Peripheral neuropathy can be caused by damage to peripheral nerves outside of the brain and spinal cord. Symptoms may include numbness, tingling, pain or weakness in the hands, feet, arms and legs. Peripheral neuropathy has many potential causes including diabetes, nutritional deficiencies, toxins, infections and autoimmune disorders. Evaluation may involve neurological exams, nerve conduction studies and biopsies. Treatment depends on the underlying cause but aims to relieve symptoms and prevent further nerve damage when possible.
Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health, depending on the type of nerve affected
Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health, depending on the type of nerve affected
By the end of this presentation, learners will be able to:
Develop and refine a differential diagnosis for peripheral neuropathy.
Discuss the workup for common & typical cases.
Perform a comprehensive diabetic foot exam by ADA/NDEP standards.
Treat painful peripheral neuropathy.
By the end of this presentation, learners will be able to:
Develop and refine a differential diagnosis for peripheral neuropathy.
Discuss the workup for common & typical cases.
Perform a comprehensive diabetic foot exam by ADA/NDEP standards.
Treat painful peripheral neuropathy.
Guillain-Barré syndrome (GBS) can be described as a collection of clinical syndromes that manifests as an acute inflammatory polyradiculoneuropathy with resultant weakness and diminished reflexes.
Although the classic description of GBS is that of a demyelinating neuropathy with ascending weakness, many clinical variants have been well documented in the medical literature.
"Demystifying Common Neurological Disorders: A Primer for Future Healthcare Professionals with Dr. Ganesh"
🌐 Greetings, aspiring healthcare professionals! I'm Dr. Ganesh, and today, we're embarking on an educational journey tailored for undergraduate students in medicine, nursing, and pharmaceutical sciences. We'll be demystifying some of the common neurological disorders, laying the groundwork for your future careers in healthcare.
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.
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- 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
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.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
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
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.
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
9. Peripheral neuropathy is caused by damage to your
peripheral nerves. Peripheral nerves are nerves that
are not located in the brain or spinal cord. They are
found throughout your body and help you feel
things. They also control the function of your organs.
The damage is usually to nerves in the hands, feet,
arms, and legs.
11. Peripheral neuropathy may be classified in a varieties of
ways-
according to the
1.number of nerves affected
Mononeuropathy
Mononeuritis multiplex
Polyneuropathy
2.the type of nerve cell affected
motor
sensory
autonomic
12. Mononeuropathy means a process affecting a single
nerve.
Mononeuritis multiplex (multiple mononeuropathy
and/or multifocal neuropathy) affects several or
multiple nerves.
Polyneuropathy describes diffuse, symmetrical
disease, usually commencing peripherally.
13. The course may be
- acute, chronic, static, progressive,
relapsing or towards recovery.
Polyneuropathies are motor, sensory,
sensorimotor and autonomic.
21. Exact cause is unknown
Theories behind Neuropathy
High Glucose Concentration
Chemical changes in nerves
Damaged blood vessels
Genetic Disposition
22. Depends on part of body being affected.
Diffuse Peripheral
Pain
Numbness and tingling in the limbs
Sensitivity to touch
More susceptible to feet injury and infections
Loss of Balance and Control
Loss of sensation
Diffuse Autonomic
Bladder infections
Stomach disorders
dizziness
23. Localized neuropathy
Pain in front of thigh, lower back, chest stomach and behind
eyes
Double vision
Paralysis of one side of the face
24. Based upon symptoms
Pain Assessment
Screening Test for lost sensation
Nerve Conduction Study
Electromyography
Ultrasound
Nerve Biopsy (extreme cases)
25. Treat symptoms and not neuropathy
Manage your glucose levels
Drug Therapy can be used but is not suggested
Pain Medication
Early treatment more successful and reversing
damage. Later stages of neuropathy irreversible
26. the peripheral nerves have been damaged by too
much alcohol use. The peripheral nerves transmit
signals between the body, the spinal cord, and the
brain.
Thiamine, folate, niacin, vitamins B6 and B12, and
vitamin E are all needed for proper nerve function.
Drinking too much can alter levels of these nutrients
and affect the spread of alcoholic neuropathy.
Fortunately, abstaining from alcohol can help restore
your nutritional health.
27. Alcoholic neuropathy can affect both movement and
sensation. Symptoms range from slight discomfort to major
disability. Although the condition is not life threatening, it
can decrease your quality of life. Some areas of the body
affected by alcoholic neuropathy include:
numbness
tingling and burning
prickly sensations
muscle spasms and cramps
muscle weakness and atrophy
28. Alcoholic neuropathy is the result of damage to these
nerves. The damage may be the direct result of long
periods where you drank too much alcohol.
Nutritional problems linked to alcohol use, such as
vitamin deficiency, can also cause nerve damage.
29. nerve biopsy
nerve conduction tests
upper GI and small bowel series
neurological examination
electromyography
esophagogastroduodenoscopy (EGD)
kidney, thyroid, and liver function tests
complete blood count (CBC)
30. vitamin supplements to improve nerve health (folate,
thiamine, niacin, and vitamins B6, B12, and E)
prescription pain relievers (tricyclic antidepressants and
anticonvulsants)
medication for people with problems urinating
physical therapy to help with muscle atrophy
orthopedic appliances to stabilize extremities
safety gear, such as stabilizing footwear, to prevent
injuries
special stockings for your legs to prevent dizziness
31. Disorders of peripheral nerves are the most common
neurological complications of systemic amyloidosis;
an illness where a protein called amyloid is deposited
in tissues and organs. Amyloidosis can affect
peripheral sensory, motor or autonomic nerves and
deposition of amyloid lead to degeneration and
dysfunction in these nerves.
32. The typical symptoms of amyloid neuropathy are due
to sensory and autonomic dysfunction. Patients may
experience painful paresthesias (unusual sensations),
numbness and balance difficulties due to sensory
dysfunction and persistent nausea, vomiting,
diarrhea, constipation, incontinence, sweating
abnormalities or sexual dysfunction due to autonomic
nerve involvement.
33. Diagnosis of amyloid neuropathies is based on
history, clinical examination and supporting
laboratory investigations. These include
electromyography with nerve conduction studies,
skin biopsies to evaluate cutaneous nerve innervation,
and nerve and muscle biopsies for histopathological
evaluation. In cases of familial amyloidosis, genetic
testing in the blood may be useful.
34. Treatment of amyloid neuropathies is directed at both
preventing further deposition of amyloid in
peripheral nerves and treating painful symptoms.
Depending on the type of amyloid protein, patients
may benefit from liver or bone marrow transplant.
Neuropathic pain due to amyloid neuropathy can be
treated with anti-seizure medications,
antidepressants, or analgesics including opiate drugs.
In severe painful conditions patients may be referred
to the Blaustein Chronic Pain Clinic for a
multidisciplinary approach to pain management.
35.
36. Most common type ---
Acute inflammatory demyelinating polyneuropathy
(AIDP)
Symptoms and Signs
Muscles weakness – facial and orophyrengial
cardiac arrhythmias, GI stasis, urinary retention, and
pupillary changes. An unusual variant (Fisher variant)
may cause only ophthalmoparesis, ataxia, and areflexia.
45. Mycobacterium leprae – coolest tissue in the body
Tuberculoid (high-resistance) leprosy – single patch of
hypoesthesia or anesthetic skin in any location
Lepromatous (low resistance) leprosy – numerous bacilli, wide
spread skin thickening, cutaneous anesthesia, anhydrosis
sparing axilla, groin and skin beneath the scalp hair
46. Nerve root disorders result in segmental radicular
deficits (eg, pain or paresthesias in a dermatomal
distribution, weakness of muscles innervated by the
root). Diagnosis may require neuroimaging,
electrodiagnostic testing, and systemic testing for
underlying disorders. Treatment depends on the cause
but includes symptomatic relief with NSAIDs, other
analgesics, and corticosteroids.
71. Axillary lesion : weak triceps and radial innervated m.
Mid-upper arm lesion : ‘Saturday night palsy’ (spiral
groove or intermuscular septum) : wrist drop, normal
triceps, variable motor and sensory deficit
Posterior interosseous : weak extensor of thumb and
other fingers, no sensory loss
Superficial radial n. : terminal cutaneous br.
76. Femoral nerve (L2,3,4)
• Mix sensorimotor
• Quadriceps femoris or knee
extensor
• Weakness of hip flexor in
intraabdominal lesion
• Sensory deficit over
anteromedial aspect of thigh
and perhaps leg
• Absent or diminished knee
jerk
79. Composed of 2 main nerves of leg : common peroneal
and tibial nerve
Paralysis of all muscles below knee plus hamstrings
and for high lesion, external rotators of thigh
Sensory loss below knee except anteromedial aspect
of leg and foot
80. Common peroneal nerve
• Foot-drop
• Paralysis of anterior and
lateral compartment of leg
• Sensory loss over dorsum
of foot and toes and
anterolateral aspect of leg
83. Medial division of sciatic nerve
Lesions at ankle
Tarsal tunnel syndrome
Pain and paresthesia in sole
Paralysis of intrinsic muscles of foot
Tenderness of Tinel’s sign at flexor retinaculum
Sural nerve compression syndrome
Pure sensory
Numbness on lateral aspect of foot
87. Clinical features :
postauricular pain (few days)
lower motor neuron facial weakness
impaired taste
hyperacusis
88.
89. Bell’s palsy : idiopathic, HSV 1
Ramsay Hunt syndrome : external ear pain with presence of
herpes zoster vesicles in auditory canal and pinna, VZV
Trauma : blunt impact to temporal bone
Middle ear infection : otitis media (infrequent in ATB era),
mastoid pain persist after acute infection resolved
Neoplasm : rarely compressed by CPA tumor but due to
surgery for tumor removal
90. Management
Reassurance – not a stroke
Short course of prednisolone 60 mg/day
Prognosis :
complete recovery 75%
satisfactory 15%
poor function 10%