Clavicular head originates on the medial 1/3rd of the clavicle.
Both insert on the mastoid process of the temporal bone.
Unilateral contraction laterally flexes the neck and rotates the head to turn the face to the opposite side.
Bilateral contraction extends the neck at the base of the head (if the posterior fibers contract) or, flexes the neck so that the chin moves toward the sternum (if the anterior fibers contract).
Sternocleidomastoid divides the cervical region into anterior and posterior triangles.
Trapezius
Originates on the external occipital protuberance, the nuchal ligament over the cervical vertebrae, and the spinous processes of the thoracic vertebrae; it inserts along the lateral 1/3rd of the clavicle and also the acromion and spine of the scapula.
Trapeziuseither adducts, rotates, elevates, or depresses the scapula based on which muscle fiber region contracts.
Platysma:
Originates on the superficial fascia over the superior shoulder and chest, and inserts into the skin and muscles of the mandible; it depresses the skin of the neck and lower lip and angle of the mouth.
Because of their actions on the larynx and hyoid bone, the infrahyoid muscles are involved in swallowing and speech.
Deep muscles:
Sternothyroid
Originates on the manubrium of the sternum and the first costal cartilage and inserts on the oblique line of the thyroid cartilage; it depresses the larynx. It overlies the trachea.
Thyrohyoid
Originates on the oblique line of the thyroid cartilage
Inserts on the body of the hyoid
Depresses the hyoid and elevates the larynx
Superficial muscles:
Sternohyoid
Originates on the manubrium and the medial end of the clavicle
Cartilage type is determined by matrix and fiber components.
Hylaine Cartilage
The most common type in the body.
Matrix
Glassy, pink-staining, gel-like matrix comprises a ground substance of proteoglycan aggregates, chondronectin, and water.
Isogenous groups of chondrocytes are housed within lacunae; the darker staining ring around the lacuna is the cartilage capsule.
Invisible type II collagen fibers.
Locations:
Sternal ends of the ribs, many articular surfaces, the tracheal rings, the larynx, and the nasal septum.
Hyaline cartilage is also the skeletal precursor during development.
Functions:
At the articular surfaces, hyaline cartilage provides a smooth surface for free movement; elsewhere, such as in the nasal septum, it provides structural support.
Elastic Cartilage
Shares many similarities with hyaline cartilage.
Matrix
Very light staining
Chondrocytes in lacunae
Elastic fibers create a dark-staining network around the lacunae
Locations:
Auditory tubes, epiglottis, and external ear
Functions
Elastic fibers provide flexibility with recoil; for example, when you bend your external ear, it moves easily, but snaps back into place when released.
Fibrocartilage (aka, fibrous cartilage)
Highly organized appearance.
Collagen fibers
Tightly packed, thick bundles of type I and type II collagen fibers run in parallel.
Lacunae and chondrocytes lie in rows between the collagen bundles.
Locations
Intervertebral discs, the pubic symphysis, and the joint capsules
Functions:
Provides tensile strength and resistance to compression; its dense nature allows it to bear a weight, as in the intervertebral discs.
Integumentary system serves to both protect the body and assist in the maintenance of homeostasis.
Comprises the skin, which divides into:
The Epidermis
The Dermis
The Skin Accessory Organs (derivatives): hair, glands, and nails
EPIDERMIS
Superfical to Deep:
Stratum corneum
Outermost layer; it comprises numerous rows (25-30) of flat, dead cells.
Contain keratin.
Continually sloughed.
Stratum lucidum
Comprises clear-appearing cells.
Lack nuclei and organelles.
Contain keratin and eleidin.
Stratum granulosum
Comprises 3-5 rows of cells that contain keratohyaline granules.
Help form the keratin cells of the epidermis.
Stratum spinosum
Comprises, most notably, several rows of keratinocytes.
They are called prickle cells due to their spiny appearance.
Within the stratum spinosum layer, desomosomes exist, which form intercellular bridges.
Stratum basale
Forms the deepest layer of the epidermis.
It comprises a single layer of cuboidal keratinocytes that are active in cellular reproduction (mitosis).
Responsible for hair growth
Occurs when stratum basale generates new hair cells that push the old, keratinized hair cells through the follicle to form hair fibers.
Note that melanocytes and Merkel cells also exist within this layer.
Melanocytes are responsible for the formation of melanin, which derives from tyrosine.
“Come Let’s Get a Sun Burn”
Use the “Come Let’s Get a Sun Burn” to remember the layers
Come – Corneum
Let’s – Lucidum
Get a – Granulosum
Sun – Spinosum
Burn – Basale
TYPES OF SKIN
Thin skin
Most ubiquitous form of skin
Thin skin lacks a stratum granulosum and stratum lucidum and has a relatively small amount of stratum corneum.
75 to 150 μm thick.
Thick skin
Restricted to discrete areas that are commonly traumatized.
Key regions: palms and soles.
Thick skin contains both stratum granulosum and stratum lucidum.
Has a prominent stratum corneum.
400 to 600 μm thick.
DERMIS AND SKIN ACCESSORY ORGANS
Papillary layer, with dermal papillae
Forms a thin layer of loose connective tissue with finger-like projections, called dermal ridges (aka dermal papillae).
They interdigitate with the epidermal down-growths (epidermal papillae) — they form fingerprints.
Reticular layer
Forms the bulk of the dermis.
It comprises a dense layer of collagen bundles and elastic fibers
(as opposed to the papillary layer, which is loosely constructed)
Hypodermis
Superficial fascia layer (and not a layer of the skin).
ACCESSORY ORGANS
Derivatives/appendages of the skin.
Hair
Shaft, root, and dermal papilla.
Hair follicle invaginates the epidermis.
The outer root sheath of the hair follicle is continuous with the epidermis.
Hair follicle comprises:
Hair shaft, which is the slender filament at the center of the follicle that extends above the epidermis.
Hair root, which is the expanded region of the hair follicle, deep within the dermis at the root of the hair follicle.
Dermal papilla, which contains the capillary network that nourishes the hair follicle; not to be confused with dermal papilla that interdigiate with epidermis.
Arrector pili
Smooth muscle attached to the dermal sheath surrounding the hair follicle.
Glands
Sebaceous glands
Commonly associate with hair follicles;
Sebaceous glands are branched acinar, holocrine glands, which have a lobulated appearance.
They secrete sebum (an admixture of an oily/lipid substance and degenerating epithelial cells) into hair follicles.
Keeps hair supple, skin soft, protects against microorganisms, and maintains the hydration status of the epidermis.
Sweat Glands: Eccrine and Apocrine
Eccrine glands secrete sweat and are most prominent on the palms, soles of the feet, and forehead.
Sweat is formed through the filtration the blood into a hypotonic solution that is primarily water with small amounts of such products as salt, antibodies, metabolic waste, vitamin C, and dermcidin.
Apocrine glands are specialized, and (unlike the nearly ubiquitous eccrine glands) are confined to specific regions, namely: the axilla, areolar nipple, and perianal region.
Other apocrine, non-sweat producing glands are ceruminous glands, which lie in ear canals and secrete cerumin, and mammary glands, which produce and secrete milk.
Nails
Comprise a nail bed, nail plate, cuticle, lunula, hyponchium, and nail root.
Other stuctures:
Blood vessels
Vascularize the dermal papilla
Sensory nerve receptors
Within papillary layer
Meissner copuscles
Mechanosensitive (light touch detection)
Unmyelinated nerve fibers
Transmit pain and temperature sensation.
Within reticular layer
Pacinian corpuscles
Krause end-bulbs
Mucocutaneous (eg, oral cavity) receptors.
Clinical Correlations
Neuropathy
See Sensory Receptors
CLINICAL CORRELATIONS: COMMON SKIN LESIONS
Flat, Discolorations
Macules
Patches
Raised Lesions
Papules
Nodules
Plaques
Blisters
Vascular Lesions
Petechiae
Purpura
Ecchymosis
Infectious Lesions
Pustules
Vesicles
Venous-backflow Lesions
Varicose Veins
Stasis Dermatitis
PHASES OF HAIR GROWTH
Human hair grows at 2mm per day.
Human head has ~ 150,000 hairs.
Anagen phase
Growing phase
Catagen phase
Growth respite phase.
Telogen phase
Terminal resting phase (when hair falls out).
HAIR COLOR
Hair derives its color from the melanocytes that lie within the hair follicle basement membrane on the surface of the dermal papilla.
The bending of light when a wave travels from a medium with one refractive index to a medium with another.
LIGHT RECEPTION – OVERVIEW
Occurs within the photoreceptors of the retina, of which there are two main categories: cones and rods.
Cones detect color vision and require bright light.
Rods detect black/white (“night”) vision, so they only require low levels of illumination.
OPTIC REFRACTION
Anatomy
The cornea has a pronounced curvature and is transparent to allow for the passage of light.
Where the cornea ends, the outer layer becomes the sclera, which is opaque, so it blocks the transmission of light. The portion of the sclera we can see is the “white of the eye”; conjunctiva covers it.
The biconvex lens is also transparent and serves to focus a target on the retina, specifically on the area of maximal visual acuity: the fovea centralis of the macula.
The anterior cavity, which lies in front of the lens, contains aqueous humor.
The posterior cavity, which lies behind the lens, contains vitreous humor – it’s referred to as the vitreous chamber, or vitreous body.
Like aqueous humor, vitreous humor is primarily water, but the presence of glycosaminoglycans and collagen gives it a gel-like composition, which helps maintain the eye’s shape.
Physiology
There are 4 key anatomical components to optic refraction:
Primary mediator is:
The Cornea It comprises 70% of the power of optic refraction through its pronounced curvature and through its corneal refractive index, which is substantially higher than that of the environmental air. The refractive index is the degree to which a medium bends light.
Secondary mediators are:
Aqueous humor
The Lens
Vitreous humor
Rays of light enter the cornea and bend to ultimately converge at the macula.
LIGHT DETECTION WITHIN THE EYE
Anatomy
The uvea.
In front of the lens, lies the pigmented iris, which forms an adjustable diaphragm to funnel light through the pupil – the pigmented epithelium of the iris blocks light transmission and funnels light through the pupil.
Posterior to the iris, lies the ciliary body.
The choroid, which is a thin, brown, highly vascular layer is sandwiched between the sclera and retina; it nourishes the retina and removes heat produced during phototransduction, which is the process wherein the photoreceptors transform light into neural signal, and its brown pigment helps absorb light.
The ciliary body anchors suspensory ligaments, collectively called zonule, which stretch the lens and alter its refractive power.
The retina lies internal to the choroid.
It transitions into optic nerve when it exits the eye, posteriorly, at the lamina cribrosa.
Key aspects of the retina are: the optic nerve head and the macula, the area of highest visual acuity (in the center of it, lies the fovea centralis).
At the macula, the various retinal layers are displaced to the sides to allow light the best passage directly to the photoreceptors.
Brief notes on the Physiology of Light Detection and Phototransduction
Rays of light enter the cornea and bend to ultimately converge at the macula.
Electrical impulse, then, passes along the retina to the optic nerve.
PATHOPHYSIOLOGY OF OPTIC REFRACTION
Emmetropia refers to normal refraction.
Ametropia refers to abnormal refraction.
In myopia, objects focus in front of the retina (the eyeball is too long).
In hyperopia, objects focus behind the retina (the eyeball is too short).
In astigmatism, there is image blurring irrespective of object distance from unequal curvatures in the various parts of the cornea.
Histology of the Retina & Physiology of Phototransduction – Overview
Light reception occurs via photoreceptors within the retina.
The pigmented layer is involved in photoreceptor metabolism; it comprises retinal pigemented epithelium (commonly abbreviated RPE), which captures light not picked up by the photoreceptors.
The photoreceptor cells divide into cones and rods.
Cones provide high-resolution color vision via photoreceptors that are large, conical, active in bright light, and are located predominantly centrally within the retina, meaning in the fovea of the macula,
Rods provide low-resolution black/white (or “night”) vision via photoreceptors that are small, narrow and cylindrical, and require only dim light (low-level illumination), and are predominantly located peripherally within the retina – meaning outside of the macula.
Differences in the number of receptor subtypes and their opsins – the photoreceptor proteins the determine the color waves they capture.
For the cones, there are generally three types of the photoreceptors which contain opsins that ultimately handle either red, green, or blue light.
Rods possess one type of photoreceptor, which contains rhodopsin.
The photoreceptor cell segments, themselves, are metabolically dependent upon the pigmented epithelium for photoreceptor regeneration and waste disposal.
Interneuronal cell bodies comprise multiple cell body types and perform multiple functions, including passing forward electrical signal from the photoreceptor cells to the ganglion cells.
The ganglion cells send axons, which form the nerve fibers, which are unmyelinated so as to NOT impeded the light from passing through the retina to the photoreceptor cell layer.
Summary
Light passes through the retina and is captured by the photoreceptor cell segments where the phototransduction cascade occurs, which converts light to neural signal.
Electrical signal is passed back through the retina.
Baron Constantin von Economo first hypothesized about the anatomy of the sleep induction center when in 1916–17 he studied the clinical–pathologic correlations of patients who had died from encephalitis lethargica (aka von Economo’s encephalitis).
The parkinsonian and oculomotor manifestations found in patients with that disorder led him to postulate that:
The sleep induction center lies within the anterior hypothalamus
The area for wakefulness lies, roughly, within the posterior hypothalamus/upper brainstem
Over the next several decades, he was proven, to a large extent, correct.
THE ANATOMIC LOCATION OF THE SLEEP CENTER
The area for non-REM sleep induction lies within the anterior hypothalamus, specifically in the ventrolateral preoptic area and the median preoptic nucleus.
THE PHYSIOLOGY OF SLEEP
Thalamocortical network
Thalamocortical network generation of sleep electroencephalographic (EEG) patterns — sleep spindles and slow-wave sleep.
The reticular thalamic nuclei gate the flow of information between the thalamus and cerebral cortex, and the thalamocortical neurons drive cortical EEG patterns through, at least in part, the low-threshold spike.
The reticular thalamic nuclei causes GABAergic inhibition of thalamocortical cells.
Eventually the thalamocortical membrane hyperpolarizes more negatively than –65 mV, which causes the T-type calcium channels to open, which generates a low-threshold spike: a burst of action potentials.
The thalamocortical burst acts both on the reticular thalamic cells to facilitate their rhythmic oscillation and also on the cortical pyramidal neurons, which generate the EEG patterns observed during sleep.
After the low-threshold spike, there is a refractory period for the thalamocortical neurons.
As a byproduct of the refractory period, there is cessation of the excitatory thalamocortical inputs to such relay neurons as the lateral geniculate nucleus, which results in the phenomenon of sensory gating: the process wherein sensory stimuli that might otherwise wake us from sleep fail to reach our cerebral cortex.
REM SLEEP
The putative primary REM-promoting region lies within the pons, in what is called the sublaterodorsal nucleus in the rat and the perilocus coeruleus in the cat.
This region excites the cortex to produce the characteristic EEG pattern of REM sleep.
And also excites a constellation of nuclei called the supra-olivary medulla to produce muscle atonia during REM sleep.
REM inhibition comes from the midbrain (during wakefulness and non-REM sleep) from the ventrolateral periaqueductal gray area and the dorsal deep mesencephalic reticular nucleus, which tonically inhibit the sublaterodorsal nucleus/peri-locus coeruleus.
REM disinhibition comes from the hypothalamus, from lateral hypothalamic melanin concentrating hormone nuclei, and from the medulla, from the dorsal paragigantocellular nucleus, which suppress the REM inhibition subnuclei and frees the REM promoting region to act on the supra-olivary medulla and cerebral cortex to produce REM sleep as previously described.
The suprachiasmatic nucleus (the master timekeeper) to adjust the production and release of melatonin and, in turn, the timing of our internal clock with help from the retinohypothalamic pathway.
Orexin (aka hypocretin), which acts via the flip-flop switch, and is notably dysregulated in narcolepsy.
Wake-promoting cells that are: cholinergic, histaminergic, dopaminergic, serotinergic, noradrenergic.
SUPRACHIASMATIC CIRCUITRY & MELATONIN
Melatonin helps drive us to sleep.
Key Anatomy
The suprachiasmatic nucleus lies just above the optic chiasm in the anterior hypothalamus and the paraventricular nucleus lies above it.
Dark Phase
During the DARK phase, descending hypothalamospinal projections from the paraventricular nucleus excite the cervical spinal cord.
The cervical spinal cord, in turn, excites the superior cervical ganglion.
The superior cervical ganglion activates the production of melatonin from within the pineal body, causing its release into circulation, which helps promote sleep.
Light Phase
During the LIGHT phase, light passes along the retinohypothalamic pathway to excite the suprachiasmatic nucleus.
The suprachiasmatic nucleus inhibits the paraventricular nucleus, which causes inhibition of the production and release of melatonin, thus promoting wakefulness.
THE NEUROBIOLOGY OF WAKEFULNESS
In the 1940s and 1950s neurophysiologists Giuseppe Moruzzi and H. W. Magoun performed a series of EEG studies to prove the existence of the wakefulness center.
They described an active arousal generator in the brainstem reticular formation, coined the ascending reticular activating system, which was shown to directly and indirectly activate the cerebral cortex by way of diff use projection fibers; we addressed these intralaminar thalamic projections in the thalamus section.
Key nuclear groups
The cholinergic basal forebrain nuclei in the ventral surface of the frontal lobe (orbitofrontal gyri).
The tuberomammillary nucleus in the center of the hypothalamus: it is the sole source of histamine in the brain.
The substantia nigra and ventral tegmental area (which are dopaminergic): in the anterior midbrain.
The laterodorsal tegmental and pedunculopontine nuclei in the lower midbrain and upper pons (which are cholinergic).
The locus coeruleus (which is noradrenergic): in the posterior pons – (the largest concentration of locus coeruleus neurons lies within the pons).
The dorsal group of raphe nuclei and (serotinergic) – in the central upper pons and midbrain.
Pharmacologic corollaries
Wake-promoting
Amphetamines are adrenergic reuptake inhibitors and are stimulatory
They increase the amount of circulating monoamines.
Serotonin-norepinephrine reuptake inhibitors (as their name states) increase serotonin and norepinephrine, which are wake-promoting.
Cholinesterase inhibitors (like donepezil) are mentally energizing and used to help memory.
Sleep-inducing
Tricyclic antidepressants can be especially sedating because they often have both anti-cholinergic and anti-histaminergic properties.
Diphenhydramine (Benadryl) is an anti-histamine, so it causes drowsiness and is used in over-the-counter sleep aids.
OREXIN AND THE FLIP-FLOP SWITCH
Wakefulness
Wake-promoting cells inhibit the sleep center and that the orexigenic cells excite the wake-promoting cells: they stabilize the biphasic aspect of this physiology.
Sleep
The sleep center inhibits the wake-promoting cells and the orexin area.
Flip-Flop Circuit
An electrical engineering term for a switch that avoids transitional states; the circuit is in either one of two states but not a blend of both.
If you are tired when you lie down, you quickly fall asleep, and when you’re ready to rise, you suddenly wake up.
This is unlike most other key physiologic processes, which function along a continuum (eg, heart rate or respiratory rate).
Sleep Center
For reference, the SLEEP CENTER is the following important hypothalamic areas: the ventrolateral preoptic area and the median preoptic nucleus.
Wakefulness stabilizer
OREXIN AREA is the region in the perifornical-lateral hypothalamic populated with orexigenic cells, which form the wakefulness stabilizer.
Wake-promoting cells
Wake-promoting cells are those we addressed in our section on wakefulness neurobiology.
Be aware that there are a few different versions of the TORCHeS acronym and the infectious diseases included; we’ll use a relatively inclusive version for completeness.
Overview
This tutorial includes key infections that are transmitted from the woman to fetus or neonate during pregnancy or birth.
These infections are a significant source of fetal and neonatal mortality and childhood morbidity.
Common manifestations — Slow growth, congenital heart disease, enlarged liver and/or spleen, jaundice, microcephaly or hydrocephaly, ocular lesions, and skin rashes.
The severity of infection often depends on its timing. — Outcomes are often more severe when infection occurs early in pregnancy; for example, early infections are more likely to lead to fetal loss.
Where available, treatment should be administered as soon as possible to minimize long-term complications. TORCHEeS acronym: Toxoplasma gondii Other (including Varicella Zoster Virus, Parvovirus B 19, Listeriosis) Rubella Cytomegalovirus Herpes Simplex Virus HIV (some include HIV in the “Others” category) Syphilis (also sometimes included in the “others” category).
Be aware that the “Others” category also sometimes includes additional infectious agents, such as Zika Virus.
Toxoplasma gondii (protozoan parasite)
Infected mothers are usually asymptomatic.
Infections occurring early in a pregnancy are less likely to be passed to the offspring; however, in the cases when infection is passed to the offspring early in pregnancy, the outcomes are worse.
In addition to the non-specific signs we listed in our table, congenital toxoplasmosis is often associated with the “classic triad”: diffuse intracranial calcifications, chorioretinitis, and hydrocephaly. — Additionally, some neonates have a characteristic “blueberry muffin rash” wherein the skin is marked by raised, bluish spots. — Long-term CNS complications can develop, including intellectual disabilities, seizures, spasticity/palsies, and vision impairments.
Treatment includes anti-parasitic drugs, including pyrimethamine, sulfadiazine, and leucovorin.
Rubella virus
Infection can cause congenital rubella syndrome.
Although infection is often subclinical at birth, characteristic manifestations may develop: — Deafness, cataracts, and heart disease
Some infants have a blueberry muffin rash.
No specific treatment for congenital rubella syndrome.
The best prevention is to ensure that pregnant women are vaccinated against the virus.
Herpes Simplex Viruses 1 & 2
Congenital infections are acquired in utero, and are rare.
Neonatal infections are acquired during birth.
3 primary patterns of HSV 1 & 2 neonatal infections, all of which can include rash: — Mucocutaneous lesions are localized to the skin, eyes (conjunctivitis), and mouth (“SEM”). — In other cases, infection is localized in the CNS, and can manifest, for example, as meningitis. — In the most severe cases, infection is disseminated and can lead to multi-organ failure and death. Some authors report that the liver and lungs are especially compromised in disseminated infections.
Acyclovir is used to treat neonatal HSV.
Because we cover HIV in depth elsewhere, we’re omitting it, here. — Be aware that recurring and/or opportunistic infections during childhood may be a warning sign of HIV infection.
“Other” Varicella-Zoster Virus (aka, Human Herpes Virus 3, chickenpox).
Congenital varicella is the result of primary infection in early pregnancy; mortality is high, and offspring that survive are likely to have skin and ocular lesions, hypoplastic limbs, and CNS abnormalities.
Neonatal varicella is the result of primary infection in late pregnancy; infants often develop a vesiculopapular rash. In more severe cases, disseminated infection can lead to pneumonia, hepatitis, and encephalitis.
Treatment includes VZV immune globulin, and acyclovir is used to treat disseminated infections.
Congenital listeriosis *Occurs when pregnant women consume the bacteria Listeria monocytogenes in contaminated foods
Infection early in pregnancy often leads to fetal loss.
Infection later in pregnancy can produce neonatal infections that are categorized as early or late onset. — Early onset is associated with sepsis, pneumonia, and, in very severe cases, granulomatosis infanticeptica, which is associated with a high mortality rate. Granulomatosis infantiseptica is characterized by disseminated granulomas. — Late onset listeriosis is associated with meningitis.
Antibiotics can be used to treat congenital listeriosis.
Parvovirus B19
Infection during pregnancy is associated with anemia, and that severe anemia can lead to fetal hydrops. — Fetal hydrops is characterized by fluid accumulation in multiple fetal compartments, which can lead to respiratory distress and swelling of the abdomen.
Intrauterine red blood cell transfusions have been used to treat severely anemic fetuses.
Cytomegalovirus
Congenital infection is common in the US; approximately 1 in 200 infants born in the US is affected. — Most of these infants are asymptomatic, and only 1 in 5 with the infection will develop complications of congenital cytomegalovirus syndrome, which may not be apparent at birth. — Congenital CMV is the leading cause of birth and developmental abnormalities in the US.
Key manifestations include: deafness, blueberry muffin rash, and periventricular calcifications (as well as other CNS abnormalities).
Treatment includes ganciclovir or valganciclovir.
Syphilis
Neonates with congenital syphilis are often asymptomatic at birth.
Early and late onset illnesses.
Early onset illness is defined as the arrival of symptoms before two years of age. Common manifestations include: — Rash, “snuffles” (syphilitic rhinitis), hepatomegaly with jaundice, lymphadenopathy, and long bone abnormalities such as Wimberger’s sign (which is characterized by bilateral destruction of the medial tibial metaphysis), and CNS abnormalities.
Late onset illness, defined as after 2 years of age, is characterized by a variety of abnormalities, including: — Hearing impairment — Facial features: Frontal bossing (forehead protrusion), interstitial keratitis, saddle nose (sunken nasal bridge), short maxilla (and possibly perforated hard palate), and protruding mandible. — Dental features: Hutchison incisors have a serrated appearance, and mulberry molars are pitted on the surface. — Some patients develop skeletal abnormalities such as “saber shins,” characterized by tibias that are bowed anteriorly like saber blades, and Clutton’s joints, which are characterized by symmetrical synovitis and joint swelling (especially of the knees).
General Medicine is indeed a highly important and high weightage subject in NEET MDS Exam. It is one of the subjects which are common to both Medical and Dental Courses. Given below is the list of standard books to refer & most important topics covered under General Medicine which helps in your Preparation Planning.
Given below are the list of Questions MERITERS experts will answer that are essential for an effective and efficient preparation:
Dentowesome 