ID Flashcards
(92 cards)
1
Q
Neutropenic patient with hemoptysis?
A
Think about aspergillus, which is the most common cause of hemoptysis in neutropenic patients
2
Q
Clinical subtypes of invasive aspergillus?
A
Pulmonary
Rhinosinusitis - can get necrotic areas, epistaxis, facial pain
Tracheobronchitis - obstructive plugs, ulceration, pseudomembranes
Disseminated
3
Q
Describe the schematic breakdown for aspergillus complications
A
See evernote on aspergillus in ID section
4
Q
Risk factors for invasive pulmonary aspergillosis?
A
- Prolonged neutropenia (<500 for >10 days)
- Transplantation - in particular lung transplant and HSCT
- > 3 weeks (prolonged) high dose corticosteroid therapy
- Hematological malignancy
- chemotherapy
- Advanced AIDs
- CGD
5
Q
Treatment for invasive pulmonary aspergillosis
A
Voriconazole
6
Q
Causes of false negative TST?
A
Non-technical: Infections: - Bacteria: active TB, pertussis - Viral: HIV, VZV - Fungal (blastomycoses) - live virus (measles, mumps, polio, varicella) - Chronic kidney disease - lymphoma - Drugs - corticosteroids, TNF alpha inhibitor - Age - newborn, elderly patients - Stress--surgery, burn, mental illness
Technical:
- Related to tuberculin: improper storage, improper dilution, chemical denaturation, contamintion
- Method of administration: too little antigen, subcutaneous injection
- Factors related to reading: inexperienced reader
7
Q
Causes of false positive TST?
A
- Other mycobacterial infection
- BCG vaccination
- Allergic reaction
8
Q
For TST of 0-4 mm, in which group is this defined as positive?
A
Less than 5 years of age AND high risk for TB infection (Because of exposure)
9
Q
For TST of 5-9 mm, in which group is this defined as positive?
A
- In many of the groups where there is risk of false negative, we have a lower cut off for defining positive test
- Immunodeficiency:
- HIV and well
- Corticosteroids (>=15 mg/day x >=1 month)
- TNF alpha inhibitor
- Organ transplant
- Close contact of active contagious disease in the last 2 years
- End stage renal diseaes
- Fibronodular disease on CXR (healed TB)
10
Q
What is the typical cut off for defining a positive TST?
A
> = 10 mm
Categories:
0-4 mm
5-9 mm
>=10 mm
11
Q
If you find a non-tuberculous mycobacterium on a sputum or BAL for a patient, then is that bacteria the cause of the patient’s respiratory symptoms?
A
- It very likely is NOT the cause of the patient’s respiratory symptoms.
- Thought of as an opportunistic bacteria with low pathogenic potential, so it’s not enough to just identify NTM and label it as the cause of disease
- Challenges with labelling NTM disease just based on positive sample:
- Environmental contamination
- Transient recovery
- Colonizer
- Or could be truly pathogenic
12
Q
Treatment of PJP?
A
septra 15-20 mg/kg/day IV or po in 3-4 divided doses x 3 weeks (high dose IV septra x 21 days, but can finish with oral if patient is improving)
If PJP + moderate to severe hypoxemia (PaO2<70 on room air), then glucocorticoids
13
Q
Imaging findings of invasive pulmonary aspergillosis?
A
CXR: peipheral lung nodules
CT: halo sign, air crescent (necrosis within lung nodule)
14
Q
If suspecting fungal pulmonary infection, what cell wall antigens can be tested for?
A
- Galactomannan –>released by growing aspergillus
- Beta-D glucan
15
Q
How is TB infection defined?
How do you differentiate the types of TB infection–>latent TB versus TB disease?
A
- TB infection = positive TST
- Symptoms and radiographic findings on CXR are the key things that differentiate latent TB versus disease
- It’s no sputum culture which make that differentation
- TB disease: symptoms or signs or radiographic manifestations + positive TST
- Latent TB: positive TST, but no symptoms or signs or radiographic features
16
Q
Child >=5 years of age with exposure to TB. What is the management?
A
- Evaluate as soon as possible with physical exam, CXR, TST or IGRA
- If TST/IGRA is negative, then repeat at 8-12 weeks since the initial test could have been a false negative with early TB infection
- Unlike for children <5 years, there is no need for a window of prophylaxis
17
Q
Child <5 years of age with exposure to TB. What is the management?
A
- Evaluate as soon as possible with physical exam, CXR, TST or IGRA
- If there is no evidence of TB infection, then give a window of prophylaxis with INH
- Repeat TST/IGRA in 8-12 weeks. If the repeat test is negative and no concern about this results, then the window of prophylaxis could be stopped. If you are concerned that it’s a false negative (Eg. age, malnutrition, immunocompromised), then complete a course of treatment for latent TB (if there is no evidence of TB disease)
18
Q
Who should be tested for latent TB?
(We don’t indiscriminantly test everyone for latent TB. Testing for latent TB is based on the risk factors for progressing to TB disease). Latent TB matters if there is a high risk for developing active TB
A
- Recent infection, within the last 2 years
- Organ transplant
- HIV
- Immunosuppressive medication - TNF alpha, prolonged steroids
- primary immunodeficiency
- malignancy
- malnutrition
- Age:
- <2 years
- Adolescence
(in the absence of risk factors, the risk of progressing from latent TB to active TB is 5-10%)
19
Q
How do we treat for latent TB?
A
- In a child >=2 years of age: rifampin x 4 months (better adherence compared to other treatment regimens).
- I would assume that for a child <2 years of age–>INH x 9 months
20
Q
How does active TB usually develop?
A
- It’s usually due to reactivation of latent TB
21
Q
What are the investigations for a patient with suspected active TB?
A
- CXR
- 3 gastric aspirates or sputum sample: smear, AFB culture, drug susceptibility testing
- HIV
- Xpert MTB/RIF–>can test for rifampin resistance
22
Q
Advantage of IGRA over TST?
A
- Doesn’t cross react with most non-tuberculous mycobacteria
- Doesn’t cross react with BCG
- Doesn’t require follow up in 48-72 hours
23
Q
How do you practically decide between TST or IGRA?
A
- Kendig’s has a nice alogirthm
- For a child <5 years of age, the preferred test is TST. But if don’t believe results of TST (Eg. TST is negative but you are very suspicious or TST is positive but you think it’s a falsepositive), then do IGRA
- So TST and IGRA can both be used if needed
- For a child >=5 years of age: if they have had BCG, then the preferred test is IGRA. If they will not return for follow up, then preferred test is IGRA. Otherwise, the preferred test is TST.
- If you don’t believe results of TST, then do IGRA
- IGRA is either reported as positive, negative or indeterminate
(uptodate recommends not using IGRA in <2 years of age)
24
Q
How is TB treated?
A
- Empiric treatment: INH, rifampin, ethambutol, PZA = RIPE x 2 months, then RI x 4 months (this is while you are waiting to figure out suspcetibility profile).
- If you figure that the TB is fully susceptible, then you can get rid of ethambutol
Treatment Modification after knowing susceptibility profile:
- Fully Susceptible, intrathoracic TB: RIP (rifampin, INH, PZA) x 2 months (initiation phase), then 4 months RI (continuation phase) for minimum total duration of 6 months (It’s handy that ethambutol is not part fo the empiric treatment, since it can be harder to monitor visual symptoms in children)
o Treat for 9 months if cavities on CXR or positive sputum culture after 2 months of treatment
25
What are side effects associated with TB treatment?
Rifampin: orange discoloration of secretions, hepatitis, drug interactions (especially with drugs metabolized by liver, so can't take rifampin with ivacaftor containing CFTR modulators), rash (hypersensitivity reaction).
INH: peripheral neuropathy (so need to take pyridoxine = B6)
P: hepatoxicitiy, arthralgia. “Most common cause of drug induced hepatoxicity and rash” (The "a" in the word is for arthralgia)
E: ethambutaol = eyes (optic neuritis), advise patients to report any changes in vision immediately. There should be monthly nursing assessment of vision. If patients are on ethambutol for more than the initial phase, then they should have periodic check ups with opthalmologist. Ethambutol should be used with caution in children, who are too young for monitoring.
(If you can’t think of a drug side effect, then say hepatotoxicity or rash)
- Apart from asking about side effects and periodic visual assessments, there's no other particular monitoring of side effects, no routine monitoring of liver enzymes (only if pre-existing liver disease or other hepato-toxic drugs)
26
TB disease versus infection?
TB disease = active TB
| Infection could be latent TB or active TB
27
Fully susceptible intrathoracic TB is treated for 6 months. When would you decide for a longer duration of treatment?
* patients with cavities on initial chest x-ray or cavities on CXR within first 2 months of therapy (then treat for total of 9 months minimum)
* positive sputum cultures after 2 months of treatment = culture positive after 2 months (the minimum duration of therapy should be 9 months)
* Discontinuing RMP or PZA due to side effects. (Rifampin is considered a cornerstone of TB therapy and should not be stopped for minor side effects)
* Having cavity on CXR at the end of therapy (extend total treatment duration to 9 months)
Extrapulmonary TB such as CNS, Disseminated/miliary, bone and joint:
- Treatment duration of 9-12 months
Pulmonary TB in patients with HIV:
- optimal treatment duration is not known
28
What are the features to consider when deciding if a patient with active TB is infectious?
- Sputum status: smear positive, culture positive
- symptomatic
- treatment for <2 weeks
- if treatment for >2 weeks with no evidence of treatment response (eg. no clinical improvement, no sputum conversion from smear positive to smear negative)
-multi-drug resistant TB and not receiving adequate treatment
(this assessment of infectiousness does not impact the approach to dealing with an exposed individual)
29
What is the treatment of latent TB?
- rifampin x 4 months, as per 2018 NEJM article, which specifically studies children 0-18 years ofa ge
- for a child <2 years of age-->I might be a bit more conservative and go with INH x 9 months (I think uptodate mentioned this), but I think either option is fine as long as source is mentioned
30
When a child is the first identified case of TB, what is important to remember in terms of finding the original case?
- Kids usually get infected by adults
31
After inhalation of TB bacilli, how does primary infection progress in children?
- Either form a caseating granuloma
OR
- Primary complex = primary focus, local tuberculous lymphangitis, enlarged lymph nodes
32
What are the manifestations of intrathoracic TB and how is this different adults?
- Most TB disease in children is from the primary infection, as opposed to from reactivation, which is more common in adults (and more common if primary infection is after puberty)
- Isolated lymphadenopathy (most of these kids are relatively well)
- Progressive primary infection-->looks like an airspace infiltrate on CXR. Can rupture into airway-->endobronchial disease or into pleura-->pneumothorax
- Bronchial disease-->airway narrowing, distal hyperinflation, atelectasis, secondary pneumonia
- Complicated lymph node disease (various consequences of lymph node obstruction)
- Acute pneumonia
33
Where does reactivation TB tend to happen?
- Posterior segment of upper lobes > superior segement lower lobes due to higher oxygen tension
(The primary infection such as with development with Ghon complex equally affects all regions of the lung, since the primary infection is from inhaling bacilli, as opposed to hematogeneous spread)
34
What are the features of a ghon/primary complex?
primary focus, local tuberculous lymphangitis, enlarged lymph nodes
35
Radiographic features of TB disease?
Primary disease:
- Can be seen in any lung zone. (This is the more common subtype in children. Therefore I would not use lung zone as a way to discriminate likelihood of TB).
- Lymphadenopathy
- Infiltrate, which could be lobar infiltrate
- Calcified lesion where granuloma or Ghon complex formed (tuberculoma)
- Can have cavitation, though this less likely than with reactivation TB
- calcified lymph nodes
- pleural effusion
- hyperinflation or atelectasis from airway disease
Reactivation:
- cavitation
- patchy consolidation
- location
1. posterior segments of the upper lobes
2. superior segments of the lower lobes
36
Radiographic features of latent TB?
- Most patients with latent TB have NORMAL CXR
Radiographs demonstrating stable upper lobe fibro-nodular disease or calcified granulomas are considered to demonstrate evidence of previous active TB and indicate the patient is at increased risk of reactivation-->it may be hard to make this differentiate that a particular lesion is stable, would need sputum cultures to help differentiate
37
What are life-threatening complications of respiratory papillomatosis?
- Airway obstruction
| - Malignant transformation
38
What is the most common organism causing bacterial tracheitis? Treatment?
- #1 is staph aureus
- others: H. influenzae, Moraxella cattharalis, strep pneumonia
- Treatment: ceftriaxone (third generation cephalosporin) + vanco
- Technically would need a rigid bronch for gold standard diagnosis, bronch also enables removal of pseudomembranes and intubation (Which about 50% of patients need)
39
What are clinical findings of CGD?
- Marked lymphadenopathy
- Hepatosplenomegaly
- Infection:
- pneumonia
- dermatitis
- suppurative lymph nodes
40
What are the most common types of infection in patients with CGD?
- Pneumonia is the MOST common
- Any kind of abscess
- Sucutaneous
41
What are the most common causes of pneumonia in CGD patients?
- #1 is aspergillus
- #2 is staph aureus
- other fungal: PJP, candida
- Other bacteria: burkholderia, serratia, nocardia, atypical mycobacteria
42
What are imaging findings of invasive pulmonary aspergillosis?
- Consolidation
- Nodules, which may have surrounding hypoattenuation (due to hemorrhage. this is called the halo sign). There may or may not be cavitation of nodules
- peribronchial infiltrate
- ground glass opacity
- pleural effusion
43
What are the stages of development of a parapneumonic effusion?
- Exudative
- Fibropurulent
- Organizational
44
How does endemic mycoses usually present?
- Either asymptomatic OR influenza illness with respiratory symptoms (chest pain, cough)
- Endemic mycoses happen in immunocompetent or compromised patients
45
Imaging findings of an endemic mycoses?
- Nodules (potentially with calcification if remote infection)
- Lymphadenopathy, which can cause airway obstruction and unilateral wheeze
- Cavitation
- Infiltrate
- A lot of overlap in the above features with TB
- (Blasto does not cause lymphadenopathy)
46
What's different about treatment of blastomycoses?
- You actually need to treat all cases of blasto, regardless of severity in children, since there is a higher chance of disseminated disease
47
Endemic mycoses and geographic location?
- Coccidio - valley fever, southern U.S. so California, Arizona, New Mexico, Northern Mexico
- Central U.S. is histo
- Eastern U.S. and great lakes is Blasto
- In Canada (ontario, manitoba, quebec)-->histo, blasto
48
What are the challenges with diagnosing and treating NTM infection?
- NTM is actually an OPPORTUNISTIC pathogen so there are very specific criteria to actually say it's the cause of a patient's pulmonary symptoms
- Kendig's mentions that even if NTM is the cause of a patient's disease, you need to consider risks and benefits of treatment. If treatment is not done properly-->poor adherence can cause treatment emergent resistance and there can be lots of side effects from treatment
49
With which pulmonary conditions are patients at risk for NTM?
- CF
- Non-CF bronchiectasis
- Alpha 1 antitrypsin
- COPD
- Pneumococciniosis
- Various immunodeficiencies
50
ADD in questions from other site
to do
51
Does a negative serologist test for echinonoccus rule out the diagnosis?
Nope
52
Which viruses cause respiratory papillomatosis and what are long term complications?
- 6, 11 which have low oncogenic potential
- - Recurrence, this is known to occur even after surgical removal
- Distal involvement
- Dysphonia
- Chronic cough
- Stridor, OSA
- Dysphagia
53
HIV patient is seen for chronic respiratory symptoms. DDx?
- Airway: bronchiectasis, BO, asthma/airway hyper-reactivity
- Interstitial: lymphoid interstitial pneumonitis
- chronic infection - TB, NTM
- aspiration--eg. candidal esophagitis
- pulmonary hypertension
- malignancy- kaposi sarcoma, lymphoma
54
contraindications for live attenuated influenza vaccine?
- immunocompromised
- severe asthma
- pregnancy
- child receiving ASA
- defer the vaccine if there is nasal congestion, which would affect ability to delivery vaccine
(egg allergy is no longer a contraindication)
55
Intrinsic immunity features of respiratory system and most important immunoglobulin for immunity in mucous?
- Aerodynamic filtering done by the nose, including nasal turbinates, adenoids and tonsils – based on particulate size
- Respiratory mucous, airway surface liquid layer and mucociliary clearance
- Airway reflexes: eg. Sneezing, coughing and bronchoconstriction
- macrophages
Ig A. Secretory IgA is the most predominant Ig isotype present in airway secretions and important for the mucosal response. Functions include: neutralising viruses & exotoxin, enhancing lactoferrin & lactoperoxidase activities and inhibits microbial growth
56
acute complications of pulsed steroid therapy?
- CVS: BP changes - Hypotension/Hypertension, arrhythmias, circulatory collapse, cardiac arrest, sudden death, flushing
- CNS: Headaches, seizures, altered behaviour (mood alteration, hyperactivity, psychosis, disorientation), sleep disturbances
- Metabolic: Hyperglycemia, Hypokalemia
- Immune: increased risk of infections
- Anaphylactic shock (ass’d with the succinate ester of methylprednisolone)
57
Alternates to septra for PJP prophylaxis?
- penatmidine - IV or nebulized
- atovaquone
- dapsone
58
Causes of pneumonia in the following age groups:
- newborns
- 1-6 months
- 6-12 months
- 1-5 years
- older than 5 years
- overall, viruses are the most common cause of pneumonia
- Newborn: GBS, E. coli, RSV
- 1-6 months: general pneumonia bugs, unique: bordatella pertussis, Chlamydia trachomatis, ureaplasma urealyticum
- 6-12 months: general pneumonia bugs, except for atypicals
- >=1 years (interestingly, kendig's put this whole age group in this category): Strep pneumo, mycoplasma pneumonia, chlamydia pneumonia
- general pneumonia bugs: strep pneumono, haemophilus influenza, moraxella cattharalis, staph aureus
59
treatment for community acquired pneumonia?
amoxicillin 80-90 mg/kg/day x 7-10 days
60
What is the difference between abscess and necrotizing pneumonia?
- complicated pneumonia = empyema, abscess, necrotizing pneumonia
- necrotizing pneumonia = necrosis/liquefaction within lung, see areas of lucency within consolidation. (but this is not organized into an abscess, which is well demarcated)
- abscess = thick walled cavity containing puss, you will see an air fluid level
- similar organisms that cause all types of complicated pneumonia: strep pneumo, staph aureus (including MRSA), klebsiella pneumonia, pseudomonas, strep pyogenes, (nocardiac can cause lung abscess)
- for all of them, there will be a prolonged duration of antibiotics:
reatment for all Complicated Pneumonia (uptodate):
*
for complicated pneumonia: third generation cephalosporin + either clinda (communicated MRSA or anaerobes) or vancomycin for MRSA
*
Duration of treatment depends on the complication:
*
Parapneumonic effusion/empyema: I would just follow the same approach below
*
Necrotizing pneumonia: continue antibiotics for at least 2 weeks after afebrile and improving; this will generally correspond to about 4 weeks of treatment
*
Lung abscess: most resolve spontaneously by draining into the tracheobronchial tree
*
continue antibiotics for at least 2 weeks after afebrile and improving; this will generally correspond to about 4 weeks of treatment
*
If fails to improve:
*
Needle aspiration or percutaneous catheter aspiration —“if fails to improve after 72 hours of antibiotics"
*
Need to do at least 3 weeks of IV antibiotics before considering lobectomy
61
Patient with parapneumonic effusion. How do you decide if chest tube is needed or not?
- Small (<10 cm or <1/4 hemithorax)-->antibiotics, no need for chest tube insertion
- Moderate: >1/4 to <1/2 hemithorax -->management depends on extent of cardiorespiratory compromise. If not very sick, then IV antibiotics. If cardiorespiratory compromise, then follow algorithm for large effusion
- Large (>1/2 thorax): chest U/S to assess size of effusion + loculation-->drainage. If fluid is not loculated-->chest tube +/- fibrinolytic, or VATS. If fluid is loculated: chest tube + fibrinolytic or proceed directly to VATS
62
complications of lung abscess?
empyema
bronchopleural fistula
intra-cavitary hemorhage
63
Lyte's criteria?
- pleural fluid/serum protein >0.5
- pleural fluid/serum LDH >0.6
- pleural LDH >2/3 upper limit of normal serum LDH
- only need to meet 1 of these criteria for fluid to be an exudate
64
Examples of transudative and exudative pleural effusions?
- transudate: cardiac, renal, liver, SVC obstruction
- exudate: empyema, parapneumonic, chylothorax, malignancy, connective tissues and vasculitis, pancreatitis, hypothyroidism
65
When will CXR normalize in a complicated pneumonia?
Empyema:
* Normalize in 2/3 of children by 3 months post
*
Normal in 90% of children by 6 months
*
Normal in 100% of children by 18 months
- I think we can extrapolate the above to complicated pneumonia
- For non-complicated pneumonia, takes 4-6 weeks for radiographic resolution
66
Basic immunology investigations for a patient?
CBC+differential, immunoglobulins IgG, A, M, E, vaccine titres (IgG tetanus, diptheria, H. flu), IgG subclasses, flow cytometry, mitogen stimulation, HIV , neutrophil oxidative burst test
- things we don't usually send: CH50
67
Child with TB. What other infections should they be screened for?
- consider screening for HIV
68
Sputum sample being sent for TB investigations. What should it be sent for?
- mycobacterial smear, culture, Xpert MTB/Rifampin Xpert (this is a rapid PCR test to identify TB and test for rifampin resistance). it is endorsed by WHO as a first line test
69
HIV patient presenting with acute respiratory symptoms and diffuse infiltrates. Differential?
- Bacterial pneumonia, TB, mycobacteria
- Viral - RSV, paraflu, influenza, CMV
- fungal - PJP**
- acute on chronic presentation of chronic lung disease:
- interstitial pneumonia: LIP, NSIP
- malignancy: kaposi, lymphoma
- pulmonary hypertension
70
Bacterial causes of pleural effusion
- strep pneumo
- staph aureus
- strep pyogenes
- H. flu
- TB
- Pseudomonas
- Mycoplasma pneumonia
- chlamydia pneumonia
71
Approach to PBB?
- key points: chronic cough, as opposed to acute bronchitis
- antibiotic of choice is amox-clav
* Chronic wet/productive cough (>4 weeks duration) not related to an underlying disease, no specific cough pointers:
*
Trial of treatment with 2 weeks of antibiotics targeting common respiratory pathogens--H. flu, Strep pneumo, Moraxella cattharalis
*
If the cough improves after 2 weeks, then it's a diagnosis of PBB
*
If no improvement after 2 weeks, then can try an additional 2 weeks of antibiotics
*
For PBB, we can differentiate between clinically-based diagnosis versus microbiologically based (>=10^4 cfu/mL of respiratory bacteria)
*
Increased risk of chronic lung disease like bronchiectasis if the cough doesn't respond to 2-4 weeks of antibiotic treatment and would need to consider further investigations like bronchoscopy +/- CT should be done, aspiration, immunodeficiency
72
What is the most common type of pulmonary infection in HIV?
- Bacterial pneumonia
| - TB
73
Echinococcus genus (hydatid organism)-->how is it passed on? What is the treatment?
- Passed to humans by contact with eggs in feces of definitive host (eg. fox, wolf) or close contact with canine or sheep
- Treatment: surgical resection, or percutaneous drainage with treatment with albendazole, which also potentially used after treatment. For Canadian variety, may ok to just use medical treatment and not surgical
74
Post exposure prophylaxis for varicella?
Red Book algorithm
Immune or not?
Any contraindications to vaccine, which is ideally within 5 days?
If can't get vaccine, are they within 10 day time frame for VZIG?
75
What does and duration of prednisone is defined as immunosuppression?
>=2 mg/kg/day x 14 days
76
What is the evidence for high flow in bronchiolitis?
CPS statement re: evidence in general:
- Extensive neonatal literature that there is decreased need for intubation and ventilation. (They don’t go into details about specific disease conditions)
- Pediatric studies have suggested reduced need for intubation, but studies were inadequately powered to show difference in mortality or length of icu stay. (They don’t specify these pediatric conditions)
Bronchiolitis:
NEJM 2018:
- Largest RCT to date
- Infants <12 months of age requiring oxygen for bronchiolitis were randomized to either receive low flow oxygen therapy or high flow at 2 L/kg/min
- Primary outcome: therapy escalation
- Secondary outcome: various including transfer to ICU, mortality, length of stay, intubation
- Finding: children on high flow were less likely to have an escalation in therapy compared to children on low flow, but there were no differences in any of the secondary outcomes, such as transfer to ICU
- Key critiques:
- The jump from high flow to further escalation is perceived as a bigger jump than from low flow to high flow, so this could explain the differencethey try and account for the difference in RR before escalation of therapy by doing a sensitivity analysis
- The presence of an ICU on site also affected decision for escalation of therapybut they also try and account for this with sensitivity analysis
77
Radiographic signs for Echinococcus
1) Meniscus sign/crescent sign
2) Cumbo sign/onion peel (double air layer appearance/onion peel/double arch)
3) Water lily
4) serpent sign
5) cavity
6) well defined round opacity (due to uncomplicated cyst, no rupture)
4) U/S: same as CXR + honeycomb appearance, ball of wool sign, cyst wall calcification
78
3 major forms for Echinococcus
Cystic (predominant form affecting lungs)
Alveolar
Polycystic
(two major organs affected are liver and lung. In children, lung is more commonly affected)
79
Treatment for Echinococcus
U/S guided aspiration of cysts
Surgery
Drugs: Albendazole or Mebendazole
80
Mechanisms of Acute Flaccid Paralysis causing lung disease
Atelectasis
Aspiration
Hypoventilation/respiratory muscle weakness
Secondary infection
Guillam Barre = autonomic neuropathy - cardiac failure - pulmonary edema
81
Causes of Acute Flaccid Paralysis
```
Enterovirus: polio and non-polio enteroviruses, D68 (anterior horn cell)
West Nile (anterior horn cell)
Guillain Barre (axon demyelination)
Adenovirus (anterior horn cell)
Botulism (NM junction)
Tetanus (NM junction)
Spinal cord compression
```
82
What are features of an airborne isolation room?
- negative pressure ventilation
- door closed at all times
- no opening of windows
- bathroom and hygeine area for patient
- handwashing sink for healthcare staff
- exhaust of air goes to outside of the building
- air has to go through HEPA filter before going to general circulation
- healthcare workers must wear N95 and be fit tested
83
Infectious disorders that cause GBS?
Often prior infection, resulting in molecular mimicry:
- Campylobacter jejuni - most important
- Mycoplasma pneumonia
Viruses- CMV, EBV, HIV, Influenza
- post vaccination, such as influenza
84
What organisms is a patient with CGD at risk of?
recurrent infections with catalase positive bacteria or fungi
The mnemonic "cats Need PLACESS to Belch their Hairballs" can be used to memorise the catalase-positive bacteria (and Candida and Aspergillus, which are fungi): nocardia, pseudomonas, PJP, listeria, aspergillus, candida, E. coli, staphylococcus, serratia, B. cepacia and H. pylori.[52] (so some common CF bugs like Pseudomonas and Burkholderia can actually be seen in CGD patients)
85
Where are endemic fungi located in Canada?
BC: cryptococcus
Manitoba: blastomycoses
Ontario: blasto and histo
Quebec: blasto and histo
86
What sorts of infections are patient with neutropenia at risk for?
Neutropenia:
- Decreased number of neutrophils: chemotherapy induced neutropenia
- Decreased function of neutrophils: CGD, steroids
- At risk for infection with bacteria and fungi
- Chemotherapy induced neutropenia: risk of infection with own bacteria such Strep, Staph. G - like E. coli, Klebsiella, Pseudomonas and Fungi like aspergillus
- CGD: see above
87
What infections are patients with impaired humoral immunity at risk of?
- Mostly bacteria, in particular encapsulated (Strep pneumo, Neisseria, Haemophilus, GBS, salmonella) and some virus (like enterovirus)
88
What infections are patients with cell mediated immunity problems at risk of?
Intracellular pathogens:
Viruses: CMV, VZV, EBV, community viruses (eg. RSV)
Fungi: PJP, aspergillus, endemic fungi
Intracellular bacteria like nocardia
Mycobacteria
Parasites: toxoplasma gondii and strongyloides
89
Conditions needing airborne precautions?
```
Active pulmonary TB (specify that it is active and pulmonary)
VZV
Measles
SARS - severe acute respriatory syndrome
small pox
```
90
Why is diphtheria deadly?
- Airway obstruction: diphtheria makes a toxin which destroys tissue and causes membranous pharyngitis-->these membranes can extend to larynx and can cause airway obstruction OR pharyngeal membrane can get dislodged and obstruct airway
- toxin also causes:
- myocarditis/cardiomyopathy
- sepsis
- secondary pneumonia
91
If suspicious of diptheria, do you wait for laboratory confirmation before giving anti-toxin?
No.
Diphtheria antitoxin to neutralize circulating toxin (administer before lab confirmation).
· Antibiotics (penicillin or erythromycin x 14d) to eradicate the organism, stop toxin production and reduce transmission, but do not replace antitoxin.
92
Most common cause of croup (D)
Parainfluenza
