Pathophysiology of Kochs Disease

(Tuberculosis)
Predisposing Factors: Precipitating Factors:
Age - Occupation (e.g Health Workers)
!!unosuppression - "epeated close contact #$ infected persons
o Prolonged corticosteroid therapy - ndefinite substance abuse %ia &
'yste!ic nfection: - recurrence of infection
o Diabetes (ellitus
o )nd-stage "enal Disease
o *& or AD' infection
)+posure or inhalation of infected
Aerosol through droplet nuclei
(e+posure to infected clients by coughing,
snee-ing, tal.ing)
Tubercle bacilli in%asion in the apices of the
/ungs or near the pleurae of the lo#er lobes
0ronchopneu!onia de%elops in the lung tissue
(Phagocytosed tubercle bacilli are ingested by !acrophages)
bacterial cell #all binds #ith !acrophages
arrest of a phagoso!e #hich results to bacilli replication
1ecrotic Degeneration occurs
(production of ca%ities filled #ith cheese-li.e
!ass of tubercle bacilli, dead 203s, necrotic lung tissue)
drainage of necrotic !aterials into the
tracheobronchial tree
(eruption of coughing, for!ation of lesions)
PRIMARY INFECTION
/esions !ay calcify (4hons 3o!ple+)
and for! scars and !ay heal
o%er a period of ti!e
Tubercle bacilli i!!unity de%elops
(2 to 6 weeks after infection)
(!aintains in the body as long as li%ing
bacilli re!ains in the body)
Ac5uired i!!unity leads to further gro#th
Of bacilli and de%elop!ent of ACTIVE INFECTION
SINS AN! SYMPTOMS
Pul!onary 'y!pto!s: 4eneral 'y!pto!s:
Dyspnea - Fatigue
1on-producti%e or producti%e cough - anore+ia
*e!optysis (blood tinge sputu!) - 2eight loss
3hest pain that !ay be pleuritic or dull - lo# grade fe%er #ith chills and
3hest tightness s#eats (often at night)
3rac.les !ay be present on auscultation
2ith (edical nter%ention 2ithout (edical inter%ention
)arly detection$ diagnosis of the dse "eacti%ation of the tubercle bacilli
(ulti-antibacterial therapy (Due to repeated e+posure to infected
Fi+ed- dose therapy ndi%iduals, !!unosuppression)
T0 DOT' (Direct Obser%ed Therapy) SECON!ARY INFECTION
034 %accination
'e%ere occurrence of lesions in the lungs
1o "ecurrence "ecurrence
3a%itation in the lungs occurs
oo" Pro#nosis $a" Pro#nosis
Acti%e infection is spread throughout
the body syste!s
(infiltration of tubercle bacilli in other organs)
TB of the Bones
Potts Disease
Renal TB
')&)") O336"")13) OF
1F)3TO1
3lient beco!es clinically ill
0AD P"O41O''
!EAT%
PAT%OP%YSIO&OY
1a!e of Patient: &an.enlee/loren
Diagnosis: Acute 0ronchitis777
0ronchitis !eans that the tubes that carry air to the lungs (the bronchial tubes) are infla!ed and
irritated8 2hen this happens, the tubes s#ell and produce !ucus8 This !a.es you cough8
Acute bronchitis usually co!es on 5uic.ly and gets better after 9 to : #ee.s8 (ost healthy people #ho
get acute bronchitis get better #ithout any proble!s8 'ee a picture of acute bronchitis8
Pat'o(')sio*o#)
n nor!al breathing, air is dra#n in through the bronchial passages and do#n into the increasingly fine
net#or. of tubing in the lungs called the al%eoli, #hich are !any !illions of tiny sacs surrounded by
capillaries8 These absorb the o+ygen and transfer it into the blood8 2hen to+ins such as s!o.e are breathed
into the lungs, the particles are trapped and cause a locali-ed infla!!atory response8 3he!icals released
during the infla!!atory response (e8g8, elastase) can brea. do#n the #alls of al%eoli (al%eolar septu!)8 This
leads to fe#er but larger al%eoli, #ith a decreased surface area and a decreased ability to absorb o+ygen and
e+ude carbon dio+ide by diffusion8 The acti%ity of another !olecule called alpha ;-antitrypsin nor!ally
neutrali-es the destructi%e action of one of these da!aging !olecules8
After a prolonged period, hyper%entilation beco!es inade5uate to !aintain high enough o+ygen le%els in the
blood8 The body co!pensates by %asoconstricting appropriate %essels8 This leads to pul!onary hypertension,
#hich places increased strain on the right side of the heart, #hich in turn leads to peripheral ede!a as blood
bac.s up in the syste!ic circulation and fluid is forced into the tissues8
)!physe!a occurs in a higher proportion in patient #ith decreased alpha ;-antitrypsin (A;AT) le%els (alpha
;-antitrypsin deficiency, A;AD)8 n A;AD, infla!!atory en-y!es (such as elastase) are able to destroy the
al%eolar tissue (the elastin fibre, for e+a!ple)8 (ost A;AD patients do not de%elop clinically significant
e!physe!a, but s!o.ing and se%erely decreased A;AT le%els (;<-;=>) can cause e!physe!a at a young
age8 n all, A;AD causes about 9> of all e!physe!a8 *o#e%er, s!o.ers #ith A;AD are in the highest ris.
category for e!physe!a8
PAT%OP%YSIO&OY
&iruses (corona %irus,
influen-a %irus)
Heat and smoke inhalation
The pathogens directly attach
the tracheobronchial tree8
nfla!!ation of tacheobronchial tree
The air#ays beco!e infla!ed and narro#ed fro!
capillary dilatation, increased!ucus production
Ac+te
$ronc'its
O+t*ook
To understand 3OPD, it helps to understand ho# the lungs #or.8 The air that you breathe goes do#n your
#indpipe into tubes in your lungs called bronchial tubes or air#ays8
2ithin the lungs, your bronchial tubes branch into thousands of s!aller, thinner tubes called bronchioles8
These tubes end in bunches of tiny round air sacs called al%eoli (al-&))-uhl-eye)8
'!all blood %essels called capillaries run through the #alls of the air sacs8 2hen air reaches the air sacs, the
o+ygen in the air passes through the air sac #alls into the blood in the capillaries8 At the sa!e ti!e, carbon
dio+ide (a #aste gas) !o%es fro! the capillaries into the air sacs8 This process is called gas e+change8
The air#ays and air sacs are elastic (stretchy)8 2hen you breathe in, each air sac fills up #ith air li.e a s!all
balloon8 2hen you breathe out, the air sacs deflate and the air goes out8
n 3OPD, less air flo#s in and out of the air#ays because of one or !ore of the follo#ing:
The air#ays and air sacs lose their elastic 5uality8
The #alls bet#een !any of the air sacs are destroyed8
The #alls of the air#ays beco!e thic. and infla!ed8
The air#ays !a.e !ore !ucus than usual, #hich tends to clog the!8
Figure A sho#s the location of the lungs and air#ays in the body8 The inset i!age sho#s a detailed
cross-section of the bronchioles and al%eoli8 Figure 0 sho#s lungs da!aged by 3OPD8 The inset
i!age sho#s a detailed cross-section of the da!aged bronchioles and al%eolar #alls8
n the 6nited 'tates, the ter! ?3OPD? includes t#o !ain conditions@e!physe!a (e!-fi-')-!a) and
chronic bronchitis (bron-K-tis)8 (1ote: The Diseases and 3onditions nde+ article about bronchitis
discusses both acute and chronic bronchitis8)
n e!physe!a, the #alls bet#een !any of the air sacs are da!aged, causing the! to lose their
shape and beco!e floppy8 This da!age also can destroy the #alls of the air sacs, leading to fe#er
and larger air sacs instead of !any tiny ones8 f this happens, the a!ount of gas e+change in the
lungs is reduced8
n chronic bronchitis, the lining of the air#ays is constantly irritated and infla!ed8 This causes the
lining to thic.en8 /ots of thic. !ucus for!s in the air#ays, !a.ing it hard to breathe8
(ost people #ho ha%e 3OPD ha%e both e!physe!a and chronic obstructi%e bronchitis8 Thus, the
general ter! ?3OPD? is !ore accurate8
Pat'o(')sio*o#)
Acute bronchitis often follo#s a cold or infection8 The earliest clinical feature of bronchitis is increased
secretion of !ucus by sub!ucosal glands of the trachea and bronchi8 Da!age caused by irritation of the
air#ays leads to infla!!ation and infiltration of the lung tissue by neutrophils8 The neutrophils release
substances that pro!ote !ucosal hypersecretion8