitis, impaired immune function
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125
Q

copper use in body

A

required for function of many enzymes

126
Q

copper deficiency characteristics

A

anemia, bone demineralization, and blood vessel fragility

127
Q

What is one of the first messengers involved in acid secretion?

A

gastrin

128
Q

What cell activates the proton pump in the stomach to produce acid?

A

parietal cells

129
Q

What are three second messengers used to activate parietal cells?

A

ACh, Histamine, and gastrin

130
Q

What are three second messengers used to activate parietal cells?

A

ACh, Histamine, and gastrin

131
Q

Which messenger provides negative feedback in acid secretion?

A

somatostatin

132
Q

What are ulcers caused by?

A

depletion of mucus layer by inhibition of prostaglandins

133
Q

what are adverse effects of sodium bicarbonate?

A

systemic alkalosis, fluid retention

134
Q

What are adverse effects of calcium carbonate?

A

hypercalcemia, nephrolithiasis, milk-alkali syndrome

135
Q

What are adverse effects of aluminum hydroxide?

A

constipation, hypophosphatemia,

136
Q

What are the adverse effects of magnesium hydroxide?

A

diarrhea

137
Q

What is the MOA of cimetidine?

A

competitive antagonist of H2 histamine receptor
reduce gastric acid secretion in response to histamine, gastrin, acetylcholine

138
Q

What are the second generation H2 blockers?

A

ranitidine, famotidine, nizatidine

139
Q

What is the difference between cimetidine and famotidine?

A

1st gen vs 2nd gen H2 blockers
- 2nd gen has:
- longer half life
- fewer effects on CYP 450 system
- greater potency
- absorbed quickly

140
Q

what cell and second messenger are stimulated/released even when on a PPI?

A

G cell; Gastrin

141
Q

What cell and second messenger are not stimulated/ released when on a PPI?

A

D cell; somatostatin (no negative feedback)

142
Q

What is the difference between omeprazole and esomeprazole?

A

omeprazole- racemic mixture; less potent
esomeprazole– purified s enantiomer; more potent (more expensive)

143
Q

MOA of PPIs?

A
  • 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
Q

What is a risk of discontinuing PPIs?

A

rebound hypersecretion of gastric acid; hypergastrinemia

145
Q

Which drug class is most effective in reducing acid in the stomach?

A

PPIs

146
Q

Which drug class can tolerance be built to?

A

H2 antagonists

147
Q

What are risks of PPI therapy?

A

vitamin B12 deficiency
decreased Ca2+ absorption/ increased bone fractures

148
Q

What is sucralfate?

A

a mucosal protective agent; forms protective barrier at ulcer site.

149
Q

What is the use of misoprostol?

A

semi-synthetic prostaglandin; reduced acid secretion; enhance mucus and bicarbonate secretion
can be used in combination with chronic NSAIDS

150
Q

Why is bismuth subsalicyclate used for h pylori treatment?

A

coating agent in the stomach; anti inflammatory and antibacterial properties

151
Q

What is bismuth subsalicylate used for?

A

nausea, heartburn, indigestion, upset stomach, diarrhea, h-pylori treatment

152
Q

what antibiotics are commonly used to treat H. pylori?

A

metronidazole, tetracycline, amoxicillin, and clarithromycin

153
Q

What controls the smooth muscles in the gut?

A

the enteric nervous system

154
Q

how do bulk and osmotic laxatives work?

A

form hydrophilic mass and increase water in the intestinal lumen which stimulates stretch receptors and increases peristalsis

155
Q

How do stool softeners work?

A

acts as a surfactant and lubricant; make passage easier and decrease water absorption

156
Q

how do secretory/stimulant laxatives work?

A

irritation of mucosa affects fluid secretion/absorption balance and induces peristalsis

157
Q

What is gastroparesis?

A

neuropathy during diabetes or Parkinson’s disease

158
Q

what is metoclopramide?

A

D2 dopamine receptor antagonist

159
Q

How does metoclopramide work?

A

block of D2 receptors in myenteric plexus leads to increased acetylcholine release; also produces anti-emetic effects

160
Q

What are the centrally acting opioid receptor antagonists

A

naloxone, naltrexone, nalmefene

161
Q

What are the peripherally acting opioid receptor antagonists?

A

naloxegol, alvimopan, naldemedine

162
Q

What is lubiprostone?

A

type II chloride channel activator

163
Q

What are linaclotide (linzess) and plecanatide (trulance)?

A

peptide activators of guanylate cyclase C

164
Q

What are opiates used as anti-diarrheals?

A

diphenoxylate + atropine (lomotil) – active in CNS
and loperamide (imodium) – activates Mu opiod receptors in GI

165
Q

What are 5-HT3 receptor antagonists used for?

A

block activity of afferent nerves from stomach and small intestine to prevent nausea and vomiting

166
Q

What is ondansetron?

A

a 5-HT3 receptor antagonist

167
Q

What are side effects of ondanstron

A

constipation

168
Q

What are some antihistamines/ anticholinergics that can be used as antiemetics?

A

Diphenhydramine, meclizine, scopolamine

169
Q

What are the D2 dopamine receptor antagonists that have anti-emetic and sedative properties?

A

metoclopramide, prochlorperazine, promethazine, droperidol

170
Q

risk factors of GERD

A

obesity, tobacco smoking, pregnancy, delayed gastric emptying, genetic predisposition, nonalcoholic fatty liver disease, major depressive disorder, asthma

171
Q

What is one medication that reduces the LES pressure?

A

tetracycline

172
Q

What are medications that directly irritate esophageal mucosa?

A

aspirin, bisphosphonates, NSAIDS

173
Q

What are the three main clinical presentations of GERD? (all 3 must be present for diagnosis)

A

heartburn, regurgitation/belching, and reflux chest pain

174
Q

What are extraesophageal symptoms of GERD?

A

chronic cough, laryngitis, wheezing, asthma

175
Q

What are the alarm symptoms for GERD?

A

dysphagia (difficulty swallowing), painful swallowing, bleeding, weight loss

176
Q

what is barrett’s esophagus?

A

thickening of the esophagus lining

177
Q

first-line prevention and treatment of GERD

A

lifestyle modifications

178
Q

first-line agent to neutralize acid

A

antacids

179
Q

first-line agent to reduce gastric acid secretion

A

H2RAs and PPIs

180
Q

Which GERD medications are PRN?

A

antacids and sometimes H2RAs

181
Q

Which GERD medications are scheduled?

A

PPIs and sometimes H2RAs

182
Q

What is always first line treatment for GERD?

A

lifestyle mods to address triggers

183
Q

how long is the OTC trial for GERD before referring?

A

2 weeks

184
Q

How long is a rx trial of PPI before switching?

A

8 weeks

185
Q

What can be avoided to improve gerd symptoms?

A

fatty meals, carbonated beverages, excessive exercise

186
Q

What are other recommendable lifestyle modifications for GERD?

A

eat smaller meals, lose weight, stop smoking, sleep with head elevated, sleep on left side

187
Q

How do antacids work?

A
  • maintain pH>4 and increase LES pressure; offer immediate symptomatic relief
188
Q

Which antacids cause constipation?

A

Calcium and aluminum

189
Q

Which antacid causes diarrhea?

A

magnesium

190
Q

What are side effects all antacids can cause?

A

N/V

191
Q

What are drugs that commonly interact with antacids?

A

antimicrobials, levothyroxine, iron, steroids, digoxin

192
Q

When should interacting medications with antacids be taken?

A

2 hours before or 4-6 hours after antacids

193
Q

What is the maximum frequency of all antacids

A

up to 4x/day

194
Q

which antacid medications cannot be given to children?

A

Alka-seltzer and pepto-bismol

195
Q

What is the MOA for H2RAs?

A

reversible inhibition of histamine receptors

196
Q

Which H2RA has many drug-drug interactions and is not commonly used?

A

cimetidine

197
Q

What are side effects of H2RAs?

A

headache, dizziness, fatigue, constipation or diarrhea, confusion/delerium, agitation, B12 deficiency with long-term use

198
Q

What are the clinical pearls of H2RAs?

A

tachyphylaxis occurs with long-term use
on beer’s criteria
not as efficacious as PPIs
useful for nocturnal symptoms

199
Q

MOA for PPIs

A

irriversible inhibition of proton/potassium ATPase

200
Q

What is Dexilant

A

Dexlansoprazole; newer PPI; dual release formulation allows 2 different onsets; can be taken without regard to meals

201
Q

How long is OTC treatment with PPIs?

A

2 weeks only; if needed for longer or if needed again before 4 months, refer

202
Q

Omeprazole release

A

only immediate release PPI when combined with sodium bicarbonate

203
Q

What is omeprazole/ esomeprazole metabolized by?

A

CYP 2C19

204
Q

What drugs do PPIs increase the effect of?

A

methotrexate, phenytoin, warfarin

205
Q

What drugs do PPIs decrease the effect of?

A

iron, bisphosphonates, HIV drugs, clopidogrel

206
Q

What are potential long-term side effects of PPIs?

A

Hypomagnesemia, bone density decrease/fractures, vitamin B12 deficiency, chronic kidney disease (rare)

207
Q

Which PPI interacts with clopidogrel?

A

omeprazole/ esomeprazole

208
Q

When is sucralfate recommended for GERD?

A

in pregnancy

209
Q

What are the options for combination therapy?

A

antacids and H2RAs
PPIs and H2RAs

210
Q

How should PPIs be discontinued?

A

taper to decrease hypergastrinemia

211
Q

Which medications are on beers criteria?

A

both PPIs and H2RAs

212
Q

In pregnancy, what is the desired order of treatment for reflux?

A

lifestyle modifications&raquo_space; antacids/ sucralfate&raquo_space; H2RAs&raquo_space; PPIs (last line; any except omeprazole)

213
Q

What is first line treatment in those lactating

A

antacids&raquo_space; PPIs and H2RAs found in breast milk

214
Q

alarm symptoms of GERD in children

A

weight loss, fever, seizure, persistent vomiting/diarrhea

215
Q

non-pharm options for children

A

thickening formula/food, decreasing volume of intake, milk free diet, positioning therapy

216
Q

What antacids should be avoided in those younger than 12?

A

aluminum or bismuth subsalicyclate

217
Q

safe OTC options for children?

A

simethicone and probiotics

218
Q

Where is the common site of damage for H. Pylori induced ulcer?

A

D>S

219
Q

Where is the common site of damage for NSAID or stress-induced ulcers?

A

S>D

220
Q

what type of ulcer presents with epigastic pain?

A

H. Pylori

221
Q

Which type of ulcer is generally the most deep

A

NSAID-induced

222
Q

What type of ulcers generally result in more bleeding?

A

NSAID and Stress

223
Q

What are aggressive risk factors for PUD

A

pepsin, NSAIDS, H. Pylori, gastric acid

224
Q

What are protective factors for PUD?

A

blood flow to mucosa, bicarbonate, prostaglandins and mucus

225
Q

In what type of ulcer does food relieve the pain?

A

duodenum

226
Q

in what type of ulcer does food worsen the pain?

A

stomach

227
Q

what is the general treatment regimen for h.pylori

A

PPI plus 2-3 antibiotics

228
Q

What is the preferred regimen for h. pylori?

A

quadruple therapy: PPI BID, bismuth subsalicyclate, metronidazole, tetracycline x10-14 days

229
Q

What is helidac?

A

convenience packaging of the bismuth quadruple (14 day therapy)

230
Q

What is pylera?

A

3 in 1 capsule of the bismuth quadruple (10 day therapy) PPI is separate

231
Q

How long should PPIs be used for h. pylori therapy?

A

14 days; should not be continued indefinitely

232
Q

bismuth salts MOA

A

topical bactericidal effect; improves ulcer healing by inhibiting aggressive factors and increasing protective factors

233
Q

adverse reactions of metronidazole

A

avoid alcohol due to N/V

234
Q

adverse effect of levofloxacin

A

tendon rupture, mental status change, QTC prolongation

235
Q

What class is levofloxacin?

A

fluoroquinolone

236
Q

adverse effect of amoxicillin

A

GI upset (N/V) diarrhea; take with food to help alleviate

237
Q

adverse effect of tetracycline and doxycycline

A

photosensitivity

238
Q

amoxicillin class

A

penicillin

239
Q

tetracycline and doxycycline class

A

tetracyclines

240
Q

clarithromycin class

A

macrolide

241
Q

azithromycin class

A

macrolide

242
Q

adverse effect of clarithromycin

A

QTC prolongation, photosensitivity, GI upset

243
Q

what can probiotics be used for?

A

prophylaxis for h.pylori colonization; supplement to antibiotic therapy

244
Q

What therapies are no longer recommended in the US due to resistance?

A

clarithromycin based therapies

245
Q

How do NSAIDs increase the risk of PUD?

A

by reducing protective factors such as prostaglandins (impaired mucosal defense)

246
Q

What is included in prophylaxis of NSAID induced PUD?

A

PPIs, H2RAs (duodenal ulcer only), misoprostol

247
Q

What is included in treatment of NSAID induced PUD?

A

PPIs, H2RAs, sucralfate

248
Q

When is misoprostol used?

A

As prophylaxis only (prostaglandin analogue)

249
Q

When is sucralfate used?

A

For an NSAID induced ulcer; administer on an empty stomach 2 hours before or 4 hours after other meds

250
Q

What is the preferred non-selective agent?

A

Naproxen

251
Q

What is the preferred cox-2 specific agent?

A

celecoxib

252
Q

Which agent is less likely to cause ulcers?

A

celecoxib

253
Q

Which agent has the least cardiovascular risk?

A

naproxen

254
Q

When are H2RAs used for NSAID induced ulcers?

A

for prophylaxis or treatment; duodenal ulcer prevention only

255
Q

What is the result of an increase in intestinal motility?

A

diarrhea

256
Q

what is the result of a decrease in intestinal motility?

A

constipation

257
Q

what is acute diarrrhea?

A

less than 14 days

258
Q

what is persistent diarrhea?

A

> 14 days

259
Q

What is chronic diarrhea?

A

> 30 days

260
Q

What is secretory diarrhea characterized by?

A

large stool volumes; caused by laxatives, not altered by fasting

261
Q

What is an example of osmotic diarrhea

A

lactose intolerance

262
Q

characteristics of osmotic diarrhea

A

improves with fasting state

263
Q

what is exudative diarrhea characterized by?

A

inflammatory diseases of the bowel; large stool volumes

264
Q

most common causes of diarrhea in the US

A

salmonella, norovirus

265
Q

complications of diarrhea

A

inconvenience, social isolation, dehydration, electrolyte imbalance (may cause cardiac arrythmia)

266
Q

diet management in diarrhea

A

most important for osmotic diarrhea; do not stop feedings in those with bacterial diarrhea; BRAT diet x24 hours

267
Q

non-pharmacologic diarrhea treatment

A

diet, fluid/electrolyte replacement

268
Q

pharmacologic diarrhea treatment

A

antimotility agents; loperamide; short term use only; do not use with bacterial diarrhea

269
Q

absorbents

A

used in people with chronic diarrhea who have trouble forming solid stools; psyllium (metamucil) and fibercon

270
Q

antisecretory agents

A

reduce secretions in the gut; bismuth subsalicyclate

271
Q

Symptoms of constipation

A

cramping, bloating, lumpy and hard stools, straining, and sense of incomplete evacuation or blockage

272
Q

acute constipation classification

A

less than 3 bowel movements per week

273
Q

chronic constipation causes

A

medications, obstruction, metabolic, neurological, systemic, psychiatric, slow transit, evacuation disorder

274
Q

long-term use of what medication(s) may cause constipation

A

analgesics/ NSAIDs (short term use of opioids can cause constipation), antacids, antihistamines, antimuscarinics, verapamil, clonidine, CA channel blockers, diuretics

275
Q

When to refer for constipation

A

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
Q

lifestyle modifications for constipation

A

6-8 glasses of water/day, add high fiber foods slowly (20-30g fiber/day), prunes (contains sorbitol), fresh kiwi

277
Q

When are the best times to defecate?

A

first thing in the AM, within 30 minutes of meals

278
Q

Bulk laxatives and examples

A

psyllium (metamucil), methylcellulose (citrucel), calcium polycarbophil (fibercon)

279
Q

Bulk laxatives MOA

A

forms emollient gels which retain water, swell, and stimulates stretch receptors

280
Q

bulk laxatives advantages/disadvantages

A

best for softening stools, well tolerated.
need adequate fluid intake, not ideal for bedridden patients, gas formation, impact on drug absorption

281
Q

Surfactants/ Emollients

A

Docusate

282
Q

Docusate MOA

A

decrease fecal surface tension; stool softener

283
Q

Saline laxatives examples and uses

A

MOM; Mg citrate; draws fluid into colon and stimulates motility. used for acute constipation; quick onset

284
Q

Hyperosmotic agents examples

A

glycerin suppositiories, Miralax (PEG)

285
Q

hyperosmotic agents use

A

chronic constipation; softens and stimulates BM

286
Q

Stimulant laxatives MOA

A

locally stimulates enteric nerves which stimulates contractions and mobility; increase in fluid and Na secretion into the lumen

287
Q

stimulant laxatives examples

A

senna, bisacodyl

288
Q

stimulant laxatives use

A

in patients with motility disorders, in patient who use opiods

289
Q

lubiprostone brand name and MOA

A

amitiza; chloride channel activator (increases fluid movement into intestinal lumen)

290
Q

when to use lubiprostone

A

in patients who do not respond to /tolerate other laxatives

291
Q

linaclotide brand name and MOA

A

linzess; increase chloride and bicarbonate secretions into the intestinal lumen; guanylate cyclase-c receptor activator

292
Q

plecanitide brand name and MOA

A

trulance; guanylate cyclase-c receptor activator

293
Q

how to relieve acute constipation

A

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
Q

chronic constipation steps

A

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
Q

what should be used for constipation in pregnancy?

A

diet, fiber, docusate (senna for severe cases)

296
Q

what should be used in diabetes?

A

preokinetic agents and stimulants

297
Q

what should be used in patients on opiods?

A

stimulants, docusate, lactulose, or PEG prn
AVOID bulk forming laxatives
opioid receptor antagonists

298
Q

what two drugs can be used in patients who use opioids for constipation? (last line)

A

methylnaltrexone (relistor) (SC injection) and naloxegol (movantik) (oral tablet)

299
Q

What types of laxatives are used for GI procedures?

A

hyperosmotics and saline laxatives

300
Q

Which class of laxatives are most effective at softening the stool?

A

bulk laxatives

301
Q

IBS syndrome definition/ characteristics

A

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
Q

alarming features/ referral necessary

A
  • rectal bleeding
  • weight loss
  • iron deficient anemia
  • nocturnal symptoms
  • family history of colorectal cancer, IBD, or celiac disease
303
Q

IBS non-pharmacologic treatment

A
  • avoid foods that make symptoms worse
  • increase fiber, water, aerobic exercise, avoid postponing defecation
304
Q

pharmacologic treatment

A
  • 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
Q

for treatment of IBS constipation:

A

soluble fiber psyllium (increase stool volume); polyethylene glycol (osmotic laxative)

306
Q

second line for IBS constipation:

A

hyoscyamine (anticholinergic anti-spasmodic; on beers list); dicyclomine (improves abdominal pain)

307
Q

IBS constipation last line:

A

SSRIs (citalopram, escitalopram, fluoxetine, paroxetine, sertraline) reduces visceral sensitivity

308
Q

other medications that help with constipation (last line)

A

linaclotide and lubiprostone

309
Q

treatment of IBS diarrhea predominant

A

manage stress plus lactose and caffeine free diet; avoid foods that increase symptoms

310
Q

stepwise treatment of IBS-D

A

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
Q

viberzi (eluxadoline) use

A

reduce abdominal pain and diarrhea in IBS-D patients

312
Q

TCAs

A

antidepressants used in IBD-D predominant (notriptyline and amitryptyline)

Therapeutics (7 decks)

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