2. TUBERCULOSIS
- A chronic infectious disease which can affect all
organs of the human body, but more often the lungs.
3. CAUSATIVE AGENT OF TUBERCULOSIS
Four types of mycobacteria:
1.Mycobacterium tuberculosis
2. Bovine (Mycobacterium bovis),
3.Bird (Mycobacterium avium),
4.M intracellulare complexes (or MAC)
cold-blooded.
For human pathogens are the first two
types.
5. TUBERCULOSIS Epidemiology
Infection source: ill people and animals (mainly cattle).
Ways of infection contamination:
- aerogenous (thus the special role is played by airborne and
dust infections),
- alimentary (with food),
- contact, i.e. through the injured skin, mucous membranes,
- transplacentary (seldom).
15. TUBERCULOSIS
Morphological substrate of
tuberculosis - pockets of various sizes
(from milliary to tuberculoma 2-4 cm in
diameter or more), subject to caseous
(curd) necrosis without melting or
encapsulation of exposed melt to form a
cavity - the cavity in different organs and
ulcers on mucous membranes.
19. PRIMARY TUBERCULOSIS
Variants of course:
1. attenuation of the primary tuberculosis foci and the healing of the
primary focus;
2. progression of primary tuberculosis with generalization of the
process;
3. chronic course.
22. PRIMARY TUBERCULOSIS
Hematogenous form of progression developed when
mycobacteriae enter the blood from the primary affect or
caseous-modified lymph nodes and disseminate in the
organism.
27. PRIMARY TUBERCULOSIS
Lymphogenous form of progression
(generalization) – involvment of
bronchial, bifurcative, paratraheal, suprar
and subclavian, cervical and other lymph
nodes. Lymphatic nodes are
hyperplastic, enlarged in diameter by 1 -
5 cm, they have a caseous focus.
28. PRIMARY TUBERCULOSIS
Growth of primary affect – it is more severe
progression form and is characterized by
caseous necrosis of perifocal inflammation
zone.
Primary acinar tuberculosis focus transforms
into lobular, then into segmental, lobar
(development of lobar caseous pneumonia
or primary pulmonary cavern).
29. PRIMARY TUBERCULOSIS
Mixed form of progression:
develops in weak patients after acute infections, in avitaminosis, hunger
and oth.
It is characterized by large primary focus, caseous bronchoadenitis,
sometime with resolution of necrotic mass and fistula formation. In both
lungs there are multiple tuberculosis foci.
30. PRIMARY TUBERCULOSIS
Outcomes of progression:
in negative cases death due to common generalization of process
and tuberculosis meningitis;
in positive cases progression stops: exudative inflammation
transform into proliferative, focus is encapsulated and calcificated.
31. PRIMARY TUBERCULOSIS
Peculiarities of primary chronic tuberculosis of lungs:
1) total caseous necrosis of lymph nodes;
2) inclination to generalization with metastatic foci of extra
pulmonary tuberculosis formation;
3) hematogenous generalization of infection is accompanied with
tuberculosis inflammation of serous coats (Tuberculosis polyserosiris –
Plevritis, pericarditis) and activity of process in lymph nodes.
32. PRIMARY TUBERCULOSIS
Chronic primary tuberculosis arises in case of slowly progressive
wavy course of specific process. It results in organism sensibilization:
increase of it`s sensitivity to nonspecific agents and development of
paraspecific reactions (diffuse and nodular proliferation of lymphocytes
and macrophagocytes, fibrinoid changes in blood vessel wall,
hyperplastic changes of hemopoietic tissue, disproteinosis, sometime
amyloidosis.
33. HEMATOGENOUS TUBERCULOSIS
Arises and develops in organism after primary infection and healing, but
in patients secondary foci or not full healed foci are kept in different
organs and lymph nodes. Due to action of negative factors and
hypersensitivity to tuberculosis latent process exacerbation arises.
Subvariants:
1) generalized hematogenous tuberculosis;
2) hematogenous tuberculosis with lungs lesion mainly;
3) hematogenous tuberculosis with extrapulmonary lesions mainly.
34. HEMATOGENOUS TUBERCULOSIS
Generalized hematogenous tuberculosis is severe form of disease in
which multiple tuberculosis tuberculum and necrotic foci appear.
Depending on morphological substrate its 3 kinds are distinguished:
I. Acute tuberculosis sepsis (necrotic type),
II. Acute general miliary tuberculosis,
III. Acute general large focal tuberculosis .
35. HEMATOGENOUS TUBERCULOSIS
Hematogenous tuberculosis with lungs
lesion mainly – most frequent form of pulmonary
tuberculosis.
Variants:
а) acute miliary lung tuberculosis;
б) chronic miliary lung tuberculosis;
в) chronic large focal tuberculosis of lungs.
36. HEMATOGENOUS TUBERCULOSIS
Chronic large focal tuberculosis of lungs is one of
intermediate form of hematogenous tuberculosis with kept
immunological features (appear in adult persons).
Main morphological signs:
1. symmetric damage of both lungs;
2. mainly corticopleural localization of pathological process in
lungs;
3. predominance of proliferative reactions;
4. development of diffuse net sclerosis;
5. development of emphysema;
6. hypertrophy of right heart;
7. absence of inclination to destruction;
8. formation of caverns in the borderline zones of lungs and their
symmetric localization;
9. presence of extrapulmonary metastatic foci.
46. TUBERCULOSIS
COMPLICATIONS
In primary tuberculosis: tuberculosis meningitis, pleuritis,
pericarditis, peritonitis.
In tuberculosis of bones: sequesters, abscess, deformations,
fistula.
In secondary tuberculosis complications are provided by
caverns: hemorrhage, rupture of wall and spreading into pleural cavity
(empyema and pneumothorax).
Amyloidosis (complication of chronic purulent processes).
49. TUBERCULOSIS
Causes of death
-the progression of a specific process, accompanied by severe intoxication
and degeneration of parenchymal organs; swelling of the brain in the
generalization of tuberculosis and miliary tuberculosis with tuberculous
meningitis hydrocephalus in fibrosis in the soft meninges;
-increasing with the development of renal failure, uremia with bilateral renal
tuberculosis;
-pulmonary bleeding from vascular wall cavity arrozirovannyh with the
progression of pulmonary tuberculosis may be;
-amyloid-lipoid nephrosis with progressive renal amyloidosis in general;
chronic pulmonary heart disease, against which may develop acute
pulmonary heart disease on the left type.
50. Office of Vitebsk region State service of medical forensic examinations. № 216 forensic examination of
a corpse
FORENSIC MEDICAL DIAGNOSIS: Bilateral apical caseous pneumonia with abscess
formation. Focal tuberculosis more harmful lobe of right lung. MBT + (smear). Swelling of the
brain. Serous pericarditis. Serous diffuse myocarditis. Sacral bedsore. Arterial hypertension:
myocardial hypertrophy, the increase in the size and weight of the heart, not constrictive
coronarosklerosis, diffuse small focal cardiosclerosis, arteriolonephrosklerosis. Atherosclerosis
of the aorta (II Stage, 2 nd degree) and the base of the brain vessels. Steatosis. Liver fibrosis
second degree.
53. Sepsis is a generalized infection with
immunosuppressive properties,
characterized by polyetiology and the
acclivity
- of flow, which has some differences
from other infectious diseases.
54. Etiological features of
sepsis
Sepsis, polyetiologicaly has a variety of
pathogens: Streptococcus, pneumococcus,
meningococcus, Pseudomonas aeruginosa,
Mycobacterium tuberculosis, fungi and other
microorganisms, but most often staphylococci,
Klebsiella, Streptococcus and Pseudomonas
aeruginosa.
56. The clinical features of sepsis
In the course of the disease is not cyclical.
Regardless of the pathogen during
monotonous. process:
1. very acute - acute (up to 2 or 3 days of
lightning);
2. acute - up to 6 weeks;
3. subacute - more than 6 weeks (long);
4. chronically.
57. The clinical features of
sepsis
Clinical signs of sepsis may be:
-fever, chills, severe sweating;
-tachypnea over 20 breaths per minute;
-GNI disorder: insomnia, psychosis,
hallucinations;
-hypotension, rapid pulse;
-on the skin - petechial rash;
-in the blood: anemia, leukocytosis, leukocyte shift
to the left, the increase in erythrocyte
sedimentation rate;
-violation of diuresis: oliguria, anuria possible.
58. Immunological differences of
sepsis:
Fail to develop immunity.
Pathological differences of sepsis:
Local and general changes do not
have specific features, whereas
other infections have
characteristic changes.
59. Pathological anatomy of
sepsis
Local changes:
Develop from the “entrance gate" of infection (septic
focus). From the septic focus infect the lymphatic and
blood vessels throughout the body, getting into the
bloodstream.
In the case of spread through the lymphatic system arise
lymphangitis, lymphadenitis, may be lymphothrombose.
In the case of distribution by the circulatory system occur
phlebitis. Violation of the integrity of the endothelium of
the veins leading to the formation of blood clots, often
purulent.
Festering in the removal of a blood clot becomes an embolus
- peddler of bacterial infection (thrombosebacteriamia
embolus).
61. Septic focus. Phlegmonous-ulcerative appendicitis
а – infiltration of leukocytes,
б – the destroyed mucosa.
в – in the lumen of the appendix pus.
62. Pneumonia with abscess formation. The lumen of the
bronchus (a) and the cavity of many of the alveoli (b) are
filled with pus.
63. Thrombosebacteriamia embolism. Pustular or
apostematose nephritis. On the left - in the context of
renal abscesses are seen. Right - on the surface of the
kidney visible ulcers.
64. Bacterial thrombotic embolism - purulent nephritis. and - in the
hearth of suppurative bacterial emboli are seen melting. b -
the vessels around the abscess rapidly expanded and more
fulfilling.
66. Pathological anatomy of sepsis
General changes in the organs in sepsis:
1. dystrophic,
2. inflammatory,
3. hyperplastic.
Common degenerative changes occur in the
liver, kidneys, myocardium, muscle,
central nervous system. Frequently
degenerative changes go into
necrobiotic that end necrosis.
73. Hydropic degeneration of hepatocytes. в - on-site vacuole
EPS m - modified mitochondria РБ - the remnants of
ribosomes.
74. Pathological anatomy of
sepsis
Terms and inflammatory changes
Presented mediate (interstitial) productive inflammation:
Characterized by the presence of cellular infiltrate in the
stroma of the organ.
With the progression
of interstitial inflammation occurs sclerosis and damaged
parenchyma of the organ.
At the heart valves may be polypus-
ulcerative endocarditis. The valve is loose, pieces
of it can come off and become an embolus.
Inflammatory changes are observed in the vessels -
multiple vasculitis, it is one of the causes of hemorrhage.
75. Pathological anatomy of
sepsis
Hyperplastic processes.
Yellow marrow becomes red: in the blood increases the
number of immature white blood cells (leukemoid
reaction).
There is hyperplasia of the lymph nodes, they increase in
size with the advent of the reactive centers.
The spleen is flabby, is red and gives ample scraping the
pulp (septic spleen).
Bacterial intoxication leads to an increase in the liver,
jaundice may occur
78. Hyperplasia of lymph node and spleen. Visible
accumulation of macrophages (macrophage
reaction).
79. Hyperplasia of the lymph node. Visible clusters
plasmoblast stained Brochette pink.
80. Classification of sepsis
Takes into account three features:
etiology;
the entrance gate;
clinical and morphological.
On the etiology distinguish streptococcal,
staphylococcal, pneumococcal,
gonococcal, Pseudomonas, and other
bacterias. The most common are
staphylococcus and Pseudomonas
aeruginosa.
81. Classification of sepsis
Depending on the entrance gate. Prerequisite
for the development of sepsis is the
formation of a septic focus.
Septic focus can be formed directly in the
implementation of the pathogen. Such a
center, and sepsis, is called the primary.
In other cases, the septic focus can evolve
from a common source of infection
(pneumonia with prolonged, chronic otitis,
furunculosis). Such a septic focus, and
sepsis, caused by them is called secondary.
Secondary sepsis is a complication of
infectious disease.
82. Localization of septic focus
pulmonary (most
common in nosocomial infections associated
with intubation);
umbilical (primary focus is localized in the umbilical
wound or umbilical vein);
skin;
urinogenous;
tonsilogenny;
mother (may be associated with criminal abortion,
childbirth);
otogenic (due to a primary septic focus in the ear due
to exacerbation of chronic otitis media).
cryptogenic.
85. Pathological anatomy of septicemia
No septic focus;
hemolytic jaundice, icteric skin and sclera;
hemorrhagic lesions (hemorrhagic syndrome);
hyperplasia of lymphoid and hematopoietic tissues,
resulting in increased spleen, which is called "septic"
(abundant scraping), lymph nodes increase, bone
marrow hyperplasia (myelogram shift to the left).
in parenchymatous organs (liver, kidney, heart), an
intermediate inflammation, increased vascular
permeability of the tissue.
develop fibrinoid changes of vessel walls, allergic
vasculitis.
86. Bacterial (septic, toxic-
infectious) shock
Bacterial shock can be defined as a condition
caused by microorganisms and their toxins,
stimulates the activity of endogenous release
of biological substances, leading to
hypotension, disorders of central
hemodynamics and microcirculation,
dramatically reducing the oxygen in the
tissue perfusion.
89. Aggravating factors of bacterial
shock
rough handling in the septic focus
(necrectomy, ligation with damage to
granulation)
rapid intravenous administration of
large doses of antibiotics that have
antibacterial properties.
97. Septic (bacterial) Endocarditis
By the nature of the flow divided into:
Acute, up to 2 weeks;
Subacute, up to 3 months;
The protracted, lasting months or years.
Presence or absence of underlying disease are divided
into:
Arising on intact valves - primary septic endocarditis
(20-30% of cases).
Evolving in the modified (perverse) valves - secondary
bacterial endocarditis (in 70-80% of cases, often
against a background of rheumatic heart disease).
98. Pathological anatomy of septic
endocarditis
Heart. In 75% of the cases affects the aortic valve (alone or
in combination with mitral and others). On the valve there
is polypous-ulcerative endocarditis. On the surface of the
ulcer is formed thrombus. Often calcification occurs (post
necrotic calcification). The newly formed connective
tissue deforms the wing valves and forms a heart defect.
In the interstitial tissue infarction are found nodules
(granulomas) develop myocarditis.
In the vascular system, particularly in the microvasculature
are visible alterative, productive change: plazmorragiya
and fibrinoid necrosis of endo-and perivasculities with the
growth of connective tissue around the vessel.
Inflammatory changes lead to the formation of aneurysms
and their subsequent rupture. Especially dangerous
aneurysm in the brain.
101. Pathological anatomy of septic
endocarditis
The spleen is enlarged with infarcts of various limitations,
as the spleen is affected first. Symptoms of
hypersplenism: leucocytopenia, thrombocytopenia, and
anemia.
Light struck a third of patients in the form of a heart attack
(pulmonary embolism), pneumonia, pulmonary vasculitis,
which manifests itself nonspecific pneumonia.
Kidneys. It often occurs as immunocomplex
glomerulonephritis (hematuria, proteinuria. Cylindruria,
hypertension, edema).
In the brain, heart attacks occur both on the grounds of
thromboembolism and hemorrhage due to aneurysm
rupture. In all patients, an infectious-toxic
encephalopathia: headache, lethargy, and insomnia
occurs.
102. Peripheral symptoms of septic
endocarditis
The appearance of petechiae in the field squeezing of the skin.
Petechiae in the conjunctiva of the eye from the inner corner of the
lower eyelid.
Osler nodules (a manifestation of septic vasculitis)
- painful thickening on the palmar surface of the brush from
the millet seed to a pea.
Drumsticks (thickening of the phalanges) due to the soft tissues -
the proliferation of connective tissue, swelling of the periosteum.
Hemorrhages in the skin (Janeway spots).
Jaundice (hemolytic).
Frequent thromboembolic complications. If
you take multiple thromboembolism in nature, this process is
called thromboembolic syndrome.
