Inflammation is the body's response to injury or infection and can be either acute or chronic. Acute inflammation is short-lived, occurring over minutes to days, and is characterized by redness, swelling, heat, pain, and loss of function due to exudation of fluid, proteins, and immune cells. Chronic inflammation lasts longer, over days to months, and involves accumulation of lymphocytes, plasma cells, and macrophages with fibrosis and tissue proliferation. Common types of acute inflammation include serous, fibrinous, and suppurative, characterized by fluid, fibrin, or pus accumulation respectively. Chronic inflammation can result from prolonged acute inflammation or persistent infection/exposure and involves mononuclear cell infiltration and tissue destruction.
Acute inflammation is the early response of tissues to injury and involves vascular and cellular events. The vascular events include vasodilation, increased vascular permeability allowing plasma proteins to leave circulation, and accumulation of leukocytes from the blood vessels into tissues. The principal leukocytes in acute inflammation are neutrophils. The cellular events in acute inflammation help destroy, dilute or isolate injurious agents. Mediators of acute inflammation include histamine, prostaglandins, nitric oxide, complement factors and cytokines. Acute inflammation is rapid in onset, relatively short in duration and aims to return tissues to normal function.
Inflammation can cause systemic effects like fever, increased white blood cell count, and changes in plasma proteins. It is normally regulated to prevent harm, but severe inflammation from massive cytokine release can cause shock. Acute inflammation presents as different patterns (catarrhal, serous, fibrinous, membranous, allergic, hemorrhagic) depending on site and characteristics of escaped plasma. Suppurative inflammation is caused by pyogenic bacteria and results in pus formation in structures like abscesses, boils, and carbuncles.
This document discusses inflammation. It defines inflammation as the body's local response to injury or infection aimed at eliminating the cause of injury and initiating repair. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. The early response involves vasodilation and increased permeability, causing swelling. The late response involves neutrophils in acute inflammation and macrophages in chronic cases, which work to destroy pathogens and initiate healing. Understanding inflammation is important for diagnosing conditions like appendicitis and treating diseases.
Inflammation is the body's response to injury or infection that is characterized by redness, swelling, heat, pain, and loss of function. The cardinal signs of inflammation are caused by increased blood flow, increased vascular permeability, and leukocyte infiltration at the site of injury or infection. Acute inflammation typically involves neutrophils and resolves within 48 hours, while chronic inflammation involves mononuclear cells and persists for longer than 48 hours. Inflammation can lead to abscess formation, progression to chronic inflammation, resolution, or repair through scarring or fibrosis.
aetiology of inflammation; types of inflammation; how inflammation occur; cells involve in inflammation; role of wbc in inflammation; outcome of inflammation; how inflammation associated with immunity, clotting system, complementary system kinin system, how inflammation is associated with oral cavity; disease associated with inflammatory system
Chronic inflammation is inflammation of prolonged duration that involves ongoing active inflammation, tissue injury, and simultaneous healing. It can be caused by persistent infections, prolonged exposure to toxic agents, or autoimmunity. Morphologically, it is characterized by infiltration of mononuclear cells like macrophages, lymphocytes, and plasma cells, as well as ongoing tissue destruction and attempts at repair through angiogenesis and fibrosis. Chronic inflammation involves recruitment and accumulation of macrophages from the blood and their activation, leading to effects like increased cytokine production. Other cells like mast cells, lymphocytes, plasma cells, and eosinophils may also be present. Granulomatous inflammation features collections of macrophages that form granulomas. Chronic inflammation can also cause systemic effects through the acute
Acute inflammation is the early response of tissues to injury and involves vascular and cellular events. The vascular events include vasodilation, increased vascular permeability allowing plasma proteins to leave circulation, and accumulation of leukocytes from the blood vessels into tissues. The principal leukocytes in acute inflammation are neutrophils. The cellular events in acute inflammation help destroy, dilute or isolate injurious agents. Mediators of acute inflammation include histamine, prostaglandins, nitric oxide, complement factors and cytokines. Acute inflammation is rapid in onset, relatively short in duration and aims to return tissues to normal function.
Inflammation can cause systemic effects like fever, increased white blood cell count, and changes in plasma proteins. It is normally regulated to prevent harm, but severe inflammation from massive cytokine release can cause shock. Acute inflammation presents as different patterns (catarrhal, serous, fibrinous, membranous, allergic, hemorrhagic) depending on site and characteristics of escaped plasma. Suppurative inflammation is caused by pyogenic bacteria and results in pus formation in structures like abscesses, boils, and carbuncles.
This document discusses inflammation. It defines inflammation as the body's local response to injury or infection aimed at eliminating the cause of injury and initiating repair. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. The early response involves vasodilation and increased permeability, causing swelling. The late response involves neutrophils in acute inflammation and macrophages in chronic cases, which work to destroy pathogens and initiate healing. Understanding inflammation is important for diagnosing conditions like appendicitis and treating diseases.
Inflammation is the body's response to injury or infection that is characterized by redness, swelling, heat, pain, and loss of function. The cardinal signs of inflammation are caused by increased blood flow, increased vascular permeability, and leukocyte infiltration at the site of injury or infection. Acute inflammation typically involves neutrophils and resolves within 48 hours, while chronic inflammation involves mononuclear cells and persists for longer than 48 hours. Inflammation can lead to abscess formation, progression to chronic inflammation, resolution, or repair through scarring or fibrosis.
aetiology of inflammation; types of inflammation; how inflammation occur; cells involve in inflammation; role of wbc in inflammation; outcome of inflammation; how inflammation associated with immunity, clotting system, complementary system kinin system, how inflammation is associated with oral cavity; disease associated with inflammatory system
Chronic inflammation is inflammation of prolonged duration that involves ongoing active inflammation, tissue injury, and simultaneous healing. It can be caused by persistent infections, prolonged exposure to toxic agents, or autoimmunity. Morphologically, it is characterized by infiltration of mononuclear cells like macrophages, lymphocytes, and plasma cells, as well as ongoing tissue destruction and attempts at repair through angiogenesis and fibrosis. Chronic inflammation involves recruitment and accumulation of macrophages from the blood and their activation, leading to effects like increased cytokine production. Other cells like mast cells, lymphocytes, plasma cells, and eosinophils may also be present. Granulomatous inflammation features collections of macrophages that form granulomas. Chronic inflammation can also cause systemic effects through the acute
Definition of inflammation, Causes, Signs of inflammation, Types of inflammation, Triple response, Phagocytosis, Transudate or Exudate, Difference between transudate and exudate, Granuloma and Granulomatous inflammation
Inflammation is the body's response to injury or infection. It involves both vascular changes and cellular events at the site of injury or infection. The vascular changes include transient vasoconstriction, followed by vasodilation and increased vascular permeability, leading to exudation of fluid proteins from blood vessels into tissues. This exudate carries antibodies, complement proteins, and cells to help fight infection and begin repair. The cardinal signs of inflammation - redness, heat, swelling, pain, and loss of function - result from these vascular and cellular processes.
Inflammation is the protective response of tissues to injury or infection. The document outlines the key aspects of acute and chronic inflammation including:
1) The mediators of acute inflammation such as histamine, prostaglandins, and cytokines which cause redness, swelling, heat and pain.
2) Chronic inflammation is characterized by persistence of the inflammatory response and attempts at repair/regeneration. It involves lymphocytes, plasma cells and macrophages.
3) Granulomatous inflammation forms distinct nodules or granulomas that wall off chronic infections or foreign materials.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
This document summarizes the key differences between acute and chronic inflammation. Acute inflammation is an initial rapid response to injury or infection that involves increased blood flow and immune cell infiltration. It is typically short-lived and resolves within days. Chronic inflammation is a prolonged response lasting weeks or longer that can cause ongoing tissue damage. It involves different immune cells and may have no obvious symptoms, increasing risk for serious diseases like cancer if left unaddressed.
1. Acute inflammation is rapid in onset and short in duration, characterized by fluid and protein exudation and neutrophil accumulation. Chronic inflammation is slower in onset and longer lasting, characterized by mononuclear cell infiltration, ongoing tissue destruction, and attempts at repair through fibrosis.
2. The key features of acute inflammation are vasodilation, increased vascular permeability, and recruitment of leukocytes from the blood vessels to the site of injury. Chronic inflammation features mononuclear cell infiltration, persistent tissue damage, and attempts to repair through fibrosis and angiogenesis.
3. Granulomatous inflammation is a pattern of chronic inflammation seen with certain infections, featuring focal collections of activated macrophages that develop an epithelial-like appearance known
Chronic inflammation is characterized by prolonged inflammation lasting weeks or months, where tissue injury and attempts at repair occur simultaneously. It can be caused by persistent infections, prolonged exposure to toxic agents, or autoimmunity. Morphologically, it features infiltration by mononuclear cells like macrophages and lymphocytes, ongoing tissue destruction, and attempts at healing through fibrosis and angiogenesis. Chronic inflammation is regulated by various cell-derived mediators like cytokines, eicosanoids, and reactive oxygen species, as well as plasma-derived mediators like components of the complement, coagulation, and kinin systems. Granulomatous inflammation forms microscopic nodules called granulomas in an attempt to contain hard to eliminate infectious agents.
Acute inflammation is the early response of tissue to injury and is characterized by changes in the microcirculation such as increased fluid exudation and leukocyte emigration from blood vessels to the injured area. It is typically short in duration and aims to remove the injurious agent. The major causes include infections, tissue necrosis, foreign bodies, and burns. Acute inflammation exhibits cardinal signs of pain, heat, redness, swelling, and loss of function and involves vascular changes like increased permeability and blood flow as well as cellular components like leukocytes that release inflammatory mediators. The morphological patterns of acute inflammation depend on the type and extent of tissue response. Outcomes range from resolution to fibrosis, abscess formation, or progression to
Inflammation is the protective response to eliminate the cause of cell injury and damaged tissue. It is characterized by redness, heat, swelling, pain, and loss of function. The signs are caused by increased blood flow and vascular permeability. Inflammation can be acute, lasting minutes to days, or chronic, lasting weeks or months. Acute inflammation involves recruitment of leukocytes from the bloodstream to fight infection at the site of injury. Chronic inflammation is prolonged and involves tissue destruction by mononuclear cells and attempts at healing through fibrosis. Mediators like cytokines prolong the inflammatory response.
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. The main events of acute inflammation are vascular events like vasodilation and increased permeability, and cellular events involving leukocyte recruitment and activation. This results in an inflammatory cell-rich exudate. Acute inflammation can resolve, repair through regeneration or fibrosis, lead to suppuration or pus formation, or progress to chronic inflammation. Examples include acute appendicitis, meningitis, and pneumonia.
Acute inflammation in pathologic basis of diseasesoyovwipedro2
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. The main events of acute inflammation are vascular events like vasodilation and increased permeability, and cellular events involving leukocyte recruitment and activation. This results in an inflammatory cell-rich exudate. Acute inflammation can resolve, repair through regeneration or fibrosis, lead to suppuration or pus formation, or progress to chronic inflammation. Examples include acute appendicitis, meningitis, and pneumonia.
This document discusses different patterns of inflammation. It describes acute and chronic inflammation, and outlines several morphological patterns including serous, fibrinous, suppurative, ulcerative, pseudomembranous, catarrhal, and granulomatous inflammation. Each pattern is characterized by the type of inflammatory exudate produced, such as watery fluid, fibrin deposits, or pus accumulation. Examples are provided of diseases associated with each inflammatory pattern.
Lyme disease is caused by the spirochete Borrelia burgdorferi and transmitted through tick bites. It involves three stages: stage 1 causes a characteristic rash and flu-like symptoms near the site of the bite; stage 2 results in secondary skin or neurological lesions as the bacteria spreads; stage 3 may cause long-term arthritis. Clostridial infections include gas gangrene caused by Clostridium perfringens and tetanus caused by C. tetani. Chlamydial infections, such as trachoma, are transmitted sexually and involve an intracellular life cycle. Rickettsial diseases infect endothelial cells and cause symptoms from vascular damage. Fungal infections include candidiasis, where
1. Inflammation is the body's normal response to injuries or infections where immune cells travel to the injured or infected site and cause inflammation.
2. Acute inflammation occurs immediately after injury and is characterized by increased blood flow, vascular permeability, and recruitment of immune cells.
3. Chronic inflammation lasts weeks to months where active inflammation, tissue damage, and healing occur simultaneously, such as in autoimmune diseases or infections unable to be cleared.
Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, pain, and loss of function. It involves increased blood flow, exudation of fluid, and emigration of leukocytes. The goals are to remove harmful stimuli, limit tissue damage, and initiate repair. Acute inflammation is short-lived and has beneficial effects like fighting infection, but can also cause harmful tissue swelling and pain.
Inflammation is the body's response to harmful stimuli and involves increased blood flow, swelling, heat, redness, and pain. The goals of inflammation are to eliminate the initial cause, remove damaged cells, and initiate tissue repair. The cardinal signs of inflammation come from Latin and include pain, heat, redness, swelling, and loss of function. Acute inflammation lasts less than 48 hours and involves neutrophils, while chronic inflammation lasts longer and involves mononuclear cells. Acute inflammation may resolve, progress to chronic, lead to abscess formation, or result in tissue repair through scarring.
Inflammation is the body's response to injury or infection that involves vascular and cellular events. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. Inflammation can be either acute (minutes to days) or chronic (weeks to months). Chemical mediators like histamine, prostaglandins, and leukotrienes are released during inflammation and cause changes like increased vascular permeability and leukocyte migration. Repair after inflammation occurs through regeneration of tissues like skin, or through healing by scar formation. Healing involves granulation tissue formation, angiogenesis, fibroblast proliferation and extracellular matrix deposition.
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. It involves both vascular and cellular events over a short period of time. The vascular events include increased blood flow and permeability, which leads to fluid leakage. The cellular events involve leukocyte recruitment to the site through adhesion molecules and chemotaxis, followed by activation and phagocytosis of microbes. Acute inflammation can manifest morphologically as serous, fibrinous, purulent or hemorrhagic inflammation. It typically resolves through resolution or repair, but can also lead to suppuration or progress to chronic inflammation.
The document summarizes key aspects of acute and chronic inflammation. Acute inflammation is triggered by various stimuli and involves increased blood flow, vascular permeability, and leukocyte migration. It aims to eliminate injurious agents. Chronic inflammation arises from persistent infections, toxins, or autoimmunity and is characterized by mononuclear cell infiltration and attempts at repair through fibrosis. Nutrition can impact inflammation through deficiencies, essential fatty acids, antioxidants, and factors related to over-nutrition like obesity.
Definition of inflammation, Causes, Signs of inflammation, Types of inflammation, Triple response, Phagocytosis, Transudate or Exudate, Difference between transudate and exudate, Granuloma and Granulomatous inflammation
Inflammation is the body's response to injury or infection. It involves both vascular changes and cellular events at the site of injury or infection. The vascular changes include transient vasoconstriction, followed by vasodilation and increased vascular permeability, leading to exudation of fluid proteins from blood vessels into tissues. This exudate carries antibodies, complement proteins, and cells to help fight infection and begin repair. The cardinal signs of inflammation - redness, heat, swelling, pain, and loss of function - result from these vascular and cellular processes.
Inflammation is the protective response of tissues to injury or infection. The document outlines the key aspects of acute and chronic inflammation including:
1) The mediators of acute inflammation such as histamine, prostaglandins, and cytokines which cause redness, swelling, heat and pain.
2) Chronic inflammation is characterized by persistence of the inflammatory response and attempts at repair/regeneration. It involves lymphocytes, plasma cells and macrophages.
3) Granulomatous inflammation forms distinct nodules or granulomas that wall off chronic infections or foreign materials.
INTRODUCTION
HISTORY
CAUSES OF INFLAMMATION
CLASSIFICATION
ACUTE INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
OUTCOMES OF ACUTE INFLAMMATION
CHRONIC INFLAMMATION
INFLAMMATORY DISEASES
REFERENCES
This document summarizes the key differences between acute and chronic inflammation. Acute inflammation is an initial rapid response to injury or infection that involves increased blood flow and immune cell infiltration. It is typically short-lived and resolves within days. Chronic inflammation is a prolonged response lasting weeks or longer that can cause ongoing tissue damage. It involves different immune cells and may have no obvious symptoms, increasing risk for serious diseases like cancer if left unaddressed.
1. Acute inflammation is rapid in onset and short in duration, characterized by fluid and protein exudation and neutrophil accumulation. Chronic inflammation is slower in onset and longer lasting, characterized by mononuclear cell infiltration, ongoing tissue destruction, and attempts at repair through fibrosis.
2. The key features of acute inflammation are vasodilation, increased vascular permeability, and recruitment of leukocytes from the blood vessels to the site of injury. Chronic inflammation features mononuclear cell infiltration, persistent tissue damage, and attempts to repair through fibrosis and angiogenesis.
3. Granulomatous inflammation is a pattern of chronic inflammation seen with certain infections, featuring focal collections of activated macrophages that develop an epithelial-like appearance known
Chronic inflammation is characterized by prolonged inflammation lasting weeks or months, where tissue injury and attempts at repair occur simultaneously. It can be caused by persistent infections, prolonged exposure to toxic agents, or autoimmunity. Morphologically, it features infiltration by mononuclear cells like macrophages and lymphocytes, ongoing tissue destruction, and attempts at healing through fibrosis and angiogenesis. Chronic inflammation is regulated by various cell-derived mediators like cytokines, eicosanoids, and reactive oxygen species, as well as plasma-derived mediators like components of the complement, coagulation, and kinin systems. Granulomatous inflammation forms microscopic nodules called granulomas in an attempt to contain hard to eliminate infectious agents.
Acute inflammation is the early response of tissue to injury and is characterized by changes in the microcirculation such as increased fluid exudation and leukocyte emigration from blood vessels to the injured area. It is typically short in duration and aims to remove the injurious agent. The major causes include infections, tissue necrosis, foreign bodies, and burns. Acute inflammation exhibits cardinal signs of pain, heat, redness, swelling, and loss of function and involves vascular changes like increased permeability and blood flow as well as cellular components like leukocytes that release inflammatory mediators. The morphological patterns of acute inflammation depend on the type and extent of tissue response. Outcomes range from resolution to fibrosis, abscess formation, or progression to
Inflammation is the protective response to eliminate the cause of cell injury and damaged tissue. It is characterized by redness, heat, swelling, pain, and loss of function. The signs are caused by increased blood flow and vascular permeability. Inflammation can be acute, lasting minutes to days, or chronic, lasting weeks or months. Acute inflammation involves recruitment of leukocytes from the bloodstream to fight infection at the site of injury. Chronic inflammation is prolonged and involves tissue destruction by mononuclear cells and attempts at healing through fibrosis. Mediators like cytokines prolong the inflammatory response.
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. The main events of acute inflammation are vascular events like vasodilation and increased permeability, and cellular events involving leukocyte recruitment and activation. This results in an inflammatory cell-rich exudate. Acute inflammation can resolve, repair through regeneration or fibrosis, lead to suppuration or pus formation, or progress to chronic inflammation. Examples include acute appendicitis, meningitis, and pneumonia.
Acute inflammation in pathologic basis of diseasesoyovwipedro2
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. The main events of acute inflammation are vascular events like vasodilation and increased permeability, and cellular events involving leukocyte recruitment and activation. This results in an inflammatory cell-rich exudate. Acute inflammation can resolve, repair through regeneration or fibrosis, lead to suppuration or pus formation, or progress to chronic inflammation. Examples include acute appendicitis, meningitis, and pneumonia.
This document discusses different patterns of inflammation. It describes acute and chronic inflammation, and outlines several morphological patterns including serous, fibrinous, suppurative, ulcerative, pseudomembranous, catarrhal, and granulomatous inflammation. Each pattern is characterized by the type of inflammatory exudate produced, such as watery fluid, fibrin deposits, or pus accumulation. Examples are provided of diseases associated with each inflammatory pattern.
Lyme disease is caused by the spirochete Borrelia burgdorferi and transmitted through tick bites. It involves three stages: stage 1 causes a characteristic rash and flu-like symptoms near the site of the bite; stage 2 results in secondary skin or neurological lesions as the bacteria spreads; stage 3 may cause long-term arthritis. Clostridial infections include gas gangrene caused by Clostridium perfringens and tetanus caused by C. tetani. Chlamydial infections, such as trachoma, are transmitted sexually and involve an intracellular life cycle. Rickettsial diseases infect endothelial cells and cause symptoms from vascular damage. Fungal infections include candidiasis, where
1. Inflammation is the body's normal response to injuries or infections where immune cells travel to the injured or infected site and cause inflammation.
2. Acute inflammation occurs immediately after injury and is characterized by increased blood flow, vascular permeability, and recruitment of immune cells.
3. Chronic inflammation lasts weeks to months where active inflammation, tissue damage, and healing occur simultaneously, such as in autoimmune diseases or infections unable to be cleared.
Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, pain, and loss of function. It involves increased blood flow, exudation of fluid, and emigration of leukocytes. The goals are to remove harmful stimuli, limit tissue damage, and initiate repair. Acute inflammation is short-lived and has beneficial effects like fighting infection, but can also cause harmful tissue swelling and pain.
Inflammation is the body's response to harmful stimuli and involves increased blood flow, swelling, heat, redness, and pain. The goals of inflammation are to eliminate the initial cause, remove damaged cells, and initiate tissue repair. The cardinal signs of inflammation come from Latin and include pain, heat, redness, swelling, and loss of function. Acute inflammation lasts less than 48 hours and involves neutrophils, while chronic inflammation lasts longer and involves mononuclear cells. Acute inflammation may resolve, progress to chronic, lead to abscess formation, or result in tissue repair through scarring.
Inflammation is the body's response to injury or infection that involves vascular and cellular events. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. Inflammation can be either acute (minutes to days) or chronic (weeks to months). Chemical mediators like histamine, prostaglandins, and leukotrienes are released during inflammation and cause changes like increased vascular permeability and leukocyte migration. Repair after inflammation occurs through regeneration of tissues like skin, or through healing by scar formation. Healing involves granulation tissue formation, angiogenesis, fibroblast proliferation and extracellular matrix deposition.
Acute inflammation is characterized by five signs: redness, heat, swelling, pain, and loss of function. It involves both vascular and cellular events over a short period of time. The vascular events include increased blood flow and permeability, which leads to fluid leakage. The cellular events involve leukocyte recruitment to the site through adhesion molecules and chemotaxis, followed by activation and phagocytosis of microbes. Acute inflammation can manifest morphologically as serous, fibrinous, purulent or hemorrhagic inflammation. It typically resolves through resolution or repair, but can also lead to suppuration or progress to chronic inflammation.
The document summarizes key aspects of acute and chronic inflammation. Acute inflammation is triggered by various stimuli and involves increased blood flow, vascular permeability, and leukocyte migration. It aims to eliminate injurious agents. Chronic inflammation arises from persistent infections, toxins, or autoimmunity and is characterized by mononuclear cell infiltration and attempts at repair through fibrosis. Nutrition can impact inflammation through deficiencies, essential fatty acids, antioxidants, and factors related to over-nutrition like obesity.
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga
GASTROINTESTINAL INFECTIONS AND GASTRITIS
Osvaldo Bernardo Muchanga
Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
Among the factors that lead to the occurrence of gastrointestinal infections are the hygienic and sanitary deficiencies that characterize our markets and other places where raw or cooked food is sold, poor environmental sanitation in communities, deficiencies in water treatment (or in the process of its plumbing), risky hygienic-sanitary habits (not washing hands after major and/or minor needs), among others.
These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
Gastritis and Gastric Health
Gastric Health is one of the most relevant concerns in human health, with gastrointestinal infections being among the main illnesses that affect humans.
Among gastric problems, we have GASTRITIS AND GASTRIC ULCERS as the main public health problems. Gastritis and gastric ulcers normally result from inflammation and corrosion of the walls of the stomach (gastric mucosa) and are generally associated (caused) by the bacterium Helicobacter pylor, which, according to the literature, this bacterium settles on these walls (of the stomach) and starts to release urease that ends up altering the normal pH of the stomach (acid), which leads to inflammation and corrosion of the mucous membranes and consequent gastritis or ulcers, respectively.
In addition to bacterial infections, gastritis and gastric ulcers are associated with several factors, with emphasis on prolonged fasting, chemical substances including drugs, alcohol, foods with strong seasonings including chilli, which ends up causing inflammation of the stomach walls and/or corrosion. of the same, resulting in the appearance of wounds and consequent gastritis or ulcers, respectively.
Among patients with gastritis and/or ulcers, one of the dilemmas is associated with the foods to consume in order to minimize the sensation of pain and discomfort.
Discover the benefits of homeopathic medicine for irregular periods with our guide on 5 common remedies. Learn how these natural treatments can help regulate menstrual cycles and improve overall menstrual health.
Visit Us: https://drdeepikashomeopathy.com/service/irregular-periods-treatment/
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
Pictorial and detailed description of patellar instability with sign and symptoms and how to diagnose , what investigations you should go with and how to approach with treatment options . I have presented this slide in my 2nd year junior residency in orthopedics at LLRM medical college Meerut and got good reviews for it
After getting it read you will definitely understand the topic.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
Nano-gold for Cancer Therapy chemistry investigatory projectSIVAVINAYAKPK
chemistry investigatory project
The development of nanogold-based cancer therapy could revolutionize oncology by providing a more targeted, less invasive treatment option. This project contributes to the growing body of research aimed at harnessing nanotechnology for medical applications, paving the way for future clinical trials and potential commercial applications.
Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
4. Patterns of Inflammation
Acute
* Short duration (minutes-days) with exudation of
fluid & plasma proteins, and emigration of
neutrophils into tissue.
Chronic
* Longer duration (days-months) with tissue
accumulation of lymphocytes, plasma cells, &
macrophages plus variable proliferation of blood
vessels, fibrosis and necrosis.
5. Inflammation: essential definitions
Exudation = Escape of fluid, proteins, and blood
cells from vessels into tissues
Exudate = Inflammatory fluid, high protein
concentration and sp.gr. > 1.020
Transudate = Watery fluid, low protein concentration
and sp. gr. < 1.012
Oedema = Excess fluid in tissues & excess fluid
in serous cavities lined by mesothelium
(pleural, pericardial, peritoneal)
Pus = Inflammatory exudate rich in
neutrophils and cell debris
6. Cardinal Signs of Inflammation
Redness : Hyperaemia.
Warm : Hyperaemia.
Pain : Nerve, Chemical
mediators.
Swelling : Exudation
Loss of Function: Pain
7. Function of inflammatory exudates
1-Dilute the invading microorganism and its
toxins.
2-Bring antibodies through the plasma to the
inflamed area for neutralization.
3-Bring leukocytes that engulf the invading
microorganisms.
4-Bring fibrinogen through the plasma, which is
converted, to fibrin mesh, helping in trapping the
microorganism and localize the infection.
5- Initiate the process of repair
9. Pathogenesis
Vascular events
* Changes in Vascular Flow and Caliber
* Increased Vascular Permeability
Cellular events
* Extravasation of Leukocytes
• In lumen of blood vessel (3 phases):
– Margination
– Rolling
– Adhesion
• Transmigration of leukocytes
• Migration into interstitium toward injury site by
locomotion along a chemical gradient: Chemotaxis
* Phagocytosis
16. TRANSUDATE AND
EXUDATE
TRANSUDATE
Filtrate of blood plasma
without changes in endothelial
permeability.
Non-inflammatory edema
<1gm/dl protein
pH <7.3
Few cells,mainly mesothelial
Eg:congestive cardiac failure
EXUDATE
Edema of inflamed tissue
associated with increased
permeability
inflammatory edema
>3.5gm/dl protein
pH>7.3
Many cells,inflammatory as
well as parenchymal
Eg:purulent exudate such as
pus
18. SEROUS INFLAMMATION:
Serous inflammation is marked by the
outpouring of a thin fluid
* e.g. the skin blister resulting from a burn or viral
infection represents a large accumulation of
serous fluid
19.
20.
21. FIBRINOUS INFLAMMATION
More severe injuries and
More greater vascular permeability,
Larger molecules such as
* fibrinogen pass the vascular barrier, and fibrin
is formed and deposited
22. FIBRINOUS PERICARDITIS(GROSS)
Exudation of a protein-
rich fluid into a cavity
leads to a transudate. The
fibrin in this fluid can
form a fibrinous exudate
on the surfaces. Here, the
pericardial cavity has been
opened to reveal a
fibrinous pericarditis with
strands of stringy pale
fibrin between visceral
and parietal pericardium.
23. FIBRINOUS INFLAMMATION
* A fibrinous exudate is characteristic of
inflammation in the lining of body cavities, such as
the meninges, pericardium and pleura
24. FIBRINOUS INFLAMMATION
Fibrinous exudates may be removed by
fibrinolysis
But when the fibrin is not removed, it
may stimulate the in-growth of
fibroblasts and blood vessels and thus
lead to scarring (organization)
25. SUPPURATIVE OR PURULENT
INFLAMMATION
Characterized by the production of large amounts
of pus or purulent exudate consisting of
neutrophils, necrotic cells, and edema fluid
Certain bacteria (e.g., staphylococci) produce this
localized suppuration and are therefore referred
to as pyogenic (pus-producing) bacteria
27. Acute Appendicitis(Gross)
Here is acute
appendicitis with
Yellow to tan exudate
and
Hyperemia, including
The peri-appendiceal
fat superiorly, rather
than a smooth,
glistening pale tan
serosal surface.
29. PYOGENIC MENINGITIS(GROSS)
A purulent exudate is
seen beneath the
meninges in the brain
of this patient with
acute meningitis from
Streptococcus
pneumoniae infection.
The exudate obscures
the sulci.
31. Pyogenic Meningitis(Micro)
Microscopically, a
neutrophilic exudate is seen
involving the meninges at
the left, with prominent
dilated vessels.
There is edema and focal
inflammation in the cortex
to the right.
This acute meningitis is
typical for bacterial
infection.
33. LOBAR PNEUMONIA(MICRO)
At medium power
magnification, numerous
neutrophils fill the alveoli
in this case of acute
bronchopneumonia in a
patient with a high fever.
Pseudomonas aeruginosa
was cultured from
sputum.
Note the dilated
capillaries in the alveolar
walls from vasodilation
with the acute
inflammatory process.
36. Suppurative inflammation. A, A subcutaneous bacterial
abscess with collections of pus. B, The abscess contains
neutrophils, edema fluid, and cellular debris.
39. KIDNEY ABSCESS(MICRO)
This is an ascending
bacterial infection
leading to kidney
abscess.
Numerous PMN's are
seen filling renal
tubules across the
center and right of this
picture.
40. Lung Abscess(Gross)
Here is lung abscess, in
the upper lobe of this left
lung.
An abscess is a
complication of severe
pneumonia, most
typically from virulent
organisms such as S.
aureus.
44. Cellulitis
It is an acute diffuse suppurative inflammation
caused by streptococci, which secrete
hyaluronidase & streptokinase enzymes that
dissolve the ground substances and facilitate the
spread of infection.
Sites:
* Areolar tissue; orbit, pelvis, …
* Lax subcutaneous tissue
45. Ulcers
An ulcer is a local defect of the surface
of an organ or tissue that is produced by
the sloughing (shedding) of
inflammatory necrotic tissue
46. Ulceration can occur only when tissue necrosis and
resultant inflammation exist on or near a surface
Epithelial Defect
Fibrinopurulent exudates
Granulation tissue
Fibrosis
Necrotic base
48. Systemic Effects of Inflammation
Fever
Fever is produced in response to Pyrogens
What are pyrogens?
* act by stimulating prostaglandin synthesis in the
vascular and perivascular cells of the hypothalamus.
Bacterial products (called exogenous pyrogens),
stimulate leukocytes to release cytokines such as
IL-1 and TNF (called endogenous pyrogens) that
increase the enzymes (cyclooxygenases) that
convert AA into prostaglandins.
49. Outcomes of acute inflammation
Fig. 3-24, Pathologic Basis of Disease, 6th ed, WB Saunders, 1999.
50. Chronic inflammation
Chronic inflammation is inflammation of
prolonged duration (weeks or months) in
which inflammation, tissue injury, and
attempts at repair coexist, in varying
combinations.
Types of chronic inflammation
1. Chronic non specific inflammation
2. Chronic specific inflammation: It includes
granulomatous inflammation
51. Causes of chronic inflammation
Prolonged acute inflammation or repeated bout of
acute inflammation may lead to the presence of
more mononuclear cells and chronic
inflammation.
52. Causes of chronic inflammation
Persistent infection by microorganisms that are
difficult to eradicate such as mycobacteria, certain
viruses, fungi and parasites. These often evoke
delayed-type hypersensitivity reaction.
Immune-mediated inflammatory diseases: Include
autoimmune diseases & allergic diseases. May
show mixture of acute and chronic inflammation.
Prolonged exposure to potentially toxic agents,
either exogenous (e.g. silicosis) or endogenous
(e.g. atherosclerosis).
53. CHRONIC INFLAMMATION
Morphologically, characterized by:
Infiltration by mononuclear cells i.e. macrophages,
lymphocytes, and plasma cells.
Tissue destruction.
Attempts at healing by connective tissue
replacement of damaged tissue accompanied by
angiogenesis and in particular, fibrosis.
54.
55. Chronic non specific inflammation
It is seen affecting any organ for a
prolonged period of time.
It is characterized by diffuse infiltration
with mononuclear inflammatory cells.
Examples:
1. Chronic nonspecific cervicitis
2. Chronic cholecystitis
3. Chronic osteomyelitis
60. CHRONIC OSTEOMYELITIS
There is fibrosis of
the marrow space
accompanied by
chronic inflammatory
cells.
There can be bone
destruction with
remodeling.
61. Granulomatous inflammation
Granulomatous inflammation is the
ditinctive pattern of chronic inflammation.
It is caused by organisms which are difficult
to eradicate and induce immune response
known as delayed hypersensitivity.
Immune reactions usually lead to
development of granuloma, which is a
cellular attempt to contain an offending
agent.
62. GRANULOMA
Granuloma is a focus of chronic inflammation
consisting of a microscopic aggregation of
macrophages that are transformed into epithelium
like cells- epithelioid cells surrounded by a collar
of mononuclear leukocytes, principally
lymphocytes and occasionally plasma cells.
Frequently, epithelioid cells fuse to form giant
cells, having many nuclei arranged either
peripherally (Langhans-type) or haphazardly
(Foreign body-type).
Older granuloma develop an enclosing rim of
fibroblasts and connective tissue.
63. Defination
Chronic Inflammation- Defined as a
prolong process in which tissue destruction
and inflammation occurs at the same time.
Granuloma-Defined as a circumscribed
,tiny,lesion,about 1mm in diameter
,composed predominantly of collection of
modified macrophages called epitheloid
cells and rimmed at the periphery by
lymphoid cells.
64. Tuberculosis Mycobacterium
tuberculosis
Caseating granuloma
(tubercle)
Leprosy Mycobacterium leprae AFB in macrophages;
noncaseating granuloma
Syphillis Treponema pallidum Gumma(enclosing wall of
histiocytes; plasma cells)
Cat-scratch disease Gram neg bacillus Round or stellate granuloma
Crohn disease Immune reaction against
intestinal bacteria, self
antigens
Occasional noncaseating
granuloma in the wall of
intestine
Sarcoidosis Unknown etiology Noncaseating granulomas
with abundant activated
macrophages
Inorganic metals
,dusts,silicosis
Foreign body Granuloma with foreign body
type giant cells.
66. GRANULOMATOUS INFLAMMATION(MICRO,L.P.)
The focal nature of
granulomatous
inflammation is
demonstrated in this
microscopic section of
lung in which
there are scattered
granulomas in the
parenchyma.
71. Actinomycosis
Causative Agent is Bacterium
Actinomycosis Israeli..
Gross-Painless mass at jaw cervicofacial,
pulmonary, ileocecal region.
The mas has discharging sinuses draining
yellow sulfur granules with centrsl necrotic
area.
73. Repair
The injured tissue is replaced through regeneration
of native parenchymal cells, by filling of the
defect with fibrous tissue (scarring) or, most
commonly, by a combination of these two
processes.
Granulation tissue
It is formed during the process of repair.
Grossly, pink & granular soft tissue formed at the
surface of the wounds and is characterized by
proliferation of blood vessels & fibroblasts and
with some degree of inflammatory cells infiltrate .
74.
75.
76. GRANULATION TISSUE(H.P.)
At high
magnification,
granulation
tissue has
capillaries,
fibroblasts, and a
variable amount
of inflammatory
cells (mostly
mononuclear).
77. GRANULATION TISSUE
Healing of
inflammation often
involves in growth of
capillaries and
fibroblasts. This forms
granulation tissue.
Here, an acute
myocardial infarction
is seen healing.
78. Pathological aspects of repair
Repair will be abnormal in following
conditions:
1. Deficient scar formation: Wound
dehiscence (or rupture) and ulceration.
2. Excessive formation of the repair
components: Hypertrophic scar and
keloid.
3. Formation of contractures.
79. Cont…
Hypertrophic scar shows excess amount of
collagen deposits.
Keloid is overgrowth of scar tissue beyond
the boundaries of original wound healing. It
shows excessive hyalinisation.
82. Definition
• TB (Tuberculosis) is potentially fatal
contagious disease that can affect almost
any part of the body but is mainly an
infection of the lung.
• Tubercle-Round nodule/swelling
• Osis-Condition
83. Etiology
• Mycobacterium Tuberculosis from the
family Mycobacteiaceae.
• First discovered by Robert KOCH in 1882.
• So called as KOCH BACILLI.
• Although classified as gram positive but its
reaction is weak.
92. Lung, Ghon complex - In the radiograph and in the photograph, a
calcified, well-circumscribed nodule in the left lung represents an old
healed focus of primary tuberculosis; these are characteristically
peripheral in location. In addition, other calcified nodules can be seen in
the radiograph in the left hilar region -This is a former focus of infection
by TB in draining lymph nodes.
•CALCIFIED
LYMPHNODE
•SUBPLEURAL
NODULE
93. •Caseous
necrosis
•Zone of
epitheloid
cells
Lung, left, caseous necrosis - Low power
There is a large central area of caseous necrosis, which is seen as
granular pink structureless material with complete destruction of the lung
parenchyma. The caseous material is surrounded by a cellular zone that
contains epithelioid cells and giant cells. These cells are seen at a higher
magnification in the next image. At the periphery, some alveolar spaces
can be seen.
94. In this higher magnification of the lung lesion, caseous necrosis is seen
as pink granular structureless material that has destroyed the lung
alveoli. Epithelioid cells surrounding the caseous material are
elongated cells with indistinct cell boundaries. Individual epithelioid
cells are difficult to see in this lesion. A large multinucleated giant cell
is clearly visible. The cells with dark round nuclei are lymphocytes.
95. Testis, granulomatous inflammation - High power Granulomatous
inflammation with caseous necrosis.
•Caseous
necrosis
•Epitheloid
histiocytes
96. Lymph node, noncaseating granulomas - Low power. This image is of a
lymph node from a patient with sarcoidosis and is provided here for
comparison with the caseating granulomas of tuberculosis. Each of these
clusters of pink cells is a granuloma composed of interlacing epithelioid
cells and giant cells. Note the absence of caseous necrosis. While
granulomas in sarcoidosis do not have caseous necrosis, it should be
remembered that early lesions in tuberculosis may also have
noncaseating granulomas. .
•GRANULOMA
•GIANT CELL
97. - Lung, left, acid-fast stain - High power Reddish rods = acid-fast
bacteria (Mycobacterium tuberculosis) seen within an area of caseous
necrosis
98.
99. Lung, tuberculosis, secondary (reactivation) - The cavities in the upper
lobes are the pathologic and radiographic findings in secondary, or
reactivation, tuberculosis. The major bronchi have been opened to reveal
mucosal hyperemia, which indicates congestion or inflammation of the
bronchial mucosa. In addition, patchy consolidation is present in the
upper lobe; this may represent either superimposed bronchopneumonia
or progressive
•CYSTIC CAVITIES
•PATCHY
CONSOLIDATION
100. Spleen, miliary tuberculosis - Gross, cut surface This cut surface of the
spleen shows multiple light tan areas of caseous necrosis, which look
like multiple small abscesses grossly. Miliary tuberculosis may occur in
patients after either primary or secondary (reactivation) tuberculosis
103. EXTRAPULMONARY TB
Often due to reactivation or re-infection.
REACTIVATION:
Common
Represents breakdown of immunity
REINFECTION:
Due to partial immunity.
Load of bacteria to cause this must be relatively large.
104. MODE OF SPREAD OF EXTRA PULMONARY TB
Primary
focus
Bacteria invade pulmonary
vein in vicinity
Bacteria try to
invade systemic
circulation
Impaired Phagocyte
Function
M
E
T
A
S
T
A
S
I
S
Kidney
Adrenals
Fallopian tubes
Epididymis
Bones & Joints
Tendon Sheaths
105. Tuberculous Lymphadenitis
Commonest form of extra pulmonary TB.
Cervical lymphadenopathy most common.
Nodes are firm and often matted due to periadenitis.
Common cause of pyrexia of unknown origin
106. Stages Of Cervical Lymphadenitis
Enlargement
Matting
Cold Abscess Formation
Burst abscess in deep fascia
(Collar Stud Abscess)
Sinus Formation.
(1)
(2)
(3)
(4)
(5)
107. CNS Tuberculosis
Organisms reach brain via blood.
Common in HIV patients
1) TB Meningitis
2) Tubercular Abscess (Tuberculoma)
109. Abdominal TB
It may be Primary or secondary.
Swallowing of sputum in patients with active
tuberculosis causes sec. TB
Most common site - Terminal Ileum
Types Of Intestinal TB:
1. Ulcerative
2. Hyperplastic
3. TB Peritonitis
4. TB Lymphadenitis
111. TB Bones and Joints
Occurs secondary to lypho-haematogenous
dissemination from primary focus and later
reactivation.
Most commonly involves Spine (Pott’s Spine)
Tuberculous arthritis and Ankylosis.
115. MILIARY TB
Haematogenous spread
Millet sized casseous necrosis 2-3mm foci
Involvement of multiple organs
Rapid spread and detioration occurs in a
short period of time
116. MAC COMPLEX
Mycobacterium avium intracellulare
complex
More common in soil,water,dust and
domestic animals
More seen in AIDS with CD4
lymphocytes<60 cells/mm3
Abundant acid fast bacilli seen within
macrophages involve LN,lung,liver,spleen
Granulomas,lymphocytes, tissue destruction
is rare
120. Lepromin Test
Used for classifying leprosy on basis of
immune response
Early reaction: induration within 24 to 48
hrs
Delayed granulomatous lesion: After 3 to 4
wks
Pts with tuberculoid leprosy give positive
lepromin test and lepromatous leprosy pts
are negative