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Z-Advanced Pharmacology > Final Exam - Section VII > Flashcards

Final Exam - Section VII Flashcards

1
Q

Define tremor, chorea, ballismus, athetosis, and dystonia?

A
  • Tremor: Rhythmic movement around a joint; tremor at rest is a hallmark of Parkinsonism.
  • Chorea: Muscle jerks in various areas
  • Ballismus: Violent abnormal movements.
  • Athetosis: Slow, writhing, twisting movements.
  • Dystonia: abnormal posture
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2
Q

What is the relationship between the basal gangila, thalamus, and motor cortex?

A

Motor cortex- sends information the the muscles for movement and to the basal ganglia cells, which relay information to the thalamus.
Thalamus- sends signals to the motor cortex to slow down or enhance movement, fine tuning them.
Basal ganglia - regulates activity of the thalamus, primarily by the substantia nigra (SN). The SN releases dopamine which inhibts and excites information to the thalamus.

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3
Q

What is the pathology of movement related disorders?

A

The substantia nigra dopaminergic neurons are degraded, leading to decreased dopamine levels.
Dopamine is inhibits muscle movements.

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4
Q

What are the common signs of Parkinson’s disease?

A

TRAP
T- tremor
R - rigidity
A - akinesia; loss or impairment in power of voluntary movement
P - posture and balace instability

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5
Q

What is the function of synuclein?
Describe the conditions where abnormal synuclein is found?

A

Found in the substatia nigra that is normally diffuse within the cell. In Parkinson’s, synuclein is misfoldied and aggregated together called Lewy bodies.
Lewy Bodies are found in Parkinsons, and Alzheimers.

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6
Q

What is the MOA of Levodopa?
Why is it given with carbidopa?

A
  • Levodopa is a prodrug that is converted to dopamine in the body, but only 1-3% cross into the brain
  • Carbidopa increases crossing of the BBB to 10% by preventing breakdown by DOPA decarboxylase and COMT in the periphery
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7
Q

What are the adverse effects of levodopa and their treatments?

A
  • Anorexia
  • Dyskinesias
  • Tachycardia, a fib (low incidence)
  • N/V - improved with carbidopa
  • Depression, anxiety, hallucinations, delusions (high incidence)
    -Made worse by carbidopa
    -Can be treated with Pimavanserin (Nuplazid), an antipsychotic that is an inverse agonist of the 5-HT2a receptor in the visual cortex.
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8
Q

What is the MOA of apomorphine?

A

Derivative of morphine that is a dopamine agonist

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9
Q

What is the “On-Off” Phenomenon?

A

Periods of increased mobility, followed by marked akinesia; associated with long term Levodopa use

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10
Q

What is the pathogenesis of Huntington’s disease?
Treatments?

A
  • GABA is reduced in the basal ganglia
  • Tetrabenazine - dopamine receptor antagonist
  • Dopamine receptor blockers (Haloperidol)
  • Genetic counseling, speech and physical therapy
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11
Q

Diagram the cell damage pathways (COX and LOX)

A
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12
Q

Describe the two different COX isoforms?

A
  • COX-1 – Always present allows for important homeostatic functions in the GI tract, renal tract, platelet function, and macrophage differentiation. Inhibition undesirable
  • COX-2 - expressed due to stimulation and leads to inflammatory response
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13
Q

Describe the MOA of aspirin’s irreversible inhibition?

A

Irreversibly blocks COX-1 by acetylation of serine 529.
This prevents arachidonic acid interacting with COX.
This prevents formation of TXA2 and platelet aggregation

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14
Q

What is the black box warning for NSAIDS?

A

Increased risk of cardiovascular events (MI, stroke) and GI bleeding

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15
Q

What are the benefits and drawbacks of COX-2 selective inhibitors?
Drug?

A

Benefits: No effect on COX-1 functions (less GI upset, no impact on platelet aggregation)
Drawbacks: Increased risk of serious CV events due to inhibition of PGI2
Celecoxib

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16
Q

What are the indications for diclofenac and indomethacin?

A

Indomethacin
* Rheumatism
* Gout
* Patent ductus arteriosus
Diclofenac
* Reduce arthritic pain
* Comes in a topical form

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17
Q

Why is acetaminophen not an NSAID?

A

It selectively inhibits COX-2 in the CNS and does not have much effect on the arachidonic acid pathway in the periphery
It has no anti-inflammatory effects

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18
Q

Describe the acute and chronic effects of glucocorticoids?

A

Acute is good, chronic is bad
Attributed to cortisol levels

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19
Q

What is the MOA of glucocorticoids?

A
  • Inhibit immune response by blocking transcription/translation
  • Increases Annexin-1 which suppresses phospholipase A2 and leukotriene response
  • Increases secretory leukoprotease inhibitor (SLPI)
  • Increases IL-10 - immunosuppressive enzyme
  • Decreases NFkB which is proinflammatory
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20
Q

What are DMARDs?

A

Disease Modifying Anti-Rheumatic Drugs
Used to reduce inflammation and decrease damage to bones and joints

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21
Q

List the 3 biologic DMARDs and their MOA?

A
  • Abatacept (Orencia) - Blocks T cell activation
  • Rituximab (Rituxan) - Depletes B-lymphocytes
  • Adalimumab (Humira) - anti TNF-alpha
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22
Q

Describe the 3 main fibers for sensation transmission?

A
  • A beta fiber (myelinated) – transmits non-noxious mechanical stimuli
  • A delta fiber (myelinated) - transmits noxious heat and mechanical stimuli like sharp pain. Produces initial reflex response.
  • C fiber (unmyelinated) - transmits noxious heat, chemical, and mechanical stimuli (slow, burning pain).
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23
Q

Describe the 3 tracts in the CNS?

A
  • Spinothalamic - (primary pain pathway) transmits signal through the thalamic nuclei to the somatosensory cortex.
  • Spinoreticular - (emotional sensation) transmits signal through the reticular formation of the pons, then thalamus, then somatosensory cortex.
  • Spinomesencephalic - Mu opiod receptors in the periaqueductal (PAD) grey matter of the brainstem can release endorphins to supress pain signaling.
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24
Q

What are the endogenous opiods and their receptors?

A
  • Endorphins – highest affinity for mu opioid receptors
  • Enkephalins – highest affinity for delta receptors
  • Dynorphins – Highest affinity for kappa receptors

All ligands can bind to each receptor, they differ in affinity

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25
Q

What are the pharmacokinetics of opiods?

A

A: well absorbed, many routes
D: Highly perfuses tissues; accumulates
M: Varies
E: mainly urine (drug tests)

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26
Q

How do opiods reduce pain sensation?

A
  • Bind to receptors in brain and spinal cord
  • Reduce neurotransmitter release (Glutamate, ACh, NE, serotonin, substance P)
  • Hyperpolarize postsynaptic neurons
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27
Q

What are the different organ system effects of the opiods?

A
  • CNS - analgesia, euphoria, sedation, respiratory depression, miosis (always, no tolerance)
  • CV - bradycardia (CNS), tachycardia (meperidine, demerol)
  • GI - constipation (no tolerance)
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28
Q

What are the specific applications for opioids?

A
  • Analgesia
  • Acute Coronary Syndrome
  • Acute pulmonary edema
  • Cough
  • Diarrhea (loperamide)
  • Shivering (demerol)
  • Anesthesia
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29
Q

What is the degree of tolerance for the different opiod effects?

A
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30
Q

What drugs are phenanthrenes?

A
  • Morphine, codeine, oxycodone
  • Dilaudid
  • Heroin
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31
Q

What drugs are phenylheptylamines?

A

Methadone

32
Q

What drugs are phenylpiperidines?

A
  • Fentanyl
  • Meperidine (Demerol)
  • Tramadol
  • Loperamide
33
Q

What are percodan and percocet made of?

A

Percodan: Oxycodone and aspirin
Percocet: Oxycodone and acetaminophen

34
Q

What are the opiod antagonists?

A

Naloxone - opiods
Naltrexone - EtOH
Naloxegol - antagonizes GI effects

35
Q

What are the sleep aids and their receptor target?

A
  • Zolpidem (ambien) and Lunesta
  • GABAa receptor
36
Q

What are the anxiolytics and their receptor target?

A
  • Buspirone
  • 5HT1A receptors
37
Q

What are the sedative-hypnotic benzodiazepines and their receptor target?

A
  • Diazepam and midazolam
  • GABAa receptors
38
Q

What is ethanol’s target receptor?

A
  • Increases action of GABA at GABAa receptors
  • Inhibits glutamate to open NMDA channels
39
Q

Describe/draw the biochemical metabolism of ethanol?

A
  • Normal pathway is alcohol dehydrogenase pathway
  • Chronic users also utilize the microsomal ethanol-oxidizing system (MEOS)
40
Q

What is the management of alcohol-use disorders?

A
  • Alcohol counseling
  • Naltrexone (long acting opioid antagonist)
  • Acamprosate - decrease desire for alcohol
  • Disulfram (antabuse) - causes toxic effects of acetaldehyde rapidly
41
Q

What are the sedative-hypnotic barbituates and their receptor target?

A
  • Phenobarbital, thiopental, methohexital
  • GABAa receptor at level of cell wall
42
Q

Explain the drug development phases?

A
43
Q

What are the puported benefits of echinacea?

A

Improvement in cold symptoms like rhinovirus by increasing WBC and cytokines. Inhibits COX enzymes.

44
Q

What are the puported benefits of garlic?

A
  • HMG-CoA Reductase inhibition (not significant)
  • antiplatelet, antimicrobial, antineoplastic (minimal supporting data)
45
Q

What are the puported benefits of ginkgo?

A

Increased blood flow, free radial scavenger, increased CNS receptors, decreased fibril formation

46
Q

What are the puported benefits of St. John’s Wort?

A

Antidepressant, increases CYP450, should not be taken with MAOI’s or SSRI’s

47
Q

List the purported benefits of ginseng, milk thistle, and saw palmetto

A
48
Q

What are the 3 traditional cancer treatments?

A

Surgery, radiation, chemotherapy

49
Q

Define Primary, Adjuvant, and Neoadjuvant Chemotherapy.

A
  • Primary - chemotherapy, limit spread
  • Neoadjuvant - surgery primary treatment, chemo used pre and post surgery to reduce tumor size
  • Adjuvant - Surgery and chemo used equally, goal is disease free survival
50
Q

What is the MOA of alkylating agents and drug examples?

A

Alkylates DNA causing cross linkage, abnormal base pairing, and DNA strand breakage lead to decreased cell proliferation.
Cyclophosphamide (most common), chlorambucil (least toxic)

51
Q

Describe the MOA of cisplatin and important side effects, as well as the most common uses

A

Forms reactive platinum complex causing intra strand and interstrand cross links, damagind DNA, preventing cell proliferation.
Has severe SA of emesis, neuropathy, ototoxicity, and nephrotoxicity.
Used for testicular cancer and many solid tumor cancers

52
Q

What is the MOA of methotrexate?

A

Inhibits dihydrofolate reductase, interfering with DNA/RNA synthesis

53
Q

What are the antineoplastic antimetabolites?

A

6-MP, 5-FU

54
Q

What are the plant based antineoplastics?

A

Vincristine, Paclitaxel

55
Q

What are the antineoplastic antibiotics?

A

Dactinomycin, doxorubicin, bleomycin

56
Q

What are the antineoplastic hormonal agents?

A

Corticosteroids, tamoxifen, fulvestrant

57
Q

What are the miscellaneous antineoplastics?

A

Imatinib, trastuzumab, rituximab

58
Q

What drugs work on the dopamine metabolism pathway and their MOA?

A
  • Pramipexole – agonizes dopamine receptors to increase the release of dopamine
  • Tolcapone – COMT inhibitor, preventing breakdown of dopamine
  • Selegeline – Selective MAO-B inhibitor preventing the breakdown of dopamine
  • Carbidopa - Inhibits dopamine breakdown in periphery by blocking DDC and COMT
59
Q

List an important application for nitrosoureas.

A

Crosses the BBB to treat meningeal/brain tumours

60
Q

What are the innante, nonspecific host defenses?

A
61
Q

What is the acquired, specific host defense?

A
62
Q

List the 5 immune system cytokines and their function?

A
  • Interleukins (ILs) - Signal among leukocytes
  • Interferons (IFNs) - Antiviral proteins that may act as cytokines
  • Growth factors - Proteins that stimulate stem cells to divide
  • Tumor necrosis factor (TNF)-
    Secreted by macrophages and T cells to kill tumor cells and regulate immune responses and inflammation
  • Chemokines - Chemotactic cytokines that signal leukocytes to move
63
Q

What is primary immunodeficiency?
Examples?

A
  • Born with hyposensitivies
  • DiGeorge Syndrome: No thymus (no T cells)
  • Agammaglobinemia: No B cells (no antibodies)
  • Severe combined immunodeficiency disorder (SCID): No B or T cells
64
Q

What is secondary immunodeficeny?
Examples?

A
  • Acquired hyposensitivity
  • Acquired Immune Deficiency Syndrome (AIDS)
65
Q

What are the 4 types of hypersensitivities?
Examples?

A
  • Types I-IV
  • A - anaphylaxis, allergies
  • C - cytotoxic (blood incompatability)
  • I - Immune complex (rheumatoid arthritis)
  • D - delayed (graft rejection)

I-III antibodies, IV T cells

66
Q

What is autoimmunity?

A

Immune response against normal, healthy tissue

67
Q

Describe SLE, MS, MG, and DM?

A
  • SLE – autoantibodies against DNA
  • MS – Autoantibodies and T-cells against neurons, myelin
  • MG – Destruction of ACh receptors
  • Pancreas (Islets) - Insulin-dependent Diabetes mellitus;
    Cytotoxic T cells attack beta cells (Insulin)
68
Q

What are the glucocorticoids?
MOA?

A
  • Prednisone, dexamethasone, and hydrocortisone
  • Suppress immune response by interfering with cell cycle of B & T cells
69
Q

What is calcineurin?

A

Necessary for T-cell receptor signaling and activation

70
Q

What is cyclosporines class and uses?

A
  • Peptide antibiotic, calcineurin inhibitor
  • Transplant, GVHD
71
Q

What is tacrolimus class and uses?

A
  • Macrolide antibiotic
  • Can be topical for atopic dermatitis or psoriasis
72
Q

What is the class, MOA, uses, and side effects of azathioprine?

A
  • Cytotoxic agent
  • Antimetabolite targeting rapidly proliferating cells
  • Metabolized by xanthine oxidase (XO) to mercaptopurine
  • Graft rejection, lupus, RA, Crohn’s, MS
  • Main side effect – leukocytopenia caused by bone marrow suppression
73
Q

How does cyclophosphamide cause tissue toxicity and cell death?

A

Alkylating agent

74
Q

What are the immunosupressive antibodies?

A

Muromonab, RhoGAM, adalimumab

75
Q

What category is sirolimus, mycophenylate mofetil, and thalidomide derivaties?

A

Additonal agents

Z-Advanced Pharmacology (17 decks)

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