abx and anti-parasites Flashcards
sheehy Gi
describe the functions of the two C. Dif toxins
Toxin A= enterotoxin= diarrhea
Toxin B= cytotoxin= cytotoxic to the colonic cells
what is the trx for C Dif
cessation of inciting abx
supportive care
fecal transplant
vancomycin OR
metronidazole OR
fidaxomicin
which medication is the preferred trx (name and class) for C Dif
vancomycin = glycopeptide
which med (name and class) do you give for C Dif when oral administration doesn’t work for patients
Metronidazole- 5-nitroimidazole
what is the trx (name and class) for recurrent C Dif
fidaxomicin= macrolide
what are the key meds (name and class) to trx H Pylori
PPI- omeprazole
5-nitroimidazole- metronidazole
Bismuth compounts- bismuth subsalicylate
tetracycline
E. hystolitica complications
portal blood circulation
liver abscesses
pulmonary abscesses and often death
what drugs will eliminate E. hystolitica
(5 nitroimidazoles) metronidazole if extraluminal amebiasis
OR tinidazole, which is better tolerated
metronidazole AND tinidazole if luminal amebicide
what drugs(name and class) will eradicate intestinal carriage of E. hystolitica
what are adverse effects?
paromomycin (aminoglycoside) > iodoquinol (8-hydroxyquinolines)
NO EFFECT ON EXTRAINTESTINAL ORGANSIMS: 99% stay in intestine and excreted via feces
rash, pruritis
how does giardia interact with the small intestine
it coats the small intestine and inerferes with fat absorption (creeping fat)
NO BLOOD IN STOOLS
trx for giardia
correct fluids and electrolytes
first line= tinidazole (5 nitroimidazoles)
nitazoxanide
when do you use nitazoxanide
MOA, kinetics, adverse effects
giardia
will inhibit pyruvate-ferredoxin oxidoreductase, needed for anaerobic E metabolism
rapid absorption
flatulence, enlarged salivary glands, yellow eyes, dysuria, bright yellow urine
Cryptosporidium parvum with immunocompromised
immunocompetent- self limiting
compromised= severe life threatening diarrhea
trx for cryptosporidium
anti-diarrheal –> loperamide
fluid management
antimicrobial –> nitazoxanide > paromomycin (aminoglycoside)
what is the trx for Cryptosporidium in HIV patients
antiretroviral therapy + nitazoxanide
what is the trx for Cryptosporidium in non-HIV, immunocompromised patients
reduced immunosuppressants and nitazoxanide
describe the body’s response to works/nematodes
no immune response to the worms, just respond to dead worms and eggs
elevation of eosinophils
dx with visualization of microscopic eggs in feces
the two hookworms are..?
sx of a hookworms infection
necator americanus + ancylostoma duodenale
diarrhea abd pain weight loss anemia intense itching at site of penetration
sx of ascaris lumbricoides
abd cramping,
malnutrition
worm invasion
differentiate the life cycle of a hookworm vs ascaris lumbricoides vs strongyloides stercoralis vs trichuris trichiura vs enterobius vermicularis
hookwork penetrate skin –> lungs –> coughed and swallowed–> intestine –> eggs in feces
ascaris lumbricoides is CONSUMED –>penetrate intestine–> lung–> coughed swallowed –> –> intestine –> EGGS in feces
strongyloides penetrate skin –> lungs –> coughed and swallowed–> intestine –> HATCHED LARVAE excreted in stools
tri tri eggs ingested via food –> hatch in small intestine –> migrate to cecum–> mature, hatch thousands of egg over a YEAR
enterobius –> eggs ingested –> mature in cecum, ascend large intestine –> females go to perianal area at night–>eggs infectious 4-6 hrs later
sx of strongyloides steroralis
anemia
weight loss
vomiting, diarrhea
abd pain
what immunosuppressive medications can lead to severe autoinfection in the setting of strongyloides steroralis
prednisone
asthma
how do you dx a strongyloides infection
larvae in feces
sign difference in lifecycle of trichuris trichiura vs other works
no transit through the intestinal wall
no lung involvement
no eosinophilia
no auto-infection
transmission methods of enterobius vermicularis
how do you diagnose
hand to mouth via severe perianal itching
scotch tape test
what are the broad spectrum oral anti-helminthic agents
MOA
kinetics
adverse effects
albendazole, mebendazole, thiabendazole
MOA= inhibit micro-tubule synthesis–> paralysis
are prodrugs
THIABENDAZOLE ONLY= rapidly absorbed, largely excreted, can be ingested or absorbed from skin
THIABENDAZOLE ONLY= most toxic of the three, dizzy, anorexia, irreversible liver failure, fatal Stevens-Johnson syndrome
ivermectin anti-helminth
MOA
kinetic
AEs
intensify GABA-mediated signal transmission in peripheral Ns of the nematode
kinetics= rapidly absorbed, oral only, excreted in feces
AEs= no combine w other GABA altering drugs= barbituates, benzodiazepines, valproic acid
pyrantel pamoate antihelminth
MOA
kinetics
AEs
MOA= NMSK blocker, cause Ach release and inhibit cholinesterase–> paralysis and explusion
kinetics= poorly absorbed, half of the administered dose will be excreted unchanged in feces
AEs= –
which drugs are used to trx N. americanus + A. duodenale (hookworms)
primary= albendazole
alternate= mebendazole, pyrantel pamoate
poor= ivermectin
trx of A lumbricoides
primary= albendazole or mebendazole
alternate= ivermectin
trx of S stercoralis
primary= ivermectin
alternate= albendazole
no longer primary= thiabendazole
trx of T. trichiura
primary= mebendazole
alternate= abendazole
second alternate= ivermectin
trx of E. vermicularis
primary= albendazole, mebendazole, pyrantel pamoate
how does schistosoma infect
invade venous system through exposed skin, found in fresh water
portal V
Schistosoma japonicum
geography
resides where
deposit eggs where
easter asia
Vs in intestinal tract
eggs in feces
Schistosoma mansoni
geography
resides where
deposit eggs where
south america and africa
Vs in intestinal tract
eggs in feces
schistosoma haematobium
geography
resides where
deposit eggs where
africa
in Vs around bladder
deposit in urine
life cycle of schistosoma (blood flukes)
eggs hatch water mature in a snail leave snail infect humans mate in the intrahepatic portion of the portal venous system mates move to intestine orbladder enter lumen to be excreted
clinical manifestations of schistosoma
dermatitis immediately
katayama fever (4-8 weeks) chronic fibrosis (years)
trx for schistosoma
MOA
kinetics
AE
praziquantel
MOA= increase permeability of cell membrane to Ca –> paralysis, dislodgement, death
kinetics: oral admin, rapid absorb, excreted in urine
AE= immediate= drowsy, lassitude, fatigue
after days, low grade fever, pruritis, rash
life cycle of cestodes= tapeworms
ingested through undercooked meat containing larvae
freshwater tapeworm ingested by raw freshwater fish
cause –> anemia
diphyllobothrium latum
extra-intestinal tapeworm infection, ingested from dog feces
echinococcus granylosus
trx for cestodes
praziquantel
niclosamide- an alternative for most tapeworms
albendazole
niclosamide
MOA
kinetics
uncouples ox phos, block glucose uptake–> parasite death
kinetics= oral admin,
