Mitral regurgitation is caused by abnormalities of the mitral valve leaflets, chordae tendineae, or annulus that prevent complete coaptation of the leaflets during systole. The main causes include degenerative diseases like mitral valve prolapse or rheumatic heart disease. Severe mitral regurgitation can lead to left atrial and ventricular dilation and dysfunction over time if left untreated. Echocardiography is the main imaging modality used to assess severity based on regurgitant jet area and velocity. Surgery is recommended for symptomatic patients or asymptomatic patients with severe regurgitation and abnormal ventricular size or function. Mitral valve repair is preferred over replacement when possible due to better long-
Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction
Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
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
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
2. ANATOMY
The mitral valve apparatus consists of
• the anterior and the posterior leaflets ,
• the mitral annulus (fixed and dynamic)
• The chordae tendinae
• Papillary muscles
• Underlying myocardium
6. Rheumatic Heart Disease
Usually associated with stenosis and
fusion of the commissures
Retractile fibrosis of leaflets and
chordae, causing loss of coaptation.
Secondary dilatation of the mitral
annulus tends to further decrease the
coaptation.
7. Degenerative
Mitral annular calcification is common
in the elderly population
Accelerated by hypertension, Old
Age and diabetes.
Connective tissue diseases such as
Marfan and Hurler syndromes.
8. Mechanisms
Abnormal movement of the leaflets
into the left atrium (LA) during systole
Caused by inadequate chordal
support (elongation or rupture) and
excessive valvular tissue.
Myxomatous degeneration -
characterized by redundant, floppy
leaflets and associated with
progressive MR.
10. Infective Endocarditis
approx. 5 %of cases of severe MR.
Vegetations may produce mild MR by
interposition between leaflets.
Severe endocarditic MR is usually
related to ruptured chordae and less
frequently to destruction of mitral tissue
(edges or perforation)
11. Ischemic and Functional MR
Consequence of LV wall dysfunction (ischemia,
scarring, aneurysm, cardiomyopathy, or
myocarditis,)
The coaptation of intrinsically normal leaflets is
incomplete.
The pattern of mitral valve (MV) deformation from
the medial to the lateral side is asymmetrical in
ischemic MR, whereas it was symmetrical in
nonischemic MR of cardiomyopathy.
12. Responds to vasodilators or improvement
of ischemia-is a result of a reversal of
adverse LV geometry.
Rupture of papillary muscle produces MR
because of the flail leaflet.
80 percent of cases involves the
posteromedial papillary muscle.
Complete rupture is rapidly fatal without
surgery, and partial- or single-head rupture
of the papillary allows emergency surgery.
13. Other causes
(1) connective tissue disorders Marfan
syndrome, Ehlers-Danlos syndrome,
pseudoxanthoma elasticum, osteogenesis
imperfecta, Hurler disease, SLE, and
anticardiolipin syndrome;
(2) cardiac trauma penetrating or
nonpenetrating
(3) myocardial disease—hypertrophic
cardiomyopathy, amyloidosis, or sarcoidosis;
(4) endocardial lesions caused by
hypereosinophilic syndrome, endocardial
fibroelastosis, carcinoid tumors, ergot toxicity,
radiation toxicity, diet or drug toxicity
(5) congenital cleft mitral valve, corrected
transposition
(6) cardiac tumors.
14. Hemodynamics – Severity
Parameters
The abnormal coaptation creates a
regurgitant orifice during systole.
The systolic pressure gradient between the
LV and LA is the driving force of the
regurgitant flow, which results in a regurgitant
volume.
May be expressed as the regurgitant
fraction.
15. Torricelli principle, states that flow through
an orifice varies by the square root of the
pressure gradient across that orifice:
MRV= MROA* constant* Ts*√ (LVP-LAP)
The pressure gradient between the LV and
LA begins with mitral closure (simultaneous
to S1) and persists after closure of the aortic
valve (S2) until the mitral valve opens.
16. MR induces a low-pressure form of
volume overload as a result of ejection
into the LA.
Moderate MR when the regurgitant
fraction is in the range of 30 to 50 %
severe MR - regurgitant fraction >50%
17. Orifice Area
In Functional MR (dilated cardiomyopathy) -
constant decrease in OA throughout systole.
In MVP, OA is small in early systole,
increasing substantially in midsystole, and
decreasing mildly during LV relaxation.
In Rheumatic MR, constant regurgitant OA
during most of systole.
19. MR & AR Comparison
The volume overload is usually less severe in MR than
in AR, despite a larger regurgitant gradient and orifice
Due to shorter duration of regurgitation during the
cardiac cycle in MR than in AR
The LV is unloaded in both early and late systole by
ejection into the low-pressure LA; whereas in AR, the
excess volume is ejected into the high-pressure aorta
only in early systole.
The lower LV mass and mass-to-volume ratio in
patients with MR as compared to AR.
20. LA Dynamics
LA pressure is mainly determined by LA compliance.
Dynamics Acute
Compensated
MR
Chronic
Compensated
MR
LA Compliance
(Volume)
Less or No
compliance
Compliant -
Dilated
LA Pressure High Relatively Low
or Even Normal
LA/LV Gradient Lesser More
Regurgitant
Volume
Tends to be
lesser
As LA dilated,
tends to be more
Murmur Early/Holosystoli
c
Holosystolic
21.
22.
23. Role of ACE I
Efficacy of ACE inhibitor in papillary
muscle dysfunction or dilated
cardiomyopathy produces a decrease in
LV size and improved LV geometry and
thereby regurgitant OA
This benefit is not observed with
rhuematic MR or Mitral Valve Prolapse
24. MR – Chronic Compensated
In c/c MR adrenergic system provides
inotropic support (important mech. of
compensation)
Norepinephrine release increases
directly with increase in end systolic
volume.
25. MR Chronic Decompensated
Stage
muscle dysfunction has developed,
impairing ejection fraction, diminishing
both TSV and FSV.
EF, although still “normal,” has
decreased to 0.55.
LAP is reelevated because less
volume is ejected during systole,
causing a higher ESV.
26. Clinical presentation
Usual symptoms -Fatigue and mild dyspnea
on exertion (rapidly improved by rest.)
Severe dyspnea on exertion ,PND, frank
pulmonary edema, or even hemoptysis in
decompensation.
Severe symptoms may be triggered by a
new onset of AF, an increase in degree of
MR, the occurrence of endocarditis or
ruptured chordae, or a change in LV
compliance or function.
27. Severe Presentations
A/c MR - dramatic symptoms-with pulmonary edema or
ccf
subside with administration of a diuretic, afterload
reduction, and increased LA compliance with time.
Abrupt chordal rupture - sudden onset of atypical
chest pain and dyspnea
rupture of papillary muscle in of a/c MI - cardiogenic
shock or a severe pulmonary edema.
Pulmonary edema may also be observed in transient
severe papillary muscle dysfunction.
28. Physical examination
BP is usually normal. Carotid upstroke is brisk;
Wide Pulse Pressure.
Hyperdynamic Apical Impulse – down & out –
LV enlargement.
An apical thrill is characteristic of severe MR.
Systolic expansion of the enlarged left atrium
causes a late systolic thrust in the parasternal
region,-confused with RV enlargement.
29. Auscultation
S1 is included in the murmur and is usually
normal but may be increased in rheumatic
disease.
Wide splitting of S2 due to the shortening of
LV ejection and an earlier A2 due to reduced
resistance to LV ejection.
In patients with MR who have severe
pulmonary hypertension, P2 is louder than
30. The abnormal increase in the flow rate
across the mitral orifice during the rapid
filling phase is associated with an S3,
(not due to heart failure) ; may be
accompanied by a brief diastolic rumble.
Midsystolic clicks are markers of valve
prolapse.
31. Systolic Murmur
Most often holosystolic, including 1st and
2nd heart sounds.
Blowing type but may be harsh(MVP)
The maximum intensity is usually at the
apex, and it may radiate to the axilla in
anterior leaflet prolapse, degeneration
affecting primarily the anterior leaflet.
32. In posterior leaflet prolapse, the jet is usually
superiorly and medially directed and the
murmur radiates toward the base of the
heart.
In MI, severe MR may be totally silent.
Murmurs of shorter duration usually
correspond to mild MR; they may be mid or
late systolic in mitral valve prolapse or early
systolic in functional MR.
33. Murmer is increased by squatting ,
isometric excercises
Decreased by amyl nitrite inhalation
and valsalva
34. Clinical Severity Parameters
Systolic Thrill over apex
Large LV indicates severe MR
Presence of S3
Flow MDM across non stenotic Mitral
valve.
35. ECG
The principal ECG findings are
left atrial enlargement and AF.
Wide notched P waves – P Mitrale
ECG evidence of LV enlargement
occurs in 1/3rd of patients with severe
MR.
Tall R in V5 V6 but S in V1 is small
15 % of patients -evidence of RV
hypertrophy.
36. CXR
Cardiomegaly may be present in c/c
MR or in ischemic or functional MR .
LA body and appendage dilatation is
frequent, but giant LA is rare.
annular calcification, seen as a C-
shaped density below the posterior
leaflet, is frequent.
signs of pulmonary hypertension or
pulmonary edema are rarely
observed.
37.
38. Doppler echocardiography
High-velocity jet in the LA during systole
Severity of the regurgitation is a function of the
distance from the valve that the jet can be
detected.
Area of the mitral jet >8 cm2 indicates severe
MR.
Severity Predictor: Vena Contracta defined as
the narrowest cross-sectional area of the
39.
40. Echocardiography
Quantification of LV end-diastolic and
end-systolic dimensions, wall
thickness, and ejection fraction and
fractional shortening.
M-mode diameter or volume can
assess the LA size by two-dimensional
echocardiography
42. Rheumatic MR is characterized by
thickening of the leaflets and chordae.
The posterior leaflet has reduced mobility,
whereas the anterior leaflet may be doming if
commissural fusion is associated.
Degenerative MR, prolapse -the
passage of valvular tissue beyond the
annulus plane in the long-axis view
43. The valve leaflets are diffusely thickened
leaflets and excessive valvular tissue
and increased echogenicity of the
annulus - mitral annular calcification.
Flail segments appear as complete
eversion of the segment with or without
the small floating echo of ruptured
chordae
44. Treatment (medical)
IE prophylaxis
Rhuematic fever prophylaxis
If AF rate control with digoxin and beta
blockers
Anticoagulation in AF
Vasodilators in acute MR and
cardiomyopathy- ACE inhibitors
Beta blockers may be used – but no
definite evidence
45. Surgery Indications
American College of Cardiology/American Heart Association
Guidelines for Surgery for Nonischemic Severe Mitral Regurgitation
Class I (evidence and/or general agreement that surgery is
useful and effective)
Symptoms cause by MR (acute or chronic)
Asymptomatic patients with severe MR and mild-moderate LV
dysfunction defined as an —Ejection fraction 30–60% and —
End-systolic dimension 45–55 mm
Class IIa (conflicting evidence and/or divergence of opinion but
the weight of evidence/opinion favors surgical intervention)
Asymptomatic patients with normal LV function and —Atrial
fibrillation or —Pulmonary hypertension (>50 mmHg at rest of
>60 mmHg with exercise)
Asymptomatic patients with —Ejection fraction 50–60% or —
End-systolic dimension 45–55 mm
Severe left ventricular dysfunction (ejection fraction <30% and/or
end-systolic dimension >55 mm) if chordal preservation is highly
likely
46.
47. Post op outcome
Mitral valve repair is better
Maintains continuity of valve with
papillary muscles
Hence maintains LV geometry and
maintains EF
Operative mortality 1-2 % (5-10 with
MVR)
AF may persist - anticoagulation