Qs for med students
Lecture three - Microbiology
Done By : Baylsan Bataineh
PNS Microbiology
1. Clostridium tetani (Tetanus)
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Epidemiology
• Decreased incidence due to vaccination (Booster required every 10 years)
• Risk factors: Injuries (e.g., rusty nail) , Lack of vaccination , Elderly (>65 years) → waning immunity
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General Features
• Gram +ve, obligate anaerobic, spore-forming bacillus. Produces:Tetanospasmin (main toxin) , Tetanolysin
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Pathogenesis
• Spores enter through ( wounds , accidental puncture wounds , burns , umbilical stumps , frostbite & crushed
body parts ) → germinate.
• Tetanospasmin: Travels via retrograde transport to CNS. Blocks release of GABA & glycine from
inhibitory neurons (Renshaw cells).
• Result → loss of inhibition → muscle overactivity ( increased muscle tone ) & hypersympathetic state
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Clinical Manifestations
• Types: Generalized (most severe) , Localized , Cephalic & Neonatal
• Features of Generalized type : Trismus (lockjaw, masseter rigidity) , Risus sardonicus (increased tone in
the orbicularis oris ) & Opisthotonos (arched back)
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Diagnosis : Clinical (history + exam) , Culture is difficult and not useful.
Complications : Death mainly due to respiratory muscle paralysis.
Treatment : Antitoxin / Antibiotics: Penicillin
Prevention : Tetanus toxoid vaccine every 10 years.
2. Clostridium botulinum (Botulism)
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Gram-positive, strict anaerobic, spore-forming bacillus. Produces 7 toxins (A–G).
Most lethal food poisoning (mortality 12–20%).
Types of Botulism : Foodborne , Infant , Wound , Iatrogenic & Inhalational / undetermined
Epidemiology
• Foodborne → canned/fermented foods ( pickles, kimchi )
• Infant → honey ingestion ( ‫ )العسل أصال ممنوع للي عمرهم تحت السنة‬, or through placenta
• Wound → injection drug use of black tar heroin
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Qs for med students
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Pathogenesis : Toxin fills up the presynaptic cleft → blocks acetylcholine release at neuromuscular junction.
Botulinum toxin : Descending flaccid paralysis , absorbed in (GI , blood & Neuromuscular synapse)
Symptoms (4D’s) :
• Diplopia : double or blurred vision
• Dysphagia : difficulty swallowing
• Dysphonia : difficulty voice production
• Dysarthria : speech articulation
• Neuromuscular symptoms
• Respiratory paralysis
• No fever : because Neuromuscular junction has a low density of immune cells ( ‫ما في إشارات كافية انه يصير‬
‫)رد فعل مناعي‬
➢ Infant Botulism:
• Ingestion of food (honey or corn syrup) which contaminated with spores
• Constipation
• Difficulty swallowing
• Muscle Weakness Floppy baby syndrome
➢ Wound Botulism ( puncture wounds deep ) : Fever (from wound inflammation) & ↑ WBC
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Diagnosis
• Clinical presentation (bilateral cranial neuropathies + descending paralysis).
• Toxin detection in: Serum , Leftover Food , brain scan , spinal fluid examination & nerve conduction test
• Culture → difficult (anaerobic, low yield)
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Treatment
• Antitoxin
• Supportive care (mainstay)
• Infant: BabyBIG (immune globulin)
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Prevention : Proper food preparation , No vaccine available
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Same toxin used in:
o Botox (cosmetic use) ‫مع التقدم بالعمر والتعرض للشمس بقلل تجدد خاليا الجلد وبنفس الوقت العضالت في حالة انقباض مستمر‬
‫بيجي هون دور البوتوكس بحقنوه النه بعمل شلل مؤقت (كذا شهر) لعضالت الوجه مكان ما بنحقن‬
o Treats dystonia, achalasia, spasms
o Can be used as bioterrorism agent ( ‫)بستخدموه كسالح بيولوجي الصابة االفراد بالشلل‬
3. Listeria monocytogenes
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Gram-positive, non–spore forming rod
Intracellular organism
No complex nutritional requirements
Resistant to: Cold , Heat , pH extremes & Bile
Grows at 4°C (refrigerator)
Sources : Soil, animals ( dairy cattle , household pets )
Also present in Foods: Meats , Cold cuts (‫ )السنيورة والتيركي والمرتديال‬, Soft cheeses & Coleslaw
Killed by pasteurisation or cooking
High-Risk Groups : immunocompromised , Pregnant , Elderly , Neonates , fetuses (‫)بياخد العدوى من المشيمة‬
In LAB : Growth at 0–4°C , Tumbling motility (22–28°C) , It grows in Umbrella or mushroom fashion
Virulence Factor :
o Listeriolysin O (LLO) : Breaks phagosome , Allows escape into cytosol , Enables intracellular survival
Pathogenesis : Survives inside macrophages by: Preventing phagosome-lysosome fusion
-2-
Qs for med students
•
At risk
In Pregnant women, infection usually occurs in the 3rd trimester when cell-mediated immunity decreases Fever,
chills and headache in mother, organism can be recovered in the amniotic fluid, placenta.
‫ تنتقل هذه البكتيريا غالبًا‬.Listeria monocytogenes ‫ تكون الحامل أكثر عرضة لإلصابة ببكتيريا‬،‫ خاصة في المراحل المتقدمة‬،‫ خالل الحمل‬o
.‫صا األجبان غير المبسترة ومنتجات األلبان غير المعالجة حراريًا‬
ً ‫ خصو‬،‫ملوثة‬
ّ ‫عبر تناول أطعمة‬
.‫ لذلك يُنصح بتجنب هذه األطعمة أثناء الحمل وااللتزام باألغذية اآلمنة والمبسترة‬،‫ اإلصابة قد تكون خطيرة ألنها يمكن أن تؤثر على الجنين‬o
o Bacteria infect the fetus and 22% of cases result in neonatal death. (transmitted trans placentally)
o Neonatal meningitis can result about 2 weeks post partum.
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4. Leprosy (Mycobacterium leprae)
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Prefers cool temperatures
Affects: Skin , Mucous membranes & superficial nerves – “glove & stocking “ Loss of sensation
Cannot be grown in vitro
Transmission : Respiratory secretions , Skin lesions of patients
Reservoir : Armadillos (especially in U.S.)
Types of Leprosy :
1. Lepromatous Leprosy : Diffuse skin involvement , Leonine facies , High bacterial load ( communicable) ,
Low cell-mediated immunity with Strong Th2 response . More severe (can be fatal)
2. Tuberculoid Leprosy : hairless skin plaques , Low bacterial load . High cell-mediated immunity with
Strong Th1 response
•
Diagnosis : Skin/nerve biopsy (AFB + granuloma) , PCR
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Qs for med students
Lecture 4 - Microbiology
Done By : Baylsan Bataineh
Rabies & Arboviruses
1. Rabies
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is a zoonotic encephalitis caused by neurotropic viruses of the Lyssavirus genus , Rhabdoviridae family
Infection starts in the peripheral nervous system and then spreads to the central nervous system
Epidemiology
• One of the oldest diseases with the highest case-fatality rate.
• ~3.3 billion people live in endemic areas.
• ~25,000–159,000 deaths/year (WHO ~59,000).
• Mostly affects children <15 years.
• 99% of cases → due to rabid dog bites.
• Can be transmitted via tissue or organ transplantation.
• In developing areas where canine rabies remains common, most cases from dog bites
• National rabies → animals reservoirs (bats, raccoons, skunks, foxes).
Microbiology
• Bullet-shaped, single-stranded RNA virus ( order mononegavirales )
• Family: Rhabdoviridae, Genus: Lyssavirus.
• Has: Helical nucleocapsid , Lipoprotein envelope & Glycoprotein spikes (G protein) (absent at blunt end)
Pathogenesis
Initial infection:replicates locally to increases the viral load (inoculum) before entering the nervous system.
After sufficient replication, the virus enters peripheral nerves, (targets neurons with (ACh receptors))
Mechanism of neuronal entry: ‫مهم‬
1. Virus binds to ACh receptors.
2. Enters the neuron via receptor-mediated endocytosis (clathrin-coated pits).
3. Travels inside endosomes along microtubules toward the cell body (soma).
4. Endosomes naturally acidify, releasing the virus into the cytoplasm.
Negri Bodies ( Diagnostic feature)
• Found in: Hippocampal pyramidal cells , Cortex & Purkinje cells ( less frequently)
• Eosinophilic cytoplasmic inclusions containing viral nucleocapsids.
Spread of infection:
• Virus moves centrally to the CNS → causes severe disease.
• Then spreads back to peripheral tissues, especially: Salivary glands → high viral concentration in saliva.
Critical timing (VERY IMPORTANT):
• Before entering nerves: RIG (Rabies Immune Globulin) + vaccine → effective to prevent the spread
• After reaching peripheral nerves: Prevention becomes difficult
• After reaching CNS: Disease is almost always fatal
Qs for med students
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Virus stability: Inactivated by:
o pH < 3 or > 11
o UV light, sunlight
o Drying (desiccation)
o Chemicals (formalin, phenol, ether, trypsin, β-propiolactone) and many detergents
Paralytic Rabies
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characterized by ascending flaccid quadriparesis and coma
Affects spinal cord (mainly) , brain stem ( lesser extent)
Segmental Demyelination in peripheral nerves & resembles acute inflammatory polyneuropathy (GuillainBarré syndrome)
May cause: Myocarditis due to catecholamine storm (not direct viral damage).
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Diagnosis
• Clinical suspicion after animal bite ( fever, hydrophobia, aerophobia , agitation, autonomic overactivity
with hypersalivation , coma & paralysis)
• Lab methods:
o Direct immunofluorescence (skin biopsy)
o RT-PCR (saliva/skin)
o Detectiob of antivirus Antibodies (serum/CSF)
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Prevention
• Immediate: Wound cleaning , Rabies Immune Globulin (RIG) & Vaccine
• Given during incubation period (most critical point).
• Bat rabies causes the majority of human cases in the United States, and
postexposure prophylaxis depends on the type of exposure and
availability of the animal for rabies diagno
• Pre-exposure prophylaxis : For (Veterinarians , Lab workers & High-risk travelers)
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Therapy : No effective antiviral treatment
Death occurs within days to 2 weeks after symptoms
2. Arboviruses
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Transmitted by Mosquitoes, ticks, flies
~400 viruses (Include: Flaviviruses , Togaviruses & Some Bunyaviruses & Reoviruses)
Clinical Range : Mild fever → severe (Encephalitis , Hemorrhagic fever)
Zika Virus
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Flavivirus
Transmission: Mosquito (Aedes) , Sexual or via transfusion (vertical)
Clinical
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Mild fever
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Complications
1.
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Conjunctivitis
Congenital microcephaly
Diagnosis : RT-PCR , Serology
Treatment : Supportive only , no defintive treatment
2.
Miscarriage
Itchy rash (20%)
Qs for med students
SARS-CoV-2
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RNA Beta-coronavirus
Targets: intrapulmonary epithelial cells
Uses: ACE2 receptor
Origin not known from bats in Wuhan china ‫الصينيين يلي ضاقت فيهم الدنيا وراحوا اكلوا خفافيش‬
Pathophysiology Stages : ‫مش مهم‬
1. Early infection
2. Pulmonary phase → hypoxia, ARDS
3. Hyperinflammatory phase → DIC / Myocarditis / Multi-organ failure
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Transmission : Mainly respiratory droplets
High infectivity in: Presymptomatic phase
Neurological Effect : Brain fog: Memory problems , Poor concentration
PPE for Healthcare Workers ‫اهم شي تعرفوا انه الزم نحمي يلي بشتغلوا بالقطاع الصحي وبتعرضوا للمصابين‬
• Hand hygiene
• PPE: Gown , Gloves , Eye protection & Mask (N95 if aerosol)
• Documentation required
• Chlorine-based disinfection
Covid-19
‫ركزوا ع يلي عليهم مربعات احمر‬
Anatomy | ‫تشريح‬
Lecture 21
Nervous System
Done By :
Ayham abo al heja
Smell & Taste
#Olfaction:
• Olfaction (the sense of smell) is mediated by the olfactory nerve (cranial nerve I), the first of the twelve
cranial nerves. It is a purely special sensory nerve, transmitting olfactory information from the nasal cavity to
the brain.
• The perception of odor requires volatile odorant molecules to reach the olfactory mucosa, which is located in
the superior part of the nasal cavity, covering the superior nasal concha, the upper nasal septum, and the roof
of the nasal cavity. Efficient odor detection depends on a specialized pattern of nasal airflow that carries
odorant molecules toward this olfactory region.
# Olfactory Pathway Components
◼ Olfactory receptor cells → located in the olfactory epithelium
◼ Olfactory nerves
◼ Olfactory bulb
◼ Olfactory tract
◼ Olfactory striae (medial and lateral)
◼ Olfactory cortex (including the piriform cortex and related regions)
◼ Output targets of the olfactory cortex (e.g., limbic system and orbitofrontal cortex)
Airflow Distribution in the Nasal Cavity
• Airflow within the nasal cavity is not evenly distributed:
• Approximately 50% of inhaled air passes through the middle meatus
• About 35% passes through the inferior meatus
• Only 15% of total airflow passes through the olfactory region
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Nasal Mucosa:
◼ The nasal mucosa is divided into two main regions: the respiratory mucosa and the olfactory mucosa, each
with distinct structure and functions.
◼ Respiratory epithelium:
◼ It is thick, ciliated highly vascular and contains mucous glands & goblet cells
◼ It lines the lower part of the nasal cavity (from skin of vestibule to the superior concha)
Respiratory epithelium:
• This epithelium plays an essential role in conditioning inspired air through three main processes:
• Humidification: The air is moistened by secretions from mucous and seromucous glands as well as goblet
cells.
• Filtration: Dust particles and microorganisms are trapped in mucus and transported toward the nasopharynx
by the coordinated beating of ciliary action.
• Warming: Inspired air is warmed by an extensive submucosal vascular plexus within the lamina propria.
➢These mechanisms help protect the lower respiratory tract by ensuring that inhaled air is clean, moist, and
close to body temperature
Olfactory epithelium:
➢ The olfactory epithelium is a specialized neuroepithelium responsible for detecting odorants. It contains
olfactory receptor neurons, which are primary sensory (first-order) neurons.
➢ This epithelium is located in the upper part of the nasal cavity,
including:
• The roof of the nasal cavity
• The upper part of the nasal septum (medial wall)
• The superior nasal concha and adjacent sphenoethmoidal recess on the lateral wall
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Olfactory Mucosa and Receptor Cells
• The olfactory mucosa contains olfactory receptor neurons, s upporting (sustentacular) cells, and basal stem cells.
• Olfactory receptor neurons are bipolar neurons, meaning they have two projections from the cell body:
• Dendritic process: Extends to the epithelial surface and forms an olfactory knob, from which 10–30 nonmotile cilia project into the mucus layer covering the epithelium. Odorant molecules dissolve in this mucus and
interact with receptors on these cilia.
• Axonal process: A thin unmyelinated axon that passes through the cribriform plate of the ethmoid bone to
synapse in the olfactory bulb
Olfactory Mucosa:
➢ A distinctive feature of the olfactory system is its ability to regenerate neurons. Olfactory receptor neurons
typically have a lifespan of approximately 30–60 days. Basal stem cells within the olfactory epithelium
differentiate into new receptor neurons to replace damaged or aging cells
➢ However, with advancing age, the efficiency of neuronal regeneration may decline, and cumulative damage
can lead to a gradual reduction in the sense of smell (age-related hyposmia)
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Olfactory Nerve Stimulation
➢ Olfactory receptors can be stimulated through two main airflow pathways: orthonasal and retronasal
olfaction
◼ Orthonasal airflow: This occurs during inhalation through the nostrils, when air carrying odorant molecules
moves from the anterior nares toward the olfactory epithelium located in the superior part of the nasal cavity.
◼This pathway is primarily responsible for the perception of environmental odors.
◼ Retronasal airflow: This occurs mainly during eating and drinking, when volatile odorant molecules released
from food in the oral cavity travel through the nasopharynx to the nasal cavity, reaching the olfactory
epithelium. Retronasal olfaction contributes significantly to the perception of flavor, integrating smell with
taste.
Olfactory Nerve (Cranial Nerve I)
• Each olfactory receptor cell is a bipolar neuron that has an axon extending from its basal surface.
• As these axons leave the receptor cells, they join with axons from other receptor neurons, forming small
bundles of nerve fibers called olfactory nerve rootlets. Collectively, these bundles form the olfactory nerve
(cranial nerve I).
• The olfactory nerve fibers pass superiorly through 15–20 small foramina in the cribriform plate of the
ethmoid bone to reach the cranial cavity. These nerve bundles are surrounded by meningeal coverings (pia,
arachnoid, and dura mater) as they pass through the skull.
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Olfactory Bulb
• Each olfactory bulb lies on the inferior surface of the frontal lobe, lateral to the crista galli and superior to the
cribriform plate of the ethmoid bone.
• The olfactory bulb is an ovoid structure that contains several types of neurons, the most important being the
mitral cells, which act as second- order relay neuron
• Inside the bulb are specialized structures called glomeruli. In these glomeruli, axons of olfactory receptor
neurons synapse with the dendrites of mitral cells and tufted cell
◼ The olfactory bulb is highly organized and contains several layers:
1. Glomerular layer
2. External plexiform layer
3. Mitral cell layer
4. Internal plexiform layer
5. Granular cell layer
Olfactory Tract and Olfactory Striae
•Initial processing of olfactory information occurs in the olfactory
bulb, which contains interneurons and mitral cells.
•The axons of mitral cells leave the olfactory bulb and form the olfactory tract
❑ The olfactory tract runs posteriorly along the inferior
surface of the frontal lobe in a groove called the olfactory sulcus.
❑ Near the optic chiasm, the olfactory tract divides into two main bundles called
olfactory striae:, the medial olfactory stria and the lateral olfactory stria
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Lateral Olfactory Stria
• Carries most olfactory fibers.
• Projects to the primary olfactory cortex, mainly the piriform cortex, uncus,and
adjacent parahippocampal (hippocampal) gyrus on the same side (ipsilateral).
• Responsible for conscious perception of smell
Medial Olfactory Stria
• Curves toward the midline.
• Some fibers cross to the contralateral olfactory bulb through the anterior commissure.
• Others project to parts of the limbic system.
• Plays a role in reflex, emotional, and instinctive responses to odors.
➢ The olfactory pathway is unique because primary olfactory signals reach the cerebral cortex without first
synapsing in the thalamus. However, secondary projections from the olfactory cortex later reach the thalamus,
which then relays information to the orbitofrontal cortex for odor identification.
Olfactory Cortex
◼ The olfactory cortex is not a single structure but a group of cortical areas that
receive direct input from the olfactory bulb. These areas are mainly located in
the medial temporal lobe.
• Major components include:
• Piriform Cortex
• Located near the lateral olfactory stria
• Considered the primary olfactory cortex
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• Amygdala
• Located anterior to the inferior horn of the lateral ventricle.
• Involved in emotional responses to odors, especially fear and aversion.
• Entorhinal Cortex
• Located in the anterior part of the parahippocampal gyrus.
• Plays an important role in memory formation and odor-associated memories
Functional Connections
• Olfactory signals are interpreted in the olfactory cortex, located mainly in the temporal lobe and the basal
part of the frontal lobe.
•From there, projections extend to:
•The limbic system → emotional responses to smells
•The hypothalamus → autonomic and instinctive reactions
•The orbitofrontal cortex → conscious identification and discrimination of odors
Sensory Adaptation
How long do you think sensory
adaptation occurs for the sense of smell?
Sensory Adaptation
Olfactory receptors undergo sensory adaptation RAPIDLY
◼Sense of smell drops by up to 50% within 5 seconds after stimulation
◼Within a minute the receptors may become insensitive to a given odor
Gustatory Pathway:
Taste Sensation - Gustation
• Gustation (taste) is considered one of the most primitive and evolutionarily
conserved sensory systems. It plays an important role in detecting nutrients and
protecting the body from harmful substances.
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• Traditionally, five primary taste modalities are recognized:
• Sweet
• Sour
• Salty
• Bitter
• Umami (savory taste associated with amino acids such as glutamate)
• Some researchers have proposed additional taste qualities, such as fatty taste
(oleogustus) and carbonation detection, but there is no full consensus that
these represent independent primary taste modalities
Biological and Evolutionary Role of Taste
Taste functions as an adaptive protective mechanism that helps organisms evaluate food before ingestion.
• Bitter tastes are often associated with potentially toxic substances found in plants.
• Sour tastes may indicate unripe or spoiled foods.
• Sweet tastes typically signal energy-rich nutrients such as sugars.
Thus, taste perception helps guide food selection and avoidance of harmful substances
Taste Perception Before Birth
• During fetal life, the fetus swallows amniotic fluid, which
contains various nutrients including:
• Glucose
• Fructose
• Fatty acids
• Amino acids
• Experimental studies have shown that:
• Adding glucose to amniotic fluid increases fetal swallowing and movement, indicating a positive taste
response.
• Introducing bitter substances reduces fetal swallowing, suggesting early aversive taste perception.
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• These observations indicate that gustatory sensory mechanisms are functional during prenatal development
and may influence early feeding behavior.
Taste buds
Taste buds
Circumvallate papillae
◼ These papillae lie in a V - shaped row immediately anterior to the sulcus terminalis
◼ The shape of the papillae resembles a (truncated cone ). The base that attaches onto the tongue is the
narrower end and the broader apex is coated with stratified squamous epithelium.
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Filiform Papillae
◼ These are the commonest papillae on the tongue, and cover the majority of the anterior two thirds
of the tongue.
◼ They are small and conical , and do not contain taste buds.
They comprise a core of irregular connective tissue, which is covered by a keratinized epithelium featuring
secondary processes, they are overlapped into a brush like dense layer of processes. For proper food grip and
handling in mouth.
Fungiform Papillae
◼ These are named fungiform as they resemble mushrooms.Lying at their core is connective tissue.
◼ They are located on the superior surface of the tongue, and are dotted around the surface. Lying on them
are numerous tastebuds that are able to discern sweetness, sourness, saltiness, bitterness and umami.
Foliate Papillae
◼ These are vertical, relatively short and lie on either side and back of the tongue.
◼ They can be located anterior to the palatoglossal arch. They are coated with non- keratinized epithelium and
hence are softer than other papillae. They have numerous taste buds .
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Peripheral Taste Pathways
◼ Lingual:
• Signals of first-order taste neurons travel are carried by three cranial nerves:
• Facial nerve (CN VII) – anterior 2/3 of the tongue
• Glossopharyngeal nerve (CN IX) – posterior 1/3
• Vagus nerve (CN X) – epiglottis, pharynx and most posterior epiglottis
Facial nerve:
◼ Taste sensations from the anterior two-thirds of the tongue and soft
palate reach the geniculate ganglion. From there, fibers travel via
the intermediate nerve to the pontomedullary junction, enter the
solitary tract, descend, and synapse in the solitary nucleus.
Glossopharyngeal and Vagus Nerves:
◼ Taste fibers from cranial nerves IX and X have their cell bodies in
the petrosal ganglion (IX) and the inferior ganglion (X),
respectively. These fibers enter the medulla, descend within the
solitary tract, and terminate in the adjacent solitary nucleus.
Cranial nerve
Tongue/oral Region
Gangilon
Facial nerve (CN VII)
Anterior 2/3 of the
tongue and soft plate
Geniculate ganglion
Posterior 1/3 of the
tongue
Petrosal ganglion
Glossopharyngeal nerve
(CN IX)
Pathway
Fibers travel via the
chorda tympani and
intermediate nerve,
enter the
pontomedullary
junction, join the
solitary tract,
descend, and
synapse in the
solitary nucleus.
Fibers enter the
medulla, descend
within the solitary
tract, and terminate
in the adjacent
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solitary nucleus.
Vagus nerve(CN X)
Epiglottis pharynx and
most posterior tongue
Inferior(nodose)ganglion
Fibers enter the
medulla, descend in
the solitary tract,
and synapse in the
solitary nucleus
Central Pathway
1. From the nucleus of the solitary tract (NST) in the medulla oblongata, taste signals are transmitted via
second-order neurons to the ventral posteromedial (VPM) nucleus of the thalamus.
2. Third-order neurons project from the VPM to the primary gustatory cortex, located in the insula and frontal
operculum, where conscious taste perception occurs
➢ The taste pathway is primarily ipsilateral, meaning that signals from one side of the tongue are processed
mostly on the same side of the brain
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Special senses – Vision
‫ ادرﺳﻮا ﻣﺤﺎﺿﺮة ال‬، ‫ ﻗﺒﻞ ﻣﺎ ﺗﺒﺪأوا ﺑﺎﻟﻤﺤﺎﺿﺮة‬: ‫ﻧﺼﯿﺤﺔ‬
‫ ﺑﺎﻻﻧﺎﺗﻮﻣﻲ‬The Eyeball and Optic Nerve
Introduction
✓ Vision is one of the most important special senses in humans and, along with audition, is the basis for
most human communication.
✓ Along with hearing considered a dominant sense , as it’s impairment significantly decreases the quality
of the life .
✓ The visual system detects and interprets electromagnetic waves between 400 and 750 nm long, which
constitutes visible light
✓ The eye can distinguish two aspects of light, its brightness (or luminance) and its wavelength (or
color).
✓ Light enters the eye and impinge on photoreceptors in a specialized sensory epithelium, the retina.
✓ The photoreceptors include rods and cones.
✓ Rods have high sensitivity ( even a single photon of light can activate them ) for detecting low light
‫ ﻣﮭﻢ‬intensities but do not provide well-defined visual images, nor do they contribute to color vision. Rods
operate best under conditions of reduced lighting (scotopic vision). Rods are responsible for dark
vision ‫ما تعطيني تفاصيل للرؤية‬
✓ Cones, by contrast, are not as sensitive to light as rods are and thus operate best under daylight
‫ ﻣﮭﻢ‬conditions (photopic vision). Cones are responsible for high visual acuity and color vision . Cones
produce high-resolution images
✓ Information processing within the retina is performed by retinal interneurons, and the output signals
are carried to the brain by the axons of retinal ganglion cell ( RGC).
✓ The axons travel in the optic nerves; there is a partial
crossing in the optic chiasm that results in all input from one
side of the visual space being directed to the opposite side of
the brain.
✓ Posterior to the optic chiasm, the axons of retinal ganglion cells pass
through the optic tracts and synapse in nuclei of the brain.
✓ The main visual pathway in humans is through the lateral
geniculate nucleus (LGN) of the thalamus.This nucleus
projects through the visual radiation to the visual cortex.
✓ Other visual pathways project to the superior colliculus, pretectum, and hypothalamus, and these
structures participate in orientation of the eyes, control of pupil size, and circadian rhythms,
respectively.
The Eye structure
‫ﻗﺮاءة‬
The wall of the eye is composed of three concentric layers:
1. The outer layer, or the fibrous coat, includes the transparent cornea, with its epithelium (the
conjunctiva), and the opaque sclera.
2. The middle layer, or vascular coat, includes the iris and the choroid.The iris contains both radially
and circularly oriented smooth muscle fibers, which make up the pupillary dilator and sphincter
muscles. The choroid is rich in blood vessels that support the outer layers of the retina, and it also
contains pigment.
3. The innermost layer of the eye is the retina, which is embryologically derived from the diencephalon
and is therefore part of the central nervous system (CNS).
✓ Light enters the eye through the cornea and passes through a series of transparent fluids.
✓ These fluids and structures consist of the cornea (major refractive area), aqueous humor, lens (can
‫ﻣﮭﻢ‬
change shape and vary its refractive power ,thus, the lens is responsible for adjusting the optical
focus of the eye), and vitreous humor.
✓ Aqueous humor pressure, which is normally less than 22 mm Hg, determines the pressure within the
eye.
✓ The vitreous humor is a gel composed of extracellular fluid that contains collagen and hyaluronic acid.
-
The vitreous humor is responsible for maintaining the stability of the shape of the eye
Muscular control of the eye
A number of functions of the eyes are under muscular control.
1. Externally attached extraocular muscles ( aim the eyes toward an
appropriate visual target and are innervated bythe [CN]III),(CNIV),and
(CNVI)nerves.
2. The muscles in the ciliary body (secretes aqueous humor) control
lens shape and thereby the focus of images on the retina.
3. The pupillary dilator and sphincter muscles allow the iris to control
the amount of light entering the eye, similar to the diaphragm of a camera.The dilator is activated by
the sympathetic nervous system (Mydriasis), whereas the sphincter and ciliary muscles are controlled
by the parasympathetic nervous system (Miosis) (through CN III)
4. Suspensory ligaments (or zonule fibers), which attach to the wall of the eye at the ciliary body, hold the
lens in place.
‫ﻣﮭﻢ‬
When the muscles in the ciliary body are relaxed, the tension exerted by the suspensory ligaments flattens the
lens (less convex) (distant objects). When the ciliary muscles contract, the tension on the suspensory
ligaments is reduced; this process allows the somewhat elastic lens to assume a more spherical shape (near
objects) .
Eye protection
1. The eye is well protected from injury by the bony walls of the orbit.
2. The cornea is moistened and kept clear by tears that pass from the lacrimal gland
3. Blinking helps keep the cornea moist (Renewing of the tear film, Mechanical protection)
Accomodation
✓ A process by which the refractive power of the eye changes
to focus objects at different distances on the Retina.
✓ It is done by changing the curvature of the lens
‫ﻣﮭﻢ‬
Far ( distant ) objects
Near objects
Lens shape
Less convex
More convex (more spherical)
ciliary body
Relaxed
Contracted
suspensory ligaments
Contracted
Relaxed
✓ It depends on the action of the ciliary body and the suspensory ligaments
Retina
✓ The 10 layers of the retina. It’s the neural part of the eye
✓ The retina begins with the pigmented epithelium (layer 1), which is just inside the choroid.
✓ the pigmented epithelium main functions are:
1) provide nutrients and remove waste from the photoreceptors;
2) Phagocytosis
3) Regeneration of visual pigments
- Photoreceptors , Bipolar cells , Horizontal cells (Inhibitory) , Amacrine cells ( Inhibitory) ,
Retinal Ganglion cells
Rods and Cones
‫ﻣﮭﻢ‬
✓ rods and cones synapse on bipolar cells, which synapse on the ganglion cells.
1.Few cones synapse on a single bipolar cell, which synapses on a single ganglion cell. This arrangement is the
basis for the high acuity and low sensitivity of the cones. In the fovea, where acuity is highest, the ratio of
cones to bipolar cells is 1:1.
2. Many rods synapse on a single bipolar cell. As a result, there is less acuity in the rods than in the cones.
There is also greater sensitivity in the rods because light striking any one of the rods will activate the bipolar
cell.
Responsible for low visual acuity: rods. / Responsible for high sensitivity to light: rods
Horizontal and amacrine cells form local circuits with the bipolar cells. ( usually are inhibitory )
Pigments in the photoreceptors
✓ The pigment found in the of rods is rhodopsin. Rhodopsin is comprised of retinal, an aldehyde of
vitamin A, and a protein called opsin (Absorb at 500 nm)
✓ Rods: Rhodopsin (purple pigment) → vision in dim light → no color vision.
✓ Cones: Photopsins → responsible for color vision
✓ Three variants of visual pigment (each contains retinal and an opsin) are found in cones, and these cone
pigments absorb best at 437 nm (blue), 533 nm (green), or 564 nm (red).
✓ A few retinal ganglion cells contain melanopsin rather than rhodopsin or cone pigments.The axons of
these neurons project to the suprachiasmatic nuclei of the hypothalamus
✓ These signals are then relayed to the pineal gland to help regulate the circadian rhythm
✓ Rhodopsin is formed when a retinal isomer, 11- cis retinal, is combined with a glycoprotein opsin.
✓ When rhodopsin absorbs light, it is "boosted" to a higher energy state.This boost causes a series of
‫ﻣﮭﻢ‬
chemical changes that lead to isomerization of 11-cis retinal to all-trans retinal.
✓ Separation of all-trans retinal from opsin causes bleaching of the visual pigment
Steps of photoreception in the rods
✓ Photoreceptors are partially depolarized when they are inactive (in the dark). This is opposite to most
sensory receptors, where activation usually causes depolarization
✓ In darkness, photoreceptors are slightly depolarized (around -40 mV) because cGMP-gated Na+
‫ﻣﮭﻢ‬
channels in their outer segments are open, thereby increasing the membrane potential toward the Na+
1.
2.
3.
4.
5.
equilibrium potential.This net influx of Na+ results in a continuous current,
called the dark current ( partially depolarised >> inactive )
Light on the retina converts 11-cis retinal to all- trans retinal, a process
called photoisomerization.
- A series of intermediates is then formed, one of which is
metarhodopsin II.
- Vitamin A is necessary for the regeneration of 11-cis rhodopsin.
Deficiency of vitamin A causes night blindness.
Metarhodopsin II activates a G protein called transducin (Gt), which in turn
activates a cyclic guanosine monophosphate phosphodiesterase.
Phosphodiesterase catalyzes the conversion of cyclic guanosine
monophosphate (cGMP) to 5′-GMP, and cGMP levels decrease.
Decreased levels of cGMP cause closure of Na+ channels, decreased inward
Na+ current, and, as a result, hyperpolarization of the photoreceptor cell
membrane. Increasing light intensity increases the degree of
hyperpolarization.
When the photoreceptor is hyperpolarized, there is decreased release of the excitatory transmitter
glutamate.There are two types of glutamate receptors on bipolar and horizontal cells, which determine
whether the cell is excited or inhibited.
✓ What is different in vision compared with other sensory systems is the action of photoreceptors.
Photoreceptors are activated by hyperpolarization rather than depolarization
✓ Ionotropic glutamate receptors are excitatory. If decreased release of glutamate from the
photoreceptors interacts with ionotropic receptors, there will be hyperpolarization (inhibition) because
there is decreased excitation.
✓ Metabotropic glutamate receptors are inhibitory. If decreased release of glutamate from
photoreceptors interacts with metabotropic receptors, there will be depolarization (excitation) because
there is decreased inhibition.
✓ bipolar can have both
✓ The narrower the visual field, the higher the visual acuity,
and the wider the field, the lower the resolution. This is
because when photoreceptors are activated by light, their
‫ ﻣﮭﻢ‬glutamate release decreases. The bipolar cells respond
differently depending on their receptor type: those with
ionotropic receptors become hyperpolarized (inhibited),
while those with metabotropic receptors become
depolarized (activated). The ratio of depolarized ON bipolar
cells to hyperpolarized OFF bipolar cells, together with the
size of the receptive field, determines the visual acuity and
resolution.
Color Vision - trichromacy theory (depend on the proportion of activated color cones )
✓ The three visual pigments in the cone outer segments have opsins that differ from the opsin found in
rhodopsin.As a result of these differences, the three types of cone pigments absorb light best at different
wavelengths (Blue, Green, and Red).
✓ These differences in absorption efficiency are presumed to account for color vision because a suitable
mixture of three colors can produce any other color.
✓ At least two different kinds of cones are required for color vision. (Trichromates and Dichromates)
Visual Adaptation
✓ Light adaptation, which occurs rapidly, within seconds, favors cone vision ( phototopic vesion)
because the rhodopsin in rods bleaches (separates from its opsin) more readily than the cone pigments
do.
✓ In dark adaptation, a process that results in an increase in visual sensitivity. Cones adapt more rapidly
to darkness than rods do, thus, cones do not function when the ambient light level is low. By contrast,
rods adapt to darkness slowly, but their sensitivity increases.
✓ Within 10 minutes in a dark room, rod vision is more sensitive than cone vision
PROCESSING OFVISUAL INFORMATION INTHE RETINA
✓ In a sense, the processing of visual information in the retina involves the formation of three images. The
first image, formed by the action of light on the photoreceptors, is changed to a second image in the
bipolar cells, and this in turn is converted to a third image in the ganglion cells.
✓ In the formation of the second image, the signal is altered by the horizontal cells, and in the
formation of the third, it is altered by the amacrine cells.There is little change in the impulse pattern
in the lateral geniculate bodies, so the third image reaches the occipital cortex.
Clinical insight
‫اﻟﺪﻛﺘﻮرة ﺣﻜﺖ اﻗﺮأوه اﻟﻜﻢ‬
Hearing (audition) is considered one of the dominant senses,
as it plays a fundamental role in:
● Communicating with the surrounding environment
● Understanding speech and language
● Improving quality of life
Hearing impairment can lead to a significant decline in quality of life.
Audition (hearing) is the process by which sound waves are:
1. Collected by the outer ear
2. Transmitted through the middle ear
3. Converted into neural signals in the inner ear
4.
Interpreted by the auditory cortex
Sound energy → Mechanical vibration → Electrical signal → Perception
Sound is a pressure wave produced by vibration.
‫(ﺧﻼل اﻟوﺳط‬Pressure waves)‫( ﺗﻧﺗﻘل ﻋﻠﻰ ﺷﻛل ﻣوﺟﺎت ﺿﻐط‬Mechanical vibrations) ‫اھﺗزازات ﻣﯾﻛﺎﻧﯾﻛﯾﺔ‬
Important properties:
●
●
●
Frequency:
○
Measured in Hertz (Hz)
○
Determines pitch
○
Normal hearing range: 20 Hz – 20,000 Hz ‫ﻣدى اﻟﺳﻣﻊ اﻟطﺑﯾﻌﻲ ﻟﻼﻧﺳﺎن‬
○
Speech frequencies: 300 – 3500 Hz ‫اﻟﻣدى اﻟذي ﯾﺗﺣدث ﺑﮫ اﻹﻧﺳﺎن‬
Intensity:
○
Measured in Decibels (dB)
○
Determines loudness ‫ﺗﻌﺑر ﻋن ﻋﻠو اﻟﺻوت‬
○
Typical speech intensity: ~65 dB
Noise damage:
○
>100 dB may damage hair cells
○
>120 dB may cause pain and permanent damage (permanent loss of hearing)
Presbycusis = age-related hearing loss
Characteristics:
●
Gradual loss of high-frequency hearing ‫ﻣﻊ اﻟﺗﻘدم ﻓﻲ اﻟﻌﻣر ﯾﻔﻘد اﻟﺷﺧص ﻗدرﺗﮫ ﻋﻠﻰ ﺳﻣﺎع اﻷﺻوات اﻟﺣﺎدة‬
●
Degeneration of hair cells ‫اﻟﻣﺳؤوﻟﺔ ﻋن إﻧﺗﺎج اﻹﺷﺎرات اﻟﻌﺻﺑﯾﺔ اﻟﺗﻲ ﺗﻧﺗﻘل ﻟﻘﺷرة اﻟدﻣﺎغ‬
●
Reduced basilar membrane sensitivity
Page 1 of 6
‫ ﺗﻘل ﺣﺳﺎﺳﯾﺗﮭﺎ ﻣﻊ اﻟﺗﻘدم ﻓﻲ اﻟﻌﻣر وﺗﺻﺑﺢ ﻏﯾر ﻗﺎدرة ﻋﻠﻰ ﺗﻣﯾﯾز اﻟﺗرددات‬,‫ ﻣﺳؤول ﻋن ﺗﻣﯾﯾز ﺗرددات اﻟﺻوت اﻟﻣﺧﺗﻠﻔﺔ‬Basilar membrane ‫ال‬
(high-frequency / high pitch) ‫اﻟﻌﺎﻟﯾﺔ ﻟﻠﺻوت =< اﻟﺷﺧص ﯾﺻﺑﺢ ﻏﯾر ﻗﺎدر ﻋﻠﻰ ﺗﻣﯾﯾز ال‬
●
Difficulty understanding speech
Usually affects frequencies >2000 Hz.
The ear has three main parts:
1. Outer ear → collects sound
2. Middle ear → amplifies sound
3. Inner ear → converts sound into neural signals
Sound signals are transmitted to the auditory cortex, where they are processed to detect the frequency,
intensity, and location of the sound.
Outer Ear
Components:
●
Pinna (auricle)
●
External auditory canal
Functions:
●
Collects sound waves
●
Directs sound toward tympanic membrane
●
Assists in sound localization ‫اﻋرف اﺣدد ﻣﺻدر اﻟﺻوت‬
●
Cerumen (ear wax) protects the canal from infection and debris
Middle Ear
The middle ear is an air-filled cavity.
Main structures:
●
Tympanic membrane
●
Auditory ossicles: *the smallest bones in human body
○
Malleus
○
Incus
○
Stapes
The stapes footplate attaches to the oval window of the cochlea To transmit sound vibrations to the cochlea(part of
inner ear)
The middle ear acts as an impedance matching system.
Main mechanisms of amplification:
1. Lever action of ossicles Resonating
2. Surface area difference between: when the ear transmitted from tympanic membrane which has a large surface
area to oval window which has small surface area, sound is amplified
a. Tympanic membrane
b. Oval window
The eardrum (tympanic membrane) is much larger than the oval window, which connects to the cochlea. When sound vibrations hit
the eardrum, the same force is concentrated onto the smaller area of the oval window. This surface area difference increases the
Page 2 of 6
pressure of the vibrations, allowing the sound to be transmitted more efficiently into the cochlear fluid and enhancing the
perception of sound.
These mechanisms increase sound pressure transmitted to cochlear fluid In the outer and middle ear, sound is
transmitted through air, while in the inner ear, it is transmitted through fluid.
Sequence of sound conduction:
Sound waves → Tympanic membrane vibration → Ossicles movement → Stapes pushes oval window → Movement of
cochlear fluid(redistribution) → Basilar membrane vibration They contain the hair cells (the receptor cells) that generate
electrical signals, which are then transmitted to the auditory cortex.
Inner Ear
The inner ear contains:
●
Bony labyrinthe
Cochlea
Vestibule
Semicircular canals
●
Membranous labyrinth
Scala media
Sensory organs for hearing and balance
The inner ear is filled with specialized fluids
The cochlea is a spiral structure responsible for hearing.
Contains three compartments:
●
●
●
Scala vestibuli
Scala media (cochlear duct)
Scala tympani
The scala media contains the sensory organ of hearing
Two types of fluid exist in the cochlea:
●
●
Perilymph
○ Located in scala vestibuli and scala tympani
○ Similar composition to CSF
Endolymph
○ Located in scala media contain hearing apparatus
○ High K+ concentration ‫ﻣﮭم‬
The ion responsible for transmitting auditory signals is potassium (K⁺), not sodium (Na⁺), which
distinguishes it from other types of action potential in the nervous system
○
Produced by stria vascularis
Page 3 of 6
The organ of Corti is the sensory receptor for hearing.
Located on the basilar membrane.
Components:
●
●
●
●
Inner hair cells
Outer hair cells
Tectorial membrane
Supporting cells
Hair Cells
Hair cells convert mechanical vibration into electrical signals.
●
●
Inner hair cells
○ Primary sensory receptors
○ Responsible for auditory perception
Outer hair cells
○ Amplify basilar membrane movement
○ Improve frequency discrimination ‫ﯾﺳﺎﻋد ﻓﻲ ﺗﻣﯾﯾز طﺑﯾﻌﺔ اﻟﺗردد‬
Auditory nerve fibers arise from: Spiral ganglion neurons
Key facts:
●
●
●
~32,000 afferent fibers ‫ﺗﻧﻘل اﻹﺷﺎرات ﻟﻠﻘﺷرة اﻟﺳﻣﻌﯾﺔ‬
90% connect to inner hair cells
Signals travel via Cranial Nerve VIII (vestibulocochlear nerve)
‫ﻓﯾدﯾو ﻟﻠﺗوﺿﯾﺢ‬
Steps of auditory transduction:
1.
2.
3.
4.
5.
Basilar membrane vibrates
Hair cell stereocilia bend
Ion channels open
Hair cells depolarize
Neurotransmitter is released
Sound waves reach the tympanic membrane (large surface area)→ Vibrations are transmitted through the ossicles
(resonance and amplification)→ Sound reaches the oval window (small surface area)→ Pressure increases and sound is
amplified→ Vibrations enter the cochlea→ Redistribution (movement) of cochlear fluid occurs→ Movement reaches
the basilar membrane (contains the organ of Corti)→ Basilar membrane vibrates→ Hair cells bend→ Stereocilia
movement opens or closes ion channels (depolarization or hyperpolarization)→ Neurotransmitters are released→
Signals are transmitted or inhibited
Hair Cell Electrical Response
Bending of stereocilia changes K+ conductance.
●
●
Bending toward kinocilium:
○ Increased K+ entry
○ Depolarization
Bending away from kinocilium:
Page 4 of 6
○
Hyperpolarization
Depolarization causes:
●
●
●
Opening of voltage-gated Ca²⁺ channels
Ca²⁺ influx
Release of glutamate
Glutamate stimulates cochlear nerve fibers → Action potentials travel to brain
Opening of K⁺ channels → Depolarization→ Opening of voltage-gated Ca²⁺ channels→ Ca²⁺ influx→ Binding of Ca²⁺ to
receptors on synaptic vesicles→ Exocytosis of neurotransmitters (glutamate)→ Glutamate (an excitatory
neurotransmitter) is released→ Stimulation of cochlear nerve fibers→ Generation of action potentials→ Signals travel
to the auditory cortex
Different regions of the basilar membrane detect different frequencies.
●
●
Base of cochlea:
○ Narrow and stiff
○ Detects high frequencies
Apex of cochlea:
○ Wide and flexible
○ Detects low frequencies
How does stiffness play a role ?
High-frequency sounds stimulate stiff regions of the basilar membrane, while low-frequency sounds stimulate more
flexible region
This arrangement is called tonotopic organization.
Auditory signals travel through:
1.
2.
3.
4.
5.
6.
Cochlear nerve
Cochlear nuclei
Lateral lemniscus
Inferior colliculus
Medial geniculate nucleus (thalamus)
Auditory cortex do the final processing to the signal
Located in the temporal lobe.
Functions:
●
●
●
●
Sound perception (detect frequency, intensity, location)
Speech recognition ‫اذا ﻛﺎن اﻟﺻوت ﻋﺑﺎرة ﻋن ﻛﻼم ﺗﻘوم اﻟﻘﺷرة اﻟﺳﻣﻌﯾﺔ ﺑﻔﮭم ھذا اﻟﻛﻼم اﻟﻣﻧطوق ﺑﻠﻐﺔ ﻣﻌﯾﻧﺔ‬
Sound localization ‫ﺗﺣدد ﻣﺻدر اﻟﺻوت‬
Integration of auditory information
Auditory information is integrated with higher brain functions, allowing sounds to be linked with memory, emotions,
language, and behavior.
In the auditory association areas, sounds are interpreted and given meaning based on previous experience. This helps in
Page 5 of 6
forming and recalling memories.
Different sound signals can also be combined to produce meaningful information, such as understanding speech.
Auditory input is connected to emotional centers in the brain, so certain sounds can trigger emotional responses, such
as fear or alertness.
It is also linked to motor functions, where sudden sounds can produce protective reflexes, such as moving away from
danger.
Overall, this integration allows sound to influence understanding, memory, emotions, and behavior.
.Both ears are represented in each hemisphere
‫ﻛل اذن ﺗﺑﻌث اﺷﺎرات اﻟﻰ ﻛل ﻧﺻف ﻣن ﻧﺻﻔﻲ اﻟدﻣﺎغ‬
The vestibular system maintains balance.
‫ ﻣﺳؤول ﻋن اﻟﺗوازن واﻟﻣﺣﺎﻓظﺔ ﻋﻠﻰ ﺟودة اﻟﻧظر ﺣﺗﻰ ﻻ ﺗﺧﺗل أﺛﻧﺎء ﺣرﻛﺔ اﻟرأس‬،‫ﻣوﺟود ﻓﻲ اﻷذن اﻟداﺧﻠﯾﺔ‬
Functions:
●
●
●
Detect head movement
Maintain posture
Stabilize vision during movement
Works closely with:
●
●
●
Visual system
Cerebellum ‫ﻣﺳؤوﻟﺔ ﻋن اﻟﺗوازن‬
Proprioceptive system ‫ﻣﺳؤول ﻋن اﻟوﻋﻲ ﺑوﺿﻌﯾﺔ اﻟﺟﺳم وﻣوﻗﻊ اﻟﺟﺳم ﺑﺎﻟﻧﺳﺑﺔ ﻟﻠﻣﺣﯾط‬
Components of vestibular apparatus:
●
●
●
●
●
●
●
●
Semicircular canals
The sensory epithelium in a semicircular canal is called a crista ampullaris, or ampullary crest An ampullary crest
consists of a ridge that is covered by epithelium in which there are vestibular hair cells embedded in gelatinous
structure called the cupula .. These hair cells are innervated by primary afferent fibers of the vestibular nerve,
which is a subdivision of the eighth cranial nerve
The canals are filled with endolymph and are bathed in perilymph
The cupula has the same specific gravity as endolymph, and thus it is unaffected by linear acceleratory forces,
such as that exerted by gravity
Detect rotational (angular) acceleration
Otolith organs
○ Saccule
○ Utricle
○ Detect linear acceleration and gravity
The sensory epithelia of the otolith organs are called the macula utriculi and the macula sacculi
It contains numerous otoliths ("ear stones") composed of calcium carbonate crystals. Together, the gelatinous
mass and its otoliths are known as an otolithic membrane. The otoliths increase the specific gravity of the
otolithic membrane to about twice that of the endolymph
‫اﻟدﻛﺗورة ﺗﻘول اﻟﺗزﻣوا ﺑﺎﻟﺳﻼﯾدات‬
‫م حمد ا له‬
Page 6 of 6
Temperature regulation
.‫ وﻓﻲ آﺧﺮ اﻟﻤﺤﺎﺿﺮة ﻣﻠﺨﺺ ﺷﺎﻣﻞ‬،pathways ‫ ﻟﺘﺴﮭﯿﻞ ﻓﮭﻢ ﺑﻌﺾ اﻟـ‬AI ‫أﺿﻔﺖ ﺻﻮر ﻣﻦ اﻟـ‬
.‫ اﻗﺮأوا اﻟﻤﻠﺨﺺ وإن ﺷﺎء ﷲ ﻣﺎ رح ﯾﻄﻠﻊ ﻋﻨﮭﻢ‬،‫إذا ﻣﺎ ﻟﺤﻘﺘﻮا ﺗﺪرﺳﻮا اﻟﻤﺤﺎﺿﺮة ﻛﻠﮭﺎ‬
Normal core temperature
✓ Body temperature is a regulated variable that must be maintained within the normal range to prevent
damage to the body
✓ 35.9–37°C (if measured orally)
✓ 36.4 oC – 37.5 oC (rectally)
✓ Body temperature is controlled by balancing heat production and heat loss.
❖ Body heat is produced by :
a. Basic metabolic processes – increase ATP
b. Food intake ( specific dynamic action ) - Thermogenic effect of food intake (the heat
produced during digestion, absorption, and metabolism of food)
c. Muscular activity
❖ Body heat is lost by :
a. Radiation and conduction ( 70%)
b. Vaporisation of sweat (27%)
c. Respiration (2%)
d. Urination and defection (1%)
Sources of heat gain and heat loss from the body
A. Heat production
✓ Heat is a principle by-product of metabolism.
✓ Each cell contributes to the basal metabolic rate through its metabolic activity
✓ Thyroxine is one of the most important hormones that regulate metabolic rate
✓ The main factors that determine the rate of heat production (metabolic rate of the body):
1. Basal rate of metabolism of all the cells of the body. ‫الحد األدنى من الطاقة التي تنتجها الخاليا‬
2. Extra rate of metabolism caused by muscle activity (including muscle contractions caused by
shivering)
▪ Shivering is the most potent mechanism for increasing heat production.
▪ Cold temperatures activate the shivering response, which is controlled by the posterior
hypothalamus.
▪ α-Motoneurons (lower motor neuron of the brain stem and spinal cord) and γ-motoneurons
are activated, causing contraction of skeletal muscle and heat production.
▪ α-motoneurons innervate extrafusal skeletal muscle fibers, while γ-motoneurons innervate
intrafusal fibers in the muscle spindle (sensory receptors).
▪ Shivering is an involuntary increase in skeletal muscle activity, which significantly increases
heat production and raises body temperature
3. Extra metabolism caused by the effect of thyroxine (and, to a less extent, growth hormone and
testosterone) on the cells.
4. Extra metabolism caused by the effect of epinephrine, norepinephrine and sympathetic
stimulation on the cells.
▪ Cold temperatures activate the sympathetic nervous system, leading to:
1. Release of epinephrine and norepinephrine, which cause vasoconstriction. This
reduces blood flow to the skin, increases insulation, and helps prevent heat loss,
thereby maintaining or increasing body temperature.
2. Activation of β3-adrenergic receptors in brown adipose tissue, which increases
metabolic rate and heat production through stimulation of mitochondrial uncoupling
protein 1 (UCP1). Exercise promotes the conversion of white fat into brown-like fat.
Brown adipose tissue is very powerful in burning glucose and fatty acids. The higher
the amount of brown fat, the higher the metabolic rate. That is why cold showers are
considered beneficial.
5. Extra metabolism needed for digestion, absorption, and storage of food (thermogenic effect of
food).
B.
Heat loss
✓ Rate of heat loss depends on:
1. how rapidly heat can be conducted from where it is produced in the body core to the skin
2. how rapidly heat can then be transferred from the skin to the surroundings.
✓ The skin, the subcutaneous tissues, and especially the fat of the subcutaneous tissues act together as a
heat insulator for the body.
✓ Blood flow to the skin from the body core provides heat transfer.
Heat-loss mechanisms
i.
Radiation (heat waves)
ii.
Evaporation
iii.
Conduction
Heat-loss mechanisms - response to heat
1. Heat loss by radiation and convection increases when the ambient temperature increases.
- This response is controlled by the anterior hypothalamus.
- Increases in temperature >>> decreased sympathetic tone of cutaneous blood vessels>>> increase
blood flow through the arterioles and increasing arteriovenous shunting of blood to the venous
plexus near the surface of the skin >>> heat loss by radiation and convection.
2. Heat loss by evaporation depends on the activity of sweat glands, which are under sympathetic
muscarinic control.
- Sweat glands are innervated by sympathetic cholinergic fibers, which are an exception to the usual
adrenergic sympathetic system
3. reduction of shivering, which decreases skeletal muscle activity and heat production
4. decreasing metabolic rate through lowering the effects of thyroxine, epinephrine, and norepinephrine, as
well as reducing brown fat activity
Feature
Hypothalamic Center
Cutaneous Vessels
Muscle Activity
Hormonal Response
Sweat Glands
Brown fat
Main Mechanism
Cold Response (Heat Gain)
Posterior Hypothalamus
Vasoconstriction (decreases blood
flow to skin to save heat)
Shivering (most potent heat
producer via alpha & gamma
neurons)
Increased Thyroxine &
Epinephrine (increases BMR)
Inhibited (inactive)
UCP1 Activation (Non-shivering
thermogenesis)
Metabolism & Muscle Contraction
‫ملخص‬
Heat Response (Heat Loss)
Anterior Hypothalamus
Vasodilation (increases blood flow
to skin to lose heat)
Muscle relaxation (decreased tone
to lower metabolism)
Decreased metabolic hormones
Activated (via Sympathetic
Muscarinic control)
Inactive
Radiation & Evaporation
Regulation of sweating by autonomic nervous system
1. Stimulation of the anterior hypothalamus-preoptic area in the brain by excess heat causes
sweating.
2. The nerve impulses from this area are transmitted in the autonomic pathways to the spinal cord
and then through sympathetic outflow to the skin
everywhere in the body.
AI
3. Sweat glands are innervated by cholinergic nerve
fibers that run in the sympathetic nerves along
with the adrenergic fibers. ( Acetylcholine)
4. So sweat glands can also be stimulated to some
extent by epinephrine or NE circulating in the
blood (ex.: in exercise).
Temperature-Decreasing Mechanisms When the Body Is Too Hot
✓ Vasodilation of skin blood vessels
✓ Sweating
✓ Decrease in heat production
• Inhibition of shivering and chemical thermogenesis.
Temperature-Increasing Mechanisms When the Body Is Too Cold
✓ Skin vasoconstriction throughout the body
• Caused by the stimulation of the posterior hypothalamic sympathetic centers.
✓ Piloerection
• (not important in human beings).
✓ Increase in thermogenesis.
Hypothalamic set point for body temperature
✓ The hypothalamus is the major integrator and controller of body temperature
✓ The temperature of the body is regulated almost entirely by nervous negative feedback mechanisms, and
almost all these operate through temperature-regulating centers located in the hypothalamus (preoptic
and anterior hypothalamic nuclei of the hypothalamus).
✓ Temperature detectors ( sensors in hypothalamus and skin) are also needed
✓ Posterior hypothalamus integrates the central and peripheral temperature sensory signals
✓ Temperature sensors on the skin and in the hypothalamus “read” the core temperature and relay this
information to the anterior hypothalamus.
✓ The anterior hypothalamus compares the detected core temperature to the set-point temperature.
- If the core temperature is below the set point, heat- generating mechanisms are activated by the
posterior hypothalamus.
- If the core temperature is above the set point, mechanisms for heat loss are activated by the
anterior hypothalamus.
AI
Fever ‫مهم‬
✓ Fever means a body temperature above the usual range of normal.
✓ It can be caused by abnormalities in the brain itself or by toxic substances that affect the temperature
regulating centers (such as bacterial diseases, brain tumors, heatstroke).
✓ Many proteins, breakdown products of proteins, and certain other substances, especially
lipopolysaccharide toxins released from bacterial cell membranes cause the set-point of the
hypothalamic thermostat to rise.
- These substances are called pyrogens.
✓ Some pyrogens can act directly and immediately on the hypothalamic temperature-regulating center to
increase its set-point.
- During a fever, pyrogens increase the set point of body temperature in the anterior hypothalamus. As
a result, the current body temperature is lower than the new set point, which triggers heat production
mechanisms and raises body temperature, leading to fever.
✓ Other pyrogens function indirectly and require several hours (ex.: endotoxins of
gram-negative bacteria).
✓ Phagocytic cells digest bacterial products and then release cytokines. One of the
most important is interleukin-1 (IL-1; endogenous pyrogen, leukocyte pyrogen).
✓ Several experiments have suggested that interleukin-1causes fever by first inducing
the formation of one of the prostaglandins, mainly prostaglandin E2, or a similar
substance, which acts in the hypothalamus to elicit the fever reaction.
- During a bacterial infection, toxic substances (exogenous pyrogens) trigger the
activation of the inflammatory cascade. This leads to the production of
prostaglandins, which act on the anterior hypothalamus to increase the set point
of body temperature.
✓ Fever may be also caused by lesions to the hypothalamus.
✓ Fever can be treated by targeting prostaglandin production. Cortisol and other steroids can reduce
prostaglandin synthesis, but steroids are not regularly used for fever. Instead, NSAIDs are commonly
used, as they inhibit cyclooxygenase (COX) and block prostaglandin production. Paracetamol can also
be used, but NSAIDs are more potent.
✓ The difference between NSAIDs and steroids:
❖ NSAIDs:
▪ Inhibit cyclooxygenase → reduce prostaglandins
▪ Also act on other inflammatory cytokines
▪ Stronger antipyretic effect than paracetamol
▪ First-line treatment for fever
❖ Steroids:
▪ Reduce prostaglandin synthesis by suppressing the
inflammatory cascade
▪ Not first-line for fever
▪ First-line treatment for general inflammatory
condition
‫ بس اقرأوهم احتياط‬، ‫ما قرأتهم‬
Adrenergic Agonists & Antagonists
Adrenergic Agonists (Sympathomimetics)
:‫ وﺗﻨﻘﺴﻢ إﱃ‬،adrenergic receptors
‫ﻫﻲ اﻷدوﻳﺔ اﻟﺘﻲ‬
1) Direct-Acting Adrenergic Agonists
:‫ وﺗﻨﻘﺴﻢ إﱃ‬،‫ﺗﻌﻤﻞ ﻣﺒﺎﺷﺮة ﻋﲆ اﻟﻤﺴﺘﻘﺒﻼت‬
Alpha Adrenergic Agonists (‫أ‬
Selective:
³1 agonist:
Phenylephrine :‫ﻣﺜﺎل‬
vasoconstriction
blood pressure :‫اﻟﻮﻇﻴﻔﺔ‬
³2 agonist:
Clonidine :‫ﻣﺜﺎل‬
sympathetic outflow ‫ ﺗﻘﻠﻴﻞ‬+ analgesia :‫اﻻﺳﺘﺨﺪام‬
Non-selective (³1 + ³2):
Oxymetazoline :‫ﻣﺜﺎل‬
nasal decongestant (vasoconstriction) :‫اﻻﺳﺘﺨﺪام‬
Beta Adrenergic Agonists (‫ب‬
Non-selective (´1 + ´2):
Isoproterenol :‫ﻣﺜﺎل‬
Selective:
´1 agonist:
Dobutamine :‫ﻣﺜﺎل‬
heart rate & contractility
:‫اﻻﺳﺘﺨﺪام‬
´2 agonist:
Albuterol :‫ﻣﺜﺎل‬
bronchodilation (asthma, COPD) :‫اﻻﺳﺘﺨﺪام‬
´3 agonist:
Mirabegron :‫ﻣﺜﺎل‬
overactive bladder (
Mixed
&
urination) :‫اﻻﺳﺘﺨﺪام‬
Agonists (‫ج‬
Epinephrine Norepinephrine :‫أﻣﺜﻠﺔ‬
‫ ﻓﻲ اﻟﺠﺴﻢ‬endogenous ligands ‫ ﻫﺬه‬:‫ﻣﻼﺣﻈﺔ‬
2) Indirect-Acting Adrenergic Agonists
:‫ ﺑﻞ ﺗﺰﻳﺪ اﻟﻨﻮاﻗﻞ اﻟﻌﺼﺒﻴﺔ‬،‫ﻻ ﺗﺮﺗﺒﻂ ﻣﺒﺎﺷﺮة ﺑﺎﻟﻤﺴﺘﻘﺒﻞ‬
Releasing agents:
Amphetamine (drug of abuse) :‫ﻣﺜﺎل‬
Reuptake inhibitors:
Cocaine (drug of abuse) :‫ﻣﺜﺎل‬
3) Mixed-Acting (Direct + Indirect)
:‫أﻣﺜﻠﺔ‬
Ephedrine
Pseudoephedrine
nasal decongestant :‫اﻻﺳﺘﺨﺪام‬
Adrenergic Antagonists (Blockers)
‫ﻫﻲ اﻷدوﻳﺔ اﻟﺘﻲ‬
1) Mixed
&
Blockers
:‫أﻣﺜﻠﺔ‬
Carvedilol
Labetalol
hypertension + heart failure :‫اﻻﺳﺘﺨﺪام‬
2) Alpha Blockers
Non-selective (α1 + α2):
Phenoxybenzamine
Phentolamine
Selective (α1):
Prazosin
Terazosin
‫ ﺑﺸﻜﻞ ﺷﺎﺋﻊ‬selective α2 blockers ‫ ﻻ ﻳﻮﺟﺪ أدوﻳﺔ ﺗﺴﺘﺨﺪم ﻛـ‬:‫ﻣﻼﺣﻈﺔ‬
3) Beta Blockers
Non-selective (β1 + β2): Propranolol
Selective (β1): Metoprolol , Atenolol
Hypertension , Heart failure , Cardiac conditions :‫اﻻﺳﺘﺨﺪام‬
Adrenergic Receptors ‫ﻣﺮاﺟﻌﺔ ﺳﺮﻳﻌﺔ ﻟﻠـ‬
1 Receptors
‫ اﻷوﻋﻴﺔ اﻟﺪﻣﻮﻳﺔ‬:‫اﻟﻤﻮﻗﻊ‬
Vasoconstriction :‫اﻟﺘﺄﺛﻴﺮ‬
Peripheral resistance
Blood pressure
1 Receptors
‫ اﻟﻘﻠﺐ‬:‫اﻟﻤﻮﻗﻊ‬
Heart rate (tachycardia)
:‫اﻟﺘﺄﺛﻴﺮ‬
Contractility
2 Receptors
Bronchodilation :‫اﻟﺘﺄﺛﻴﺮ‬
Vasodilation (in skeletal muscles )
‫اﻟﻀﻐﻂ‬
‫اﻟﻤﻘﺎوﻣﺔ‬
‫اﻟﺪم ﻳﻤﺸﻲ ﺑﺴﻬﻮﻟﺔ‬
(Vasodilation)
‫ﻟﻤﺎ اﻷوﻋﻴﺔ‬
3 Receptors
urination
‫ ﺑﺎﻟﺘﺎﻟﻲ‬Relaxation of bladder :‫اﻟﺘﺄﺛﻴﺮ‬
Dopamine Receptors (ً ‫ ﺧﺼﻮﺻﺎ‬D1)
dopamine receptors ‫ ﺑﻞ أﻳﻀﺎ ً ﻋﲆ‬،´ ‫ و‬³ ‫اﻟﺪوﺑﺎﻣﻴﻦ ﻻ ﻳﻌﻤﻞ ﻓﻘﻂ ﻋﲆ‬
D1 Receptors
:‫اﻟﻤﻮﻗﻊ‬
Renal circulation
Mesenteric circulation
:‫اﻟﺘﺄﺛﻴﺮ‬
Vasodilation
blood flow ‫ﻟﻬﺬه اﻷﻋﻀﺎء‬
Vasopressors
Vasoconstriction ,,
Blood pressure ,,
Tissue perfusion
:‫ﻣﺎ ﻫﻲ؟ أدوﻳﺔ ﺗﻌﻤﻞ ﻋﲆ‬
Shock :‫ﺗﺴﺘﺨﺪم ﺑﺸﻜﻞ أﺳﺎﺳﻲ ﻓﻲ‬
‫؟‬Shock ‫ﻣﺎ ﻫﻮ‬
‫ إﱃ اﻷﻧﺴﺠﺔ‬Significant decrease in blood perfusion:‫ ﻫﻮ‬:‫اﻟﺘﻌﺮﻳﻒ‬
‫واﻷﻋﻀﺎء‬
(hypoperfusion ‫)ﻣﻤﻜﻦ ﻳﻜﻮن اﻟﻀﻐﻂ ﻃﺒﻴﻌﻲ ﻣﻊ وﺟﻮد‬
‫ ﻟﻜﻦ‬hypotension ‫ ﻏﺎﻟﺒﺎ ً ﻳﻜﻮن ﻣﻌﻪ‬:‫ﻣﻼﺣﻈﺔ‬
Shock ‫أﻧﻮاع‬
1) Hypovolemic Shock
Blood volume
:‫اﻟﺴﺒﺐ‬
Hypotension + Hypoperfusion :‫ و اﻟﻨﺘﻴﺠﺔ‬.. Hemorrhage ,, Dehydration :‫أﻣﺜﻠﺔ‬
2) Cardiogenic Shock
hypoperfusion ‫ﻟﻜﻦ ﻓﻲ‬
blood pressure ‫ ﻣﻤﻜﻦ ﻳﻜﻮن‬:‫ ﻣﻼﺣﻈﺔ‬.… ‫ اﻟﻘﻠﺐ ﻏﻴﺮ ﻗﺎدر ﻋﲆ ﺿﺦ اﻟﺪم ﺑﺸﻜﻞ ﻛﺎﻓﻲ‬:‫اﻟﻤﺸﻜﻠﺔ‬
3) Vasodilatory (Distributive) Shock
‫ ﺷﺪﻳﺪ‬Vasodilation :‫اﻟﺴﺒﺐ‬
Hypotension + Hypoperfusion :‫ … اﻟﻨﺘﻴﺠﺔ‬Septic shock (sepsis) :‫أﻫﻢ ﻣﺜﺎل‬
4) Obstructive Shock
Tension pneumothorax ,, Cardiac tamponade ,, Pulmonary embolism :‫ أﻣﺜﻠﺔ‬.. ‫ ﻳﻤﻨﻊ ﺗﺪﻓﻖ اﻟﺪم‬Obstruction :‫اﻟﺴﺒﺐ‬
‫؟‬Shock ‫ﻛﻴﻒ ﻧﻘﻴﻢ‬
:‫ﻣﺆﺷﺮات ﻣﻬﻤﺔ‬
Blood pressure .. Tissue perfusion ,, Lactate:
Lactate
‫ دﻟﻴﻞ ﻋﲆ‬hypoperfusion
Mean Arterial Pressure (MAP)
shock ‫اﻟﻤﺮﻳﺾ ﻣﺎ زال ﻓﻲ‬
‫ إذا أﻗﻞ‬.. mmHg 65 ≤ ‫ ﻻزم ﻳﻜﻮن‬..
perfusion
:‫ﻳﻌﺘﺒﺮ‬
‫اﻟﻌﻼج‬
(ً ‫أول ﺧﻄﻮة )أﺳﺎﺳﻴﺔ ﺟﺪا‬
IV Fluid Resuscitation
Crystalloids :‫ﻧﻌﻄﻲ‬
Normal saline (NaCl) ,, Ringer lactate :‫أﻣﺜﻠﺔ‬
perfusion ‫ﻟﺘﻌﻮﻳﺾ ﻧﻘﺺ‬
‫ ﻧﻌﻄﻲ‬first-line ‫ﻫﻲ‬
:‫إذا ﻟﻢ ﻳﺘﺤﺴﻦ اﻟﻤﺮﻳﺾ ﺑﻌﺪ اﻟﺴﻮاﺋﻞ ﻧﻨﺘﻘﻞ إﱃ‬
Vasopressors
Vasopressors :‫اﻟﻔﺮق ﺑﻴﻦ‬
Vasoconstriction ,,
Blood pressure :‫ﺗﻌﻤﻞ ﻋﲆ‬
Inotropes‫و‬
Cardiac contractility
,, :‫ﺗﻌﻤﻞ ﻋﲆ‬
‫؟‬Vasopressors ‫ﻣﺘﻰ ﻧﺴﺘﺨﺪم‬
perfusion ‫ وﻣﺎ ﺗﺤﺴﻦ اﻟﻀﻐﻂ أو‬IV fluids ‫ أﻋﻄﻴﻨﺎ‬:‫إذا‬
Vasopressors ‫ ﻧﺒﺪأ‬:‫ وإذا أﻗﻞ‬MAP
65 :‫أﻫﻢ ﻧﻘﻄﺔ اﻟﻬﺪف‬
First-line Vasopressor
(septic shock ً ‫ )ﺧﺼﻮﺻﺎ‬shock‫ ﻳﺴﺘﺨﺪم ﻓﻲ ﻣﻌﻈﻢ أﻧﻮاع ال‬guidelines
:‫ ﻫﻮ‬Norepinephrine
Vasopressors in Shock
‫ اﻟﻤﺴﺘﺨﺪﻣﺔ‬Vasopressors ‫أﻫﻢ‬
Norepinephrine (‫ )اﻷول‬,, Epinephrine ,, Dopamine ,, Phenylephrine ,, Vasopressin (‫ )ﻟﻦ ﻳﺘﻢ ﺷﺮﺣﻪ ﺑﺎﻟﺘﻔﺼﻴﻞ‬,, Dobutamine
Norepinephrine :ً ‫أوﻻ‬
(septic shock
) shock
first-line vasopressor
:‫ ﻫﻮ‬First-line treatment ‫ال‬
Mechanism: Potent -adrenergic agonist
(‫ )أﻗﻮى ﻋﲆ اﻷﻟﻔﺎ‬α > β :‫ ﻟﻜﻦ ﻧﺸﺎﻃﻪ ﻋﲆ‬mixed ‫ﺻﺤﻴﺢ اﻧﻪ‬
Effects: Vasoconstriction ‫ﻗﻮي‬
BP ‫ زﻳﺎدة‬perfusion
Less tachycardia , Less arrhythmias :‫ ﻳﺴﺒﺐ‬Dopamine , Epinephrine :‫ ﻣﻘﺎرﻧﺔ ﻣﻊ‬:‫ﻣﻴﺰة ﻣﻬﻤﺔ‬
Epinephrine :ً ‫ﺛﺎﻧﻴﺎ‬
Mechanism: Non-selective ( + ) (the same thing
Effects:
Cardiac index ,, Vasoconstriction
‫ وﻻ آﺧﺮ ﺧﻴﺎر‬First-line :‫ ﻟﻴﺲ‬:‫اﺳﺘﺨﺪاﻣﻪ‬
norepinephrine ‫ ﻓﻤﻤﻜﻦ ﻧﻀﻴﻔﻪ ﻣﻊ‬norepinephrine
Dopamine :ً ‫ﺛﺎﻟﺜﺎ‬
‫ إذا اﻟﻤﺮﻳﺾ‬:‫ﻳﺴﺘﺨﺪم‬
Mechanism: ‫ﻳﻌﻤﻞ ﻋﲆ‬: Dopamine receptors,, ‫و‬
:(Dose-dependent effects) ً ‫ﻣﻬﻢ ﺟﺪا‬
receptors
Low dose: ‫ ﻳﻌﻤﻞ ﻋﲆ‬D1 receptors
Vasodilation
Renal blood flow
High dose:
´ receptors ‫ و‬³ :‫ﻳﻌﻤﻞ ﻋﲆ‬
Heart rate ,,
Stroke volume
ً ‫ﻧﻘﻄﺔ ﻣﻬﻤﺔ ﺟﺪا‬
renal perfusion
septic shock
low-dose dopamine
‫ ﺑﻴﻌﻤﻞ‬:Pharmacologically :‫رﻏﻢ إﻧﻪ‬
:‫ ﻟﺬﻟﻚ‬morbidity ‫ أو‬mortality ‫ ﻻ ﻳﻮﺟﺪ ﺗﺤﺴﻦ ﻓﻲ‬:Clinically :‫ﻟﻜﻦ‬
High risk of arrhythmias :‫ و ﻟﻪ‬norepinephrine ‫ و ﻳﻤﻜﻦ إﺿﺎﻓﺘﻪ ﻣﻊ‬first-line ‫ ﻟﻴﺲ‬:‫اﺳﺘﺨﺪاﻣﻪ‬
Phenylephrine :ً ‫راﺑﻌﺎ‬
Mechanism: Selective 1 agonist
Effects:Vasoconstriction ‫ﻓﻘﻂ‬
(minimal cardiac effect) ‫ﻻ ﺗﺄﺛﻴﺮ ﻋﲆ اﻟﻘﻠﺐ‬
Heart rate (Reflex bradycardia)
Contractility: ‫ﻻ ﻳﺘﺄﺛﺮ‬
Cardiac output: ً ‫ﻗﻠﻴﻼ‬
‫ﻣﻤﻜﻦ ﻳﺒﻘﻰ ﻧﻔﺴﻪ أو‬
Peripheral vascular resistance
Blood pressure (systolic & diastolic)
first-line ‫ ﻟﻴﺲ‬:‫اﺳﺘﺨﺪاﻣﻪ‬
:‫ﻳﺴﺘﺨﺪم ﻓﻲ ﺣﺎﻻت ﺧﺎﺻﺔ‬
:‫إذا اﻟﻤﺮﻳﺾ‬
tachycardia ‫ﻋﻨﺪه‬
(heart rate ‫ )ﻣﺎ ﺑﺪﻧﺎ ﻧﺰﻳﺪ‬ischemia ‫أو‬
Dobutamine :ً ‫ﺧﺎﻣﺴﺎ‬
Mechanism: 1 agonist
(vasopressor
) Inotropic drug :‫ﻧﻮﻋﻪ‬
‫ ﻟﻤﺎ ﻛﻞ اﻟﺨﻴﺎرات اﻷﺧﺮى ﺗﻔﺸﻞ‬:‫أو‬
(‫ )أﻫﻢ ﺗﺄﺛﻴﺮ‬Contractility
:‫اﻟﺘﺄﺛﻴﺮات‬
Cardiac output
Heart rate (‫)زﻳﺎدة ﺧﻔﻴﻔﺔ‬
α receptors ‫ ﻻ ﺗﺄﺛﻴﺮ ﻣﺒﺎﺷﺮ ﻋﲆ‬:‫ﻋﲆ اﻷوﻋﻴﺔ‬
Peripheral resistance: ً ‫ﻗﻠﻴﻼ‬
‫ﺑﺴﻴﻂ‬
‫( ﻏﺎﻟﺒﺎ ً ﻻ ﻳﺘﻐﻴﺮ «««««« ﻣﻤﻜﻦ‬reflex)
‫ ﻻ ﻳﺘﻐﻴﺮ ﺑﺸﻜﻞ ﻛﺒﻴﺮ و ﻣﻤﻜﻦ‬:ً ‫ ﻏﺎﻟﺒﺎ‬:Blood Pressure ‫ﻋﲆ‬
(‫ )ﺿﻌﻒ ﺿﺦ اﻟﻘﻠﺐ‬Cardiogenic shock :‫ ﻓﻲ‬:‫اﺳﺘﺨﺪاﻣﻪ‬
hypoperfusion ‫ ﻟﻜﻦ ﻣﺎ زال ﻫﻨﺎك‬, ‫ أﺻﺒﺢ ﻣﻘﺒﻮل‬BP :‫ إذا‬:‫أو‬
Dobutamine ‫ ﻻ ﻧﻌﻄﻲ‬Hypotension :‫ إذا اﻟﻤﺮﻳﺾ ﻋﻨﺪه‬:ً ‫ﻧﻘﻄﺔ ﻣﻬﻤﺔ ﺟﺪا‬
‫ﻟﻮﺣﺪه‬
‫ﻳﺮﻓﻊ اﻟﻀﻐﻂ‬
Vasopressor :‫ ««««« اﻟﺴﺒﺐ‬Vasopressor ‫ ﻧﻌﻄﻲ ﻣﻌﻪ‬:‫ﻻزم‬
Dobutamine
‫ ﻳﺰﻳﺪ‬contractilit
Vasopressors ‫ﻣﻼﺣﻈﺎت ﻣﻬﻤﺔ ﻋﻦ‬
‫ ﻓﻘﻂ‬ICU ‫( ﺗُﻌﻄﻰ ﻓﻲ‬1
vasopressor = Indication for ICU admission ‫اﻟﺤﺎﺟﺔ إﱃ‬
(Continuous BP monitoring ,, Infusion pump ) ‫ ﻣﺴﺘﻤﺮ‬Monitoring ‫ﻻﻧﻬﺎ ﺗﺤﺘﺎج‬
Invasive blood pressure monitoring :‫ ﻧﺴﺘﺨﺪم‬:‫ﻓﻲ ﻛﺜﻴﺮ ﺣﺎﻻت‬
Large veins (central line) :‫ ﻋﺎدي «««ﻻزم‬IV ‫ ﻻ ﺗُﻌﻄﻰ ﻋﺒﺮ‬Central Line ‫( ﺗُﻌﻄﻰ ﻋﺒﺮ‬2
Extravasation
‫ ﺑﺪل اﻟﺪم‬tissue ‫ﻣﺎ ﻫﻮ؟ ﺧﺮوج اﻹﺑﺮة ﻣﻦ اﻟﻮرﻳﺪ ووﺻﻮل اﻟﺪواء إﱃ اﻟـ‬
‫ﻣﺎذا ﻳﺤﺪث؟‬
Severe vasoconstriction
Tissue necrosis :‫ﻣﻤﻜﻦ ﻳﺆدي إﱃ‬
:vasopressors ‫إﻋﻄﺎء‬
‫ﻟﻴﺲ إﺟﺮاء ﺑﺴﻴﻂ‬
:‫ﻳﺤﺘﺎج‬
‫ﻛﺎدر ﻣﺘﻤﺮّس‬
(Critical care) ‫ﻣﺮاﻗﺒﺔ دﻗﻴﻘﺔ‬
(‫ ﺑﻄﺮﻳﻘﺔ وﺻﻔﻴﺔ‬Summary Table) ‫ﻣﻘﺎرﻧﺔ اﻟﺘﺄﺛﻴﺮات‬
(Extravasation Antidote)
:‫اﻟﺴﺆال‬
:‫ ﻟـ‬extravasation ‫إذا ﺣﺪث‬
Norepinephrine
Epinephrine
‫ﻣﺎذا ﻧﻌﻄﻲ؟‬
Phentolamine :‫اﻟﺠﻮاب‬
-blocker ‫ﻟﻤﺎذا؟‬
vasoconstriction ‫ ﻳﻌﺎﻛﺲ ﺗﺄﺛﻴﺮ‬Vasodilation :‫ﻳﻌﻤﻞ‬
2026/4
NS, BRIEF TEAM / MOHAMMAD BANIHANI, MD
This content includes:
Slides, dr.’s record and
Past-Years Questions
❖ Multiple Sclerosis: is an autoimmune inflammatory demyelinating disease of the CNS that is a leading
cause of disability in adults.
❖ The risk factors include:
o Ages between 20 and 40 years are at higher risk
o Women are at higher risk
o Family history
o Low level of Vitamin D (low sun exposure) → associated with aggressive MS, therefore,
all MS patients should take Vitamin D.
o Smoking
o Certain infections (EBV)
❖ Multiple sclerosis attack: Patient-reported symptoms or objectively observed signs typical of an acute
inflammatory demyelinating event in the CNS, current or historical, with duration of at least 24 hours, in
the absence of fever or infection. ‫مهم‬
❖ Common presentations suggestive of Clinically Isolated Syndrome (CIS):
o Optic neuritis: Painful subacute unilateral visual loss that present as visual blurring.
o Brainstem or cerebellar syndrome
- Diplopia due to ophthalmoplegia
- Ataxia with nystagmus, facial sensory symptoms, vertigo & paroxysmal symptoms.
o Spinal cord syndrome: …
o Incontinence, dysarthria, dysphagia … many other symptoms that doctor didn’t mention
❖ If MS is highly suspected → next step is MRI with contrast (to see if there are active and inactive lesions)
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NS, BRIEF TEAM / MOHAMMAD BANIHANI, MD
❖ McDonald criteria for diagnosis of MS:
❖ CSF examination shows Oligoclonal bands & elevated IgG index
❖ Treatment of relapsing remitting MS:
 During acute attack: give Glucocorticoids (Intravenous methylprednisolone 1000 mg daily for 3-5 days
without oral tapering)
- Relapses include functionally disabling symptoms with objective evidence of neurological
impairment, sensory attacks are often not treated (symptomatic relief)
- Improves short term outcomes, but has no effect on disease activity or long-term disability
- Do Plasma exchange if there is significant neurological deficit (speech problem…)
 Disease-modifying therapy (injectable therapies for disease modification in MS)
-
-
Leads to relapse rate reduction, reduction in new T2 lesions & Gd enhancement, MRI activity, relative
reduction in EDSS score.
Interferon (can lead to Flulike symptoms, Injection site reaction…), Natalizumab (Humanized monoclonal
AB that increase the risk of PML (JC virus)), Glatiramer acetate…
❖ Pregnancy & MS: ‫مهم‬
Pregnancy decreases the risk of relapses (protective effect). But there is an increase in disease
exacerbations in early postpartum period (the first 3 month after delivery).
‫ نسأل هللا أن يوفقكم جميعًا ويسدّد خطاكم‬،‫تم بحمد هللا‬
Mohammad M banihani, MD
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