Practical D.Maher.pdf

Special sense MR 0 1. Superficial reflexes A- Corneal reflexes  Tool: piece of sterile cotton  Test: Touching the cornea with tapered piece of cotton from lateral side while the subject is looking up & in (at the operator)→ response: closure of eye lids on both sides  Afferent: ophthalmic division of trigeminal  Efferent: facial nerve.  Importance: test integrity of………… 1 B- Pupillary light reflex Tool / stimulus light torch Test Direct a source of light into one eye from behind to shine on one eye , then observe the response Receptors photoreceptors Afferent optic nerve→ optic chiasma→ optic tract (No relay in LGB of the thalamus) Center pretectal nucleus of midbrain Efferent & Pretectal nucleus  EWN of both sides Preganglionic fibers in oculomotor Effector nerves  ciliary ganglion  postganglionic ciliary nerves  contraction of both organs constrictor pupillae muscles Response Direct pupillary light reflex: pupil constriction of the stimulated eye Indirect or consensual light reflex: pupil constriction of unstimulated eye, due to:  Partial crossing at optic chiasma  bilateral innervation of EWN from pretectal nucleus Argyll-Robertson pupil:  Cause: neurosyphilis due to lesion in pretectal nucleus.  Manifestations: No Pupillary constriction on light reflex (loss of light reflex) Pupillary constriction on near reflex (normal accommodation reflex) 2 C- Near Response (Near Reflex) Near Response (Near Reflex) Changes occurring on looking to near object 1. Accommodation Contraction of ciliary muscle (supplied by postganglionic ciliary nerve) ↑dioptric power of the lens to focus the image of near object on retina 2. Convergence Contraction of medial recti muscles of both eyes (supplied by motor fibers of inward deviation 3rd ) to focus images of near object on fovea centralis of each eye. 3. Miosis Contraction of 2 constrictor pupillae muscles to increase depth of focus  Pathway of near response: Receptors rods & cones Afferent Optic nerve  optic chiasma (crossing of nasal fibers)  optic tract  relays in lateral geniculate body of thalamus.  optic radiation  visual sensory area (17)→ visual association area (18, 19)  then to Center superior colliculus in midbrain Efferent From superior colliculus to both Edinger Westphal nucleus (EDW)  preganglionic parasympathetic in oculomotor nerves→ ciliary ganglion  postganglionic ciliary nerves  contraction of ciliary muscle (accommodation) and pupilloconstrictor muscle (miosis) o Motor fibers of oculomotor nerve  contraction of medial recti  convergence o Parasympatholytic drug (atropine): paralyses accommodation (cycloplegia) & pupil dilation. Accommodation Definition ↑ dioptric power of the lens via ↑ curvature → to focus image of near object on retina. Mechanism During rest:  relaxed Lens surrounded by elastic capsule →tend to be spherical → pulled by tension of suspensory ligament → cause flat lens During near vision: < 6 meters: Ciliary muscle contracts: Radial muscle fibers Circular fibers When contract: pull peripheral insertion of lens When contract → ↓tension on the lens → more ligaments forward →↓tension on lens. spherical lens 3 Purkinje Sanson’s image using a candle (3 image test) Tests for accommodation  Dark room  Hold a candle in front of & on one side of the subject’s eye  Ask him to look at a distant object  Observe the images of the candle that are formed in the eye:  Small clear upright image (a) → at anterior surface of the cornea  Large faint upright image (b) → at anterior surface of lens  Small inverted image ) (c )→ at posterior surface of the lens  On asking the patient to look to a nearby object After accommodation: only the 2nd image becomes smaller, clear & closer to image (a)  Cause: As accommodation occurs mainly due to ↑curvature of the anterior surface of lens Observation if you repeat the experiment with 70 years old patient: 2nd image will not change due to loss of accommodation(presbyopia) Observation if you repeat the experiment with oculomotor nerve lesion: 2nd image will not change due to loss of accommodation as oculomotor nerve is the efferent for the near reflex Observation if you repeat the experiment after putting atropine: 2nd image will not change due to loss of accommodation due to blockage of muscarinic receptors Determination of the near point:Nearest point seen clearly with maximum accommodation= 8 cm at 10y old 100 cm at 70 years (↑with age) due to loss of accommodation 4 Demonstration of physiological blind spot Optic Disc  Exit of optic nerve from the retina  3mm nasal (medial) to macula  Contains no rods and cones→ cause physiological blind spot = physiological scotoma Test dot & cross experiment (card)  General rule of examination  Close right eye  Look at the cross by the left eye (cross present on the right side)  Moving the paper closer to the face,  At a certain distance: o The dot (temporal) disappears from the visual field and then reappear because its image is falling on the blind spot of the eye  Each eye should be examined separately as to avoid the masking effect of other eye on blind spot 5 Visual Fields  Field of external world can be seen by one eye (keeping fixed gaze)  Not circular (irregular oval)  limited medially by the nose  superiorly by the roof of the orbit  Extends  50 degrees upwards,  80 degrees downwards,  60 degrees nasally  90 degrees temporally.  Binocular vision= Overlap of both central parts of both visual field  Visual field is divided into 4 quadrant though the fixation point (nasal, temporal) (upper, lower)  Scotoma: loss of small area of visual field (physiological scotoma???)  Measured by Perimeter (mapping of visual field) technique = perimetry Confrontation method: the examiner compares his field with that of the patient  Examine the facing eye while closing the other one  Sit facing the patient with a distance of 60 cm  both eyes on the same level  Move a finger from the periphery in different directions and ask the patient when seeing it.  He must see it nearly at the same time as the examiner  Repeat the test on the other eye 6 Neural pathway of vision (Visual Pathway) Photoreceptors rods & cones  bipolar cells  ganglionic cells (axons form optic nerve) Nasal retina receives rays from temporal visual field and vice versa. Upper half of the retina receives light rays from lower visual field and vice versa. Optic nerve → Optic chiasma (nasal fibers cross / temporal fibers on ipsilateral side) Optic tract Carries impulses from opposite halves of visual fields of both eyes. LGB of thalamus  optic radiation  primary visual sensory (striate) cortex (area 17) in occipital lobe primary visual Right visual cortex receives from right halves of both retina cortex (area 17, i.e. temporal of same side & nasal of opposite side. striate cortex) : (Carry impulses from opposite halves of both visual field) Upper halves of retina: represented superiorly/ lower portions: inferiorly. Peripheral parts of retina: represented anteriorly Macula: represented posteriorly at occipital pole & widely  Hemianopia= blindness of half of visual field Heteronymous Homonymous Bitemporal Binasal Loss of the same halves of both visual field Loss of both temporal  Quadrantanopia= blindness of one quadrant  Scotoma= patchy loss of field of vision Lesions of visual pathway: site???? or drawing the lesion???? Unilateral lesion in the optic nerve Blindness of corresponding eye. Direct light reflex is lost in blind eye. Lesion at center of optic chiasma (e.g pituitary bitemporal hemianopia tumor) (heteronymous) Lesion at the lateral side of optic chiasma binasal hemianopia (heteronymous) Lesions at optic tracts or geniculate body Contralateral homonymous hemianopia Lesion of optic radiations Contralateral homonymous hemianopia or contralateral quadrant-anopia. Unilateral lesion of the occipital cortex (area 17) contralateral homonymous quadrant-anopia with macular sparing Macula: widely represented in visual cortex+ extensive blood supply Fibers from upper and lower quadrants of both sides of the retinae and maculae are represented on the occipital cortex above and below calcarine fissure 7 Lesion above or below the fissure result in quadratic visual field defect Retro-chiasmal lesion cause homonymous hemianopia or quadrant-anopia. To localize the lesion of the visual pathway, elicit the light reflex on the blind half of retina  If light reflex is absent: lesion in optic nerve, chiasma, tract before the fibers branch off  If light reflex is intact: lesion is beyond optic tract 8 Visual acuity  Shortest distance by which 2 lines can be separated and still perceived as 2 lines.  Depends on refractive power & density of photoreceptors, the visual angle (angle at nodal point) Requirements:  2 points make visual angle of 1 minute at the nodal point of the eye (space on retina 4.5um)  2 images fall on 2 cones separated by at least one un-stimulated cone Fovea centralis has the greatest visual acuity in photopic vision Mid peripheral portion of the retina the greatest visual acuity in scotopic vision Test: Subject at 6 meter (20 feet) =d (distance)/ cover one eye/ with & without glasses (MR) Normal acuity is 6/6) or 20/20 (if you use the standard in feet) (d/D) distance from where subject can read / normal subject can read  Snellen’s letter chart  Landolt’s chart 9 Error Myopia Hypermetropia Presbyopia Near sightedness Far sightedness Definition/problem Parallel rays Parallel rays ↓ power of accommodation by focus in front of retina focus behind retina aging Cause ↑ refractive power of ↓ refractive power ↓elasticity of lens by age due to the eye of the eye protein denaturation Long eye ball > normal Short eye ball Near point: < 10 cm > 10 cm Near point: recede away from eye Far point < 6 meter Normal by Far point: does not change accommodation Correction Concave (Divergent) Convex convex lens for near vision only lens (Convergent) lens Astigmatism: irregularity of corneal /less commonly lens curvatures in various planes. egg shaped Light rays in certain meridian are refracted to focus (different from that of other meridian) Power of lens system (MR) is different in different axes →inability to focus on horizontal or vertical lines at the same time For astigmatism: astigmatism chart 6 m (20 feet): some spokes appear sharp & dark, others appear blurred and lighter Like spokes of wheel Emmetropic eye: distant object can seen clearly while ciliary muscles are relaxed 10 11 Test for color vision Ishihara’s Chart Test (colored plates) Color vision is Function of the cones Mechanism of color vision: (Young-Helmholtz theory) trichromatic theory of color vision Color blindness (achromatopsia) Definition inability to perceive portion of spectrum or to discriminate between colors. Cause Congenital sex-linked recessive disease (X-linked). Males (8%) more affected than females (0.4 %). Types of color blindness A- Color anomaly (Anomalous Trichromats): Has 3 cones but weakness in one color (red, or green or blue) Protanomaly Deuteranomaly Tritanomaly weakness of red color weakness of green color weakness of blue color. (most common) B-Color anopia: loss of perception of one or more primary color Dichromatic: 2 cones working, one affected, match color spectrum by mixing only 2 primary colors. Protanopia Deuteranopia Tritanopia Red blindness green blindness blue blindness (rare) Monochromatic: one cones working, Match color spectrum by varying intensity of one primary color Colored number on background of colored spots Confusion in differentiating the color in color blindness= fails to read the number or deviates from zigzag line (trace the path) 12 13 MHR 0 Hearing tests ( ) Amplitude (intensity) of sound measured by decibel (dB)= 20 𝑙𝑜𝑔 =` ( )  Minimal intensity heard = zero db Range of normal frequency heard by humans = 20- 20000 Hz. e.g. if audiogram showed that he lost 40 db, how many times, he can hear more than threshold pressure Tuning fork tests: To differentiate between conductive & nerve deafness.  High frequency [short arm] tuning fork Weber test Rinne Test Procedure Base of the vibrating tuning fork Base of a vibrating tuning fork is placed on is placed on vertex of the skull mastoid process until bone conduction is over. Then the tuning fork is held in air next to ear Normal finding Sound is heard equally in both sound is heard in air after bone conduction ears is over conduction deafness sound is heard better in sound in not heard in air in diseased ear (one ear) diseased ear, after bone conduction is over. due to absence of masking effect of environmental noise on diseased side nerve deafness Sound is heard better in normal both bone and air conduction are impaired (one ear) ear sound is heard in air after bone conduction is over as long as nerve deafness is partial Explain why normally air conduction is better than bone conduction? Air conduction allows amplification 22 times (Impedance matching) a. Force collected over large area of tympanic membrane is concentrated over smaller area of footplate of stapes in oval window → ↑ pressure (17 times). b. Ossicles act as a lever→ ↑ pressure 1.3 fold 1 Pure tone audiometry device: audiometer  Significance of air conduction audiogram (sound given to external ear): measure the sensitivity of the entire hearing mechanism (external, middle, sensory neural of cochlea and auditory nerve)  Significance of bone conduction audiogram: measure only the sensitivity of sensory neural mechanism) From the case, draw the expected air, bone conduction? with symbol A- Conduction deafness: Inability to hear sounds due to  Causes: ear wax, perforated ear drum, otosclerosis  Explain your answer:  Bone conduction curve shows normal threshold for hearing  Air conduction curve shows increased threshold for hearing, due to impaired amplification of sound)= curve is shifted downward 2 B- Nerve deafness: Inability to hear sounds due to  Congenital defect in cochlea  Ototoxic drugs (streptomycin)  Presbycusis: age-related, progressive sensorineural hearing impairment of high frequency sounds in elderly individuals.  Explain your answer:  Both bone & air conduction curves show increased threshold for hearing (both curves shifted downwards) 3 Indications and clinical significance pure tone evaluation 1. Subjective hearing loss 2. Cases with risk factors for hearing loss 3. Identify degree of hearing loss 4. Abnormal auditory perception 5. Ear trauma or otologic diseases 6. Tinnitus 7. Ototoxic monitoring protocol 8. Speech delay in children Gold standard for determining type, degree, configuration of hearing loss including the amount of conductive compared to sensorineural hearing loss THE SENSE OF TASTE: ‫ اﻟﻨﻈﺮي‬note 4 Motor nervous system M Motor nervous system Function: generation and control of voluntary & reflex movement Organization Central apparatus Peripheral apparatus Cortex, AHC , axons , NMJ, muscle Cerebellum, basal ganglia, Descending tracts (as pyramidal system) Types of motor neurons Upper motor neurons (UMN) Lower motor neurons (LMN) (Pyramidal and extra-pyramidal tracts) (Motor nerves to skeletal muscles) Originate from cortex and brain stem → synapse with cells of (LMN) M Motor nuclei of cranial nerves (3, 4, 5, 6, 7, 9, 10, 11, 12) Spinal motor neurons (AHCs) Clinical importance of motor examination a) Diagnosis of different neurological disorders b) Localization of site of lesion c) Differentiate UMNL and LMNL Required tools 1- Tongue depressor (for assessment of palatal reflex, pharyngeal or gag reflex) 2- Measuring tapes (for assessment of muscle bulk) 3- Percussion hammer (for assessment of tendon reflex) 4- Pencil torch light (for assessment of light reflex) 1. Examination of muscle bulk A. Bulk 1. General rule + relaxation 2. Inspect, palpate (observe symmetry and shape for evidence of wasting, hypertrophy, tenderness) 3. Measuring tape for circumference with from fixed points (compare both sides) 4. Compare thenar and hypothenar eminence with your owns M  Abnormal findings Wasting/ atrophy of the muscle Hypertrophy (decrease muscle bulk) LMNL Exercise (symmetrical distribution + normal tone +↑power) Ischemia Myopathy (localized hypertrophy + decreased power) Lack of use ???? Description of wasting Unilateral or bilateral More distal or proximal Symmetrical or asymmetrical  Carpal tunnel syndrome? 2. Muscle power Active movement against resistance Upper extremities (segmental distribution) Shoulder abduction C5 (deltoid) Elbow flexion C5 , 6 Elbow extension C7 Fist grasp C8 Fingers abduction C8 + T1 Lower extremities Hip flexion L2 Knee extension L3 + 4 Foot dorsiflexion L4 + 5 M Foot planter flexion S1 Grading of the muscle power (manual muscle testing scale) Zero No Muscle activation (complete UMNL or LMNL) 1 Trace Muscle activation as twist, without achieving full range of motion 2 Muscle activation with gravity eliminated, achieving full range of motion 3 Muscle activation against gravity, full range of motion 4 Muscle activation against examiner’s some resistance, full range of motion 5 Muscle activation against examiner’s full resistance, full range of motion 3. Muscle tone Muscle tone: reflex continuous, sub-tetanic, alternating partial contraction (state of tension) Base of muscle tone: Static stretch reflex Muscle tone: not cause fatigue because: a. Alternating b. Sub-tetanic (constant low level of contraction) c. Red muscle fibers (involved), contract slowly & sustain force for long time. importance of muscle tone 1. General rule + relaxation 2. Passive flexion & extension (movement) of the limb at various joints and observe resistance Elbow joints Wrist joints (examined also by shaking method) Knee joints The neck M Hip joint (rolling of the extended leg by external & internal rotation) 3. Compare right and left side  Abnormal finding Hypotonia= flaccidity , hyporeflexia Hypertonia = spasticity or rigidity LMNL UMNL (recovery), Anxiety., Hyperthyroidism Shock stage of UMNL Other causes, Neocerebellar syndrome, myxedema Forms of hypertonia  Clasp knife spasticity (lengthening reaction): immediate↑ in resistance then sudden release In UMNL Due to ↑ gamma motor neurons discharge (Withdrawal of supraspinal inhibition)  Lead-pipe rigidity = continuous resistance to bending throughout movement (?)  Cogwheel Rigidity = series of catches (intermittent resistance) during passive movement ? Spasticity Rigidity Chronic UMNL Parkinsonism Area 6 lesion Other basal ganglia lesion Affect antigravity muscles Affect all muscles Clasp knife Cog wheel (interrupted) , lead pipe (continuous) Clonus No clonus Hyper-reflexia Normal Increase gamma Increase alpha & gamma No tremors Static tremors 4. Examination of reflexes Involuntary, unplanned sequence or action in response to stimulus Components of reflex arc: Reflex arc: The functional unit of the nervous system  Components:  Stimulus  Receptor (sensory organ): where impulse is initiated   Afferent neuron Center: One or more synapse in CNS Type of reflexes: M o Monosynaptic reflex (simplest reflex) (one synapse) o Polysynaptic reflex: one or more interneurons between afferent & efferent  Efferent neuron  Effector organ  Response A- Superficial reflexes: a- Corneal & light reflexes: see later b- Palatal reflex:  Tool: tongue depressor  Stimulus: Ask the patient to say “ah” ,Touching soft palate on either side of the midline with tongue depressor  Afferent: IX  Center: medulla  Efferent: X  Response: retraction (elevation) of the palate c- Pharyngeal (gag) reflex  Stimulus: Touching posterior pharyngeal wall, tonsillar area, base of the tongue, with tongue depressor  Afferent: IX  Center: medulla  Efferent: X  Response: contraction of pharyngeal muscles, elevation of soft palate  Importance: evolutionary reflex prevent swallowing of foreign objects and prevent shocking d- Abdominal reflexes:  Tool: slightly sharp pin (pin of percussion hammer)  Stimulus: supine position stroking the relaxed abdomen in all quadrants with  Center:  Upper abdominal reflexes → T7-10   Lower abdominal reflexes → M T10- 12 Response: contraction of abdominal muscle, deviation of umbilicus toward the stimulated quadrant  Response may be hidden by obesity or limited by abdominal scar e- Plantar (Babinski) reflex: Polysynaptic superficial spinal reflex  Stimulus: supine position, knee slightly bent, thigh rotated, lateral side of the foot rests on couch scratch lateral aspect of the sole with key (firm pressure not painful) starting from the heel towards the little toe & then along the bases of the toes medially to the base of the big toe  Center: sacral 1-2 (examine integrity of the center)  Response: plantar flexion of big toe (downward movement), other toes flex and come together  Abnormal response: Babinski sign: primitive response reappear following injury of pyramidal fibers  Dorsiflexion of big toe (up) + Fanning of other toes  Causes of Babinski sign: o Physiological: infants (1st year) [unmyelinated pyramidal tract] - deep sleep o Pathological: pyramidal tract lesion (UMNL) - deep general anesthesia - coma - recovery stage of spinal shock B- Deep reflexes [tendon jerks]: spinal, monosynaptic deep reflexes. How to test:  Examined muscle: uncovered, put in position that causes slight stretch to the muscle, Completely relaxed  Reinforcement (potentiate reflex if no response) via Jendrassik’s phenomenon  Clasp his hands and pull them apart in lower limb jerks  grinding the teeth in upper limb jerks  clinch fist for fraction of minutes before the test Response is increased by stimulation of gamma efferent Compare Types of jerks Center Position (how can we assess……) Ankle jerk Sacral 1-2 Dorsi-flexion of the ankle Contraction of gastrocnemius Subject kneels on a chair+ feet muscles projecting over the edge Extension of the foot M Striking (tap) Achilles tendon at level of the ankle Put some tension on gastrocnemius muscle by pressing on great toe Knee jerk Lumbar 3-4 Sitting with legs free (knee 90) Contraction of quadriceps Strike the patellar tendon just below Extension of the leg patella (knee cap) Biceps jerk Cervical 5-6 Flexed forearm 120 & support the arm Contraction of biceps tap over your thumb [ placed on biceps flexion of forearm tendon] Triceps jerk Cervical 6-7 Supine position+ elbow bent Twitch of triceps muscle Arms lies loosely across the abdomen not contract strong enough to Flexed forearm 90 cause movement Tap over the triceps tendon 2 inch above the elbow Explain how can we assess tendon jerk in the upper limb G+  Base of this reflex/ Principle: dynamic stretch reflex  in Exaggerated reflex: we can also observe clonus, lengthening reaction  clonus: regular rhythmic contractions of the muscle when it is subjected to sudden maintained stretch M Type of S mulus Aﬀerent Center Eﬀerent Response reﬂex Ophthalmic division Corneal reﬂex Superﬁcial Brain stem Facial nerve of (V) Palatal reﬂex Superﬁcial Glossopharyngeal Brain stem Vagus nerve nerve (Cranial IX) (Cranial X) Upper Superﬁcial Posterior roots of Thoracic spinal Anterior roots of spinal nerves cord segments spinal nerves abdominal (T7-T8) (T7-T8) reﬂex Lower Superﬁcial Posterior roots of Thoracic spinal Anterior roots of spinal nerves cord segments spinal nerves abdominal (T10-T12) (T10-T12) reﬂex Biceps reﬂex Deep 1ry endings C5 &C6 α-motor ﬁbers (spinal cord) Knee Jerk Deep 1ry endings L3&L4 α-motor ﬁbers (spinal cord) Achilles reﬂex Deep 1ry endings S1 &S2 α-motor ﬁbers (spinal cord) Light reﬂex Deep Light Optic nerve Brain stem Oculomotor Miosis (cranial nerve I) (Midbrain) nerve(cranial UMNL M LMNL nerve III) Possible causes Cerebrovasular strokes due to Lesion of the AHCs as in poliomyeli s hemorrhage or thrombosis in the or damage of motor nerves e.g. carpal posterior limb of internal capsule tunnel syndrome. (damage of both pyramidal and extrapyramidal ﬁbers) Muscle Bulk Absence Of Signiﬁcant Was ng because Marked Was ng (Disuse Atrophy) due paralyzed muscles are s ll innervated to the inability of the muscles to and can contract reﬂexly. Also spas city contract neither reﬂexly nor saves them from disuse. voluntarily. Muscle tone Hypertonia: Clasp Knife Type ? due Hypotonia or atonia: ﬂaccid paralysis unopposed hyperac ve facilitatory due to re cular forma on and ves bular nuclei, interrup on of the stretch reﬂex s mula ng the gamma motor neurons, facilita ng the stretch reﬂex. Deep Reﬂexes Exaggerated Absent Correlate the possible findings in the muscle bulk in LMNL to its pathophysiological basis. Marked Muscle-Wasting (Disuse Atrophy) due to the inability of the muscles to contract neither reflexly nor voluntarily 5. Coordination of movement observe all movements if progress smoothly depends on: proprioceptors, Integrity of dorsal columns, Cerebellum, State of muscle tone Of upper limb Of lower limb Finger-nose test: ask the patient to touch his nose with each index finger Heel-knee test: Finger-finger test (finger of the other hand) Place heel of one limb on the Draw a large circle in air opposite knee then slide along Dysdiadokokinesia anterior surface of the tibia Arm pulling test towards the ankle  Normal response: brake movement at appropriate time Abnormal: neocerebellar syndrome  Abnormal: Rebound phenomenon: inability to "put on" the brake Due to absence of timing, cause: neocerebellar syndrome (braking action is lost) planning action of cerebellum Other manifestations: nystagmus (can not fix his eye), kinetic tremor M What is meant by Ataxia? Incoordination of movements due to errors in rate, range, direction of movement in absence of paralysis. Types: sensory, motor ataxia Manifestations of motor ataxia (neocerebellar syndrome)? 6. Examination of the Gait Types of gait Occur in Spastic gait Circumduction (hemiplegic) gait in Unilateral UMNL Scissoring gait (paraplegic) in Bilateral UMNL Hypertonia due to increase gamma discharge due to loss of supra spinal inhibition Plantar reflex: babinski High steppage (stamping Sensory ataxia degeneration of dorsal column (absence of proprioception) gait) As in [tabes dorsalis] +ve Romberg’s sign [inability to maintain erect position with closed eyes Zigzag [drunken] gait Neocerebellar lesion Shuffling Parkinson’s disease Waddling LMNL M 7. Look for any involuntary (abnormal) movements as tremors , chorea Reflexes in frog To identify and locate the centers controlling the reflex and to demonstrate basic motor activity (reflex action) I-Reflexes in frog with intact CNS CNS center Experimental procedure Observations Intact Cerebral Observe the normal posture and spontaneous activity Voluntary movements cortex Brain stem Place the frog on its back Corrects its posture reflexes Place it on a tilted (inclined) board Tries to creep Postural & Put the frog in sink half filled with H2O Swimming corneal reflexes Corneal reflex Eye blinking Spinal reflexes Pinch or prick foot of the frog Withdrawal reflex Dip one leg in the beaker containing solution of Crossed extensor in high moderate conc. hydrochloric or acetic acid conc. M Dip one leg in the beaker containing solution of diluted scratch reflex Sulfuric acid II-Decerebrated frog (mid-brain frog)  Method: Cutting the head between the eyes & tympanic membrane.  RESULT: spinal & postural reflexes are present Only voluntary movement is lost (cortical motor effect) III-Decapitated frog (spinal frog)  Method: cutting the head below (behind) tympanic membrane (below brain stem) or pithing needle damaging the brain stem (single pithed) (double pithed)  RESULT: stage of spinal shock i.e. absent reflexes for few minutes. Spinal cord reflexes are only present after the stage of spinal shock [scratching & flexor withdrawal] loss of……………… spinal cord reflexes: Decapitated frog in spinal shock & Double pithing M Sensory nervous system Neurological examina on is evalua on of a person's nervous system integrity When neurological examina on is needed?  Following trauma  early iden ﬁca on of nervous system damage  Follow the progression of a disease  The pa ent is presen ng with numbness or weakness Neurological examina on includes………………………………………… Sensa on Feeling produced by change in the environment or by applica on of s mulus to receptors or nervous pathway: Types General (soma c via soma c aﬀerent , organic mediated by autonomic aﬀerent ), special, emo onal Soma c sensa ons 1. Mechanical a) Tac le  Touch (crude, ﬁne)  Pressure  Vibra on  Stereognosis  Tickle, itch b) Posi on sense (sta c, kine c) 2. Thermal (cold, warm) 3. Pain (cutaneous, deep, visceral, neuropathic) Pathways Dorsal Column Spinothalamic (Ventrolateral) Tract Receptors Unimodality (mechanoreptor) Polymodality ………………… Carry Carries mechanical sensations Carries different sensations a. Fine touch and pressure. a. Crude touch and pressure b. Position b. Tickle and itch c. Vibration c. Pain d. Stereognosis & graphesthesia d. Temperature Afferents Thick myelinated Aα and Aβ Thin myelinated Aδ Unmyelinated C fibers 1st DRG, fibers ascend upwards Dorsal root ganglia (DRG). Order ipsilateral (same side) as dorsal Neurons column (gracile and cuneate tracts) 2nd Order Gracile and cuneate nuclei in medulla Ipsilateral posterior horn cells of spinal cord. Neurons on the same side  Fibers carrying pain and temperature cross Fibers then cross to the opposite side immediately in front of central canal → ascend as In sensory decussation and ascend lateral spinothalamic tract as medial leminscus  Fibers carrying crude touch, tickle, itch sensations cross farther from central canal → ascend as ventral spinothalamic tract 3rd neuron ventrobasal (VBN) nuclei of thalamus→ sensory radiation →end in somatic sensory cortex How can you test the integrity of dorsal column pathway? Assess the sensa ons carried by this pathway: ﬁne touch, propriocep on & vibra on Examina on of soma c sensa on subjec ve General rules: To test for any sensa on: Wash your hands Introduce your self Pa ent: relaxed , in comfortable surrounding Explain the examina on, (assure him that is not painful), The pa ent should be asked whether abnormal sensa ons are experienced, or he/ she experienced any pain before examina on Take his consent Exposure of the examined part Examina on: eyes closed, Compare both sides: right & le / proximal & distal parts of the body Mechanical sensa ons A) TACTILE SENSATIONS 1. Touch A- Crude touch (feeling of clothes, hair comb): Touch with poor intensity discrimina on and localiza on)  Tool: Piece of co on or brush of hammer  Test: touched diﬀerent parts with…………. o Ask the pa ent if he feels the touch, and to iden fy the touched point  Receptors: Free nerve ending, hair end organ  Aﬀerent: A δ  Pathway: Ventral spinothalamic tract  Importance: Diagnosis of some neurological disorders as area examined correlated with speciﬁc dermatome Impaired in ventral spinothalamic tract lesion B. Fine touch: Touch with high intensity discrimina on and localiza on  Tool: …………………………..  Test: ……………………………  Receptors: Meissner’s & Merkel’s  Aﬀerent: Aβ  Pathway: Dorsal column 3 tests for ﬁne touch with eyes closed 1. Tac le localiza on (Topognosis): ability to localize tac le s muli with …. Tool: blunt (non-sharp) object Test: G+ closed eyes+ Touched diﬀerent parts, Ask the pa ent to localize the touched point + compare Importance: Test intact sensory pathway and cor cal sensory areas 2. Tac le (2 points) discrimina on: Ability to feel 2 touched points simultaneously, as 2 separate points with closed eyes provided that they are separated by threshold distance  Tool; weber’s compass and pair of caliper  G+ closed eyes  Start with 2 points wide apart  ↓ distance un l the pa ent feel one point  measure in mm  Most accurate: tongue (1mm), ps of ﬁngers & lip= 2-4mm, dorsum of ﬁngers (4 -6mm), Palm (8-12 mm)  Least accurate: back= 30-40 mm Factors aﬀect 2-point discrimina on (less threshold distance) (diﬀerence between ﬁngers and back)? 1. ↑number of receptors 2. small recep ve ﬁeld. 3. less convergence 4. larger area of cor cal representa on. Importance: Measure tac le acuity , abolished in cor cal damage 3. Texture of material 2. Pressure sensa on and weight discrimina on ability to feel the weight (crude pressure) and to dis nguish between diﬀerent weights (ﬁne pressure)  Tools: diﬀerent weights  Test: G +E+ Place diﬀerent weights in hands, Ask the pa ent to iden fy the varia on of weights  Receptor: Pacinian corpuscles and spray type endings  Aﬀerent: Aᵟ for crude & Aᵝ for ﬁne  Pathway: Dorsal column 3. Vibra on  Tool tuning fork of long arms low frequency tuning fork (128-256)  Test Vibra ng Tuning fork placed on bony prominences [to magnify the s mulus]. Proceed from upper parts of the body downwards. the clavicle, p of the shoulder, elbow, wrist, dorsum of the hand, anterior chest wall, anterior superior iliac spine, patella, bial tuberosity, lateral and medial malleoli and the base of the big toe Ask the pa ent how he feels the sensa on and iden fy when vibra on stop  Receptor: Meissner ‘corpuscle (80 c /sec), Pacinian corpuscles (500 c /sec)  Aﬀerent: Aβ  Pathway: Dorsal column Men on the clinical importance of the vibra on sense? Very sensi ve parameter of polyneuropathy o Impaired vibra on sense is early diagnos c sign in subacute combined degenera on of spinal cord (degenera on of posterior column) e.g. a) pernicious anemia (vit B12 deﬁciency) b) Tabes dorsalis (reduced a er introduc on of penicillin in the treatment of syphilis) c) Hemi sec on of the spinal cord due to trauma, tumors, abscesses Pa ent feels the tuning fork as cold object. o It localizes lesions of spinal cord. 4. Stereo gnosis Definition: ability to iden fy familiar objects, placed on hand with closed eyes, depends on Past experience Tool: familiar object (keys or coins) Test: Test peripheral sensa ons ﬁrst Place any familiar object in the hand (key, coins), Ask pa ent to iden fy the object , compare Receptor: mixture of tac le , pressure, temperature receptors Afferent: Aβ Pathway: Dorsal column Clinical importance: test Intact sensory pathways, cor cal sensory areas, Processing center in parietal lobe Astereognosis (Impaired stereognosis): early sign of cor cal damage (SSI & associa on area of parietal lobe), also aﬀected in diseases aﬀec ng dorsal column Determine somatic sensations that require intact cortical sensory function Stereognosis, tac le localiza on (topognosis) & 2 points discrimina on; 5. Graphesthesia Definition: it is the ability to recognize symbols wri en on the skin Grahanesthesia: absence of this sensa on Tools: pencil or dull pin Test: ask the pa ent to iden fy le ers or numbers wri en on the skin Importance: assessment of cor cal sensory func on provided that the individual sensory modali es are intact Propriocep ve sensa on examina on: - No tools required Test: Show the pa ent, with eyes open, the posi on of his big toe`(dorsiﬂexion, planter ﬂexion). Move the big toe of the pa ent from the sides and ask him if he feels it moving (kine c posi on sensa on) and if so in which direc on (sta c posi on sensa on). ask him if he feels it moving & in which direc on. Receptor Slowly adap ng: Muscle spindle in skeletal muscles , Golgi tendon organs in tendons, Ruﬃni endings in joint capsules Rapidly adap ng: Paccinian corpuscles in joint Aﬀerent Aα (mainly), Aβ Pathway: Dorsal column importance of proprioceptive sensation: Define Romberg sign Assess the integrity of dorsal column pathway. Romberg sign: the pa ent can’t maintain erect posi on with closed eyes → suggests impaired propriocep on (peripheral neuropathy / dorsal column lesion as in ….. Losing balance can be deﬁned as increased body sway, placing one foot in the direc on of the fall, or even falling. 1. The pa ent is asked to remove his shoes and stand with his two feet together. The arms are held next to the body. 2. The clinician asks the pa ent to ﬁrst stand quietly with eyes open, and subsequently with eyes closed. The pa ent tries to maintain his balance. 3. For safety, it is essen al that the observer stand close to the pa ent to prevent poten al injury if the pa ent were to fall. Define Sensory ataxia Deﬁni on: Incoordina on of voluntary movements without paralysis Cause: loss of propriocep on (Tabes dorsalis, pernicious anemia → posterior column damage) Character: → high steppage (or stamping) gait & +ve Romberg's sig II- Temperature sensa on: Tools 2 test tubes containing warm (not more than 45) & cold water (not less than 5) Test touch diﬀerent parts , Ask subject to iden fy the temperature diﬀerences Receptor free nerve ending Aﬀerent C ﬁbers (for warm) and A ﬁbers (for cold) Pathway lateral spinothalamic tract Importance more sensi ve measure of subtle dysfunc on than pain tes ng III- acute Pain sensa on: Tool: sharp pin Test: elicit the sensa on of pain by pin , record the results Receptor: free nerve endings Aﬀerent: Aᵟ Pathway: lateral spinothalamic tract Importance impaired pain sensa ons in peripheral neuropathy (stocking glove pa ern) Define abnormal pain sensation that could be found during neurological assessment 1. hyperalgesia Exaggerated pain response: Primary hyper-algesia Secondary hyper-algesia Site at injured skin (sunburned skin) in normal skin surrounding the site of injury area surrounding sunburned skin Cause Sensitization of peripheral Central sensitization of neighboring pain neurons nociceptors by inflammatory by the sensitized nociceptors mediators→ ↓pain threshold Accompanied by allodynia (exaggerated pain response to nonpainful stimuli). e.g. caused by central sensitization of neighboring tactile neurons. 2. Hypoalgesia : reduced pain sensation 3. Analgesia: Inability to feel pain sensation Clinical importance of somatic sensory examination 1- Vibra on sense → for polyneuropathy 2- Stereognosis → for cor cal sensory func on (astereognosis → early sign of cor cal pathology) 3- Iden fy aﬀected sensory pathway (dorsal column or ventrolateral spinothalamic) 4- Localiza on of site of the lesion What is the glove and stock hypothesia? Cause: Vitamin B12 deﬁciency or diabe c neuri s Manifesta on: symmetric polyneuropathy in hands & LL “Glove & stock" Sensory disturbance: numbness, ngling, burning & --- tac le sensa on then total sensory loss Deﬁne the diﬀerence between topognosis and stereognosis and their clinical importance Tool Tested examina on Sensory pathway Sensation Receptors Type of afferent The name of pathway Tools to be used fibers Crude touch A Ventral spinothalamic tract Cotton Fine touch Aβ fibers. Dorsal column Blunt non sharp object Two points Aβ fibers Dorsal column Weber's compass discrimination Vibration Aβ fibers Dorsal column Tuning fork Proprioception Paccinian Aα (mainly) & Aβ fibers Dorsal column No tools required corpuscles, Muscle spindles in skeletal muscle ,Golgi tendon organs in tendons, Ruffini endings in joint capsule and tissues around joint Stereognosis Mixture of tactile Aβ fibers Dorsal column Familiar objects e.g receptors Key Acute Pain Free nerve fibers Lateral spinothalamic A pin endings Temperature Free nerve A and C fibers Lateral spinothalamic Test-tubes Olfactory nerve CN-I Optic nerve CN-II Oculomotor CN-III, trochlear (CN-IV) & abducent (CN-VI) Ask the patient if Examine visual acuity using Snellen chart Examine the eye movement noticed any recent or Landolt chart changes in smell sense Examine visual field by confrontation test Check if there is ptosis (drooping of the eyelids) Examine light reflex Abolish the action of frontalis muscle by pressing over Smell & identify familiar Examine color vision by Ishihara chart superior orbital muscle then ask the patient to open his non irritant odors as eye coffee and peppermint Third nerve palsy Sympathetic palsy while the eyes closed in The patient can’t open his The patient can partially comparison (each eye + dilated fixed pupil open his eyes + miosis nostril examined alone) Examine the size and reaction of the pupil to light and near object In third nerve palsy →dilated fixed pupil Trigeminal nerve CN-V Examine facial sensation (touch and pain) including the forehead , cheek and lower jaw in the distribution of each branch Examine the corneal reflex in comparison fashion Examine the muscles of mastication by asking the patient to chew , bit and move jaw side to side Facial nerve CN- Vistibulocochlear Glossopharyngeal Vagus nerve CN-X Spinal accessory Hypoglossal nerve VII nerve CN-VIII nerve CN-IX nerve CN- XI CN- XII Examine taste in Examine hearing Examine taste in Elicit palatal reflex Ask the patient to Ask the patient to anterior 2/3 of the by tickling watch 2 posterior 1/3 of Elicit gag reflex shrug his move his tongue tongue to 3 cm by each the tongue. shoulders and (protruding the ear then against tongue) Examine Observe upward resistance push the tongue movement of Perform Weber movement of soft (trapezius) into the cheek forehead and and Rinne tests palate on saying mouth “ah” Ask the patient to Asking patient to Ask the patient to turn his head to Raise eyebrows stand and walk in Elicit gag reflex the side and then Close eyes upright position against resistance Show teeth & smile (observe balance Note ability to (sternomastoid) Buff out cheeks disturbance) swallow Diagnosis: Herpes zoster neuralgia caused by reactivation of varicella-zoster virus (VZV), the same virus that causes varicella (chickenpox). The virus remain dormant within dorsal root ganglia for years What is the cause of pain? On reactivation herpes virus attacks DRG causing irritation of pain afferents leading to severe pain in dermatomal segment supplied by the infected ganglion. What is the cause of the skin rash? Virus migrates with neuronal cytoplasmic flow towards the peripheral axons to their cutaneous terminals causing skin rash Explain why the symptoms are unilateral? Virus affects dorsal root ganglion at one side What is the predisposing factor for this condition in this case? Decline of immunity. He takes an immunosuppressive twice daily for his multiple sclerosis, Diagnosis: Diabetic peripheral neuropathy Neurodegenerative disorder caused by chronically high blood glucose What are the proposed criteria for diagnosing diabetic neuropathy? High blood glucose Bilateral, Distal symmetrical polyneuropathy Length dependent (affecting long fibers) Small fibers are usually affected first (spinothalamic sensations) Large fiber sensation is affected later. Other causes of polyneuropathy must be excluded Is there evidence of peripheral nervous system involvement in this case? Yes, Symptoms: burning and tingling in his feet Signs: hyperesthesia of both feet as well as decreased vibratory sensation What is the most probable diagnosis? Diabetic neuropathy What is the cause of such a condition in this patient? And how it affects the sensory nervous system High blood sugar causes microangiopathy (small blood vessels) that supply nerves with nutrients Facial muscles are innervated peripherally by ipsilateral 7th cranial nerve and centrally by the contralateral cerebral cortex. Central innervation bilateral for the upper face (forehead muscles) Unilateral for the lower face both central and peripheral lesions paralyze the lower face. Peripheral lesions (facial nerve palsy) affect also upper face Central facial palsy Peripheral facial palsy Paralysis of the lower half of one side of the face Paralysis of the whole one side of the face Caused by a stroke →damage of upper motor neurons Causes are viral infections, trauma, surgery, of the facial nerve diabetes, local infections, tumor, immunological disorders, or drugs Identify the affected cranial nerve in this case. Justify your answer Right facial nerve (cranial nerve VII) as it supplies the muscles of the face Inability to close her right eye Excessive lacrimation, Dropping of food from the mouth Inability to brush her teeth due to deviation of the mouth to the left side. Identify the possible risk factors for this condition. Obesity, hypertension and diabetes mellitus that are associated with microangiopathy. Clarify whether this affection is due to either LMNL or UMNL? LMNL as the upper part of the face is affected Enumerate the possible causes of this condition highlighting the most common cause Idiopathic/Bell Palsy (70%): Most commonly, Trauma: Fractures involving temporal bone Neoplasia: as parotid malignancies, facial and acoustic neuromas Infection: Viral, Herpes Zoster infection Outline how to manage this case Eye care: Artificial tears, prevention of corneal ulceration. Physiotherapy: Facial massage + exercises Medical treatment: anti-inflammatory drugs , antiviral , corticosteroids (( take care the patient is diabetic) Electrophysiological studies can be helpful in assessment of prognosis ENDOCRINE 2024 Growth Hormone (GH) (Somatotropin) Origin: acidophilic cell of anterior pituitary Physiological Functions of Growth Hormone A- Metabolic effects Describe the mechanism by which this hormone exerts its effect on skeletal muscle? 1. On protein metabolism anabolic ↑amino acid uptake, Stimulates DNA transcription ,,↑RNA translation , Protein sparing 2. On carbohydrate metabolism: hyperglycemic a. ↓glucose uptake and utilization in skeletal muscles and fat cells, ↓affinity of insulin receptor b. ↑glucose production by the liver 3. On fat metabolism: a. ↑lipolysis (hyperlipidemia)→increase fatty acid utilization by the muscle b. fatty liver & ↑release of acetoacetic acid into body fluids Hyperglycemia, hyperinsulinemia, hyperlipidemia and impaired insulin action= "insulin resistance" B-Effect of growth hormone on growth ????? ↑ protein synthesis, cell division and proliferation 1. On soft tissues Stimulate growth of all soft tissues , Erythropoiesis , positive nitrogen balance. 2. On bone and cartilage GH stimulates cartilaginous growth at epiphysis indirectly via Somatomedin secreted by liver?????? (somatomedin site of release, primary site of action GH →↑insulin secretion to enhance its anabolic effect Regulation of GH Secretion GH Increased by???????? GH Decreased by 1- Hypothalamic control GHRH GHIH (Somatostatin) 2- Feedback control: a. Ultra-short feedback: GHRH on itself. b. Short loop feedback: GH inhibits GHRH c. Long loop feedback control: IGF-1(somatomedin)→ ↑ GHIH secretion??? Effect of somatomedin on GH 3- Caloric supply ↓blood glucose & FFA level ↑blood glucose & FFA Fasting/ Starvation (Ghrelin) Obesity Exercise, Stress aging Protein meal 4- Hormones Sex hormones as estrogens Cortisol 5- Others during first 2 hours of deep sleep 1 Disturbances of GH Function A- Effects of Hypofunction 1. Pituitary Dwarfism: short stature (100-120 cm) ❖ Causes: a. GHRH deficiency. b. GH deficiency. c. IGF-1 local secretion by chondrocytes deficiency (normal or high GH) d. Lévi-Lorain dwarf: hereditary inability to form somatomedin C (normal or high GH)????????? e. Laron dwarf: gene mutation of GH receptor →defective receptor →GH insensitivity?????????? normal or high serum GH and low serum IGF-I levels which fail to rise after exogenous GH administration. ❖ Manifestations: a. Arrested growth →↓ size of trunk & extremities→ well proportioned Span = height Vertex to symphysis = symphysis to heel b. Normal sexually c. Normal mentally, some are intelligent but unstable psychologically. ❖ Treatment: Human GH by recombinant DNA technology. 2. Pituitary infantilism: deficiency of gonadotrophic hormones & GH→ dwarfism + hypogonadism. Differential Diagnosis of Dwarfism???????? Achondroplasia dwarf Thyroid dwarf (cretin) The most common clinical form of dwarfism. Cause: autosomal dominant gene mutation for Cause: deficiency of thyroid hormones fibroblast growth factor receptor–3: FGFR-3. during infancy Manifestations: Manifestations: Physically: disproportionate Physically: Dwarf, Disproportionate in Normal Trunk , Short Limbs visceral size in relation to skeletal size. Mentally and sexually: retarded 2 Hypersecretion of GH due to Acidophilic pituitary adenoma leads to: (cause??????????) Depending on the age 1- Gigantism???? 2- Acromegaly???????? ↑GH before adolescence (before ↑GH after adolescence (after ossification) union of epiphysis with the shaft) No linear growth of long bones Overgrowth of all bones: Overgrowth of all bones in thickness, especially terminal skeleton Tall = 200 cm Skull: box shaped, prominent supra- ciliary ridges, cheeks, nasal bones Symmetrical (proportionate) Mandible: protrusion (prognathism), teeth separation(no teeth growth). Skin & soft tissues (nose & lips): overgrowth →wrinkling Vertebrae → kyphosis due to over-weight (Osteoarthritis) Hands, feet, fingers, digits→ large & broad Overgrowth of soft tissues Overgrowth of soft tissues (muscles & viscera) Symmetrical At first: strong muscle At first: strong muscle Later weak due to inadequate muscular development later weak due to over stretch. relative to bony & visceral enlargement. General manifestations in Gigantism and Acromegaly: a. Hyperglycemia, glucosuria, DM (blood glucose???) Comment on patient HbA1c???? mechamism??? b. Goiter ???????????? (abnormalities in thyroid) c. Structural similarity between GH & prolactin In males: gynecomastia & In females: galactorrhea d. Pituitary enlargement →press on optic chiasma??????→ bitemporal hemianopia???????????? (Visual defect , lesion in visual pathway) Can be diagnosed by confrontation test and perimetry e. Hypogonadism due to pressure by the tumor on basophils secreting gonadotropins f. Ends by panhypopituitarism (destruction of all cells of the pituitary). g. ↑ secretion of 4-hydroxy proline in urine (indicator of excessive soft tissue growth)?????????????? of value in assessing the development and treatment of acromegaly. NB: Acromegaly may occur on top of gigantism (if not treated): Acromegalic Giant?????????? Treatment????????/ : microsurgical removal of the tumor or by irradiation of pituitary gland Correlate the symptoms and signs to the endocrine disorder related to this case??? Symptoms + signs in the case then hormone disorder+ mechanism changes in her facial features, …………….. ,……. … all are due to increase bone thickness and increase growth of soft tissue. vision was reduced … Bi-temporal hemianopia due to pressure on optic chiasma 3 Identify the possible laboratory investigation required in this patient Serum GH (not very significant due to pulsatile secretion), serum IGF-1, glucose suppression test. Insulin provocation test Arginine vasopressin test Prolactin Origin: acidophilic cells of anterior pituitary. Function A- In female On breast On ovary 1- Milk secretion (↑casein & lactalbumin 1- anovulation, Infertility & amenorrhea , production) irregular menses????????? inhibit release of GnRH inhibit effect of gonadotrophic hormones on ovaries Regulation / control of PRL Secretion 1- Hypothalamus a. Prolactin inhibiting hormone (dopamine) →cause tonic inhibition of prolactin (non-secretion period) b. Negative feedback (indirect): Prolactin →↑ dopamine secretion →that ↓ prolactin secretion 2- Clinical use Dopamine agonists (e.g. Dopamine receptor blockers (e.g. chlorpromazine) bromocriptine)??????? ↓PRL secretion in hyperprolactinemia Stimulate PRL secretion in hypo-prolactinemia Disturbance of PRL Secretion Hypo-prolactinemia (rare) in case of pituitary damage → cause inability to lactate after labor. Hyperprolactinemia: Adenoma of anterior pituitary→↑ prolactin secretion ❖ Effects: ↑PRL level antagonizes action of GnH on gonads (ovaries/ testis) In females Infertility, Amenorrhea ↓libido Galactorrhea (no or irregular) menses (Milk production in non-lactation period) In males Hypogonadism & sterility ↓libido Gynecomastia??? irregular menstruation and pain the breast, recurrent headaches and milky discharge of her nipples, prolactin levels 800ng investigation to be done? MRI brain to diagnose pituitary tumor 4 Panhypopituitarism Simmond’s disease (in both sexes) Sheehan's syndrome (in females after severe post-partum hemorrhage). ????????????? ❖ Cause: atrophy of adenohypophysis →↓ secretion of all pituitary hormones →2nd↓of thyroid, adrenal & gonadal functions. ❖ Manifestations: 1- ↓GH function: Generalized premature senility (progeria): a. Premature graying of scalp hairs b. Dry & wrinkled skin. c. Shrunken hands & feet. 2- ↓thyroid function: decreased (BMR) & anemia. 3- ↓Adrenal cortex function: hypoglycemia, hypotension 4- ↓Gonadotrophic hormones: amenorrhea in females, and sterility in males. Regulation of ADH Secretion ADH ↑by ADH ↓by Osmolarity ↑ plasma osmolarity 1% ↓ plasma osmolarity Blood volume ↓blood volume (Hypovolemia) →↓ABP Hypervolemia Drugs Morphine and nicotine,. Ethyl Alcohol Others Stress α- adrenergic agonists Disturbance of ADH A- Deficiency of ADH secretion: (Diabetes insipidus) Types Central diabetes insipidus Nephrogenic diabetes insipidus Cause Lesion in supraoptic nucleus Congenital defect of renal V2 receptors a. X-linked mutation of V2 receptor gene → defect in production of cAMP b. Autosomal mutation of aquaporin2 gene Manifestations 1. Polyuria (diabetes) & very diluted solutes (tasteless) (insipidus) 2. Polydipsia→ keeps patient healthy Depressed thirst sensation by loss of consciousness→ cause fatal dehydration B- Syndrome of inappropriate ADH secretion (SIADH) Cause: ↑ADH from posterior pituitary or ectopic source as malignant tumor (bronchogenic carcinoma) Manifestations: Water retention, Hyponatremia, ↑urine osmolarity, Edema. 5 Regulation of Thyroid function/ Hormones Diagram?????????? 1. Hypothalamic regulation: TRH (via hypothalamic-hypophyseal portal circulation) 2. TSH: 3. Feedback of thyroid hormones: ↑T3 &T4 →↓TSH either by 6 Disturbances of thyroid gland function Hypofunction: hypothyroidism Hyperfunction: hyperthyroidism. ✓ Primary: of thyroid origin. ✓ Secondary: of pituitary origin. ✓ Tertiary: of hypothalamic origin. HYPERTHYROIDISM: THYROTOXICOSIS HYPOTHYROIDISM Causes: Causes: 1. Thyroid over-activity: 1- Thyroidal (primary): Acute Thyroiditis (irritation) Congenital absence of thyroid gland or biosynthesis thyroid Tumor or nodule Maternally transmitted (antithyroid drugs). Her thyroid contained 3 nodules, (multinodular goiter) Chronic iodine deficiency (rare) Grave's disease (auto antibodies) due to supplementation of table salt with iodides. TSH-R [stim] Ab (not controlled by TRH) Iatrogenic: ↑antithyroid drugs/ surgical removal/ 2. Supra-thyroidal: (2nd)(↑TSH). overdose of radioactive iodine in hyperthyroidism. Thyrotrope pituitary tumor (↑TSH). Chronic thyroiditis: destruction of thyroid tissue by Resistance of thyroid receptors in pituitary viruses or antibodies (autoimmune = Hashimoto). (TSH- (gene mutation) R[block] Ab, Tg Ab, TPO Ab → no negative feedback effect of thyroid hormones. 2- Supra-thyroidal: 3. Extrathyroidal activity: Pituitary (↓TSH) (secondary). Ectopic thyroid tissue or Hypothalamic (↓TRH) (tertiary). Excessive administration of thyroid hormones by error Factitious thyroiditis Subclinical hyperthyroidism is low or suppressed TSH with normal T3 and T4 levels. Toxic multinodular goiter is an enlarged thyroid gland due to formation of multiple nodules. Toxic Adenoma is characterized by presence of a solitary nodule. Both of them are due to mutations involving the TSHR in areas of thyroid gland 7 Symptoms HYPERTHYROIDISM Adult HYPOTHYROIDISM BMR ↑BMR 60- 100 %→ heat intolerance??? ↓BMR, → ↓body temp.→↑ susceptivity to cold weather????? Explain low temperature Skin: Warm, Flushed (VD), ↑sweating Skin: coarse, Dry ↓body weight: energy loss > energy gain ↑body weight due to ↓BMR, ↓lipolysis??? despite ↑appetite and hyperphagia. accumulation of subcutaneous mucoproteins & mucopolysaccharides →non-pitting edema.???? CNS ↑excitability of nervous system. examination of deep tendon reflex Hypo-reflexia (prolonged reflex time). Irritable, nervousness Fine tremors due to ↑ response of RAS to catecholamine??????????????? CVS ↑HR (tachycardia) ???& CO, due to: ↓Heart rate (bradycardia) Direct stimulation of SAN. Decrease direct effect of thyroid on SAN Thyroxine sensitizes SAN to catecholamines. ↓ metabolism & VR ↑metabolism →↑VR and reflex tachycardia (Bainbridge reflex). ABP: Hypotension due to decrease SV, HR ↑systolic, due to ↑stroke volume & CO. ↓diastolic: due to peripheral VD. ↑pulse pressure ???? Respiration ↑ respiratory rate ↓ respiratory rate (brachypnea) GIT ↑ motility (diarrhea) ↓ motility (constipation) Eye Exophthalmos: (diagnostic sign)????? name Cause: Cytotoxic autoantibodies against extra-ocular muscles → hypertrophy of extra ocular muscles & retro-orbital connective tissues Complications: ↑ Pressure On optic nerve→ atrophy &blindness. Laboratory ↓plasma cholesterol ↑ plasma cholesterol explain findings: ↓plasma cholesterol via ↑LDL receptors on liver & ↑secretion its secretion in bile & differentiate between 1ry and 2ry stools hypothyroidism?? Via TSH ↑T3 and T4 + ↓TSH in ↓T3 & T4 + ↑TSH in Thyroidal (1ry hyperthyroidism) & 1ry hypothyroidism = thyroid origin).????? Extra-thyroidal hyperthyroidism Explain high level of TSH????? ↑T3 & T4 + ↑TSH in 2ry and 3ry hyperthyroidism ↓T3 & T4 + ↓TSH in Radioiodine thyroid uptake and scan using 2ry or 3ry hypothyroidism (hypothalamic) an I-123 isotope 8 Identify the possible diagnosis. Justify your answer Diagnosis (endocrine disorder) + supported symptoms & signs It may be secondary (decreased TSH leads to not palpable thyroid) or primary with auto- antibodies (TSH receptor blocking antibodies). Specific age dependent effects in hypothyroidism a- Cretinism: occurs in children since birth or early childhood, characterized by: Special features: o Wide nasal bridge, enlarged lips with a protruded tongue, o Supraclavicular pad of fat o Abdominal bulging + umbilical hernia Delayed mentally (Idiot): o Inability to learn in proper age (very low IQ) o unable to sit, stand, and control his urine & stools. Delayed physically: o Dwarf o Delayed fontanel’s closure & teeth eruption (delayed milestones) Delayed sexually: o impotent & sterile (if he lives to adult age) b – Myxedema: occurs in adults, characterized by: ↑susceptibility to cold Absent outer 1/3 of the eyebrows Husky voice Depressed Mental functions: drowsy with prolonged reaction time. Depressed Sexual functions: due to slight atrophy of the gonads. What is goiter, and would you expect to find goiter in this case? Explain your answer. Goiter is enlargement of thyroid gland. Yes, high levels of TSH will increase the gland size. 9- Describe a suitable treatment for this patient. Thyroid replacement therapy (levo-thyroxin). 9 Disturbance of function of Parathormone A- Hyperparathyroidism 1. Primary hyperparathyroidism Cause tumor of parathyroid. Characters Hypercalcemia is the hallmark ↑plasma calcium →↓neuromuscular excitability (↓excitability of nerves, weak contractions). bone fracture due to osteoporosis, hypertension and kidney stones. 2. Secondary hyperparathyroidism Cause hyperplasia of parathyroid glands in response to ↓serum calcium level: a. ↓intestinal calcium absorption: ↓calcium intake Vitamin D deficiency

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