Angioedema is rapid swelling of subcutaneous tissues caused by increased vascular permeability. There are four main types: allergic angioedema caused by allergens, drug-induced non-allergic reactions, idiopathic angioedema of unknown cause, and hereditary angioedema (HAE) caused by C1 inhibitor deficiency. HAE is treated with C1 inhibitor concentrate, icatibant, or ecallantide while other types may be treated with antihistamines, steroids, and epinephrine if anaphylaxis is possible. Early airway management is important as angioedema can affect the tongue, larynx, and uvula and potentially cause
Ludwig's Angina is an infective condition of the floar of mouth above and below the mylohyoid muscle. Tongue is raised, mouth remains open and there may be compromised airway and require tracheostomy. Treatment is medical in the form of antibioticsand pain killers and surgical in the form of incision and drainage.
To download my ANIMATED presenation VISIT
https://www.dropbox.com/s/5rfb35jcq45uexa/ANIAngioedema.pptx?m
To watch my ANIMATED vedio presentation VISIT
www.youtube.com/watch?v=hlqNGUGphuk
Thank you
Ludwig's Angina is an infective condition of the floar of mouth above and below the mylohyoid muscle. Tongue is raised, mouth remains open and there may be compromised airway and require tracheostomy. Treatment is medical in the form of antibioticsand pain killers and surgical in the form of incision and drainage.
To download my ANIMATED presenation VISIT
https://www.dropbox.com/s/5rfb35jcq45uexa/ANIAngioedema.pptx?m
To watch my ANIMATED vedio presentation VISIT
www.youtube.com/watch?v=hlqNGUGphuk
Thank you
Shock: types of shock, treatment - General Medicine - ATOTDr. Salman Ansari
Topic: Shock
Faculty: Medicine
Course: BSc ATOT - 2nd year
Definition
Types of shock with examples
Hypovolemic shock
Cardiogenic shock
Septic shock
Clinical features
Treatment of shock
this presentation includes all the parts of shock. its definition classisfication, types of shock, pathophysiology, and additiionaly also includes clinical emergencies such as anaphylactic shock and syncope. hope this helps everyone.
Dr satyaki Verma
Dept of perio
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.
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.
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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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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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
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.
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.
2. What is angioedema?
• Heinrich Irenaeus Quincke (1842 –1922) was
a German doctor. He introduced the
lumbar puncture and in 1882 was the
first to recognise angioedema.
William Osler remarked in 1888
that some cases may have a
hereditary basis
3. What is angioedema?
• It is the rapid swelling of the dermis,
subcutaneous tissue, mucosa and submucosal
tissues
• It is very similar to urticaria
• You can try to differentiate through history
and examination
• Etiologies of angioedema are divided into
mast cell mediated and non-mast cell
mediated
4.
5. What is angioedema?
• Non pitting, rapid onset, self limiting swelling
• Results from increased vascular permability
• Generally resolves in 24-48 hours
• But has the potential to ruin your day (and the
patient’s)
6. What are the types of angioedema?
The causes of angioedema depend on the type
of angioedema a patient has:
1) acute allergic angioedema
2) non-allergic drug reactions
3) idiopathic angioedema
4) hereditary angioedema (HAE) / acquired C1
inhibitor deficiency
7. Acute allergic angioedema
• Almost always occurs with urticaria within 1-2
hours of exposure to the allergen
• Nuts, shellfish, milk, eggs
• Drugs, e.g. penicillin, NSAIDS, vaccines
• Radiocontrast media
• Natural rubber latex e.g. gloves, catheters
• Reactions will recur with repetitive exposures
or exposure to cross-reactive substances
8. Non-allergic drug reactions
• Onset may be days to months after taking the
medication
• Commonly ACE inhibitors
• Cascade of effects via kinin production and
nitric oxide generation
• Occurs without urticaria
9. ACE inhibitors increase bradykinin activity >>> Transient
vasodilation >>> fluid in extracellular space
The incidence of angioedema from ACE inhibitors ranges in
the literature from 0.1 to 2.2%
(Allergy Asthma Proc 30:11–16, 2009; doi: 10.2500/aap.2009.30.3188)
10. Idiopathic angioedema
• Similar to acute allergic but angioedema keeps
on recurring and often no known cause is
found
• Usually occurs with urticaria
• 30-50% of this type of angioedema may be
associated with some types of autoimmune
disorders including SLE
http://www.dermnetnz.org/reactions/angioedema.html
11. Hereditary angioedema (HAE)
• 3 types:
Type 1 and II mutation of C1NH gene on chromosome 11,
(encoding C1 inhibitor protein)
Type III mutation in F12 gene on chromosome 12,
(encoding coagulation factor XII)
• Type 1 results in low levels and function of circulating C1
inhibitor;
• Type II has normal levels of C1 inhibitor protein but
reduction in function
• Occurs in 1 in 50,000 males and females (rare)
• Decreased C1 inhibitor activity leads to excessive kallikrein,
which in turn produces bradykinin, which we know is a
potent vasodilator
12. Acquired C1 inhibitor deficiency
• Acquired during life rather than inherited
• May be due to B-cell lymphoma or antibodies
against C1 inhibitor
• Treatment is the same as HAE
13. Acquired and Hereditary:
• Patients often experience no symptoms until they reach
puberty
• Swellings can occur without any provocation
• Sometimes local trauma, vigorous exercise, emotional
stress, alcohol, and hormonal factors
• Some may get a transitory prodromal non-itchy rash,
headache, visual disturbance or anxiety
• Face, hands, arms, legs, genitals, digestive tract and airway
may be affected; swellings spread slowly
• Abdominal cramps, nausea, vomiting, difficulty breathing
• Urticaria does not usually occur
14. Treatment
There isn’t much treatment out there…but
AIRWAY!
AIRWAY!
AIRWAY!
HAVE A LOW THRESHOLD FOR INTUBATION
USE CLINICAL EXAMINATION
15. Investigations
There are no point-of-care tests! Treat what you see and from the patient’s history.
Bedside
Fiberoptic laryngoscopy
Laboratory - Identify underlying cause (help with long term management):
C1 esterase inhibitor (C1-INH) assays (low/ abnormal in HAE)
C4 levels (low in HAE attacks, usually normal between attacks)
serial tryptase levels (may be elevated in anaphylaxis/ mast cell-mediated angioedema)
Imaging
CT abdomen may show evidence of angioedema in patients presenting with abdominal pain:
CT neck primarily has a role in excluding conditions that may mimic angioedema (e.g. soft tissue
infection)
16. Specific treatments
FFP – approx 40 case reports only. Limited evidence.
possible therapy for ACEI-related angioedema
FFP contains ACE, which degrades bradykinin
Therapies for HAE
– icatibant — a bradykinin 2 receptor inhibitor
– ecallantide — a kallikrein inhibitor (kallikrein is the enzyme that produces bradykinin)
– C1-INH concentrate
Role of adrenaline, steroids and antihistamines….
• unlikely to be be effective for ACEI-related angioedema
– this a bradykinin-mediated condition, not related to mast cell degranulation
– many ACEI-related angioedema cases can be managed by observation alone, without
pharmacotherapy or intubation
…..Should be adminstered if the underlying cause of angioedema is uncertain (i.e.
anaphylaxis is possible)
17. Treatment
• H1 antihistamine e.g IV
chlorpheniramine 10 mg or diphenhydramine
25–50 mg
• Limited evidence for adding in H2 blocker e.g
ranitidine IV 50mg
• Intravenous corticosteroids e.g. hydro-
cortisone 200 mg or methylprednisolone 50–
100 mg
• Adrenaline IM 1:1000
19. Disposition
Consider admission to hospital in the following situations
(Winters et al, 2013):
• previous history of angioedema
• tongue edema
• pharyngeal edema (palate, uvula)
• laryngeal edema / upper airway oedema
• lack of improvement during stay in ED
Patients with isolated angioedema of the face or lips and
be usually be observed in ED for 4 to 8 hours for
progression of symptoms, then discharged
20. Conclusion
• 4 main types of angioedema
• Pharmacological treatment is limited
• Early airway management is key
Guidelines:
http://www.aaem.org/em-resources/position-statements/2006/clinical-practice-guidelines
http://lifeinthefastlane.com/ccc/angioedema/
Pedrosa M, Prieto-García A, Sala-Cunill A; Spanish Group for the Study of Bradykinin-Mediated
Angioedema (SGBA) and the Spanish Committee of Cutaneous Allergy (CCA). Management of
angioedema without urticaria in the emergency department. Ann Med. 2014 Dec;46(8):607-18.
doi: 10.3109/07853890.2014.949300. PubMed PMID: 25580506.