This document discusses the evaluation and management of coma. It begins by defining coma as prolonged unresponsiveness. It then describes the anatomy of arousal centered around the ascending reticular activating system. Assessment of coma involves the Glasgow Coma Scale and examining for signs of increased intracranial pressure. Common causes of coma include metabolic derangements, structural lesions of the brainstem or supratentorial regions. Management involves stabilizing ventilation, circulation, controlling seizures, reducing intracranial pressure and maintaining temperature. Detailed neurological examination can help localize lesions through assessment of reflexes, eye movements, respiratory patterns and posture.
Coma is defined and the anatomy of consciousness explained. The various levels of arousal, AVPU scale and Glasgow Coma Scale described. The differential diagnosis of coma discussed are coma with & without focal deficits and the meningitis syndrome.
The various aspects of history discussed in details. The examination part includes the general examination, Brainstem reflexes, motor functions with the signs of lateralisation and meningeal irritation signs.
The basic lab investigations, Imaging and special investigations like CSF examination, EEG discussed.
Elevated intracranial pressure and its management explained.
Coma is defined and the anatomy of consciousness explained. The various levels of arousal, AVPU scale and Glasgow Coma Scale described. The differential diagnosis of coma discussed are coma with & without focal deficits and the meningitis syndrome.
The various aspects of history discussed in details. The examination part includes the general examination, Brainstem reflexes, motor functions with the signs of lateralisation and meningeal irritation signs.
The basic lab investigations, Imaging and special investigations like CSF examination, EEG discussed.
Elevated intracranial pressure and its management explained.
Pediatric Coma
Introduction
Disorders of Consciousness
Coma Mimics
Etiologies
Evaluation
Brainstem Reflexes
Pediatric Glasgow Coma Scale
Management
Coma Sequelae
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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.
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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
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- Prix Galien International Awards Ceremony
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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.
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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.
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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.
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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
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
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neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
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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.
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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
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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
4. Really Simple Neuroanatomy
Arousal: where is it localized?
Ascending Reticular Activating System (ARAS) ‘core of the brainstem’
receives input from numerous somatic afferents
projects to midline thalamic nuclei (which are in a circuit with cortical structures)
and the limbic system
5. GLASGOW COMA SCALE
Eye opening Best Motor Response
4 – spontaneous 6 – obeys
3 - to speech 5 - localizes
2 - to pain 4 - withdraws
1 – none 3 – abnormal flexion
Verbal Response 2 – abnormal extension
5 – oriented 1 - none
4 - confused conversation
3 - inappropriate words
2 - incomprehensible sounds
1 - none
5
The sum obtained in this scale is used to the assess Coma and Impaired consciousness
Mild is 13 through 15 points Moderate is 9 to 12 points Severe 3 through 8 points
Patients with score less than 8 are in Coma
6. Coma - Aetiology
Metabolic:-
Ischemic hypoxic
Hypoglycaemic
Organ failure
Electrolyte disturbance
Toxic
Structural:-
Supratentorial bilateral
Unilateral large lesion with transtentorial
herniation
Infratentorial
8. Supra tentorial mass lesion
differential characteristics
Initiating signs usually of focal cerebral
dysfunction
Signs of dysfunction progress rostral to caudal
Neurologic signs at any given time point to
one anatomic area - diencephalon, midbrain,
brainstem
Motor signs are often asymmetrical
10. Infratentorial Mass Lesions
Differential Characteristics
History of preceding brainstem dysfunction or sudden onset of
coma
Localizing brainstem signs precede or accompany onset of
coma and always include oculovestibular abnormality
Cranial nerve palsies usually present
“Bizarre” respiratory patterns common, usually present at onset of
coma
Plum and Posner, 1982
11. Why coma management?
Common medical emergency 3-5%
Large proportion of comatose patient recover
Untreated coma may lead to further brain damage
12. Emergency treatment
Maintain ventilation oxygenation
Maintain circulation
Control seizure
Reduce icp
Maintain temperature
Control hypoglycemia
13. Maintain ventilation
Insert oral airway
Clean oropharyngeal secretion
Insert cuffed endotracheal tube if apnea, hypoventilation or liable to
aspirate
Mechanical ventilation if apnea or raised intracranial pressure
14. Maintain circulation
If hypotenstion ( <90mmHg systolic)
Replace fluid:
Saline if hyperglycemia or suspected stroke, diabetes
Dextrose saline or isolyte if undiagnosed
Vasopressor if low systolic pressure inspite of fluid
Hypertension: Betablocker, Nitroglycerine or Nitropruside
18. HISTORY
Inquire about-
i. History of diabetes
ii. Hypertension
iii. Head injury
iv. Convulsions
v. Alcohol or drug use
vi. Circumstances in which patient was found
vii. Medications in hospitalized patient like anesthetics, sedatives,
antiepileptic, opiates, antidepressants, antipsychotics.
18
19. GENERAL EXAMINATION
1. SIGNS OF TRAUMA- a) Racoon eyes
b) Battle`s sign
c) CSF rhinorrhea or otorrhea
2. BLOOD PRESSURE- Hypertension suggests-
a) Hypertensive encephalopathy
b) Intracerebral haemorrhage
Hypotension suggests-a) Myocardial infarction
b) Septicemia
c) Addison disease
d) Alcohol or barbiturate intoxication
e) Internal haemorrhage.
19
20. 3. PULSE- Bradycardia with periodic breathing and hypertension (CUSHING REFLEX) suggests
raised ICP.
4. TEMPERATURE- Hypothermia suggests-
a) Alcohol or barbiturate intoxication
b) Myxedema
c) Advanced tubercular meningitis
d) Peripheral circulatory failure
Hyperthemia suggests- a) Systemic infection
b) Meningoencephalitis
c) Heat stroke
d) Anticholinergic drugs abuse
20
21. 5. SIGNS OF MENINGEAL IRRITATION-
a) Meningitis
b) SAH
6. FUNDUS- a) Raised ICP (Papilledema)
b) SAH ( retinal haemorrhages,disc swelling)
c) Hypertensive encephalopathy
7. SKIN INSPECTION- a) Rash suggests menigococcemia, staphylocoocal
endocarditis, typhus, RMSF
b) Excessive sweating suggest hypoglycemia or shock
c) Diffuse petechiae suggest TTP, DIC, fat embolism
21
22. NEUROLOGICAL ASSESMENT
Observation first without examiner intervention.
Simply watch posture of limbs and body, position of head and eyes, presence
or absence of spontaneous movements on one side, rate and depth of
respiration.
Yawning and spontaneous shifting of body position indicates minimal degree
of unresponsiveness.
Multifocal myoclonus almost always indicate metabolic disorder.
Assess responsiveness by noting patient`s reaction to calling his name, or to
noxious stimuli such as supraorbital or sternal pressure.
Glasgow coma scale allows rapid assessment and allows to track neurological
changes over time.
22
23. POSTURE IN COMATOSE PATIENT
Decerebrate rigidity: consists of opisthotonus, clenching of jaws, stiff
extension of limbs with internal rotation of arms & plantar flexion of feet.
Precise correlation between extensor posturing & level of lesion is rarely
possible because extensor posturing arises in variety of settings: midbrain
compression, cerebellar lesions, metabolic, drug intoxication etc.
Decorticate rigidity: arms in flexion and adduction and legs extended
signify lesion rostral to midbrain.
Extensor posture of arms with weak flexor responses of legs is seen with
lesions at level of vestibular nuclei (medulla)
23
26. AS A RULE, WHEN THESE BRAINSTEM ACTIVITIES ARE PRESERVED,
PARTICULARLY THE PUPIL REACTIONS AND EYE MOVEMENTS, COMA MUST BE
ASCRIBED TO BILATERAL HEMISPHERAL DISEASE. THE CONVERSE, HOWEVER,
IS NOT ALWAYS TRUE, AS A MASS IN THE HEMISPHERES MAY BE THE
UNDERLYING CAUSE OF COMA BUT NONETHELESS PRODUCE BRAINSTEM
SIGNS BY INDUCING TRANSTENTORIAL HERNIATION.
26
27. PUPILLARY REACTIONS
Symmetrically reactive round pupils: Exclude midbrain damage.
Enlarged and unreactive pupil (>5 mm): Intrinsic midbrain lesion (ipsilateral) or
by ipsilateral mass.
Oval and slightly eccentric pupils: Early midbrain or third nerve compression.
Bilateral dilated and unreactive pupils: Severe midbrain damage by
transtentorial herniation or anticholinergic drugs toxicity (atropine, TCA).
Reactive bilaterally small but not pin point (1-2.5 mm): Metabolic
encephalopathies or thalamic haemorrhages.
Very small but reactive pupil (less than 1 mm) : Opioid or barbtiturate
overdose or bilateral pontine haemorrhage.
27
28. EYE MOVEMENTS
In light coma of metabolic origin, eyes rove conjugately from side to side in
random fashion. These movements disappear as coma deepens.
Adducted eye at rest: 6th nerve palsy. If it is bilateral it is due to raised ICT.
Abducted eye at rest: 3rd nerve palsy.
Downward and inward deviation of eyes: Lesions of thalamus and upper
midbrain.
Eyes turn toward convulsing side in focal seizures.
28
29. OCULAR BOBBING: Brisk downward and slow upward movements of the
eyes associated with loss of horizontal eye movements is diagnostic of
lesions in midbrain and pons.
OCULAR DIPPING: Slow downward followed by faster upward movement
in patients with normal horizontal gaze and it indicates diffuse cortical
anoxic damage and drug intoxication.
29
30. OCULO-CEPHALIC REFLEX
Also called Doll`s-eye movement.
Elicited by briskly turning or tilting the head.
Response in coma of metabolic origin or that due to bihemispheral structural
lesions consist of conjugate movements of eyes in the opposite direction.
Positive response indicates-
i. Oculomotor, abducent, midbrain and pons are intact.
ii. There is loss of cortical inhibition on brainstem that normally holds these
movements in check.
Absent reflex indicates damage within brainstem but also can be due to
profound overdose of sedatives or anticonvulsants.
30
31. RESPIRATORY PATTERNS
Slow, shallow, regular breathing: metabolic or drug depression.
Cheyne-Stokes respiration: Massive supratentorial lesions, B/L
cerebral lesions & mild metabolic disturbance.
Central neurogenic hyperventilation: Lesions of lower midbrain &
upper pons either primary or secondary to transtentorial herniation.
Apneustic breathing: Lower pontine lesions.
Biot`s or ataxic breathing: Lesions of dorsomedial part of medulla.
Agonal gasps: B/L lower brainstem damage & terminal respiratory
pattern.
31
32. PATHOLOGICAL ANATOMY OF COMA
Only if cerebral lesions are bilateral and extensive, then consciousness will
be impaired.
Unilateral mass lesions like infarct or hemorrhage if are causing coma, it
means compression of midbrain and subthalamic region of RAS has
occurred.
Either lateral displacement or herniation of temporal lobe can cause their
compression.
Even small lesions in upper brainstem and thalamus are sufficient to cause
coma.
32
33. Onset of coma-
i. Sudden onset- vascular origin especially brainstem stoke or SAH.
ii. Rapid progression from hemispheric signs to coma- intracerebral
haemorrhage.
iii. Protracted course- tumor, abscess, chronic SDH.
iv. Coma preceded by confusional or agitated state & without lateralizing signs-
metabolic cause.
v. REMEMBER FRONTAL AND OCCIPITAL HEMORRHAGES ARE LESS LIKELY TO
DISPLACE DEEP STRUCTURES AND TO CAUSE COMA THAN ARE CLOTS OF
EQUIVALENT SIZE IN THE PARIETAL OR TEMPORAL LOBES
33
34. LABORATORY STUDIES AND IMAGING
Complete blood count
Random blood sugar
RFT, LFT
Serum electrolytes
Urine examination for specific gravity, glucose, acetone & protein content.
ABG analysis
Chest X-Ray
ECG
CT or MRI Scan
Lumbar Puncture
EEG
34
35. TAKE HOME MESSAGE
Remember clinical analysis of comatose patient is urgency.
Evaluate for airway, breathing & circulation.
History & systematic general and neurological assessment will help a lot.
Presence or absence of brainstem reflexes helps to localize the lesion.
Evaluate for imminent herniation.
Implement rapid & systematic investigation and take prompt therapeutic
action.
35