Midterm 2 Flashcards
1
Q
selectively toxic
A
antibiotics are selectively toxic to bacteria without being toxic to eukaryotic organisms
“magic bullet” concept
they can still have unintended side effects which are:
- age dependent
- cell development
- metabolism dependent
- allergy
2
Q
what do penicillins treat
A
narrow spectrum
only gram (+)
3
Q
what do ampicillins treat
A
they are broad spectrum
treat gram (+) and gram (-)
4
Q
isoniazid treats
A
very narrow spectrum
5
Q
bacteriostatic antibiotics
A
prevents bacterial growth -> immune response able to get rid of the pathogen
6
Q
bactericidal antibiotics
A
kill the pathogens
7
Q
how to measure antibiotic effectiveness
A
- in vitro tests for antibiotic effectiveness
- Minimal inhibitory concentration (MIC) -> uses disk diffusion assays (Kirby-bauer assay), the zone of inhibition is measured around filter-paper disks impregnated with 12 antibiotics
- Minimal bactericidal concentration (MBC) -> requires further plating to determine if any cell survived
8
Q
how to determine if an antibiotic is clinically useful
A
clinical considerations
- drugs concentration in tissue based on its half-life > MIC at all times during the treatment
- higher doses than MIC or multiple doses to keep the levels > than lab MIC
chemotherapeutic index = ratio of the toxic dose to therapeutic dose (the high the chemotherapeutic index, the safer the drug)
- therapeutic dose = minimum dose per kg of body weight that stops growth
- toxic dose = maximum dose tolerated by the pt
synergism and atagonism
- combinations of antibiotics can be synergistic or antagonistic
9
Q
minimal inhibitory concentration (MIC)
A
the lowest concentration of an antimicrobial agent that prevents visible growth go a microorganism after overnight incubation
10
Q
synergistic drugs
A
drugs that have greater effectiveness when used together
ex. aminoglycoside and vancomycin
11
Q
antagonistic drugs
A
interfere with each other and decrease effectiveness
ex, penicillin and macrolides
12
Q
empirical therapy
A
refers to the antimicrobial regimen used when a clinical diagnosis of infection has been made and delay in initiating therapy to get microbio results would be inappropriate
ex. meningitis diagnosis has been made and are waiting to see what antibiotic would be best to use, there are charts that say what abx is best to use while waiting -> cefotaxime is the most common for meningitis
13
Q
directed therapy
A
directed antimicrobial regimens are prescribed to target a specific pathogen, usually informed by the results of microbiological tests
14
Q
3 ways of classifying antibacterial agents
A
- bactericidal or bacteriostatic
- target sites
- chemical structure
15
Q
antibiotic target sites
A
metabolic inhibitors -> sulfonamides, trimethoprim, metronidazole
DNA replication inhibitors -> quinolones
RNA polymerase inhibitors
Cell wall inhibitors -> penicillins, cephalosporins, vancomycin
cell membrane damage
protein synthesis inhibitors -> macrolides (50S), clindamycin (50S), tetracyclines (30S), aminoglycosides (30S)
16
Q
cell wall inhibitors (abx)
A
abx targeting cell wall biosynthesis generally kill only growing cells
17
Q
penicillin-binding proteins
A
enzymes that produce peptide cross links in peptidoglycan
a normal part of bacterial cells -> important for cell wall synthesis
these proteins are the primary target for beta-lactam abx to kill the bacteria cell
18
Q
beta lactam antibiotics
A
penicillins, cephalosporins, carbapenems, and monobactams
inhibit bacterial cell wall synthesis
contain a beta-lactam ring in their chemical structure
19
Q
drugs that target the bacterial membrane
A
gramicidin and polymyxin
pokes holes in the bacterial cytoplasmic membrane and is an effective way to kill bacteria
20
Q
Protein synthesis inhibitors
A
Rifampin
selectively binds to bacterial RNA polymerase and prevents newly made mRNA from exiting the enzyme
21
Q
antiviral drugs
A
harder to identify viral targets that provide selective toxicity -> there are fewer antiviral agents than antibacterial agents
the spectrum of activity is linked to its molecular target
inhibiting DNA synthesis is the mode of action for many antiviral agents, although they work only for DNA viruses and retroviruses
22
Q
list of viruses
A
- influenza
- herpes simplex virus
- varicella-zoster virus
- Hepatitis B
- Hepatitis C
- cytomegalovirus
- respiratory syncytial virus
- HIV
23
Q
antiviral agents effective against HIV
A
protease inhibitors
- nelfinavir
- lopinavir
Entry inhibitors
- maraviroc
HIV treatments regimens
- HAART (highly active antiretroviral therapy) combination drug therapy, now called antiretroviral therapy (ART)
24
Q
anti fungal agents
A
there are 6 categories available
polyenes -> disrupts membrane integrity
- nystatin
- amphotericin B
azoles -> interferes with ergosterol synthesis
- triazoles
- imidazole
allylamines -> interferes with ergosterol synthesis
- terbinafine
- lamisil
echinocandins -> blocks fungal cell wall synthesis
- caspofungin
griseofulvin
flucytosine
25
aims of antiviral therapies
- blocking viral entry
- targeting viral enzymes -> inhibiting DNA synthesis
- interfering with viral replication
- vaccine development
- combination therapies
26
sample collection
sample collection is used to identify what pathogen is causing the infection
- there is risk of sequelae with some bacterial infections, its important to identify pathogen quickly
- antimicrobial susceptibility should be known before antibiotics are prescribed -> empirical abx tx is often started before lab testing is completed -> increases chance of antibiotic resistance
- is useful for epidemiological surveillance
27
sampling from sterile body sites
- blood
- CSF
- pleural fluid
- synovial fluid
- peritoneal fluid
- any tissues from internal organs
28
blood cultures
collected by venipuncture into bottles
bacterial growth induces fluorescence
29
CSF culture
is collected by a lumbar puncture (spinal tap)
direct microscopy and culture
30
pleural, synovial, and peritoneal fluid culture
collected by aspiration
- pleural fluid = thoracentesis
- synovial fluid - arthrocentesis
- peritoneal fluid = paracentesis
direct microscopy and culture
31
samples from sites with normal microbiota
samples from skin, abscess, throat, and nasopharyngeal sites
deep wound abscesses are sampled via needle aspiration
special nasopharyngeal swabs are used
32
specimens of lung contents
sputum comes from the bronchi, bronchioles, and trachea, and is the result of inflammation
a bronchoalveolar lavage can be used if pt is having trouble producing sputum
33
urine collection
normal microbiota exist in the bladder but are anaerobic and not easily cultural
skin microbiota may contaminate "clean catch" urine samples
catheterization ensures aseptic collection of samples directly from the bladder
34
diagnostic assays
lab tests performed on bodily samples to identify and measure specific biomarkers used to help diagnose conditions
35
sensitivity and specificity diagnostic tests
sensitivity = dense net, will catch all true positives, but also may misidentify some (false positives)
specificity = looser net, ensure only true positives are detected (reduced amount of false positives), but miss some true positives (false negatives) -> very accurate when positive
36
Point of care (POC) tests
sensitivity may be sacrificed for rapid results
advantages
- no culturing is required
- clinicians can immediately prescribe the right abx
- pts can avoid taking unnecessary abx
- can quickly determine a chain of infection in pts with similar symptoms
disadvantages
- no data about pathogen abx sensitivity
- increased risk of clinician becoming infected
- multiple infections may be overlooked if the initial test is positive
37
chocolate agar
contains lysed blood to support the growth of fastidious bacteria (has complex or particular nutritional requirements)
38
hektoen agar
contains lactose, peptone, bile salts, thiosulfate, iron salts, and two pH indicators
39
MALDI-TOF MS
matrix assisted laser desorption ionization - time of flight mass spectrometry (MALDI-TOF MS) os used to probe bacterial biochemistry
each pathogen has a specific protein composition that defines its own unique protein signature or fingerprint
prints out something the kind of looks like and ECG
40
polymerase chain reaction (PCR)
most widely used molecular method in the lab
DNA primers can be made for specific pathogens
- multiple sets of DNA primers can identify individual genes from a pathogen for more specific typing
useful for pathogens that are hard to grow or slow to grow
occurs in a cyclic process of denaturation, annealing, and extension -> creates multiple copies of the target DNA
41
quantitative reverse transcription - polymerase chain reaction (qRT-PCR)
is used routinely for the high-throughput diagnosis of viral pathogens such as WNV (West Nile virus)
42
enzyme-linked immunosorbent assay (ELISA)
detects antibodies or antigens
antibody capture
- add in antigen into the patient serum, if mixture turns colourful the antibody is present in the pts serum
- the rate of conversion of the substrate to coloured product is proportional to the amount of antibody present in the pts serum
antigen capture
- antibody is attached to the plate surface
- antigen from patients serum will be captured by the antibody on the plate
- enzyme-conjugated antibody is then added
- if the antigen is present, the conjugated antibody will be captured by the complex, adding substrate will yield a coloured product
43
clinical indicators of infections
fever
- temp > than 38.3 defines fever of unknown origin
- for every 1 degree increase in temp, the HR rises by 15-20 beats/min
lymphadenopathy (swollen lymph nodes)
- important to note location, size (>1cm is abnormal), tenderness, consistency, and matted nodes
- localized lymphadenopathy -> 55% head and neck, 14% inguinal, 5% axillary
skin exam
- essential for identifying specific rashes that help narrow infection diagnosis -> must do front and back
lab diagnositics
- serologic tests, antigen tests, and molecular diagnostics
- tests should complement, not replace history and physical examinations
44
lab indicators of infection
inflammatory markers
- ESR (erythrocyte sedimentation rate) -> indirect measure of inflammation, it changes slowly
- CRP -> direct measure of inflammation (changes rapidly)
elevated ESR (>100 mm/h) indicates serious underlying disease
pathogen-specific testing
- sample collection
- culture
- serology/ antigen testing/ PCR
- radiology
45
anatomy of the skin
epidermis - superficial layer (has 5 layers)
-> stratum corneum, stratum lucidum, startum granulosum, stratum spinosum, stratum basale(deepest layer)
-> langerhans cells
-> basal cells
-> melanocytes
-> dead keratinocytes
dermis - deep layer
-> connective tissue
-> cells
-> blood vessels, nerves, hair follicles, sweat glands
46
skin rash
change in colour and texture of the skin
can be caused by a reaction to a toxin produced by
- a pathogen
- damage to the skin by the pathogen
- an immune response
47
exanthem rash
widespread skin rash accompanied by systemic symptoms
fever, malaise, headache
48
enanthem rash
rash on mucous membranes
49
viral infections of the skin
measles
German measles (rubella)
fifth disease (erythema infectiosum)
roseola
chickenpox
shingles
cold sores
warts
small pox
hand, foot, and mouth disease
produces rashes and warts, often blotchy red spots
are cytolytic and cytoproliferative
50
bacterial infections of the skin
folliculitis, furuncle, carbuncle
scalded skin syndrome
necrotizing fasciitis
erysipelas
cellulitis
acne
cytolytic -> produce toxins
forms rash and pus formations, necrotizing
51
fungal infections of the skin
dermatophytosis
tinea versicolor
candidiasis
causes rashes and desquamative (flaky skin)
52
macular
aka erythematous
flat! and red
<1cm in diameter
53
papular
small, solid, and elevated
<1cm in diameter
54
maculopapular
a papule that is reddened
55
pustular
a skin lesion filled with pus
56
vesicular
small blisters are formed
57
bulla
a large fluid filled blister, >1cm
58
nodule
a solid, raised lesion, typically round, may be red
>1cm
59
petechial rash
small pinpoint red or purple spots
due to broken capillaries
60
purpuric rash
larger purple of red areas of skin
more extensive spots than petechial rashes
61
classifications for bacterial infections of skin and soft tissue
- primary pyodermas
- infections associated with underlying conditions of the skin
- necrotizing infections
62
pyodermas
a group of superficial bacterial skin infections -> commonly caused by staphylococcus aureus or streptococcus species
folliculitis
furunculosis
carbuncle
impetigo
erysipelas
cellulitis
necrotizing fasciitis
myonecrosis
63
staphylococcal scalded skin syndrome
aka SSSS
in neonates is caused by a toxin (exfoliatin) from S. aureus disrupting skin desmosomes (structure where cells are attached)
64
staphylococcal toxic shock syndrome
caused by S. aureus
65
is staphylococcus epidermis coagulase + or -
it is coagulase negative, meaning it doesn't
produce coagulase
66
staphylococcus aureus coagulase + or -
is is coagulase positive, meaning it produces the enzyme coagulase which causes blood plasma to clot
67
staphylococci
is a normal inhabitant of the nares
can infect a cute and gain access to the dermis via a hair follicle
68
folliculitis
staphylococcal skin infection -> S.aureus infection of hair follicles can be superficial or deep
pathogenesis:
folliculitis is a minor infection of a hair follicle -> furuncle (boil), boils may rupture and drain pus -> carbuncle (large located abscess), particularly in diabetics
diagnosis
clinical diagnosis
treatment
- resolve on their own
- topical abx (mupirocin or fusidic acid)
- abx and drainage
- oral cephalexin or cloxacillin (7-10 days) -> these are first-line empirical therapies for community-acquired SSTIs
69
MRSA abx
vancomycin is the treatment of choice
70
impetigo
a superficial infection of the skin
etiology = S. aureus or group A beta-haemolytic streptococci (sometimes both)
epidemiology = principally associated with childhood
there are two main types of impetigo
- nonbullous: starts as a superficial bump -> papule and vesicle -> pustules on erythematous skin -> fluid from the pustules leaks out as they break open (fluid is a honey colour)
- bullous -> vesicles grow larger and become bullae that are full of clear yellow fluid
clinical features
- honey coloured crusted lesions develop mainly on face around nose and spread by auto inoculation
lab diagnosis
-> culture of swabs of lesions
tx
-> topical treatment often sufficient (mupirocin)
71
streptococcus pyogenes
the human nasopharynx and parts of the skin are the natural reservoir for S. pyogenes
has several virulence factors:
- has exotoxins -> streptococcal pyogenic exotoxins (SPEs): they are super antigens, massive amounts = high levels of inflammation = shock
-SPEs are associated with scarlet fever, streptococcal toxic shock syndrome, and necrotizing fasciitis
-hemolysin -> lyses RBCs, these streptococci are sub classified into groups A-O according to cell wall antigens
72
acne vulgaris
etiology = propionibacterium acnes
results from keratin blocked hair -> sebaceous follicles or pores called comedones -> can be open (blackheads) or closed (whiteheads)
factors that contribute to acne development
- genetic predisposition
- hormones
- gram positive bacterium -> propionibacterium acnes -organism uses the triglycerides in sebum as nutrients
tx of severe cases is tetracycline combined with topical antiseptics
73
erysipelas
- caused by S. pyogenes
- acute infection
small erythematous patch -> fiery-red shiny plaque
involves super layer of the dermis, then spreads to the superficial lymphatics
swollen lymph nodes, fever, systemic symptoms
erysipelas rash
- may appear on the face but is most commonly seen on the lower extremities
lab diagnosis
- blood cultures and skin aspirates may be positive in approximately 25% of pts
tx
- benzylpenicillin or macrolide (erythromycin or clarithromycin) or clindamycin
74
cellulitis
most frequently caused by S. pyogenes, but can be caused by a number of other bacterial species
uncomplicated, non-necrotizing inflammation of the dermis
characterized by localized pain, swelling, tenderness, erythema with a poorly defined edge**, and warmth
develops slowly and involves deeper levels of the dermis including subcutaneous fat and connective tissue
often a complication of a wound infection
75
ALT-70
used to help diagnosis cellulitis
predicts cellulitis over other conditions
76
necrotizing fasciitis
flesh eating disease
type 1 = polymicrobial
type 2 = one microorganisms, usually S. pyogenes and sometime S. aureus
other organisms that can cause necrotizing fasciitis include clostridium perfringens (soil) and vibrio vulnificus (immunocompromised)
pathogenesis - bacteria penetrates the skin -> produce enzymes and toxins -> local subcutaneous tissue destruction and systemic toxicity
clinical features - rapidly spreading cellulitis with necrosis, fever, systemic toxicity, hypotension, and shock -> high mortality
tx
- rapid and aggressive surgical removal of the affected tissue (debridement)
abx
- clindamycin, metronidazole, and gentamicin
77
LRINEC
scale test for diagnosing necrotizing soft tissue infections
incorporates data present at admission
- CRP
- WBC count
- hemoglobin
- serum sodium
- serum creatinine
- serum glucose
score greater than of equal to 6 is associated with a high risk of necrotizing infection
high score = surgery
lower score = treat with abx
78
gangrene
dry gangrene occurs when blood supply to tissue is cut off
wet gangrene occurs due to an infection
localized necrosis (tissue death)
- can effect an internal or external part of the body
- anaerobic infections affecting the genital area (Fournier's gangrene) and infections caused by clostridium species can produce large amounts of gas
cause by clostridium perfringens -> highly fermentative, it is a true saprophyte
C. perfringens -> enzymes and exotoxins -> rapid spread -> hemolysis -> gas gangrene or myonecrosis -> septic shock
clinical features
- cellulitis with necrotic areas
- bullae with foul smelling drainage and gas gangrene
- tissue crepitus due to gas production, fever, and toxemias evolve as myositis develops
79
how fungal infections of the skin are diagnosed
- clinical appearance
- microscopic examination of potassium hydroxide (KOH) preparations of skin flakes or hair -> the KOH destroys the skin cells but no the wall of mycelia or spores and they can be seen under a light microscope
fungi can also be cultured on a special selective medium called sabouraud agar
80
dermatophytes
cause fungal skin infections
love cool/warm, moist, keratinized tissues -> skin, hair, nails
epidermophyton, trichophyton, and microsporum cause the majority of infections
81
names of fungal skin infections
tinea capitis = scalp -> primarily in small children
tinea corporis = body -> ringworm ring shaped itching lesions -> ring expands as the fungus grows outward
tinea cruris = groin/jock itch
tinea pedis = foot
tinea unguium = nails
82
tinea versicolor
long term infection of the skin
prevalent mostly in warm, moist climates
caused by a yeast of the genus Malassezia -> not a dermatophyte
pathogenesis:
round yeast converts to hyphal form -> invades stratum corneum
lesions of tinea versicolor are small with a sharp border and hypo pigmented skin
83
upper respiratory tract infections
- rhinitis
- sinusitis (rhino sinusitis)
- pharyngitis (with or without tonsillitis)
- otitis
- laryngitis
- epiglottitis
84
lower respiratory tract infections
- croup (laryngotracheobranchitis)
- bronchitis/bronchiolitis
- pneumonia
- TB
85
requirements for upper RT infections
self-limited irritation and swelling of the upper airways with associated cough with no proof of pneumonia, lacking a separate co edition to account for the pt symptoms, or with no hx of COPD/ emphysema/ chronic bronchitis
involves the nose, sinuses, middle ear, pharynx, and larynx
86
acute otitis media (AOM)
50% caused by respiratory viruses
these are the common bacterial causes:
streptococcus pneumoniae
H. influenzae
moraxella catarrhails
group A beta-hemolytic streptococci
S. aureus
acute inflammation of the middle ear cause be infection
impaired drainage of middle ear fluid -> predispose to viral or bacterial infection -> may result in edema and blockage of the Eustachian tube -> fluid/pus collection and pain
most infections of self-limiting but abx such as amoxicillin or erythromycin my be required
87
acute infectious rhinitis/sinusitis
usually caused by viral rather than bacterial agents
common causes:
- the common cold virus group -> rhinoviruses, adenoviruses, coronaviruses, parainfluenza virus, RSV
- influenza virus
cardinal symptoms (10 days or longer)
- clear to mucopurulent nasal discharge
- nasal obstruction/ congestion
- headache (facial pressure)
other symtoms
- gradual
- runny nose
- sneezing
- fever, malaise, fatigue, general aches (not very common)
S+S > 10 days with no improvement = bacterial
tx
- amoxicillin and clavulanate + intranasal corticosteroids
88
secondary bacterial infection
persistent facial pain, edema, purulent drainage, and fevers
89
influenza etiology
incubation period 1 to 4 days, and symptoms usually resolve in 7 to 10 days
influenza viruses A,B, C
influenza A is divided into subtypes based on envelope glycoproteins
90
pharyngitis
inflammation of the mucous membranes on the oropharynx (medical term for sore throat)
it is infectious
bacterial or viral (more commonly viral)
viral:
- transmission is by aerosol and direct contact
bacterial:
- approximately 5-10% of the population carries streptococcus pyogenes in the pharynx
most cases of pharyngitis occur in children under 5
91
pharyngitis etiology
50-80% of pharyngitis (sore throat) is viral in origin
- predominantly rhinovirus, influenza, adenovirus, coronavirus, parainfluenza
more severe cases tend to be bacterial and may develop after an initial viral infection
most common bacterial infection is group A beta-hemolytic streptococci (5-36%)
92
cold vs flu
Cold
- gradual symptom onset
- fever is rare
- slight aches
- uncommon to have chills
flu
- symptoms are abrupt
- fever is usual
- aches is usual
- chills is fairly common
93
influenza complications from untreated viral pharyngitis
influenza is viral
respiratory
- viral pneumonia
- secondary bacterial pneumonia
- otitis media
- sinusitis
muscular
- rhabdomyolysis
- myositis
neuro
- encephalitis
- meningitis
- transverse myelitis
- Guillain-barre syndrome
94
clinical manifestations of pharyngitis
viral
- flu-cold like symptoms
- erythema associated with pharyngitis
- odynophagia (painful swallowing)
- low fever <38
- concurrent conjunctivitis
bacterial
- sore throat and odynophagia
- high fever >38
- tonsillar exudates
- painful cervical adenopathy
- pharyngeal erythema
- ear pain
- no cough of flu like symptoms
95
complications of untreated bacterial pharyngitis
peritonsillar abscesses
scarlet fever
rheumatic fever
acute glomerulonephritis
96
evaluating for pharyngitis
WBC counts = not useful for etiology differentiation
nasopharyngeal swabs for rapid antigen detection or RT-PCR (influenza gold standard) -> if negative it is likely the common cold
rapid antigen detection tests (RADT) is specific for group A beta-hemolytic streptococci
-> positive = tx should be initiated
-> negative = throat culture should be obtained and should guide tx
lymphocytosis (>50%) = suggest infectious mononucleosis
97
streptococcal sequelae
caused by the immune response to the bacteria
antibodies cross-react with host cells in an autoimmune reactions -> can cause serious sequelae like:
acute rheumatic fever
- high fever
- damage to heart, joints, skin, nervous system
- common in 4-9 years old (2-3 weeks after initial infection)
glomerulonephritis
- hematuria and proteinuria
- high BP
98
treatment for pharyngitis
hydration therapy is crucial
bacterial
- 6-10 day course of oral amoxicillin (eradication of bacterial carriage and prevents rheumatic fever)
- if adherence is a problem -> single IM dose of penicillin G
- corticosteroids not recommended
- oral cephalosporins, clarithromycin, and clindamycin can be used if hypersensitive to amoxicillin
viral
- if influenza -> antiviral therapy within 48 hours of symptoms onset reduces risk of complicatiosn
- oseltamivir or zanamivir
- amantadine?
- vaccination is the most effective method of preventing influenza
99
pneumonia
infection of the lung tissue
inhalation, aspiration, and hematogenous spread are the 3 main ways that bacteria reach the lungs
its a serious infection in which air sacs fill with pus and other liquid
100
community acquired pneumonia
non-hospitalized or > 48 hrs after hospitalization
most common
101
hospital acquired pneumonia
it presents clinically <48 hours after hospitalization
102
ventilator associated pneumonia
is presents > 48 hours after endotracheal intubation
most common in ICU
103
aspiration pneumonia
results from aspiration of colonized upper RT secretions
most common in IV drug users, pathogens come from the oral cavity, throat or GI tract)
104
pneumonia risk factors
impaired lung defences
- poor cough/gag reflex
- impaired mucociliarly transport
- immunosuppression
increased risk of aspirations
- impaired swallowing
105
pneumonia prediction scales
PSI
CURB-65
IDSA-ATS (ICU admission)
105
pneumonia clinical presentation
- cough +or - sputum,
- pleuritic chest pain
- dyspnea
- tachypnea
- tachycardia
elderly often present atypically -> altered LOC is sometimes only sign
evidence of lung consolidation -> dullness to percussion and/or crackles
106
pneumonia lab tests and investigations
- pulse oximetry (resp distress)
- CXR + or - CT -> shows distribution (lobar consolidation or interstitial pattern)
- CBC and differential, electrolytes, urea, Cr, ABG (if in resp distress), troponin/CK, LFT, urinalysis
- sputum gram stain and culture, blood C&S
107
atypical pneumonia
- influenza type A and B
- covid 19
- RSV
- rhinovirus
- adenovirus
diagnosis
- clinical findings overlap overall with typical pneumonia and it is challenging to identify without lab confirmation
-> RT-PCR
-> bilateral mulitlobular ground-glass opacities and interstitial inflammation
108
treatment for pneumonia
neuraminidase inhibitors (oseltamivir) or endonuclease inhibitor (baloxavir marboxil) for influenza
corticosteroids
supportive care
109
blood tests for pneumonia
- Would test for troponin, CRP, ESR, proca
- PMN → Immature neutrophils (shift to left, increase in bands)
- Viral infections can decrease lymphocytes
110
pulmonary tuberculosis
infection by the bacillus M. tuberculosis
one third of the world's population is infected with M. tuberculosis
the increase in incidence is related to poverty, population displacement, HIV, and drug resistance
111
pulmonary tuberculosis etiology
grows slowly = culture could start to appear after 1 -12 weeks
infections are spread usually by inhalation of "droplet nuclei" -> rarely by ingestion
incubation period is 4 - 16 weeks
112
TB clinical features
when active
- chronic cough
- hemoptysis
- weight loss
- malaise
- night swear
113
Lab diagnosis for TB
acid-fast (ZN) stain or fluorescent rhodamine-auramine die
culture on special media for up to 12 weeks
114
treatment for TB
combinations of up to 4 anti-mycobacterial drugs
initial phase for 2 months
- isoniazid
- rifampicin
- pyrazinamide
- ethambutol
continuous phase
- 4 months of rifampicin and isoniazid
115
primary TB
the initial infection of TB
often asymptomatic and localized
116
secondary TB
reactivation of TB
typically more severe and affects upper lobes of the lungs
117
lymphadenopathy
swelling of lymph nodes
118
lymphadenitis
inflammation of lymph nodes
119
lymphangitis
inflammation of the lymph vessels
120
systemic viral infections
infectious mononucleosis
burkitts lymphoma
cytomegalovirus infections
dengue fever
121
systemic bacterial infections
SIRS
bacteremia
sepsis
septicemia
septic shock
plague
Lyme disease
Rocky Mountain spotted fever
122
bacterial infections of the heart
subacute bacterial endocarditis
infectious endocarditis
acute bacterial endocarditis
prosthetic valve endocarditis
123
systemic inflammatory response syndrome (SIRS)
medical emergency characterized by rapid heart rate, breathing rate, and abnormal WBC count
124
