This document discusses the four main types of hypersensitivity reactions:
Type I is an immediate reaction mediated by IgE antibodies. It causes conditions like allergic asthma.
Type II involves antibodies binding to antigens on a person's own cells, activating complement and causing cell lysis. It includes conditions like autoimmune hemolytic anemia.
Type III occurs when immune complexes are deposited in tissues, activating complement and causing inflammation and tissue damage. Examples are serum sickness and lupus nephritis.
Type IV is a delayed reaction mediated by T cells and monocytes/macrophages. It causes conditions like contact dermatitis and tuberculosis.
Type II Hypersensitivity-Antibody mediated cytotoxic HypersensitivityAnup Bajracharya
Type II Hypersensitivity is antibody-mediated immune reaction in which antibodies (IgG or IgM) are directed against cellular or extracellular matrix antigens with the resultant cellular destruction, functional loss, or damage to tissues.
Type II Hypersensitivity-Antibody mediated cytotoxic HypersensitivityAnup Bajracharya
Type II Hypersensitivity is antibody-mediated immune reaction in which antibodies (IgG or IgM) are directed against cellular or extracellular matrix antigens with the resultant cellular destruction, functional loss, or damage to tissues.
Immediate or Type I hypersensitivity is a rapid immunological reaction occurring in a previously sensitized individual that is triggered by the binding of an antigen to IgE antibody on the surface of mast cells.
Autoimmunity is the system of immune responses of an organism against its own healthy cells and tissues. Any disease that results from such an aberrant immune response is termed an "autoimmune disease".
A. There are three types of immunological disorders
1. Hypersensitivity
2. Autoimmune disease
3. Immunodeficiency
B. Hypersensitivity reactions to usually harmless substances are often called allergies or allergic reactions
Immunity is the ability of the body to protect against all types of foreign bodies like bacteria, virus, toxic substances etc. As it protects us from diseases it is also called disease resistance. Immunity is done by immune system which is a complex network of lymphoid organs such as bone marrow, thymus, spleen etc. It is mainly of two types- Natural and Acquired immunity.
Immediate or Type I hypersensitivity is a rapid immunological reaction occurring in a previously sensitized individual that is triggered by the binding of an antigen to IgE antibody on the surface of mast cells.
Autoimmunity is the system of immune responses of an organism against its own healthy cells and tissues. Any disease that results from such an aberrant immune response is termed an "autoimmune disease".
A. There are three types of immunological disorders
1. Hypersensitivity
2. Autoimmune disease
3. Immunodeficiency
B. Hypersensitivity reactions to usually harmless substances are often called allergies or allergic reactions
Immunity is the ability of the body to protect against all types of foreign bodies like bacteria, virus, toxic substances etc. As it protects us from diseases it is also called disease resistance. Immunity is done by immune system which is a complex network of lymphoid organs such as bone marrow, thymus, spleen etc. It is mainly of two types- Natural and Acquired immunity.
Hypersensitivity can be defined as a state of altered immune response against an antigen characterized by hyper reactivity leading to immunopathology
Hypersensitivity reactions require a pre-sensitized (immune) state of the host.
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
Hypersensitivity Update .pdf Immunology and Microosmanolow
Immunology is the study of the immune system and is a very important branch of the medical and biological sciences. The immune system protects us from infection through various lines of defence.
1. Type I Hypersensitivity:
Type I hypersensitive reactions are the commonest type among all types which is mainly induced by certain type of antigens i.e. allergens. Actually anaphylaxis means “opposite of protection” and is mediated by IgE antibodies through interaction with an allergen
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
- 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
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
2. Introduction
Generally the immune system is protective
Protective mechanisms may result in severe
damages to tissues and may lead to death
When?
Severe damages may occur when the immune
system responded in exaggerated or
inappropriate form.
3. Classification
Coombs and Gell classification
1-Type I - immediate ( atopic, or anaphylactic)
2-Type II - antibody-dependent
3-Type III - immune complex
4-Type IV - cell-mediated or delayed
4.
5. Type I - immediate (or atopic, or anaphylactic)
Type I hypersensitivity is an allergic reaction provoked by
re-exposure to a specific antigen.
Exposure may be by ingestion, inhalation, injection,
or direct contact.
The reaction is mediated by IgE antibodies and
produced by the immediate release of histamine,
tryptase, arachidonate and derivatives by basophils
and mast cells..
6. This causes an inflammatory response
leading to an immediate (within seconds to
minutes) reaction.
The reaction may be either local or systemic.
Symptoms vary from mild irritation to sudden
death from anaphylactic shock.
Treatment usually involves epinephrine,
antihistamines, and corticosteroids
9. Type II - antibody-dependent
In type II hypersensitivity, the antibodies produced
by the immune response bind to antigens on the
patient's own cell surfaces.
The antigens recognized in this way may either be
intrinsic ("self" antigen, innately part of the patient's
cells) or extrinsic (absorbed onto the cells during
exposure to some foreign antigen, possibly as part
of infection with a pathogen
10. IgG and IgM antibodies bind to these antigens to
form complexes that activate the classical pathway
of complement activation for eliminating cells
presenting foreign antigens (which are usually, but
not in this case, pathogens).
As a result mediators of acute inflammation are
generated at the site and
membrane attack complexes cause cell lysis and
death. The reaction takes hours to a day.
13. Type III - immune complex
In type III hypersensitivity:
soluble immune complexes (aggregations of
antigens and IgG and IgM antibodies) form in the
blood and are deposited in various tissues
(typically the skin, kidney and joints)
This may trigger an immune response
according to the classical pathway of
complement activation.
The reaction takes hours to days to develop
15. Type IV Hypersensitivity
Type IV hypersensitivity is often called
delayed type as the reaction takes two to
three days to develop.
Unlike the other types, it is not antibody
mediated but rather is a type of cell-
mediated response.
16. Some clinical examples:
Contact dermatitis (poison ivy rash, for example)
Temporal arteritis
Symptoms of leprosy
Symptoms of tuberculosis
Transplant rejection
19. Type I hypersensitivity is also known as
immediate or anaphylactic
hypersensitivity.
The reaction may involve skin (urticaria and
eczema), eyes (conjunctivitis), nasopharynx
(rhinorrhea, rhinitis), bronchopulmonary
tissues (asthma) and gastrointestinal tract
(gastroenteritis)
20. The reaction may cause a range of
symptoms from minor inconvenience to
death.
The reaction usually takes 15 - 30 minutes
from the time of exposure to the antigen.
sometimes it may have a delayed onset
(10 - 12 hours).
21. Immediate hypersensitivity is mediated by
IgE.
The primary cellular component in this
hypersensitivity is the mast cell or
basophil.
The reaction is amplified and/or modified
by platelets, neutrophils and eosinophils.
A biopsy of the reaction site demonstrates
mainly mast cells and eosinophils.
22. Mechanism:
The mechanism of reaction involves preferential
production of IgE, in response to certain antigens
(allergens).
IgE has very high affinity for its receptor on mast
cells and basophils.
A subsequent exposure to the same allergen cross
links the cell-bound IgE and triggers the release of
various pharmacologically active substances
Cross-linking of IgE Fc-receptor is important in mast
cell triggering. Mast cell degranulation is preceded by
increased Ca++ influx, which is a crucial process;
ionophores which increase cytoplasmic Ca++ also
promote degranulation, whereas, agents which
deplete cytoplasmic Ca++ suppress degranulation.
24. Mast cells may be triggered by other stimuli
such as
-Exercise,
-Emotional stress
-Chemicals (e.g., photographic developing
medium, calcium ionophores, codeine, etc.),
-Anaphylotoxins (e.g., C4a, C3a, C5a, etc.).
These reactions are not hypersensitivity
reactions although they produce the same
symptoms.
26. Type II hypersensitivity is also known as cytotoxic
hypersensitivity and may affect a variety of organs
and tissues.
The antigens are normally endogenous, although
exogenous chemicals (haptens) which can attach to
cell membranes can also lead to type II
hypersensitivity.
Examples:
- Drug-induced hemolytic anemia
-Granulocytopenia
-Thrombocytopenia
27. The reaction time is minutes to hours.
Type II hypersensitivity is primarily mediated
by antibodies of the IgM or IgG classes and
complement
Phagocytes and K cells may also play a role
(ADCC).
28.
29. Lab Diagnosis
Diagnostic tests include detection of circulating
antibody against the tissues involved and the
presence of antibody and complement in the
lesion (biopsy) by immunofluorescence
31. Also known as immune complex disease
occurs when immune complex (Ag-Ab) are
not removed from circulation
These complexes are deposited in various
tissues and organs such as:
- Kidneys
- Joints
- Lung
- Skin
32. Immune complex formation may occur as
a result of :
Autoimmune diseases (RA)
Persistence infection (Hepatitis virus)
Repeated inhalation of antigenic materials
33. MECHANISM
Step 1
Large quantities of
soluble antigen-
antibody complexes
form in the blood and
are not completely
removed by
macrophages.
34. Step 2
These antigen-
antibody complexes
lodge in the
capillaries between
the endothelial cells
and the basement
membrane.
41. Serum Sickness
- Is a disease caused by the injection of large doses of a
protein antigen into the blood and characterized by the
deposition of antigen-antibody complexes in blood vessel
walls, especially in the kidneys and joints.
43. Systemic Lupus Erythmatosus
The disease is characterized by the presence
of autoantibodies , which form immune
complexes with autoantigens and are
deposited within the kidney glomeruli
The resulting type III hypersensitivity is
responsible for the glomerulonephritis
(Inflammation of blood capillary vessels in the
glomeruli)
45. Type IV hypersensitivity is also known as cell
mediated or delayed type hypersensitivity.
The classical example of this hypersensitivity
is tuberculin (Montoux) reaction
Reaction peaks 48 hours after the injection of
antigen (PPD or old tuberculin). The lesion is
characterized by induration and erythema
46.
47. Type IV hypersensitivity is involved in the
pathogenesis of many autoimmune and infectious
diseases:
Tuberculosis
Leprosy
Blastomycosis
Histoplasmosis
Toxoplasmosis
Leishmaniasis
Granulomas due to infections and foreign antigens.
48.
49. Another form of delayed hypersensitivity is
contact dermatitis (poison ivy (figure 6),
chemicals, heavy metals, etc.) in which the
lesions are more papular
Type IV hypersensitivity can be classified into
three categories depending on the time of
onset and clinical and histological
presentation
50. Fig 5Type
Reaction
time
Clinical
appearance
Histology Antigen and site
contact 48-72 hr eczema
lymphocytes, followed by
macrophages; edema of
epidermis
epidermal ( organic chemicals,
poison ivy, heavy metals,
etc.)
tuberculin 48-72 hr
local
induratio
lymphocytes, monocytes,
macrophages
intradermal (tuberculin, lepromin,
etc.)
granuloma 21-28 days hardening
macrophages, epitheloid and
giant cells, fibrosis
persistent antigen or foreign
body presence
(tuberculosis, leprosy, etc.)
51. Mechanism:
The mechanism includes T lymphocytes and
monocytes and/or macrophages.
Cytotoxic T cells (Tc) cause direct damage
whereas helper T (TH1) cells secrete
cytokines which activate cytotoxic T cells,
recruit and activate monocytes and
macrophages, which cause the bulk of the
damage
The delayed hypersensitivity lesions mainly
contain monocytes and a few T cells.
52. Diagnosis
Diagnostic tests in vivo include delayed
cutaneous reaction (e.g. Montoux test )
In vitro tests for delayed hypersensitivity
include mitogenic response, lympho-
cytotoxicity and IL-2 production.
Corticosteroids & other immunosuppressive
agents are used in treatment.
Editor's Notes
Figure 12.20. Serum sickness is a classic example of a transient immune complex-mediated syndrome. An injection of a foreign protein or proteins leads to an antibody response. These antibodies form immune complexes with the circulating foreign proteins. The complexes are deposited in small vessels and activate complement and phagocytes, inducing fever and the symptoms of vasculitis, nephritis, and arthritis. All these effects are transient and resolve when the foreign protein is cleared.