Flashcards in Module 5 Path Continued: TB Deck (41):
What is the mode of transmission in TB?
Inhalation of resp droplets
What is the most important risk factor for TB?
Who gets Primary Pulmonary TB?
Patients who get TB for the first time and are immunocompetent
stays in the lungs and forms of a granuloma
Why can primary pulmonary TB never be primary progressive TB?
Because the patients who get primary pulmonary are immunocompetent and therefore can form a granuloma
How do you form Gohns Focus?
Caseous Central Necrosis ---- Gohns Focus ( located in the lower part of the upper lobe , upper part of the lower lobe or subpleural location) ----- caseating granuloma (type IV hypersensitivity)
How do you form Gohns complex or primary complex?
Caseous necrosis is very mild, inflammation spreads to regional lymph nodes and hilar lymph nodes ---- primary complex ( Gohns focus, regional lymphatics and hilar lymph nodes)
In primary TB does the TB get contained in the lung?
Yep contained in the lung and can heal via fibrosis because collagen is laided down and you get dystrophic calcification (Therefore calcium levels are normal)
Remains dormant waiting for you to become reinfected
If you biopsy Gohn's Focus what do you see?
caseating granuloma with langhans giant cells and again these are exclusive for TB
CD4 T cells (Th1) and B cells and fibroblasts all surround granuloma
No room for PMNs because TB is chronic from day 1
Most patients are symptomatic or asymptomatic?
most about 90% are asymptomatic
What are the symptoms for primary pulmonary TB?
Coughing up blood
Usually Asian or African Immigrants
What investigations do you do if you suspected a patient has TB?
best: acid fast stain of sputum
DO NOT DO A PPD in active TB this is just a screening
can primary pulmonary TB ever become primary progressive TB?
Primary progressive becomes disseminated and miliary TB, what kind of patients can contract primary progressive TB?
First time patients who are immunocompromised and moves from the lungs to the bloodstream to everywhere else in the body
so immunocompromised patient can never get primary pulmonary TB
How does primary progressive TB present?
Multi organ failure so every organ, also can get Addison's and meningitis from this
Remember that immunocompromised patients cant form a granuloma so therefore it can not be contained in the lung and this is why it spreads and causes organ failure
If you biopsy one of these miliary foci in a patient who has primary progressive TB what do you see?
Very minimal CD4 T cells ( again because person is immunocompromised) with macrophages (containing acid fast bacilli) and no PMNS (because its chronic from the get go)
Can Primary progressive TB turn into secondary progressive TB?
Secondary pulmonary TB affects what kind of patients?
Immunocompetent patients who had primary pulmonary TB years ago and patient gets reinfected with TB and patient is still immunocompetent
Called Reinfection secondary pulmonary TB
What do you see in patients with Secondary pulmonary TB due to reinfection ?
Extensive caseous necrosis with cavitation in the APEX of the upper lobe
but again stays in the lung because patients are still immunocompetent
SO this is the only time you will see cavitations in the lung
What infections can you get from secondary pulmonary TB due to reinfection?
Aspergilloma (fungal ball)
AA amyloidosis from the chronic inflammation (therefore more dangerous then primary) liver makes SAA but its misfolded so it goes everywhere
Secondary progressive TB are seen in what kind of patients?
Patients who when initially contracted TB where immunocompetent and now for some reason the dormant bacilli bacteria has become reactivated in immunocompromised patients and becomes miliary
What do you see in secondary progressive TB due to reactivation?
Milet sized lesions (however you see these in primary progressive TB as well) -- because the immunocompromised person can not form granulomas -- no caseation/cavitation/fibrosis only extensive necrosis
What do you see on histology of patients with secondary progressive TB?
Acid fast bacili in the macrophages
What are complications of TB?
Late complication (AA amyloidosis)
Potts disease (cold abscess of the spine ruptures into paravertebral soft tissue)
Tuberculin (PPD) test measures extent of induration with an interdermal injection of tubercle protein, what is the pathogenesis of this test?
its a type IV hypersensitivity that needs CD4 T cells to come and mount a response to the injection
What are the readings for a PPD test?
>5mm: HIV, history of recent contact, chest xray with old TB scar
>10mm: IVDA, homeless, born in countries with high incidence, health care workers
>15mm: everyone else
Again this is used to screen for TB not to diagnosis
if you want to dx TB then do acid fast of sputum
What granulomas mimic that of TB?
what is the difference in granulomas of histoplasmosis and TB?
No langhans giant cells (no horseshoe appearance) in histoplasmosis
What is the etiology of histoplasmosis?
Inhalation of spores in bird and bat droppings in the ohio, appalachia, and mississippi river valley
There are three forms of histoplasmosis each card will go through the forms. 1 -->
1. Acute: Immunocompetent patients and it completely resolves
stays contained in the lungs and the PMNs take care of the fungi
patient may experience some prodromal symptoms but does spontaneously resolve
2nd form of histoplasmosis
2. Chronic: Mimics TB (fever, weight loss and cough with hemoptysis)
Immunocompetent: stays in the lungs and forms a caseating granuloma like TB in the upper lobe
on xray: multiple foci buckshot dystrophic calcification
In TB: Gohn's Focus
In histoplasmosis: multiple granulomas with buckshot
If you have a patient with a CD4 count more then 500 with fever, weight loss, night sweats and coughing blood with a chest xray of buckshot and no dissemination beyond lung, what will the biopsy show?
Caseating granuloma with central necrosis and without langhans giant cells
3rd form of histoplasmosis
3. Disseminated Immunocompromised patients
from the lung through the blood to the RES (spleen, liver, lymph node, and bone marrow)
What is the first investigation and 2nd investigation you do for Histoplasmosis?
1. Antigens in blood and urine by PCR then stain with fungal stains
2. Biopsy: budding yeast in macrophages (Increased pH to survive)
if acute you will see PMNs
What is the etiology of cat scratch disease?
Gram negative bacteria Bartonella Henselae
(Therefore action via LPS in cells wall so it can cause gram negative sepsis and septic shock and DIC)
What is the effect in patient who are immunocompetent and contract cat scratch disease?
Usually in face and upper limbs (The scratch) and its self limiting.
2 weeks -- wall off infection and suppurative granuloma in lymph nodes (type IV hypersensitivity reaction)
Present: fever, headache, malaise, tender, suppurative, warm axillary/cervical lymph nodes
Lymph node biopsy: see suppurative granuloma (PMNs and debris) -- Epitheloid cells arranged around a stellate area of necrosis composed of dead/dying PMNs
What is the effect in patient who are immunocompromised that contract cat scratch disease?
No granuloma--- disseminates ---gram negative organisms in the macrophages
Bone -- osteomyelitis and thrombocytopenia
Brain --- encephalitis
gram negative septic shock
not self limiting ppl can die
What is the etiology of Leprosy?
Inhalation of intracellular, acid fast M. Leprae
What is the tropism for leprosy?
Affects cooler areas of the body --- distal extremities, ear lobe, peripheral nerve and testes
Found within macrophages or schwann cells
There are two types of leprosy, each card will go through them. 1-->
1. Tuberculoid (Also called pauci bacilli, because they form granulomas so there are few acid fast bacilli)
---fewer skin lesions and less nerve damage because again they form granulomas ----- more commonly non caseating granulomas
more TH1 then TH2 cells
Unilateral nerve damage
2. Lepromatous (immunocompromised patients)
--more TH2 then TH1 so therefore they are unable to form granulomas
--Multi bacilli so they have symmetric nerve damage
---Lions facies and amputation of fingers (because patients cant feel fingers so continued damage and eventually the fingers fall off)
--from the fingers falling off patient are at risk for stap. aureus and septic shock (so patients die from the septic shock not the leprosy)