Pathophysiology :Pathophysiology Perception & Coordination MARIA HAZEL T. ORGANO, RN Clinical Instructor, College of Nursing


Grading System :2 Grading System QUIZ 25% PROJECT 15% LONG Test 20% FINAL Test 40% TOTAL 100%


Slide 3:3 Perception Conscious, mental registration of sensory stimulus Coordination Regulation of bodily functions & movement


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Disturbances in Perception & Coordination :6 Disturbances in Perception & Coordination


Alterations in Motor Function :Alterations in Motor Function


Herniated Intervertebral Disk :8 Herniated Intervertebral Disk Intervertebral disc: cartilaginous plate that forms a cushion between the vertebral bodies Nucleus pulposus: ball-like, soft, gelatinous cushion in the center of the disc Annulus fibrosus: fibrous ring around the disc Most common areas affected: cervical (C5-C6, C6-C7) & lumbar area (L4/L5-S1)


HERNIATED INTERVERTEBRAL DISK (Herniated Nucleus Pulposus) :9 HERNIATED INTERVERTEBRAL DISK (Herniated Nucleus Pulposus) -protrusion of nucleus pulposus of spine Prevalence: more common in adults, more common in men ,,,,, Annulus fibrosus Nucleus pulposus Permit motion bet. Vertebral bodies Shock absorber Exchange of fluid bet. Disk and capillaries


Risk Factors :10 Risk Factors Age Lifestyle – men more prone than women Trauma such as falls, accident, repeated minor stresses such as lifting


Pathophysiology :11 Pathophysiology Degenerative changes  Nucleus pulposus dries out & loses elasticity  Annulus fibrosus cracks  Trauma  Herniation of nucleus pulposus  PAIN


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Clinical Manifestations :13 Clinical Manifestations PAIN – 1st & most common – back pain that spreads down the back of the leg & over sole of foot Slight motor weakness, major weakness rare Sensory problems – paresthesias, numbness of leg & foot Diminished or (-) knee & ankle reflexes


Diagnostic Evaluation :14 Diagnostic Evaluation MRI (Magnetic Resonance Imaging) Electromyography (EMG): to localize the specific spinal nerve roots involved Neurologic Assessment – Straight Leg Test Pt is positioned supine, leg is passively raised. Normally, no pain is felt at the hamstring muscles even if leg is raised passively to 90 degrees. In slipped disk, pain may be felt at the hamstring when leg is raised 60 degrees or less


Disorders in :Disorders in Basal Ganglia & Cerebellum


PARKINSON’S DISEASEDisorder of the Basal Ganglia & Cerebellum :16 PARKINSON’S DISEASEDisorder of the Basal Ganglia & Cerebellum Chronic, progressive, degenerative disorder of the basal ganglia, affecting individuals over the age of 50 affects men more than women Cause: UK Predisposing Factors: Genetics, atherosclerosis, stroke, encephalitis, head injury


PARKINSON’S :17 PARKINSON’S Slowly progressive degenerative disorder of the nervous system characterized by tremor when muscles are at rest, slowness of voluntary movts, and increased muscle tone (rigidity) Decrease dopamine level >dopamine: an inhibitory neurotransmitter in the caudate nucleus and the putamen, playing an impt. role in integration of movt.


Signs & Symptoms :18 Signs & Symptoms bradykinesia micrographia – shrinking, slow handwriting dysphonia mask-like expression – decreased blinking, bland expression cogwheel rigidity resting tremor – disappears with purposeful movement but evident when extremities are at rest pill-rolling difficulty with balance and walking


Slide 19:19 Normal Physiology: CNS Impulse via basal ganglia(part of EPS –initiation, modulation and completion of movts & regulates autonomic movements) Helps smooth out muscle movt and coordinate changes in posture Release of dopamine Increased nerve signals to muscles


Pathophysiology :20 Pathophysiology Risk factor  Nerve cell degeneration in substantia nigra (basal ganglia)   Dopamine levels  Impaired extra-pyramidal symptoms


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HUNTINGTON DISEASE :23 HUNTINGTON DISEASE HUNTINGTON’S CHOREA Transmitted as an autosomal dominant trait with complete penetrance Chronic progressive hereditary disease of the nervous system that results in progressive involuntary choreiform movement and dementia Affects men and women of all races Each child of a parent with Huntington’s disease has 50% risk of inheriting the illness


PATHOPHYSIOLOGY :24 PATHOPHYSIOLOGY PREMATURE DEATH OF CELLS IN THE STRIATUM ( caudate and putamen)of the basal ganglia Loss of cells in the cortex, cerebellum Glutamine abnormally collected in the nucleus causing cell death Cell destruction Lack of neurotransmitters (Gamma-aminobutyric acid and acetylcholine) Dilated ventricles huntington disease


HUNTINGTON’S :25 HUNTINGTON’S CM: Early manifestations > a. Psychological >Early signs of dyskinesia > Choreiform >dystonic posturing Late Mainfestations > rigidity > akinesia >dementia


DIAGNOSTICS :26 DIAGNOSTICS Gene therapy History taking CT Scan MRI


That’s all for disorders of :That’s all for disorders of Basal Ganglia & Cerebellum


MULTIPLE SCLEROSIS :28 MULTIPLE SCLEROSIS Autoimmune disease in which a protein component of the sheath is attacked the myelin sheaths around the fibers of the axon of the neurons in the CNS are gradually destroyed, converted, to hardened sheaths called scleroses the current is short-circuited, and the affected person loses the ability to control his or her muscles and becomes increasingly disabled


Slide 29:29 commonly occurs in 20-40 yrs old, rarely having onset before age 15 or after 50 Areas frequently affected: optic nerves, chiasm and tracts, cerebrum, brain stem and cerebellum, spinal cord Epidemiology of MS hints at an interaction b/n a viral illness in the teen years and a genetic predisposition Cause: UK


Pathophysiology :30 Pathophysiology Sensitized T cells cross the blood-brain barrier Sensitized T cells remain in the CNS and promote infiltration of other agents inflammation of myelin and oligodendroglial cells that produce myelin in the CNS Plaques of sclerotic tissue appear on demyelinated axons   Demyelination further interrupts the flow of nerve impulses   Axons themselves begin to degenerate resulting in permanent and irreversible damage


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Clinical Manifestations :33 Clinical Manifestations Fatigue Depression Weakness, Numbness Difficulty in coordination Loss of balance Pain, Spasticity Visual disturbance such as burning of vision, diplopia, patchy blindness and total blindness


Diagnosis :34 Diagnosis MRI Neuropsychological testing to assess cognitive impairment


SPINAL CORD INJURY :35 SPINAL CORD INJURY disturbance of the spinal cord that results in loss of sensation and mobility Types (Cause): Trauma: automobile accidents, falls, gunshots, diving accidents, etc. Disease: polio, spina bifida, tumors, Friedreich's ataxia, etc.


Types of SCI :36 Complete injury there is no function below the level of the injury Voluntary movement and physical sensation are impossible always bilateral Incomplete injury retains some sensation below the level of the injury person may be able to move one limb more than another, may be able to feel parts of the body that cannot be moved, or may have more functioning on one side of the body than the other Types of SCI


Clinical Manifestations :37 Clinical Manifestations Neurologic Level – lowest level at which sensory & motor functions are normal Below neurologic levels: Total sensory & motor paralysis Loss of bladder & bowel control (urinary retention & bladder distention) Loss of sweating & vasomotor tone Marked reduction of BP from loss of peripheral vascular resistance


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Cervical Injuries :39 Cervical Injuries Usually result in full or partial tetraplegia C-3 vertebrae and above : Typically lose diaphragm function and require a ventilator to breathe C-4: Have some use of biceps and shoulders, but weaker than C-5 and lower C-5: May retain the use of shoulders and biceps, but not of the wrists or hands C-6: Generally retain some wrist control, but no hand function C-7 and T-1: Can usually straighten their arms but still may have dexterity problems with the hand and fingers


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Thoracic Injuries :41 Thoracic Injuries result in paraplegia – the hands, arms, head, and breathing are usually not affected T-1 to T-8: Most often have control of the hands, but lack control of the abdominal muscles so control of the trunk is difficult or impossible T-9 to T-12: Allows good trunk and abdominal muscle control, and sitting balance is very good


Lumbar and Sacral Injuries :42 Lumbar and Sacral Injuries decreased control of the legs and hips, and anus dysfunction of the bowel and bladder, sexual dysfunction


ANTERIOR CORD SYNDROME :43 ANTERIOR CORD SYNDROME Loss of pain, temperature and motor function; light touch, position an vibration sensation remain intact Causes: acute disk herniation/hyperflexion injuries; fracture-dislocation of vertebra injury to the anterior spinal artery


BROWN-SEQUARD SYNDROME (Lateral Cord Syndrome) :44 BROWN-SEQUARD SYNDROME (Lateral Cord Syndrome) Ipsilateral paralysis/paresis Ipsilateral loss of touch, pressure and vibration and contralateral loss of pain and temperature Causes: transverse transection of the cord caused by knife or missile injury; fracture-dislocation of a unilateral/ articular process or on acute ruptured disk


SPINAL SHOCK :45 SPINAL SHOCK also called NEUROGENIC shock result of loss vasomotor tone that induces generalized arteriolar and venous dilation that leads to hypotension & hypotonia Injury to medullary brainstem is caused by head injuries – direct or indirect deep general anesthesia drug overdose


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Clinical Signs :47 Clinical Signs hypotonia (flaccid paralysis) absent reflexes below level of injury B & B retention hypotension ( loss of vasomotor tone ) bradycardia loss of sweating , piloerection ,and body temperature control below the area of injury


Autonomic Dysreflexia/Hyperreflexia :48 Autonomic Dysreflexia/Hyperreflexia over-activity of the autonomic nervous system acute episode of exaggerated sympathetic reflex responses that occur in persons with SCI because of lack of control from higher brain centers occurs after spinal shock is resolved & autonomic reflexes return, usually within 1st 6 mos after injury


Pathophysiology :49 Pathophysiology irritating stimulus is introduced to the body below level of spinal cord injury  stimulus sends nerve impulses to the spinal cord  blocked by the lesion at the level of injury  impulses cannot reach brain  reflex is activated that increases activity of the sympathetic portion of autonomic nervous system  results in spasms and a narrowing of the blood vessels  rise in blood pressure  nerve receptors in the heart and blood vessels detect rise in blood pressure and send message to the brain  brain sends message to the heart, causing heartbeat to slow down and blood vessels above level of injury to dilate  brain cannot send messages below level of injury due to the spinal cord lesion and blood pressure cannot be regulated


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Causes :51 Causes overfilling of the bladder bowel that is full of stool or gas burns broken bones appendicitis other medical complications


Clinical Manifestations :52 Clinical Manifestations Increased blood pressure greater than 20 mmHg above baseline Severe pounding headache Diaphoresis and flushing above the level of the SCIs Bradycardia Pallor and gooseflesh below the level of the SCI Anxiety Bronchospasm or respiratory distress Mydriasis (abnormal dilation of the pupil) Cardiac irregularities


NEURAL TUBE DEFECTS :53 NEURAL TUBE DEFECTS occur because of a defect in the neurulation process anterior and posterior neuropores - close last; most vulnerable to defects & majority of NTDs arise in these areas a/w folate deficiencies


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Types of NTD :55 Types of NTD Anencephaly "cephalic" or head end of the neural tube fails to close, resulting in the absence of a major portion of the brain, skull, and scalp Infants are born without both a forebrain and a cerebrum The remaining brain tissue is often exposed--not covered by bone or skin infant is usually blind, deaf, unconscious, and unable to feel pain


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Slide 57:57 Encephalocele rare disorder in which an infant is born with a gap in the skull a part of one or more of the plates that form the skull does not seal, the meninges and brain tissue protrude through this gap PORENCEPHALY Cerebral cysts or cavities involving cortical tissue, which usually penetrate the white matter and communicate with a ventricle May be caused by: A developmental anomaly Vascular thromboses


Slide 58:58 HYDRAENCEPHALY Extreme form of porencephaly in which the cerebral hemispheres are almost totally absent DANDY-WALKER CYSTS Developmental malformations in which the outlets of the 4th ventricle do not open, and the 4th ventricle itself is cystic


Slide 59:59 Defect in formation of several brainstem areas consists of: elongation of the cerebellar tonsils, which protrude the foramen magnum Breaking of the colliculi thickening of the upper cervical spinal cord ARNOLD-CHIARI MALFORMATION


NEURAL TUBE DEFECTS :60 NEURAL TUBE DEFECTS Spina bifida the tube that forms the spinal cord and spine does not close properly, causing damage to the developing spinal cord Latin term which means "split spine" The spinal membranes and spinal cord may protrude through the absence of vertebral arches


Two Forms of Spina Bifida :61 Two Forms of Spina Bifida Spina Bifida Occulta - there is an opening in one or more of the vertebrae (bones) of the spinal column without apparent damage to the spinal cord ‘hidden spine split in two’ RACHISCHISIS-open spine Spina Bifida Manifesta Meningocele - meninges have pushed out through the opening in the vertebrae in a sac called the "meningocele" spinal cord remains intact Myelomeningocele - most severe form of spina bifida, in which a portion of the spinal cord itself protrudes through the back In some cases, sacs are covered with skin; in others, tissue and nerves are exposed MYELOCELE- protruding sac contains spinal cord


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CEREBRAL PALSY :65 CEREBRAL PALSY -disparate collection of disabilities that derive from perinatal brain injury -not a disease: constellation of symptoms that result from damage to the parts of the brain control muscle movts -brain damage may occur: During pregnancy After birth In early childhood


CAUSES :66 CAUSES Birth injuries 2. Poor oxygen supply to the brain before, during and immediately after birth (10-15%) 3. Pre-natal infections:rubella toxoplasmosis, cytomegalovirus 4. Premature infants are vulnerable: poorly developed BV, bleed easily 5. High levels of bilirubin 6. meningitis, sepsis, trauma, severe dehydration during early years of life


MENINGITIS :67 MENINGITIS Inflammation of the pia mater, arachnoid, and the CSF-filled subarachnoid space Inflammation of the meninges Two types: 1. ASEPTIC 2. SEPTIC Or: 1. Viral 2. Bacterial


BACTERIAL MENINGITIS :68 BACTERIAL MENINGITIS CAUSATIVE AGENT Enters the blood stream Crosses BBB Inflammation of pia mater & SA space IICP MENINGITIS Replicate in the CSF Releases endotoxins of cell wall fragments Release of inflammatory mediators Neutrophils bind to cerebral endothelial cells, toxic product release Fluid moves across capillary wall


CM: :69 CM: EARLY : petechial rash with purpuric lesion disorientation and memory impairment IICP: dec.LOC,focal motor deficits LATE: lethargy unresponsiveness coma


ASEPTIC :70 ASEPTIC CAUSES: 1. viral 2. secondary to lymphoma 3. brain abscess Viral meningitis Causes: > mumps, coxsackievirus, Eipstein-Barr virus, HS type 2 !lymphocytes in the CSF, moderately elevated CHON, sugar is normal self-limited


CM: :71 CM: Headache and fever-initial Nuchal rigidity-early (+) Kernig’s sign (+) Brudzinski’s sign Photophobia


PATHOPHYSIOLOGY :72 PATHOPHYSIOLOGY Mosquito bites Viral replication Virus goes to the CNS via cerebral capillaries Affects the brain stem and thalamus Meningeal exudates formation Meningeal irritation IICP Brain infection ENCEPHALITIS


END OF PART ONE :END OF PART ONE Don’t only rely on what the instructors are imparting you.. Value your high priced books.. Read them @ home.. Books means reading not merely stocking them up in the cabinet..


Disorders in :Disorders in Brain Function


BRAIN :75 BRAIN The brain is enclosed in the protective confines of the rigid bony SKULL The skull affords protection for the tissues BUT it can also cause ischemia & traumatic injuries Because it cannot expand to accommodate the increase in volume that occurs when there is swelling or bleeding in its confines The bony structures themselves can cause injury to NS Can cause penetrating wound


HEAD INJURY/ BRAIN INJURY & BRAIN DEATH :76 HEAD INJURY/ BRAIN INJURY & BRAIN DEATH broad classification that includes injury to the scalp, skull, and brain Traumatic brain injury is the most serious form of head injury Causes motor vehicle crashes violence falls


At Risk :77 At Risk 15-24 years and males very young (under 5 years) very old (over 75 years) Mechanisms of Injury Coup Injury – there is damage to the site of impact, the brain rebounds & strikes the opposite side of the skull Countercoup – damage to opposite side of impact, the brain is thrown against 1 side in a CONTINUOUS motion thus damaging the tissues below injury


Types of Head Injury :78 Types of Head Injury CLOSED (BLUNT) INJURY occurs when the head accelerates and then rapidly decelerates or collides with another object and brain tissue is damaged but there is no opening through the skull and dura OPEN INJURY occurs when object penetrates the skull, enters the brain and damages and soft brain tissue is path, or when blunt trauma to the head is so severe that it opens the scalp, skull, and dura to expose the brain


Types of Brain Injury :79 Types of Brain Injury Concussion jarring of brain & its sudden forceful contact with rigid skull, momentary interruption in brain fxn (+)/(-) LOC-recovery within 24 H may result to unconsciousness, amnesia no structural changes Contusion Bruising; there is structural change characterized by extravasation of blood cells Hematoma may result May lead to IICP/CVA


Slide 80:80 Laceration Tearing of tissue caused by sharp fragment or object Most serious complication – hemorrhage leading to IICP Compression of brain Resulting from fracture causing edema & hemorrhage Hemorrhage Epidural hematoma – bleeding into epidural space Subdural hematoma – venous bleeding below the dura or between the dura & SA Acute – symptoms present within 24H after injury Sub-acute – symptoms appear from several days – weeks Chronic – symptoms appear after a long time, months – years Subarachnoid hemorrhage – blood within subarchnoid space


Pathophysiology :81 Pathophysiology Vehicular accident with the involvement of the head   Brain suffers from traumatic injury  Contusion   Bleeding or swelling within the skull   Increase intracranial pressure   Blood flow obstruction to the brain   Decrease tissue perfusion   Cerebral hypoxia   Ischemia, infarction, irreversible brain damage   Brain death


Clinical Manifestations :82 Clinical Manifestations altered LOC; confusion manifestations of IICP; sudden onset of neurologic deficit pupillary abnormalities (changes in shape, size, & response t light) altered or absent gag reflex absent corneal reflex changes in vital signs (altered respiratory pattern, hypertension, bradycardia, tachycardia, hypothermia or hyperthermia) vision and hearing impairment sensory dysfunction spasticity headache movement disorders seizures


Diagnosis :83 Diagnosis Physical examination X-ray Computed tomography (CT) scan Magnetic Resonance Imaging (MRI) Cerebral angiography


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INCREASED INTRACRANIAL PRESSURE :85 INCREASED INTRACRANIAL PRESSURE the measure of cerebrospinal fluid pressure within the cranium Normal ICP ranges from 0 - 15 mm Hg A resting ICP value greater than 20 mm Hg is defined as intracranial hypertension and may be acute or chronic in nature Increased ICP can result in irreversible damage to the cranial contents by impairing blood flow and eventually cause death if left untreated


Slide 86:86 Elevation in ICP can be graded as follows:  Normal ICP                        0 - 15mm Hg Mile elevation                    16 - 20 mm Hg Moderate elevation           21 - 30 mm Hg Sever elevation                  31 - 40 mm Hg Very severe elevation       41 mm Hg and above      Normal total volume of the cranial contents (brain tissue, blood, and CSF) equals 1700 to 1900 cc This volume remains constant to assure stability of cerebral functioning


Slide 87:87 Monro-Kellie hypothesis If any one of the three cranial contents is either increased or decreased in volume, the other two components will increase or decrease inversely to maintain the consistent equal volume of 1700 to 1900 cc.  If the compensation process of the other two components is lost or impaired, ICP will increase.  As the pressure continues to increase the reticular activating system (RAS) and cranial nerves III, IV, and VI are pressed on leading to the outward symptomatology seen.


Etiology of Increased ICP :88 Etiology of Increased ICP Cerebral edema can be one of the causes for intracranial pressure to increase Other causes include: Blood clots or expanding lesions Abscess or infection Enlarged ventricles due to increased CSF volume Increased cerebral blood flow Impaired cerebral venous drainage


Diagnostic Tests :89 Diagnostic Tests CT scan Cerebral angiogram EEG Caloric testing


Clinical Manifestations :90 Clinical Manifestations Restlessness Headache, nausea, vomiting, diplopia Elevated systole Widening pulse pressure Slow PR Alteration in sensory function, motor function, language, speech


Pathophysiology :91 Pathophysiology Risk Factors Increase in intracranial pressure Obstruction of blood flow Destroy brain cells, displace brain tissue, damage delicate brain structures ischemia


BRAIN HERNIATION :92 BRAIN HERNIATION displacement of brain tissue, cerebrospinal fluid, and blood vessels outside the compartments in the head that they normally occupy deadly side effect of very high intracranial pressure, occurs when the brain shifts across structures within the skull


Slide 93:93 Causes occurs when pressure inside the skull (intracranial pressure) increases and displaces brain tissues commonly the result of brain swelling from a head injury It can also be caused by space-occupying lesions such as primary brain tumor , metastatic brain tumor , and hemorrhages or strokes that produce swelling within the brain Hydrocephalus (accumulation of fluid in the brain) can also lead to brain herniation A brain herniation itself often causes massive stroke. This results from poor blood supply to some areas of the brain and compression of vital structures that regulate your breathing and circulation. This can rapidly lead to death or brain death


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Symptoms :95 Symptoms Progressive loss of consciousness Coma Irregular breathing Respiratory arrest (no breathing) Irregular pulse Cardiac arrest (no pulse) Loss of all brainstem reflexes (blink, gag, pupillary reaction to light) Complications Permanent and significant neurologic problems Brain death


CEREBRAL EDEMA :96 CEREBRAL EDEMA excessive accumulation of water in the intra- and/or extracellular spaces of the brain Causes: head injury allergic reaction stroke acute liver disease


Types of Cerebral edema :97 Types of Cerebral edema Interstitial – mov’t of CSF across the ventricular wall Vasogenic – occurs in cond’ns that impair fxn of the BBB & allow transfer of h2o & CHON into the interstital space Cytotoxic – involves an increase in fluid in the intracellular space, occurs from water intoxication or severe ischemia, hypoxia, brain trauma


Pathophysiology :98 Pathophysiology Trauma, head injury  loss of the integrity of the blood brain barrier ↓ Inflammatory response ↓ Cerebral edema ↓ IICP ↓ Clinical Manifestations


Clinical Manifestations :99 Clinical Manifestations headaches decreased level of consciousness loss of eyesight, hallucinations psychotic behavior memory loss and coma Coma Vomiting and nausea Confusion Seizures


HYDROCEPHALUS :100 HYDROCEPHALUS abnormal accumulation of cerebrospinal fluid in the ventricles and subarachnoid spaces of the brain PROBLEM: decreased absorption or overproduction of CSF There is an  increase intracranial pressure that causes compression of the brain Causes of Hydrocephalus Overproduction of fluid by choroids plexus Obstruction of the passage of fluid in the brain ventricles or in the subarachnoid space Interference with the absorption of fluid from the subarachnoid space


Types of Hydrocephalus :101 Types of Hydrocephalus Communicating hydrocephalus/Extraventicular hydrocephalus Caused by impaired CSF resorption in the absence of any CSF-flow obstruction, block in CSF pathway Non-communicating hydrocephalus/Intraventricular Hydrocephalus caused by CSF-flow obstruction Congenital Hydrocephalus-occurs in the utero Acquired Hydrocephalus


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Clinical Manifestations :103 Clinical Manifestations Enlargement of the head Headaches Vomiting & nausea      Sleepiness or coma Urinary incontinence Dementia Gait instability


Diagnosis :104 Diagnosis Computer Tomography Scanning (CT scans) Magnetic Resonance Image (MRI scan)


STROKE :105 STROKE A sudden loss of brain function resulting from disruption of the blood supply to a part of the brain CAUSES thrombosis – a blood clot on a blood vessel of the brain or neck cerebral embolism – a blood clot or other material carried to the brain from another part of the body ischemia – decrease blood flow to an area of the brain cerebral hemorrhage – rupture of the cerebral blood vessel with bleeding into the brain tissue or spaces surrounding the brain


Risk Factors :106 Risk Factors Hypertension – the major risk factor cardiovascular diseases high cholesterol obesity diabetes smoking drug abuse alcohol consumption DM


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Types of CVA :108 Types of CVA Transient Ischemic Attack Sudden, lasts for few minutes-hours; if there are deficits, they will be resolved in time Dysarthria (slurred speech), hemiparesis, paresthesia, Amaurosis fugax – loss of vision in one eye for 2-3 mins Progressive or Evolving CVA Usually r/t occlusive (obstructive) disorder Lasts for few hrs-few days Might lead to permanent neurologic impairment Completed CVA Blood supply is totally cut off to a portion of the brain followed by permanent neurologic alterations Pt will go into coma


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Diagnosis :110 Diagnosis CT scan Cerebral angiogram EEG Caloric testing


Aneurysm :111 Aneurysm Bulge at the site of a localized weakness in the muscular wall of an arterial vessel Berry aneurysm-small saccular aneurysm Aneurysms enlarges in time leading to weakening of the vessel wall Leading to rupture CAUSE: UK


ANEURYSMAL SUBARACHNOID HEMORRHAGE :112 ANEURYSMAL SUBARACHNOID HEMORRHAGE BRAIN ANEURYSM also called a cerebral or intracranial aneurysm abnormal bulging outward of one of the arteries in the brain often discovered when they rupture, causing bleeding into the brain or the space closely surrounding the brain called the subarachnoid space, causing a subarachnoid hemorrhage can lead to a hemorrhagic stroke, brain damage and death can occur in people of all ages, but are most commonly detected in those ages 35 to 60 Women are actually more likely to get a brain aneurysm than men, with a ratio of 3:2


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Risk Factors :114 Risk Factors Cigarette smoking hypertension cocaine use heavy alcohol use Patients with a family history of first-degree relatives with subarachnoid hemorrhage are also at a higher risk


Clinical Manifestations :115 Clinical Manifestations Ruptured Cerebral Aneurysms Nausea and vomiting Stiff neck or neck pain Blurred vision or double vision Pain above and behind the eye Dilated pupils; photophobia Sensitivity to light Loss of sensation; loss of consciousness sudden onset of severe headache (frequently described as the "worst ever")


Slide 116:116 Unruptured Cerebral Aneurysms Peripheral vision deficits Thinking or processing problems Speech complications Perceptual problems Sudden changes in behavior Loss of balance and coordination Decreased concentration Short-term memory difficulty Fatigue


Diagnosis :117 Diagnosis CT scans Lumbar puncture: to detect blood in the cerebrospinal fluid (CSF) Cerebral Angiography/Tomography: to determine the exact location, size and shape of an aneurysm


ARTERIOVENOUS MALFORMATION :118 ARTERIOVENOUS MALFORMATION Defects of the circulatory system that are generally believed to arise during embryonic or fetal development or soon after birth congenital disorder of the veins and arteries that make up the vascular system Commonly cause of hemorrhage in young people range from small, local lesions to network that may cause an entire hemisphere varies in shape and location


Slide 119:119 SUBARACHNOID HEMORRHAGE may occur as a result of an AVM PATHOPHYSIOLOGY It is due to an abnormality in embryonal development that leads to a tangle of arteries and veins in the brain without a capillary bed


Clinical Manifestations :120 Clinical Manifestations Severe, unusually severe headache Loss of consciousness Pain and rigidity of the back of the neck (NUCHAL RIGIDITY) and spine due to the meningeal irritation Visual disturbances (visual loss, diplopia, ptosis) Tinnitus Dizziness Hemiparesis Formation of a clot- Neurologic deficit is shown by the patient Severe bleeding- can result in cerebral damage followed rapidly by coma and death Xanthochromia (yellow coloration of the CSF): caused by the bleeding from the AVM into the subarachnoid space


Diagnosis :121 Diagnosis Ct Scan determines the size and location of the hematoma confirm the diagnosis of an AVM Lumbar Puncture- done when the CT Scan results are negative, no evidence of increased ICP (Intracranial Pressure) and subarachnoid hemorrhage must be confirmed


SEIZURE DISORDERS :122 SEIZURE DISORDERS Seizures – sometimes called convulsions Paroxysmal motor, sensory or cognitive manifestations of spontaneous, abnormally synchronous discharges of collection of neurons in the cerebral cortex It is not a disease, but a symptom of an underlying CNS dysfunction


EPILEPTICSEIZURE DISEASE :123 EPILEPTICSEIZURE DISEASE Symptom  complex of several disorders of brain function characterized by recurring seizures There is electrical disturbance (DYSRHYTHMIA) in the nerve cells in one section of the brain causing them to emit abnormal, recurring, uncontrolled electrical discharges Causes Symptomatic: due to structural or metabolic abnormality in the brain Complications during pregnancy or birth Stroke Head injury Neurosurgical operations Bacterial or viral encephalitis Parasitical infection Alcohol Idiopathic (cryptogenic) - Unknown


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Types of seizure :125 Types of seizure Provoked – febrile seizures, precipitated by metabolic conditions(F&E imbalances, hypoglycemia, hypoxia, hypocalcemia) & those following a primary insult to the CNS (brain infections) Unprovoked – cause is undetermined


Classification of epileptic seizures :126 Classification of epileptic seizures Partial seizures – with or without LOC Generalized-onset – most common type Absence – generalized, nonconvulsive epileptic evnets (petit mal seizures) Atonic-sudden, split-second loss of muscle tone leading to slackening of the jaw, drooping of the limbs, falling to the ground (DROP ATTACKS) Myoclonic – brief involuntary muscle contractions induced by stimuli of cerebral origin, bilateral jerking of muscles Tonic-clonic – grand mal; has a vague warning & experiences a sharp tonic contractions of the muscles, clonic state then postictal phase(unconscious)


Pathophysiology :127 Pathophysiology Messages from the body   Neurons of the brain    Discharges of electrical energy    Burst when there is task to perform    Continue firing after a task is finished (unwanted discharges)    Errant cells may perform erratically    Uncontrolled abnormal discharges occur rapidly    Epileptic syndrome


Clinical Manifestations :128 Clinical Manifestations Staring episode to prolonged convulsive movements with loss of consciousness A finger or mouth may shake, or the mouth may jerk uncontrollably Talk unintelligibly Dizziness Excessive emotions of fear, anger, elation or irritability Intense rigidity of the entire body followed by alternating muscle relaxation and contraction Tongue is often chewed Incontinent of urine and stool Headaches, sore muscles Fatigue Depression Confused and hard to arouse Does not remember the episode when it is over


Diagnosis :129 Diagnosis Medical history EEG (Electroencephalography) Brain MRI (Magnetic Resonance Imaging) PET (Positron Emission Tomography)


Complications :130 Complications Physical harm Increased health problems if pregnant Cardiac arrhythmias Brady arrhythmias Permanent brain damage Death


DEMENTIA :DEMENTIA Alzheimer’s, vascular dementia, pick’s, creutzfedt-jakob, wernicke-korsakoff, huntington


ALZHEIMER’S DISEASE :132 ALZHEIMER’S DISEASE chronic, progressive, and degenerative brain disorder accompanied by profound effects on memory, cognition, and ability for self-care CAUSE: Idiopathic HALLMARK: The deposition of beta-amyloid in senile plaques and blood vessel walls, as well as the presence of neurofibrillary tangles and loss of neurons


Risk Factors :133 Risk Factors advanced age genetic factor viral infection with an incubation period of many years acetylcholine deficiency excessive aluminum autoimmunity amyloid neuritic plague formation Down’s syndrome due


Pathophysiology :134 Pathophysiology Neurofibrillary tangles & neurotic plaques deposit in the brain  Neural damage occurs primarily in the cerebral cortex  Results in decrease brain size  Cells that use acetylcholine are the ones principally affected   Enzyme involved in memory processing is decreased


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Clinical Manifestations :136 Clinical Manifestations Early stage: forgetfulness, subtle memory loss, depression Progressive stage: dementia (gradual decline in mental functioning), depression, paranoid, hostile, combative More progressive stage: needs assistance for ADL, speech impairment, sun downing, dysphagia, incontinence Terminal stage: immobility therefore requires total care, death due to complications


Diagnosis :137 Diagnosis CTS and MRI to r/o other conditions Cerebral biopsy – confirms the diagnosis of Alzheimer’s disease Nursing history


Stages of AD :138 Stages of AD Mild — At the early stage of the disease, patients have a tendency to become less energetic or spontaneous, though changes in their behavior often go unnoticed even by the patients' immediate family Moderate — As the disease progresses to the middle stage, the patient might still be able to perform tasks independently, but may need assistance with more complicated activities. Severe — As the disease progresses from the middle to late stage, the patient will undoubtedly not be able to perform even the simplest of tasks on their own and will need constant supervision. They may even lose the ability to walk or eat without assistance


VASCULAR/ MULTI-INFARCT DEMENTIA :139 VASCULAR/ MULTI-INFARCT DEMENTIA Second most common form of dementia after Alzheimer’s Disease in the elderly caused by a series of strokes that disrupt blood flow and damage or destroy brain tissue Typically begins between the ages of 60 and 75 The prevalence is higher in men than in women and it increases with age Dementia - Uneven, downward decline in mental function 3 most common nonreversible Dementias: Alzheimer’s disease, Multi-infarct Dementia, and Mixed Alzheimer’s and Multi-infarct Dementia


Risk Factors :140 Risk Factors High blood pressure Narrowing of main arteries in the neck supplying blood to the brain (Atherosclerosis) Raised cholesterol (LDL- Low Density Lipoprotein Cholesterol) Diabetes Heart Attacks (Myocardial Infarction and Ischemic Heart Disease) Irregular heart beat (Atrial Fibrillation) Smoking


Clinical Manifestations :141 Clinical Manifestations Memory problems; forgetfulness Personality changes Aphasia (impaired language ability) Abnormal behavior Dizziness Uncoordinated or weak movements Lack of concentration Withdrawal from social interaction Moving with rapid, shuffling steps Decreased interest in daily living activities Sudden involuntary laughing or crying (Emotional instability) Loss of bladder or bowel control


Diagnosis :142 Diagnosis Thorough physical exam Complete medical history Psychological Test CT Scan MRI (Magnetic Resonance Imaging)


PICK’s DISEASE :143 PICK’s DISEASE progressive rare form of dementia that typically affects the frontal and/or temporal lobes causes a slow shrinking of brain cells due to excess protein build-up Patients initially exhibit marked personality and behavioural changes, and a decline in the ability to speak coherently (echolalia, loss of initiative, hypotonia, incontinence) rather than memory deficits Cause : unknown


Pathophysiology :144 Pathophysiology Pick's Disease is the result of a build-up of protein in the affected areas of the brain. The accumulation of abnormal brain cells, known as Pick's bodies, eventually leads to changes in character, socially inappropriate behavior, and poor decision making, progressing to a severe impairment in intellect, memory and speech


Clinical Manifestations :145 Clinical Manifestations Obsessive/compulsiveness (for example, overeating or only eating one type of food) Drinking alcohol to excess (when this was not previously a problem) Withdrawal or seclusion Lack of attention to personal hygiene Sexual exhibitionism or promiscuity Indifference to events or to one's environment Easily distracted; difficulty maintaining a line of thought Reduced quality of speech: shrinking vocabulary, difficulty finding a word


CREUTZFELDT-JAKOB Disease :146 CREUTZFELDT-JAKOB Disease Transmissible Spongiform Encephalopathyvery rare and incurable degenerative neurological disorder that is ultimately fatal Pathophysiology: incompletely understood Causes Transmissible spongiform encephalopathy diseases (also known as prion diseases) - caused by a unique type of infectious agent called a prion, an abnormally structured form of a protein found in the brain bovine spongiform encephalopathy (BSE) - commonly known as “mad cow disease”


Risk Factors :147 Risk Factors a family or genetic history of CJD human growth hormone injections certain medical procedures contaminated surgical instruments some blood transfusions eating beef from certain countries How CJD is transmitted heredity certain medical procedures exposure to contaminated instruments


Clinical Manifestations :148 Clinical Manifestations dementia leading to memory loss personality changes hallucinations speech impairment jerky movements (myoclonus) balance and coordination dysfunction (ataxia) changes in gait rigid posture Seizures The symptoms of CJD are caused by the progressive death of the brain's nerve cells, which is associated with the build-up of abnormal prion proteins


Diagnosis :149 Diagnosis Electroencephalography Cerebrospinal fluid analysis MRI of the brain


WERNICKE – KORSAKOFF Syndrome :150 WERNICKE – KORSAKOFF Syndrome Korsakoff psychosis; Alcoholic encephalopathy; Encephalopathy - alcoholic; Wernicke's disease A brain disorder involving loss of specific brain functions caused by a thiamine deficiency & chronic alcoholism Condition affects males slightly more frequently than it affects female Onset is evenly distributed from 30 – 70 yrs


Causes :151 Causes Chronic alcoholism (most common) Dietary deficiencies, Prolonged vomiting Eating disorders


Stages :152 Stages Wernickes encephalopathy (“acute phase”) Degenerative brain disorder caused by the lack of thiamine Mental Confusion Vision impairment Stupor Coma Hypothermia Hypotension Ataxia


Korsakoff’s Amnesic Syndrome (“Chronic phase”) :153 Korsakoff’s Amnesic Syndrome (“Chronic phase”) Memory disorder – results from a deficiency of thiamine & Niacin Heart, vascular, and nervous system are involved Characterized by impairments in acquiring new information or establishing new memories and in retrieving previous memories   Amnesia Confabulation attention deficit disorientation vision impairment


Clinical Manifestations :154 Clinical Manifestations Confabulation Recitation of imaginary experiences to fill in gaps in memory Ataxia Confusion Memory loss Hallucinations


Diagnosis :155 Diagnosis Electrolytes Check CBC Liver associated enzyme CT brain scan (non contrast) assessment for hemorrhage, mass effect, edema and large sub acute stroke MRI of the brain with contrast Lumbar puncture/CSF analysis


HUNGTINGTON’S DISEASE :156 HUNGTINGTON’S DISEASE chronic, progressive, hereditary disease of the nervous system that results in progressive involuntary choreiform movement and dementia progressive disorder that often involves thinking and learning problems, psychological disturbances, and abnormal movements also known by the name Huntington (or Huntington's) chorea (neurological diseases that are characterized by spasmodic movements of the limbs and facial muscles) Incidence: men and women of all races Causes: A specific mutation in the HD gene called a triplet expansion causes symptoms of the condition to occur


Pathophysiology :157 Pathophysiology Premature death of cells in the striatum (caudate and putamen) of basal ganglia, the region deep w/in the brain involved in the control of movement There is also loss of cells in the cortex, the region of the brain associated w/ thinking, memory, perception and judgment and in the cerebellum, the area that coordinates voluntary muscle activity


Clinical Manifestations :158 Clinical Manifestations weight loss abnormal involuntary movement intellectual decline emotional disturbance writhing, twisting and uncontrollable movement facial movements produces tics and grimaces speech become slurred, hesistant, often expulsive dysphagia depression psychosis


Alterations in vision :Alterations in vision Glaucoma Cataract Retinal detachment


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GLAUCOMA :161 GLAUCOMA A group of ocular conditions characterized by optic nerve damage which is related to the IOP caused by congestion of aqueous humor in the eye More prevalent among people older than 40 the incidence increases with age


Risk Factors :162 Risk Factors Family history of Glaucoma African American race Older age Diabetes Cardiovascular disease Migraine syndromes Nearsightedness (myopia) Eye trauma Prolonged use of topical or systemic corticosteroids


Glaucoma :163 Glaucoma Aqueous humor helps maintain IOP & serves a nutritive, facilitating metabolism of the lens & posterior cornea. It contains a low CHON concentration, high ascorbic acid, glucose & amino acids It mediates the exchange of respiratory gases Produced by ciliary epithelium


Classifications of Glaucoma :164 Classifications of Glaucoma Open- angle glaucoma (Chronic) Most common form of glaucoma; diagnosed as early as 40-45 y/o but s/s appear at 60-65 y/o Probably d/tdegeneration of trabecular meshwork        Usually bilateral but one eye maybe more severely affected than the other Angle-closure (Pupillary Block) glaucoma or Acute Angle b/n cornea & iris is decreased thus, decreased outflow of aqueous humor into trabecular meshwork


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Pathophysiology :166 Pathophysiology Initiating events/ precipitating actors (illness, emotional stress)  Structural alterations in the aqueous outflow system  Functional alterations (Increased IOP or impaired blood flow)  Optic nerve damage → loss of nerve fibers and blood supply  Visual loss  Glaucoma


Clinical Manifestations :167 Clinical Manifestations Blurred vision or "Halos" around lights Tunnel vision – loss of peripheral vision Reddening of the eye Severe eye pain cloudy cornea (usually transparent part of the eye in front of the pupil) one eye becoming larger than the other excessive tearing (epiphora) light sensitivity (photophobia) excessive blinking (blepharospasm) strabismus (crossed or out-turned eyes) decreased vision (amblyopia)


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Diagnosis :169 Diagnosis Tonometry - involves the use of a tonometer that measures eye pressure (i.e., IOP) During tonometry, the eye is anesthetized with drops, and while the patient is examined with a slit lamp, a plastic prism is lightly pushed against the eye to measure IOP During air tonometry, a puff of air is sent onto the cornea to measure the pressure. No anesthetic eye drops are needed. Visual field test - enables the ophthalmologist to determine any loss of peripheral vision The patient places his or her chin on a stand placed in front of a computer screen. When a flash of light appears, the patient is asked to press a button. A computerized printout provides an accurate assessment of the patient's peripheral vision. Ophthalmoscopy - an ophthalmoscope is used to look directly through the pupil at the optic nerve. Its color and appearance can indicate the presence of and the extent of damage from glaucoma


Complications :170 Complications intraoperative and postoperative suprachoroidal hemorrhage visual loss


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CATARACT :176 CATARACT Clouding or increased opacity of crystalline lens very common in older people can occur in either or both eyes; It cannot spread from one eye to the other Lens - clear part of the eye that helps to focus light, or an image, on the retina *In a normal eye, light passes through the transparent lens to the retina. Once it reaches the retina, light is changed into nerve signals that are sent to the brain. The lens must be clear for the retina to receive a sharp image.


Slide 177:177 APHAKIA – absence of lens; congenital Etiology Senile Cataract – d/t aging process; most common form Congenital cataract – UK cause; present at birth Traumatic cataract – injury d/t irradiation Risk Factors Systemic disease – DM, chemical eyeburns Toxic factors – prolonged corticosteroid use


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Clinical Manifestations :180 Clinical Manifestations Painless burning of vision – may lead to uni/bilateral blindness Distorted vision Diplopia Photophobia Previously black pupil appears milky or white                      Cloudy or blurry vision; Colors seem faded Glare - Headlights, lamps, or sunlight may appear too bright Poor night vision


Diagnosis :181 Diagnosis Slit-lamp exam Snellen visual acuity test Ophthalmoscopy


RETINAL DETACHMENT :182 RETINAL DETACHMENT Separation of the light-sensitive membrane (the retina) from its supporting layers Pathophysiology Associated with a tear or hole in the retina through which the internal fluids of eye may leak, causing separation from the underlying tissues


Etiology :183 Etiology Trauma Aging process Tumors Inflammatory disorders of the eye Risk Factors Nearsightedness Family history of retinal detachment


Causes of Retinal Detachment :184 Causes of Retinal Detachment Tears or holes in the retina: fluid from the middle of the eye collects under the retina; usually due to an eye or head injury Traction on the retina: pulls the retina away from the layers beneath it; The most common cause of this problem is proliferative diabetic retinopathy, a condition that leads to the growth of scar tissue that can pull on the retina Fluid buildup under the retina: Fluid buildup causes the layers of the retina to separate, resulting in retinal detachment. Fluid buildup may be caused by inflammation or disease in the retina, the layer just beneath the retina (choroid), blood vessels, or tissues in the eye


Clinical Manifestations :185 Clinical Manifestations Floaters - Floating spots or spidery webs in front of the eyes Dark spots seen in the visual field Flashes -Flashes are visual effects where a person sees sudden flashes of light Blurred vision Blurred central vision Peripheral visual field loss Veil over visual field Blank area in visual field No eye pain; Symptoms usually in one eye only


Diagnosis :186 Diagnosis ophthalmoscopy visual acuity electroretinogram (record of electrical impulses of the retina)


GENU VARUMBowlegs :187 GENU VARUMBowlegs condition observed when a person stands with the feet and ankles together, but the knees remain widely apart Overview Infants are born bowlegged because of their folded position in the uterus. The infant's bowed legs begin to straighten once the child starts to walk and the legs begin to bear weight (about 12 to 18 months old) Normal appearance is usually attained by the time the child is three years old. At this time, a child can usually stand with the ankles together and the knees just touch. If the bowed legs persist into this period, the child is called bowlegged


Slide 188:188 Etiology: Idiopathic Cause and Risk factors bone dysplasias Severely bowed legs can be a sign of rickets, a condition caused by a vitamin D deficiency Clinical Manifestations Knees do not touch when individual stands with feet together (ankles touching) Symmetrical bowing of legs Persistence of bowed legs beyond three years of age


Slide 189:189 Diagnosis & Tests Physical examination X-rays may be necessary if the child is three years old or older, if the bowing is getting worse, if it is asymmetric, or if other findings suggest disease Bowlegs Prevention There is no known prevention other than that to avoid rickets. Make sure your child has normal exposure to sunlight and appropriate levels of vitamin D in the diet.


GENU VALGUMKnock-knees :190 GENU VALGUMKnock-knees A condition where the knees angle in and touch when the legs are straightened Persons with severe valgus deformities are typically unable to touch their feet together while simultaneously straightening the legs Etiology: Idiopathic Risk Factors Mild genu valgum is relatively common in children up to two years of age, and is often corrected naturally as children grow and develop. The condition may continue or worsen with age, particularly when it is the result of a disease, such as rickets or obesity


Congenital Hip Dysplasia :191 Congenital Hip Dysplasia abnormal formation of the hip joint in which the ball at the top of the thighbone (femoral head) is not stable in the socket (acetabulum) dysplasia can refer to a hip that is subluxatable (unstable if stressed), dislocatable (can come out of socket under stress), and currently dislocated may occur during fetal development, at delivery, or after birth CAUSE: UK


Slide 192:192 RISK FACTORS female gender first born babies babies born in the breech position (especially with feet up by the shoulders) Approximately 5-9 times more common in females than males Affects the left hip more often than the right hip


Clinical Manifestations :193 Clinical Manifestations asymmetrical thigh and buttock skin folds or creases legs appear to be different lengths hip have a decreased amount of motion walk with an abnormal gait or limp


Diagnosis :194 Diagnosis Neonatal Examination To test for hip instability, the pediatric orthopaedic surgeon will move the hip around to feel and palpate for a "clunk" as the femoral head slides out of the acetabulum (pelvis). In early infancy, instability is the most reliable sign for DDH. Hip Ultrasounds can accurately determine the stability of the hip joint enables direct imaging of the cartilaginous portions (bones that are not yet ossified) of the hip that cannot be seen on plain radiographs


CLUBFOOTCongenital Talipes Equinovarus :195 CLUBFOOTCongenital Talipes Equinovarus is when the foot turns inward and downward; seen at birth Cause: Unknown Clinical Manifestations no pain It gets worse over time, with secondary bony changes developing over years The patient walks on the outside of his foot which is not meant for weight-bearing The skin breaks down, and develops chronic ulceration and infection


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LEGG-CALVE-PERTHES Disease :197 LEGG-CALVE-PERTHES Disease disorder of the blood supply to the femoral head, the "ball" of the hip joint Incidence It can affect children of nearly in any age. It’ s common among boys ages 4 to 8. It’s four to five times more common in boys but when girls develop it, it’s more severe Diagnosis X-rays Bone scans Magnetic Resonance Imaging (MRI)


Pathophysiology :198 Pathophysiology blood supply to the femoral head is interrupted  avascular necrosis, or the death of the bone cell  femoral head collapse creating an irregular fit in the acetabulum, or socket


Clinical Manifestations :199 Clinical Manifestations Knee pain (may be the only initial symptom) Persistent thigh or groin pain Wasting of muscles in the upper thigh Apparent shortening of the leg, or legs of unequal length Hip stiffness that restricts movement in the hip Difficulty walking, walking with a limp (which is often painless) Limited range of motion


OSTEOMYELITIS :200 OSTEOMYELITIS Pyogenic infection of bone which may involve bone marrow usually caused by staphylococcus aureus, Haemophilus influenzae, pseudomonas, streptococcus & E. coli Usually affects long bones SEQUESTRUM – dead tissue caused by osteomyelitis Clinical Manifestations Abrupt onset of pain Fever Malaise Weakness of limb affected


OSTEOMALACIA/RICKETS :201 OSTEOMALACIA/RICKETS softening of the bones, caused by not having enough vitamin D, or by problems with the metabolism of this vitamin These softer bones have a normal amount of collagen that gives the bones its structure, but they are lacking in calcium Causes, incidence, and risk factors Not enough vitamin D in the diet Not enough exposure to sunlight, which produces vitamin D in the body Malabsorption of vitamin D by the intestines Use of very strong sunscreen, limited exposure of the body to sunlight, short days of sunlight, and smog are factors that reduce formation of vitamin D in the body Risk factors for osteomalacia are related to the causes. In the elderly, there is an increased risk among people who tend to remain indoors and those who avoid milk because of lactose intolerance


Slide 202:202 Signs and Symptoms Diffuse (not pinpointed to one location) bone pain , especially in the hips Muscle weakness Bone fractures that happen with very little trauma Symptoms associated with low calcium including: Numbness around the mouth Numbness of extremities Spasms of hands or feet Abnormal heart rhythms DIAGNOSIS Bone biopsy shows osteomalacia Serum vitamin D level may be low Serum calcium levels vary with the cause of the disorder Serum phosphate levels vary with the cause of the disorder Bone x-ray


PAGET’S DISEASEOsteitis Deformans :203 PAGET’S DISEASEOsteitis Deformans Etiology: Unknown Thought to be of viral origin: measles virus, respiratory syncytial virus Affected: bones, usually the femur, tibia, lower spine, pelvis, and cranium The normal process of bone growth is changed The bone breaks down more quickly, and when it grows again it is softer than normal bone Areas affected by Paget’s disease can become shorter because the bone bends With Paget’s disease the bone can also grow larger than before Risk Factors Men are more likely to be affected than women; people over age 40


Pathophysiology :204 Pathophysiology More bone resorption than normal  Osteoblasts try to keep up by making new bone  Osteoblasts is more active than osteoclasts  Osteoblasts mak excess bone that is very chaotic  New bone formed is abnormally large & deformed  New bone has irregular mosaic pattern (tight overlapping structure)  Bones become large & dense, but weak & brittle PAGET’S DISEASE


Clinical Manifestations :205 Clinical Manifestations First warning sign may be pain in or over a bone The area may feel extra warm Feeling of tiredness for symptomatic Paget’s dse deep, aching bone pain skeletal deformity (e.g. barrel-shaped chest, bowing of tibia and femur, kyphosis) changes in skin temperature pathologic fractures through diseased bone cranial nerve compressions: vertigo hearing loss with tinnitus blindness


Diagnosis :206 Diagnosis Chest X-ray Blood test measurement of serum alkaline phosphate (SAP) SAP is type of enzyme made by bone cells that is overproduced by pagetic bone When SAP is higher than usual in blood, MAY be a sign of the disease Mild increase of SAP (up to 2x the usual level): indicative of Paget’s disease OR another condition Greater than 2x the usual level: strongly suggestive of Paget’s disease Bone Scan Test that helps identify which bones have been affected by Paget’s disease Also a useful way to determine the extent and activity of the disease


SCOLIOSIS :207 SCOLIOSIS lateral curvature of the spine that has an undetermined cause, but is believed to be a genetic trait passed from generation to generation found uniformly in both males and females can be corrected if it is detected at a young age and while the bones of the spine are still growing   Idiopathic scoliosis (over 80% of cases)


4 Types of Idiopathic Scoliosis :208 4 Types of Idiopathic Scoliosis Juvenile scoliosis occurs in the 3 to 10 year old age group; often requires treatment because the deformity (curve) is at a high risk of progression Infantile scoliosis is found in children age 2 months to 3 years; relatively minor and tend to resolve spontaneously Adolescent scoliosis may require treatment if the deformity (curve) is at a high risk of progression. Treatment may consist of a brace or surgery. If the curve is not too severe, simple observation may be sufficient Adult scoliosis is generally defined as scoliosis in a patient over the age of 20 years. Adult scoliosis tends to be more symptomatic than its childhood counterpart


Pathophysiology :209 Pathophysiology It is not well understood. It seems logical to assume that scoliosis in these conditions is caused by muscle weakness; however, this conclusion is difficult to support because some conditions are accompanied by spasticity and others by flaccidity. Furthermore, no consistent pattern of scoliosis is associated with a particular pattern of weakness.


Clinical Manifestations :210 Clinical Manifestations Uneven hip and shoulder levels Unequal distance between the arms and body A prominent shoulder blade Muscle mass or humps on one side of the spine Complications Lung and heart damage Back problems Body image


Risk Factors :211 Risk Factors Sex. Curves in girls are more likely to worsen than curves in boys. Age. The younger the child when scoliosis appears, the greater the chance the curve will worsen. Angle of the curve. The greater the curve angle, the higher the likelihood that it will worsen. Location. Curves in the middle to lower spine are less likely to progress than those in the upper spine. Spinal problems at birth. Children who are born with scoliosis (congenital scoliosis) may have rapid progression of the curve. Congenital scoliosis is thought of as a birth defect in the spine itself


Diagnosis :212 Diagnosis Physical examination X-rays Shape. Curves develop side-to-side as a C- or S-shaped curve. The rotation of the spine causes the ribs and muscles near the spine to move out of normal alignment. Location. The curve may occur in the upper back area (thoracic), the lower back area (lumbar) or in both areas (thoracolumbar). Direction. The curve can bend to the left or to the right. Angle. Doctors figure out the angle of the curve using the vertebra at the apex of the curve. A normal spine, viewed from the back, is at 0 degrees — a straight line. A curve that is horizontal, or parallel to the floor, is described as at 90 degrees. Scoliosis is defined as a spinal curvature of greater than 10 degrees. Most doctors can detect even mild curves during a physical exam.


OSTEOPOROSIS :213 OSTEOPOROSIS Metabolic bone disorder characterized by decreased bone mass or density Pathophysiology: bone formation < bone resorption – makes bones fragile & porous CAUSES low vitamin D status inadequate calcium intake family history of the disease inadequate physical activity


Risk Factors :214 Risk Factors Female gender  Thin and small body frames Family history of osteoporosis Personal history of fracture as an adult Cigarette smoking Excessive alcohol consumption Poor nutrition and poor general health Low estrogen levels Chemotherapy Amenorrhea Immobility Hyperparathyroidism Loss of estrogen, due to the menopause


Slide 215:215 Diagnosis for Osteoporosis x-ray PTH level Bone scan   Clinical Manifestations fractures on the vertebral column, hip, wrist kyphosis/dowager’s hump back pain loss of height snapping sound limited mobility hunched forward or bent stature difficulty in breathing Complication: Fractures


OSTEOARTHRITIS :216 OSTEOARTHRITIS Degenerative inflammation of joints, usually affects large weight-bearing joints Cause: UK; usually unilateral Pathophysiology: increased friction causes wear & tear leading to thinning of articular cartilages – narrowing of joint space; cartilage also becomes harder & denser making mobility more difficult Clinical Manifestations painful joints enlarged tender joint shiny skin over affected joint stiff limited joint movement deformities d/t contractures HEBERDEN’S NODES – nodes on distal interphalangeal joints BOUCHARD’ S NODES – proximal interphalangeal joints


RHEUMATOID ARTHRITIS :217 RHEUMATOID ARTHRITIS is an autoimmune disease that causes chronic inflammation of the joints systemic collagen inflammatory disease but initially presents as joint pain progressive illness that has the potential to cause joint destruction and functional disability Etiologic cause: unknown Incidence rate: usually in women 20-40 y/o Diagnostic findings: laboratory findings, x-ray Clinical Manifestations joint pain, joint stiffness – bilateral & usually affects upper extremeties swelling, warmth, erythema, lack of function, malaise


Extra-articular Changes :218 Extra-articular Changes fever, weight loss, fatigue, anemia, lymph nodes enlargement Pain and swelling in your joints, especially in the smaller joints of your hands and feet Generalized aching or stiffness of the joints and muscles, especially after sleep or after periods of rest Loss of motion of the affected joints Loss of strength in muscles attached to the affected joints Fatigue, which can be severe during a flare-up Low-grade fever Deformity of your joints over time


Pathophysiology :219 Pathophysiology Sinuvitis (inflammation of synovial lining)  Pannus formation  Destruction of cartilage  Ankylosis (fusion of cartilages)  Calcification of fibrous tissue


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GOUTY ARTHRITIS :221 GOUTY ARTHRITIS an attack of a metabolic disease marked by uric acid deposits in the joints there is problem in purine metabolism causing (-) excretion of uric acid usually affects big toe affects males more, 40 up DIAGNOSIS: Ultrasound/Ultrasonography


Risk Factors :222 Risk Factors Obesity High blood pressure Tuberculosis Hypothyroidism Dehydration Complications Kidney stones Kidney failure Joint deformities Loss of Motility


Pathophysiology :223 Pathophysiology Hyperuricemia (↑ uric acid) ↓ Urate crystals deposited within the joint ↓ Inflammation ↓ Gout arthritis ↓ Normal repeated attacks ↓ Accumulation of Urate crystals in Peripheral areas of the body ↓ Worsens (kidney stones) ↓ Immunologic activity


Clinical Manifestations :224 Clinical Manifestations Pathognomonic sign: TOPHUS/TOPHI – lesion surrounded by intense inflammation PODAGRA – inflammation & pain in joint of big toe d/t tophi Recurrent attacks of acute inflammatory arthritis (polyarthritis) Uric acid nephrolithiasis Rapid onset of pain in the affected joint Warmth on the joint affected Swelling Reddish discoloration (erythema) Tenderness