Patho Exam 2 Review PDF

1.Discuss the pathophysiology, clinical manifestations, treatments, and\ complications of common eye, ear, brain, spinal cord, and peripheral nerve\ disorders. Common eye- Cataract( Congenital,Senile,Traumatic)- cloudiness of lens causing blindness. Patho: Unilateral or bilateral growth, insidious,...

1.Discuss the pathophysiology, clinical manifestations, treatments, and\ complications of common eye, ear, brain, spinal cord, and peripheral nerve\ disorders. Common eye- Cataract( Congenital,Senile,Traumatic)- cloudiness of lens causing blindness. Patho: Unilateral or bilateral growth, insidious, vitreous and aqueous humor seeping into the lens causing cloudiness. Retinal Detachment- scleral buckling surgery is the most common way to treat it. Method of closing breaks and flattening the retina. Vitrectomy(laser)sealing tissue. Glaucoma- increased ocular pressure and loss of visual field fuel to increased aqueous humor or blockage of fluid outflow. \^IOP 20 mmHg, pain and compression of retinal nerves. Open Angle, an outflow of aqueous humor is blocked at the canal of Schlemm. Closed Angle, displacement of the iris towards the cornea causing a blockage in aqueous humor. (EMERGENCY) Treatments: Miotic eye drops. Retinitis Pigmentosa- a group of genetic eye conditions that leads to incurable blindness. Progression of symptoms for RP is night blindness, tunnel vision. Loss eyesight outside. Conjunctivitis- (pink eye) (Allergenic, Bacterial/viral/fungal, Congenital) inflammation infection of the transparent membrane that lines your eyelid and eyeball. Redness and gritty sensation in your eye with itching. Accompanied by purulent drainage. Treatments: Antibiotic Eye Drops (tobramycin, steroid eye drops) Corneal Abrasion- scratch on the cornea. Symptoms- foreign body sensation of the eye, gritty eye sensation; unilateral eye watering pain; photophobia and mild erythema of the conjunctiva. Minor corneal abrasions may be asymptomatic. Diagnosis- drops of fluorescein dye in the eye. Fluorescein dye flows into the defect and glows under the lights of a Wood's lamp. Treatment: topical antibiotic ointments to prevent bacterial growth. Heals in 24 hours. Diabetic Retinopathy- changes in retina that occurs in type 1 or type 2 diabetes. Vascular changes occur caused by periodic high blood glucose levels. High levels of blood glucose cause endothelial injury throughout the body, including retinal blood vessels. This renders the blood vessel walls susceptible to arteriosclerosis, aneurysm, and rupture. Often present upon the diagnosis of diabetes. This is because blindness in adults 20 to 74 years old. Ear- **Conductive hearing loss-** poor inner bone conduction **Sensorineural hearing loss-** Meniere\'s Disease- severe dizziness, roaring sound (tinnitus), hearing loss comes and goes, pressure or pain that Affects one ear. Otosclerosis- abnormal bone growth in the middle of the ear that causes hearing loss. Prosthesis replaced stapes (surgery) typically, in young adults, more in women than men. Affects both ears. Slowly... gets worse. Medications- fluoride, calcium, or Vitamin D help slow hearing loss. Hearing aids help. Surgery to remove the stapes and replace them with a prosthesis can cure conductive heating loss. A total replacement is called stapedectomy. Brain-Multiple Sclerosis: demyelinated disorder that results in inflammation and damage to the myelin and other cells within the CNS. T-cells attack the myelinated neurons. MS is an autoimmune disease. Sclerotic plaques noted on the MRI MS disease is characterized by the remissions and exacerbations stages. Affected both the motor and sensory impairment. The most common symptoms of MS are weakness, numbness, balance problems and blurred vision. The eyes are the most common place affected by MS because the optic nerves are heavily myelinated. Also, cerebellar dysfunction leading to ataxia (gait disturbance), tremor and dysarthria (weaken of the muscle around the mouth that leads to difficulty of speech) Diagnosis for MS followed the McDonald process that required MRI, blood test. Cerebrospinal fluid should be tested for (OBCs) oligoclonal bands and IgG. EMG and evoked potential test (test to see if other disease may lead to these condition) Treatment includes: Immunosuppressives to decrease autoantibody and corticosteroids to decrease inflammation 2\. Discuss the different types of acute brain injury: DAI, concussion, and\ coup/contra-coup injury. What are the pathophysiology, clinical manifestations,\ assessment information, complications, and treatment for each? 3\. Discuss TBI. What are the pupil responses/changes in TBI? - **Traumatic Brain Injury (TBI)** refers to damage to the brain caused by an external force, such as a hit to the head TBIs can range from mild (concussion) to severe, with symptoms including headache, confusion, memory loss, and, in severe cases, loss of consciousness or coma. Pupil responses are critical indicators in assessing TBI severity. Abnormalities like unequal pupil sizes (anisocoria), sluggish or non-reactive pupils to light, or dilated pupils can suggest increased intracranial pressure, brain herniation, or damage to the brainstem. A fixed and dilated pupil on one side often indicates pressure on the cranial nerves, particularly the oculomotor nerve (cranial nerve III), and may signal severe brain injury requiring immediate medical attention. Monitoring pupil changes helps assess the progression of the injury and guides treatment decisions. 4\. Discuss the different types of headaches. How do they differ in clinical\ manifestations? - **Migraine-** throbbing pain, wanting to be in dark places the light hurts. Can be triggered by stress, lack of sleep, hormone shifts, odors, and food additives. Can be diagnosed with a severe headache lasting from 4-72 hours with throbbing pain aggravated by movement. Treatment can be medicine or botox injections - **Tension-** constant pain feels like a tight band - **Cluster-** severe episodic but no throbbing forehead, eyes teary, with head beating 5\. Describe decerebrate and decorticate posturing. What are the signs and symptoms,\ causes, and parts of the brain affected? What do these positions indicate? 6\. Differentiate between MS, Parkinson's, myasthenia, Huntington's disease, ALS ,\ Gillian-Barre causes, symptoms, pathophysiology, and long-term outcomes. **MS**:The etiology of it is that the autoimmune attacks on CNS myelin. Patho: t-cell immune injury to myelinated neurons meaning that there is damage being caused by the body's own immune system, specifically the t-cells which are one of the white blood cells that plays a key role in the immune system, immune injury referring to the damage or harm that was caused by the immune system when the immune system mistakenly targets and injures the body's own cells such as neurons. Myelinated neurons are nerve cells that have a protective covering called myelin. This myelin helps increase the speed of electrical signals transmitted along the nerve cells. Damage to this can disrupt communication between the brain, spinal cord and the rest of the body which can lead to conditions such as MS. Sclerotic plaques noted on MRI. Demyelination disturbs neuron conduction. Clinical manifestations include paresthesia, gait disturbance, leg weakness, vision loss (optic neuritis), double vision, arm weakness, vertigo. MRI lesion is diagnostic **Parkinson's: Disorder** of the brain that leads to difficulty with movement and coordination. This often develops in people over 50 and is one of the most common nervous system disorders of the elderly. Parkinson's disease occurs when the nerve cells that are in the brain that make dopamine (a neurotransmitter that controls emotions, behavior, and movement) begin to slowly be destroyed and without dopamine the nerve cells in the brain can\'t properly send messages. Unknown reason why this occurs. The Patho of it is low dopamine level in the basal ganglia, excessive action of acetylcholine, and that the disease process is progressive. Clinical manifestations are as follows; akinesia (loss of ability to move your muscles voluntarily), rigidity (stiff or inflexible muscles), resting tremor/pill-rolling hand movements. Associated manifestations are poor speech quality, 30-50% have dementia, drooling, postural instability, masklike face. Complications can be hallucinations, depression, dementia. There is no known cure, treatment is to control symptoms. Medicine controls symptoms by increasing the levels of dopamine in the brain **Myasthenia:** Patho: loss of Ach receptors at neuromuscular junction, destroyed by IgG antibodies from B- cells. This means that the loss of ach receptors which are special proteins located on muscle cells at the neuromuscular junction and this is the point where nerve cells communicate with muscle cells to trigger muscle contraction. Ach is released by nerve cells and binds to these receptors, telling the muscle to contract. In Myasthenia Ach receptors are reduced because the immune system mistakenly attacks them, causing impairment to communication between nerves and muscles. IgG antibodies are immune proteins produced by B-cells (a type of white blood cell) that normally help fight infections. In myasthenia, the body mistakenly produces IgG antibodies that target and destroy the Ach receptors on muscle cells. This is an autoimmune response, where the body attacks its own tissues. Clinical manifestations: NM fatigue which worsens with activity, eye droop, diplopia, head droop, jaw dropping, severe muscle weakness with repetitive motion. No loss of reflexes, no change in sensation. Treatment: medicine to control symptoms, chronic and progressive, No cure. **Huntington's disease: This** is a serious genetic disorder that affects the brain and nervous system. Progressively degenerative meaning that this disease worsens over time, that leads to the gradual breakdown of nerve cells in the brain. It specifically affects the nervous system, particularly areas of the brain that control movement, cognition, and emotions. Clinical manifestations are involuntary motor symptoms, emotional and behavioral symptoms, cognitive symptoms, chorea; brief irregular dancelike movements, Athetosis: twisting and writhing movements, Ballismus: thrashing motions, emotional lability, and cognitive impairment **ALS**: Amyotrophic Lateral Sclerosis is a rapidly progressive neurodegenerative disorder. Loss of upper and lower motor neuron functioning, the brain can no longer send messages to the muscles. Muscle weakness starts progressing to paralysis. Voluntary movement is now tampered; one may have difficulty breathing and swallowing. No cure **Gillian-Barre:** Antibodies begin to attack myelin sheath resulting in impulse activity. The most common cause being acute flaccid, ascending, symmetrical paralysis; polyneuropathy. Clinical manifestations are back leg pain that progresses to weakness. Additional numbness, decreased DTRs, muscle weakness. Treatment: hospitalize, plasmapheresis 7\. Discuss spinal cord injuries. Describe paraplegia, quadriplegia, hemiplegia,\ paralysis, and spinal shock. 8\. Discuss the physiology of pain. Discuss how pain sensation moves along the\ tracks/ fibers of the peripheral nerves. Discuss endorphins gate control theory. 9\. Discuss the pathophysiology, clinical manifestations, complications, and\ treatments of the following disorders of the eye: glaucoma, cataract, corneal\ abrasion, conjunctivitis, retinitis pigmentosa, stye, retinal hemorrhage/ tearing,\ macular degeneration. Identify risk factors/causes, pathophysiology, signs/\ symptoms, and treatments for each. **GLAUCOMA** -Pathophysiology: increased inter-ocular pressure from an issue with the optic nerve that causes a decrease in the outflow of aqueous humor -Clinical Manifestations: open angle\~ mild pain, gradual loss of peripheral vision closed angle\~ extreme pain -Complications: blindness -Treatments: mannitol, check level of consciousness every hour, avoid anything that causes pressure (ex: constipation, nausea, vomiting) -Risk Factors: 40-60 years, African American, eye injury **CATARACT** -Pathophysiology: excessive growth of the epithelial tissues causing cloudiness in the lens -Clinical Manifestations: blurry vison, halos at night, cloudy vison, sensitive to glare \- Complications: myopia, presbyopia, blindness -Treatments: antiglare sunglasses, surgical removal, replacement lens -Risk Factor: age, diabetes, sunlight **CORNEAL ABRASION** -Pathophysiology: a foreign body damages the epithelial surface of the cornea -Clinical Manifestations: gritty sensation, unilateral eye watering pain, photophobia -Complications: blindness, corneal ulcerations, infection -Treatment: topical ointment -Risk Factors: eye trauma, contact lens, eye protection **CONJUNCTIVITIS** -Pathophysiology: inflammation and infection of the conjunctiva -Clinical Manifestations: red/ swollen/itchy eye, purulent discharge, crust -Complications: scarring, sepsis, punctate keratitis -Treatment: wash hands before eye drops, \~bacterial: sulfacetamide, \~allergenic: steroids and antihistamines -Risk Factors: bacteria, viruses, allergies **RETINITIS PIGMENTOSA** -Pathophysiology: progressive dysfunction of predominantly rod photoreceptors with degeneration of cone photoreceptors and the retinal pigment epithelium -Clinical Manifestations: night blindness, tunnel vison, clumsiness, color blindness -Complications: visual loss, cataracts, macular edema -Treatment: glasses, gene therapy, retina implants -Risk Factors: male, genetic mutations, 10-40 years **STYE** -Pathophysiology: bacterial infection that appears at the root of the eyelash outside the eye \- Clinical Manifestations: pain, red, swelling of the conjunctiva and eye lid -Complications: cellulitis, orbital cellulitis, chalazion -Treatment: diluted boric acid, warm compresses, antibiotics -Risk Factors: poor hygiene, eye makeup, eye conditions **RETINAL HEMORRHAGE** -Pathophysiology: bleeding in the retina -Clinical Manifestations: asymptomatic, loss of vison -Complications: blindness, glaucoma, retinal tears -Treatment: lazor treatment, injections, surgery -Risk Factors: young women, oral contraceptives, systemic vascular conditions **MACULAR DEGENERATION** -Pathophysiology: degenerations of retinal photoreceptors -Clinical Manifestations: blurry spot in the middle of visual, straight lines look wavy, seeing spots -Complications: Blindness -Treatment: notify HPC, AREDS formula, no cure -Risk Factors: smoking, hypertension, age 10\. Discuss the pathophysiology, clinical manifestations, and treatments of the\ following disorders of the ear: Conductive hearing loss, Sensorineural hearing\ loss, otitis infections, Meniere's disease, tympanic rupture, and Otosclerosis. **CONDUCTIVE HEARING LOSS** -Pathophysiology: blockage of sound waves to the middle of the ear causing a muffled sound -Clinical Manifestations: \~infant: no babbling, \~toddler: monotone/ loud voice/ withdrawn behavior -Treatments: hearing aid, sign language **SENSORINEURAL HEARING LOSS** -Pathophysiology: loss of hair cells from the corti of the inner ear sounds are heard, but not understood -Clinical Manifestations: overly loud sound in one ear, noisy areas cause loss of hearing, high pitched sounds get mixed up (T's & S's) -Treatments: face patients, use gestures, hearing aids **OTITIS MEDIA** -Pathophysiology: infection of the Eustachian tubes of the middle of the ear causing fluid and inflammation -Clinical Manifestations: extreme ear pain, high fever, refusing food, not sleeping -Treatments: encourage routine vaccines, otoscopic examination, inspect tympanic membrane for redness **MENIERES DISEASE** -Pathophysiology: fluid in the ears -Clinical Manifestations: tinnitus, unilateral hearing loss, vertigo -Treatments: sodium restrictions, avoid smoking and drinking alcohol/caffine. Fall prevention **TYMPANIC RUPTURE** -Pathophysiology: fluid buildup causes a perforation -Clinical Manifestations: hearing loss, buzzing sound, earache -Treatments: antibiotics, patching **OTOSCLEROSIS** -Pathophysiology: a callus forms on one of the ossicles and causes lack of vibration so sound is not inhibited -Clinical Manifestations: hearing loss, tinnitus, vertigo -Treatments: stapedectomy\ 11. Discuss the causes-risk factors, pathophysiology, clinical manifestations,\ complications, and treatment of the different types of strokes (hemorrhagic,\ embolytic, thrombolytic), TIAs, and penumbra. **HEMORRHAGIC STROKE** -Pathophysiology: cerebral artery ruptures and can\'t bring blood to the brain tissue -Clinical Manifestations: sudden headache, weakness, vision problems -Complications: anoxic encephalopathy, death -Treatment: IV mannitol, intubation/ mechanical ventilation, neurosurgery -Risk Factors: hypertension, uncontrolled diabetes mellitus, and cigarette smoking **EMBOLYTIC STROKE** -Pathophysiology: a blood clot from elsewhere in the body travels to the brain and blocks blood flow -Clinical Manifestations: paralysis, vertigo, slurred speech -Complications: cerebral edema, dysphasia, seizures -Treatment: clot busting meds, surgical removal, aspirin/ anti platelet meds -Risk Factors: atrial fibrillation, diabetes, hypertension **THROMBOLYTIC STROKE** -Pathophysiology: blood clot (thrombus) blocks blood flow to the brain causing brain cells die -Clinical Manifestations: facial drooping, slurred speech, weakness -Complications: blood clots, pressure ulcers, cerebral edema -Treatment: blood thinner, blood sugar management, mild hypothermia -Risk Factors: obesity, smoking, immobility **TIAs** -Pathophysiology: tiny lack of oxygen, a temporary reduction of blood flow -Clinical Manifestations: memory impairment, confusion, disorientation, inability to communicate -Complications: stroke -Treatment: blood thinners, anti-platelet drugs, cholesterol lowering meds, asprin -Risk Factors: hypertension, over 55, smoking **PENUMBRA** -Pathophysiology: the area of brain tissue around the ischemic that has reduced oxygen blood flow and transport -Clinical Manifestations: sudden weakness, confusion, vison problems -Complications: death -Treatment: the penumbra system -Risk Factors: atrial fibrillation, heart disease, smoking 12\. Discuss seizure disorder. Identify causes, signs/ symptoms, and treatments.\ Discuss the phases of a seizure. Differentiate between generalized and focal\ seizure. **SEIZURES** -Pathophysiology: uncontrolled electrical discharges of neurons in the brain -Clinical manifestations: jerking movement of arms and legs, awareness, breathing -Treatment: medication, surgery, diet PHASES \- prodromal phase: warning signs before a seizure \- aura phase: visual, auditory clue happens before a major seizure \- ictal phase (seizure phase): ignition phase, period of the active seizure \- postictal phase: after the seizure, confused, disoriented, major headache, tired/sleepy GENERALIZED VS FOCAL SEIZURE Generalized: -tonic (tight and tense) \- clonic (convulsions, contractions,) \- lip smacking \- biting \- picking 13\. Discuss pathophysiology, clinical manifestations, medical treatments, and\ complications of dementia Alzheimer's disease. Identify causes, signs/ symptoms,\ and treatments. **DEMENTIA/ ALZHEIMER'S DISEASE** -Pathophysiology: plaques build up in the neuro-synapses of the brain disrupting signaling -Clinical Manifestations: irritability , mood swings, gradual memory loss, lack of environmental awareness -Treatment: fall safety, diet, no cure, donepezil -Complications: cognitive difficulties, agitation, depression -Risk Factors: family history, lifestyle (smoking/alcohol), environment factors 14\. Identify normal intracranial pressure (ICP). What vital sign changes occur with\ increased ICP? How do meningitis, cerebral edema, traumatic brain injury, or\ encephalitis contribute to ICP? Discuss the complications and medical treatment\ for ICP. What is brain stem herniation? How does it occur? Why is this serious? **ICP** -ICP is the pressure of CSF in the skull, normal ICP is 5-15 mm Hg in an adult \- Increased ICP causes blood vessels to compress and leads to cerebral hypoxia, it puts a lot of pressure on the brain stem that controls breathing and heart rate which kills the patient. \- Meningitis is an infection of the membranes that protect the brain and spinal cord when they are infected, they swell and put pressure on the brain and spinal cord increasing the ICP \- Cerebral edema is when the brain swells due to build up fluid in the brain's tissues and increases the ICP \- Traumatic brain injury may cause bleeding and results in inflammation and swelling since the brain can\'t expand due to the firmness of the skull which increases the ICP \- encephalitis occurs when a viral agent enters the brain, WBCs infiltrate the brains tissues and cerebral edema occurs increasing the ICP \- complications: stroke, seizures, death \- treatment: corticosteroids/ antibiotic medications, breathing support, draining CSF **BRAIN STEM HERNIATION** -What? A life-threatening condition when the brain is forced to shift due to increased pressure in the skull -How? Something inside the skull produces pressure that moves the brain's tissues -Why? This occurs when the brain is swelling, bleeding, or has tumors or abscesses 15\. Discuss the Glasgow coma scale. How is it used? -The Glasgow scale classifies if your patient in a coma is getting better or worse. It goes by a score, there is 4 points for eyes, 5 points for the mouth, and 6 points for the extremities. 15 is the highest score, which is normal, anything below 8 is considered neurologically unstable and put in the ICU. EYES (4): 4 points if the eyes open spontaneously, 3 if they don\'t open spontaneously but verbally, 2 if they open for pain, 1 if they don\'t open at all. MOUTH (5): 5 is alert and orientated, 4 is confused and mixing up words, 3 is speaking but not making sense just mixing random words, 2 is for moans, 1 is for no noise at all. EXTREMITIES (6): 6 means you obey commands, 5 means you localize pain, 4 means you withdrawal from pain, 3 decorticate meaning flexing extremities, 2 means you expand exterminates during painful stimuli, 1 means you do nothing during painful stimuli 16\. Discuss autonomic dysreflexia. Autonomic Dysreflexia occurs in high spinal cord injuries ABOVE T6. It\'s super deadly because it results in extreme hypertension up to 300 systolic. It comes from a full bladder, constipation, or tight clothing. The injury causes miscommunication with the spinal cord and the SNS and PNS of the autonomic nervous system. The SNS speeds up vitals and the PNS slows them down. The dysfunction causes vasodilation Above the injury site and vasoconstriction below the injury site. So, there\'s mixed signals of high blood pressure and a low heart rate. 17\. Discuss cerebral hemorrhaging. Describe a Subarachnoid hemorrhage. **CEREBRAL HEMORRHAGING** When blood accumulates rapidly in the brain disrupting the brain's tissues. It causes neuronal dysfunction and can compromise cell signaling pathways. The blood build up increases ICP, causes cerebral edema, and disrupts the blood brain barrier leading to cell death. **SUBARACHNOID HEMORRHAGE** Blood is in the subarachnoid space between the arachnoid and pia mater causing chemical meningitis which in a couple days- weeks increases ICP and can lead to a stroke. Vocabulary-Know the following terms: vertigo, Febrile, purulent, posturing, ototoxic\ drugs, cerumen, Lethargy, hematoma, photophobia, encephalitis, dyskinesia,\ demyelinated **Vertigo-** dizziness / loss of balance **Febrile-** a fever **Purulent-** pus **Posturing-** rigid body movements or holding the bodying in an abnormal way **Ototoxic Drugs-** medications that can damage the inner ear and result in hearing loss **Cerumen-** ear wax **Lethargy-** sleepiness or unresponsive and inactivity **Hematoma-** pool of blood in an organ **Photophobia-** eyes are sensitive to light **Encephalitis-** condition that causes inflammation and edema of the brain **Dyskinesia-** impaired voluntary movement **Demyelinated-** damage of the myelin sheath