Cardiac manifestations of connective tissue disorders & kawasaki disease
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kawasaki disease connective tissue disorders in children notes from nelson's textbook of paediatrics, IAP pediatric cardiology & nada's pediatric cardiology textbook
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Necrotizing fasciitis, also known as flesh-eating bacteria, is a rare but serious soft tissue infection caused by various bacteria such as Group A Strep. The bacteria spreads rapidly, destroying skin, muscles, and tissues. Common causes include skin trauma, surgery, and insect bites. Left untreated, it can cause serious illness or death by releasing toxins and destroying tissue. Aggressive treatment requires hospitalization, IV antibiotics, debridement of damaged tissue, and sometimes amputation to prevent further spread.
Hand infection by Dr.K.AmrithaAnilkumar
Hand infection is the infection caused in hand , since hand contains neurovascular bundles, muscles, bones, and ligaments.
It includes
1. Acute Paronychia
2.Chronic Paronychia
3.Terminal pulp space infection ( felon)
4.subungal infection
5. Web space infecion
6. Mid palmar space infection
7.Thenar space infection
8. Deep palmar abscess
9. Acute suppurative tenosynovitis
11. Chronic Tenosynovitis
12. Lymphangitis of the hand
13. Arthritis of hand joints
14. Subcuticular abscess
Arterial diseases by Dr. AmrithaAnilkumar
Abdominal aortic aneurysm (AAA) is an enlargement of the aorta in the abdominal region. The most common cause is atherosclerosis. It can be asymptomatic and found incidentally or symptomatic with back pain, abdominal pain, or a pulsatile abdominal mass. Complications include rupture, infection, thrombosis, embolism, and erosion of nearby structures. Treatment involves surgical repair if the aneurysm reaches a certain size.
Boils or furuncle by Dr.K.AmrithaAnilkumar
Boil is an acute staphylococcal infection of a hair follicle with perifolliculitis which usually proceeds to suppuration & central necrosis.Often boil open on its own & subsides (S. aureus infection)
Gangrene-Pathology
The document discusses different types of gangrene: wet gangrene, dry gangrene, and gas gangrene. Wet gangrene occurs when both arterial and venous blood flow are blocked, causing tissue to become infected and rotten. Dry gangrene typically affects the toes and feet of older patients due to atherosclerosis, resulting in black, mummified tissue. Gas gangrene is caused by Clostridium bacteria that enter through wounds, producing toxins and gas bubbles within tissues causing swelling and a foul odor.
Gangrene
Dr. Monika Negi discusses different types of gangrene including dry gangrene, wet gangrene, and gas gangrene. Dry gangrene results from ischemia and causes tissue to become dry and black. Wet gangrene occurs in moist tissues and is caused by blockages leading to bacterial overgrowth and tissue putrefaction. Gas gangrene develops from clostridial bacteria infecting wounds and causing muscle necrosis and gas formation. Treatment for gas gangrene requires urgent surgery, antibiotics like penicillin, and sometimes hyperbaric oxygen or amputation.
CELL INJURY-II Gangrene
Hello friends..! This is 2nd presentation of series 'CELL INJURY'.. I have tried to describe important points about 'GANGRENE' in brief so that it will be helpful for quick revision. Plzz Like, Share n Subscribe to get notifications of my next presentations.. Thank You..!!
Infectious diseases by Dr.AmrithaAnilkumar
- Ludwig's angina is a rapidly progressive polymicrobial cellulitis of the sublingual and submandibular spaces, involving the floor of the mouth and suprahyoid area of the neck bilaterally.
- It is commonly caused by dental infections and presents with diffuse painful swelling and woody induration of the mouth and anterior neck, which can lead to airway obstruction if not treated promptly with antibiotics and potentially tracheostomy.
- Complications include laryngeal edema, mediastinitis, sepsis and spread of infection to deep spaces which can become life-threatening.
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Nf PowerPoint
Necrotizing fasciitis, also known as flesh-eating bacteria, is a rare but serious soft tissue infection caused by various bacteria such as Group A Strep. The bacteria spreads rapidly, destroying skin, muscles, and tissues. Common causes include skin trauma, surgery, and insect bites. Left untreated, it can cause serious illness or death by releasing toxins and destroying tissue. Aggressive treatment requires hospitalization, IV antibiotics, debridement of damaged tissue, and sometimes amputation to prevent further spread.
Hand infection by Dr.K.AmrithaAnilkumar
Hand infection is the infection caused in hand , since hand contains neurovascular bundles, muscles, bones, and ligaments.
It includes
1. Acute Paronychia
2.Chronic Paronychia
3.Terminal pulp space infection ( felon)
4.subungal infection
5. Web space infecion
6. Mid palmar space infection
7.Thenar space infection
8. Deep palmar abscess
9. Acute suppurative tenosynovitis
11. Chronic Tenosynovitis
12. Lymphangitis of the hand
13. Arthritis of hand joints
14. Subcuticular abscess
Arterial diseases by Dr. AmrithaAnilkumar
Abdominal aortic aneurysm (AAA) is an enlargement of the aorta in the abdominal region. The most common cause is atherosclerosis. It can be asymptomatic and found incidentally or symptomatic with back pain, abdominal pain, or a pulsatile abdominal mass. Complications include rupture, infection, thrombosis, embolism, and erosion of nearby structures. Treatment involves surgical repair if the aneurysm reaches a certain size.
Boils or furuncle by Dr.K.AmrithaAnilkumar
Boil is an acute staphylococcal infection of a hair follicle with perifolliculitis which usually proceeds to suppuration & central necrosis.Often boil open on its own & subsides (S. aureus infection)
Gangrene-Pathology
The document discusses different types of gangrene: wet gangrene, dry gangrene, and gas gangrene. Wet gangrene occurs when both arterial and venous blood flow are blocked, causing tissue to become infected and rotten. Dry gangrene typically affects the toes and feet of older patients due to atherosclerosis, resulting in black, mummified tissue. Gas gangrene is caused by Clostridium bacteria that enter through wounds, producing toxins and gas bubbles within tissues causing swelling and a foul odor.
Gangrene
Dr. Monika Negi discusses different types of gangrene including dry gangrene, wet gangrene, and gas gangrene. Dry gangrene results from ischemia and causes tissue to become dry and black. Wet gangrene occurs in moist tissues and is caused by blockages leading to bacterial overgrowth and tissue putrefaction. Gas gangrene develops from clostridial bacteria infecting wounds and causing muscle necrosis and gas formation. Treatment for gas gangrene requires urgent surgery, antibiotics like penicillin, and sometimes hyperbaric oxygen or amputation.
CELL INJURY-II Gangrene
Hello friends..! This is 2nd presentation of series 'CELL INJURY'.. I have tried to describe important points about 'GANGRENE' in brief so that it will be helpful for quick revision. Plzz Like, Share n Subscribe to get notifications of my next presentations.. Thank You..!!
Infectious diseases by Dr.AmrithaAnilkumar
- Ludwig's angina is a rapidly progressive polymicrobial cellulitis of the sublingual and submandibular spaces, involving the floor of the mouth and suprahyoid area of the neck bilaterally.
- It is commonly caused by dental infections and presents with diffuse painful swelling and woody induration of the mouth and anterior neck, which can lead to airway obstruction if not treated promptly with antibiotics and potentially tracheostomy.
- Complications include laryngeal edema, mediastinitis, sepsis and spread of infection to deep spaces which can become life-threatening.
Syphilis
Treponema pallidum is a spirochete bacterium that causes the sexually transmitted disease syphilis. It has four stages: primary, secondary, latent, and tertiary. Primary syphilis presents as a chancre, while secondary syphilis causes a rash and mucous membranes lesions. Without treatment, later stages can involve the cardiovascular system, central nervous system, and other organ systems. Syphilis screening and treatment are important for preventing transmission and progression of disease.
Pyogenic abscess by Dr.K.AmrithaAnilkumar
This document discusses pyogenic abscesses, which are localized collections of pus caused by bacterial infection. It defines pyogenic abscesses and describes their causes, signs and symptoms, common sites, investigations, complications, differential diagnosis, and treatment, which involves incision and drainage after antibiotics. Common causative organisms are Staphylococcus aureus and Streptococcus pyogenes. Investigations may include blood tests and imaging like ultrasound or chest X-ray. Complications can include sepsis if not treated properly. Treatment is incision and drainage of the abscess after it has formed, along with antibiotics.
Gangrene
Gangrene is a type of tissue death caused by lack of blood supply and can be caused by blocked arteries or infection. There are several types of gangrene including dry gangrene caused by gradual arterial blockage, wet gangrene caused by sudden blockage and infection, and gas gangrene caused by Clostridium bacteria infection. Clinical features include discolored, numb skin that is dry in dry gangrene and swollen in wet gangrene, with a foul smell and crepitus in gas gangrene. Treatment depends on the type but may include antibiotics, surgery to remove dead tissue, and amputation in severe cases.
4.gangrene
Gangrene is the invasion and decay of necrotic tissue by bacteria. It most commonly affects the lungs, intestines, mammary glands, and extremities. There are two main types - dry gangrene occurs when circulation is cut off in extremities, resulting in mummified tissue. Moist gangrene happens in organs with more moisture and heat, allowing bacteria to rapidly spread and cause sepsis. Specific forms include gas gangrene caused by Clostridium bacteria entering wounds and producing toxins.
Gangrene
Gangrene, introduction, definition, causes, symptoms, types, wet and dry gangrene, morphological features.
Granuloma annulare 2.0
- A 7 year old female presented with a skin biopsy from her left gluteal region for a clinical diagnosis of granuloma annulare.
- Microscopic examination showed features consistent with granuloma annulare including hyperkeratosis, acanthosis, lymphocytic infiltration, and histiocytes surrounding degenerated collagen extending into the dermis.
- Granuloma annulare is a benign inflammatory dermatosis more common in females that involves skin and subcutaneous tissue, though the etiology is unknown.
NECROTIZING FASCIITIS, GAS GANGRENE AND SEPTIC ARTHRITIS (1).pptx
Necrotizing fasciitis is a life-threatening soft tissue infection that spreads rapidly along fascial planes. Risk factors include poor wound healing and immunosuppression. It is usually caused by bacteria like Streptococcus and Staphylococcus entering through breaks in the skin. Symptoms include severe pain, fever, and skin changes like blistering. Diagnosis involves imaging tests and the finger test, while treatment requires emergency surgery to remove dead tissue along with broad-spectrum antibiotics. Gas gangrene is caused by Clostridium bacteria contaminating wounds. It causes excruciating muscle pain and swelling along with skin discoloration and gas in tissues. Septic arthritis is a medical emergency where bacteria infect the joints
Bronciectasis
Bronchiectasis is permanent dilation of the bronchi and bronchioles due to destruction of muscle and elastic tissue, usually resulting from chronic necrotizing infections. It is characterized by a persistent cough and expectoration of copious amounts of purulent sputum. Predisposing factors include bronchial obstruction from foreign bodies or infection, congenital conditions like cystic fibrosis, and immunodeficiency states that increase susceptibility to repeated lung infections. Chronic infection and obstruction cause damage and dilation of the bronchial walls over time in a recurrent cycle. On microscopy, areas of ulceration and inflammation are seen within the bronchial walls in active disease, and fibrosis develops in chronic cases.
Gangrene
Gangrene is the death of body tissue due to reduced blood flow or bacterial infection. There are several types of gangrene including dry, wet, gas and internal gangrene. Gangrene is caused by lack of blood supply, infection, or trauma. Risk factors include diabetes, vascular disease, injury, smoking, obesity, and immunosuppression. Treatment involves removing dead tissue through surgery, antibiotics to treat infection, and hyperbaric oxygen therapy to promote healing. Preventing gangrene requires managing conditions like diabetes, losing weight, not smoking, and promptly treating infections or frostbite.
Gas gangrene by Dr.AmrithaAnilkumar
Gas gangrene is an infective gangrene caused by clostridial organisms involving mainly skeletal muscle as oedematous myonecrosis.
3 inflamm
The document summarizes the fate and types of acute inflammation, as well as chronic inflammation. Regarding acute inflammation, it can resolve and tissues return to normal, involve regression and healing of tissue damage, or progress and spread. Acute inflammation is classified as suppurative or non-suppurative. Chronic inflammation lasts a long time and can follow acute inflammation or start gradually due to infection, irritants, or autoimmunity. It involves fibrosis and different inflammatory cells than acute inflammation. Granulomas are a form of chronic inflammation involving collections of macrophages, lymphocytes, and giant cells.
Rhinolith
A rhinolith forms around a small foreign body introduced into the nose, causing inflammation and pus secretion high in calcium and magnesium. This allows mineral salts to precipitate over time, forming a stony mass. Rhinoliths typically cause unilateral nasal obstruction, foul discharge, pain, and ulceration. They appear on examination as an irregular, stony hard mass and can be seen on imaging tests. Rhinoliths are usually removed surgically under general anesthesia.
Gangrene
This document discusses gangrene, which is defined as the invasion and petrification of necrotic tissue by saprophytic bacteria. It commonly occurs in the lungs, intestines, and extremities. There are two main types of gangrene - dry gangrene and moist gangrene. Dry gangrene occurs where moisture and temperature limit bacterial growth, resulting in a dry, shriveled appearance. Moist gangrene occurs where moisture and heat allow rapid bacterial growth in tissues like the lungs and intestines, often resulting in death from sepsis, toxemia and shock. The document describes the gross and microscopic appearances of both dry and moist gangrene.
4.outcomes and morphology dr ashutosh kumar
This document discusses genetic and acquired defects that can lead to dysregulated inflammation. It describes several genetic conditions that cause defects in leukocyte adhesion, phagolysosome function, and microbicidal activity. These defects predispose to recurrent bacterial infections. The document also outlines different morphological patterns inflammation can take, such as serous, fibrinous, purulent, and ulcerative. Examples are provided of disease states that demonstrate each pattern along with images showcasing the histopathological features.
nursn cvs.pptx
This document discusses several topics related to cardiovascular and gastrointestinal systems. It provides definitions and classifications of endocarditis, atherosclerosis, infarction, and aneurysms. It also covers peptic ulcer disease, typhoid fever, and esophageal carcinoma. Key information includes causes and risk factors, pathological findings such as vegetations or atheromatous plaques, and common clinical manifestations like abdominal pain or fever.
Systemic sclerosis
Systemic sclerosis is an autoimmune connective tissue disease that affects the skin, blood vessels, and internal organs. There are two major subtypes: limited, characterized by skin changes limited to the hands, face, and CREST syndrome features; and diffuse, with generalized skin thickening. Systemic sclerosis causes fibrosis of skin and internal organs due to vascular dysfunction, immune dysregulation, and excessive collagen deposition. It commonly involves the lungs, gastrointestinal tract, kidneys, heart, and musculoskeletal system. Prognosis depends on the degree of internal organ involvement.
Systemic sclerosis
Systemic sclerosis is an autoimmune connective tissue disease that affects the skin, blood vessels, and internal organs. There are two major subtypes: limited, characterized by skin changes limited to the hands, face, and CREST syndrome features; and diffuse, with generalized skin thickening that spreads from the hands and arms. Systemic involvement can include pulmonary fibrosis/hypertension, gastrointestinal dysmotility, renal crisis, cardiac and musculoskeletal issues. The pathogenesis involves vascular dysfunction, immune dysregulation, and excessive fibrosis. Diagnosis is based on characteristic skin changes and internal organ involvement. Prognosis depends on the specific organ systems affected.
Progresive systemic sclerosis
Progressive systemic sclerosis is a disorder affecting connective tissue in the skin, internal organs, and blood vessels. It is characterized by thickening and tightening of the skin, especially in the fingers and face. It can be classified as limited or diffuse cutaneous disease depending on the extent of skin involvement. Internal organ systems commonly impacted include the lungs, heart, kidneys, and gastrointestinal tract. Management involves treatments for symptoms such as Raynaud's phenomenon, digital ischemia, reflux, and pulmonary hypertension. Prognosis depends on factors like the extent of skin and organ involvement.
Progresive systemic sclerosis
Progressive systemic sclerosis is a disorder affecting connective tissue in the skin, internal organs, and blood vessels. It is characterized by thickening and tightening of the skin, especially in the fingers and face. It can be classified as limited or diffuse cutaneous disease depending on the extent of skin involvement. Internal organ systems commonly impacted include the lungs, heart, kidneys, and gastrointestinal tract. Management involves treatments for symptoms such as Raynaud's phenomenon, digital ischemia, reflux, and pulmonary hypertension. Prognosis depends on factors like the extent of skin and organ involvement.
Diseases of sclera
Diseases of sclera
2. anatomy • Sclera posterior 5/6th opaque part of the external fibrous tunic of the eyeball.
3. • outer surface }covered by Tenon's capsule. • anterior part } covered by bulbar conjunctiva.
4. Its inner surface lies in contact with choroid with a potential suprachoroidal space in between
5. Thickness of sclera. • thinner }children and in females Sclera • thickest} posteriorly (1mm) • gradually becomes thin when traced anteriorly. • thinnest } insertion of extraocular muscles (0.3 mm). • Lamina cribrosa is a sieve-like sclera from which fibres of optic nerve pass.
6. Apertures of sclera • Anterior • Anterior ciliary vessels • Middle • four vortex veins (vena verticosae) • Posterior • Optic nerve • Long & short ciliary nerves
7. Layers of sclera sclera episclera Sclera proper Lamina fusca thin, dense vascularised layer of connective tissue fibroblasts, macrophages and lymphocytes avascular structure dense bundles of collagen fibres. innermost blends with suprachoroidal and supraciliary laminae of the uveal tract. brownish in colour presence of pigmented cells.
Aneurysms
1. An aneurysm is an abnormal dilation of a blood vessel that can be congenital or acquired due to weakening of the vessel wall.
2. Aneurysms are classified based on composition, shape, location, and pathogenetic mechanism. The most common type is atherosclerotic aneurysms, which often affect the abdominal aorta.
3. Complications of aneurysms include rupture, which can lead to fatal hemorrhaging, as well as compression of surrounding structures. timely diagnosis and treatment are important to prevent such complications.
General pathology lecture 3 cell death or necrosis
Necrosis refers to cell death in living tissue. Dead cells show changes in both the cytoplasm and nucleus, such as increased eosinophilia and swollen mitochondria. There are several types of necrosis including coagulation, liquefactive, fatty, caseous, and gangrenous necrosis. Coagulation necrosis results in hardened cells while liquefactive necrosis involves enzymatic breakdown. Caseous necrosis is characterized by soft, cheesy debris. Apoptosis is a normal and regulated form of cell death, while postmortem changes that occur after death include algor mortis, rigor mortis, livor mortis, autolysis, and putrefaction.
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Syphilis
Treponema pallidum is a spirochete bacterium that causes the sexually transmitted disease syphilis. It has four stages: primary, secondary, latent, and tertiary. Primary syphilis presents as a chancre, while secondary syphilis causes a rash and mucous membranes lesions. Without treatment, later stages can involve the cardiovascular system, central nervous system, and other organ systems. Syphilis screening and treatment are important for preventing transmission and progression of disease.
Pyogenic abscess by Dr.K.AmrithaAnilkumar
This document discusses pyogenic abscesses, which are localized collections of pus caused by bacterial infection. It defines pyogenic abscesses and describes their causes, signs and symptoms, common sites, investigations, complications, differential diagnosis, and treatment, which involves incision and drainage after antibiotics. Common causative organisms are Staphylococcus aureus and Streptococcus pyogenes. Investigations may include blood tests and imaging like ultrasound or chest X-ray. Complications can include sepsis if not treated properly. Treatment is incision and drainage of the abscess after it has formed, along with antibiotics.
Gangrene
Gangrene is a type of tissue death caused by lack of blood supply and can be caused by blocked arteries or infection. There are several types of gangrene including dry gangrene caused by gradual arterial blockage, wet gangrene caused by sudden blockage and infection, and gas gangrene caused by Clostridium bacteria infection. Clinical features include discolored, numb skin that is dry in dry gangrene and swollen in wet gangrene, with a foul smell and crepitus in gas gangrene. Treatment depends on the type but may include antibiotics, surgery to remove dead tissue, and amputation in severe cases.
4.gangrene
Gangrene is the invasion and decay of necrotic tissue by bacteria. It most commonly affects the lungs, intestines, mammary glands, and extremities. There are two main types - dry gangrene occurs when circulation is cut off in extremities, resulting in mummified tissue. Moist gangrene happens in organs with more moisture and heat, allowing bacteria to rapidly spread and cause sepsis. Specific forms include gas gangrene caused by Clostridium bacteria entering wounds and producing toxins.
Gangrene
Gangrene, introduction, definition, causes, symptoms, types, wet and dry gangrene, morphological features.
Granuloma annulare 2.0
- A 7 year old female presented with a skin biopsy from her left gluteal region for a clinical diagnosis of granuloma annulare.
- Microscopic examination showed features consistent with granuloma annulare including hyperkeratosis, acanthosis, lymphocytic infiltration, and histiocytes surrounding degenerated collagen extending into the dermis.
- Granuloma annulare is a benign inflammatory dermatosis more common in females that involves skin and subcutaneous tissue, though the etiology is unknown.
NECROTIZING FASCIITIS, GAS GANGRENE AND SEPTIC ARTHRITIS (1).pptx
Necrotizing fasciitis is a life-threatening soft tissue infection that spreads rapidly along fascial planes. Risk factors include poor wound healing and immunosuppression. It is usually caused by bacteria like Streptococcus and Staphylococcus entering through breaks in the skin. Symptoms include severe pain, fever, and skin changes like blistering. Diagnosis involves imaging tests and the finger test, while treatment requires emergency surgery to remove dead tissue along with broad-spectrum antibiotics. Gas gangrene is caused by Clostridium bacteria contaminating wounds. It causes excruciating muscle pain and swelling along with skin discoloration and gas in tissues. Septic arthritis is a medical emergency where bacteria infect the joints
Bronciectasis
Bronchiectasis is permanent dilation of the bronchi and bronchioles due to destruction of muscle and elastic tissue, usually resulting from chronic necrotizing infections. It is characterized by a persistent cough and expectoration of copious amounts of purulent sputum. Predisposing factors include bronchial obstruction from foreign bodies or infection, congenital conditions like cystic fibrosis, and immunodeficiency states that increase susceptibility to repeated lung infections. Chronic infection and obstruction cause damage and dilation of the bronchial walls over time in a recurrent cycle. On microscopy, areas of ulceration and inflammation are seen within the bronchial walls in active disease, and fibrosis develops in chronic cases.
Gangrene
Gangrene is the death of body tissue due to reduced blood flow or bacterial infection. There are several types of gangrene including dry, wet, gas and internal gangrene. Gangrene is caused by lack of blood supply, infection, or trauma. Risk factors include diabetes, vascular disease, injury, smoking, obesity, and immunosuppression. Treatment involves removing dead tissue through surgery, antibiotics to treat infection, and hyperbaric oxygen therapy to promote healing. Preventing gangrene requires managing conditions like diabetes, losing weight, not smoking, and promptly treating infections or frostbite.
Gas gangrene by Dr.AmrithaAnilkumar
Gas gangrene is an infective gangrene caused by clostridial organisms involving mainly skeletal muscle as oedematous myonecrosis.
3 inflamm
The document summarizes the fate and types of acute inflammation, as well as chronic inflammation. Regarding acute inflammation, it can resolve and tissues return to normal, involve regression and healing of tissue damage, or progress and spread. Acute inflammation is classified as suppurative or non-suppurative. Chronic inflammation lasts a long time and can follow acute inflammation or start gradually due to infection, irritants, or autoimmunity. It involves fibrosis and different inflammatory cells than acute inflammation. Granulomas are a form of chronic inflammation involving collections of macrophages, lymphocytes, and giant cells.
Rhinolith
A rhinolith forms around a small foreign body introduced into the nose, causing inflammation and pus secretion high in calcium and magnesium. This allows mineral salts to precipitate over time, forming a stony mass. Rhinoliths typically cause unilateral nasal obstruction, foul discharge, pain, and ulceration. They appear on examination as an irregular, stony hard mass and can be seen on imaging tests. Rhinoliths are usually removed surgically under general anesthesia.
Gangrene
This document discusses gangrene, which is defined as the invasion and petrification of necrotic tissue by saprophytic bacteria. It commonly occurs in the lungs, intestines, and extremities. There are two main types of gangrene - dry gangrene and moist gangrene. Dry gangrene occurs where moisture and temperature limit bacterial growth, resulting in a dry, shriveled appearance. Moist gangrene occurs where moisture and heat allow rapid bacterial growth in tissues like the lungs and intestines, often resulting in death from sepsis, toxemia and shock. The document describes the gross and microscopic appearances of both dry and moist gangrene.
4.outcomes and morphology dr ashutosh kumar
This document discusses genetic and acquired defects that can lead to dysregulated inflammation. It describes several genetic conditions that cause defects in leukocyte adhesion, phagolysosome function, and microbicidal activity. These defects predispose to recurrent bacterial infections. The document also outlines different morphological patterns inflammation can take, such as serous, fibrinous, purulent, and ulcerative. Examples are provided of disease states that demonstrate each pattern along with images showcasing the histopathological features.
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NECROTIZING FASCIITIS, GAS GANGRENE AND SEPTIC ARTHRITIS (1).pptx
NECROTIZING FASCIITIS, GAS GANGRENE AND SEPTIC ARTHRITIS (1).pptx
Similar to Cardiac manifestations of connective tissue disorders & kawasaki disease
nursn cvs.pptx
This document discusses several topics related to cardiovascular and gastrointestinal systems. It provides definitions and classifications of endocarditis, atherosclerosis, infarction, and aneurysms. It also covers peptic ulcer disease, typhoid fever, and esophageal carcinoma. Key information includes causes and risk factors, pathological findings such as vegetations or atheromatous plaques, and common clinical manifestations like abdominal pain or fever.
Systemic sclerosis
Systemic sclerosis is an autoimmune connective tissue disease that affects the skin, blood vessels, and internal organs. There are two major subtypes: limited, characterized by skin changes limited to the hands, face, and CREST syndrome features; and diffuse, with generalized skin thickening. Systemic sclerosis causes fibrosis of skin and internal organs due to vascular dysfunction, immune dysregulation, and excessive collagen deposition. It commonly involves the lungs, gastrointestinal tract, kidneys, heart, and musculoskeletal system. Prognosis depends on the degree of internal organ involvement.
Systemic sclerosis
Systemic sclerosis is an autoimmune connective tissue disease that affects the skin, blood vessels, and internal organs. There are two major subtypes: limited, characterized by skin changes limited to the hands, face, and CREST syndrome features; and diffuse, with generalized skin thickening that spreads from the hands and arms. Systemic involvement can include pulmonary fibrosis/hypertension, gastrointestinal dysmotility, renal crisis, cardiac and musculoskeletal issues. The pathogenesis involves vascular dysfunction, immune dysregulation, and excessive fibrosis. Diagnosis is based on characteristic skin changes and internal organ involvement. Prognosis depends on the specific organ systems affected.
Progresive systemic sclerosis
Progressive systemic sclerosis is a disorder affecting connective tissue in the skin, internal organs, and blood vessels. It is characterized by thickening and tightening of the skin, especially in the fingers and face. It can be classified as limited or diffuse cutaneous disease depending on the extent of skin involvement. Internal organ systems commonly impacted include the lungs, heart, kidneys, and gastrointestinal tract. Management involves treatments for symptoms such as Raynaud's phenomenon, digital ischemia, reflux, and pulmonary hypertension. Prognosis depends on factors like the extent of skin and organ involvement.
Progresive systemic sclerosis
Progressive systemic sclerosis is a disorder affecting connective tissue in the skin, internal organs, and blood vessels. It is characterized by thickening and tightening of the skin, especially in the fingers and face. It can be classified as limited or diffuse cutaneous disease depending on the extent of skin involvement. Internal organ systems commonly impacted include the lungs, heart, kidneys, and gastrointestinal tract. Management involves treatments for symptoms such as Raynaud's phenomenon, digital ischemia, reflux, and pulmonary hypertension. Prognosis depends on factors like the extent of skin and organ involvement.
Diseases of sclera
Diseases of sclera
2. anatomy • Sclera posterior 5/6th opaque part of the external fibrous tunic of the eyeball.
3. • outer surface }covered by Tenon's capsule. • anterior part } covered by bulbar conjunctiva.
4. Its inner surface lies in contact with choroid with a potential suprachoroidal space in between
5. Thickness of sclera. • thinner }children and in females Sclera • thickest} posteriorly (1mm) • gradually becomes thin when traced anteriorly. • thinnest } insertion of extraocular muscles (0.3 mm). • Lamina cribrosa is a sieve-like sclera from which fibres of optic nerve pass.
6. Apertures of sclera • Anterior • Anterior ciliary vessels • Middle • four vortex veins (vena verticosae) • Posterior • Optic nerve • Long & short ciliary nerves
7. Layers of sclera sclera episclera Sclera proper Lamina fusca thin, dense vascularised layer of connective tissue fibroblasts, macrophages and lymphocytes avascular structure dense bundles of collagen fibres. innermost blends with suprachoroidal and supraciliary laminae of the uveal tract. brownish in colour presence of pigmented cells.
Aneurysms
1. An aneurysm is an abnormal dilation of a blood vessel that can be congenital or acquired due to weakening of the vessel wall.
2. Aneurysms are classified based on composition, shape, location, and pathogenetic mechanism. The most common type is atherosclerotic aneurysms, which often affect the abdominal aorta.
3. Complications of aneurysms include rupture, which can lead to fatal hemorrhaging, as well as compression of surrounding structures. timely diagnosis and treatment are important to prevent such complications.
General pathology lecture 3 cell death or necrosis
Necrosis refers to cell death in living tissue. Dead cells show changes in both the cytoplasm and nucleus, such as increased eosinophilia and swollen mitochondria. There are several types of necrosis including coagulation, liquefactive, fatty, caseous, and gangrenous necrosis. Coagulation necrosis results in hardened cells while liquefactive necrosis involves enzymatic breakdown. Caseous necrosis is characterized by soft, cheesy debris. Apoptosis is a normal and regulated form of cell death, while postmortem changes that occur after death include algor mortis, rigor mortis, livor mortis, autolysis, and putrefaction.
General pathology lecture 3 cell death or necrosis
Necrosis refers to cell death in living tissue. Dead cells show changes in both the cytoplasm and nucleus, such as increased eosinophilia and swollen mitochondria. There are several types of necrosis including coagulation, liquefactive, fatty, caseous, and gangrenous necrosis. Caseous necrosis is a combination of coagulative and liquefactive necrosis seen in tuberculous infections, appearing as a soft, cheesy material. Apoptosis is a normal and regulated form of cell death important in development and tissue homeostasis. After death, the body undergoes changes including algor mortis, rigor mortis, livor mortis, autolysis, and putrefaction.
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- Risk factors that can lead to coronary artery blockage include hypertension, hyperlipidemia, diabetes, and smoking.
- A thrombus or embolism in a coronary artery cuts off the blood supply, causing cell death in the affected heart muscle area.
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The disease can be either localized to the skin or involve other organs in addition to the skin.
Symptoms may include areas of thickened skin, stiffness, feeling tired, and poor blood flow to the fingers or toes with cold exposure.
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This document provides an overview of non-neoplastic salivary gland disorders. It discusses various classifications of these disorders and then describes specific conditions in detail under categories such as developmental disorders, infections, traumatic/ischemic disorders, and autoimmune disorders. Key points include descriptions of common developmental disorders like ductal atresia and polycystic disease of the parotid. Infectious disorders covered include viral sialadenitis from mumps virus and bacterial sialadenitis. Conditions resulting from trauma or ischemia like cheilitis glandularis and necrotizing sialometaplasia are also summarized.
Inflammation
1. Inflammation is defined as the local response to injury characterized by fluid and leukocyte movement into tissues. Acute inflammation has a rapid onset and short duration dominated by neutrophils, while chronic inflammation has a long duration dominated by mononuclear cells.
2. The classical signs of acute inflammation are redness, heat, swelling, pain, and loss of function. Systemic effects include fever, leukocytosis, lymphadenopathy, and acute phase protein production by the liver.
3. Exudative inflammation can be serous, lymphoplasmocytic, purulent, fibrinous, or gangrenous depending on the characteristics and cellular composition of the exudate and tendency for
scleroderma disease - connective tissues
Scleroderma is a rare autoimmune disease characterized by fibrosis of the skin and internal organs. It is caused by endothelial cell damage, activation of fibroblasts, and immune system dysfunction. There are two main types: limited scleroderma affects the hands, face and forearms, while diffuse scleroderma affects the whole body. Symptoms include hardening and tightening of the skin, Raynaud's phenomenon, gastrointestinal issues, lung fibrosis, heart and kidney problems. The disease has many internal complications and no known cure. Early diagnosis and treatment of symptoms is key to improving quality of life for those affected by scleroderma.
Rheumatoid arthritis
Rheumatoid arthritis is a chronic autoimmune disorder that causes inflammation of the synovial tissue in joints, resulting in pain, stiffness, swelling and erosion of cartilage and bone. It affects around 1% of the population and is more common in women. The disease progresses through four stages, starting with swelling and pain and progressing to joint deformity and ankylosis. Treatment focuses on reducing inflammation and joint damage through medications like NSAIDs, DMARDs and corticosteroids, as well as joint protection, exercise and surgery. Nursing management addresses pain, impaired mobility, self-care needs and psychosocial impacts of the disease.
Non specific ulcers
This document provides an overview of various types of non-specific ulcers, including their causes, characteristics, and treatments. It discusses ulcers caused by trauma, arterial issues, venous issues, pressure, infection, tropical conditions, frostbite, hypertension, diabetes, mycobacteria, cancer, and more. For most ulcer types, it outlines key features like location, appearance, complications, investigations needed, and management approaches involving wound care, antibiotics, surgery, or other therapies.
Infective endocarditis
Infective endocarditis is an infection of the heart valves or endocardium that is usually caused by bacteria or fungi forming clusters called vegetations. Antibiotics are the primary treatment. It can be classified as native valve, prosthetic valve, or intravenous drug abuse-related endocarditis. Native valve endocarditis commonly affects pre-existing valve damage and is caused by various organisms. Prosthetic valve endocarditis can be early or late-onset depending on time since valve placement and causing organisms differ. Symptoms vary between subacute presentations with fever and embolic phenomena, and acute presentations with rapid valve destruction and increased risk of embolism. Diagnosis involves blood cultures, echocardiography identifying
Pharyngeal arches
The document discusses the pharyngeal arches, which form in the embryonic stage from mesoderm and include five pairs of arches. Between the arches form pharyngeal clefts lined by ectoderm and internally form pharyngeal pouches lined by endoderm. The arches give rise to muscles, bones, nerves and arteries. Abnormal development can result in conditions like branchial cysts. The pharyngeal arches also have clinical significance as their abnormal development can lead to conditions like agnathia, microstomia, mandibulofacial dystosis and Pierre Robin syndrome.
Similar to Cardiac manifestations of connective tissue disorders & kawasaki disease (20)
General pathology lecture 3 cell death or necrosis
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General pathology lecture 3 cell death or necrosis
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More from Dr. Kanishk Sharma
Anti -depressants: classification & mechanism of action
Antidepressants
Dr. Kanishk Deep Sharma
Intern
J.N. Medical College, Belagavi
Classification
Reversible inhibitors of MAO-A
Moclobemide, Clorgyline
Tricyclic antidepressants
NA + 5-HT reuptake inhibitors
Imipramine, Trimipramine, Amitriptyline
Predominantly NA reuptake inhibitors
Reboxetine, Desipramine, Nortriptyline
Selective serotonin reuptake inhibitors
Fluoxetine, Fluvoxamine, Paroxetine, Sertraline
Serotonin- Norepinephrine Reuptake Inhibitors
Duloxetine, Venlafaxine
5-HT2 Antagonist
Nefazodone, Trazodone
Atypical antidepressants
Mirtazapine, Bupropion
SSRIs & TCA
SNRIs
MAO-B Inhibitors
5-HT2 ANTAGONISTS
weak inhibitors of serotonin reuptake
block postsynaptic 5-HT2A receptors
chronic use:- desensitize 5-HT1A presynaptic autoreceptors and, thereby, increase serotonin release
Bupropion
weak dopamine and nor-epinephrine reuptake inhibitor
assists in decreasing the craving and attenuating the withdrawal symptoms for nicotine in tobacco users
Mirtazapine
enhances serotonin and nor-epinephrine neurotransmission
Block pre-synaptic alpha-2 receptors
Block 5-HT2 receptors
aetiology and pathogenesis of chronic obstructive lung disease
Chronic Obstructive Pulmonary Disease
Kanishk Deep Sharma
Roll no. 50
Definition
“A disease state characterised by progressive development of airflow limitation that is not fully reversible. The airflow limitation is usually progressive and usually results from an abnormal response of lungs to noxious particles or gases”
Airflow obstruction is defined as reduced FEV1/FVC ratio (< 0.7)
RISK FACTORS
Exposure to tobacco smoke.
most significant risk factor
Pipe smokers, cigar smokers and marijuana smokers
second-hand smoke
Nicotine stimulates sympathetic system
Decreased ciliary activity & ciliary loss
Decreased oxygen carrying capacity
Cellular hyperplasia
Production of mucus
Reduction in airway diameter
Increased difficulty in clearing secretions
People with asthma who smoke
increases the risk of COPD
Occupational exposure to dusts and chemicals
Long-term exposure to chemical fumes, vapors and dusts in the workplace can irritate and inflame lungs
Age
develops slowly over years
Genetics
alpha-1-antitrypsin deficiency
certain smokers more susceptible to the disease
Infection
Aggravates COPD progression
CHRONIC BRONCHITIS
presence of cough and sputum production for at least 3 months in each of 2 consecutive years, is not necessarily associated with airflow limitation
Hyperplasia of mucus-secreting glands in trachea and bronchi
Bronchioles are clogged with mucus and pose a physical barrier to ventilation
Increase in goblet cells
Disappearance of cilia
Chronic inflammatory changes and narrowing of small airways
Altered function of alveolar macrophages causing infections
Greater resistance to airflow increases work of breathing
Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema
EMPHYSEMA
Abnormal permanent enlargement of the air space distal to the terminal bronchioles accompanied by destruction of bronchioles
Small bronchioles become obstructed as result of
Mucus
Smooth muscle spasm
Inflammatory process
Collapse of bronchiolar walls
Recurrent infections causing inflammation, exudates & edema
Elastin & collagen destroyed
Bronchioles collapse
Trapped air cause hyperinflation & over distension
Alveolar wall & capillary destruction
Reduced surface area for oxygen diffusion
Compensatory tachypnea
Thank you
asthma medical treatment
MAST CELL STABILIZERS
BY
Mr. Kanishk Deep Sharma
MAST CELL STABILIZERS
THEY ARE CHROMONE DERIVATIVES THAT BLOCK CHLORIDE CHANNELS ESSENTIAL FOR MAST CELL DEGRANULATION
Sodium cromoglycate Ketotifen
Sodium cromoglycate
ADVERSE EFFECT
KETOTIFEN
ANTIHISTAMINIC WITH CROMOGLYCOLATE LIKE ACTION
ADVERSE EFFECT
LEUKOTRIENE ANTAGONISTS
LEUKOTRIENES
THEY ANTAGONISE RECEPTOR CYSLT1
ADVERSE EFFECT
ZILEUTON
CORTICOSTEROIDS
SYSTEMIC STEROIDS
USED IN 2 SITUATIONS
SEVERE CHRONIC ASTHMA
STATUS ASTHAMATICUS
SEVERE CHRONIC ASTHMA
WHEN NOT CONTROLLED BY BROCHODILATORS/INHALED STEROIDS
START PREDNISOLONE 20-60Mg/DAY
STATUS ASTHMATICUS
HIGH DOSE I.V. GLUCOCORTICOID, ACT IN 6-24 HRS
INHALED STEROIDS
HIGH TOPICAL LOW SYSTEMIC ACTIVITY
SHOULD BE ‘STEP 1’ FOR ALL ASTHMA PATIENTS
INDICATED WHEN B2 AGONIST REQUIRED DAILY
START 100-200 mg BD
EFFECT
SUPRESS BRONCHIAL INFLAMMATION
INCREASE PEAK EXPIRATORY FLOW RATE
NO ROLE IN ACUTE ATTACK
PEAK EFFECT IN 4-7 DAYS
DOESN’T PRECIPITATE ASTHMA, MUUSCULAR PAIN, LASSITUDE, DEPRESSION, HYPOTENSION
IN COPD
HIGH DOSE INHALED STEROIDS BENEFICIAL ONLY IN ADVANCED CASES
NO PROOF THAT THEY SLOW DISEASE PROGRESSION
ADVERSE EFFECT
EXAMPLES
BUDESONIDE
BECLOMETHASONE DIPRPIONATE
FLUTICASONE PROPIONATE
FLUNISOLIDE
CICLESONIDE
THANK YOU
Paralytic squint
PARALYTIC SQUINT
KANISHK DEEP SHARMA
ROLL NO. 50
Uncoordinated eye movement
Angle of squint varies
Motor imbalance
ETIOLOGY
Lesion of nerve
Lesion of muscles
Lesions due to
Injury
Inflammation-syphilis, disseminated sclerosis
Vascular diseases-hemorrhage, aneurysm,arteriosclerosis
Neoplasms-brain tumor
Toxins-alcohol, lead, carbon monoxide
Degeneration-chronic nuclear ophthalmoplegia
Myasthenia gravis
SYMPTOMS
DIPLOPIA
In field of action of paralyzed muscle
Long duration- suppression of false image
Vertigo & nausea
Action required towards paralysed muscle
False projection
Binocular diplopia
Secondry deviation
Defective ocular motility
Complementary head postures
Attempt to lessen diplopia
Head tilt to avoid torsion
SEQUALAE
Weakness of paretic muscle
Overacting contralateral synergistic muscle
Inhibitory palsy of contralateral antagonist
TESTS
Record of visual acuity
Ocular motility
Perimetry
Inspection of compensatory head postures
Diplopia charting
Dark room procedure
Armstrong's glasses
4ft distance, fine linear light
Primary & other positions of gaze measured
Hess charting
Explains muscle paralysis & pathological sequlae
Field of binocular fixation
Forced duction test
MANAGEMENT
Treatment of cause
Conservative measures
Vit B complex, systemic steroids
Diplopia treatment
Occluder on affected eye
SURGERIES
Muscle weakening procedure
Recession, marginal myotomy, myectomy
Muscle strengthening procedures
Resection, tucking advancement
Changing direction of muscle action
THANK YOU
Acute flaccid paralysis
ACUTE FLACCID PARALYSIS
Kanishk Deep Sharma
definition
Sudden onset of weakness or paralysis over a period of 15 days in a patient aged less than 15 years age
Ddx
poliomyelitis
Non enveloped, positive stranded RNA virus
Genus ENTEROVIRUS
family PICORNAVIRIDAE
3 antigenically distinct serotypes:-1,2,3
pathogenesis
•Entry into mouth.
•Replication in pharynx, GI tract, Local Lymphatic.
•Hematologic spread to lymphatic and central nervous system.
•Viral spread along nerve fibers.
•Destruction of motor neurons
Immunity
Initially protected by maternal antibodies for first few weeks of life
Types
Asymptomatic
Abortive Polio
Non-paralytic
Paralytic
Spinal
Bulbar
Bulbospinal
Cf- asymptomatic
• Accounts for approximately 95% of cases
• Virus stays in intestinal tract and does not attack the nerves
• Virus is shed in the stool so infected individual is still able to infect others
Cf-abortive
•Does not lead to paralysis
•Mild symptoms seen such as sore throat, fever, n/v, diarrhea, constipation ( Minor illness)
•Most recover in <1><5><4days />95% immune after 3 doses
Immunity probably lifelong
Inactivated polio vaccine
Humoral immunity and to some extend pharyngeal immunity
Duration of immunity not known with certainty
Strategies for polio eradication
Global Polio Eradication Initiative launched in 1988
Polio cases have decreased by over 99%
1988 - >125 countries
In 2010 - 4 countries
The remaining countries are Afghanistan, India, Nigeria and Pakistan
Core strategies
High infant immunization coverage with four doses of oral poliovirus vaccine (OPV) in the first year of life
Supplementary doses of OPV to all children under five years of age during national immunization days
AFP surveillance among children under fifteen years of age
Targeted “mop-up” campaigns once wild poliovirus transmission is limited to a specific focal area.
Immunisation in india
Polio Vaccination under UIP
OPVº birth
OPV1 6 wks
OPV2 10 wks
OPV3 14 wks
OPV4 16-24 Months
Pulse Polio Immunization (PPI)
The supplementary immunization activities (SIAs) in India launched in 1995
Irrespective of the immunisation status
Usually Dec & Jan – Peak transmission
aim
Providing additional OPV doses to every child aged <5><15 years who have had the onset of flaccid paralysis within the preceding 60 days
All cases that are found are investigated immediately, with collection of two stool specimens before administration of OPV.
Thyroid cancers
all types of thyroid cancers that affect human body.
anaplastic
medullary
with staging and treatment
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Learning objectives:
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Cardiac manifestations of connective tissue disorders & kawasaki disease
- 1. IN • KAWASAKI DISEASE • CONNECTIVE TISSUE DISORDERS BY:- Kanishk deep Sharma *
- 2. * *‘licks’ the skin & ‘bites’ the coronaries *1st case identified by Tomasaku Kawasaki in 1961 *“a febrile occulo-oro-cutaneo-acro- desquamatous syndrome with or without acute nonsuppurative cervical lymphadenitis”
- 3. * 1. Bilateral non-exudative bulbar conjunctival injection with limbal sparing
- 4. 2. Erythema of oral and pharyngeal mucosa with strawberry tongue and dry, cracked lips
- 5. 3. Edema & erythema of hands and feet
- 6. 4. Rash of various forms with accentuation in groin area
- 7. 5. Nonsuppurative cervical lymphadenopathy, usually unilateral with node size >1.5 cm
- 8. * •staphylococcus •streptococcus Unknown bacteria •Virus(helper role) •Genetic(predispostion) Susceptible host •Edema of endothelial & smooth muscle cells with intense inflammatory infiltration of vascular wall Immunological injury •Destruction of internal elastic lamina •Weak vessel wall aneurysm
- 9. * *Cardiac pathology divided into 4 stages 1. 0 to 10 days : Microvascular angitis 2. 12 to 25 days : Panvasculitis with aneurism development 3. 28 to 31 days : granulation of coronaries 4. 40 days to 4 yrs. : scarring
- 10. * *Gallop rhythm *Tachycardia *Mitral regurgitation *Aortic root dilatation with aortic regurgitation
- 11. *Pericardial effusion due to pericarditis *Decreased contractility
- 13. *Aortic insufficiency with aortic root dilatation
- 14. *Ventricular Tachycardia out of proportion to fever due to myocarditis
- 15. *Abnormal q wave
- 16. *Prolonged PR and/or QT interval
- 17. *Low voltage /ST-T wave changes
- 18. *cardiomegaly
- 19. *Coronary artery aneurysms are classified by Japanese ministry of health according to internal diameter as: 1. <5mm : small 2. 5-8mm : medium 3. >8mm : giant
- 20. *
- 21. 1. Osteogenesis imperfecta 2. Marfan syndrome 3. Ehler-danlos syndrome 4. Pseudoxanthoma elasticum 5. Arterial calcification of infancy 6. Congenital contractural arachnodactyly
- 22. * *Brittle bone disease *Most common genetic disorder causing osteoporosis *Autosomal dominent *Defect in type 1 collagen
- 24. * 1. Aortic & Mitral valve prolapse 2. Sometimes associated with Tetralogy of fallot & atrial septal defect
- 25. * 1. Autosomal dominant 2. Mutation in extracellular matrix protein fibrillin-1 3. Deranged elastin deposition leads to structural insufficiency
- 28. * 1. Mitral valve prolapse due to mitral valve annular dilatation and occasional calcification 2. Ventricular dysrhythmias & supraventricular arrhythmia 3. Prolonged QT interval 4. Aortic root dilatation, aneurysm & dissection 5. Aortic valve rupture 6. Progressive left heart dilatation & dysfunction 7. rarely ruptured coronaries leading to cardiac tamponade
- 29. * 1. Group of heterogeneous connective tissue disorders 2. Appearance normal at birth 3. Skin hyperelastic & fragile 4. Joint hypermobility 5. Easy bruising, scoliosis
- 30. * 1. Mitral valve prolapse 2. Tricuspid valve prolapse 3. Hemorrhage due to aortic rupture secondary to minor trauma
- 31. * *Mutation of ABCC6 gene *Accumulation of mineralized tissue in skin, retina & vessel walls *Involve endocardium or pericardium *Occlusion of cerebral & coronary arteries
- 33. * *Mutation in ENPP1 gene *Autosomal recessive *Affects infants before 1st 6 months of life *generalised calcification of the arterial internal elastic lamina *Death usually by coronary occlusion
- 35. * 1. concentric ventricular hypertrophy 2. Hypertrophy of myocardium 3. arterial calcification involving aorta and coronary arteries 4. Mitral prolapse
- 37. * *Also called as Beals syndrome *Mutation of FBN2 gene *Contractures of varying degrees at birth, usually involving large joints *Reported cases of mitral insufficiency or prolapse
- 39. *