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Pharm week 2 (infection) Flashcards

1
Q

4 things to assess on the tympanic membrane?

A
  1. Color (red)
  2. Position (displaced/bulging)
  3. Translucency (opaque)
  4. Mobility (immobile)
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2
Q

Criteria for “watchful waiting” in otitis media (4 things)

A

> 6 months old
Non severe illness (fever < 39, mild otalgia)
Uncomplicated
Parent can recognize worsening sx and seek care

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3
Q

Criteria of uncomplicated otitis media?

A
  • no episode in preceding month
  • no acute facial nerve palsy
  • no mastoiditis
  • no meningitis
  • no labyrinthitis (inflammation of middle ear (labyrinth), causes vertigo, hearing loss
  • No craniofacial abnormalities, immunodeficiencies, cardiac/pulmonary disease, Down syndrome, or hx of complicated AOM
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4
Q

What does H. influenzae and M. catarrhalis produce?

A

beta-lactamases

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5
Q

How does penicillin work?

A

Prevents cell wall synthesis in dividing organisms

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6
Q

Where does Penicillin target? (8)

A 
body fluids
joints
pleural cavities
pericardial cavities
bile
saliva
milk
placenta
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7
Q

Dorsal versus palmar of hand

A 
Dorsal= top
Palmar= underside
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8
Q

Pathogenic organism in osteomyelitis in newborn?

most common, and high risk infants

A

Staphylococcus aureus (S. aureus)

Some cases:

  • Group B. Streptococcus
  • Escherichia coli (especially with multiple bone involvement and high risk infants)
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9
Q

What drugs to avoid in pyelonephritis? (4)

A
  1. Nitrofurantoin (not adequate tissue or renal concentration)
  2. Fosfomycin : same as above
  3. Moxifloxacin: inadequate urinary levels
  4. amoxicillin and cephalexin (high e. coli resistance)
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10
Q

Examples of atopic illness? (6)

A 
Anaphylaxis
allergic rhinitis
allergic asthma
Hives
eczema (atopic dermatitis)
Some food sensitivities
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11
Q

Explain mechanism of Type I reactions? (3 points)

A
  • IgE antibody mediated
  • Runs in families
  • Hypersensitivity of an end organ (i.e. nose, bronchi) to MAST CELL production
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12
Q

Explain beta-lactam allergy and related concerns?

A

Negatives:

  • longer hospital stays
  • use of less desirable abx
  • True PCN allergy doesn’t need to avoid all beta-lactams/cephalosporins (97%) are fine
  • anaphylaxis in < 1%
  • family hx not significant factor
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13
Q

What is negative predictive value?

A

Negative predictive value is the probability that subjects with a negative screening test truly don’t have the disease.

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14
Q

Positive Predictive Value?

A

Positive predictive value is the probability that subjects with a positive screening test truly have the disease.
I.e.: you test positive for PCN allergy, you actually have a PCN allergy

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15
Q

DRESS stand for?

A 
D-drug
R-rash
E-eosinophilia
S-systemic
S-symptoms
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16
Q

What factors affect the type of reaction a patient may have to a drug?

A

1- type of antigen
2- route of exposure (IV, topical > oral)
3-end organ affected

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17
Q

End organ affected by PCN and food allergies?

A

Blood vessels

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18
Q

Example of a allergic rhinitis Type I reaction antigen?

A

Ragweed pollen

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19
Q

What is the effect of leukotrienes?

A
  • Increased vascular permeability
  • leukocyte recruitment (increase WBC adhesion to endothelium, act as a chemotactic factor)
  • Bronchoconstriction (ie. astham, allergies, anaphylaxis)
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20
Q

What does histamine do in a Type I reaction? (4)

A
  • vasodilation
  • bronchoconstriction
  • itching
  • chemotaxis of eosinophils to the site
  • RAPID
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21
Q

What drug blocks leukotriene receptors? (2)

A

Zafirlukast

Montelukast

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22
Q

Histamine receptors blocked by?

A

H1 and H2 antihistamines

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23
Q

Histamine release blocked by?

A

Cromolyn sodium

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24
Q

Anaphylactoid reactions are? Causes?

A
  • resemble anayphylaxis
  • NOT mediated by IgE
  • causes: radiocontrast dye, opioids
  • these release histamine and other compounds from mast cells
  • produce the same clinical picture with anaphylaxis but are not IgE mediated, occur through a direct nonimmune-mediated release of mediators from mast cells and/or basophils or result from direct complement activation.
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25
Q

Symptoms of serum sickness? (8)

A 
rashes
itching
arthralgia
fever
lymphadenopathy,
hypotension
shock 
glomerulonephritis
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26
Q

What type of reaction is serum sickness?

A

Type III : IgG or IgM immune complex formation

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27
Q

Examples of drugs that can cause serum sickness?

A

sulfonamides
penicillin
phenytoin
isoniazid

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28
Q

Who reacts to NSAIDS or ASA? How?

A 
20% of those with asthma
urticaria
angioedema
rhinosinusitis
asthma
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29
Q

Patient experiences a rash from penicillin. Safe option?

A

Cephalosporin

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30
Q

What does epinephrine do?

A
  • Increases peripheral vascular resistance
  • Decreases mucosal edema
  • Induces bronchodilation
  • Increases cardiac contractility and HR
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31
Q

Acetaminophen dosage (Pediatrics)

A

10-15mg/kg/dose PO q4h prn (Max 75 mg/kg/day)

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32
Q

Ibuprofen dosage (Peds)

A

10mg/kg/dose PO q 6-8h prn (Max 40mg/kg/day)

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33
Q

What are the benefits of “watchful waiting” for AOM? (3)

A
  1. Decreases cost
  2. prevent development of resistance
  3. Prevent ADR: Nausea, vomiting, rash
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34
Q

Most prevalent pathogen in AOM?

A

S. Pneumoniae (strep pneumoniae)

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35
Q

Standard Amoxicillin dosing for OAM?

A

40mg/kg/day (divided TID) x 5 days

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36
Q

S. Pneumoniae resistance risk factors?

A

< 2 years old

Had abx in the last 3 months

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37
Q

How many days of abx therapy for perforated tympanic membrane?

A

Amoxicillin x 10 days (instead of 5)

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38
Q

High dose for Amoxicillin for AOM?

A

90mg/kg/day (divided BID or TID)

Less volume/ dose may be better for kids/parents

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39
Q

Who gets high dose Amoxicillin for AOM?

A

Risk factors for S. Pneumonia resistance

6 months to 2 years old

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40
Q

Drug and dose for AOM and purulent conjuntivitis?

A

Amoxicillin- Clavulin (7:1, 200 or 400mg clavulin)

45 mg/kg/dose (divided BID) x 5 days

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41
Q

Who gets Amoxicillin-Clavulin with purulent conjunctivitis for 10 days?

A

< 2 years

perforated eardrum

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42
Q

Examples of IgE Mediated Reaction to Beta-Lactam? (3)

A
  • • Urticaria (hives)
  • • Laryngeal edema
  • • Angioedema
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43
Q

Examples of serious Non-IgE Mediated reactions to Beta-Lactam? (6)

A 
-Serum sickness 
• End organ damage
 • Severe cutaneous reactions (ie: StevensJohnsons Syndrome) 
• Hemolytic anemia 
• hepatitis 
• Interstitial nephritis
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44
Q

What are the first 2 steps after unresolved sx of AOM?

A

Check compliance

confirm diagnosis

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45
Q

How do you prevent mastoiditis?

A
  • following pt appropriately and

- initiating abx therapy for those who do not improve

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46
Q

When do you treat acute sinusitis with ABX?

A
  • worsening sx
  • no improvement after 5-7 days
  • fever >39 with purulent drainage OR
  • facial pain for 3-4 days consecutively from start
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47
Q

When are nasal corticosteroids possibly useful for acute sinusitis? (2)

A
  • recurrent

- allergic

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48
Q

Pathogens responsible for acute sinusitis?

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
  3. Moraxella Catarrhalis
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49
Q

What are benefits to amoxicillin?

A
  • good spectrum against s. pneumoniae
  • well tolerated
  • not expensive
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50
Q

Clinical presentation for Acute Exacerbation of Chronic Bronchitits?

A

Cough with absence of tachypnea or tachycardia

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51
Q

Cardinal signs of acute exacerbation of Chronic Bronchitis?

A

Cardinal signs:

Increased sputum volume

Increased sputum purulence

Worsening of dyspnea

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52
Q

First line option for treating community acquired pneumonia? CAP

A

Amoxicillin and doxycylcine

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53
Q

What needs to be done BEFORE prescribing antimicrobial therapy?

A
  1. identlfy the pathogen

2. identify local resistance patterns

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54
Q

What color does the gram negative stain?

A

RED

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55
Q

What color does the gram positive stain?

A

violet or blue

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56
Q

Characteristics of Gram Positive?

A
  • stains blue/violet
  • thick outer peptidoglycan cell wall
  • inner cytoplasmic membrane
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57
Q

MIC?

A

Minimum inhibitory concentration

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58
Q

mbc

A

minimum bactericidal concentration of a drug

used for more serious infections

59
Q

Bacteriostatic

A

Inhibits growth
MIC achieved but not MBC
MIC is lower than MBC

60
Q

Bacteriocidal

A

MIC = MBC

kills organism

61
Q

Beta Lactams: Penicillins?

A
  • Penicillin (PO/IV)
  • Cloxacillin (PO/IV)
  • Ampicillin (PO/IV)
  • Amoxicillin (PO)
  • Piperacillin (IV)
  • Ticarcillin (IV)
62
Q

Beta Lactams: Carbapenems?

A
  • Ertapenem (IV)
  • Imipenem (IV)
  • Meropenem (IV
63
Q

Beta Lactams: Glycopeptides

A

Vancomycin (PO/IV)

64
Q

Beta Lactams: Cephalosporins 1st generation

A

Cephalexin (PO)

Cefazolin (IV)

65
Q

Beta Lactams:

Cephalosporins - 2nd generation

A

Cefaclor (PO)
Cefuroxime (PO/IV)
Cefotetan/Cefoxitin

66
Q

Beta Lactams:

3rd generation - Cephalosporins

A 
Cefixime (PO)
Cefotaxime (IV)
Ceftizoxime (IV)
Ceftriaxone (IV)
Ceftazidime (IV)
67
Q

Beta Lactam: 4th generation Cephalosporins

A

Cefepime IV

68
Q

Beta Lactam: 5th generation Cephalosporins

A

Ceftobiprole (IV)

69
Q

What are the 3 parts to the autonomic nervous system?

A
  1. sympathetic
  2. parasympathetic
  3. enteric
70
Q

What cranial nerve connect the parasympathetic nervous system to the CNS?

A

III
VII
IX
X (vagus nerve)

71
Q

What does amoxicillin cover that PCN does not?

A

H. Influenzae

72
Q

What does penicillin cover?

A

Gram Positives
Strep
Some gram negatives
Non-beta lactamase producing anaerobes

73
Q

What is the advantage of Cephalosporins over PCN?

A

More stable against beta lactamase producing pathogens

74
Q

What do Carbapenems treat?

A

Gram positive and gram negatives, and anaerobes

75
Q

What do carbapenems not cover?

A

MRSA and enterococci (gram positive)

C. difficile (anaerobes)

76
Q

What does Vancomycin treat?

A 
Gram positive, 
Gram positive that produce beta lactamase
Penicillin allergy
Colitis r/t abx
MRSA
77
Q

How does Vancomycin work?

A

Binds to cell wall to prevent cell wall synthesis

78
Q

Examples of beta-lactamase inhibitors? (3)

A

Clavulanic acid
Sulbactam
Tazobactam

79
Q

What pathogens do Beta-Lactamase inhibitors help fight? (6)

A
  • Staph Aureus
  • H, influenziea
  • M. Catarrhalis
  • E. Coli
  • Klebsiella
  • B. Fragilis
80
Q

What pathogens do beta-lactamase inhibitors not help against?

A
  • Serratia pseudomonas
  • Indole + Proteus
  • Citrobacter
  • Enterobacter
    “Spice” organisms
81
Q

Benefits of Intensive dosing for Aminoglycosides

A

Once daily
advantage of PAA
Blood levels can drop below MIC
Allows some renal recovery

82
Q

What is the spectrum for Clindamycin?

A

Gram positives
Many anaerobes
Not for:
Gram Negative (i.e. H. Influenzae, enterococci, Neisseria Meningitis, mycoplasma pneumonia or aerobic gram-negative bacilli)

83
Q

3 ways that nucleic acid synthesis inhibitors work?

A
  1. Precursor synthesis (sulfonamides, trimethoprim)
  2. DNA replication (Quinolones)
  3. RNA polymerase (rifampin)
84
Q

Steven Johnson Syndrome

A

rare, serious disorder of the skin r/t drug reaction. Flu like symptoms followed by extensive skin blistering and pain.

85
Q

What drug treats Parkinson’s and how does it work?

A

Levodopa: prevents dopamine blocking

86
Q

Things to consider when choosing the correct antibiotic?

A
  1. Treat patient not the disease (only treat what is necessary)
  2. Start narrow (reduce resistance)
  3. Treat likely pathogen
    - use cultures/sensitivities if available
    - preferably get cultures prior to starting tx
  4. limit toxicity and adverse effects
  5. Is monitoring necessary/available (ie. vanco.)
  6. Consider costs
87
Q

Examples of multivalent cations? (6) what should they not be given with? (2)

A 
Iron
dairy
antacids
zinc
vitamins
sucralfate

** Don’t give with tetracyclines or fluoroquinolones

88
Q

Cardinal sx of strep throat? (4)

A

Fever > 38
tender cervical lymphadenopathy
tonsillar exudate
NO cough

89
Q

Cardinal sx of strep throat? (4)

A

Fever > 38
tender cervical lymphadenopathy
tonsillar exudate
NO cough

90
Q

Drug of choice for strep throat?

A

PCN

Erythromycin if PCN allergy

91
Q

Tx for non-limb threatening animal or human bites?

A

Amoxi clav 875 PO BID x 3-5 days

PCN allergy: doxy 100mg PO BID x 3-5 days (=/- flagyl 500mg PO BID x 3-5 days, if > 8years old)

92
Q

Stages of acne development? (4)

A

Follicular hyperkeratinization
microbial colonization with Cutibacterium acnes “cutie”
sebum production
innate and acquired immune response

93
Q

Name for drug effects that are harmful and never desirable?

A

Adverse
Deleterious
Toxic

94
Q

Where and when do idiosyncratic reactions occur ?

A

Skin, liver, haematoma poetic, and immune system‘s.
Reaction is usually delayed.
Can be life threatening.

95
Q

What makes a toxic effect reversible ?

A

Depends on the tissues ability to:

  • adapt
  • repair
  • regenerate
96
Q

What tissues regenerate easily?

A

Liver

Gastrointestinal tract

97
Q

Toxic effects that are often not reversible?

A

CNS. Neurons have a limited ability to regenerate.

98
Q

Target organs of toxicity are?

A

Where the chemical elicits it’s toxic effect

99
Q

What are some bisphosphonate drugs used for modifying bone pain?

A

Clodronate
Pamidronate
Zolendronic acid

100
Q

What is the dosage for clodronate?

A

900 mg IV q 4 weeks
or
1600-2400 mg PO daily

101
Q

Pamidronate dosage?

A

60-90 mg IV q 3-4 weeks

102
Q

Zolendronic acid dose?

A

4mg IV every 4 weeks

103
Q

What are some ADEs to watch for when giving Clodronate, Pamidronate or Zolendronic acid?

A
  • osteonecrosis of the jaw (DENTAL REVIEW BEFORE INITIATING)
  • renal impairment (= extreme caution and dose adjustment)
  • hypocalcemia (ca into bones, not enough in blood).
  • flu-like sx for 1-2 days after administration
  • **monitor renal function and Ca levels with each treatment.
104
Q

Monoclonal antibody given for bone pain in palliative patients?

A

Denosumab

120mg SC every 4 weeks

105
Q

Dosage for dexomethasone for bone pain in palliative care?

A

2-8 mg po daily tid

106
Q

Who should avoid or be careful taking tricyclic antidepressants?

A

Glaucoma
Heart disease
urinary retention
orthostatic hypotension

107
Q

Dosage of TCA’s Amitriptyline and Nortriptyline for neuropathic pain? (palliative)

A

75-150 mg PO at bedtime
(start at 10-25 mg at bedtime.
-titrate by 10-25mg every 3-7 days.

108
Q

Who should beware of TCAs for neuropathic pain?

A
  • poor cardiac function
  • severe prostatic hypertrophy
  • glaucoma
109
Q

Anticholinergic effects include:

A
  • drowsiness
  • constipation
  • dry mouth
  • urinary retention
110
Q

Tricyclic Antidepressants (4)

A

• Amitriptyline (most common)
or Nortriptyline
• Imipramine
• Desipramine

111
Q

Gabapentin dose in palliative care?

A

300-800mg PO q6- 8 hours
(start at 100-300mg at hs, Titrate upwards q 1-7 days.
Target dose range= 900-3600mg od
** after 1800 mg od = less bioavailability

112
Q

Pregabalin dosage?

A

150-300mg PO q 12 hours

  • start at 75 mg BID
  • increase q 3-7 days
  • target dose= 50-150mg daily- divided.
  • slower titration in elderly/frail
113
Q

What patient population requires a dose adjustment for both Gabapentin and Pregabalin?

A

Patients with renal impairment

114
Q

ADE’s of Pregabalin?

A

Somnolence
Dizziness
Ataxia

115
Q

What is baclofen used for? Dosage?

A

Hiccups

5-20mg PO q 6-12 hours (max 40mg/day)

116
Q

What drug can cause hiccups in the palliative care patient?

A

> 10mg daily dexamethasone

117
Q

What does evidence show for treating CNCP with opioids?

A
  • dose dependent risk for serious harm

- insufficient to show effectiveness for improving chronic pain or function

118
Q

Reason not to be a “dose-escalating” prescriber in CNCP?

A

Most patients will not have a good response to opioids for CNCP. Why chase a response by increasing the dose??

119
Q

What are realistic goals for treating CNCP?

A
  • meaningful reduction in pain
  • increased functioning
  • ensuring safety
  • set measurable goals (i.e. 9 holes of golf twice per week).
120
Q

What does the SMART approach stand for in treating CNCP?

A 
Specific
Measurable
Attainable
Relevant
Time dependent
Prior to initiating an opioid 
trial, highlight the importance 
of realistic patient 
expectations and establish 
treatment goals that include 
patient‐centered 
improvements in function
121
Q

Boundaries to set BEFORE prescribing opioids for CNCP?

A

If this medication doesn’t work we will increase it only a few times, if it still doesn’t work we will have to discontinue it and try something else.

There will be NO early refills

122
Q

How to limit your risks when prescribing opioids to patients?

A

Following strict/structured prescribing regiments

Setting rules for ALL patients

Keeping proper documentation

Follow rules/laws from prescribing authorities and colleges

123
Q

What is classic serum sickness?

A

serum sickness” describes the clinical syndrome caused by immunization of the host (human) by heterologous (nonhuman) serum proteins and subsequent illness caused by formation of immune complexes.

124
Q

What are SSLR?

A

Serum sickness-like reactions (SSLRs) present as rash, arthritis, and fever beginning several days to weeks following administration of a drug.

125
Q

Management steps for serum sickness and SSLR?

A

●The management of these reactions primarily involves discontinuation of possible culprit agents. Typically, fever and arthralgias resolve and new skin lesions stop forming within 48 hours of this intervention. This is often all that is required for patients with mild symptoms.
●Further treatments depend upon the discomfort of the individual patient. Antihistamines may be administered for symptomatic relief of pruritus. Nonsteroidal anti-inflammatory agents and analgesics may be given for symptomatic treatment of low-grade fever and arthralgias.

126
Q

What is bupropion?

A

Anti depressant. (Wellbutrin).

127
Q

Serum sickness versus SLSR? (Serum like sickness reaction)

A

Serum sickness Involves the deposit of immune complexes resulting from nonhomologous proteins.

128
Q

Isoniazid?

A

Antibacterial used to treat TB

129
Q

What is ecthyma?

A

Ecthyma — Ecthyma is an ulcerative form of impetigo in which the lesions extend through the epidermis and deep into the dermis. They consist of “punched-out” ulcers covered with yellow crust surrounded by raised violaceous margins

130
Q

Gram negative bacteria

A 
E. Coli 
Enterobacter
Pseudomonas
Proteus
Neisseria
Salmonella 
H. Pylori
131
Q

Gram positive

A 
Staphylococcus 
Streptococcus 
Enterococcus 
Lactobacillus
Listeria monocytogens
Clostridium
132
Q

Bacteria that produce beta lactamase? 6

A 
Bacteroides
Enterococcus 
H. influenzae
M. catarrhalis
Neisseria gonorrhoeae
Staphylococcus
133
Q

Examples of aminoglycins? 4
Poorly absorbed how?
Best way to administer?
Excreted how?

A 
gentamicin
tobramycin
neomycin 
streptomycin
poor gastrointestinal absorption, so intravenous or intramuscular administration is needed

excreted renally.

134
Q

Drug of choice for Malaria?

A

Chloroquine/ Aralen

135
Q

Prophylaxis dose for Malaria?

A 
Chloroquine
500 mg po per week (same day):
2 weeks prior to leaving
during travel
8 weeks after home
136
Q

Active Malaria tx:

A

Chloroquine:
1000 mg PO STAT
500mg at 6 hours and 8 hours
500mg PO daily x 2 days

137
Q

ADR of Chloroquine (10)

A 
Blindness if taken too long
hypotension
ECG changes
Headache
N/V/D
Anorexia
Malaise
Abd cramps
Visual changes
Pruritis
138
Q

Drug that decreases the effectiveness of chloroquine?

A

Ampicillin

139
Q

First line tx for COMPLICATED AECB?

A

Amoxicillin-Clavulanate 875 mg PO BID x 5-7 days

Cefuroxime 500mg PO BID x 5-10 days

Clarithromycin 500mg PO BID or XL 1g PO daily x 5-10 days

Azithromycin 500mg PO x 3 days

140
Q

Reasons not to use Azithromycin and Clarithromycin to treat AECB?

A

Poor H. Influenzae coverage

High S. Pneumoniae resistance

141
Q

First line tx for:
AECB
ABS
AOM?

A

Amoxicillin

142
Q

Why are fluoroquinolones used as a last resort for tx of UTI?

A

(Cipro) can cause permanent serious side effects:

Involves tendons

Muscles

Joints

Nerves

CNS

** Have to stop immediately if this occurs and switch to another antimicrobial

143
Q

TMP/SMX?

A

Trimethoprim/sulfamethoxazol

Bactrim
1 part TMP to 5 parts SMX. 160mg/800 (DS*= double strength)

144
Q

Cystitis tx in female

A

Hydrate
watch and wait
Nitrofurantoin (macrobid):
50- 100 mg PO QID x 5 days

pharm week 1 (8 decks)

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