This document provides an overview of cardiovascular pathology and focuses on myocardial infarction and endocarditis. It discusses the definition, etiology, pathogenesis, clinical features, investigations, and management of MI and endocarditis. It also presents an example case of a man experiencing chest pain who is found to have a dissecting aortic aneurysm.
venous drainage of head and neck and its branches are described in detail along with applied anatomy for better understanding of the anatomy and its application in oral and maxillary surgeries. knowing the anatomy and the course of the veins is crucial and helps in better locating the vein and ligating it to avoid further complications while performing a oral and maxillofacial surgeries such as in trauma fixation, tumor resection and as well as reconstruction of the defect pertaining to the maxillofacial region.
Endocarditis ( Inflammatory disease of the Heart ANILKUMAR BR
Any of the heart's three layers may be affected by an infectious process.
The diseases are named for the layer of the heart most involved in the infectious process: (Myocarditis (inflammation of the myocardium).
Endocarditis(inflammation of the endocardium) and pericardium(inflammation of the pericardium)
The usual management for all infectious diseases prevention. IV antibiotics are usually necessary once an infection in the heart has developed.
Endocarditis is an inflammation of the endocardium; it is usually limited to the membrane lining and the valves.
Theca use of endocarditis may be viral, fungal, or most commonly, bacterial.
The most common organism is Streptococcus viridans. Vegetations (growths orlesion) may cause vulvular dysfunction.
Endocarditis is inflammatory process of the endocardium, especially the valves.
This disorders carriers high morbidity and mortality rates, but outcomes can be improved greatly with early diagnosis and effective treatment.
venous drainage of head and neck and its branches are described in detail along with applied anatomy for better understanding of the anatomy and its application in oral and maxillary surgeries. knowing the anatomy and the course of the veins is crucial and helps in better locating the vein and ligating it to avoid further complications while performing a oral and maxillofacial surgeries such as in trauma fixation, tumor resection and as well as reconstruction of the defect pertaining to the maxillofacial region.
Endocarditis ( Inflammatory disease of the Heart ANILKUMAR BR
Any of the heart's three layers may be affected by an infectious process.
The diseases are named for the layer of the heart most involved in the infectious process: (Myocarditis (inflammation of the myocardium).
Endocarditis(inflammation of the endocardium) and pericardium(inflammation of the pericardium)
The usual management for all infectious diseases prevention. IV antibiotics are usually necessary once an infection in the heart has developed.
Endocarditis is an inflammation of the endocardium; it is usually limited to the membrane lining and the valves.
Theca use of endocarditis may be viral, fungal, or most commonly, bacterial.
The most common organism is Streptococcus viridans. Vegetations (growths orlesion) may cause vulvular dysfunction.
Endocarditis is inflammatory process of the endocardium, especially the valves.
This disorders carriers high morbidity and mortality rates, but outcomes can be improved greatly with early diagnosis and effective treatment.
Basic description of Infective Endocarditis from a Clinical and Microbiological point of view with description on Pathogenesis, Clinical Manifestations, Clinical and Laboratory diagnosis.
The inflammation of the heart muscles, such as myocarditis, the membrane sac which surrounds the heart called as pericarditis, and the inner lining of the heart or the myocardium, heart muscle as endocarditis are known as the inflammatory heart diseases.
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Basic description of Infective Endocarditis from a Clinical and Microbiological point of view with description on Pathogenesis, Clinical Manifestations, Clinical and Laboratory diagnosis.
The inflammation of the heart muscles, such as myocarditis, the membrane sac which surrounds the heart called as pericarditis, and the inner lining of the heart or the myocardium, heart muscle as endocarditis are known as the inflammatory heart diseases.
Intracellular accumulation (lipids, proteins, carbohydrates, pigments) ppt pdf by rohit kumar trivedi
for VIDEO LECTURE
www.youtube.com/c/rohitkumartrivedi
,intracellular accumulation ,intracellular accumulation pdf ,intracellular accumulation in cell injury ,intracellular accumulation in hindi ,intracellular accumulation of proteins ,intracellular accumulation pathology ,intracellular accumulation meaning ,intracellular accumulation of pigments ,intracellular accumulation of carbogydrates ,pathophysiology ,study pharmacy with rohit kumar trivedi ,pharmacy ,pathology ,rohit kumar trivedi
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Contains bullet-point summary of questions to be asked in medical interview / consultation based on the presenting complaint or system. Contains additional information on clinical reasoning and developing a differential diagnosis
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2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
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Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
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Read| The latest issue of The Challenger is here! We are thrilled to announce that our school paper has qualified for the NATIONAL SCHOOLS PRESS CONFERENCE (NSPC) 2024. Thank you for your unwavering support and trust. Dive into the stories that made us stand out!
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
2. Today
● overview of CV path
● some pathology of most important topics
○ MI
○ endocarditis
● an example case
3. Overview of Cardiovascular Path
●
●
●
●
●
●
●
●
●
Ischaemic Heart Disease - insufficient blood supply
○ Atherosclerosis
○ Angina pectoris
○ MI, sudden cardiac death
Hypertensive Heart Disease - pumping against elevated pressure
Valvular Disease
Inflammation / Infection of the layers of the heart
Congenital Heart Disease - embryological defects
Cardiomyopathies - acquired and genetic problems of heart muscle
Tumours
Vasculitides
Aneurysms and Dissections
(vascular vs. more heart related)
4. List of Pathological Causes
A
– autoimmune
V
– vascular
I
– infective, inflammatory
T
– traumatic
A
– acquired
M
– metabolic
I
– iatrogenic
N
– neurological, neoplastic, nutritional
C
– congenital
D
– degenerative, drugs
E
– environmental, endocrine
P
– psychosomatic
5. Overview of CV Path
●
●
●
●
●
●
●
●
●
●
what’s most important!
Ischaemic Heart Disease - insufficient blood supply
○ Atherosclerosis
○ Angina pectoris
○ MI, sudden cardiac death
Hypertensive Heart Disease - pumping against elevated pressure
Valvular Disease
Inflammation / Infection of the layers of the heart
Congenital Heart Disease - embryological defects
Cardiomyopathies - acquired and genetic problems
Tumours
Vasculitides
Aneurysms and Dissections
=> pretty much all the “vitamins”
6. Today
● overview of CV path
● some pathology of most important topics
○ MI
○ endocarditis
● an example case
7. Pathology of MI’s
●
●
●
Definition: A myocardial infaction is ischaemia of an area of cardiac
muscle, leading to necrosis of muscle tissue that can be fatal.
Aetiology: coronary artery thrombosis: disruption of existing plaque,
embolism (mainly from mural thrombus or valve vegetations), vasospasm,
increased demand on marginally perfused heart
○ risk almost 50% >65y! female sex hormones protective
Pathogenesis:
○ disruption of plaque => new clotting => thrombus↑ => occlusion of
lumen => ischaemia, irreversible after 20-40min => necrosis
○ molecular pathogenesis: loss of contractility and electrical instability
○ Buzz words: “non-contractile state”, “stunned myocardium”, “transient
cardiac failure”
8. Pathology of MI’s ctnd.
Patterns of MIs
●
●
Patterns of blood supply:
○ L CA => fatal => widow maker
○ 40-50% L ant ↓ => ant. LV wall, IV septum, apex
○ 30-40% prox. R CA => RV
○ (post. becomes post. ↓ in 90% => LV)
Relating to the heart wall:
○ Subendocardial infarction (last to receive blood at high intramural
pressure, most susceptible zone)
○ Transmural = full thickness infarction => ST ELEVATION!
○ Microscopic infarction
http://www.sciencedirect.com/science/journal/13573039/38/7
9. Pathology of MI’s ctnd.
Timing of MI morphology =>
●
●
Clinical Features:
○ severe chest pain
○ not relieved
○ …
Complications:
○ ¾ of pt. >1!
○ contractile dysfunction
○ structual dysfunction
○ electrical dysfunction
○ clotting
○ chronic: IHD, cardiomyopathy
11. Pathology of MI’s ctnd.
●
Management:
○ ABCDE + help
○ 12 lead ECG - cardiac monitor - IV access (2x antecubital, think
forward as arrest possible!)
○ Oxygen!
MONAC
○ Drugs:
Morphine+metoclopramide
O2
■ morphine
Nitrates
■ oxygen
Aspirin (if not yet given)
■ nitrates - GTN spray
Clopidogrel 300mg
■ aspirin/clopidogrel
■ fondaparinoux (FXa inhibitor)
○ PCI percutaneous coronary intervention if ST elevation or new onset
bundle branch block within 12h (if no centre nearby then clot lysis)
12. Today
● overview of CV path
● some pathology of most important topics
○ MI
○ endocarditis
● an example case
13. Pathology of Endocarditis
●
Definition: Inflammation of the endocardium, i.e. the innermost endothelial
layer of the heart that lines its chambers, potentially including heart valves,
aorta, septum, chordae tendinae or any artificial structures present in the
heart. Distinguish:
○ infective endocarditis <= discussed here
■ acute
(virulent, on normal valve)
■ subacute
(low virulence, on abnormal valve)
○ non-infective endocarditis
■ non-bacterial thrombotic endocarditis NBTE - sterile lesions
■ Libman-Sacks endocarditis - sterile lesions in patients with SLE or
antiphospholipid syndrome
14. Pathology of Endocarditis ctnd.
●
●
Aetiology:
○ 60% Strep. viridans on pre-existing damage on valve
○ 10-20% Staph. aureus on normal and damaged valves
○ HACEK
○ other: fungal, Rikettsiae, Chlamydia
○ 10% culture -ve
○ predisposing factors: valve abnormalities or T2DM, EtOH, CA, IVDU
Pathogenesis:
○ microbes entering the bloodstream settling on valves (L,R => IVDU?)
○ valves vulnerable due to lack of blood supply
3V’s
○ => vegetations
○ potential shedding of emboli
○ possible mycotic aneurysms!
15. Pathology of Endocarditis ctnd.
●
●
Vegetations: what they consist of and where the are
○ fibrin, necrotic debris, thrombi, organisms
○ subacute: less destructive, regenerative granulation tissue
predisposing to fibrosis and calcification
RHD: many small (Rheum: Aschoff bodies, small granulomatous nodules,
lymhocytes and macrophages, “Anitschkow cells”), IE: large destructive,
NBTE: medium thrombotic, LSE mixed, either side
18. Pathology of Endocarditis ctnd.
●
Management
○ eradicate infection and manage complications of valve damage
○ valve damage
■ like congestive heart failure
■ oxygen, manage BP
■ potential surgery: valve replacement
○ infection
■ long-term antibiotics
■ empirical: flucloxacillin (b-lactamase resistant pen, gram +ve
bacilli/cocci) and gentamycin (aminoglycoside, gram -ve)
■ strep: ben-pen and gentamycin
■ staph: flucloxacillin or vancomycin and rifampicin (if allergic)
■ HACEK: amoxicillin and gentamycin
19. Today
● overview of CV path
● some pathology of most important topics
○ MI
○ endocarditis
● an example case
20. A cardiovascular case
A 60 year old male was admitted with a 2h history of
persistent severe chest and interscapular pain, as well as
nausea and sweating.
On examination, he was cold and clammy. His BP was
195/115 and his HR was 90bpm and regular. Chest
sounds were clear and the heart sounds unremarkable.
22. •What is the differential diagnosis?
•What further investigations would you request?
23. • What is the differential diagnosis?
• Dissecting aneurysm
• Acute myocardial infarction
• Acute oesophageal spasm
• Pulmonary embolism
• What further investigations would you request?
Chest x-ray, US, CT, cardiac enzymes/troponin, MRI angiography, VQ
scans
24. Several hours later the pain had extended to the abdomen.
His left hand was cold and white and the left radial and
brachial pulses were absent. He had been anuric in the
last 2 hours.
26. Extension of the dissection to occlude left
subclavian and renal arteries.
27. Shortly afterwards the patient died.
At necropsy, the specimen shown in the
photograph was removed.
28. • What does the photograph show and what is
your diagnosis?
29. Formation of a blood filled space in the media of the aorta
=> dissection aneurysm.
• What is the pathogenesis of this pathological
process?
30. What is the pathogenesis of this pathological process?
•
weakening of vessel wall
•
acquired: ischaemia of the media by atherosclerosis and/or
hypotension (ischaemia of vasa vasorum, atherosclerotic
plaques have increased metalloproteases that degrade media)
•
genetic: structural abnormalities of connective tissue as in
Marfan or Ehlers Danlos Syndrome (fibrillin vs. collagen
defect) => cystic medial necrosis