This document discusses animal models for studying vulnerable plaque and atherosclerosis. It describes how the chicken, pig, mouse, and rabbit models each have advantages and limitations for replicating human disease. The mouse has been genetically modified to better model plaque development. No current animal model fully captures plaque rupture seen in humans. The rabbit model with an embedded inflatable balloon shows promise for experimentally inducing plaque rupture.
Six angiographic indicators of large thrombus burden by
Yip and colleagues,depending upon the angiographic morphology are
features indicated “high-burden thrombus formation”:
1. A cut-off pattern of occlusion
2. Accumulated thrombus proximal to the occlusion
3. A reference lumen diameter of the IRA of >4.0 mm
4. An incomplete obstruction with an angiographic thrombus with
the greatest linear dimension more than 3 times the reference
lumen diameter
5. The presence of floating thrombus proximal to the lesion
6. A persistent dye stasis distal to the occlusion
STICH (Surgical Treatment for Ischemic Heart Failure)theheart.org
- Population and treatment:
1212 patients with coronary artery disease amenable to coronary artery bypass graft (CABG) with LVEF <35%
Randomized to CABG or standard medical therapy alone
- Primary outcome:
All-cause death
STICH myocardial viability substudy:
- A substudy designed to determine whether substantial viable myocardium evident at baseline (visualized by SPECT imaging or dobutamine echo) affects all-cause mortality over five years or influences the relative effectiveness of the selected treatment strategy
See the article at http://www.theheart.org/article/1204899.do
Six angiographic indicators of large thrombus burden by
Yip and colleagues,depending upon the angiographic morphology are
features indicated “high-burden thrombus formation”:
1. A cut-off pattern of occlusion
2. Accumulated thrombus proximal to the occlusion
3. A reference lumen diameter of the IRA of >4.0 mm
4. An incomplete obstruction with an angiographic thrombus with
the greatest linear dimension more than 3 times the reference
lumen diameter
5. The presence of floating thrombus proximal to the lesion
6. A persistent dye stasis distal to the occlusion
STICH (Surgical Treatment for Ischemic Heart Failure)theheart.org
- Population and treatment:
1212 patients with coronary artery disease amenable to coronary artery bypass graft (CABG) with LVEF <35%
Randomized to CABG or standard medical therapy alone
- Primary outcome:
All-cause death
STICH myocardial viability substudy:
- A substudy designed to determine whether substantial viable myocardium evident at baseline (visualized by SPECT imaging or dobutamine echo) affects all-cause mortality over five years or influences the relative effectiveness of the selected treatment strategy
See the article at http://www.theheart.org/article/1204899.do
A stent is a small, expandable tube. During a procedure called angioplasty, the stent is inserted into a coronary artery and expanded using a small balloon. A stent is used to open a narrowed or clotted artery.
Antibody mediated rejection of solid organ allograftstashagarwal
Objectives:
Introduction of Antibody mediated rejection AMR
Role of C4d in transplant rejection
Donor specific antibodies DSA
Presentation of AMR in kidney, liver, lung and heart.
A Sinister Cause for Recurrent Syncope: Metastatic Parapharyngeal Space Tumorasclepiuspdfs
Introduction: Metastasis from oropharyngeal squamous cell carcinoma can occur in the parapharyngeal space (PPS). Syncope is an uncommon presentation of parapharyngeal space tumors. This can occur because of the extrinsic compression or infiltration of the carotid sinus or glossopharyngeal nerve. Aim: This study aims to raise awareness about this rare condition of recurrent syncope secondary to PPS tumor. We aim to share our knowledge of dealing with such a case focusing on clinical presentation, investigations, and multidisciplinary approach to management. Case Presentation: We present a case of a 68-year-old Caucasian male who was admitted to a medical ward with recurrent episodes of syncope. The underlying cause was found to be the extrinsic compression of the left carotid artery from a PPS tumor. The CT scan of the neck raised a suspicion of the left PPS malignancy. It was confirmed on fine-needle aspiration cytology to be a metastatic poorly differentiated squamous cell carcinoma. The patient was managed with best supportive care. Conclusion: In a patient presenting with recurrent syncope, PPS tumor-related carotid sinus or glossopharyngeal nerve involvement should be considered. In our patient, the best supportive care was chosen. However, in select patients, cardiac pacing may be required to prevent recurrent syncope so that curative intent treatment can be started.
Similar to Percutaneous coronary intervention by hossein (20)
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
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 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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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Hot Selling Organic intermediates
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
2. AT THE BEGINNING OF
20thCENTRY,CVD ACCOUNTED FOR
LESS THAN 10 PERCENT OF ALL
DEATHS WORLD WIDE.AT IT’S
END,CVD ACCOUNTED FOR NEARLY
HALF OF ALL DEATH IN DEVELOPED
COUNTRIES.BY 2020,CVD WILL CLAIM
25 MILLION DEATHS ANNUALLY AND
WILL SURPASS INFECTIOUS DISEASE
AS THE WORLD’S NUMBER ONE
CAUSE OF DEATH AND DISABILITES.
3. THREE COMPLEMENTARY
STRATEGIES TO REDUCE
MORBIDITY AND MORTALITY
FROM CVD:
Lowering overall burden of CVD risk factors in
the entire population through population-wide
public health measures (national campaign).
Identifying and targeting high-risk subgroup of
population who may benefit from preventive
intervention.
Resources can be allocated to acute and
chronic treatment and secondary prevention.
5. Vulnerable plaques, vulnerable myocardium, andVulnerable plaques, vulnerable myocardium, and
hypercoagulablehypercoagulable state of the blood lead tostate of the blood lead to
sudden cardiac death and acute myocardial infarction.sudden cardiac death and acute myocardial infarction.
Vulnerable
Blood
Vulnerable
Myocardium
Vulnerable
Plaque
Vulnerable
Patient
10. The vast majority of plaque of
disruptions are self-contained
and clinically silent.So plaque
disruption leading to ACS is not a
rule but an exception in a
-symptomatic patients with non-
obstructing atherosclerosis but
contributes to plaque progression
and luminal narrowing.
11. Culprit Plaque; a retrospective terminology
Vulnerable Plaque; a prospective terminology
VulnerablePlaque= FutureC ulprit Plaque
Clarification of Terminologies
14. Dangerous forms of
atherosclerotic plaques
that can rupture or
induce thrombosis and
lead to critical disruption
of blood flow.
The short answer is:
15. Proposed Histopathological and ClinicalProposed Histopathological and Clinical
Criteria for Definition of VulnerableCriteria for Definition of Vulnerable
PlaquePlaque
•• MajorMajor Criteria:Criteria:
1.1. Active Inflammation (Active Inflammation (monocytemonocyte//
macrophage infiltration)macrophage infiltration)
2.2. Thin Cap with Large Lipid CoreThin Cap with Large Lipid Core
3.3. Endothelial Denudation with SuperficialEndothelial Denudation with Superficial
Platelet AggregationPlatelet Aggregation
4.4. Fissured / Wounded PlaqueFissured / Wounded Plaque
16. Proposed Histopathological and ClinicalProposed Histopathological and Clinical
Criteria for Definition of VulnerableCriteria for Definition of Vulnerable
PlaquePlaque
•• MinorMinor Criteria:Criteria:
1.1. Superficial Calcified noduleSuperficial Calcified nodule
2.2. Glistening YellowGlistening Yellow
3.3. IntraplaqueIntraplaque HemorrhageHemorrhage
4.4. Critical StenosisCritical Stenosis
5.5. Positive Remodeling?Positive Remodeling?
17. Plaque Rupture: Definition
Structural failure of the fibrocellular cap11 that
separates an atheromatous core22 from the lumen
of an atherosclerotic artery (ie, lumen ↔ core).
11
cap defectcap defect//gapgap rupture, fissure, break, tear
not just missingnot just missing endotheliumendothelium
22
lipidlipid--richrich Greek athere, gruel (soft)
Propensity to rupture
lipidlipid--richrich corecore + → +++
no coreno core →→ no capno cap -
20. Vulnerable Plaque and Vulnerable
Patient, The Challenge of
Cardiovascular Medicine in 21st
Century
An introductory tutorial from
VP.org
In conjunction with
The Center for Vulnerable Plaque Research
University of Texas Houston and
Texas Heart Institute
23. Emerging Diagnostic Techniques
A. Invasive Techniques
Angioscopy
Intravascular Ultrasound (IVUS)
Intravascular T hermography
Intravascular Optical CoherenceT omography (OC T )
Intravascular E lastography
Intravascular and T ransesophageal MRI
Intravascular Nuclear Imaging
Intravascular E lectrical ImpedanceImaging
Intravascular T issueDoppler
Intravascular Shear Stress Imaging
Intravascular (Photonic)Spectroscopy
24. - Raman Spectroscopy
- Near-Infrared Diffuse Reflectance Spectroscopy
-Fibrousis and lipid measurement
-pH and lactate measurement
- Fluorescence Emission Spectroscopy
- Spectroscopy with contrast media
… Invasive Techniques
Intravascular (Photonic) Spectroscopy
Intra-coronary assessment of endothelial function
Intra-coronary measurement of MMPs and cytokines
25. Emerging Diagnostic Techniques
B. Non-Invasive Techniques:
A. MRI
1- MRI without contrast media
2- MRI with contrast media: Gadolinium-DPTA
2- MR Imaging of Inflammation: Super Paramagnetic
Iron Oxide (SPIO and USPIO)
3- MR Imaging of Thrombosis using monoclonal Ab
B. Electron Beam Tomography (EBT)
C. Multi-Slice Fast Spiral / Helical Computed Tomography
D. Nuclear Imaging (18-FDG, MCP-1, Annexin V, CD40)
26. Emerging Diagnostic Techniques
C. Blood Tests / Serum Markers
- CRP
- ICAM-1, VCAM, p-Selectin, sCD40-L
- Proinflamatory cytokines
- Lp-PLA2
- Ox-LDL Ab
- PAPP-A
D. Endothelial Function Test
-Intra coronary acethylcholine test
-Noninvasive flow mediated dilatation of
brachial artery
- Anti-body against endothelial cells
27. CONCLUSION
It is well established that
composition and size of lipid
core,composition and thickness of
fibrous cap, inflammatory
process,and the quantity of SMC’s
within a plaque are predictors of
plaque rupture.
29. THE IMPORTANCE OF
ANIMAL MODEL
Animal models are important to
research directed toward better
understanding of human
atherosclerosis.For this reason
much effort has been expended
to identify and characterize
species suitable as animal model.
30. Criteria needed for choosing
animal model
Susceptibility under standard system
of husbandry
Ready availability at reasonable cost
Ready trainability and size adequate
for all project lab procedure
Recognition that behavior responses
to experimental situations may
determine result
31. The ideal animal model of
human atherosclrosis:
*Should be easy to acquire and
maintain at reasonable cost
*Easy to handle
*Proper in size
*Should be reproducible in lab
*Should have well-defined genetic
characteristics
*Should share with human the
most important aspect of disease
32. THE CHICKEN AS A MODEL
*The chicken is good animal model for
atherosclerosis study because it is:
Omnivorous
Small and suitable for prolonged lab
investigation
Able to develop spontaneous atherosclerosis
Capable of producing atherosclerosis after
cholesterol feeding
Plasma level of cholesterol and triglyceride
are similar to those in human
Lipid composition of LDL , HDL and
chylomicron resemble those in human
There is no essential difference between
vascular lesion in chicken on high cholesterol
33. DISADVANTAGES OF CHICKEN
Nonmammals
Lesion site inconsistent
Complication uncommon
Intramyocardial coronary
involvement
Chicken herpes virus can be the
sources of variability
34. THE PIG AS A MODEL
* Some similarities between man and pig in
atherosclerosis:
Atherosclerosis in man and pigs develops most
frequently in aorta,coronary and intracranial arteries
The age at which lesion originate and the rate of
progression in any lesion is independent of other
The origin and distribution of coronary artery in man
and pig corresponds closely
The histological change of growth and aging that
leads to atherosclerosis of aorta and coronary
artery are closely similar
According to the mean age of death and its relation
to morphological character and size of lesion,the
sequel of atherosclerosis in man and pig also
correspond closely
35. MOUSE AS A MODEL
*As a species the mouse is highly resistant
to atherosclerosis.But through induced
mutation lines of mice have been
developed to be susceptible to
atherosclerosis,such as:
Mice that are deficient in apoE
Mice that are deficient in LDL receptor
Transgenic mice that express human apoE
Transgenic mice with transdominant mutant
form of apoE
36. pathology Comparison of atherosclerosispathology Comparison of atherosclerosis
ApoE-deficient
mouse
Human
Fatty streak with
MAC and Tcells
yes yes
Fibrous plaque with
SMC
yes yes
Lesion calcification yes yes
Oxidized apitopes
present
yes yes
Lesions at branches
and sites with
disturbed flow
yes yes
Diet responsiveness yes yes
Aneurysms observed yes yes
Plaque rupture no yes
37. NO PLAQUE RUPTURE IN
ANIMAL MODEL
Atherosclerosis plaque rupture is the
main cause of coronary thrombosis
and MI but currently,there is no animal
model of plaque disruption ?
38. THE POTENTIAL CAUSE OF LACK
OF PLAQUE RUPTURE IN MICE
May be due to small diameter of
mice aorta (<1mm) which
increase surface tension
preventing plaque rupture
39. RABBIT AS AN ANIMAL MODEL
Advantages:
Lesion well characterized
Lesion inducible with dietary
cholesterol
Reproduce rapidly
Relatively inexpensive
40. RABBIT AS AN ANIMAL MODEL
Disadvantages:
Whole body cholesterol is different from human
Lesions don’t duplicate many important features
of human
Lesions usually occur in aortic arch and thoracic
aorta
Distribution of coronary artery lesion is different
from human(proximal portions aren't involved)
Only proximal portion of carotid artery usually
involved and cerebral vessels spare
41. AN EXPERIMENTAL MODEL OF
PLAQUE RUPTURE
In rabbit model embedding inflatable
balloon in to the atherosclerotic plaque
and measuring the pressure needed to
inflate the plaque-covered balloon may
be an index of plaque mechanical
strength