Pneumonia Flashcards
What are the general clinical symptoms of pulmonary infection?
- organisms leak into blood therefore fever and chills
- yellow green sputum (plus) OO are rusty bloody sputum (blood)
- tachypnoea and pleuritic chest pain (breath in leading to stretching of the pleura leading to stress on pleura due to bradykinin and PGe2
4.D creased breath sounds and dullness at percussion. The lung is like a drum I.E.it is full of air.
If replace the air with exudate from inflammation You get decreased breath sounds and dullness to percussion
- Increased white blood cell count due to infection
In pneumonia Which Normal defences are impaired?
Cough reflex, mucociliary escalator, mucus plugging
What are the three types of pneumonia ?
Lobar – Intra-alveolar exudate leading to consolidation of an entire lobe/lobes
Bronchopneumonia – Ai infiltrates from bronchioles/small airways ––> adjacent alveoli. CXR patchy consolidation/distribution
Interstitial atypical pneumonia– inflammation @ interstitial areas of alveolar walls - involves more than one lobe = diffuse + patchy + No consolidation
What organisms cause lobar pneumonia ?
Strep pneumonia >klebsiella
What does strep pneumonia cause ?
What’s the toxin and what does it do ?
PROMS
Pneumonia LOBAR, rusty sputum, otitis media, meningitis, sinusitis
PneumoLysin toxin – – >poreforming Cell membrane
What Problems is strep pneumonia associated with?
Plasmid
Pneumonia LOBAR, chronic Liver disease, asplenia, sickle-cell disease and sepsis, mucus trapping, Ig deficient + IgA protease, diabetes
In strep pneumonia What happens as a result of asplenia?
You get decreased tuftsin and therefore decreased phagocytosis therefore an increased risk of infection
Who gets klebsiella?
Alcoholics, diabetics, old people
They aspirate intestinal flora – – >lobar pneumonia – – >abscess in the lung liver,
red current jelly sputum,
UTI I know is nosocomial,
Mucoid colonies of increased polysaccharide
What are the four phases of Lobar pneumonia?
- CONGESTION infection – – >dilates blood vessels – – >increased blood – – oedema – – >congestion
- RED HEPATIZATIONInfection – >exudate = neutrophils and blood (hence red) – >fill Alveolar space – >normal spongy lung – >solid consistency (red hepatisation)
- GREY HEPATIZATIONRed blood cell – >Breakdown – >grey hepatisation
- RESOLUTION = healing by regenerating tissue = type your new website type 22 site
What organisms cause Bronchopneumonia?
Staff aureus, haemophilus influenza, pseudomonas Aeruginosa, Moraxella Catarrhalis, legionella
What are the six toxins of staph aureus?
- Eg tampon: SUPER AG toxic shock syndrome toxin – 1: brings MHC two and T cell receptor closer outside of the antigen binding site – > Cause overwhelming release of IFN-gamma And ILL2 – >toxic shock syndrome =shock organ failure desquamation, fever vomiting rash - SOD FeVoR
- PVOL toxin Forms pore @ lung – >Haemorrhagic pneumonia & cause neutrophil apoptosis –>No phagocytosis – >necrotising fasciitis
3.alpha Haemolysin – >at low conc: Exchanges monovalent irons across the cell membrane ->apoptosis
AlphaHrmolysin @ high conc – >binds to lipid membranes – >necrosis
- Exfoliative toxins – >damages cadherins at desmosomes – >scalded skin syndrome
- enterotoxin = heat stable – >food poisoning cos not destroyed by cooking
- Prot A + FcIgG – >Decreased compliment fixing – >decreased opsonisation – >Decreased phagocytosis – >increased colonisation at the nose
What inflammatory diseases are staff aureus associated with ?
E soap
Endocarditis, Skin infections, Osteomyelitis,
Abscess @organ( forms fibrin clot around itself) = empyema + pus @ Pleural space,
bronchoPneumonia (secondary to influenza virus)
How is haemophilus influenza spread?
Aerosol droplets & respiratory secretions – >Pillie adhered to the respiratory tract – >
- Nontypeable strain + Protease IgA – > Mucosal infections E.g. bronchitis otitis media and conjunctivitis
- Type B = MOST invasive disease
H\_\_ Arthritis Epiglottitis Meningitis Otitis media Pneumonia Bronco H\_\_ I\_\_ Lung disease = chronic Sellulitis
How is pseudomonas Aeruginosa spread?
Pseudomonas Aeruginosa produces procyanin in which is a blue green pigment that has a grape like odour
Pseudomonas – >Burns, ulcers, CF/bronchiectasis, catheters biofilm – >
- @ CFLong overproduces Alignate which converts pseudomonas to mucoid pseudomonas – >increase protection to bacteria due to biofilm
- Protease IgA – >fuck mucosal surfaces
- Elastase breaks through tissue
- Exotoxin A – >inactivates elongation factor two – >decrease protein synthesis
- Rhamnolipid – >Decrease first defence
ECTHYMA GANGRNOSUM HOT TUB FOLLICULITIS
Bronco pneumonia, sepsis, external otitis, UTLA, drugs, osteomyelitis
How is Legionella spread?
Contaminated aerosolised water (20 to 45°C)
Heating systems, watercooled air-conditioning plants, water tanks/pools
– – >Legionella adheres to human respiratory epithelium via pilli + grows inside a phagocytic cells therefore Fucks mechanism
– – >Are Pontiac fever + bronchopneumonia + fever
GI issues, CMS issues (meningeal and cephalitis)
What organisms cause interstitial/atypical pneumonia?
MR ICCC
Mycoplasma pneumonia, respiratory sync your virus, influenza virus, Chlamydia pnemoniae/psittaci, Coxiella, CMV
What does Mycoplasma pneumonia cause?
@barracks +prison - Increased IgM cold agglutinins = lyses RBC – >Anaemia, headache, non-productive cough
M for MMMMMMYCO!! IgMMMMMM!!!!!
What does with the respiratory Synctial virus do?
Via F protein – >atypical pneumonia + acute otitis media
What does CMV spread?
SSUTT
Congenital – >saliva, sex, your name, transfusion, transplant (Immunosuppressants)
Pneumonia, owl inclusions, retinitis
If patient get CMV after a transplant or has an immunosuppressive problem of some sort What other infections can the patient get?
Pneumocystis Jerovici and Aspergillus
How does one get pneumocystis Jerovici?
Inhale – >pneumocystis jerovici – >pneumocystis ATYPICAL pneumonia – >
- asymptomatic
- pneumonia
- immunosuppressive – >Disease
How does influenza cause pneumonia ?
Haemagglutinatin binds to RBCs and URT cells – >Host cell proteases cleaves haemoagglutinin – >HA1 + HA2 – >HA activate Fusion– >Virus binds to cell
Neuraminidase breaks down Neuraminic acid @ mucin
Get fever, Cough, Runny nose, arthralgia, Myalgia
In kids that use aspirin get Reyes syndrome so they get liver + brain disease
@Elderly and immunocompromised flu virus weakens defence – >2nd dairy Bacterial pneumonia
What does Coxiella Burnetti cause ?
Q-fever: tick SHIT + cattle placenta – >release spores – >inhale – >atypical pneumonia
Q fever = queer because no rash/fever
What factors increase the likelihood of TB?
Poverty, HIV, drug resistance
What’s are TBs virulence factors?
Cord factor: inhibits macrophage maturation + induce TNF Alpha ( cachectin) = Weight loss
Sulfatides = inhibit phagolysosomal fusion
Explain primary tuberculosis?
Infection with TV – >nonimmune host = Child – >primary TB – >acute inflammatory reaction @long parenchyma – >mycobacterium TB = intracellular pathogen thereforemultiply in macrophage – >macrophage carried to HILAR NODES + GHON FOCUS @ midzone LUNG = GHON complex = Caseating necrosis
– >Form Caseating granuloma – >
Healed by fibrosis + calcification– >
– Defence barrier built around infection NOT killed = Latent TB equals not ill/infectious
– Immunity and HSR4 – >positive PPD tuberculin tests
@HIV, malnutrition = Death
Severe bacteraemia – >miliary tuberculosis equals disease spread – >death
Preallergic lymphatic/haematogenous dissemination – >dormant tubercle bacilli @several organs – >reactivation in adult life
Explain secondary TB?
Infection with TB because of dormant mycobacterium = reactivates due to partially immune hypersensitised host – >
Secondary TB = poor lymph drainage and high oxygen tension at the apex low = fibrocaseous necrosis – >Reactivation of TB in the Lung – >Extrapulmonary TB = Pleural effusion, tuberculous empyema
@Lymph: cervical lymphadenitis
@GU: Haematuria, sterile pyuria
@CNS: Parenchymal tuberculomas/meningitis at brain base
@bones: veritable lumbar spine equals pott disease
@GI: pain and ascites
What are the symptoms of TB?
Fever, night sweats, weight loss, haemoptysis
Explain secondary TB?
Infection with TB because of dormant mycobacterium = reactivates due to partially immune hypersensitised host – >
Secondary TB = poor lymph drainage and high oxygen tension at the apex low = fibrocaseous necrosis – >Reactivation of TB in the Lung – >Extrapulmonary TB = Pleural effusion, tuberculous empyema
@Lymph: cervical lymphadenitis
@GU: Haematuria, sterile pyuria
@CNS: Parenchymal tuberculomas/meningitis at brain base
@bones: veritable lumbar spine equals pott disease
@GI: pain and ascites
What are the symptoms of TB?
Fever, night sweats, weight loss, haemoptysis
What can Mycobacterium kansasii cause ?
Pulmonary TB-like symptoms:
- Disseminated disease at sign immunocompromised
- Upper lung cavitary disease similar to TB
What does mycobacterium Avium – intracellulare cause?
Disseminated non-TB disease @AIDS
Lymphadenitis, weight loss, fever, hepatitis, diarrhoea, bronchiectatic disease,
upper lung cavitary disease,
mid/lower lung Nodular
Treatment for TB?
1st 2 months Rifampicin, isoniazid, pyrazinamide, Ethanbutol
4months: rifampicin and isoniazid
Where is aspiration pneumonia classically seen?
What’s organisms are involved and what type?
Necrotising anaerobic bacteria + oropharynx:
Bacteroids, Fusobacterium, Peptococcus
What other risk factors for lung abscesses?
Bronchial obstruction e.g. cancer
Loss of consciousness
Alcoholism
Dental work
Aspirate oropharyngeal material – >strep/staph, Prevotella, Fusobacterium– >
Lung abscess @ right-sided usually– >
Fever cough = foul-smelling sputum
(Obstructive Lung Neoplasia) +
(Infective endocarditis – >septic embolus)
– >Lung abscess
