Lecture 11 Flashcards
Haemoptysis and abnormal chest X-ray
2.5 cm diameter cavity in chest, i.e. Hole in lung. sometimes horizontal line (liquid/puss)
(lungs split into lobes/anatomical areas, depending on the bronchi that supply them (3 lobes on right, 2 and 1/2 on left))
Lots of possibilities
Lung cancer: high probability. Main worry. Need to investigate quickly. Coughing blood, heavy smoker, 65 (peak cancer time)
TB: low probability. most people coughing up blood wont have TB as is uncommon in nz.
Pneumonia: bacterial infection of lungs. however not expressing classical features (cough, fever)- is an acute syndrome, relatively short lived. diagnosed in 5-6 days (not weeks)
Chronic Obstructive Pulmonary/Airways Disease/Emphysemia: Smoking related airways disease
- variant called Chronic bronchitis.( Cough productive of sputum every day, for 3 months periods, in 2 consecutive years
-smokers cough for a long time, and poor lung function due to smoking related airways disease
-but wouldnt have lump on x-ray) )
-Bronchiectisus
Diagnosis of Chronic Bronchitis
Cough productive of sputum every day, for 3 months periods, in 2 consecutive years
- smokers cough for a long time, and poor lung function due to smoking related airways disease
- but wouldnt have lump on x-ray)
Lungs
capacity to clean itself right down to small bronchi
Bronchiectisus
small airways (not alveoli where O2 is transferred. no 02 transferred) small airways damaged and broken and cant clean themselves. and fill up with gunk -structural damage to the lung's Conducting airways -Symptoms like above case + haemoptysis -lungs are unable to clear out infections, so people get recurrent infections. perpetuates problems and damage
TB Chest x-rays
- Normal lung can see ribs clearly anteriorly and posteriorly, with black inbetween through it
- slimy cotton wool lung= puss/inflammatory goo filling the airways
- nodular fluffiness - Heart border on left lung. lung fairly indistinctable. Normal lung tissue been eroded by (cancer/in this case TB) -lung obliterated/entirely diseased
Projected global deaths 2002-2030
- Cancer
- Ischaemic heart disease
- stroke
-chronic illnesses associated with modern living- obesity, smoking, pollution - HIV/AIDS (increasing for next 20-30 before we curb it)
- other infectious disease (communicable. decreasing rapidly)
6. - TB/Malaria (decreasing)- cases transferring categories. classified as AIDS case, not TB, even though containing both. Therefore TB still huge cause of death, but under represented.
-alot of the increased death rates due to HIV are more due to TB than HIV itself. HIV- makes the person more susceptible to HIV and more likely to die from HIV
TB Pandemic
Prominent disease around the world
1/3 of the world is infected (TB bacteria in body)
1.5 million have disease/illness at any time (less than rate of infected)
96% of TB is in the developing world (non-uniform)Africe
10 million have HIV/TB co-infection
-illustrates large number of people infected who dont have disease/illness therefore dont know they’re infected
Incidence of TB in 2014 by country (WHO)
Incidence= number of “new” cases
NZ had 7 new cases/100,000 in 2014
Canada 0-24
Tonga had 14 (double in pacific, but no real change with popn size)
Samoa had 17
Australia had 6
India had 167
China had 68
-most of TB cases in auckland, are people who were born in bangladesh, india, pakastan, china and immigrate to NZ (for work/study)
NZ’s 7 cases: mostly people who were born overseas, acquired TB overseas, came to NZ and got Sick
Mycobacterium Tuberculosis complex
- M. Tuberculosis (most common form by miles)
- M. Bovis (cow TB, causes same illnesses in human)
- M. Africanum (common in Africa)
- M. Ulcerans (common in Africa)
- multiple forms of TB exisiting. not just one species of one genus
- Discovered by Robert Koch
- used M. bovis in experiments that lead to the development of Koch’s postulates (made cows sick)
Koch 1890 postulates
“germs causing disease”
-thoughts magots spontaneously appeared
how did infections spread?
Flawed:
1. pathogen isolated from sick organisms but not healthy organisms -false as may endogenous infections
2. isolated from sick organisms in pure culture
3. should cause disease when health organism is inoculated - false: Zika more often cuases no illness than illness (didnt account for other states of disease (spectrum: no symptoms-symtoms-about to die)
4. must be re-isolated from the experimentally infected organism
Classification of Mycobacteria
2x categories of mycobacteria
1. TB
2. Non-tuberculosis mycobacteria (NTM)
a) rapid growing (lab culture growth take 1-2 days)
b) non-rapid growing (lab culture growth takes weeks)
-makes diagnosing TB hard would take sputum from someone with pnuemonia and would take weeks to grow, and only then you would know have TB
c) other (non-culturable mycobacterium. cannot culture or can only culture under very special conditions)
Leprosy: thickened plaqued ears and ruined fingers. Mycobacterium Lepry. Non-culturable. can culture in Us armadillo foot pad and trangenic mice. Not in agar plates of chicken broth. Elusive germ. PCR /genetic sequencing helped to learn more. Like colds part of body (nose, ears) bumpy plaques. biopsy can see the bacteria. Grow around nerve sheets, damages nerves (mans hands nerve sheets so damaged that whacked with hammer/burn on stove, resulting in repeated injury, couldnt feel)
-therefore hands: partially injury + partially changes when loss of bulk of nerve supply
-condition that can cure readily. but often alot of damage is done before entering the clinic
Leprosy
No transmission of Leprasy in NZ
-some in Pacific. Samoa more than others. Keribat has a high rate among children. Some cases in Africa, South east asia, india. (similar distribution to TB)
Leprosy: thickened plaqued ears and ruined fingers. Mycobacterium Lepri. Non-culturable. can culture in Us armadillo foot pad and transgenic mice. Not in agar plates of chicken broth. Elusive germ. PCR /genetic sequencing helped to learn more. Like colds part of body (nose, ears) bumpy plaques. biopsy can see the bacteria. Grow around nerve sheets, damages nerves (mans hands nerve sheets so damaged that whacked with hammer/burn on stove, resulting in repeated injury, couldnt feel)
-therefore hands: partially injury + partially changes when loss of bulk of nerve supply
-condition that can cure readily. but often alot of damage is done before entering the clinic
Transmission of TB
- TB transmitted by someone coughing and another person breathing in the bacteria e.g. singing (laryngeal TB very good at transmitting TB into the air)
- normal bacteria when coughed/sneezed form droplets/dust that dont travel much further than 1 metre
- but TB has the capacity to Float (chicken pox, measles and Nori virus can). Therefore can cough and leave the room, someone else can still contract the disease regardless of them leaving.
- spread by both direct and indirect contact (people dont need to come together) - Bacterium particle inhaled and thought to have to reach alveola, come in contact with a Pulmonary Alveolar Macrophage
- if stuck in nose/throat, less likely to develop infection
- can Drink TB, get TB of the Gut by drinking infected unpasturised cows milk (myobacterium bovis)
- Cutaneous spread of TB: catch TB through skin (no longer this extreme exposure)-historical
TB initial phase of TB infection
TB wants to be phagocytosed by WBC.
LAM (Lipoarabino mannan) on the surface of the cell stimulates/binds to the complement receptor of pulmonary macrophages (causing TB to become injested)
-TB bacteria has LAM in its cell wall
TB posses an array of factors that enable it to survive intracellularily and to induce the macrophage to remain alive
-once eaten, Inside the WBC the TB can resist being killed and live
-Macrophages (like nuetrophils) normally throw H202 or oxygen free radicals at TB to kill it. but since inside is mostly resistant to killing. Due to tough cell wall, free radical scavengers and superoxide dismutase (turns off free radical production), alter formation of toxic vessels on phagosome, so lysosome doesnt mature.
-LAM also stops macrophage from dying, tricks into staying alive, and prevent them from signalling other cells (what a cell typically does if it isnt capable of handling infection and needs to be killed, especially in viral infections). Blocks this help signal, so rest of immune system half ignores it.
TB in lymph nodes
survives within macrophage
is able to communicate to other cells to a degree but not perfectly
-other cells recruit other cells. situation is augments (similar to an acute infection) stimulates other cells. TNFa (tumour necrosis factor alpha) recruits other macrophages and immune cells.
In early stages of infection TB is carried to local lymph nodes
-dendritic cells may ingest some damaged TB proteins and take to local lymph nodes. -lung local lymph nodes located in central Hilum (where BV and bronchi come into lung) (hilum normally seen on Right X-ray as not obscured by heart border).Within few hours of infection, TB germs/proteins are presented to lymph nodes indicated problems
T lymphocytes (same as HIV) proliferate and go back to site of infection to try and help out.
Often TB has not been adequately killed by host immune cells. Instead builds a prison for TB
-in some (many) cases the immune system cannot quite kill TB and instead builds a prison of immune cells around it -granuloma
TB Granuloma:
a) Centre of necrotic muck, both living and dead TB, cell fragments and proteins (similar to puss)
b) Spherical jail build around it of Abnormally large strange looking macrophages that havent been allowed to die. sometimes multinucleated as have coallesed. still alive partially due to TB, but also partially due to:
c) CD4 Helper T Lymphocytes palicade around the outside continuously sends messages to macrophages, telling them what to do: to stay strong and stay alive.
-bodies response to Chronic infection/infection your body cannot deal with. TB cardinal learning point about chronic infections. Also parasites and sifolis bacteria and Salmonella bacteria
