1. Meniere's disease is a disorder of the inner ear that causes episodes of vertigo, hearing loss, tinnitus, and a feeling of fullness in the ear.
2. The exact cause is unknown but may involve an obstruction of the endolymphatic duct resulting in a buildup of fluid in the inner ear.
3. Treatment focuses on controlling vertigo attacks, minimizing hearing loss, and in severe cases, surgery to relieve fluid buildup such as a shunt or labyrinthectomy.
Ototoxicity is, quite simply, ear poisoning (oto = ear, toxicity = poisoning), which results from exposure to drugs or chemicals that damage the inner ear or the vestibulo-cochlear nerve (the nerve sending balance and hearing information from the inner ear to the brain).
Ototoxicity is, quite simply, ear poisoning (oto = ear, toxicity = poisoning), which results from exposure to drugs or chemicals that damage the inner ear or the vestibulo-cochlear nerve (the nerve sending balance and hearing information from the inner ear to the brain).
meniere disease is the inner ear condition which affect the patient haring and balance this ppt can help the nurses to take care of the patient affected with this disease and can be used as a study material for their examination
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
oto sclerosis is the hardning of the ear bone or abnormal spongy bone growth inside ear this topic include its definition , etiology, pathophysiology, clinical menisfestation, diagnosis and its treatment which can be used by nursing students for taking care of the patient suffering from otosclerosis and for learning for their examination and knowledge purpose
an inner ear disorder that cause episodes of vertigo
(spining) . this sildeshare contained detailed information about definition, causes, types, medical and nursing management.
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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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
2. • The disease is named after a
French doctor - Prosper Ménière who described the condition as
being characterised by sudden
attacks of
dizziness, nausea, vomiting, loss
of hearing and a buzzing in the
ears (tinnitus).
DR. RS MEHTA, BPKIHS
3. Meniers disease is a disorder of inner
ear where the endolymphatic system is
distended.
It is chracterised by
i. Virtigo
ii. Sensorial hearing loss
iii. Tinnitus and
iv. Aural fullness
DR. RS MEHTA, BPKIHS
4. Function of ear
• Hearing: Sound conduction and transmission
• Balance and equilibrium
DR. RS MEHTA, BPKIHS
5. Anatomy of ear
It consists of:
• Outer ear
• Middle ear
• Inner ear
DR. RS MEHTA, BPKIHS
7. Definition
• Meniere’s disease is a disorder of inner ear in
which the endolymphatic system is distended.
• It is also called endolymphatic hydrops.
DR. RS MEHTA, BPKIHS
8. Incidence
•
•
•
•
Male are affected more than female.
Disease is mainly unilateral.
It is more common in age group 35-60 years
About 50,000 - 100,000 people of world
develop Meniere's disease in a year.
• About 50 % of the patients who have
Meniere's disease have a positive family
history of this disease.
DR. RS MEHTA, BPKIHS
9. Etiology
•
•
•
•
•
•
•
•
•
The exact cause of Meniere’s disease is unknown.
Possible causes include:
Defective absorption by endolymphatic sac
Allergies
Sodium and water retention
Hypothyroidism
Autoimmune and viral aetiologies
Mumps
Syphilis
Head trauma
Previous infection
• Hormonal (Pregnant females are more prone)
DR. RS MEHTA, BPKIHS
12. Pathophysiology
Obstruction of endolymphatic duct/sac
Alteration in production and absorption of endolymph
Distension of endolymphatic sac
Increased in pressure and rupture of inner membranes
Vertigo, tinnitus, hearing loss( Meniere’s)
DR. RS MEHTA, BPKIHS
14. Clinical features
Cardinal symptoms of Miniere’s disease are:
• Episodic vertigo
Sudden onset
Feeling of rotation of himself/environment
• Fluctuating hearing loss
Following /accompanying vertigo
Deterioration in hearing with each attack
DR. RS MEHTA, BPKIHS
15. Cont
• Tinnitus
Low pitch roaring type
• Sense of aural fullness:
Accompany/ preceed
vertigo
DR. RS MEHTA, BPKIHS
17. Physical Examination
•
•
•
During an acute attack, the patient
has severe vertigo.
Patients are sometimes diaphoretic
and pale.
Vital signs may show elevated blood
pressure, pulse, and respiration.
DR. RS MEHTA, BPKIHS
18. • The Weber tuning fork test usually lateralized to the better
ear.
• The Rinne test is positive absolute bone conduction is
reduced in the affected ear
Weber Test:
Normal: equal hearing both sides of same type
Abnormal – Tone louder in on one side
=Conductive loss – tone louder on affected side
=SNHL – tone louder on contralateral side
Rinne test:
Normal: AC > BC
Abnormal
Negative Rinne – louder on mastoid process
Positive Rinne – Bilateral SNHL
DR. RS MEHTA, BPKIHS
20. Imaging Studies
• Magnetic resonance imaging:
Brain scan should be done to rule out
abnormal anatomy or mass lesions.
• CT scans reveal dehiscent superior
semicircular canals and/or widened
cochlear and vestibular aqueducts
DR. RS MEHTA, BPKIHS
27. Rx: summary
1. Atropine: stop attack for 20-30 Minutes
2. Bed rest in quite environment
3. Labyrinthine sedative like: Prochlorperazine (stemetil),
Idmenhydrinate (Dramamine) to control giddiness and
N/V
4. Vasodilators: Nicotinic acid, betahistamine to control
vasospasm
5. Tranquilizer and anti-depressant to relieve anxiety
6. Prphylactic antihistamine or mild sedative:
Phenobarbitone, diazepam may be helpful.
7. Steroid to reduce inflamation
8. Antibiotics: esp. Aminoglycocise groups
DR. RS MEHTA, BPKIHS
28. Nursing management
• Assess the severity and frequency of attack,
any associated ear symptoms (hear loss,
tinnitus).
• Help patient prevent from aura, so patient has
time to prepare for an attack.
• Encourage patient to lie down during attack in
safe place.
• Put side rails in the bed if patient is in bed
• Place pillow to restrict movement.
DR. RS MEHTA, BPKIHS
29. Cont..
• Administer or teach anti-vertiginous
medication and sedation medication as
prescribed
• Avoid noises and glary bright light which may
initiate attack.
• Advise patient to avoid food that cause allergy.
• Assist with ambulation when indicated.
• Provide comfort measures and avoid stress
producing activities.
DR. RS MEHTA, BPKIHS
30. Post operative instructions:
• Antibiotic and other medication are to be taken
as prescribed.
• Nose blowing to be avoided (few weeks).
• Sneezing and coughing should be done with the
mouth open for a few weeks after surgery.
• Heavy lifting, straining, and bending are to be
avoided for a few weeks after surgery.
• Minor discomfort is expected can relief by
analgesic, excessive pain should be reported to
surgeon.
DR. RS MEHTA, BPKIHS
31. • Some slightly bloody or serosanganious drainage
from the ear is normal after surgery.
• Excessive or purulent drainage should be
reported to the surgeon.
• The cotton ball in the ear can be changed as
needed but not to touch or remove any packing
from the external auditory canal.
• Post auricular suture line should be cleaned and
antibiotic oint. Applied twice daily.
• The surgeon should consult for regular air travel.
• Getting water in the operated ear must be
avoided for 2 weeks after surgery.
DR. RS MEHTA, BPKIHS
32. •
•
•
•
•
•
•
Dressing first open-3rd day
Suture removal 10th day
Head up 300 (3-10 days)
Avoid: Chewing, sneezing, coughing etc
Prevent water in ear: 6 weeks
Never put oil in ear
Hearing may be impaired for few months RT
edema, blood, fluid
• Observe complications: Facial nerve palsy (VII),
brain abscess, meningitis etc
• Avoid flying in air for 2 months
• BIPP dressing (bismuth icthymol parafin paste)
while doning mastoid surgery
DR. RS MEHTA, BPKIHS
33. Complications
• Inability to walk or function due to
uncontrollable vertigo.
• Hearing loss on the affected side.
• Possible of injury due to imbalance.
DR. RS MEHTA, BPKIHS
34. Prognosis
• The outcome varies. Meniere's disease can
often be controlled with treatment.
• The condition may get better on its own
sometimes.
• Meniere's may be chronic disabling causing
permanent hearing loss.
DR. RS MEHTA, BPKIHS