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Pharmacology > GI: Antimicrobial & Antihelminthics > Flashcards

GI: Antimicrobial & Antihelminthics Flashcards

1
Q

how are antimicrobials usually grouped?

A
  • by their MOA (MC**)

- also….by their spectrum of activity (narrow or broad or gram+ or gram-)

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2
Q

parenteral

A

anything NOT PO

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3
Q

factors involved in picking the appropriate antimicrobial agent? (5)

A
  1. ID organism
  2. Susceptibility to antimicrobials (what is organism susceptible to?)
  3. site of action/infection
  4. patient factors
  5. cost
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4
Q

how to identify the pathogenic organism?
(3)
pros/cons for each

A
  1. Gram Stain–
    * PROS: quick and tells you info about presence of an organism in sterile sites aka where it does not belong..SOME sense of what it is but not EXACTLY what organism is
    * CONS: does not tell you exact organism
  2. PCR–amplification of DNA/RNA fragments
    * PROS: ID exact bacteria
    * CONS: longer time wait
  3. MALDI-TOF: matrix-assisted laser desorption/ionization time of flight mass spectrometry–*PROS: accurate, rapid, and cost effective
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5
Q

what is the gold standard for identifying an organism?

A

CULTURES

**but they take a while to get results….. so we do rapid tests tooo

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6
Q

do you get culture before or after initiating antimicrobial tx?

A

BEFORE

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7
Q

what are some exceptions to starting ABX therapy before culture results

A

*severely ill patients
*hypotensive
*high fever
basically SEPTIC PATIENTS–bacteremia

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8
Q

define: empiric antimicrobial treatment
* why do we use it?
* what kind of antibiotic is generally used
* how do we pick abx?

A

TX based on the best clinical “guess” of what the offending organism is

  • for scenarios where delaying treatment could result in serious harm to PT or in immunocomp–>neutropenic PTs (low WBCs),
  • most common organisms that are associated with the disease process of the PT
  • get cultures… THEN right away start empiric therapy

How to pick ABX:

  1. site of infection
  2. local resistance patterns EX HP
  3. Based on clinical scenario–did they just take a recent ABx, or are they sensitive to a specific one

**the abx we choose is more broad spectrum versus narrow

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9
Q

ex of bacteria that are predictable regarding susceptibility

A

N. meningitidis

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10
Q

ex of bacteria that are not so predictable regarding susceptibility

A

enterococcus

staphylococcus

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11
Q

bacteriostatic vs bactericidal

A

static–drugs generally inhibit bacterial browth and replication at a level of drug that can be achieved by PT– then the host does the rest of the work to kill bacteria (they target the protein synthesis)

cidal–drugs kill bacteria (>99% within 12-24 hours incubation) they target cell wall

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12
Q

can one agent be bacterialcidal to one microbe and bacterialcidal to another?

A

YES

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13
Q

define minimum inhibitory concentration (MIC)
*imp for?

Define Minimum bactericidal concentration (MBC)

A

min amt of [drug] that prevents visible growth of microbe after 24 hours

  • imp for definitive treatment***
  • gives us in-vitro vs in vivo information

MBC: lowest [ ] of antimicrobial agent that results in 99.9% decline in colony county after over-night broth dilution incubations
rarely determined in clinical practice bc of time and labor***

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14
Q

drugs are carried to tissues by?

A

capillaries

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15
Q

protected sites from abx?

A

brain
eyes
joints
testes

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16
Q

what kind of drugs easily penetrate BBB

*when can other drugs pass through BBB?

A

small, not protein bound (free) lipid soluble drugs**

*others can pass easily through when there is meningeal inflammation

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17
Q

list some patient factors we consider when picking an ABX (7)

A
  1. status of immune system– what is their WBC?
  2. Renal function–dose adjustment, monitering levels
  3. Hepatic function–metabolism of drugs
  4. Perfusion/absoprtion (i.e GI tract) or DM patients
  5. Age (elderly, newborn)
  6. Pregnancy–does drug cross placenta? breast milk?
  7. risk factors for multi-drug resistance (recent abx use, hospitalization, nursing home, immunocomp)
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18
Q

every single time you prescribe an abx (usually inpatient setting vs outpatient), what levels should you always know?

A

BUN
creatinine
AKA know their renal function!!!!!!!

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19
Q

which ABX is generally least toxic?

A

PCNs

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20
Q

which ABX is generally highly toxic?

A

Chloramphenicol

think of it like CLOROX=TOXIC

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21
Q

when do we give abx PO?

A

for mild infections
when enteral absorption not compromised
MC outpatient

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22
Q

when do we give abx parenteral?

A
  • drugs poorly abs by GI tract
  • severe infections–>higher serum [ ] are needed to tx
  • transitioning hospitalized PT from IV to PO (before they are discharged)
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23
Q

dosing schedule based on?

A
  • pharmacokinetics (MOA and effects)

- pharmdynamics (ADME)

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24
Q

is dose a measure of drug exposure?

why/why not

A

no

*drug [ ]s fluctuate in patients

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25
Q

what is concentration-dependent killing
*achieved how?

give two abx examples

A

increasing the drug [ ] from 4 to 64 fold increases bacterial killing (higher you go.. more bacteria you kill)

once daily dosing bolus

EXs: aminoglycosides and daptomycin ****

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26
Q

time dependent killing

  • define
  • achieved how?
  • ex?
A

amt of time that drug is above the MIC–predicting the efficacy
*achieved by extended or continuous infusions

EX: Beta-lactams should be above MIC >50-60% of the time

NO increase in the rate of killing with increased [ ]
*NOT [ ] dependent but TIME !!!!

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27
Q

post abx effect

  • define
  • highest with which abx?
  • does not occur with which abx?
A

continued suppression/delayed regrowth of bacteria even when the drug levels fall below MIC

highest with: fluoroquinolones and aminoglycosides
does NOT occur with: B-lactams and gram (-) bacilli

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28
Q

list the antibiotic spectra

A

narrow
extended
broad

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29
Q

narrow spectrum abx

ex?

A

act on 1 or limited number of organisms

EX: isoniazid for TB

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30
Q

extended spectrum

ex?

A

range of activity is gram+ and gram-

EX: ampicillin

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31
Q

broad spectrum abx
ex?
se?

A

act against a wide variety of microbial species
EX: quinolones, tetracyclines

SE: can drastically alter and/or destroy normal flora–leading to C. Diff (super infection)

32
Q

pros to using just a single abx agent

A
  • reduce superinfection
  • reduce toxicity
  • reduce resistance
33
Q

examples when we need to combine antimicrobials?

pros
cons

A
  1. when agents have synergistic effects– when combined they create increase effect in killing/and or inhibiting bacterial growth
  2. very very very sick/complicated cases–ID gets involved— identification of organism is not found yet— as we get more and more info– slowly taper off one abx and then the other

CONS:

  • interference
  • contributes to resistance
34
Q

complications of abx (3)

*ex for each

A
  1. hypersensitivity: immune system rxn to either the metabolic b/d of drug or related to rates of infusion
    EX: Red Man Syndrome
  2. direct toxicity–high serum levels of abx can cause toxicity directly to cell
  3. superinfection– esp with use of broad spectrum abx–alter normal flora of body–allowing for opportunistic infections
35
Q

which abx can cause red man syndrome

A

vancomycin

36
Q

which abx can cause cell toxicity

A

aminoglycosides can cause ototoxicity

37
Q

ABX resistance

-define

A

when the maximal amt of drug tolerable by the PT fails to prevent microbial growth

38
Q

how can bacteria become resistant to abx

A

altering their genes

altering protein expressions

39
Q

what are helminths

A

parasitic worms

  • multicellular parasites
  • life cycle w/in and outside human hosts
40
Q

Ascaris lumbricoides

A

roundworm

41
Q

Necatur Americanus

A

hookworm

42
Q

Enterobius vermicularis

A

pinworm

43
Q

Trichuris trichiuria

A

whipworm

44
Q

roundworm

A

Ascaris lumbricoides

45
Q

Necatur Americanus

A

hookworm

46
Q

pinworm

A

Enterobius vermicularis

47
Q

whipworm

A

Trichuris trichiuria

48
Q

termatodes

A

flukes or flatworms

49
Q

flukes or flatworms

A

termatodes

50
Q

Cestodes

i.e Taenia solium

A

tapeworms

51
Q

tapeworms

A

Cestodes

i.e Taenia solium

52
Q

Mebendazole

MOA
Contra
SE
Indications

A

MOA: bind to free beta-tubulin–>inhibiting microtuble synthesis and glucose uptake–then the dead parasite is expelled in feces

contra in pregnancy (but can be used in 2-3 tri if needed)

SE: mild abd pain, diarrhea

NOT avail in US****

Indications: infections caused by whipworm, pinworms, hookworms, and roundworms AKA NEMATODES– first line but not in US

53
Q

Albendazole

MOA
Indications
absoprtion–when to take it w and w/o food
Metabolized
SE
prolonged use can lead to? Have to monitor?
COntras

A

MOA: bind to free beta-tubulin–>inhibiting microtuble synthesis and glucose uptake

indications: cestodes**,
* Effective against nematodes–, roundworms, hookworm, whipworm
* tapeworms

Absoprtion: POOR after PO—

  1. systemic infection: take with a fatty meal– incrs abs by 5x
  2. w/o food for intraluminal parasitic infections

Metabolized: heavily hepatic

SE:

  • mild within 1-3 days of use
  • N/V
  • HA

Prolonged use (when tx of some cestodes) :

  • transaminitis (hepatitis from elevated liver enzymes)
  • agranulocytosis
  • pancytopenia
  • Have to monitor LFTs and CBC

Contra:

  • pregnancy.
  • but can be used 2/3 tri
54
Q

Pyrantel Pamoate

  • indications
  • admin route
  • MOA
  • absoprtion good or bad
  • SE
  • only good for what kind of infections?
A

INDS
*pinworms (Enterobius vermicularis) KIDS
*Hookworms (Necator americanus and ancylostoma duodenale)
*roundsworms
AKA NEMATODES

Admin: PO–

MOA:
*acts as a depolarizing, NM blocking agent–>causes release of AcH and inhibition of AcHE–>leading to worm paralysis and expulsion in feces

ABS:

  • poorly absorbed after PO
  • why its only used for intestinal infections**

SE:

  • N/V/D
  • usually well tolerated
55
Q

Ivermectin

  • admin route
  • metabolized
  • indications
  • ineffective for?
  • MOA
  • Abs
  • peak? *T 1/2
  • contra
  • SE
A

Routes: PO** or topical

INDS:

  • *TOC for cutaneous larva migrans, strongyloidiasis and onchocerciasis (river blindness) AKA NEMATODES
  • *other filarial worms
  • *scabies
  • *lice aka pediculosis

Ineffective in tx of hookworms*

MOA: Opens glutamate-gated chloride channel receptors–Cl- influx into cell–>hyperporlorization–>paralysis/kills worm

Routes of admin: PO

Absoprtion: the drug is lipophillic but does NOT cross BBB when it is given PO

Peak: 4-5 hrs

T1/2: LONG–57 hours

Metabolized: heavily in liver

COntra: pregnancy and lactating women and children <5

SE:

  • generally well tolerated
  • BUT if treating for Onchocerciasis— can lead to tx-induced encephalopathy *****
56
Q

Praziquantel

  • indication
  • MOA
  • routes of admin
  • abs
  • metabolized
  • excreted
  • SE
  • drug-drug interactions (what causes incr in its levels and what causes incr in its metabolism)
  • contra
A

IND: TOC for schistosomiasis (trematodes) and Taenia (cestode)

MOA: increases cell membrane’s permeability to CA2+—->paralyzes parasite

Routes: PO (with food)

absoprtion: rapid

Metab: heavily liver

Excreted: urine

SE:

  • dizziness
  • HA
  • malaise
  • GI upset

Phenytoin can increase its metabolism

Cimetidine can increase its levels

CONTRA:
*eye infection due to Taenia (cestode) bc can cause irreversible damage when the parasite is killed

57
Q

Diethylcarbamazine
*Indications

  • MOA
  • route of admin
  • excretion
  • absorption
  • SE
  • Caution with what dz
A

indications: filariasis (Wuchereia bancrofti, Brugia malayi, Brugia timori AKA NEMATODES

MOA: kills microflariae and has activity against the adult worm

route: PO–give with meals

excreted in urine

ABS: rapidly after PO with meals

SE:

  • N/V
  • fever
  • arthralgia
  • HA

*caution with Onchocerciasis

58
Q

organisms invovled with Filaraisis

A

Wuchereia bancrofti, Brugia malayi, Brugia timori AKA NEMATODES

*live in lymphatic system–why it causes the severe edema/ elephantitis

59
Q

TOC for elephantitis/ filariasis

A

Diethylcarbamazine

60
Q

list the three major groups of helminths

A

nematodes
trematodes
cestodes

61
Q

what is a helminth

A

worm

62
Q

nematodes infect where in the body

A

intestines
blood
tissues

63
Q

list the drugs used to treat nematodes

A 
Mebendazole 
Pyrantel Pamoate 
Thiabendazole 
Ivermectin 
Diethylcarbamazine
64
Q

List the drugs used to treat trematodes

A

Praziquantel

65
Q

List the drugs used to treat cestodes

A

Albendazole

Praziquantel

66
Q

Thiabendazole

  • indications
  • route of admin
  • SE
A

INDS: Cutaneous Larva Migrans (NEMATODE)
*broad spectrum

  • topical application only
  • SE: many toxic SE, so it has been discontinued in many countries
67
Q

tx of choice for Cutaneous Larva Migrans

A

Ivermectin

Thiabendazole— also but it has such toxic SE that is has been discontinued in many countries

68
Q

while treating onchocerciasis– the pt develops fever, HA, dizziness somnolence and hypotension

  1. what drug is causing this rxn?
  2. what can be given to allieviate the symptms?
A

TX INDUCED ENCEPHALOPATHY from Ivermectin

TX: steroids or antihistamines

69
Q

name antifilarial drugs

A

Diethylcarbamazine
Ivermectin
Albendazole

70
Q

what drugs can be used in combo for preventative measures for endemic areas with filariasis

A

Diethylcarbamazine + Albendazole
OR

Ivermectin + Albendazole

71
Q

what medication are we cautious about when txing Onchocerciasis aka river blindness
WHY?

A

Diethylcarbamazine

*can accelerate blindness and

72
Q

drugs used to tx river blindness aka Onchocerciasis

A

ivermectin*** and/or albendazole

*Avoid Diethylcarbamazine as much as possible

73
Q

what are trematodes

how are they characterized.

A

flukes
leaf-shaped FLATWORMS
*characterized by the tissue they infect–liver lung intestinal or blood

74
Q

tx for Pinworms or Enterobiasis

A

Mebendazole (if not in us)

In US– Pyrantel Pamoate

75
Q

tx for roundworm dz or Ascariasis

A

Albendazole
Menbendazoe
or Pyrantel Pamoate

76
Q

tx for Taenia solium

aka?

A

Praziquantel

AKA pork tapeworm

77
Q

neurocysticercosis

A

Taenia solium aka pork tapeworm

Pharmacology (28 decks)

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