Module 5 Path Continued: TB

Question 1

What is the mode of transmission in TB?

Answer 1

Inhalation of resp droplets

Question 2

What is the most important risk factor for TB?

Answer 2

HIV

Question 3

Who gets Primary Pulmonary TB?

Answer 3

Patients who get TB for the first time and are immunocompetent
stays in the lungs and forms of a granuloma

Question 4

Why can primary pulmonary TB never be primary progressive TB?

Answer 4

Because the patients who get primary pulmonary are immunocompetent and therefore can form a granuloma

Question 5

How do you form Gohns Focus?

Answer 5

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)

Question 6

How do you form Gohns complex or primary complex?

Answer 6

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)

Question 7

In primary TB does the TB get contained in the lung?

Answer 7

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

Question 8

If you biopsy Gohn’s Focus what do you see?

Answer 8

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

Question 9

Most patients are symptomatic or asymptomatic?

Answer 9

most about 90% are asymptomatic

Question 10

What are the symptoms for primary pulmonary TB?

Answer 10

Fever 
Weight Loss
 Night Sweats 
Coughing up blood 
Usually Asian or African Immigrants

Question 11

What investigations do you do if you suspected a patient has TB?

Answer 11

First: x-ray
best: acid fast stain of sputum
DO NOT DO A PPD in active TB this is just a screening

Question 12

can primary pulmonary TB ever become primary progressive TB?

Answer 12

Nope

Question 13

Primary progressive becomes disseminated and miliary TB, what kind of patients can contract primary progressive TB?

Answer 13

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

Question 14

How does primary progressive TB present?

Answer 14

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

Question 15

If you biopsy one of these miliary foci in a patient who has primary progressive TB what do you see?

Answer 15

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)

Question 16

Can Primary progressive TB turn into secondary progressive TB?

Answer 16

NOPE never

Question 17

Secondary pulmonary TB affects what kind of patients?

Answer 17

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

Question 18

What do you see in patients with Secondary pulmonary TB due to reinfection ?

Answer 18

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

Question 19

What infections can you get from secondary pulmonary TB due to reinfection?

Answer 19

Aspergilloma (fungal ball)
AA amyloidosis from the chronic inflammation (therefore more dangerous then primary) liver makes SAA but its misfolded so it goes everywhere

Question 20

Secondary progressive TB are seen in what kind of patients?

Answer 20

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

Question 21

What do you see in secondary progressive TB due to reactivation?

Answer 21

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

Question 22

What do you see on histology of patients with secondary progressive TB?

Answer 22

Acid fast bacili in the macrophages

Question 23

What are complications of TB?

Answer 23

Pneumonia 
Lung Abscess
Empysema 
Pleural thickening 
Aspergilloma 
Late complication (AA amyloidosis) 
Potts disease (cold abscess of the spine ruptures into paravertebral soft tissue)

Question 24

Tuberculin (PPD) test measures extent of induration with an interdermal injection of tubercle protein, what is the pathogenesis of this test?

Answer 24

its a type IV hypersensitivity that needs CD4 T cells to come and mount a response to the injection

Question 25

What are the readings for a PPD test?

Answer 25

> 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

Question 26

What granulomas mimic that of TB?

Answer 26

Histoplasmosis

Question 27

what is the difference in granulomas of histoplasmosis and TB?

Answer 27

No langhans giant cells (no horseshoe appearance) in histoplasmosis

Question 28

What is the etiology of histoplasmosis?

Answer 28

Inhalation of spores in bird and bat droppings in the ohio, appalachia, and mississippi river valley

Question 29

There are three forms of histoplasmosis each card will go through the forms. 1 –>

Answer 29

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

Question 30

2nd form of histoplasmosis

Answer 30

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

Question 31

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?

Answer 31

Caseating granuloma with central necrosis and without langhans giant cells

Question 32

3rd form of histoplasmosis

Answer 32

3. Disseminated Immunocompromised patients

from the lung through the blood to the RES (spleen, liver, lymph node, and bone marrow)

Question 33

What is the first investigation and 2nd investigation you do for Histoplasmosis?

Answer 33

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

Question 34

What is the etiology of cat scratch disease?

Answer 34

Gram negative bacteria Bartonella Henselae

Therefore action via LPS in cells wall so it can cause gram negative sepsis and septic shock and DIC

Question 35

What is the effect in patient who are immunocompetent and contract cat scratch disease?

Answer 35

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

Question 36

What is the effect in patient who are immunocompromised that contract cat scratch disease?

Answer 36

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

Question 37

What is the etiology of Leprosy?

Answer 37

Inhalation of intracellular, acid fast M. Leprae

Question 38

What is the tropism for leprosy?

Answer 38

Affects cooler areas of the body — distal extremities, ear lobe, peripheral nerve and testes
Found within macrophages or schwann cells

Question 39

There are two types of leprosy, each card will go through them. 1–>

Answer 39

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
   Immunocompetent patients

Question 40

2 –>

Answer 40

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)

Question 41

On a biopsy of the skin or nerve what would you see for Tuberculoid and lepromatous?

Answer 41

Tuberculoid: non caseating granuloma
Lepromatous: more skin lesions, no granuloma, Virchow cells/foamy cells/lepra cells (all activated macrophages containing organism + lipid)