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Pharm II > PharmII_Exam2 > Flashcards

PharmII_Exam2 Flashcards

1
Q

Which receptor does Diphenhydramine(benadryl) blocks?

A

It blocks H1 selectively

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2
Q

Name two drugs that can cause degranulation independent release of histamine?

A

Morphine

Tubocurarine

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3
Q

What two H receptors act in the CNS and Cardiovascular system?

A

H1 and H2

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4
Q

What is the antihistamine effect in the CNS?

A

Sedation
Depression
Anti-cholinergic effects
Stimulation (nervousness and restlessness)

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5
Q

What are the cardiovascular effects of histamine?

A

Decrease in blood pressure (H1 and H2)

Increase in heart rate (H2)

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6
Q

What are the bronchiole effect when antihistamine is present?

A

Bronchoconstriction (H1 receptors)

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7
Q

What are the GI effects of antihistamines?

A

H1 - intestinal contraction

H2 - Parietal cells secrete HCl

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8
Q

Describe the three parts in the wheal and flare response?

A
  1. reddening of the area - vascular smooth muscle dilation
  2. Edematous wheal - endothelium
  3. Red irregular flare surrounding the wheal - axon reflex.
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9
Q

What is the hypersensitivity response?

A
  1. Bronchoconstriction
  2. Hypotension, tachycardia
  3. Increase in capillary permeability
  4. Edema
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10
Q

Give me an example of a popular physiologic antagonist?

A

Epinephrine

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11
Q

What are the three ways to block histamine reaction?

A
  1. Physiological antagonist
  2. Competitive antagonists
  3. Inhibit the release
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12
Q

What is a summary of the 1st generation H1 antagonists?

A

More sedating

More autonomic receptor blockade.

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13
Q

Name the 4 categories of 1st generation antagonists?

A
  1. Ethanolamines
  2. Piperazine Derivatives
  3. Alkylamines
  4. Phenothiazines
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14
Q

What is so special about Ethanolamines?

A

More sedating.
More Anti-muscarinic actions
Motion sickness blockage

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15
Q

What separates the Piperazine Derivatives from the other H1 antagonists?

A

They are longer acting.

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16
Q

What is so special about Alkylamines and Phenothiazines?

A

They are more potent

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17
Q

What separates the 2nd generation drugs from the first?

A

They are less sedating.

They do not cross the BBB as easily or not at all

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18
Q

What are the two category of drugs found in 2nd gen antagonists?

A

Piperidines

Miscellaneous

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19
Q

What is Allegra used for?

A

Allergic rhinitis.

This is a 2nd generation H1 antagonists.

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20
Q

Does H1 1st gen or 2nd gen drugs last longer?

A

2nd gen drugs.

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21
Q

Which 2nd generation drug contains the most sedation out of the generation?

A

Zyrtec

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22
Q

What conditions are antihistamines really good for?

A

Allergic rhinitis

Urticaria

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23
Q

What condition is antihistamine not good for?

A

Bronchial asthma

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24
Q

Which generation do you give to ppl suffering from Allergic rhinitis and chronic Urticaria

A

2nd

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25
Q

What drug is the best for motion sickness?

A

Scopolamine.

Drugs like Dromazine and promethazine are used

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26
Q

T/F?

Antihistamines are used in sleeps aids?

A

True.

Sold OTC due to sedating effects.

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27
Q

What age does the child have to be to use anti-histamine?

What is the exception?

A

Over two years old.
Zyrtec can be used over 6 months.
Anti-histamines lead to seizures

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28
Q

Name the four topical agents for anti-histamines?

A

Olopatadine
Azelastine
Bepotastine
Levocabastine

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29
Q

What percentage of headaches do tension headaches compose of?

A

90%

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30
Q

How can primary headaches be classified as?

A

Tension
Migraine
Cluster

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31
Q

What drug do you use to treat gout?

A

NSAIDs

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32
Q

T/F?

Acetaminophen is a NSAID?

A

False

It has no anti-inflammatory properties

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33
Q

What are some adverse effects in NSAIDs?

A

Mild to moderate GI irritation
Hepatotoxicity
Nephrotoxicity

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34
Q

What are the three components found in prostanoids?

A

Prostaglandins
Thromboxanes
Prostacyclin

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35
Q

What occurs in phase I?

A

WBC bind to endothelial cells.

Become active, infiltrate

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36
Q

What occurs in phase 2?

A

WBC are activated for phagocytosis or lysosomal enzyme release

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37
Q

What occurs in phase 3?

A

Endothelial injury, tissue damage and inflammatory stimulus amp results.

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38
Q

Tell me about the enzyme COX 1?

A

It is constitutively expressed in all cells.

Housekeeping enzyme found in most cells

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39
Q

Tell me about COX2

A

It is an inducible enzyme.

You have to turn it on. Tissue damage will turn it on.

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40
Q

Tell me about COX-3

A

It is actually a splicing form of COX-1

It’s function is unknown.

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41
Q

Prostanoid effect in the vascular system?

A

Thromboxane A2 = vasoconstriction

PGE2 and PGI2 = vasodilators

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42
Q

Prostanoid effect on GI?

A

Activate GI smooth muscle

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43
Q

Prostanoid effect on Airways?

A

PGs relax the airways

TXA2 and PGF2-alpha contracts

44
Q

What happens if you block the COX1 mech in the GI?

A

You increase the amount of HCl that is released leading to ulcers.
Usually there is mucosal protection without this block.

45
Q

What is the action of prostanoids in platelets?

A

PGE1 and PGEI2 inhibit the aggregation of platelets.

TXA2 stimulates the aggregation

46
Q

What does a low dose of aspirin do in platelets?

A

It inhibits thromboxane A2 formation.

This is the cardioprotective effect

47
Q

T/F?

Loop diuretics will get reduced with the use of prostanoids?

A

True

48
Q

Effects of prostanoids in the eye?

A

It lowers IOP

49
Q

T/F?

The effects of aspirin are reversible?

A

False.
They are irreversible. Its effects are longer than that predicted by its 1/2 life.
The COX enzyme must be re-synthesized to return normal function.

50
Q

Symptomatic relief is provided by NSAIDs in which of the three categories?

A

Anti-inflammatory

51
Q

What percentage does NSAIDs reduce the chances of getting colon cancer?

A

By 50%

52
Q

Tell me about the relation COX-2 have with thrombotic events?

A

COX 2 does not mess with TXA2
COX2 does suppress PGI2
WHen u suppress PGI2, u lead to an activation of platelets and cause potential thrombotic events.

53
Q

T/F?

THe metabolism of aspirin is saturable?

A

True

ANother drug that is saturable is phenytoin

54
Q

How long is a patient told not to take NSAIDs before surgery?

A

7 days.

Because it takes 8-11 days for platelets to regenerate.

55
Q

Which drug is Reye’s syndrome linked to?

A

Aspirin
It is given to children with viral infections and fever.
Instead give the child acetaminophen or ibuprofen.

56
Q

T/F?

It is perfectly OK to use aspirin in gout?

A

False!!!

Aspirin does not eliminate uric crystals

57
Q

What are some adverse effects of aspirin intoxication?

A 
Headache
Dizziness
Tinnitus
Hearing loss
................
58
Q

Which drug is more potent than aspirin but not more efficacious?

A

Indocin

59
Q

What is so special about Clinoril?

A

Half as potent as Indocin.
Suppresses familial intestinal polyposis
INhibit the development of colon, breast, and prostate cancer.

60
Q

Which drug is better tolerated than aspirin?

A

Tolectin
It is also just as efficacious.
It is indicated for use for rheumatic disease including the juvenile form

61
Q

What drug can be used in place of opioids like morphine and is as efficacious for postoperative pain?

A

Toradol

62
Q

T/F?

U can take ibuprofen while breastfeeding?

A

False

63
Q

Which propionic acid has an increased Cardiovascular risk compared to a placebo with long term usage?

A

Naproxen

64
Q

Which propionic acid derivative is the most potent?

A

Ketoprofen

65
Q

Why do we use Cox2?

A

To prevent adverse GI effects and platelet actions

66
Q

Which cylcooxygenase inhibitor class have a black box warning?

A

all NSAIDs that inhibit COX-2 (nonselective COx inhibitors and COX-2 selective agents),
except for aspirin - has cardioprotective features

67
Q

Which two cox inhibitors were pulled from the market due to cardiovascular effects?

A

Vioxx

Bextra

68
Q

T/F?

Acetaminophen has peripheral effects?

A

False
It does not inhibit peripheral COX enzymes. Does not inhibit platelet aggregation.
No severe GI problems.

69
Q

What population is acetaminophen good in?

A

Elderly

Young children

70
Q

How do you treat toxicity from Acetaminophen?

A

Gastric lavage
Addition of sulfhydryl compounds to replenish glutathione.
N-actylcysteine

71
Q

What is the therapeutic approach to treat gout?

A
  1. Reduce inflammation
  2. Increase the elimination of Uric acid
  3. Decrease the production of Uric acid
72
Q

What is the function of colbenemid in gout?

A

Reduce the pain and inflammation.

73
Q

MOA of colbenemd?

A

It binds to and blocks tubulin.

prevents its polymerization preventing leukocyte migration and phagocytosis of uric acid crystals.

74
Q

which two classes of NSAIDs don’t work in gout?

A

Salicylates and tolectin

75
Q

Which NSAID is the best to use in gout?

A

Indocin.

Inhibits phagocytosis of urate crystals.

76
Q

MOA of allopurinol?

A

Inhibits xanthine oxidase which Prevents uric acid biosynthesis

77
Q

Analgesic efficacy is mediated via which receptor?

A

Mew receptors

78
Q

Which area in the brain contains a high concentration of

opioid receptors that facilitate feelings of euphoria.

A

Nucleus accumbens

79
Q

T/F?

Opioid withdrawal is life-threatening?

A

False

Alcohol and morphine is life threatening.

80
Q

I should never give a patient an opioid due to its dependcence levels!

A

Despite the propensity for abuse and the development of dependence, these drugs should never be withheld as analgesics.

81
Q

Which pain reacts well to opiates?

A

Nociceptive pain.

Stimulation of nociceptors along intact neural pathways.

82
Q

Which pain does opiates react poorly to?

A

Neuropathic pain.

May need to increase the dose to have an effect.

83
Q

T/F?
Ascending pain pathway- Opioids inhibit the ascending pathway at the dorsal horn (spinal) and at the thalamus
(supraspinal).

A

True

84
Q

Are the kappa receptors found in ascending or descending pathway?

A

Desceinding.

They work oppositely form the mew receptor

85
Q

Stimulation of descending pathway will do what?

A

Inhibit the ascending pathway.

86
Q

When sensory input is high, is there more or less respiratory distress?

A

Less!!!

Ex: someone is injured; the sensory input is gonna be mad high. As the pain goes away, the sensory input will increase.

87
Q

Cimetidine

A

H2 antagonist

used for their ability to reduce acid secretions

88
Q

T/F?

Chronic postoperative pain or pain from inflammation is well-controlled by NSAIDs?

A

True

89
Q

What does PGI2 do?

A

Normally suppresses platelet activation, so inhibiting it can cause
platelet over activation aka Thrombotic events. (this is why Vioxx and Bextra were withdrawn)

90
Q

T/F?
COX-2 selective agents and p-aminophenol derivatives are less harmful to the stomach because COX-1 is responsible for buffering stomach acid.

A

True

91
Q

Secondary use for indocin?

A

closure of patent ductus arteriosis in premature babies

92
Q

Diflusnisal

A
  • Dental and cancer pain
  • Better anti inflammatory than aspirin
  • Used as an analgesic with less auditory, GI, and platelet side effects.
93
Q

T/F?

It is OK to use acetaminophen on any kind of gout?

A

False

Due to the fact that acetaminophen has no anti-inflammatory properties.

94
Q

Which agents are better tolerated than aspirin and indomethacin

A

Propionic acids
Efficacy is similar to the sals.
The sals are cheaper

95
Q

Peroxicam?

A

Advantage is long 1/2 life so only single daily dose

96
Q

Give me two examples of uricosuric agents?

A

Probenecid

Sulfinpyrazone

97
Q

How long do you wait after a gouty attack to start a patient on probenecid and sulfinpyrazone?

A

Wait 2-3 weeks.
U use these drugs when patient has had several acute attacks or if urate levels are very high and an attack is inevitable.

98
Q

Febuxostat

A

A new drug that is more effective at lowering serum ureate levels than allopurinol.
THere are hepatic problems causing death.

99
Q

Name two examples of xanthine oxidase inhibitors?

A

Allopurinol

Febuxostat

100
Q

Diclofenac

A

Relatively high potency agent with selectivity for COX 2

101
Q

Meloxicam

A

Selective for COX 2.

Comparable efficacy with less GI effects.

102
Q

Etodolac

A

Slightly selective for COX 2

Useful for post op pain.

103
Q

What is an AE for etodolac?

A

Temporary renal problems.

104
Q

Celebrex

A

Similar efficacy as other NSAIDs with fewer adverse GI effects
Pfizer has said that the prothrombotic effects seen with Vioxx don’t happen at therapeutic doses of celebrex.

105
Q

When do you start a patient on prophylactic treatment for migraines?

A

If patient experiences more than three migraine attacks per month

Pharm II (7 decks)

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