Pulmonary stenosis (also called pulmonic stenosis) is when the pulmonary valve (the valve between the right ventricle and the pulmonary artery) is too small, narrow, or stiff. Symptoms of pulmonary stenosis depend on how small the narrowing of the pulmonary valve is
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Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
CARDIAC TAMPONADE ( Cardiac emergency) • Cardiac Tamponade is a life threatening complication caused by excessive accumulation of fluid in the pericardium. Or • Compression of all cardiac chambers due to excessive accumulation of pericardial fluid leading to compromised cardiac out put.
commonly used for medical students, and helpful to use this ppt to study for them, and also a common man can understand very easily what is coarctation of aorta.
Pulmonary stenosis (also called pulmonic stenosis) is when the pulmonary valve (the valve between the right ventricle and the pulmonary artery) is too small, narrow, or stiff. Symptoms of pulmonary stenosis depend on how small the narrowing of the pulmonary valve is
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
CARDIAC TAMPONADE ( Cardiac emergency) • Cardiac Tamponade is a life threatening complication caused by excessive accumulation of fluid in the pericardium. Or • Compression of all cardiac chambers due to excessive accumulation of pericardial fluid leading to compromised cardiac out put.
commonly used for medical students, and helpful to use this ppt to study for them, and also a common man can understand very easily what is coarctation of aorta.
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
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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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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2. DEFINITION
Aortic Regurgitation (AR), is due to damage or dysfunction of the aortic valve
of the heart that causes blood to flow in the reverse direction during
ventricular diastole, from the aorta into the left ventricle. As a consequence
the cardiac muscle is forced to work harder than normal.
3.
4. SIGNS AND SYMPTOMS
Symptoms of aortic insufficiency are:
1) Dyspnea on exertion
2) Orthopnea
3) Palpitations
4) Chest pain
5) Cyanosis (in acute cases)
In the long run, blood can accumulate the left
atrium and cause congestion in the lungs then after
years there can be congestion in the right atrium.
5. CAUSES
Over 80% of cases are idiopathic, but otherwise may result from
1) Aging
2) Aortic dissection
3) Reactive arthritis
4) Systemic hypertension
5) Infective endocarditis
Other Genetic dispositions.
Left Ventricular Heart Failure due to AR, due to congestion in the lungs,
right ventricle becomes dilated called Biventricular or globular heart
failure and patient will require transplantation.
6. PATHOPHYSIOLOGY
The mechanism of aortic regurgitation (AR), comprises the pressure in the left
ventricle decreases below the pressure in the aorta, the aortic valve is not able to
completely close. This causes a leaking of blood from the aorta into the left ventricle.
This means that some of the blood that was already ejected from the heart
is regurgitating back into the heart.
This regurgitant flow causes a decrease in the diastolic blood pressure in the
aorta, and therefore an increase in the pulse pressure. Since some of the blood that
is ejected during systole, regurgitates back into the left ventricle during diastole,
there is decreased effective forward flow.
Aortic regurgitation causes volume overload.
The volume overload causes left ventricular hypertrophy (LVH).
7. COMPLICATIONS
Heart failure may become severe and life-threatening.
Infection of the valve (endocarditis) is an uncommon complication. (Abnormal
valves are more prone than normal valves to infection.) Unless promptly treated,
endocarditis can cause serious illness.
8. DIAGNOSIS
The diagnosis of aortic regurgitation a common test for the evaluation of the
severity is echocardiography.
Chest X-ray can assist in making the diagnosis, showing left ventricular
hypertrophy and dilated aorta.
ECG typically indicates left ventricular hypertrophy.
Cardiac chamber catheterization assists in assessing the severity of
regurgitation and any left ventricular dysfunction.
9.
10. PATIENTS COMPLAINTS
Characteristic Signs:
Chest pain (angina) when patient exerts. (This occurs because of reduced blood flow
to the coronary arteries.)
Forceful heartbeats which they may feel as the sensation of having a 'thumping heart'
(palpitations).
Dizziness.
Shortness of breath, tiredness and fluid retention in various tissues of the body if the
patient has developed heart failure.
11. INSPECTION
De muse or symptom of muse - nodding of the head
Corrigan’s sign – dancing of carotid artery
Miosis and mydriasis – pupil contraction and dilation
Quincke’s sign – blood filling under the nails
*After hypertrophy characteristics signs appear
12. PALPATION
During AR, there is more blood in the left ventricle. Therefore, the left ventricle has to
work harder in order to pump blood into the aorta. In due time, the left ventricle
undergoes hypertrophy and the point of maximal impulse - will move to the left
and down.
15. AUSCULTATION
The murmur of AR occurs in diastole (diastolic murmur), usually as a high-
pitched sound that is loudest at the left sternal border. The duration of the
murmur correlates better with the severity of AR than does the loudness of
the murmur.
Systolic dysfunction
Auscultation may reveal an S3 gallop if LV dysfunction is present.
16. MEDICATION
If the backflow of blood is mild and you have no symptoms then you may not need any
treatment. If you develop symptoms or complications, various medicines may be advised to
ease the symptoms. Surgery may be advised if symptoms become worse.
Medication may be advised to help ease symptoms of heart failure if heart failure develops.
For example:
Diuretics usually help if you are breathless. They make the kidneys produce more urine. This
gets rid of excess blood and fluid which may build up in the lungs or other parts of the body
with heart failure.
Angiotensin-converting enzyme (ACE) inhibitors are medicines which help to reduce the
amount of work the heart does and to ease symptoms of heart failure.
Antibiotics to prevent endocarditis.
17. REFERENCES
Bekeredjian, Raffi; Grayburn, Paul A. (2005-07-05). "Valvular Heart Disease Aortic
Regurgitation“. Circulation. 112 (1): 125–134. doi:10.1161/CIRCULATIONAHA.104.488825. ISSN 0009-
7322. PMID 15998697.
Jump up^ "Aortic Regurgitation. Healt "Aortic insufficiency: MedlinePlus Medical
Encyclopedia". www.nlm.nih.gov. Retrieved 2016-05-16.
^ Jump up to:a b c d e f g h i Chapter 1: Diseases of the Cardiovascular system > Section: Valvular Heart
Disease in: Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine (Step-Up Series).
Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7153-6.
h Information and treatment | Patient". Patient. Retrieved 2016-06-04.
Kumar, Vinay; Abbas, Abul K.; Aster, Jon C. (2012-05-01). Robbins Basic Pathology. Elsevier Health
Sciences. p. 331. ISBN 1455737879.
Jump up^ Topol, Eric J.; Califf, Robert M. Textbook of Cardiovascular Medicine. Lippincott Williams &
Wilkins. p. 381. ISBN 9780781770125 Retrieved 4 June 2016.