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GI2 E1 > abx and anti-parasites > Flashcards

abx and anti-parasites Flashcards

sheehy Gi

1
Q

describe the functions of the two C. Dif toxins

A

Toxin A= enterotoxin= diarrhea

Toxin B= cytotoxin= cytotoxic to the colonic cells

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2
Q

what is the trx for C Dif

A

cessation of inciting abx
supportive care
fecal transplant

vancomycin OR
metronidazole OR
fidaxomicin

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3
Q

which medication is the preferred trx (name and class) for C Dif

A

vancomycin = glycopeptide

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4
Q

which med (name and class) do you give for C Dif when oral administration doesn’t work for patients

A

Metronidazole- 5-nitroimidazole

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5
Q

what is the trx (name and class) for recurrent C Dif

A

fidaxomicin= macrolide

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6
Q

what are the key meds (name and class) to trx H Pylori

A

PPI- omeprazole

5-nitroimidazole- metronidazole

Bismuth compounts- bismuth subsalicylate

tetracycline

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7
Q

E. hystolitica complications

A

portal blood circulation
liver abscesses
pulmonary abscesses and often death

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8
Q

what drugs will eliminate E. hystolitica

A

(5 nitroimidazoles) metronidazole if extraluminal amebiasis
OR tinidazole, which is better tolerated

metronidazole AND tinidazole if luminal amebicide

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9
Q

what drugs(name and class) will eradicate intestinal carriage of E. hystolitica

what are adverse effects?

A

paromomycin (aminoglycoside) > iodoquinol (8-hydroxyquinolines)
NO EFFECT ON EXTRAINTESTINAL ORGANSIMS: 99% stay in intestine and excreted via feces

rash, pruritis

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10
Q

how does giardia interact with the small intestine

A

it coats the small intestine and inerferes with fat absorption (creeping fat)

NO BLOOD IN STOOLS

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11
Q

trx for giardia

A

correct fluids and electrolytes

first line= tinidazole (5 nitroimidazoles)
nitazoxanide

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12
Q

when do you use nitazoxanide

MOA, kinetics, adverse effects

A

giardia
will inhibit pyruvate-ferredoxin oxidoreductase, needed for anaerobic E metabolism

rapid absorption

flatulence, enlarged salivary glands, yellow eyes, dysuria, bright yellow urine

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13
Q

Cryptosporidium parvum with immunocompromised

A

immunocompetent- self limiting

compromised= severe life threatening diarrhea

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14
Q

trx for cryptosporidium

A

anti-diarrheal –> loperamide

fluid management

antimicrobial –> nitazoxanide > paromomycin (aminoglycoside)

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15
Q

what is the trx for Cryptosporidium in HIV patients

A

antiretroviral therapy + nitazoxanide

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16
Q

what is the trx for Cryptosporidium in non-HIV, immunocompromised patients

A

reduced immunosuppressants and nitazoxanide

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17
Q

describe the body’s response to works/nematodes

A

no immune response to the worms, just respond to dead worms and eggs
elevation of eosinophils

dx with visualization of microscopic eggs in feces

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18
Q

the two hookworms are..?

sx of a hookworms infection

A

necator americanus + ancylostoma duodenale

diarrhea
abd pain
weight loss
anemia
intense itching at site of penetration
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19
Q

sx of ascaris lumbricoides

A

abd cramping,
malnutrition
worm invasion

20
Q 
differentiate the life cycle of a hookworm vs 
ascaris lumbricoides vs 
strongyloides stercoralis vs
trichuris trichiura vs
enterobius vermicularis
A

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

21
Q

sx of strongyloides steroralis

A

anemia
weight loss
vomiting, diarrhea
abd pain

22
Q

what immunosuppressive medications can lead to severe autoinfection in the setting of strongyloides steroralis

A

prednisone

asthma

23
Q

how do you dx a strongyloides infection

A

larvae in feces

24
Q

sign difference in lifecycle of trichuris trichiura vs other works

A

no transit through the intestinal wall
no lung involvement
no eosinophilia
no auto-infection

25
Q

transmission methods of enterobius vermicularis

how do you diagnose

A

hand to mouth via severe perianal itching

scotch tape test

26
Q

what are the broad spectrum oral anti-helminthic agents
MOA
kinetics
adverse effects

A

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

27
Q

ivermectin anti-helminth

MOA
kinetic
AEs

A

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

28
Q

pyrantel pamoate antihelminth

MOA
kinetics
AEs

A

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= –

29
Q

which drugs are used to trx N. americanus + A. duodenale (hookworms)

A

primary= albendazole

alternate= mebendazole, pyrantel pamoate

poor= ivermectin

30
Q

trx of A lumbricoides

A

primary= albendazole or mebendazole

alternate= ivermectin

31
Q

trx of S stercoralis

A

primary= ivermectin

alternate= albendazole

no longer primary= thiabendazole

32
Q

trx of T. trichiura

A

primary= mebendazole

alternate= abendazole

second alternate= ivermectin

33
Q

trx of E. vermicularis

A

primary= albendazole, mebendazole, pyrantel pamoate

34
Q

how does schistosoma infect

A

invade venous system through exposed skin, found in fresh water

portal V

35
Q

Schistosoma japonicum

geography
resides where
deposit eggs where

A

easter asia

Vs in intestinal tract

eggs in feces

36
Q

Schistosoma mansoni

geography
resides where
deposit eggs where

A

south america and africa

Vs in intestinal tract

eggs in feces

37
Q

schistosoma haematobium

geography
resides where
deposit eggs where

A

africa

in Vs around bladder

deposit in urine

38
Q

life cycle of schistosoma (blood flukes)

A 
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
39
Q

clinical manifestations of schistosoma

A

dermatitis immediately

katayama fever (4-8 weeks)
chronic fibrosis (years)
40
Q

trx for schistosoma

MOA
kinetics
AE

A

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

41
Q

life cycle of cestodes= tapeworms

A

ingested through undercooked meat containing larvae

42
Q

freshwater tapeworm ingested by raw freshwater fish

cause –> anemia

A

diphyllobothrium latum

43
Q

extra-intestinal tapeworm infection, ingested from dog feces

A

echinococcus granylosus

44
Q

trx for cestodes

A

praziquantel
niclosamide- an alternative for most tapeworms
albendazole

45
Q

niclosamide

MOA
kinetics

A

uncouples ox phos, block glucose uptake–> parasite death

kinetics= oral admin,

GI2 E1 (19 decks)

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