This document defines and describes different types of vasculitis. It begins by defining vasculitis as inflammation of blood vessel walls. The two main ways of classifying vasculitides are by the size of blood vessels involved and the presence or absence of ANCA. Small vessel vasculitis can be ANCA-positive (e.g. Wegener's granulomatosis, Churg-Strauss syndrome) or ANCA-negative (e.g. Henoch-Schönlein purpura). Medium vessel vasculitides include polyarteritis nodosa and Kawasaki's disease. Large vessel vasculitides include giant cell arteritis, Takayasaki's disease, and poly
Vasculitis syndrome an approach -and-basic principles of treatmentSachin Verma
Vasculitides are a hetrogenous group of conditions characterized by inflammation and necrosis of blood vessels.
A broad group of syndromes may result from this process,since any type,size, and location of vessel may be involved.
Vasculitis syndrome an approach -and-basic principles of treatmentSachin Verma
Vasculitides are a hetrogenous group of conditions characterized by inflammation and necrosis of blood vessels.
A broad group of syndromes may result from this process,since any type,size, and location of vessel may be involved.
Scleroderma
It is the sclerosis of skin characterized by appearance of circumscribed or diffuse ,fibrous thickening and hardening of areas that are hidebound to underlying tissues.
AI disorder( autoimmune disorder)
Spectrum is wide with localized and systemic forms.
Erythroderma is defined as the scaling erythematous dermatitis involving 90% or more of the cutaneous surface.
Also known as exfoliative dermatitis
Idiopathic exfoliative dermatitis – also known as the “red man syndrome”, is characterized by marked palmoplantar keratoderma, dermatopathic lymphadenopathy,increased IgE.
Increased skin perfusion leads to
Temperature dysregulation >
Resulting in skin loss and hypothermia >
High output state >
Cardiac failure
BMR raises to compensate for heat loss
Increased dehydration due to transpiration (similar to burns)
All lead to negative nitrogen balance and characterized by edema, hypoalbuminemia, loss of muscle mass.
Cutaneous involvement is very common in the different types of vasculitis. Skin lesions may be the only manifestation or may occur in the context of systemic disease
Scleroderma
It is the sclerosis of skin characterized by appearance of circumscribed or diffuse ,fibrous thickening and hardening of areas that are hidebound to underlying tissues.
AI disorder( autoimmune disorder)
Spectrum is wide with localized and systemic forms.
Erythroderma is defined as the scaling erythematous dermatitis involving 90% or more of the cutaneous surface.
Also known as exfoliative dermatitis
Idiopathic exfoliative dermatitis – also known as the “red man syndrome”, is characterized by marked palmoplantar keratoderma, dermatopathic lymphadenopathy,increased IgE.
Increased skin perfusion leads to
Temperature dysregulation >
Resulting in skin loss and hypothermia >
High output state >
Cardiac failure
BMR raises to compensate for heat loss
Increased dehydration due to transpiration (similar to burns)
All lead to negative nitrogen balance and characterized by edema, hypoalbuminemia, loss of muscle mass.
Cutaneous involvement is very common in the different types of vasculitis. Skin lesions may be the only manifestation or may occur in the context of systemic disease
Different types of vasculitis have characteristic patterns of blood vessel involvement.However vasculitis is a systemic illness.The symptoms of vasculitis depend on the particular blood vessels that are involved by the inflammatory process
A brief description of a very common illness affecting babies and children. Characterized by fever, heart complications, lymphadenopathy, skin rash and strawberry tongue. Useful information for doctors, medical students, dermatologists, residents, nurses. Helpful for students appearing for USMLE, MRCP, FCSP and MCPS exams. References include Rooks, Textbook of Dermatology
Hypertensive retinopathy is a very important topic for PG examinations of all types. Especially, the fundal changes are important; Keith and Wegner Grading is also a repeated topic in PG. This slide represents all information in a compressed fashion. Have fun!
Nephrotic syndrome happens when damage to your kidneys causes these organs to release too much protein into your urine.
Nephrotic syndrome isn’t itself a disease. Diseases that damage blood vessels in your kidneys cause this syndrome.
Nephrotic syndrome is characterized by the following:
A high amount of protein present in the urine (proteinuria)
high cholesterol and triglyceride levels in the blood (hyperlipidemia)
Low levels of a protein called albumin in the blood (hypoalbuminemia)
Swelling (edema), particularly in your ankles and feet, and around your eyes.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
3. Definition
• Vasculitis is a histological term describing inflammation of the
vessel wall.
• Characterized by widespread vasculitis leading to systemic
symptoms and signs, generally requiring treatment with
corticosteroids and/ or immunosuppressive drugs.
• Two main features are helpful in classifying these
vasculitides:-
– The size of the blood vessels involved
– The presence or absence of anti-neutrophil cytoplasmic antibodies (ANCA) in
the blood
6. PMR & GCA
• Polymyalgia rheumatica (PMR) and giant cell
(temporal) arteritis are systemic illnesses of the
elderly.
• Both are associated with the finding of a giant cell
arteritis on temporal artery biopsy.
7. Polymyalgia rheumatica (PMR)
PMR causes a sudden onset of severe pain and stiffness of the
shoulders and neck, and of the hips and lumbar spine.
These symptoms are worse in the morning, lasting from 30
minutes to several hours.
Clinical history is usually diagnostic and the patient is always
over 50 years old.
Approximately one-third of patients develop systemic features
of tiredness, fever, weight loss, depression and occasionally
nocturnal sweats.
8. Investigation of PMR
A raised ESR and/or CRP is a hallmark of this condition.
Serum alkaline phosphatase and γ-glutamyltranspeptidase
may be raised as markers of the acute inflammation.
Anaemia often present.
Temporal artery biopsy shows giant cell arteritis in 10–30% of
cases, but is rarely performed unless GCA is also suspected.
9. Giant cell arteritis
GCA is inflammatory granulomatous arteritis of large
cerebral arteries which occurs in association with
PMR.
The patient may have current PMR, a history of
recent PMR, or be on treatment for PMR.
10. Clinical features of GCA
It is extremely rare under 50 years of age.
Presenting symptoms include:
Severe headaches
Tenderness of the scalp or of the temple
Claudication of the jaw when eating
Tenderness and swelling of one or more temporal or occipital arteries.
The most feared manifestation is sudden painless temporary or
permanent loss of vision in one eye due to involvement of the
ophthalmic artery.
Systemic manifestations of severe malaise, tiredness and fever
occur.
11. Investigation of GCA
• A temporal artery biopsy from the affected side is the
definitive diagnostic test. This should be taken before, or
within 7 days of starting, high doses of corticosteroids.
• Anemia may be present
• ESR is usually raised and the CRP very high.
• Liver biochemistry: Abnormalities occur, as in PMR
12. Histological features of GCA
The histological features of GCA are:
Cellular infiltrates of CD4+ T lymphocytes, macrophages and giant cells
in the vessel wall.
Granulomatous inflammation of the intima and media
Breaking up of the internal elastic lamina
Giant cells, lymphocytes and plasma cells in the internal elastic lamina.
13. Treatment of PMR or GCA
Corticosteroids produce a dramatic reduction of symptoms of
PMR within 24–48 hours of starting treatment, provided the
dose is adequate.
This treatment should reduce the risk of patients who have
PMR developing GCA.
In GCA, corticosteroids are obligatory because they
significantly reduce the risk of irreversible visual loss and
other focal ischaemic lesions, but much higher doses are
needed than in PMR.
14. Sometimes biopsy is not obtainable, so the treatment should
not be delayed, especially if there have already been episodes
of visual loss or stroke.
PMR: 10–15 mg prednisolone as a single dose in the morning.
GCA: 60–100 mg prednisolone, usually in divided doses.
Most patients will eventually be able to stop corticosteroids
after 12–18 months.
Calcium and vitamin D supplements and sometimes
bisphosphonates are necessary to prevent osteoporosis while
high-dose steroids are being used
15. Takayasu’s disease
This is rare, except in Japan.
It is of unknown aetiology and occurs in females.
There is a vasculitis involving the aortic arch as well as other major arteries.
There is also a systemic illness, with pain and tenderness over the affected
arteries.
Absent peripheral pulses and hypertension are common.
Corticosteroids help relieve symptoms.
Treatment may require a surgical bypass to improve perfusion of the affected
areas.
Eventually heart failure and strokes may occur but most patients survive for at
least 5 years
17. Polyarteritis nodosa (PAN)
Classical PAN is a rare condition which usually occurs in
middle-aged men.
its occasional association with hepatitis B antigenaemia
suggests a vasculitis secondary to the deposition of immune
complexes.
Pathologically, there is fibrinoid necrosis of vessel walls with
microaneurysm formation, thrombosis and infarction.
18. Clinical features
These include fever, malaise, weight loss and myalgia.
These initial symptoms are followed by dramatic acute
features that are due to organ infarction.
Neurological: mononeuritis multiplex is due to
arteritis of the vasa nervorum.
Abdominal: pain due to arterial involvement of the
abdominal viscera, mimicking acute cholecystitis,
pancreatitis or appendicitis. Gastrointestinal
haemorrhage occurs because of mucosal ulceration.
19. Renal: presents with haematuria and proteinuria.
Hypertension and acute/chronic kidney disease
occur.
Cardiac: coronary arteritis causes myocardial
infarction and heart failure. Pericarditis also
occurs.
Skin: subcutaneous haemorrhage and gangrene
occur. A persistent livedo reticularis is seen in
chronic cases. Cutaneous and subcutaneous
palpable nodules occur, but are uncommon.
Lung: involvement is rare.
20. Investigations
Blood count: Anaemia, leucocytosis and a raised ESR
occur.
Angiography: Demonstration of microaneurysms in
hepatic, intestinal or renal vessels if necessary.
Other investigations: as appropriate (e.g. ECG and
abdominal ultrasound), depending on the clinical
problem. ANCA is positive only rarely in classic PAN.
21. Treatment
Is with corticosteroids, usually in combination
with immunosuppressive drugs such as
azathioprine.
22. Kawasaki’s disease
• This is an acute systemic vasculitis involving medium-sized
vessels, affecting mainly children under 5 years of age.
• It is very frequent in Japan, and an infective trigger is
suspected.
• It occurs worldwide and is also seen in adults.
23. Clinical features
Fever lasting 5 days or more
Bilateral conjunctival congestion 2–4 days after onset
Dryness and redness of the lips and oral cavity 3 days after onset
Acute cervical lymphadenopathy accompanying the fever
Polymorphic rash involving any part of the body
Redness and oedema of the palms and soles 2–5 days after onset
24.
25. Diagnosis
The persistent fever plus at least 4/5 features should be present to make
the diagnosis, or < 4 if coronary aneurysms can be seen on two
dimensional echocardiography, MRI or angiography.
Cardiovascular changes in the acute stage include pancarditis and
coronary arteritis leading to aneurysms or dilatation.
Anti-endothelial cell autoantibodies are often detectable.
Other features include diarrhoea, albuminuria, aseptic meningitis and
arthralgia and, in most, there is a leucocytosis, thrombocytosis and a
raised CRP.
26. Treatment
• Is with a single dose of high-dose intravenous
immunoglobulin (2 g/kg), which prevents the
coronary artery disease, followed after the acute
phase by aspirin 200–300 mg daily.
• There is no evidence that steroid treatment improves
the outcome.
31. Wegener’s granulomatosis
It is characterized by lesions involving the upper respiratory tract, lungs and kidneys.
It often starts with severe rhinorrhoea, with subsequent nasal mucosal ulceration
followed by cough, haemoptysis and pleuritic pain.
Etiology is unknown
Single or multiple nodular masses or pneumonic infiltrates with cavitation are seen
on chest X-ray.
The typical histological changes are usually best seen on renal biopsy, which shows
necrotizing microvascular glomerulonephritis.
This disease responds well to treatment with cyclophosphamide 150–200 mg daily.
Rituximab is also being used.
A variant of Wegener’s granulomatosis called ‘midline granuloma’ affects the nose
and paranasal sinuses and is particularly mutilating; it has a poor prognosis.
32. Churg–Strauss syndrome
This condition classically occurs in males in their 4th decade, who present
with rhinitis and asthma, eosinophilia and systemic vasculitis.
The aetiology is uncertain.
Typically, it involves the lungs, peripheral nerves and skin, but renal
involvement is uncommon.
Transient patchy pneumonia-like shadows may occur.
Skin lesions include tender subcutaneous nodules as well as petechial or
purpuric lesions.
ANCA is usually positive.
The disease responds well to corticosteroids.
33. Microscopic vasculitis (polyangiitis)
This involves the kidneys and the lungs where
it results in recurrent haemoptysis.
ANCA is usually positive.
35. Henoch–Schönlein Purpura
• This clinical syndrome comprises a characteristic skin rash, abdominal
colic, joint pain and glomerulonephritis.
• Approximately 30–70% have clinical evidence of renal disease with
haematuria and/or proteinuria
• The renal lesion is a focal segmental proliferative glomerulonephritis,
sometimes with mesangial hypercellularity.
• In more severe cases, epithelial crescents may be present.
• Immunoglobulin deposition is mainly IgA in the glomerular mesangium
distribution, similar to IgA nephropathy.
• There is no treatment of proven benefit; steroid therapy is ineffective.
• Treatment is usually supportive but with crescentic GN aggressive
immunosuppression has been tried with variable outcome.
36.
37. Leucocytoclastic vasculitis
• (LCV) is the most common cutaneous vasculitis affecting small vessels.
• This usually appears on the lower legs as a symmetrical palpable purpura.
• It can be caused by drugs (15%), infection (15%), inflammatory disease
(10%) or malignant disease (<5%) but often no cause is found (55–60%).
• Investigations are only necessary with persistent lesions or associated
signs and symptoms.
• LCV often settles spontaneously, treatment with analgesia, support
stockings, dapsone or prednisolone may be needed to control the pain
and to heal up any ulceration.