HOW TO MANAGE PATIENTS WITH VERTIGO?
Andradi S.
Department of Neurology. University of Indonesia, Jakarta
disampaikan dalam Simposium PIT IDI Kota Bogor
Vertigo is a subtype of dizziness in which a patient inappropriately experiences the perception of motion (usually a spinning motion) due to dysfunction of the vestibular system.
Vertigo is a subtype of dizziness in which a patient inappropriately experiences the perception of motion (usually a spinning motion) due to dysfunction of the vestibular system.
1. Identify the difference between vertigo, disequilibrium,, near-syncope, and Undifferentiated dizziness.
2. Identify helpful tests to distinguish peripheral from central vertigo.
3. Understand how to treat different kinds of vertigo
1. Identify the difference between vertigo, disequilibrium,, near-syncope, and Undifferentiated dizziness.
2. Identify helpful tests to distinguish peripheral from central vertigo.
3. Understand how to treat different kinds of vertigo
Vertigo –the dizzy patient an evidence-based diagnosis and treatment strategySachin Verma
Vertigo is a symptom of illusory movement and not a diagnosis .It is due to asymmetry of vestibular system due to damage or dysfunction of the
Labyrinth and vestibular nerve, or
Central vestibular structures in the brainstem
disampaikan pada sesi husnudzan dalam rangkaian #JamborePelajar #AkuIndonesia Ma'arif Institute, PAUDNI Lembang, 26 Desember 2014.
mohon maaf karena uploading versi PPT gagal terus tersebab koneksi di lokasi, jadi PDFnya dulu ya.
Media Sosial, Manfaat dan Risiko (Presentasi di SMP Sekolah Alam Bogormataharitimoer MT
Disampaikan pada sesi Internet Sehat Festival SALAM
6 Desember 2014.
Presentasi ini diunggah dalam format PDF, jika memiliki bandwidth yang memungkinkan, akan diunggah format PPT-nya agar mudah dimodifikasi oleh siapa saja yang memerlukan.
PENEGAKAN DISIPLIN KEDOKTERAN OLEH MKDKI & CONTOH KASUSmataharitimoer MT
PENEGAKAN DISIPLIN KEDOKTERAN OLEH MKDKI & CONTOH KASUS
Dipresentasikan oleh Dr. SABIR ALWY, SH, MH
Wakil Ketua MKDKI
pada PIT VI IDI Kota Bogor | 10 Nopember 2013
Dr kanadi s penanganan nyeri dismenorea (pit idi bogor) 2013 finalmataharitimoer MT
Dipresentasikan oleh Kanadi Sumapradja
Departemen Obstetri dan Ginekologi Fakultas Kedokteran Universitas Indonesia – RS Dr. Cipto Mangunkusumo
pada PIT VI IDI Kota Bogor | 10 Nopember 2013
Muntah pada Anak
Dipresentasikan oleh DR. dr. Dwi Prasetyo, SpA(K), M.Kes
Departemen Ilmu Kesehatan Anak
FK UNPAD/ RS Hasan Sadikin Bandung
pada PIT VI IDI Kota Bogor | 10 Nopember 2013
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
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.
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
4. Body Balance is Controlled by 3 Sensory Systems:
Vestibular, Visual, Proprioceptive
VISUAL
(Eye)
VESTIBULAR
PROPRIOCEPTIVE
(Muscle, joint, skin)
(Labyrinth)
CENTRAL NERVOUS SYSTEM
(Coordination, integration)
Control of eye
movement
Postural control
by muscle
BALANCE
dysfunction
Imbalance /Dizziness
Goebel JA. Otolaryngol Clin North Am 2000;33:483–93.
Shepard NT, Solomon D. Otolaryngol Clin North Am 2000;33:455–69
6. DIZZINESS : Frequency
40% Peripheral vestibular dysfunction
10% Central brainstem vestibular lesion
25% Presyncope or disequilibrium
15% Psychiatric disorder
10% Unknown cause
December 4, 2001, Swedish Family Medicine, Dobrina Okorn, MD
7. OUTLINES
1. Vertigo vs Dizziness
2. Vertigo:
- Types
- Causes
3. Approach to Management of Patients with Vertigo
- Diagnosis
- Treatment
8. VERTIGO
Vertigo is an ilusion of movement in which a subject feels
him-/herself or the surrounding object is moving.
Two types:
I. Vestibular Vertigo ( “spinning” vertigo / “true” vertigo)
Vestibular dysfunction
II. Vertigo Nonvestibular (“non-spinning” vertigo)
Visual dysfunction
Proprioceptive dysfunction
9. VERTIGO
VESTIBULAR vs NONVESTBIULAR
VESTIBULAR
(vestibular system)
NONVESTIBULAR
(visual & proprioceptive)
Sensation
Spinning, rotating
Swaying, floating, rocking
lightheaded
Duration
Episodic
Constant
Precipitating factor
Head or body movement
Stress, hiperventilation,
cardiac arrhythmia
Associated symptoms
Nausea, vomit, tinitus,
deafness, oscillopsia
Paleness, paresthesia,
syncope
12. Balance requires information of similar
intensity from both vestibular systems
Head movement
Activation of cells
in left
vestibular system
Activation of cells
in right vestibular
system
Central nuclei
10
10
Normally, the input from left and right vestibular
system is of similar intensity (e.g. of size ‘10’)
16. VESTIBULAR VERTIGO
PERIPHERAL vs CENTRAL
Symptom
Peripheral
Central
Vertigo episodes
Mild severe
Chronic and
unremitting
Symptom onset
Sudden
Gradual
Imbalance
Mild/mod.
Severe
Nausea, vomiting
Severe
Varying
Auditory symptoms
Common
Rare
Neurological symptoms
Rare
Common
Changes in mental status/
consciousness
Infrequent
Sometimes
Compensation/resolution
Rapid
Slow
Baloh RW. Otolaryngol Head Neck Surg 1998;119:55–9. Puri V, Jones E. J Ky Med Assoc 2001;99:316–21.
18. OUTLINES
1. Vertigo vs Dizziness
2. Vertigo:
- Types
- Causes
3. Approach to Management of Patients with Vertigo
- Diagnosis
- Treatment
19. Approach to Management of Patient with Vertigo
Patient complaint (pusing, mabuk)
Step 1
Verify : “VERTIGO” or NOT?
No
Yes
step 2
Identify : TYPE of VERTIGO
Step 3
Establish: DIAGNOSIS / ETIOLOGY
Step 4
Planning
THERAPY
Headache, stress,
other dizziness
20. STEP 1 and STEP 2
Verifying and Identifying Types of Dizziness
QUESTION :
“Apakah anda terasa mau pingsan ?” ( “Pingsan / fainting”)
• PRESYNCOPE
“Apakah anda merasa kedua tungkai tidak stabil, dan menjadi stabil kalau
duduk ?”
• DYSEQUILIBRIUM
(“ Jatuh / falling”)
“Apakah lingkungan anda kelihatannya berputar, atau anda sendiri terasa
berputar ?”
- VESTIBULAR VERTIGO”
(“ Berputar / spinning”)
“ Apakah merasa lingkungan bergoyang, atau anda sendiri terasa
bergoyang ?”
• VERTIGO NONVESTIBULAR
(“Melayang / light-headed”)
“Apakah anda merasa gugup atau cemas ?
• PSYCHOGENIC
(“ Melayang / light-headed”)
21. STEP 3
ESTABLISHING DIAGNOSIS AND ETIOLOGY OF
VERTIGO
1. History taking
2. Physical examination
a. General PhysicaL Examination
b. Routine Neurologic Examination
c. Bed-side Neuro-otologic examination
3. Investigations (as indicated)
- ENG, EEG, EMG, CTScan, MRI, MRA
- Laboratory
22. 1. HISTORY TAKING
Sensation
- Spinning, rocking, swaying, swimming, light-headed ?
Temporal profile
- Onset, duration, course.
Head/body position
- Occurs on lying, turning, rising, sitting up, standing, nodding,
bending, head turning
Associated symptoms
Tinnitus, deafness, cranial nerves
symptoms, hemiparesis, hemihipesthesia, hemiataxia.
Past history
- Head injury, stroke, cardiac and pulmonar disorders, CNS
infection, ENT diseases, psychiatric disorder.
Medication
Drugs that may give rise to dizziness, including
garamycin, sedative, tranquilizer.
23. 2. PHYSICAL EXAMINATIONS
a. General Physical Examinations
Searching for pathology related to current dizziness complaint:
- Hypertension, hypotension
- Cardiovascular disorder
- Pulmonary disease
- Malignancy
24. 2. PHYSICAL EXAMINATION
b. Routine Neurologic Examination
- Mental
- Cranial nerves
- Motor system
- Sensory system
- Autonomic system
25. 2. PHYSICAL EXAMINATION
c. Bedside Neurootologic Examination
I. Otologic examination
II. Hearing testing
III. Vestibular examination
29. 1. EYE MOVEMENT TESTS
- Aim: to evaluate Vestibulo-ocular Reflex (VOR)
- Manifestation: Nystagmus
- Examinations:
- ● Spontaneous nystagmus
- ● Gazed-evoked nystagmus
- ● Head thrust test
- ● Head shaking test
- ● Dix Hallpike ( for BPPV)
30.
31. 2. EXAMINATION OF BALANCE AND COORDINATION
A. Test for BALANCE
1. Seated : hold out arms and legs, eyes open/eyes closed
2. Stand: Romberg test, sharpened Romberg test
3. Gait :
broad-based gait
4. Tandem walking, past-pointing, Fukuda test, Babinski-Weil test.
B. Test for COORDINATION (cerebellum)
1. Upper extremity
a. Finger- to- nose
b. Finger-nose-finger
c. Adiadochokinesis
d. Rebound phenomen
2. Lower extremity
a. Heel-knee-shin
b. Repetitive heel tapping
c. Rebound phenomenon
3. Ocular dysmetria
32. THERAPY OF VERTIGO
I. Etiologic
Pharmacologic therapy
Surgery
II. Symptomatic
Pharmacologic therapy
III. Rehabilitative
Vestibular Rehabilitation Therapy (VRT)
IV. Prevention of aggravating factor
Diet control
Life-style modification
V. Physical Conditionng Exercise
38. Vestibular Suppressant
Clinical evidence
Drugs with sedative effect may disturb central
compensation mechanism
Ideal Drug
√ Effective in suppressing vertigo
√ Non-sedative
does not disturb central
compensation
39. Ideal Vestibular Suppressant
a. Ca antagonist : Flunarizin
b. Vasodilator : Betahistine
c. Tranquilizer : diazepam, haloperidol,
sulpiride, clonazepam
d. Antihistamin : Difenhidramine, meclizine.
a, c, d
b (Betahistine)
Sedative effect !!
- No sedative effect !!
41. VESTIBULAR REHABILITATION THERAPY (VRT)
TYPES
I. Specific VRT for BPPV
II. Balance exercises
III. Gaze Stabilization Exercises
IV. Visual Dependence Exercises
V. Physical conditioning exercise
45. b. Epley maneuver
30 sec
30 sec
30 sec
Other name:
• Canalith repositioning
• Particle repositioning
46. c. Brandt Daroff maneuver
-Each position 30 sec or vertigo subsides
in < 30 sec
-If Vertigo >30 sec sit up 30 sec other
side
Time
Exercise Duration
--------------------------------------------Morning
5X
10 min
Noon
5X
10 min
Evening
5X
10 min
---------------------------------------------
48. PREVENTION OF AGGRAVATING FACTOR
Control of Nutrition and Life-style:
-
• Adequate food and diet
-
• Avoid excessive alcohol, tobacco
-
• Medicine: sedative, ototoxic, opioid
-
• Sleeping, working position.
49. V. PHYSICAL CONDITIONING EXERCISE
Recommend doing one or more of the following, 3 times a week:
- Walking on a treadmill (1 mile)
- Brisk walking outdoors (1 mile or more)
- Riding a stationary bicycle
- Swimming
51. Therapeutic Modalities Options:
1. Symptomatic treatment
2. Treatment for Specific Conditions
3. Rehabilitative therapy
4. Prevention of aggravating factor
SINGLE THERAPY
or
INTEGRATED THERAPY ?
52. Single Therapy
•Etiologic or Specific treatment is paramount, but it does not offer
the patient a significant improvement or vertigo symptoms
resolution when used alone
• Symptomatic drug therapy bring improvement in 75.1% of the
patients with peripheral vestibulopathies and 39.8% of the
patients with central vestibular disorders
• Vestibular rehabilitation therapy were efficient in 51.1% of
patient when used alone
• Diet and feeding habit change improve vertigo in 42.2% patients
with vestibulopathies
Gananca et al. Brazilian Journal of Otorhinolaryngology 2007;73(1):12-8
53. INTEGRATED THERAPY
Integrated Vestibular Therapy (IVT)
A combination therapeutic modalities of Specific
Treatment, Symptomatic Treatment, Vestibular
Rehabilitaton Therapy, Diet Control and Life-style
changes, brought about 96 % of vertigo improvement.
54. CONCLUSIONS
Balance function depends on the integrity of vestibular, visual and
somatosensory systems.
Disorder of these system (s) leads to dizziness, which includes 4 types:
Vestibular Vertigo, Nonvestibular Vertigo, Presyncope, and Disequilibrium.
Treatment of vertigo includes etiologic, symptomatic, vestibular
rehabilitative therapies, dietary and life habit control, and conditioning
physical exercise.
Integrated Vestibular Therapy (IVT) proved to bring better resolution of
vertigo compared to single therapy