Tuberculosis is caused by the bacterium Mycobacterium tuberculosis. It most commonly affects the lungs. Risk factors include malnutrition, poverty, crowding, and immunocompromised states. Transmission occurs via airborne droplets from the lungs of active cases. Diagnosis involves microscopy, culture, molecular tests, chest imaging and the Mantoux skin test. Complications include cavitary lesions, caseous pneumonia, and disseminated disease. Treatment requires long-term antibiotic therapy.
Pulmonary TB is a bacterial infection of the lungs that can cause a range of symptoms, including chest pain, breathlessness, and severe coughing. Pulmonary TB can be life-threatening if a person does not receive treatment. People with active TB can spread the bacteria through the air.
Pulmonary TB is a bacterial infection of the lungs that can cause a range of symptoms, including chest pain, breathlessness, and severe coughing. Pulmonary TB can be life-threatening if a person does not receive treatment. People with active TB can spread the bacteria through the air.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
Tuberculosis is a communicable chronic granulomatous disease caused by Mycobacterium tuberculosis , where the center of the granuloma is Caseous necrosis
It usually involves the lungs but may affect any organ or tissue in the body
Airborne spread of droplet nuclei
TB
Tuberculosis
Extra-pulmonary TB.
As of 2017, about two billion people worldwide are infected with Mycobacterium tuberculosis, the causative pathogen of tuberculosis disease, commonly known as ‘TB’.
However, for the vast majority, (90-95%) of infected individuals, the infection is contained by the immune system and cannot multiply.
In other words, the TB disease remains latent, or dormant, as opposed to active, which usually causes symptoms and can easily be transmitted to others.
When the host’s immune system becomes compromised, e.g. due to HIV or malnutrition and aging, TB can reactivate, and become very serious, especially if the infection spreads through the body.
Moreover, people with active TB can easily infect 10-15 other people via close contact within a year.
Mycobacteria are slender, rod-shaped, and need high levels of oxygen to survive, i.e., “strict aerobes”.
They possess a waxy cell wall that is capable of retaining dyes even when exposed to alcohol.
Thus they are referred to as “acid-fast”, appearing as bright- red colored rods when a Ziehl–Neelsen stain is used.
The wall also makes them incredibly hardy and allows them to resist weak disinfectants and survive on dry surfaces for months.
M. tuberculosis is usually transmitted via inhalation, which is how they gain entry into the lungs.
Although we breathe in all sorts of viruses and bacteria all the time, we have defenses that take care of most of them.
For one, the air that we breathe in is turbulent in the upper airways and drives most bacteria against mucus which is then cleared pretty quickly.
Ultimately, though, TB can avoid the mucus traps and make its way to the deep airways and alveoli where we have macrophages that eat up foreign cells, digest and destroy them.
With TB, they recognize foreign proteins on their cell surface, and phagocytize them, or essentially package them into a space called a phagosome.
In most cases, the macrophage then fuses the phagosome with a lysosome, which has hydrolytic enzymes that can pretty much break down any biochemical molecule.
TB’s tricky, though, and once inside the macrophage, they produce a protein that inhibits this fusion, which allows the mycobacterium to survive.
It doesn’t just survive, though, it proliferates and creates a localized infection.
At this point, somebody has developed primary tuberculosis, which means that they have signs of infection soon after being exposed to TB.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
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is the oldest recreational drug and likely contributes to more morbidity,
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5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
3. Introduction:
• It is a Chronic Granulomatous inflammatory
infectious disease caused by Mycobacterium
tuberculosis in humans.
4. Etiology:
CAUSATIVE ORGANISM
• Tubercle bacillus or Koch’s bacillus called
Mycobacterium tuberculosis causes tuberculosis in
the lungs and other tissues of the human body.
• The organism is a strict aerobe and thrives best in
tissues with high oxygen tension such as in the apex
of the lung.
• Out of various pathogenic strains for human disease
included in Mycobacterium tuberculosis complex,
currently the most common is M. tuberculosis
hominis (human strain).
5. • M. tuberculosis bovis (bovine strain) used to
be common pathogen to human beings during
the era of consumption of unpasteurised milk
but presently constitutes a small number of
human cases
• Infection with M. avium-intracellulare (avian
or bird strain) is common in patients with
HIV/AIDS
6. Risk Factors:
• More common in developing countries of Asia,
Africa and Latin America.
• Malnutrition.
• Inadequate medical care.
• Poverty.
• Crowding.
• Chronic debilitating conditions like uncontrolled
diabetes.
• Alcoholism and immunocompromised states.
• In the western countries, there has been a
resurgence of tuberculosis due to HIV-AIDS.
7. Mode of Transmission:
• Human beings acquire infection with tubercle bacilli
by one of the following routes:
1. Inhalation of organisms present in fresh cough
droplets or in dried sputum from an open case of
pulmonary tuberculosis.
8. 2. Ingestion of the organisms leads to
development of tonsillar or intestinal
tuberculosis.
9. 3. Inoculation of the organisms into the skin
may rarely occur from infected postmortem
tissue.
10. 4. Transplacental route results in development
of congenital tuberculosis in foetus from
infected mother and is a rare mode of
transmission.
12. Pathogenesis of Tuberculosis:
EVOLUTION OF TUBERCLE
• The sequence of events which take place when
tubercle bacilli enters body:
TUBERCLE BACILLI ENTRY
If bacilli enters through blood
Neutrophils are evoked initially which
are rapidly destroyed by the organisms.
Later by macrophages and T cells.
If the tubercle bacilli are inhaled into the
lung alveoli
Macrophages predominate the picture
from the beginning.
13. Tubercle Bacilli engulfment by Macrophages
Macrophages try to kill the bacteria or die away themselves.
Macrophages present bacilli to CD4+T lymphocytes
Activated lymphocytes release lymphokines.
IL-1, IL-2, Interferon-γ TNF-α
PROLIFERATION OF
MORE T CELLS ACTIVATES MACROPHAGES FIBROBLAST PROLIFERATION
If Poorly degradable bacilli are present
14. ACTIVATED MACROPHAGES TRANSFORM TO
EPITHELIOID CELLS AFTER 2-3 DAYS
SOME MACROPHAGES, UNABLE TO DESTROY TUBERCLE
BACILLI, FUSE TOGETHER AND FORM MULTINUCLEATED
GIANT CELLS.- LANGHAN TYPE
Around the mass or cluster of epithelioid cells and a few giant
cells, a zone of lymphocytes and plasma cells is formed which
is further surrounded by fibroblasts.
The lesion at this stage is called HARD TUBERCLE due to
absence of central necrosis.
15. • Within 10-14 days, the centre of the cellular mass
begins to undergo caseation necrosis, characterized
by cheesy appearance and high lipid content.
• This stage is called SOFT TUBERCLE which is the
hallmark of Tuberculous lesions
Caseation Necrosis
16. ***
• The soft tubercle which is a fully-developed
granuloma with caseous centre does not favour
rapid proliferation of tubercle bacilli.
• Acid-fast bacilli are difficult to find in these
lesions and may be demonstrated at the
margins of recent necrotic foci and in the walls
of the cavities.
17. Fate of Tubercles:
The fate of a granuloma is variable:
1. COLD ABSCESS:
- The caseous material may undergo liquefaction and
extend into surrounding soft tissues, discharging the
contents on the surface.
- This is called cold abscess although there are no pus
cells in it.
18. 2. SINUS TRACTS:
- In tuberculosis of tissues like bones, joints,
lymph nodes and epididymis, sinuses are
formed and the sinus tracts are lined by
Tuberculous granulation tissue.
19. 3. SIZE INCREASE:
- The adjacent granulomas may coalesce
together enlarging the lesion which is
surrounded by progressive fibrosis.
20. 4. CALCIFICATION & OSSIFICATION:
- In the granuloma enclosed by fibrous tissue,
calcium salts may get deposited in the caseous
material (dystrophic calcification) and
sometimes the lesion may even get ossified
over the years.
dystrophic calcification
21. Types of Tuberculosis:
• Infection with tubercle bacilli is of 2 main
types:
1. Primary Tuberculosis.
2. Secondary Tuberculosis.
22. 1. Primary Tuberculosis:
• The infection of an individual who has not
been previously infected or immunised is
called Primary Tuberculosis or Ghon’s
complex or Childhood Tuberculosis.
23. Sites:
• The most commonly involved tissues for
primary complex are:
- Lungs and Hilar lymph nodes.
• Other tissues which may show primary
complex are
- Tonsils and Cervical lymph nodes
- Small intestine and mesenteric lymph nodes.
24. Primary complex or Ghon’s complex
• Primary complex or Ghon’s complex is the lesion
produced in the tissue of portal of entry with foci in
the draining lymphatic vessels and lymph nodes.
25. Ghon's Complex in Lungs:
• It consists of 3 components:
1. Pulmonary component
- It is 1-2 cm solitary area of primary Tuberculous foci.
- Subpleural focus in the upper part of Lower lobe.
2. Lymphatic vessel component
- Lymphatics draining the lung lesion contain
phagocytes containing bacilli.
3. Lymph node component
- Enlarged hilar and tracheo-bronchial lymph nodes in the
area drained.
- The affected lymph nodes are matted and show caseation
necrosis.
26.
27. Fate Of Primary Tuberculosis
• Primary complex may have one of the following
sequelae:
1. Fibrosis, Calcification and Ossification.
28. 2. Progressive primary tuberculosis:
• Caseous material is disseminated through
bronchi to the other parts of the same lung or
the opposite lung.
29. 3. Primary Miliary Tuberculosis:
• Bacilli may enter the circulation through
erosion in a blood vessel and spread by
haematogenous route to other tissues and
organs.
• The lesions may be seen in organs like the
liver, spleen, kidney, brain and bone marrow.
30. 3. Progressive Secondary Tuberculosis:
• Lowered resistance (AIDS) and increased
hypersensitivity of the host, the healed lesions
of Primary tuberculosis may get reactivated.
• The bacilli lying dormant in acellular caseous
material or healed lesion are activated and can
cause secondary TB.
31. Secondary Tuberculosis
• The infection of an individual who has been
previously infected or sensitized is called
– Secondary TB, or
– Post-Primary or
– Reinfection or
– Chronic Tuberculosis.
32. The infection may occur from:
1. Endogenous source such as reactivation of
dormant primary complex; or
2. Exogenous source such as fresh dose of
Reinfection by the tubercle bacilli.
• Secondary tuberculosis occurs most commonly
in lungs.
• Other sites and tissues which can be involved
are lymph nodes, tonsils, pharynx, larynx,
small intestine and skin.
33. • Infection with M. avium-intracellulare occurs
more frequently in cases of AIDS.
• Patients with HIV infection previously
exposed to tuberculous infection have
particularly high incidence of reactivation of
primary tuberculosis.
34. Morphological Features of Secondary TB
• The lesions in secondary pulmonary
tuberculosis usually begin as 1-2 cm apical
pleura.
• It occurs by lymphohaematogenous spread of
infection from primary complex to the apex of
the affected lung where the oxygen tension is
high and favourable for growth of aerobic
tubercle bacilli.
• The pattern of lesions in such cases is similar
to that of primary tuberculosis.
35. FATE OF SECONDARY PULMONARY TUBERCULOSIS
1. The lesions may heal with fibrous scarring
and calcification.
36. 2. The lesions may produce progressive
secondary pulmonary tuberculosis with the
following pulmonary and extrapulmonary
involvements:
i) Fibrocaseous tuberculosis
ii) Tuberculous caseous pneumonia
iii) Miliary tuberculosis
iv) Tuberculous empyema
37. FIBROCASEOUS TUBERCULOSIS:
• The original area of tuberculous undergoes peripheral
healing and massive central caseation necrosis which
may:
SOFT CASEOUS LESION WITHOUT
DRAINAGE INTO A BRONCHUS OR
BRONCHIOLE TO PRODUCE A
NON-CAVITARY LESION
(CHRONIC FIBROCASEOUS
TUBERCULOSIS).
BREAK INTO A BRONCHUS
FROM A CAVITY
(CAVITARY OR OPEN FIBROCASEOUS
TUBERCULOSIS)
38. CAVITARY OR OPEN FIBROCASEOUS
TUBERCULOSIS
CHRONIC FIBROCASEOUS
TUBERCULOSIS
39. PROGNOSIS OF CAVITARY OR OPEN FIBROCASEOUS TUBERCULOSIS
The cavity may communicate with bronchial tree and becomes
the source of spread of infection
(‘OPEN TUBERCULOSIS’).
May implant tuberculous lesion on the mucosal
lining of air passages producing
ENDOBRONCHIAL
AND ENDOTRACHEAL TUBERCULOSIS.
Ingestion of sputum containing
tubercle bacilli from
endogenous pulmonary lesions
may produce
LARYNGEAL AND
INTESTINAL
TUBERCULOSIS.
41. TUBERCULOUS CASEOUS PNEUMONIA
• The caseous material from a case of secondary
tuberculosis in an individual with high degree of
hypersensitivity may spread to rest of the lung
producing caseous pneumonia
42. MILIARY TUBERCULOSIS
• This is lymphohaematogenous spread of
tuberculous infection from primary focus or later
stages of tuberculosis.
• The spread may occur to systemic organs or
isolated organ.
• The spread is either by entry of infection into
pulmonary vein producing disseminated or
isolated organ lesion in different extra-pulmonary
sites (e.g. liver, spleen, kidney, brain, meninges,
genitourinary tract and bone marrow).
43.
44.
45. TUBERCULOUS EMPYEMA
• The caseating pulmonary lesions of
tuberculosis may be associated with empyema.
• Empyema may heal by fibrosis and obliterate
the pleural space (thickened pleura by chronic
pleuritis).
• Occasionally, pleural cavity may contain
caseous material and develop into tuberculous
empyema.
46. TUBERCULOUS EMPYEMA
• The caseating pulmonary lesions of
tuberculosis may be associated with empyema.
• Empyema may heal by fibrosis and obliterate
the pleural space (thickened pleura by chronic
pleuritis).
• Occasionally, pleural cavity may contain
caseous material and develop into tuberculous
empyema.
48. Clinical Features:
SYSTEMIC FEATURES:
• FEVER, NIGHT SWEATS, FATIGUE, LOSS OF
WEIGHT AND APPETITE.
REFERABLE TO LUNGS:
- PRODUCTIVE COUGH
- HAEMOPTYSIS,
- PLEURAL EFFUSION,
- DYSPNOEA,
- ORTHOPNOEA etc.
49.
50. Diagnosis of Tuberculosis
• The diagnosis is made by the following tests:
i) AFB microscopy of diagnostic specimen
such as sputum, aspirated material.
52. iii) Molecular methods- PCR.
iv) Complete Haemogram- Lymphocytosis
and raised ESR.
v) Radiographic procedures e.g. chest X-ray
showing characteristic hilar nodules and other
parenchymal changes).
53. vi) Mantoux skin test:
• This test is done by intradermal injection of
0.1 ml of tuberculoprotein, purified protein
derivative (PPD).
54. Delayed type of hypersensitivity develops in individuals
who are having or have been previously infected with
tuberculous infection which is identified as an indurated
area of more than 15 mm in 72 hours.
55. • The test may be
• FALSE POSITIVE:
- in atypical mycobacterial infection and
- previous BCG vaccination,
• FALSE NEGATIVE:
- in weakened immune system.
- sarcoidosis,
- some viral infections,
- Hodgkin’s disease,
- Recent tuberculous (8-10 weeks of exposure) infection
56. CAUSES OF DEATH IN PULMONARY TUBERCULOSIS
• Pulmonary insufficiency,
• Pulmonary haemorrhage,
• Sepsis due to disseminated miliary
tuberculosis,
• Cor Pulmonale
• Secondary Amyloidosis.