Pharmacology Week 4-6 Flashcards

1
Q

1 in how many Australians reported having….
-osteoarthritis?

-osteoporosis or osteopenia?

A
  • osteoarthritis 1 in 11 more so in F

- osteoporosis 1 in 5

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2
Q

People with back pain and problems were how many more times likely to experience…..

  • poor health?
  • very high psychological distress?
  • very severe pain?
A
  • PH: 3.2X
  • PD: 1.8x
  • SP: 2.4X
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3
Q

People with arthritis were how many more times likely to experience…..

  • poor health?
  • very high psychological distress?
  • very severe pain?
A
  • PH: 2.7x
  • PD: 1.8X
  • SP: 2.3X
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4
Q

People with osteoporosis were how many more times likely to experience…..

  • poor health?
  • very high psychological distress?
  • very severe pain?
A
  • PH: 2.0X
  • PD: 1.9X
  • 3.0X
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5
Q

Ankylosing spondylitis, psoriatic arthritis, reactive arthritis, enteropathic arthritis are all examples of what type of musculoskeletal disorder?

A

spondyloarthropathies

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6
Q

autoimmune disease that features painful swelling and stiffness in joints that is a systemic condition

A

rheumatoid arthritis (RA)

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7
Q

What happens at the cellular level in rheumatoid arthritis (RA)?

T cells invade the _____________ and produce _________ and _________

A

synovial membrane

interleukin-2

interferon

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8
Q

interleukin-2 and interferon signal a cascade reaction leading to an overproduction of ______________ which constitute the pivotal event leading to chronic inflammation

A

pro-inflammatory cytokines, mainly TNF-, IL-1 and IL-6

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9
Q

What are the stages of Rheumatoid arthritis?

A

1) synovitis
2) pannus formation
3) fibrous ankylosis
4) bony ankylosis

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10
Q

What is the general pharmaceutical management of Rheumatoid arthritis?

A

Disease Modifying Anti-Rheumatic Drugs (DMARDs)

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11
Q

What are the 3 main areas of pharmacological management of rheumatoid arthritis?

A
  • pain management w/ analgesics
  • disease modification with DMARDS w/ corticosteroids
  • aggressive management of co-morbidities such as cardiovascular risk factors
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12
Q

reduce or eradicate synovial inflammation and thus prevent joint damage

A

disease modifying anti-rheumatic drugs (DMARDs)

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13
Q

When should a response with DMARDs therapy be expected?

A

apparent within 12 weeks

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14
Q

What is the most common DMARDs choice?

A

Methotrexate (MTX) in active cases which also is a common cancer drug

(combination therapy results in superior outcomes)

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15
Q

Methotrexate….
-what is it

  • onset of action:
  • often prescribes with:
A
  • anti inflammatory, immunomodulatory and cytotoxic action
  • w/in 3-6 weeks
  • folic acid to reduce adverse effects
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16
Q

What are common adverse effects with methotrexate?

A
  • nausea
  • increase in rheumatoid arthritis
  • mouth ulcers
  • rash
  • reversible hair loss
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17
Q

conventional synthetic DMARD that is an antimalarial that possesses anti-inflammatory and possibly immunosuppressive activity

A

hydroxychloroquine

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18
Q

What is the benefit to taking hydroxychloroquine too MTX?

A

better tolerated but less effective

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19
Q

What is the response onset of hydroxychloroquine?

A

2-6 months

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20
Q

Common adverse effects with hydroxychloroquine:

A
  • nausea/ anorexia/ diarrhoea
  • rash/ alopecia
  • abdominal cramps
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21
Q

infrequent adverse effects if hydroxychloroquine:

A
  • absent deep tendon reflexes
  • muscle weakness
  • neuromyopathy
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22
Q

What are the indications to use sulfasalazine?

A
  • rheumatoid arthritis

- ulcerative colitis & chrons disease

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23
Q

Biological DMARDs (bDMARDs) are also known as…….

A

cytokine modulators

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24
Q

bDMARDs can act in different ways including….

A
  • directly against pro-inflammatoy cytokines (TNF, IL-1 and IL6)
  • act through B or T lymphocytes to decrease cytokine production
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25
Q

When are bDMARDs indicated?

A
  • severe active RA
  • psoriatic arthritis
  • juvenile RA
  • ankylosing spondylitis
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26
Q

What drugs are used to help with pain but does not modify the disease?

A

analgesics

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27
Q

if there is no inflammation what drug can be used in place of analgesics?

A

paracetamol

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28
Q

What are types of analgesics?

A
  • paracetamol
  • NSAID (ibuprofen)
  • opiods
  • fatty acid supplements (fish oil)
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29
Q

What is the dosage of DHA and EPA (fatty acid supplement) from fish oil are recommended a day to have an anti-inflammatory effect?

A

> 2.7g/day

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30
Q

Why are corticosteroids not always used to treat RA?

A

limited by adverse effects

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31
Q

What are the 3 main ways corticosteroids are used in RA?

A
  • as an initial bridging therapy
  • in the management of acute flares
  • in combination with DMARDs when DMARds therapy is suboptimal
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32
Q

What are the effects corticosteroids have?

A
  • anti-inflammatory
  • immunosuppressant
  • metabolic effects
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33
Q

glucocorticoids are diabetogenics meaning…..

A
  • they can aggravate diabetes
  • unmask latent diabetes
  • cause insulin resistance
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34
Q

cortisol is important for…. (corticosteroids)

A
  • carbohydrate metabolism
  • protein metabolism
  • fat metabolism
  • calcium balance
  • blood pressure and stress response
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35
Q

synthesis of corticosteroids…

-cholestrol –>

A

hydrocortisone (cortisol)

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36
Q

what controls the corticosteroid release?

A

-hypothalamic and pituitary control in adrenals

circadian rhythm and ultradian rhythm

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37
Q

steroids can block protein production (transrepression) which inhibit COX2 which causes an….

A

inflammatory effect

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38
Q

pregnancy and rheumatoid arthritis…give the class of drug

  • NSAID
  • corticosteroids
  • fish oil and paracetamol
A
  • category C
  • Category A

can be used during pregnancy

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39
Q

Osteoarthritis is NOT an autoimmune disorder but a disorder of “______________”

A

wear and tear

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40
Q

What happens during osteoarthritis?

A

there is an imbalance between the synthesis and degradation of articular cartilage

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41
Q

What is the pharmacological treatment for osteoarthritis?

  • oral
  • topical
A
  • oral: paracetamol and NSAID(more effective than paracetamol)
  • topical: NSAID, topical capsaicin (main ingredient in chili)
42
Q

What is just as effective as NSAID for osteoarthritis?

A

exercise

43
Q

What was the conclusions from a study testing the efficacy and safety of paracetamol for spinal pain and osteoarthritis?

A

found that paracetamol was ineffective for LBP and minimal support for people with osteoarthritis

44
Q

What intra-articular injections can be used for the treatment of osteoarthritis?

A

corticosteroid (one joint –> ok)

-hyaluronan (conflicting evidence)

45
Q

Was fish oil effective in reducing pain levels in a low dose or high dose?

A

more effective in a LOW dose (there was no added benefit to osteoarthritis in taking a high dose fish oil supplement)

46
Q

What is the first line of pharmacological treatment for …..neck pain (acute)?
LBP?

A
  • NSAIDs and paracetamol

- NSAIDs (short term); found no evidence for paracetamol, corticosteroids orally, or muscle relaxants (in chronic cases)

47
Q

a majority of LBP patients will recover within________________?

A

3 months

48
Q

What is recommended in treating LBP?

A

non-pharmacological treatment with superficial heat, massage, acupuncture, or spinal manipulation

49
Q

what. did the Cochrane review state in relation to LBP and paracetamol intervention

A

paracetamol does not produce better outcomes than placebo for people with acute LBP

50
Q

condition with too much uric acid forming monosodium rate crystals in tissues

A

gout

51
Q

what are common risk factors for gout

A

obesity, purine rich diets, genetic factors, renal impairment, osteoarthritis ageing

52
Q

How is uric acid formed?

what is the catalyst?

A

dietary and endogenous purine precursors

enzyme xanthine oxidase

53
Q

how does diet affect gout?

A

purine rich diet shifts from plasma to joint capsule and crystals accumulate in joint

54
Q

What is the management plan for acute gout?

A
help with pain by
1) maximum dose of NSAID
-prednisone 
(3 days)
-colchicine (4 days)
55
Q

What is the management plan for chronic gout?

A
  • low purine diet/ limit alcohol intake
  • introduce rate-lowering drug: allopurinol
  • prevent exacerbation of allopurinol titration: colchicine or NSAID
56
Q

What drug is used to reduce uric acid production by inhibiting xanthine oxidase and lowering plasma and urinary rate concentrations?

What is an adverse effect?

A

allopurinol (progout)

-maculopapular or itch rash

57
Q

What drug inhibits neutrophil migration, chemotaxis, adhesion, and phagocytosis in inflamed area?

it also reduces inflammation reaction to crystals but has NO effect of uric acid production or excretion

What are common adverse effects?

A

colchicine (cologout/ lengout)

-GI common adverse effects, myopathy, myalgia, rhabdomyolysis

58
Q

systemic condition characterized by low bone mass and deterioration in bone microarchitecture (bone quality)

A

osteoporosis

59
Q

What are pharmacological therapies for managing osteoporosis?

-preventing primary/secondary fractures?

A

-an oral or IV biophosphonate

60
Q

What drugs mechanism of action decreases bone resorption by inhibiting osteoclasts?

A

biophosphonates (drone-dronic)

61
Q

What should be supplemented for osteoporosis (if low)?

A

Vitamin D and calcium

62
Q

What is used to treat neuropathic pain of fibromyalgia?

A

pregamblin

63
Q

What are the classes of drugs for conditions affecting the GIT?

A
  • antidiarrhoeals
  • laxatives
  • drugs for IBS
  • antispasmodics
  • antiemetics
  • drugs for IBD
64
Q

indigestion also known as

A

dyspepsia

65
Q

What drugs are used to treat dyspepsia?

A
  • antacids

- acid suppression: H2 antagonist and protein pump inhibitor (PPI)

66
Q

chronic and relapsing condition where exposure of the esophagus to refluxed contentes

A

GORD (gastro-esophageal reflux disease)

67
Q

What drugs are used to treat GORD?

A
  • proton pump inhibitor (PPI)
  • H2 antagonists (histamine 2)
  • antacids
68
Q

What bacteria is related to stomach ulcers? what what is the treatment

A

Helicobacter pylori

-2 antibacterials improves eradication

69
Q

what is the treatment for NSAID related ulcers?

A

-stop NSAID, but if not possible, PPI and misoprostol (cytotec)

70
Q

what is used to prevent NSAID related ulcers?

A

PPI, double dose H2 antagonists and misoprostol

71
Q

in stomach, what produces prostaglandins?

A

COX-1

72
Q

what inhibits COX1 enzymes leading to frequent upper gastro-intestinal side effects (bleeding and ulceration)

A

NSAID

73
Q

What does COX 1 prostaglandins stimulate?

A

stimulate mucus and bicarbonate secretions dn cause vasodilation

74
Q

What is the mechanism of action for antacids?

A

base + acid = salt and water

-weak bases react with gastric acid to neutralize it (raise the pH of the stomach)

75
Q

What are indications for antacids?

A

dyspepsia, peptic ulcer disease (PUD), GORD

76
Q

What are adverse effects to antacids and what is the cause?

A
  • constipation (Ca and Al) and diarrhea (Mg)
  • belching, flatulence (carbonate)
  • alkalosis (bicarbonate)
77
Q

Mylanta and gaviscon are types of …….

A

antacids

78
Q

Rantidine (Zantac) is a type of …..

A

H2 receptor antagonist (histamine 2)

79
Q

what drug competitively blocks H2 receptors, which reduce gastric acid secretion

A

H2 receptor antagonist

80
Q

what are indications for using H2 receptor antagonists?

Adverse effects?

A
  • dyspepsia, PUD, GORD, stress-ulcer prophylaxis (ranitidine)
  • no adverse effects
81
Q

omeprazole (loser), esomeprazole (Nexium), and pantoprazole (somac) are types of …

A

protein pump inhibitors (PPI)

82
Q

what do PPI do?

A

irreversibly inactivate the H+ and K+ ATPase enzyme system (protein pump_ suppressing both stimulated and basal acid secretion

83
Q

what are indications for using PPI?

A

dyspepsia, peptic ulceration disease (PUD), GORD, H. Pylori eradication, scleroderma esophagus, prevention and treatment for upper GI adverse effects of NSAID

84
Q

What are adverse effects for PPI?

A
  • headache, nausea, vomiting
  • diahhrea, constipation, flatulance
  • mylagia, myopathy, arthralgia
  • decreased B12 absorption (long term use)
  • increase risk of osteoporosis- related fractures
85
Q

infrequent defecation (usually <3 times/week), often with straining and passage of hard, uncomfortable stools

A

constipation

86
Q

drugs used to treat diarrhea in Australia

A
  • oral rehydration salts (hydralyte)

- antidiarrheals (imodenium, bulking agents, opioids, adsorbents, probiotics, zinc)

87
Q

antidiarrheals the reduce motility?

A

opioids (Imodium)

88
Q

Common types of laxatives?

A
  • bulking agents
  • stool softeners-stimulants
  • suppositories and enemas
  • osmotic
89
Q

bisacsdyl (dulcolax) and Senna (senokot, coloxyl with Senna) are types of…

A

laxatives (stimulants)

90
Q

How do laxatives work?

A

direct stimulation of nerve ending or irritating mucosa to increase intestinal motility
(can cause abdominal cramps)

91
Q

where is the vomiting center located?

A

medulla if the brainstem (mechanical and chemical stimulus from the GIT can initiate nausea and vomiting)

92
Q

What is used to treat nausea and vomiting?

A

dopaminergic, histaminic, cholinergic, opined, neurokinin, and serotonergic (5HT3) receptor systems

93
Q

metoclopramide (maxolon), and domperidone (motilium) drugs are used for…

A

dopamine antagonists

94
Q

what do dopamine antagonists do?

A

block dopamine receptors in the CTZ, leading to anti nausea and antiemetic action

95
Q

adverse effects of gomapmine antagonists?

A

extra pyramidal side effects–> similar to Parkinsons shaking (decreased) dopamine

96
Q

antiemetics mean..

also, what is included in the vestibular apparatus?

A

motion sickness

M1 and H1 receptors

97
Q

what are the 2 types of antiemetics?

A
  • anticholinergics

- antihistamines (sedation)

98
Q

unknown etiology and common causing lower abdominal pain, flatulance, and diarrhea that can alternate with constipation

A

IBS

99
Q

what are the 2 main types of inflammatory bowel disease (IBD)?

A
  • ulcerative colitis (rectum and colon)

- Chrons disease (mouth to anus)

100
Q

What drugs can be used for IBD?

A

-corticosteroids
-5-aminosalicylates
-immunisupressants
-biological drugs
(monoclonal antibodies)