In this PPT u will know about Tuning Fork and its types.
u can also know the principle , purpose , procedure and implications of types of tuning fork test.
hope this will help you all.
u can suggest me for better
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In this PPT u will know about Tuning Fork and its types.
u can also know the principle , purpose , procedure and implications of types of tuning fork test.
hope this will help you all.
u can suggest me for better
@ - anantarun27@gmail.com
DEFINATION
ATIOPATHOGENESIS
FEATURE AND PREDISPOSING FACTER
SYMPTOMS
DIAGNOSIS
DEFFERENTIAL DIAGNOSIS
TREATMENT
Also known as Singer’s or Screamer's Nodes
Vocal cord nodules are benign growths on both vocal cords that are caused by vocal abuse
They appear symmetrically on the free edge of vocal cord
At the junction of anterior 1/3 and posterior 2/3 *area of maximum vibration of vocal cord.
Please find the power point on Meniere's disease. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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2 Case Reports of Gastric Ultrasound
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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- 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. Menieres disease, also called
endolymphatic hydrops , is disease of
inner ear where endolymphatic system
is distended with endolymph.
It is characterized by
1) vertigo
2) sensory neural hearing loss
3) tinnitus
4) aural fullness
3. The main pathology is distension of endolymphatic
system, mainly affecting the cochlear duct (scala
media) and saccule and to lesser extend the utricle
and semicircular canals.
The dilatation of cochlear duct is such that it may
completely fill the s. Vestibuli, there is marked
bulging of reissners membrane,which may even
herniate through halicotrema in the apical part of
s. Tympani.
4. The distended saccule may come to lie
against the stapes footplates.
The utricle and saccule may show out
pouching into semicircular canal.
5. Exact cause of menieres disease is not yet
known. Various theory have been postulated.
It is possible that menieres disease is
multifactorial, resulting in common end poin of
endolymphatic hydrops with classical
presentation
This can be result of
1) increased production of endolymph
2) decreased absorbtion of endolymph
3) both of above
6. Normally endolymph is carried by
endolymphatic duct to sac where it is absobed.
Obstruction of endolymphatic sac and duct
may responsible for raised endolymph
pressure.
Ischaemia of sac may be responsible for poor
vascularity and thus poor absorbtion by sac.
Distension of membranous labyrinth leads to
rupture of reissners membrane thus mixing of
perilymph and endolymph,which is responsible
for attack of vertigo.
7. There is sympathetic overactivity resulting in
spasm of internal auditory artery and its
branch, thus interfaring with the function of
cochlear and vestibular sensory
neuroepithelium. This responsible for
deafness and vertigo.
Anoxia of capillaries of stria vascularis also
causes increased permeability, with
transudation of fluid and increased
production of endolymph.
8. Allergen may be a foodstuff or an inhalant. In
these case, inner ear act as a “shock organ”
producing excess of endolymph
Nearly 50% of patient with menieres disease
have concomitant inhalant or food allergy.
4). SODIUM AND WATER RETENSION
5). HYPOTHYROIDISM – About 3% cases are
due to hypothyroidism. such case benefit
from thyroid replacement theraphy.
9. It is also suggested on basis of experimental
and cliniacal observation.
summary:-
10. Commonly seen in the age group of 35-60
yesrs.
Male are more affected than female.
Usually, disease is unilaterally but other ear
may affected after few years.
Cardinal symptoms is:-
a) episodic vertigo
b) fluctuating hearing loss
c) tinnitus
d) sense of aural fullness
11. It comes in attacks.
The onset is sudden.
Patient gets feeling of rotation of himself or his
environment.
Sometimes, there is “to and fro” or “up and down”
movement.
Attack comes in clusters, with periods of spontaneous
remission lasting for weeks, months and years.
Usually an attack is sccompanied by nausia and
vomiting with ataxia nystagmus.
Usually there is no warning symptoms of ongoing
attack of vertigo but sometimes patient may feel a
sense of ear fullness, change in character of tinnitus
and discomfort in ear.
12. Severe attacks may be accompanied by other
symptoms ofvagaldisturbances such as
abdominal cramps, cold sweats, pallar and
bradycardia.
Some case show tullio phenomenon.
It is a condition where loud sounds or noise
produce vertigo and is due to distended
saccule lies against stapes footplate. it is also
seen in when three functioning windows in
ear.
13. It is usually accompanies vertigo or may presede
it.
Hearing improves after the attack and may be
nomal during the periods of of remission.
Improvement in hearing during remission may
not be complete, some hearing loss being
added in every attack leading to slow and
progressive deterioration of hearing which is
permanent.
DISTORTION OF SOUND – some patients
complain of distorted hearing. A tone of
perticular frequency apear normal in one ear
and of higher in other leading to diplacusis
Intolerance to loud sound.
14. It is low pitched roaring type and aggrevated
during acute attacks.
Sometimes, it has a hissing character.
It may persist during period of remission.
Change in intensity and pitch of tinnitus may
be the warning symptom of attack.
4. SENSE OF EAR FULLNESS:- like other
symptoms it also fluctuats. It may accompany
or before an attack of vertigo.
15. Patient often shows signs of emotional upset
due to fear of repitition of attacks.
Earlear, emotional stress was considerd the
cause of menieres disease.
16. OTOSCOPY:- No abnormality seen in
tympanic membrane.
NYSTAGMUS:- it is seen only durig acute
attack. Quick component of nystagmus is
towards the unaffected ear.
TUNNING FORK TEST:- indicates SNHL.
Rinne test is positive.
Absolute bone conduction is reduced in
affected ear.
Weber lateralised to better ear.
17. 1. PURE TONE AUDIOMETRY:- Indicates SNHL
A) In early stage:- low frequency affected and curve is
rising type
B & C) Later stage:- higher frequencies are involved curve
becomes flate or falling type
18. 2. ELECTROCOCHLEOGRAPHY:- It shows changes
diagnostic of menieres disease.
normally, ratio of summating paotential (SP) to
action potential is 30%. But in menieres disease
SP/AP ratio is greater than 30%
19. 3. GLYCEROL TEST:-
The test has a diagnostic and prognostic value.
Glycerol is dehydrating agent. When given orally, it
reduce endolymph pressure so that improvement
in hearing.
Patient is given glycerol (1.5ml/kg) with an equal
amount of water with a little flavouring agent like
lemon juice.
Audiogram and speech discrimination score are
recorded before and 1-2 hours after ingestiom of
glycerol.
An improvement of 10 dB and gain of 10% in
discrimination score makes the test positive.
There is also improvement in tinnitus and sense of
aural fullness.
20. 4. SPEECH AUDIOMETRY:-
descrimination score is usually 55-85%
between the attacks but discrimination ability
much impaired during and immedietely
following an attack.
5. SPECIAL AUDIOMETRIC TEST:- they indicate the
cochlear nature of disease.
A). Recruitment test is positive.
B). Short increment sensitivity index (SISI) score
is better than 70%in two third of patient (normal
15%)
C). Tone deacay test:- there is decay of less
than 20 dB.
22. Only cochlear sign and
symptoms of MD are
present
Vertigo is absent
In these case there is block
at the level of ductus
reuniens, so that
endolymph pressure is
limited to cochlea only.
Level of
block
23. Also called tumerkins otolithic crisis.
It is due to deformation of otolithic membrane of
utricle or saccule due to change in endolyphatic
pressure
In these case there is sudden drops attack without
lack of consciousness.
There is not vertigo and fluctuations in hearing
loss.
Patient gets a feeling of having been pushed to the
ground.
It is uncommon manifestion of of MD and occurs
either early or late couse of disease.
24. Here symptoms of MD are seen in reverse order.
First progressive deterioration of hearing
followed by an attack of vertigo, at which time
hearing recovers.
D). VESTIBULAR HYDROPS
In this varient only vastibular symptoms of MD
seen and cochlear symptoms are normal.
25. CLASSIFICATION Guidelines were given by AAOHNS.
.Certain meniers-
confirmed by histopathology
Definite Meniere’s –
> 2 spontaneous attacks of vertigo each lasting > 20
min
Hearing loss documented by PTA on atleast 1
occasion
Tinnitus or aural fullness on affected side
Probable Meniere’s –
> 2 spontaneous attacks of vertigo + U/L hearing loss
+ tinnitus + aural fullness, all at the same time
Possible Meniere’s –
> 2 attacks of spontaneous attacks of vertigo without
any auditory impairment
26.
27. GENERAL MEASURE:-
1) Reasurance. Patients anxiety can be relieved by
reasurance and by expalaing the true nature of
disease
2) Cessation of smoking. Nicotine causes
vasospasm. Smoking should be completely
stopped. For some pationts, this may be only
tratment
3) Low salt diet.
4) avoid axcessive intake of water.
5) avoid over intke of alcoho, coffee and tea.
6) Avoid stress and bring a lifestyle chamge
28. During the acute attack, patient is
apprenhensive. Head movements provoke
giddiness. Therefore t/t consist of:
1) REASSURANCE And psychological support to
stop anxiety and worry.
2) BED REST with head supported on pillow to
prevent excessive movements.
3) IV FLUID and electrolyte administration to
combat their loss due to vomiting.
29. 4)VESTIBULAR SEDATIVES to relieve vertigo. They
should be given intravenously or intramuscularly
because of vomiting. Drug used in acute attack are
Dimenhydrinate:- 50 mg iv stat
Prochlorperazine:- 10 mg iv or 12.5 mg im
Diazepam:- 5-10 mg iv. It reduce anxiety. Also
supress medial vestibular activity.
Atropine:- 0.4 mg subcutaneosly
30. 5) vasodilators:- carbogen (5% Co2 with 95%
O2) is a good cerebral vasodilator and its
inhalation improves labyrinthine circulation.
31. 1). VESTIBULAR SEDATIVE:-
prochlorperazine 10 mg TDS Orally for 2 month
than dose reduced
to
5mg tds orally for 1 month
2). VASODILATORS Betahistine 8-16 mg TDS
orally. It icrease labyrinthine blood flow by
releasing histamine in the body.
3). DIURETICS furosamide 40 mg taken alternate
day with potassium supplement helps to control
recurrent attacks, if not controlled by above
measures. hydrochlorthiazide 12.5mg daily can
also be used
32. 4). ELIMINATION OF ALLERGENS:- Sometimes, a
food or inhalant allergen is responsible for
attacks.
it should be found and eliminated or
desensitisation done.
5). HORMONES:- shoud be directly fine out
endocrinal disorder like hypothyroidism,
appropriate replacement therapy given.
About 80% case can be effectively managed by
medical theraphy alone
33. Gentamycin is maily vestibulotoxic.
It has been used biweekly injection into middle
ear. Drug is absorbed through the round window
and causes destruction of vestibular labyrinth.
60-80% patients gets some relief from
symptoms.
Hearing loss in 4-30% patients withthis mode of
therapy.
34. It is a wick made og polyvinyl acetate
It directly delivers drug from external canal to
inner ear through roound wibdow. So patient
can avoid repeated intratymoaniv injection.
35. 1) CONSERVATIVE PROCEDURES:- they are used
in case where vertigo is disabling but hearing is
still useful and need to be preserved.
a) endolymphatic sac decompression
b) endolymphatic shunt operation
c) sacculotomy
d) cochleosacculostomy
e) section of vestiblar nerve
d) ultranic destruction of vestibular labyrinth
36. 1).DECOMPRASSION OF ENDOLYMPHATIC SAC
sucess rate is 81.6%
Donaldson line:- a imaginary line passing through
horizontal scc and bisects the posterior scc.this is
landmark for endolymphatic sac,which is located
below and along this line.
37. 2). ENDOLYMPHATIC SHUNT OPERATION.
A tube is put, connecting endolymphatic sac with
subarachnoid space, to drain excess endolymph.
38. 3) SACCULOTOMY:- (ficks operation)
It is puncturing the saccule with a needle
through stapes footplate.
A distended saccule lies against stapes
footplate, can be easily penetrated.
39. 4).SECTION OF VESTIBULAR NERVE:-
The nerve is exposed by retrosygmoid or
middle cranial fossa aproach and selectively
sectioned.
It control vertigo but preserves hearing.
5). Ultrasonic destruction of vestibular
labyrinth. cochlear function is preserved.
40. 2). DESTRUCTIVE PROCEDURE:- they totally
destroy cochlear and vestibular function so it is
used only when cochlear function is not
serviceable.
Labyrinthectomy:-
Membranous labyrinth is completely destroyed.
It give relief from attacks of vrtigo.
41. It is observed that intemittent positive pressure
deliverd to inner ear fluid brings relief from
symptoms of MD.
Intemittend positve pressure wave can be delivered
through an instrument called meniett device.
A prerequisite for this thearpy is insertion of
grommet tube so that device can deliver pressure
pressure waves to round window membrane via
grommet tube.
42. Pressure wave passes through perilymph and
causes reduction o in endolymph pressure by
redistributing it through endolymphatic sac or
the blood vessels.
43. Used for 5 minute 3 times a day.
Patient can self administer the treatment at home.