TB Flashcards

(34 cards)

1
Q

what feature of TB bacteria make them resistant to enzymes released by macrophages after phagocytosis

A

thick waxy cell wall

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2
Q

what is latent TB

A

tb more likely tobe spread in over crowded living conditions
when someone is infected with TB but develops immunity &
doesnt develop the disease
-they have TB bacteria which do not multiply
-they arent unwell and show no symptoms
-they cannot pass the disease onto others

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3
Q

active TB

A

-has bacteria which can actively multiply
-will be sick, show symptoms and can pass it onto others

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4
Q

3 weeks into primary TB, what happens

A

cell mediated immunity begins

immune cells surround site of infection and from a GRANULOMA

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5
Q

granuloma

A

attempt to wall off foreign substances like pathogens so they cant spread

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6
Q

what happens to tissue inside granuloma as a result of it

A

dies, caseous necrosis

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7
Q

what is the area of dead tissue called

A

ghon focus

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8
Q

ghon complex

A

TB reaches hilar lymph nodes by extension of ghon focus or through lymph and causes caseation there aswell

caseating tissue along with lymph node=ghon complex

usually in lower lobes of the lungs

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9
Q

what happens next to tissue encapsulated by granuloma

A

undergoes fibrosis & calcifies

this produces scar tissue that can be seen via x-rays

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10
Q

ranke complex

A

calcified ghon complex

in some cases the TB micro bacteria are killed by the immune system & dont come back

in other cases the bacteria are still viable just walled off, if the hosts immune system becomes compromised the ghon focus can become reactivated & infection can be spread to either one or both upper lobes of the lungs
(upper lobes where oxygen levels are the greatest, better for TB)

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11
Q

what happens if TB reactivates and spreads

A

memory cells recognise tb and release cytokines to control new outbreak, but this causes more caseous necrosis which form cavities this time allowing the bacteria to disseminate or spread through airways or lymphatic channels to other areas of the lungs

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12
Q

systemic miliary TB

A

Cavities in new areas of caseous necrosis after cytokines released can allow TB to spread to other areas of the lungs causing bronchopnemonia or spread via the vascular system infecting nearly every other tissue in the body

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13
Q

kidneys

A

lots of white blood cells in kidneys can lead to a high conc in urine

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14
Q

meninges of brain

A

can lead to meningitis

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15
Q

lumbar vertebrae

A

potts disease

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16
Q

adrenal gland

A

addisons disease

adrenal glands dont produce enough hormones like cortisol and aldosterone, fatigue, skin darkening

17
Q

liver

A

hepatitis

can lead to cirrhosis orcancer

18
Q

cervical lymph nodes

A

lymphadentitis in the neck

19
Q

testing for TB

A

-PPD skin test
-tuberculin (part of TB bacteria) injected into skin, if person has already been exposed to TB their immune system will react & produce a small localised infection within 48-72 hours

test positive if theres a large enough area of inflammation and hardening of tissue

this test only shows if patient has previously been exposed to TB
DOESNT show if its latent or active

20
Q

interferon gamma release assays

A

-look for evidence in blood of previous exposure to TB proteins
-more specific to tb than other mycobacterial infections than ppd skin tests
-unlikely to show positive due to having tb (bcg) vaccine in the past

-if ppd skin test or interferon gamma release assay test comes back positive patient may get chest x-ray
to look for signs of active tb disease

-samples from sputum or broncheolar lavage can be collected & sent for staining and pcr to check for evidence of tb

21
Q

treatment of latent tb

A

-single drug taken for long period of time like isoniazid for 9 months

22
Q

treatment of active tb

A

-combinations of different antibiotics used
-results in patients being non-infectious usually within a few weeks
-as infectious patients kept in negative pressure rooms
-visitors required to wear masks
that cant filter out oil aerosols
but can filter out all other aerosols, including tb
-still kept on drugs even after no longer infectious

23
Q

antibiotic resistant TB

A

-becoming more common
-wont be killed by usual antibiotics
-identify which strain is present in patient to see if its antibiotic resistant
-use multiple drugs at once to prevent antibiotic resistance developing (less survivors that can reproduce passing on alleles that give them resistance to an antibiotic)
-medications need to be used for entire course of therapy
so that all tb is killed

24
Q

specific vs non specific immune respone

A

non-specific=same response regardless of the pathogen
use of inflammation, interferons and phagocytosis

specific=response specific to a particular pathogen

25
how is the immune system able to recognise specific pathogens
antigens on their cell surface glycoproteins that can be recognised by the immune system as self or non-self
26
inflammation
-surrounding area of wound swollen, warm and painful -mast cells respond to tissue damage by secreting the molecule histamine -histamine=chemical signalling molecule that allows communication between cells
27
what does histamine stimulate?
vasodilation-increasing blood flow through capillaries -vasodilation capillaries walls become leaky/more permeable allowing fluid to enter the tissues and create swelling -more permeable capillaries causes phagocytes to leave bloodstream and engulf foreign particles -cell releases cytokines, cell signalling molecules that trigger an immune response in the area
28
interferon function
-part of non-specific immune reponse -anti-viral proteins released when cells are infected with viruses -prevent viruses from spreading to uninfected cells -inhibit production of viral proteins which prevents virus from replicating -activate WBCS involved in specific immune response which can destroy infected cells -they increase non-specific immune response e.g. by increasing inflammation
29
phagocytosis
-WBCS -remove dead cells and invasive microorganisms by engulfing and digesting them-phagocytosis -travel around body in blood stream and leave blood through capillary walls
30
how do phagocytes attack pathogens?
-recognise antigen on cell surface of pathogens as being non-self -ENDOCYTOSIS-->cell surface membrane of phagocyte reaches out around pathogen, engulfing it -pathogen trapped inside phagosome/phagocytic vacuole -lysosome fuses with phagosome releasing digestive enzymes into phagosome -digestive enzymes (including lysozyme) digest the pathogen -after pathogen digested the phagocyte will present the antigens of the pathogen on its CELL SURFACE MEMBRANE - now the phagocyte is an APC -presentation of antigens initiates the specific immune response
31
how're phagocytes attracted to the infected area?
by chemicals released by pathogens or by chemicals released by the body cells under attack like histamine
32
tubercles
tissue infected by tb infection undergoing caseous necrosis and being encased in a granuloma bacteria dormant in tubercles
33
first symptoms of tb
-fever -fatigue -coughing -lung inflammation
34
later effects
extensive damage to lungs which can lead to death due to respiratory failure can enter bloodstream where it can spread to organs causing organ failure