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.
DIC is not a disease entity but an event that can accompany various disease processes. It is an “Acquired” Pathological process. Widespread activation of the clotting cascade lead to formation of blood clots in small blood vessels throughout the body causing a compromise of tissue blood flow leading to multiple organ damage MOD. The coagulation process consumes clotting factors and platelets,normal clotting is disrupted and severe bleeding can occur from various sites. Patients with DIC should be treated at hospitals with appropriate critical care units (ICU) with available Subspecialty expertise, such as hematology, blood bank, or surgery. Patients who present to hospitals without those capabilities and who are stable enough for transfer should be referred expeditiously to a hospital that has those resources. Treatment of DIC includes the underlying disorder, supportive treatment and hemostatic Therapy.
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.
DIC is not a disease entity but an event that can accompany various disease processes. It is an “Acquired” Pathological process. Widespread activation of the clotting cascade lead to formation of blood clots in small blood vessels throughout the body causing a compromise of tissue blood flow leading to multiple organ damage MOD. The coagulation process consumes clotting factors and platelets,normal clotting is disrupted and severe bleeding can occur from various sites. Patients with DIC should be treated at hospitals with appropriate critical care units (ICU) with available Subspecialty expertise, such as hematology, blood bank, or surgery. Patients who present to hospitals without those capabilities and who are stable enough for transfer should be referred expeditiously to a hospital that has those resources. Treatment of DIC includes the underlying disorder, supportive treatment and hemostatic Therapy.
The Lonely Voices of Autoimmune Disease: Believe It or NotDrBonnie360
Content and Visual Design by Tiffany Simms
Due to the invisible nature of autoimmune diseases, many of its patients look normal and healthy. This presents a challenge for patients’ social sphere, a struggle when seeing doctors for diagnosis, and a lack of general awareness and knowledge of all autoimmune diseases. Despite the many statistics on autoimmune disease, it’s time to put a voice to the numbers.
We present to you, a snippet of our shocking Stanford MedicineX Workshop Survey (http://bit.ly/1JyIvKd) responses.
Believe it or not, these are the real experiences and words of the lonely voices of autoimmune 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
download link : https://www.dropbox.com/s/5c69pkpkass8sk1/Vasculitides%20AND%20ANTI-GBM.ppt?m
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
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- WOMEN’S HEALTH: FERTILITY PRESERVATION
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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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
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2. Vasculitis
DEFINITION
Vasculitis are a heterogeneous group of diseases characterized by
Inflammation , necrosis and damage to blood vessel walls , often with
associated organ involvement.
The vessel lumen is usually compromised, and this is associated with
ischemia of the tissue supplied by the involved vessel.
Any type, size, and location of blood vessel may be involved.
Vasculitis may be primary ( sole manifestation of a disease)
or may be secondary( component of another primary disease)
Vasculitis may be confined to a single organ, such as the skin,
or it may simultaneously involve several organ systems
3. Classification of Vascilites
Large vessel
.Giant cell arteritis &/or Polymyalgia rheumatica.
• Takayasu's arteritis
Medium vessel
Classical polyarteritis nodosa
• Kawasaki disease (in childhood)
Small vessel
• Microscopic polyangiitis
• Wegener's granulomatosis
• Churg-Strauss syndrome
• Henoch-Schönlein purpura
• Mixed essential cryoglobulinaemia
Others as Behcets disease.
4. PATHOPHYSIOLOGY AND
PATHOGENESIS of Vasculitis
• Generally, most of the vasculitic syndromes are assumed to be
mediated at least in part by immunopathogenic mechanisms
that occur in response to certain antigenic stimuli
• it is unknown why some individuals might develop vasculitis
in response to certain antigenic stimuli,whereas others do not.
• It is likely that a number of factors are involved in the
ultimate expression of a vasculitic syndrome. These include
the genetic predisposition, environmental exposures, and the
regulatory mechanisms associated with immune response to
certain antigens.
5. deposition of immune complexes in vessel walls is the most
widely accepted pathogenic mechanism of vasculitis.
• The actual antigen contained in the immune complex has only
rarely been identified in vasculitic syndromes.
• In this regard, hepatitis B antigen has been identified in some
patients with systemic vasculitis, most notably in polyarteritis
nodosa .
• The syndrome of essential mixed cryoglobulinemiais strongly
associated with hepatitis C virus infection
6. • . The mechanisms of tissue damage in
immune complex–mediated vasculitis
• antigen-antibody complexes are formed and are deposited in
vessel walls .
• The deposition of complexes results in activation of
complement components, particularly C5a, which is strongly
chemotactic for neutrophils.
• These cells then infiltrate the vessel wall, phagocytose the
immune complexes, and release their intracytoplasmic
enzymes, which damage the vessel wall.
• As the process becomes subacute or chronic,mononuclear
cells infiltrate the vessel wall.
• This will compromise of the vessel lumen with ischemic
changes in the tissues supplied by the involved vessel.
7. Clinical features of Vasculitis
• The clinical features of vasculitis are due to a combination of
local tissue ischaemia (caused by vessel inflammation and
narrowing) and the systemic effects of widespread
inflammation.
• Systemic vasculitis should be considered in any patient with
fever, weight loss, fatigue, evidence of multisystem
involvement, rashes, raised inflammatory markers and
abnormal urinalysis.
• Early diagnosis and management are essential to prevent
irreversible organ damage.
• .
8. Clinical Features of Vasculitis include
Constitutional symptoms Gastrointestinal
Bowel ischemia and ⁄or infarction
Fever
Weight loss Renal
Fatigue Glomerulonephritis
Nephrotic syndrome
purura
Renovascular involvement
Livido reticularis Hypertension
Digital infarction
Neurologic
Musculoskeletal Mononeuritis multiplex
Arthralgia Visual disturbance
Arthritis Stroke
Cardiovascular
pulselessness and ⁄or bruits Laboratory abnormalities
common in large vessel disease Anemia
Claudication Eosinophilia
Aneurysms Elevated acute phase reactions
Pulmonary Renal insufficiency
Alveolar hemorrhage Active urinary sediment
Nodules
9. • Vasculitis may be difficult to distinguish from
- widespread malignancy.
- occult sepsis (particularly subacute bacterial endocarditis &
meningococcal septicaemia).
- cholesterol emboli.
- atrial myxoma .
-antiphospholipid syndrome.
The key to recognition is the presence of multisystem
involvement
12. Investigations in Vasculitis
• If vasculitis is suspected, the diagnosis should ideally be
confirmed by tissue biopsy.
• Skin biopsies are easily obtained.
• Nasal septal tissue can be taken from areas of ulceration or
granulation.
• Muscle biopsy is positive in about 50% of patients with muscle
pain.
. The most important bedside test is the urine dip test for protein
and blood, and subsequent microscopy, since the prognosis of
vasculitis is often determined by the degree of renal
involvement. In patients with abnormal renal function and active
urinary sediment, renal biopsy should be considered.
13. • Visceral angiography
to detect microaneurysms (e.g. classical polyarteritis nodosa)
is most useful where involved tissue is not available to biopsy.
• ESR usually elevated in vasculitis
• CRP
• C-ANCA & p-ANCA
14. • Antineutrophil cytoplasmic antibodies (ANCA)
• are directed against enzymes present in neutrophil granules.
• Two main patterns of immunofluorescence are distinguished:
cytoplasmic (c-ANCA) and perinuclear (p-ANCA).
• c-ANCA are usually directed against proteinase 3 and are
particularly associated with Wegener's granulomatosis and Churg-
Strauss syndrome.
• p-ANCA are usually directed against myeloperoxidase and
associate with microscopic polyangiitis.
• However, positive ANCAs occur in many other diseases, including
malignancy, infection (bacterial and HIV), inflammatory bowel
disease, RA, lupus and pulmonary fibrosis. Therefore, the diagnosis
of these conditions cannot be made or refuted on the ANCA test
alone.
16. GIANT CELL ARTERITIS (GCA)
(Temporal Arteritis)
• GCA also known as temporal arteritis or cranial arteritis
• is a large vessel vasculitis predominately affecting branches of
the temporal and ophthalmic arteries.
• The mean age of onset is 70 years .
• 4:1 female:male ratio.
17. Clinical features of Giant cell arteritis
• The onset of symptoms may be abrupt but is often
insidious over the course of several weeks or months.
• The most important clinical features are:
1- Headache. This is usually the first symptom and is often
localised to the temporal or occipital region, with scalp
tenderness.
2- Jaw pain. This is brought on by chewing or talking and is
due to ischaemia of the masseters.
18. 3-Visual disturbance.
The most important complication of GCA is monocular blindness
which is almost never reversible
The optic nerve head is supplied by the posterior ciliary artery,
vasculitis of which leads to occlusion and acute anterior
ischaemic optic neuropathy.
Damage to the optic nerve results in loss of visual acuity and field,
reduced colour perception and pupillary defects.
Sudden visual symptoms in one eye, leading rapidly to blindness,
constitute the most common pattern.
On fundoscopy the optic disc may appear pale and swollen with
haemorrhages, but these changes may take 24-36 hours to
develop.
Once blindness has occurred corticosteroids have a negligible
effect but are indicated to prevent blindness in the other eye.
19. 4- There may be associated constitutional
symptoms of anorexia, fatigue, weight
loss, fever, depression and general malaise.
5- Occasionally presentation is with
neurological complications that include
transient ischaemic attacks, brain-stem
infarcts and hemiparesis.
20. Investigations
• The ESR usually elevated above 50 mm/hour in 90% of cases. ( in
some cases the ESR may be normal mainly in those with acute
presentationis , in the this situation the CRP may be more helpful ,&
usually elevated ).
• Temporal artery biopsy should be obtained.
corticosteroid treatment should not be delayed whilst the biopsy is
organised.
Characteristic biopsy findings are fragmentation of the internal
elastic lamina with necrosis of the media in combination with a
mixed inflammatory cell infiltrate (lymphocytes, plasma cells and
eosinophils).
However, 'skip' lesions are common and a negative biopsy does not
exclude the diagnosis.
21. Management of GCA
• If GCA is suspected, systemic corticosteroid (prednisolone 60
mg daily) should be started immediately to prevent visual loss.
• Steroid reduction should be guided by symptoms and ESR,
aiming for approximately 10 mg daily by 6 weeks. Thereafter,
doses should be reduced by 1 mg per month
• Maintenance therapy is required for at least 1 year, and
occasionally for the rest of the patient's life.
• Relapse occurs in 30%, and is an indication to restart high-
dose steroids with additional immunosuppressive agents,
typically azathioprine or methotrexate
22. • . Patients with known GCA should be advised to take
60 mg prednisolone and seek prompt medical advice
should they experience any recurrence of headache
or visual disturbance.