Infectious Diseases & Adverse Drug Reactions Flashcards

1
Q

Describe an algorithm for managing a patient with suspected infection.

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2
Q

What are the 9 Antimicrobial Stewardship Clinical Care Standards?

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3
Q

What is the antibiotic creed? (MINDME)

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4
Q

How do we choose the right antimicrobial?
- Pathogen factors (3)
- Drug factors (8)
- Patient factors (7)

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5
Q

What are the 6 human pathogens?

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Human Pathogens
1. Bacteria
2. Viruses
3. Fungi
4. Protozoans
5. Helminths
6. Ectoparasites

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6
Q

Human pathogenic bacteria:
What are the 3 main Aerobic Gram-positive cocci & examples of each?

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7
Q

Human pathogenic bacteria:
What are the 2 main Aerobic Gram-positive bacilli & examples of each?

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8
Q

Human pathogenic bacteria:
What are the 2 main Anaerobes & examples of gram positive/negative?

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9
Q

Human pathogenic bacteria:
What is the main Aerobic Gram-negative cocci & examples?

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Aerobic Gram-negative cocci
– Neisseria inc N. meningitidis, N. gonorrhea, Moraxella catarrhalis, other NB Brucella, Pasteurella, Haemophilus & HACEK are Gram negative cocci-bacilli

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10
Q

Human pathogenic bacteria:
What are the 7 main Aerobic Gram-Negative Bacilli & examples?

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11
Q

Human pathogenic bacteria - Examples of:
- Spirochaetes?
- Mycoplasmataceae?
- Chlamydiaceaa & Rickettsiales

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12
Q

Bacterial antimicrobials - Which inihibit:
- Cell wall synthesis (6)?
- Protein synthesis (7)?
- Nucleic acid (3)?

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13
Q

What are the 5 Most common clinical indications for antibiotics?

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14
Q

Where can you find Microbiology & Antimicrobials sources of information?

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15
Q

Staph aureus bacteraemia
- Mortality?
- Tx?

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16
Q

Which anitbiotics cover staph aureus?
- Primary? (3)
- Secondary? (3)
- Broad spectrum agents with staphylococcal cover (not MRSA) (3)?

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17
Q

Explain the Evolution of drug resistance in S. aureus

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18
Q

Core antibiotics for MRSA?

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19
Q

How can the following present:
- Skin and soft tissue infection?
- Urogenital infections?
- GIT infections?
- Intra-abdominal sepsis?
- Respiratory Tract?
- Bone & joint infections?
- Neurological infections?
- Febrile Syndromes?

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20
Q

What are 5 Limitations of testing for infectious diseases?

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Limitations of Testing
1. Timing relative to disease (e.g incubation etc)
2. Access to site of infection / organism
3. Sensitivity of test
4. Quality of specimen
5. Prior antimicrobial therapy (antibiotics prior to taking specimen reduces yield by 50%)

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21
Q

What are your options for microbiology testing?
What are the

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22
Q

What are 3 types of cultures?
Which are selective (1) and which are non-selective, sterile (3) and non-sterile (3)?

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23
Q

Urine m/c/s
- What is it used for?
- Is urine sterile?
- Why do we need to take a mid-stream urine for m/c/s?
- What results indicate an infection?
- What results indicate contamination?
- Reasons for false positive?
- Reasons for false negative?

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24
Q

What are the indications for blood cultures?
How is the specimen collected?
When do we need 3 sets?

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25
Q

When are the following swabs used?

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26
Q

Nasopharyngeal samples
- Which specific testing is needed for Bordetella?
- Which specific testing is needed for Resp viruses?

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27
Q

Faeces
- How to collect?
- Routine testing?
- 3 additional tests?
- Selective culture?

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28
Q

CSF Cultures
- Collection method?
- Routine testing?
- Additional testing?

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29
Q

What is the purpose of serology testing?
- How long does Legionella take to seroconvert?

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30
Q

Which antibodies can we detect in response to infectious agents?

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31
Q

HIV Serology?

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??

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32
Q

CMV Serology

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??

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33
Q

What is the definition of fever?
What is the definition of Pyrexia of unknown Origin?

A

Fever: > 37.5o
PUO: Unexplained fever despite extensive investigation for longer than 2-3 weeks

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34
Q

Causes of Atypical Fever Syndromes
- 3 Non-infectious causes of fever?
- 2 Atypical infections?
- 2 Atypical presentations?

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35
Q

Define:
- Bacteraemia?
- Septicaemia?
- Septick Shock?
- Underlying pathophysiology?

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36
Q
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37
Q

What are 4 bacteria that can cause rapid overwhelming sepsis and death in normal hosts?

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38
Q

What do you need to find out on history for infectious diseases?

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39
Q

What are you looking for on physical examination in suspected infectious diseases?

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40
Q

Which investigations should you consider in patients with suspected infection?

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41
Q

Why are we worried about sepsis in an asplenic patient?
5 pathogens?

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42
Q

What factors do we need to consider when choosing which antibiotic to use?
- Bug?
- Drug?
- Patient?

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43
Q

What are the most common clinical indications for antibiotics?

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44
Q

Which human pathogenic bacteria cause most infections?

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45
Q

Bacterial antimicrobials - main classes and examples of each?

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46
Q

Which antibiotics would you give for gram negative bacteria?
- 1st line?
- 2nd line?
- tertiary?

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47
Q

What are the core antibiotics to be used for Enterobacteriacea?

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48
Q

What are the core antibiotics to be used for Enterobacteriacea- ESBL / AmpC?

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49
Q

What are the core antibiotics to be used for Pseudomonas aeruginosa?

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50
Q

What are the broad spectrum gram negative antibiotics?
- first line? (3)
- alternatives? (2)

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51
Q

Which antibiotics would you use for staph:
- primary? (5)
- secondary? (3)
- broad spectrum with anti-staph cover (not MRSA)? (4)

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52
Q

5 Core antibiotics for MRSA?

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53
Q

What are your core antibiotics for streptococci?

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54
Q

Core antibiotics for Enterococci?

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55
Q

Core antibiotics for Anaerobic bacteria?

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56
Q

9 Factors to Consider When Selecting an Antibiotic?

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57
Q

What are your oral only antibiotics? (5)
Which antibiotics are iv only?
Which is available rectally? (1)

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58
Q

Which antibiotics have OK vs. POOR CSF penetration?

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59
Q

List some adjuvant measures in the management of infection.
- Physical measures?
- Address primary causes?

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60
Q

What are 5 situations in which you would not give antibiotics?

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61
Q

What are the most common problems reported by returning travellers?

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62
Q

Approach to returned traveller:
- Which 4 potentially fatal infections need to be ruled out?
- What are 6 targeted investigations to perform?

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63
Q

Discuss the incubation periods of the main imported diseases:
- Short incubation period <7days? (6)
- Long incubation period >7days? (9)

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64
Q

What are your top 4 Major Tropical Infections?
5 Other important tropical infections?

A
65
Q

Tuberculosis:
- Epidemiology?
- Site of Primary infection?
- Sites of Post-primary infection? (2)
- Sites of Reactivation infection? Extrapulmonary?
- Where does most TB come from in Australia?

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66
Q

TB:
- Transmission?
- 5 Factors that increase infectiousness?

A
67
Q

TB:
- Diagnosis?
- Treatment?

A

TB Tx
- DOTT
- IREP 2 months
- IR 4 months
- Quinolones, macrolides, streptomycin for MDR

68
Q

What is Glandular Fever?
- Epidemiology?
- Aetiology?
- Transmission?

A

Glandular Fever = Infectious mononucleosis (Kissing disease) = Epstein-Barr Virus

69
Q

What is the pathophysiology of Glandular Fever?

A

EBV infects B lymphocytes in mucosal epithelium (e.g., oropharynx, cervix) via the CD21 receptor → infected B lymphocytes induce a humoral (B-cell) as well as a cellular (T-cell) immune response → an increased concentration of atypical lymphocytes in the bloodstream, which are CD8+ cytotoxic T cells that fight infected B lymphocytes.

70
Q

What are the clinical features of Glandular Fever?
- Incubation period?
- Clinical Course?
- S&Ss?

A

Splenomegaly can lead to a potentially life-threatening splenic rupture!

In most cases, a maculopapular rash occurs due to empiric administration of aminopenicillins, and not due to EBV infection.

71
Q

How is Glandular Fever diagnosed?

A
72
Q

List 7 differential diagnoses for glandular fever/Mononucleosis?

A

Mononucleosis-like syndromes
1. Streptococcal pharyngitis, tonsillitis
2. Acute HIV infection
3. CMV infection (CMV mononucleosis)
4. Viral hepatitis
5. Toxoplasmosis
6. Diphtheria
7. Acute leukemia

73
Q

Describe the management for Glandular Fever/IM/EBV?

A
74
Q

Complications of Glandular Fever:
- 5 Nervous System?
- 4 Hematological?
- 7 Other body systems?
- 4 Associated malignancies?

A

Other organ systems:
1. Upper airway obstruction due to oropharyngeal inflammation and enlarged lymph nodes
2. Splenic rupture
3. Oral hairy leukoplakia (typically in HIV patients)
4. Acute renal failure
5. Pericarditis/myocarditis
6. Pneumonia
7. Otitis media

75
Q

Ross River Fever/Virus
- Epidemiology?
- Pathogen
- Vectors?
- Resevoirs?
- Route of transmission?
- Clinical features: classid triad?

A

Epidemiology
- Found predominantly in Australia, Papua New Guinea, the Solomon Islands, and other parts of Southeast Asia.
- Outbreaks during summer and early autumn.

Aetiology:
- Pathogen: Ross River virus (RRV)
- Vectors: mosquitoes (Aedes vigilax, Aedes camptorhynchus, Culex annulirostris, and Aedes aegypti)
- Reservoirs: wallabies, kangaroos, possums, horses
- Route of transmission: Mosquito bite, Human-mosquito-human transmission, Human-to-human: blood transfusions from an infected host

76
Q

Ross River Virus
- Diagnostics? (4)
- Differentials? (2)
- Treatment? (4)
- Complications? (2)

A

Diagnostics
1. Laboratory studies: ↑ ESR
2. Serology (gold standard): IgM and/or rising levels of IgG antibodies detected using ELISA
3. PCR
4. Viral culture

Differential diagnosis
1. Barmah Forest virus
2. Chikungunya virus

77
Q

Dengue
- Epidemiology?
- Pathogen?
- Transmission?

A

Epidemiology of Dengue
- Distribution: tropical regions worldwide, particularly Asia (e.g., Thailand)
- Incidence: Most common viral disease affecting tourists in tropical regions, ∼ 400 million infections per year worldwide

Pathogen: Dengue virus (Serotype: DENV 1–4). RNA virus of the genus Flavivirus
Transmission route - Vector-borne: mosquitoes most commonly from the species Aedes aegypti

78
Q

Clinical Features of Dengue?

A
  • If symptoms appear more than 2 weeks after returning from a dengue-endemic region, it is very unlikely that dengue is the cause.
  • Severe dengue is more frequent in individuals who experience a repeat infection with a second serotype, especially serotype 2.
79
Q

Clinical features of Severe Dengue?
Clinical features of Dengue Shock Syndrome?

A
80
Q

Diagnosis of Dengue:
- 5 Lab tests?
- Confirmation of Acute Phase diagnosis? (4)
- Confirmation of Convalescent Phase diagnosis? (3)

A

Laboratory tests
1. Leukopenia
2. Neutropenia
3. Thrombocytopenia
4. ↑ AST
5. Hct significantly increased or decreased in DHF (due to plasma leakage)

81
Q

3 Differential diagnoses for Dengue fever?
- Treatment of Dengue?

A
  1. Chikungunya fever and other viral hemorrhagic fevers
  2. Malaria
  3. Zika virus infection

Severe hemorrhagic manifestations with shock and death as well as decreased neutrophil and platelet counts are more indicative of Dengue fever than Chikungunya fever.

82
Q

Prevention of Dengue?

A
83
Q

Define: Cellulitis.
- Clinical features?

A

Cellulitis: local infection of the deep dermis and subcutaneous tissue

84
Q

Cellulitis:
- Pathophysiology?
- Aetiology?
- 3 Diagnostics?

A

Pathophysiology of Cellulitis
- Entry is commonly via a minor skin injury.
- May also be secondary to a systemic infection.
- In cellulitis, the most common point of entry for the pathogen is a small skin lesion (e.g., interdigital tinea pedis).

Aetiology
- Beta-hemolytic streptococci: mostly group A Streptococcus (S. pyogenes)
- Less common pathogens for cellulitis:
- S. aureus
- Pasteurella multocida (gram-negative, encapsulated coccobacillus): secondary to dog and cat bites.

GAS is the most common cause of nonpurulent skin and soft tissue infections (i.e., erysipelas, cellulitis).

85
Q

Treatment for Cellulitis?

A

General principles
- Empiric antibiotic therapy active against streptococci and S. aureus is the mainstay of treatment for nonpurulent SSTIs.
- Treatment should also include the control of any predisposing factors (e.g., edema, fungal infections).

Antibiotic therapy
- Systemic antibiotic therapy is usually required.
- Empiric regimens should usually cover Streptococcus spp. and S. aureus.
- Antibiotics should be targeted against gram-positive pathogens and provide broad-spectrum coverage in severe cases.

Supportive care
- Elevation of the affected limbs.
- Rest and acute pain management as needed.

86
Q

Primary amebic meningoencephalitis:
- Pathogen?
- Route of infection?
- Clinical features?
- Diagnosis?
- Treatment?
- Prognosis?

A

Cerebral amebiasis: A rapidly fatal necrotizing encephalitis results from infection with Naegleria species, and a chronic granulomatous meningoencephalitis has been associated with infection with Acanthamoeba. The amebae may be difficult to distinguish morphologically from activated macrophages. Methenamine silver or PAS stains are helpful in visualizing the organisms, although definitive identification ultimately depends on immuno- fluorescence studies, culture, and molecular methods.

87
Q

Salmonellosis (salmonella gastroenteritis)
- 3 Pathogens?
- 5 Pathogenic features?
- Transmission?
- Incubation period?
- Prevention?

A
88
Q

What are the 7 clinical features of Salmonella gastroenteritis?
- 4 Complications?

A

**Clinical features of Salmonella gastroenteritis **
1. Duration: 3–7 days
2. Fever (usually resolves within 2 days) & chills
3. Headaches
4. Myalgia
5. Severe vomiting
6. Abdominal pain
7. Inflammatory (watery-bloody) diarrhea

89
Q

Differential diagnosis of community acquired infectious diarrhoea?

A
90
Q

Outline the management for salmonella gastroenteritis?

A
  • Antibiotic treatment of nontyphoidal Salmonella enteritis is not indicated for otherwise healthy patients without risk factors for complications.
  • Initial intravenous therapy is recommended in the following situations:
    1. when oral therapy is not possible
    2. in children aged 1 to 3 months
    3. in patients with bacteraemia, endovascular infection or osteoarticular infection.
91
Q

What is Streptococcal pharyngitis?

A

Streptococcal pharyngitis, which is the major antecedent of poststreptococcal glomerulonephritis, is marked by edema, epiglottic swelling, and punctate abscesses of the tonsillar crypts, sometimes accompanied by cervical lymphadenopathy. Swelling associated with severe pharyngeal infection may encroach on the airways, especially if there is peritonsillar or retropharyngeal abscess formation.

92
Q

What are the clinical features of streptococcal pharyngitis?

A
  • More common in school-aged children and adolescents, but can occur in younger children and adults.
  • Clinical features include abrupt onset of symptoms, fever (above 38°C), tender cervical lymphadenopathy, tonsillar exudate, and the absence of cough, rhinorrhoea or nasal congestion.
93
Q

List 8 Red flags for tonsillopharyngitis?

A
  1. Trismus
  2. Drooling
  3. Asymmetric tonsils
  4. Displaced uvula
  5. Unilateral facial swelling
  6. Muffled or “hot potato” voice
  7. Clinical features of sepsis
  8. Immunosuppression

Trismus and change in voice quality indicate the formation of potentially life-threatening peritonsillar abscess!

94
Q

Discuss the diagnosis of streptococcal pharyngitis?

A

Clinical evaluation
- Assess for clinical features of acute bacterial tonsillopharyngitis, acute viral tonsillopharyngitis, and differential diagnoses of acute tonsillopharyngitis.
- Proceed to immediate treatment if red flags for tonsillopharyngitis or clinical features of airway compromise are present.
- Routine testing for GAS is not recommended for children < 3 years old, as their prevalence of GAS pharyngitis and risk of developing subsequent acute rheumatic fever are both low. Consider testing only if specific risk factors (e.g., close household contact) are present.
- Testing for GAS infection is not recommended in patients with clinical features that strongly suggest acute viral tonsillopharyngitis.

95
Q

Describe the role of Rapid strep test and Throat culture in the diagnosis of GAS pharyngitis?

A

Throat culture
Indications
1. Confirmatory test to definitively rule out GAS infection in symptomatic children and adolescents with a negative RADT
2. Recurrent or chronic tonsillitis

Findings: Causative bacteria and their antibiotic susceptibility
Time to result: 24–48 hours

96
Q

What is the Centor Score?

A

= A set of criteria used to estimate the probability that pharyngitis is streptococcal (i.e., caused by group A Streptococcus).
- Rationale: Estimate the likelihood of acute bacterial pharyngitis based on clinical features alone.
- Clinical scoring systems cannot replace RADT or throat culture to make the diagnosis of GAS pharyngitis due to a lack of accuracy.
- Clinical applications: Identifying patients with a low likelihood of GAS infection, thereby minimizing unnecessary diagnostic tests and antibiotic therapy. The use of scoring systems to identify patients with a high likelihood of bacterial pharyngitis in order to treat empirically without testing is controversial.

97
Q

Describe the treatment for streptococcal pharyngitis?

A

Supportive care
- Ensure adequate hydration.
- Consider household remedies such as salt-water gargles.
- Consider oral topical local anesthetics: e.g., benzocaine lozenges, phenol throat sprays, compounded mouthwash.
- Analgesics and antipyretics

Amoxicillin therapy in patients with infectious mononucleosis can trigger a maculopapular and/or morbilliform rash. Reserve antibiotics for patients with confirmed bacterial tonsillopharyngitis (e.g., positive rapid strep test or throat culture), whenever possible.
Avoid aspirin in children due to the risk of Reye syndrome.

98
Q

List 7 Suppurative complications of Streptococcal pharyngitis and 3 non-suppurative complications.

A
  • Antibiotic therapy for GAS pharyngitis can decrease the risk of rheumatic fever but does not affect the risk of PSGN.
  • Streptococcus “ph”yogenes is the most common cause of bacterial pharyngitis, which can result in rheumatic “phever” and poststreptococcal glomerulonephritis.
  • Rheumatic fever occurs in ∼ 3% of untreated cases of GAS infection.
99
Q
A
100
Q

HHV-2
- Subtype?
- Overview?
- Seroprevalence?
- Modes of Transmission? (2)
- Characteristics?
- 5 Diseases?
- Management?

A
101
Q

HHV-3
- Subtype?
- Overview?
- Seroprevalence?
- Modes of Transmission? (2)
- Characteristics?
- 5 Diseases?
- Management?

A
102
Q

HHV-4
- Subtype?
- Overview?
- Seroprevalence?
- Modes of Transmission? (2)
- Characteristics?
- 5 Diseases?
- Management?

A
103
Q

HHV-5
- Subtype?
- Overview?
- Seroprevalence?
- Modes of Transmission? (2)
- Characteristics?
- 5 Diseases?
- Management?

A
104
Q

HHV-6&7
- Subtype?
- Overview?
- Seroprevalence?
- Modes of Transmission? (2)
- Characteristics?
- 5 Diseases?
- Management?

A
105
Q

HHV-8
- Subtype?
- Overview?
- Seroprevalence?
- Modes of Transmission? (2)
- Characteristics?
- 5 Diseases?
- Management?

A
106
Q

What are the 3 groups of herpes viruses?

A
107
Q

Herpes Simplex Virus Infections
- 2 Serotypes?
- Prevalence?
- Transmission?
- Type of infection?

A
108
Q

Herpes Simplex Virus Infections
- Pathophysiology?
- 5 Diseases?
- 5 Diagnostics?

A

HSV related diseases
1. Herpes labialis (cold sores)
2. Genital herpes (herpes genitalis)
3. Herpetic gingivostomatitis
4. Eczema herpeticum
5. Herpetic whitlow

109
Q

What is Malaria?
- Distribution?

A

Distribution
- Most cases of malaria occur in tropical Africa (West and Central Africa).
- Transmission also occurs in other tropical and subtropical regions such as South and Southeast Asia, and Central and South America.

110
Q

Which pathogen causes Malaria?
- Vector?
- Host?
- 4 Groups with partial resistance to malaria?
- 5 plasmodium species & the disease they cause? fever spike?

A
111
Q

Describe the lifecycle of the Plasmodium?

A
112
Q

Malaria
- Incubation period?
- Course?
- General symptoms?
- Organ-specific symptoms?

A

Impaired consciousness, shock, and abnormal bleeding are signs of severe malaria that requires immediate IV treatment.

113
Q

Describe an approach to the diagnosis of suspected malaria?
- 3 Routine Lab ixs and their findings?
- 2 types of parasitological testing?

A

Routine laboratory studies
1) CBC: Changes in multiple parameters may occur.
- Hemolytic anemia: ↓ Hb, ↓ haptoglobin, ↑ LDH, ↑ indirect bilirubin, ↑ reticulocytes
- Thrombocytopenia
- Leukocytosis or leukopenia are uncommon except in severe disease.

2) CMP: Hypoglycemia can occur in severe malaria.
3) Urinalysis: Hemoglobinuria may occur with intravascular hemolysis.

114
Q

What are the 5 Developmental stages of Plasmodium in RBCs and their appearance under microscopy?

A
115
Q

Severe Malaria
- Description?
- Aetiology?
- Pathophysiology?
- Criteria: Clinical findings & Laboratory results?

A

Description: potentially fatal manifestation or complication of malaria
Aetiology: most commonly a result of falciparum malaria
Pathophysiology: Infected erythrocytes occlude capillaries, which can lead to severe organ dysfunction.

116
Q

How do you manage severe malaria?
- Approach?

A

Approach
1. Check for criteria for severe malaria.
2. Treat severe malaria immediately with IV artesunate.
3. Treat uncomplicated malaria based on species, resistance patterns, and degree of chemoprophylaxis.
4. Report all confirmed malaria to public health authorities.

117
Q

Overview of treatment of uncomplicated malaria?

A

Treatment of uncomplicated malaria
Agent selection based on:
1. Infecting Plasmodium species
2. Prior use of chemoprophylaxis
3. Likelihood of chloroquine-resistance

Additional considerations in P. vivax and P. ovale
1. Check G6PD activity levels.
2. Give primaquine or tafenoquine to eradicate hypnozoites dormant in hepatocytes.

118
Q
A
119
Q
A
120
Q
A
121
Q

List 4 Mechanisms of Antimicrobial Resistance?

A
122
Q

Describe 6 Implications of Antimicrobial resistance?

A
123
Q

Indications & Efficacy of the Influenza vaccine?

A

All people ≥6 months of age are recommended to receive annual influenza vaccine.
Efficacy - While vaccine effectiveness (VE) can vary, recent studies show that flu vaccination reduces the risk of flu illness by between 40% and 60% among the overall population during seasons when most circulating flu viruses are well-matched to those used to make flu vaccines. In general, influenza vaccine effectiveness has been found to vary between 30-60%. This implies that, on average, a vaccinated person is 30-60% less likely to experience the outcome being measured (e.g. influenza leading to attendance at a general practice or hospitalisation) than an unvaccinated person.

124
Q

Who should get the pneumococcal vaccine?

A

The Australian Immunisation Handbook recommends pneumococcal vaccination for specific groups including:
1. routine vaccination in infants and children
2. non-Indigenous adults aged 70 years and over
3. Aboriginal and Torres Strait Islander adults aged 50 years and over
4. children, adolescents and adults with risk conditions for pneumococcal disease

125
Q

What are the symptoms and signs of acute HIV seroconversion?

A

Acute HIV seroconversion refers to the initial phase of HIV infection when the body starts producing detectable antibodies against the virus. During this phase, individuals may experience a variety of symptoms and signs, which can resemble those of other viral illnesses. It’s important to note that not everyone who acquires HIV infection will experience symptoms during seroconversion, and the presence or absence of symptoms cannot be used to conclusively diagnose HIV.
General considerations
- There are no clinical features specific to HIV infection.
- In early HIV infection, patients are often asymptomatic.
- Incubation period: usually 2–4 weeks
- Infectiousness: two peaks (1st peak: within the first months after infection; 2nd peak: during AIDS-stage)

126
Q

What are 4 specific tests for HIV?

A

There are several tests used for the detection and diagnosis of HIV infection. These tests are designed to detect antibodies, antigens, or genetic material (RNA or DNA) related to the HIV virus.

127
Q

Discuss the diagnostic and screening tests for HIV?

A
128
Q

Diagnostic Algorithm for HIV?
Time to positivity of HIV diagnostic tests?

A
129
Q

Outline an approach to the diagnosis of syphillis?

A

Approach
Order both nontreponemal tests and treponemal tests for:
1. Patients with clinical features of syphilis
2. Individuals with risk factors for syphilis infection
3. Pregnant individuals at the first prenatal visit
4. Order direct detection in patients with suitable skin lesions, e.g., exudative chancre, condyloma.
5. Consider additional studies (e.g., lumbar puncture) based on the clinical assessment.

130
Q

Describe the Nontreponemal tests (NTT) for Syphillis
- 3 Indications?
- Mechanism?
- 2 Types?
- Accuracy?

A

False-Positive results on VDRL with Pregnancy, Viral infection (e.g., EBV, hepatitis), Drugs (e.g., chlorpromazine, procainamide), Rheumatic fever (rare), Lupus, and Leprosy

131
Q

Treponemal tests (TT) for Syphillis
- 2 Indications?
- Mechanism?
- 3 Types?
- Accuracy?

A
132
Q
A
133
Q

What is a drug interaction?

A

In general, water-soluble kidneys are excreted by the kidneys.

134
Q

What are the 3 types of drug interactions?

A
135
Q

Pharmaceutic Drug Interactions:
- What are they? Where do they occur?
- 1 example of a Binding interaction?
- 3 examples of Precipitation interactions?

A

Pharmaceutical = Reactions between chemical constituents – eg. Binding agents – not so common with oral meds (exception = iron supplements, iron will bind to tetracycline, give not with other meds).

136
Q

What are 3 types of Pharmacodynamic drug interactions? Give 2 examples of each.

A
137
Q

Pharmacodynamic Drug Interactions
- Give 3 examples of drugs which have same/similar toxicities?

A
138
Q

Pharmacokinetic Drug Interactions: Absorption
- Give 5 examples of pharmacokinetic drug interactions associated with absorption?

A
  • Iron supplements = dark stools & constipation –> Take every other day
  • Cholestyramine = not commonly used but good for statin intolerant patients for lipid lowering
  • Opiates = delayed gastric emptying –> Therefore, don’t bother with oral meds after because most need gastric emptying before small bowel absorption (except aspirin, get absorbed across stomach wall).
  • Need Gastric pH to absorb iron therefore people on PPIs can become iron deficient.
139
Q

Pharmacokinetic Drug Interactions: Distribution
- Describe how protein binding can cause drug interactions?
- 3 Clinically significant examples?

A

More of a theoretical issue

140
Q

Pharmacokinetic Drug Interactions: Metabolism
- What is the major organ for drug metabolism?
- Phase I vs. Phase II?

A
  • Phase I = trying to make the more lipid-solube drug more polar - Where you see most of the interactions – eg. Cytochrome P450 system most commonly implicated.
  • Phase II = conjugation (eg. Glucoronate – helps with excretion)
  • Drug interactions are most significant when they have a low therapeutic index – ie. If there is a bit more induction then it becomes toxic, no longer at a therapeutic dose – eg. Warfarin (low dose = ineffective but too high = bleeding).
  • Antibiotics + Warfarin - Antibiotics = usually sick so affects diet but also changes gut flora which influenced Vitamin K bioavailability.
141
Q

List 4 Inducers of Cytochrome P450?
List 4 Inhibitors of Cytochrome P450?

A
142
Q

Which 2 CYP450 enzymes can interact with some antipsychotics/antidepressants?
Which test can be performed to check a persons level of CYP450 enzymes?

A

2D6 and 3A4 = interact with some antipsychotic and antidepressants – has come up in exams!!
Genetic screening test = tests for the levels of cytokines so you can adjust your meds.

143
Q

What effect does alcohol have on the liver?
Why does this increase the hepatoxicity of paracetamol?
Ie. Why is paracetamol-induced hepatotoxicity common in alcoholics?

A
144
Q

Pharmacokinetic Drug Interactions: Elimination
- What is the major organ for drug elimination?
- Example of an elimination drug interaction?
- Example of a drug transport elimination interaction?

A

NSAIDs = change prostaglandin metabolism, prostaglandin balance is important for renal medullary blood flow – where lots of tubular absorption and excretion takes place.

145
Q

Which 2 patient groups are at high risk of significant drug interactions?

A
146
Q
A
147
Q

What are 4 Drug Factors associated with a high risk of significant drug interactions?

A
148
Q

Why do we need to document prescriptions?
List 9 types of drug charts?

A

Documentation of Prescription
- Communicates the prescription between medical, nursing, and pharmacy
- Acts as a legal record of medical administration

149
Q

What are 6 factors to take into account when writing up a drug chart?

A
150
Q

List 10 High risk drugs associated with errors?

A

TPN = Total Parental Nutrition

151
Q

What are 5 causes of drug chart/prescribing errors?

A
152
Q

What is the second most common type of medication error?
What are 6 factors that affect drug dosage?

A
153
Q

What are the 10 commonest causes of adverse drug reactions seen in hospital medical practice?

A

Adverse drug reactions (ADRs) are unwanted and harmful effects that occur as a result of medication use. In hospital medical practice, several factors contribute to the occurrence of ADRs. Here are some of the commonest causes of ADRs seen in hospitals:

154
Q

What is the management of drug-induced allergy including anaphylaxis?

A
155
Q

List 6 major drug interactions commonly seen in hospital practice.

A
  1. Warfarin and Antibiotics
  2. Simvastatin and Macrolide Antibiotics
  3. Digoxin and Verapamil
  4. Statins and Cyclosporine
  5. Proton Pump Inhibitors (PPIs) and Clopidogrel
  6. Monoamine Oxidase Inhibitors (MAOIs) and Serotoninergic Medications
156
Q

Explain the following drug interactions commonly seen in hospital practice:
1. Warfarin and Antibiotics
2. Simvastatin and Macrolide Antibiotics
3. Digoxin and Verapamil

A
157
Q

Explain the following drug interactions commonly seen in hospital practice:
1. Statins and Cyclosporine
2. Proton Pump Inhibitors (PPIs) and Clopidogrel
3. Monoamine Oxidase Inhibitors (MAOIs) and Serotoninergic Medications

A