This document discusses the different types of hypersensitivity reactions:
1. Type I reactions are immediate and antibody-mediated, involving IgE. They cause conditions like allergic asthma and anaphylaxis.
2. Type II reactions are cytotoxic and involve IgG/IgM binding to cell surfaces and activating complement. They can lyse cells.
3. Type III reactions involve soluble immune complexes activating complement and causing inflammation. They include serum sickness.
4. Type IV reactions are delayed, cell-mediated responses involving sensitized T cells and cytokines. They cause conditions like contact dermatitis.
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.
BP-605T, Pharmaceutical biotechnology, Structure of immunoglobulins, classification of immunoglobulins, explanation of structure of immunoglobulin, digestion with proteolytic enzymes, Fab region, Fc region, role of different immunoglobulin classes, structure of IGM, IGA, IGG, IGE, IGD, Light chain, heavy chain, kappa, lambda, papain enzyme, pepsin enzyme
This topic covers the brief introduction of Ag and Ab in detail. Types and functions of Ig is explained in detail. Paraproteinemias is explained with simple pictures.
by Dr. N.Sivaranjani, MD
Hypersensitivity reactions are exaggerated or inappropriate immunologic responses occurring in response to an antigen or allergen. Type I, II and III hypersensitivity reactions are known as immediate hypersensitivity reactions because they occur within 24 hours of exposure to the antigen or allergen.
Cell mediated immunity also known as T cell immunity. it is developed by cell mediated responses and it does not involve any antibodies. Cell mediated immunity is offered by T lymphocytes and it starts developing when T cells come in contact with the antigens. In the Cell mediated immunity T cell plays one of the important role for the process of crosstalk with other immune system as well as to signal B cells to produce the antibody mediated immune response. Primary function of cell mediated response-
1) Eliminate intracellular pathogens.
2)Eliminate tumor cells.
T cells regulate proliferation and activity of other cells of the immune system : B cells, macrophages, neutrophil, etc.
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
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.
BP-605T, Pharmaceutical biotechnology, Structure of immunoglobulins, classification of immunoglobulins, explanation of structure of immunoglobulin, digestion with proteolytic enzymes, Fab region, Fc region, role of different immunoglobulin classes, structure of IGM, IGA, IGG, IGE, IGD, Light chain, heavy chain, kappa, lambda, papain enzyme, pepsin enzyme
This topic covers the brief introduction of Ag and Ab in detail. Types and functions of Ig is explained in detail. Paraproteinemias is explained with simple pictures.
by Dr. N.Sivaranjani, MD
Hypersensitivity reactions are exaggerated or inappropriate immunologic responses occurring in response to an antigen or allergen. Type I, II and III hypersensitivity reactions are known as immediate hypersensitivity reactions because they occur within 24 hours of exposure to the antigen or allergen.
Cell mediated immunity also known as T cell immunity. it is developed by cell mediated responses and it does not involve any antibodies. Cell mediated immunity is offered by T lymphocytes and it starts developing when T cells come in contact with the antigens. In the Cell mediated immunity T cell plays one of the important role for the process of crosstalk with other immune system as well as to signal B cells to produce the antibody mediated immune response. Primary function of cell mediated response-
1) Eliminate intracellular pathogens.
2)Eliminate tumor cells.
T cells regulate proliferation and activity of other cells of the immune system : B cells, macrophages, neutrophil, etc.
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
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
The presentation includes an overview of hypersensitivity and type 1 hypersensitivity with certain pictures elaborating the mechanism. The presentation also talks about asthma very briefly as an example of type 1 hypersensitivity.
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Antibiotic Stewardship by Anushri Srivastava.pptxAnushriSrivastav
Stewardship is the act of taking good care of something.
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
WHO launched the Global Antimicrobial Resistance and Use Surveillance System (GLASS) in 2015 to fill knowledge gaps and inform strategies at all levels.
ACCORDING TO apic.org,
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
ACCORDING TO pewtrusts.org,
Antibiotic stewardship refers to efforts in doctors’ offices, hospitals, long term care facilities, and other health care settings to ensure that antibiotics are used only when necessary and appropriate
According to WHO,
Antimicrobial stewardship is a systematic approach to educate and support health care professionals to follow evidence-based guidelines for prescribing and administering antimicrobials
In 1996, John McGowan and Dale Gerding first applied the term antimicrobial stewardship, where they suggested a causal association between antimicrobial agent use and resistance. They also focused on the urgency of large-scale controlled trials of antimicrobial-use regulation employing sophisticated epidemiologic methods, molecular typing, and precise resistance mechanism analysis.
Antimicrobial Stewardship(AMS) refers to the optimal selection, dosing, and duration of antimicrobial treatment resulting in the best clinical outcome with minimal side effects to the patients and minimal impact on subsequent resistance.
According to the 2019 report, in the US, more than 2.8 million antibiotic-resistant infections occur each year, and more than 35000 people die. In addition to this, it also mentioned that 223,900 cases of Clostridoides difficile occurred in 2017, of which 12800 people died. The report did not include viruses or parasites
VISION
Being proactive
Supporting optimal animal and human health
Exploring ways to reduce overall use of antimicrobials
Using the drugs that prevent and treat disease by killing microscopic organisms in a responsible way
GOAL
to prevent the generation and spread of antimicrobial resistance (AMR). Doing so will preserve the effectiveness of these drugs in animals and humans for years to come.
being to preserve human and animal health and the effectiveness of antimicrobial medications.
to implement a multidisciplinary approach in assembling a stewardship team to include an infectious disease physician, a clinical pharmacist with infectious diseases training, infection preventionist, and a close collaboration with the staff in the clinical microbiology laboratory
to prevent antimicrobial overuse, misuse and abuse.
to minimize the developme
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Medical Technology Tackles New Health Care Demand - Research Report - March 2...pchutichetpong
M Capital Group (“MCG”) predicts that with, against, despite, and even without the global pandemic, the medical technology (MedTech) industry shows signs of continuous healthy growth, driven by smaller, faster, and cheaper devices, growing demand for home-based applications, technological innovation, strategic acquisitions, investments, and SPAC listings. MCG predicts that this should reflects itself in annual growth of over 6%, well beyond 2028.
According to Chris Mouchabhani, Managing Partner at M Capital Group, “Despite all economic scenarios that one may consider, beyond overall economic shocks, medical technology should remain one of the most promising and robust sectors over the short to medium term and well beyond 2028.”
There is a movement towards home-based care for the elderly, next generation scanning and MRI devices, wearable technology, artificial intelligence incorporation, and online connectivity. Experts also see a focus on predictive, preventive, personalized, participatory, and precision medicine, with rising levels of integration of home care and technological innovation.
The average cost of treatment has been rising across the board, creating additional financial burdens to governments, healthcare providers and insurance companies. According to MCG, cost-per-inpatient-stay in the United States alone rose on average annually by over 13% between 2014 to 2021, leading MedTech to focus research efforts on optimized medical equipment at lower price points, whilst emphasizing portability and ease of use. Namely, 46% of the 1,008 medical technology companies in the 2021 MedTech Innovator (“MTI”) database are focusing on prevention, wellness, detection, or diagnosis, signaling a clear push for preventive care to also tackle costs.
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The dimensions of healthcare quality refer to various attributes or aspects that define the standard of healthcare services. These dimensions are used to evaluate, measure, and improve the quality of care provided to patients. A comprehensive understanding of these dimensions ensures that healthcare systems can address various aspects of patient care effectively and holistically. Dimensions of Healthcare Quality and Performance of care include the following; Appropriateness, Availability, Competence, Continuity, Effectiveness, Efficiency, Efficacy, Prevention, Respect and Care, Safety as well as Timeliness.
CHAPTER 1 SEMESTER V PREVENTIVE-PEDIATRICS.pdfSachin Sharma
This content provides an overview of preventive pediatrics. It defines preventive pediatrics as preventing disease and promoting children's physical, mental, and social well-being to achieve positive health. It discusses antenatal, postnatal, and social preventive pediatrics. It also covers various child health programs like immunization, breastfeeding, ICDS, and the roles of organizations like WHO, UNICEF, and nurses in preventive pediatrics.
CHAPTER 1 SEMESTER V - ROLE OF PEADIATRIC NURSE.pdfSachin Sharma
Pediatric nurses play a vital role in the health and well-being of children. Their responsibilities are wide-ranging, and their objectives can be categorized into several key areas:
1. Direct Patient Care:
Objective: Provide comprehensive and compassionate care to infants, children, and adolescents in various healthcare settings (hospitals, clinics, etc.).
This includes tasks like:
Monitoring vital signs and physical condition.
Administering medications and treatments.
Performing procedures as directed by doctors.
Assisting with daily living activities (bathing, feeding).
Providing emotional support and pain management.
2. Health Promotion and Education:
Objective: Promote healthy behaviors and educate children, families, and communities about preventive healthcare.
This includes tasks like:
Administering vaccinations.
Providing education on nutrition, hygiene, and development.
Offering breastfeeding and childbirth support.
Counseling families on safety and injury prevention.
3. Collaboration and Advocacy:
Objective: Collaborate effectively with doctors, social workers, therapists, and other healthcare professionals to ensure coordinated care for children.
Objective: Advocate for the rights and best interests of their patients, especially when children cannot speak for themselves.
This includes tasks like:
Communicating effectively with healthcare teams.
Identifying and addressing potential risks to child welfare.
Educating families about their child's condition and treatment options.
4. Professional Development and Research:
Objective: Stay up-to-date on the latest advancements in pediatric healthcare through continuing education and research.
Objective: Contribute to improving the quality of care for children by participating in research initiatives.
This includes tasks like:
Attending workshops and conferences on pediatric nursing.
Participating in clinical trials related to child health.
Implementing evidence-based practices into their daily routines.
By fulfilling these objectives, pediatric nurses play a crucial role in ensuring the optimal health and well-being of children throughout all stages of their development.
Defecation
Normal defecation begins with movement in the left colon, moving stool toward the anus. When stool reaches the rectum, the distention causes relaxation of the internal sphincter and an awareness of the need to defecate. At the time of defecation, the external sphincter relaxes, and abdominal muscles contract, increasing intrarectal pressure and forcing the stool out
The Valsalva maneuver exerts pressure to expel faeces through a voluntary contraction of the abdominal muscles while maintaining forced expiration against a closed airway. Patients with cardiovascular disease, glaucoma, increased intracranial pressure, or a new surgical wound are at greater risk for cardiac dysrhythmias and elevated blood pressure with the Valsalva maneuver and need to avoid straining to pass the stool.
Normal defecation is painless, resulting in passage of soft, formed stool
CONSTIPATION
Constipation is a symptom, not a disease. Improper diet, reduced fluid intake, lack of exercise, and certain medications can cause constipation. For example, patients receiving opiates for pain after surgery often require a stool softener or laxative to prevent constipation. The signs of constipation include infrequent bowel movements (less than every 3 days), difficulty passing stools, excessive straining, inability to defecate at will, and hard feaces
IMPACTION
Fecal impaction results from unrelieved constipation. It is a collection of hardened feces wedged in the rectum that a person cannot expel. In cases of severe impaction the mass extends up into the sigmoid colon.
DIARRHEA
Diarrhea is an increase in the number of stools and the passage of liquid, unformed feces. It is associated with disorders affecting digestion, absorption, and secretion in the GI tract. Intestinal contents pass through the small and large intestine too quickly to allow for the usual absorption of fluid and nutrients. Irritation within the colon results in increased mucus secretion. As a result, feces become watery, and the patient is unable to control the urge to defecate. Normally an anal bag is safe and effective in long-term treatment of patients with fecal incontinence at home, in hospice, or in the hospital. Fecal incontinence is expensive and a potentially dangerous condition in terms of contamination and risk of skin ulceration
HEMORRHOIDS
Hemorrhoids are dilated, engorged veins in the lining of the rectum. They are either external or internal.
FLATULENCE
As gas accumulates in the lumen of the intestines, the bowel wall stretches and distends (flatulence). It is a common cause of abdominal fullness, pain, and cramping. Normally intestinal gas escapes through the mouth (belching) or the anus (passing of flatus)
FECAL INCONTINENCE
Fecal incontinence is the inability to control passage of feces and gas from the anus. Incontinence harms a patient’s body image
PREPARATION AND GIVING OF LAXATIVESACCORDING TO POTTER AND PERRY,
An enema is the instillation of a solution into the rectum and sig
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2. Immunopathology
Exaggerated immune response may lead to different
forms of tissue damage
1) An overactive immune response:
produce more damage than it prevents
e.g. hypersensitivity reactions and graft rejection
2) Failure of appropriate recognition:
as in autoimmune diseases
3. Hypersensitivity Reaction
Hypersensitivity or allergy
* An immune response results in exaggerated reactions
harmful to the host
* There are four types of hypersensitivity reactions:
Type I, Type II, Type III, Type IV
* Types I, II and III are antibody mediated
* Type IV is cell mediated
4. Classification
• Based on time required for a sensitized host to
develop clinical reactions on re – exposure
➢ Immediate
➢ Delayed
• Based on different mechanisms of pathogenesis
➢ Type 1 ( IgE mediated)
➢ Type 2 (cytotoxic or cell stimulating)
➢ Type 3 (immune complex)
➢ Type 4 ( cell mediated)
5. Immediate hypersensitivity
Appears and recedes
rapidly
Induced by antigens by
any route
B cell or Antibody
mediated
Delayed hypersensitivity
Appears slowly, lasts longer
Induced by antigens
intradermally or skin contact
T cell mediated
6. Type I: Immediate hypersensitivity
* An antigen reacts with cell fixed antibody (Ig E)
leading to release of soluble molecules
An antigen (allergen)
soluble molecules (mediators)
* Soluble molecules cause the manifestation of disease
* Systemic life threatening; anaphylactic shock
* Local atopic allergies; bronchial asthma, hay fever
and food allergies
7. Pathogenic mechanisms
* First exposure to allergen
Allergen stimulates formation of antibody (Ig E type)
Ig E fixes, by its Fc portion to mast cells and basophils
* Second exposure to the same allergen
It bridges between Ig E molecules fixed to mast cells
leading to activation and degranulation of mast cells
and release of mediators
8. Pathogenic mechanisms
• Three classes of mediators derived from mast cells:
1) Preformed mediators stored in granules (histamine)
2) Newly sensitized mediators:
leukotrienes, prostaglandins, platelets activating factor
3) Cytokines produced by activated mast cells, basophils
e.g. TNF, IL3, IL-4, IL-5 IL-13, chemotactic factors
* These mediators cause: smooth muscle contraction,
mucous secretion and bronchial spasm, vasodilatation,
vascular permeability and edema
9. Anaphylaxis
* Systemic form of Type I hypersensitivity
* Exposure to allergen to which a person is previously sensitized
* Allergens:
Drugs: penicillin
Serum injection : anti-diphtheritic or anti-tetanic serum
anesthesia or insect venom
* Clinical manifestations:
Shock due to sudden decrease of blood pressure, respiratory distress
due to bronchospasm, cyanosis, edema, urticaria
* Treatment: corticosteroids injection, epinephrine, antihistamines
10. Mechanism of anaphylaxis
IgE molecules bind to the surface
receptors of mast cells and
basophils
Shocking dose
Antigen combines with cell bound
IgE
Cross linking between adjacent
antibody molecules
Increased permeability of cells to
calcium ions
Degranulation
Release of inflammatory
mediators
11. Atopy
• Local form of type I hypersensitivity
• Exposure to certain allergens that induce production of specific Ig E
* Allergens :
Inhalants: dust, tree or pollens, mould spur.
Ingestants: milk, egg, fish, chocolate
Contactants: wool, nylon, animal fur
Drugs: penicillin, salicylates, anaesthesia, insect venom
• There is a strong familial predisposition to atopic allergy
• The predisposition is genetically determined
12. 4. Skin allergy:
4. Common disease of type I hypersensitivity
1. Systemic anaphylaxis: a very dangerous syndrome
1) Anaphylactic drug allergy :penicillin
2) Anaphylactic serum allergy :
2. Respiratory allergic diseases :
1) Allergic asthma:acute response, chronic response
2) Allergic rhinitis
3. Gastrointestinal allergic diseases :
The lack of SIgA protein
hydrolase
Undigested
protein
Allergen
14. Type 2 Reaction: cytolytic and cytotoxic
Ig G and rarely Ig M antibodies
Bind to antigenic cell
Lysis of cell
➢ Cell surface antigens
(autoimmune anaemia's)
➢ Adsorption of antigens on
cell surface (drugs)
➢ Cell surface receptor and
disrupts normal function
(Graves disease)
16. 2. Mechanism of Type II hypersentivity
1. Surface antigen on target cells
Target cells: Normal tissue cell, changed or modified self tissue cells
2.Antibody, complement and modified self-cell
Antigen : Blood group antigen, Common antigen,
Self-antigen modified by physical factors or infection
Drug antigen,
Antigen-antibody complex
Activate complement Lyses target cells
Opsonic phagocytosis Destroy target cells
Stimulating or blocking effect Promote /suppress the target cell function
17. Antigen or hapten on cell
Antibody (IgG, IgM)
Activate complement
Lyse target cell
Opsonic phagocytosis NK , phagocyte Stimulate / block
Destroy target cell ADCC
Target cell injury Change the function of Target cell
Mechanism of Type II hypersensitivity
18. Free Ag + Primed Ab Larger immune complex
Deposit in tissue or blood vessel wall
Inflammation
Type III hypersensitivity
19. Type 3 reactions – immune complex diseases
Antigen – antibody complexes
Complement activation
Release of inflammatory
mediators
Increased vascular
permeability
Infiltration with neutrophils
20. • The reaction may be general (e.g., serum sickness) or
may involve individual organs including skin (e.g.,
systemic lupus erythematosus, Arthus reaction), kidneys
(e.g., lupus nephritis), lungs (e.g., aspergillosis), joints
(e.g., rheumatoid arthritis) or other organs.
• This reaction may be the pathogenic mechanism of
diseases caused by many microorganisms.
Type III hypersensitivity
21. • The reaction may take 3 - 10 hours after exposure to the
antigen .
• It is mediated by soluble immune complexes.
• They are mostly of the IgG class, although IgM may also
be involved.
• The antigen may be exogenous (chronic bacterial, viral
or parasitic infections), or endogenous (non-organ
specific autoimmunity: e.g., systemic lupus
erythematosus, SLE).
• The antigen is soluble and not attached to the organ
involved
Type III hypersensitivity
22. • PMNs and macrophages bind to immune
complexes via FcR and phagocytose the
complexes.
BUT
• If unable to phagocytose the immune
complexes can cause inflammation via C’
activation ---> C3a C4a, C5a and "frustrated
phagocytes".
Type III hypersensitivity
24. Mechanism of type III hypersensitivity
Formation of the intermediate immune complex
Deposition of the intermediate immune complex
Tissue injury by the immune complex
25. Common diseases of type III hypersensitivity
1. Local immune complex disease
Arthus reaction :Experimental local reaction,
Necrotic vasculitis , Ulcer
Human local reaction: Insulin-dependent diabetes mellitus (IDDM)
2. Acute systemic immune complex disease
serum sickness
Anti-serum Ab+Ag systemic tissue injury, fever, arthritis, skin rash
Penicillin, Sulfanilamide
Acute immune complex glomerulonephritis : Streptococcus
infection
3. Chronic immune complex disease
Rheumatoid arthritis
26. Interaction of primed T cells and associated antigen
Infiltration of Mononuclear Cells, Inflammatory response
Type IV hypersensitivity (Delayed)
27. Type 4 –Delayed hypersensitivity
Sensitized T cells
Contact with specific
antigen
Release cytokines
Effects on leucocytes,
macrophages and tissue
cells
28. Mechanism of type IV hypersensitivity
Formation of effector and memory T cells
Inflammation and cytotoxicity caused by effector T cells
1) Inflammation and tissue injury mediated by CD4+Th1
Release chemokines and cytokines
Immune injury mainly caused by infiltration of mononuclear cells and
lymphocytes
2) Cytotoxicity of CD8+CTL
29. Antigen T cell
(CD4+,CD8+)
Secondary
contact
Induce
PrimedT cell
CD4+
T cell
CD8+
T cell
Release
Cytokines
IL-2
TNF-b
INF-g
TF
MCF
MIF
MAF
SRF
Directly kill target cells
Infiltration of
monocyte and Mf
Proliferation ofT cell
Exudation and edema
Cytotoxicity
Inflammation characterized by infiltration of Mf , monocyte,
and tissue injury
Mechanism of type IV hypersensitivity
30. Delayed hypersensitivity reactions
Type Reaction time
Clinical
appearance
Histology
Antigen and
site
Contact
dermatitis
48-72 hr eczema
lymphocytes,
followed by
macrophages;
edema of
epidermis
epidermal
(organic
chemicals,
poison ivy,
heavy
metals, etc.)
tuberculin 48-72 hr
local
induration
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.)
31. DIAGNOSIS AND TREATMENT
• Diagnostic tests in vivo include delayed cutaneous
reaction (e.g. Mantoux test and patch test (for contact
dermatitis).
• In vitro tests for delayed hypersensitivity include
mitogenic response, lympho-cytotoxicity and IL-2
production.
• Corticosteroids and other immunosuppressive agents
are used in treatment.
32. Common disease of type IV hypersensitivity
1) Infectious delayed type hypersensitivity
OT( Old Tuberculin ) test
2) Contact dermatitis :
Paint, drugs, water blister, dermatitis
33. Comparison of Different Types of hypersensitivity
characteris
tics
type-I
anaphylactic
type-II
(cytotoxic)
type-III
(immune
complex)
type-IV
(delayed type)
antibody IgE IgG, IgM IgG, IgM None
antigen exogenous cell surface soluble tissues & organs
response
time
15-30 minutes minutes-hours 3-8 hours 48-72 hours
appearance wheal & flare
lysis and
necrosis
erythema and
edema, necrosis
erythema and
induration
histology
basophils and
eosinophil
antibody and
complement
complement and
neutrophils
monocytes and
lymphocytes
transferred
with
antibody antibody antibody T-cells
examples
allergic asthma,
hay fever
erythroblastosis
fetalis,
Goodpasture's
nephritis
Arthus reaction,
serum sickness,
farmer's lung
disease
tuberculin test,
poison ivy,
granuloma