The document discusses infective endocarditis, which is an infection of the inner lining of the heart chambers and heart valves. It describes the types of infective endocarditis as native valve, prosthetic valve, or intravenous drug abuser infective endocarditis. It covers the typical causative organisms, pathophysiology, clinical manifestations, diagnosis and treatment of this condition.
Please find the power point on Infective Encocarditis . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Please find the power point on Infective Encocarditis . I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
infective endocarditis
pathology medicine
high yield topic
revision notes based on high yield topic
last minute revision notes
types complication treatment
vegetations
native valve endocarditis
infective endocarditis
pathology medicine
high yield topic
revision notes based on high yield topic
last minute revision notes
types complication treatment
vegetations
native valve endocarditis
Seminar of Endocarditis by Sudeep,(Pharm.D.)SUDEEP
Presentation of Endocarditis.
Pharmaco therapeutics of disease endocarditis(Inflammation of endocardium).
Definition,causes,etiology,symptoms and treatment of disease.
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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
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3. Infection of the endocardial surface of heart
characterized by
- Colonization or invasion of the heart valves
(native or prosthetic) or the mural endocardium
by a microbe,
- leading to formation of bulky, friable
vegetation composed of thrombotic debris and
organisms
- often associated with destruction of
underlying cardiac tissue.
7. ACUTE ENDOCARDITIS
SUBACUTE
ENDOCARDITIS
Destructive and
tumultuous infection,
frequently of a
previously normal
heart valve, with a
highly virulent
organism
Hematogenous seeding
Organisms of low
virulence causing
infection in a
previously abnormal
heart, particularly on
deformed valves.
Disease appear
insidiously and pursue
a protracted course of
weeks to month
9. Staphylococcus aureus (35%) : Either healthy or
deformed valves, IV drug abusers
(polymicrobial), devices
Streptococcus viridans (32%) : Native but
previously damaged/abnormal valves
Enterococci (8 %)
S. epidermidis (4%): Prosthetic valve
endocarditis, devices
G –ve bacilli of HACEK group (4%)
Yeast and Fungi(1%)
Culture negative endocarditis (5 %)
10. Pathology
◦ NVE (native) infection is largely confined to leaflets
◦ PVE (prosthetic) infection commonly extends
beyond valve ring into annulus/periannular tissue
Ring abscesses
Septal abscesses
Fistulae
Prosthetic dehiscence
◦ Invasive infection more common in aortic position
and if onset is early
03-03-2020 12
11. Portal of entry:
◦ Dental / Surgical Procedures
◦ Contamination by IV drug use
◦ Obvious infections (RS/Skin)
◦ Occult source from gut, oral cavity
◦ Trivial injuries.
◦ Intravascular catheter infection
◦ Nosocomial wounds
◦ Invasive procedures
12. Turbulent blood flow within the heart -
most often (but not always) – patient has
risk factors for this
Turbulent blood flow disrupts valve surface
(endocardium) to produce suitable (sticky)
site for bacterial attachment
Platelet deposition + fibrin may lead to
non-bacterial thrombus or vegetation
Bacteraemia – delivers organisms to the
damaged (sticky) endocardial surface
resulting in adherence & colonisation
Eventual invasion of valve leaflets results in
infected vegetation (sheath of fibrin &
platelets, ideal conditions for further
bacterial multiplications, protection from
polymorphs) 03-03-2020 14
14. Feature Acute Subacute
Underlying Heart
Disease
Heart may be normal RHD,CHD, etc.
Organism S. aureus, Pneumococcus
S. pyogenes,
Enterococcus
viridans
Streptococci,
Entercoccus
03-03-2020 16
22. 03-03-2020 24
1. Nonspecific
2. Nonblanching
3. Linear reddish-brown lesions found under the nail bed
4. Usually do NOT extend the entire length of the nail
24. Blood cultures: Echocardiography
Key diagnostic investigation
in infective endocarditis.
Isolation of microorganism
from culture is important for
diagnosis and also for
treatment.
At least 3 sets of samples
should be taken from
different venepuncture sites
over 24 hours.
It can identify the
presence and size of vegetations,
detect intracardiac complications
and
assess cardiac function.
Transthoracic
echocardiography is
noninvasive and has high
specificity for visualising
vegetations.
Transesophageal
echocardiography is more
sensitive than TTE. It can
detect small vegetations,
prosthetic endocarditis and
intra cardiac complications.
25.
26.
27. Definitive Endocarditis if,
- Two major or,
- One major and three
minor or,
- five minor
Possible Endocarditis if,
- One major and one minor
or,
- Three minor
28. Positive blood culture
◦ Typical organism from two cultures
◦ Persistent positive blood cultures taken >
12 hours apart
◦ Three or more positive cultures taken over
more than 1 hour.
Endocardial involvement
◦ Positive echocardiographic findings of
vegetations
◦ New valvular regurgitation
◦ Myocardial abscess
◦ New partial dehiscence of prosthetic valve
29. 1. Predisposition: Predisposing
valvular or cardiac abnormality
2. Intravenous drug misuse
3. Pyrexia ≥38°C (≥100.4°F)
4. Embolic phenomenon
5. Vasculitic/ immunologic
phenomenon
6. Blood cultures suggestive: -
organism grown but not achieving
major criteria
7. Suggestive echocardiographic
findings
30. Antimicrobial Therapy
Therapy requires identification
of specific pathogen and its
susceptibility to antimicrobials.
Empirical therapy should be
started as soon as possible
targeting most likely pathogens.
Bactericidal drugs should be
used.
31. Resolution of fever occurs in 5
to 7 days. If fever persists
patient should be evaluated for
complications like paravalvular
abscess and extracardiac
abscess.
Serologic abnormalities resolve
slowly and do not reflect
response to treatment.
32. Antibiotic regimen for infective endocarditis
Streptococci
Benzyl penicillin (2-3 million units 4 hourly) 4-6 weeks
Gentamicin (1mg/kg 8-12 hourly) 4-6 weeks
(ceftriaxone & vancomycin)
Enterococci
o Ampicillin sensitive
Ampicillin (2 g 4 hourly) 4-6 weeks, and
Gentamicin (1mg/kg 8-12 hourly)
o Ampicillin resistant
Vancomycin(1g 12hourly) 4-6 weeks, and
Gentamicin (1mg/kg 8-12 hourly)
33. Staphylococci
o Penicillin sensitive
Benzyl penicillin I.V(2-3 Munits 4 hourly)
+ gentamicin
o Penicillin resistant but methicillin sensitive
Flucloxacillin I.V (2g 4 hourly )
o Both penicillin and methicillin resistant
Vancomycin I.V (1g 12 hourly) and
Gentamicin
34. Surgery
Indications
patients with direct extension of infection to
myocardial structures.
Prosthetic valve dysfunction.
Congestive heart failure.
Badly damaged valves.
IE caused by fungi or gram-ve or resistant
organisms.
Large vegetations on echocardiography
Recurrent embolic attacks.
35. Prophylaxis
High risk category
prosthetic cardiac valves
Previous bacterial endocarditis, even in
absence of heart disease.
Complex cyanotic congenital heart
disease(TGA,TOF)
Surgically constructed systemic pulmonary
shunts.
36. Moderate risk category
Rheumatic and other valvular dysfunction
Congenital cardiac malformations
Hypertrophic cardiomyopathy
Mitral valve prolapse with valvular
regurgitation
37. High risk lesions
◦ Prosthetic valves
◦ Prior IE
◦ Cyanotic congenital heart
disease
◦ PDA
◦ AR, AS, MR,MS with MR
◦ VSD
◦ Coarctation
◦ Surgical systemic-pulmonary
shunts
Intermediate risk
◦ MVP with murmur
◦ Pure MS
◦ Tricuspid disease
◦ Pulmonary stenosis
◦ ASH
◦ Bicuspid Ao valve with no
hemodynamic
significance
03-03-2020 42
Lesions at highest risk
38. Regimen for IE prophylaxis
Standard oral regime
Amoxicillin 2 g 1hr before procedure
Inability to take oral medication
Ampicillin 2g IV or IM 1hr before procedure
Penicillin allergy
Clindamycin 600 mg
Clarithromycin 500 mg
Cephalexin 2 g.