winter final Flashcards
1
Q
Chloroquine and Hydroxychloroquine
A
Blood Shizonticides anti malarial drug
- acts on RBC form, no affect on tissue forms, affects the bugs ability to feed( cannot digest hemoglobin),drugs ability to raise ph of malarial food vacuoles, prophylaxis for all forms
- clinical cure for all malaria, radical cure for falciparum and . malaria, resistant forms of falciparum are developing( transport pumps remove drug from the parasite
- oral, well abs, accumulated in melanin rich tissues i.e. skin and retina, met in liver(caution in liver DS), 6-7d t.5
- tox-less than quinine-dizzy headache tinitus, GI upset(take w/food), renal and corneal tox(monitor sight),
- immunologic- skin rashes, blood dycrasias, lupus like syndrome, CONTRA IN pts with porphyria or psoriasis
2
Q
Blood Shizonticides
A
Chloroquine
hydroxychloroquine
Quinine and Quinidine Gluconate
Mefloquine
3
Q
special property of Hydroxychloroquine
A
Anti inflammatory at high doses
- used in RA and Lupus
- malaria dose is 310, Anti inflame dose is 400-600
4
Q
Quinine and Quinidine Gluconate
A
- anti malarial drug -Blood Shizonticides
- MOA-interferes with plasmodial digestion of hemogllobin, used in chloroquine resistant Falciparum
- found in cinchona bark -old drug, acts on all erythrocyte forms(schizonticidal forms), gametocytocidal in vivid and p. malaria,
- oral, t.5=5-16 hours
- other action- analgesia and antipyretic similar to aspirin, GI irritation-nvd, blurred vision, auditory deafness(tints and deafness)
- tertogenic and abortion, depressant effect on heart, mild neuromuscular blockade
_cinchonism- syndrome of toxicity resembles salicylism- Headache, Nausea, dizzy, blurred vision, tinnitus)
5
Q
Mefloquine
A
- anti malarial drug -Blood Shizonticides
- used in chloroquine resistant Falciparum treatment and prophylaxis, acts on all erythrocyte forms(schizonticidal forms)
- MOA similar to chloroquine, interferes with plasmodial digestion of hemoglobin
- rapid resistance in some strains, only oral b/c irritating, can use in preg
- tox-seizures and aggravate latent psycosis- NO USE in pts w/ history of mental illness or epilepsy
- potential cardiac (myocardial depression) and CNS toxicities, use caution in pts w/ cardiac psychiatric, or epilepsy disorders
6
Q
inhibitors of folic acid synthesis and utilization
A
pyrimethamine
Proguanil
7
Q
Artemisinin analogues
A
artemether plus lumafantrine - isolated from chinese herbal medicine
- anti malarial drug -Blood Shizonticides
- generates free radicles that kill paracyte
- GI irritation and headache
- Drug of choice in combo w/ pyrimethamine and sulfadoxone others to treat chloroquine resistant strains
8
Q
pyrimethamine
A
anti malarial
inhibits DHFR mainly on the Erethrocyte forms, some affect on tissue and pre RBC stages and cryptomerozoites
- prophylaxis for chloroquine resistant P.F strains
- used in combo w/ sulfonamides PYRIMETHAMINE PLUS SULFADOXINE (-sulfonamide MOA- inhibit dihydropteroate synthase stoping conversion of PABA–> dihydropteroic acid) (used for presumptive treatment)
- used w/ artemisinin analogues for CR P.F
9
Q
Proguanil
A
anti malarial
casual prophylaxis treatment
inhibits DHFR mainly on the Erethrocyte forms, some affect on tissue and pre RBC stages and cryptomerozoites
- prophylaxis for chloroquine resistant P.F strains
- used in combo w/ sulfonamides PYRIMETHAMINE PLUS SULFADOXINE (-sulfonamide MOA- inhibit dihydropteroate synthase stoping conversion of PABA–> dihydropteroic acid) (used for presumptive treatment)
- used w/ artemisinin analogues for CR P.F
10
Q
Atovaquine plus proguanil
A
new combination anti malarial drug
- atovaquone- acts to depolarize parasites MITO and inhibits E- transport
- RARE SE- Headache and ab pain- not sure preg use
- alternative to doxy and mefloquine prophylaxis against CR P.F, daily dose, rather expensive
11
Q
tetracyclines
A
alternative anti malarial
broad spectrum bacteriostatic agent to inhibit protein synthesis by binding to the 30S subunit of ribosomes, and blocking amino acyl T-RNA to Bind and add AA
- excreted via renal filter(10-50%), in bile
- resistance- increased efflux pumps, Tet(AE) conver resistance to G- to tetra, doxy and minocycline, production of protein to prevent binding to 30S tet(M) ,enzymatic inactivation
- USE-not 1st choice for G+, G- aerobes, or anaerobes
- drugs of choice for- spirochetes(Lyme Ds), clamidia, Rickettsiae(RMSF)(DOXY), Mycoplasm pneumo, brucella, H pylori, peridontitis
12
Q
tissue schizonticides
A
Primaquine
13
Q
Primaquine
A
anti malarial -tissue schizonticides
- active against tissue forms of all species of plasmodia, MAIN EFFECT IS TO KILL TISSUE FORMS OF VIVAX AND OVALE–> radical cure for these
- gametocytocidal
- little RBC form effect, not used for prophylaxis b/c of toxicities
- TOX- mild w/ acute use, increased w/ chronic use
- GI upset, CNS-headache and dizzyness, HEMOLYTIC ANEMIA- in G6PD pts, avoid in preg
14
Q
preferred drugs to treat Enterobius vermicularis (pinworms
A
Albendazole
- Pyrantel
- rigid standards of personal hygiene
15
Q
preferred drugs to treat Ascaris lumbricoides
A
- 2nd most common in US, most common in world, night soil, wandering worms, surgery may be needed for wanders
- asymptomatic infections-Albendazole
- Heavy infections- Pyrantel(causes worm paralysis)
16
Q
preferred drugs to treat hookworms (nectar americanus)
A
Albendazole,
-also used to treat creeping eruptions
17
Q
preferred drugs to treat Tapeworms
A
drugs affect the scolex
- T. Saginata(beef)= praziquantil
- T solium (pork)= praziquantil( along with a purgative Mg sulfate)
- Neurocysticercosis-dexamethazone2 d b4 anti helminth and albendazole and prazaquantil
18
Q
Albendazole
A
anti helminth drug
5% orally absorbed and metabolite from liver responsible for systemic effects
- MOA- binds to free B tubulin, inhibits microtubule polymerization and microtubule dependent Glucose uptake, doesn’t bind well to human B tubulin
- NVD, teratogenic potential, can resign LFTs and Leukopenia
19
Q
Pyrantel
A
available OTC, anti helminth, Broad spec used against many nemotodes
- MOA-activation of the cholinergic nicotinic receptor in the muscle of nematodes-> depolarizing muscular blockade-> worms become paralyzed and expelled from GI tract
- GI most common-NV cramps, RARE but serious liver failure, use in preg and child
20
Q
Praziquantel
A
- oral with wide tissue breakdown including CNS, metabolite and drug eliminated in kidney
- works again Neuroshistosomiasis, broad spec against schistosomes(trematodes) and tapeworms
–MOA-induces muscle contraction and spastic paralysis of the musculature of worms via increased calcium ion influx, with cestadoes causes the sucker to become dislodged
SE- Dizzy drowsy Headache, decreased alertness are most common, GI NV ab pain, increased LFTs, avoid with preg, low grade fever and rash
21
Q
Antiprotozoals
A
Metronidazole Idoquinol Paromomycin Nitazoxanide -opportunistic infections with protozoa are prominent in infants, individuals with cancer, transplant recipients, those receiving immunosuppressive drugs, and persons with acquired immunodeficiency syndrome (AIDS)
22
Q
preferred drugs entamoeba histolytica
A
Idoquinol, paromomycin-asymptomatic carriers(luminal drugs)-
-symptomatic(tissue amebiside and Luminal acting drugs)) metronidazole plus Idoquinol or paromomycin
23
Q
preferred drugs for Giardia
A
- metronidazole
- nitazoxanide
24
Q
preferred drugs for cryptosporidiosis
A
nitazoxamide
-paromomycin
25
metronidazole
- good oral and so not used in luminal phase, used in symptomatic pts
- MOA- Cidal drug, gets reduced w/in and binds to intracellular macromolecules( DNA)--> inhibits DNA synthesis
-uses- anaerobic bacteria Bacteroides fragilis and the gram positive rod Clostridium difficile.
protozoans entomeba histolytica, Trichomonas vaginalis, and Giardia lamblia
-SE-disulfram like interaction with alcohol, increases effect of oral anticoags, Nausea , headache, dry mouth, vomit Dhrea, carcinogenic in rodents
26
Iodoquinol
luminal or contact amebicide
-MOA- unknown, not well absorbed and excreted in feces
USE- sed in combination with
Metronidazole to treat symptomatic infections and used alone to treat asymptomatic carriers.
-SE-neurotoxinc if given >2g/day for > 20 days, loss of vision and optic neuritis, safe inpreg
27
Paromomycin sulfate
anti amoeba
- poor oral abs most excreted in feces,luminal or contact amebicide
- MOA- aminoglycoside--> inihbits protein synthesis via binding to the 30 S subunit
- Uses- E histolytic-(alone for asymptomatic, in combo w/ metronadazole for symptomatic or extraluminal amebiasis
- Drug of choice in AIDS pts w/ cryptosporodiosis
- se-GI-anorexia NV increased motility, abdominal cramping, nephron and ototox and neuromuscular blockade
28
Nitazoxanide
MOA- converted first to active metabolite tizoxanide
- interferes with anaerobic energy metabolism by inhibiting pyruvate:ferredoxin 2-oxidoreductase enzyme dependent electron transfer reaction which is important for organisms dependent on anaerobic metabolism (e.g. Cryptosporidium parvum, Giardia lamblia)
- USE- dhrea from crypto in immunocompetent children1-11 yo, adolescent and adults
USE- dhrea from giardia in pts >1yo
SE-ab pain , dhrea, N and headache
no mutogentic/carcinogenic effects( unlike metronidazole)
29
alkylating agents
```
-CCNS, cells most susceptible in late G1 and S
Mechlorethamine
Cyclophosphamide
Carmustine
Cisplatin
```
able to transfer reactive alkyl group to DNA-> cytotoxic effect, alkylation of DNA reacts w/ N7 on Guanine and alkylated purine,
- miscoding of DNA, incomplete repair, leads to cross linking of DNA strands and inability for separate
- toxicity-vessicant at injection, acute-NV phlebitis, chronic- bone marrow supression
30
Mechlorethamine hydrochloride
anti cancer drug, alkalating agent
- forms cross links between DNA, at the N7 of guanine,
- results in miscoding of DNA, incomplete repair of alkylated segments, excessive cross linking and inability to separate
nitrogen mustard, bis chlorethyl amine
CCNS- M and G1 most sensitive
--toxicity-vessicant at injection, acute-NV phlebitis, chronic- bone marrow supression
31
Cyclophosphamide (CTX)
CCNS,anti cancer drug
derivative of Mechlorethamine, requires activation by P450 to active metabolite ALDOPHOSPHAMIDE
- forms cross links between DNA, at the N7 of guanine,
- results in miscoding of DNA, incomplete repair of alkylated segments, excessive cross linking and inability to separate
-USE acute chronic leukemia, immunosupressive-RA, transplant
--toxicity-vessicant at injection, acute-NV phlebitis, chronic- bone marrow supression
32
Carmustine
Nitrosurea, CCNS anti cancer drug (BCNU)
_bifunctional alkylator , nonspecific, highly lip soluble
_USE- Brain tumors, hodgkins and non hodgkins lymphomas
--toxicity, acute-NV phlebitis, chronic- leukopenia and thrombocytopenia
33
Cisplatin
CCNS anti cancer drug
- Platinum complex, G1 most specific(STILL CCNS),
- bifunctional alkylating agent, inter and intra strand cross linking, disrupts double helix
-TOX-Nephrotoxic and ototoxic
also acute-NV phlebitis, chronic- bone marrow supression
34
Antimetabolites
```
-CCS agents
Methotrexate
Mercaptopurine
Fluorouracil
Cytarabine
```
-metabolized instead of normal substrate, compete with normal metabolites, affect nucleotide and nucleic acid synthesis
35
Methotrexate
- CCS agent S phase -anti cancer drug, folic acid analogue
- MOA- inhibits DHFR-> blocking folic acid synthesis--> inability to convert deoxyuridylate to thymidylate
- leucovorin(foilinic acid) protects normal cells
- poor CNS penetrate, 50% BOUND TO PLASMA PROTEIN
- TOX- acute-NVD, delayed- BM suppression, go/oral ulcer, alopecia, hepatotox
- USE- leukemia and psoriasis and RA
36
Mercaptopurine
CCS agent S phase, Purine analogue, sulfhydryl substituted analogue of hypoxanthine
-MOA- inhibts enzymes of purine interconversion--> purine nucleoside systhesis inhibition, converted by HGPRT to 6-thioinosinic acid
---metabolized by xanthine oxidase----
-toX- cute-NVD, delayed- BM suppression, cholestatic jaundice
37
Fluorouracil
pyrimidine analogue
CSS anti cancer agent, S phase,
- converted to 5-deoxyuridine-> binds to thymidylate synthetase covalently, blocks conversion of deoxyuridylate to thymidylate the rate limiting step in DNA synthesis
- no acue tox, -nausea oral ulcers and BM supression
38
Cytarabine
pyrimidine analogue
CSS S pahse anti cancer agent,
- converted to cytarabine triphosphate inhibiting DNA polymerase via compete w/ deoxycitidine triphosphate
- Delayed TOX- NV BM suppress, megaloblastosis, leukopenia, thrombocytopenia
39
Natural anti cancer products
Anthracycline Antibiotics: Daunorubicin Hydrochloride, Doxorubicin Hydrochloride
Vinca Alkaloids, Epipodophylotoxins and Taxanes: Vinblastine Sulfate, Vincristine Sulfate, Etoposide, Paclitaxel
40
Anthracycline
antibiotic anticancer drugs CCNS( but most effective in S phase)
Daunorubicin Hydrochloride, Doxorubicin Hydrochloride
- MOA- intercalate and bind to DNA--> unwinding of DNA--> destroy the DNA template, anti tumor activity at tetracycline ring
- TOX- Acute- NV, red urine, tissue necrosis, delayed- BM suppression, CARDIOMYOPATHY
- USE- used in combination with other drugs to synergize effects
41
Vinblastine sulfate
CCS M phase specific anti cancer drug
- MOA- bind to tubulin and disrupt the mitotic spindle, prevents segregation of chromosomes in metaphase
- TOX-acute- NV PHLEBITIS, DELAYED-neurologic( peripheral neuropahty and BM depression
42
Vincristine sulfate
CCS M phase specific anti cancer drug
- MOA- bind to tubulin and disrupt the mitotic spindle, prevents segregation of chromosomes in metaphase
- TOX-acute-local reactivity, DELAYED-neurologic (peripheral neuropahty), constipation andalopecia and mild BM depression
43
Etoposide
CCS for G2 phase anti cancer drug
derivative of podophyllotoxin- MOA forms complexes with topoisomerase II and DNA-->DNA breaks w/o resealing--> cell death
-TOX- A- NVD D- leukopenia, alopecia
44
Paclitaxel
CCS anti cancer drug specific to M and G2 phase from bark of yew tree
- MOA- antimicrotubule agent, rather than inhibit microtubule assembly like vincristine and vinblastine it promotes microtubule assembly to stabilize membranes
- TOX- A: NV D- BM suppression, hypersensativity , peripheral neuropathy, alopecia
45
Prednisone
| dexamethazone
adrenocorticosteroid
MOA- Binds to cytosolic receptors (complex) and affect DNA and RNA and protein synthesis
2. Suppresses lymphocytes and macrophages
TOX- CUSHINGS SYNDROME
46
Tamoifen
CCS agent specific to G1 phase, non steroids anti estrogen
MOA- competitive inhibitor of estrogen inhibitor in estrogen sensative tissues-> receptors are nuclear transcription factors
- tox- most common are menopausal
- short term- hot flash fatigue, NV, vag dryness
- LONG term- visual disturbance, vag bleed, ocular tox, thrombotic effect, thrombocyto/leukopenia
- MOST SERIOUS- possible tumor promoting, endometrial cancer
-USE- Estrogen R positive breast cancer, reduces risk of recurrence of breast cancers
47
imatinib mesylate
tyrosine kinase inhibitor CCS at G1 phase
- inibits Bcr-Abl tyrosine kinase inhibitor preventing phosphorylation, inhibits cell proliferation and induce apoptosis in leukemia and CML
- TOX- A- ab pain NVD, D- fatigue joint pain, muscle pain
USE-acute lymphocytic leukemia, Ph+ chronic myeloid Leukemia
48
Trastuzumab
monoclonal AB, CCS at G1 phase
- Humanized monoclonal Ab that binds to human epidermal growth factor(EGF) Her-2, blocking EGF and down regulating receptors tyrosine kinase activity, causing G1 cycle arrest
- TOX- A-NVD, D- anemia, neutropenia, infection, fatigue
_USE- adjuvant in breast cancer w/ overexertion of HER-2, metastatic breast cancer-in combo w/ paclitaxel first line for HER-2 overexpressing cancer
49
amphetamine
CNS effects- stimulation and increased arousal and stir via reticular activating system
-euphoria - some may get paranoid and dysphoria
-delay in fatigue induce decline in performance
-rebound effect
-psychological and physical dependence, withdraw symptoms of fatigue lethargy and depression
-amphetamine psycosis- similar to schizo
-supressed apatite
this card sucks
50
d-amphetamine
sympathomimetic effects and toxicities
this and amphetamine- irreversible degeneration of dopamine and serotonin pathways
MOA- enhanced release and (lesser effect ) to decrease re uptake of NE and DA, stimulate direct reward centers, decreased levels of DA in reward centers(chronic)
-MET- enhanced excretion in acidic urine
51
Lisdexafetamine
prodrug amphetamine bound to lysine
moderate rate of conversion leading to a lower abuse potential
-USed in ADHD
52
methamphetamine
presence of methyl group increases lipid absorption and increases lipid solubility, produce intense effect on brain and widely abused
53
methylphenidate
similar to amphetamine used in the treatment of ADD, has a paradoxical effect and effects the locus creels and increase focus attention
54
Cathinone
found in the leaves of the Khat plant of east africa and the middle east
-most recently synthetic form has marketed as bath salts
55
ephedrine
natural product found in herbal preps, has sympathomemetic actions
56
Modafanil
newer drug for narcolepsy and shift work disorder
MOA unclear, technically not amphetamines but have similar effects
57
armodafanil
newer drug for narcolepsy and shift work disorder
MOA unclear, technically not amphetamines but have similar effects
58
Cocaine
a hell of a drug
59
caffiene
methylxanthine with some effects
this and theophylline used to treat apnea in preterm infants
60
strychnine
spinal cord stimulant
potent convulsant in rat poison
-antagonist at glycine receptors the spinal cord and other CNS areas, removing post synaptic inhibitory property--> toxic seizures
treatment - symptomatic and diazepam to control seizure
61
tetanus toxin
spinal cord stimulate fro clostridium
- produces generalized tetanus and tonic convulsions similar to strychnine
- inhibits the release of glycine from renshaw cells in SC
-treatment-symptomatic and diazepam for seizures and appropriate anti microbe therapy
62
Preferred drug for Trichomonas vaginalis
metronidazole
