Exam 3 Study Guide PDF

Module 8: Orthopedic Osteoarthritis (3 questions) ● Bone/joint inflammation ● Wear and tear condition involving cartilage and bone ● Degenerative joint disease ● Most affect joints: larger joints that carry the most weight and most repetitive action (injury) ● X-Ray ○ Joint space narrowing ■ Thinnin...

Module 8: Orthopedic Osteoarthritis (3 questions) ● Bone/joint inflammation ● Wear and tear condition involving cartilage and bone ● Degenerative joint disease ● Most affect joints: larger joints that carry the most weight and most repetitive action (injury) ● X-Ray ○ Joint space narrowing ■ Thinning or loss of cartilage ○ Subchondral bone erosion ■ Bone erosion below cartilage ● OA → break down joint cartilage → inflammation → irregular growth of new bone (bone spurs, osteophytes) → pain when they grind on other bones and sensory nerves → may restrict range of motion for joint ● Early cartilage swelling = reflects an effort by cartilage to repair itself ● Late cartilage loses elasticity → flaking or shredding of cartilage ● OA in the knee begins medially then progresses laterally ● Increased inflammation → swelling, pain, stiffness ● Change in weight bearing = disuse → muscular atrophy on the opposite side (unaffected side) ● Person at risk for secondary OA ○ Mechanical injury: repeated joint stress, wear and tear, athletes, runners ● Person at risk for primary OA ○ Age + … ○ Decreased cartilage volume, cartilage thins ○ Decreased vascular supply to cartilage ○ Decreased proteoglycans ■ Compound that holds water in the cartilage → able to give rather than crack ○ DNA/genetics ● CLASS ACT ○ Chief complaint: worsening chronic pain ○ A: “gel phenomenon” = stiffness r/t thickening of synovial fluid r/t inactivity ■ Crepitus (bone grinding on bone) ○ T: morning/sedentary lasting less than 30 min (gel phenomenon) ○ Tx: get up + more ○ Physical exam: impaired physical mobility r/t loss of muscle mass and strength association with abnormal weight bearing and disuse. Decreased ROM. ● Treatment ○ Goal: correct altered anatomy to restore physiology ○ Weight control ■ Take stress off joints ○ Analgesia ■ NSAIDs, cushioning w/ hyaluronic acid injections ○ Platelet Rich Plasma ■ Inject into the knee to activate growth factors ○ Knee replacement = arthroplasty Rheumatoid Arthritis (1 question) ● Autoimmune involving synovial membrane → synovitis ● ACPA definitive diagnosis ● Bilateral involvement in smaller joints Osteoporosis (3 questions) ● Thinning of bones … Demineralization ● Bones become porous because osteoclasts > osteoblasts ● High Risk ○ Post menopausal women ■ Decreases estrogen → osteoclasts > osteoblasts ● Men ○ ¼ men over the age of 50 have or at risk for osteoporosis ○ Men generally have a greater bone density than women; bone loss begins later and advances more slowly ○ Highest risk: thin white males over the age of 65 ○ Pathological fracture r/t osteoporosis ○ Visceral obesity in men ■ Visceral fat → adipokines (weaken bones) → inflammation → osteoclast activity ● Related Concerns ○ Pathological fracture caused by thinning of bone matrix primarily spongy bone ○ Fractures: ■ vertebrae, wrists, hips (intertrochanteric area) ○ Kyphosis: ■ Stooped posture, loss of height, collapse change in contour, fracture in vertebral bodies ● Prevention ○ Screening for osteopenia (small deficient bone) ○ Routine osteoporosis screening of all women over 65 or postmenopausal under 65 with risk factors ○ No recommended screening for men (unless they have risk factors) ○ Ultrasound bone density screen (ankle) ○ Bone Mineral Density Scan (DEXA scan) → T score ■ Lumbar Vertebrae and femoral neck ■ Normal > -1 (best is 0) ■ Osteopenia - 1 to 2.5 ■ Osteoporosis < 2.5 ○ Resistance exercises to build bone as muscle pulls ○ Dietary calcium and Vitamin D ● Treatment ○ Goal is to remineralize ○ Calcium and Vitamin D ○ Resistance exercises ○ Decrease osteoclast activity with medication (alendronate) ● Special cases of bone demineralization ○ Renal failure ■ Decrease in active Vitamin D + increase in serum phosphorus (does not get filtered) → decrease in calcium ○ Long term high dose of glucocorticoids ■ Less formation of bone r/t absorption of calcium from GI tract ○ Chronic malabsorption ■ Doesn’t absorb Vitamin D + calcium ■ Roux en Y Fractures (5 questions) ● The stress on the bone is more than the bone can absorb ● Etiologies ○ Trauma / sudden injury ○ Constant pounding → stress fracture ○ Pathological fracture (disease, multiple myeloma, osteoporosis, osteomyelitis, osteosarcoma) ● Signs and Symptoms ○ Pain ○ Tenderness ○ Swelling ○ Loss of function, deformity, unnatural position ● Classification ○ Location: proximal, midshaft, distal ○ Direction/pattern: transverse, oblique, spiral, comminuted, impacted, segmental ○ Incomplete “greenstick”: does not go through all the way ○ Open: comes out of the skin ■ Osteomyelitis r/t concern ○ Impacted vs compression ■ Impacted = telescoping ■ Compression = vertebral disc collapse ● Treatment ○ Immobilization w/ 1st aid ■ Limit soft tissue injury and injury to blood vessels and nerves ■ Keep fat from being released into circulation → fat emboli ○ Reduce fracture ■ Pull into anatomical alignment ○ Fix in anatomical position ■ Maintained with plates, pins, and screws ● Special Case ○ Fractures in elderly ○ Decreased ability to withstand stress on bones → fractures with less trauma Orthopedic Compartment Syndrome (6 questions) ● Condition of increased pressure within a limited space that compromises circulation and function of the tissues in the space ● Neurovascular complication of fractures ● Increased volume → increased pressure → compression of blood vessels and nerves → vessels in compartment have decreased oxygen supply → ischemia → muscle necrosis and nerve loss of sensation ● Compartment ○ Myofascial compartment: muscle and fascia that surrounds it ○ Fascia: connective tissues, fibrous webs that surrounds and supports muscle ● Early Signs and Symptoms ○ Pain with passive muscle movement ■ Ischemic muscles → anaerobic metabolism → lactic acid build up → pain on passive movement ○ Increased volume from inflammatory fluid or bleeding → increased pressure → ischemia: pain → numbness or tingling ● Late Signs and Symptoms ○ Pale, cool skin ○ Increase in volume or decrease in size of compartment → increased pressure → decrease arterial blood supply → pale cool skin ○ Pallor r/t occluded blood supply → less hemoglobin at surface ● ● ● ● ○ Polar r/t occluded blood supply → less heat at surface ○ Paresthesia r/t poorly oxygenated nerves conduct poorly/not at all ○ Pulses are diminished/absent r/t occluded arteries that are unable to transmit a pulse Etiology ○ Any situation that would increase the volume or pressure in the extravascular spaces → occlusion of arterial blood supply → ischemia → complain of pain ○ → compression of nerves → numbness and tingling and anesthesia (no sensation) Diagnosis ○ Measure compartment pressure ○ Needle is placed in compartment and pressure is measured ■ Normal = near 0 mmHg ■ Compression > 30 mmHg Treatment ○ Reduce the pressure of the compartment ○ Split cast, remove occlusive dressing ○ Closed fracture that is casted ■ Open cast up ○ Fasciotomy: make the container bigger ■ Increasing size → decrease pressure → relieve s/s ○ Goal: ■ No complaints of pain on passive movement/stretch ■ Absence of paresthesia no n/t ■ Skin is pink, warm, strong pulses, brisk cap refill Non-orthopedic compartment syndrome ○ Inflammation in spaces with limited ability to stretch ○ Very swollen leg ○ Hypernatremia ■ Fluid shiting increasing intracranial pressure ○ Glaucoma ■ Increase aqueous humor, increase pressure on optic nerve Osteomyelitis (1 question) ● Inflammation in the bone or bone marrow related to infection ● Risk factors ○ Downward extension: vascular ulcer with PAD or infected surgical wound ■ Decubitus ulcer: downward extension of bone ○ Open fractures: break in nonspecific immune barrier of skin ● Signs and Symptoms ○ Not manly early manifestations ○ Increase temperature ○ Increase WBC ○ Increase neutrophils ○ Pain ○ Swelling ○ Skin = red and warm ○ Elevated ESR and CRP ○ Inability to bear weight ○ Pain, bone tender to palpation, reduced joint movement ○ Soft tissue swelling (late) ○ Suspicious X ray ○ Positive blood culture ● Definitive diagnosis ○ Bone biopsy ● Treatment ○ Antibiotics based on specific organism (sensitive) ○ Local debridement: removal of infected tissue ○ Surgical treatment: limited amputation Paget’s Disease (2 questions) ● Chronic disorder that causes bones to grow larger and become weaker than normal. The disease usually affects just one or a few bones. The bones most commonly affected include pelvis and skull ● Osteoclast activity ○ Osteoclasts are more active than osteoblasts ○ Disorganized bone regrowth ● Signs and symptoms ○ Bone or joint pain ○ Sciatica ○ Peripheral neuropathy ○ Loss of movement in limbs, balance problems ○ Bowel incontinence ○ Osteoarthritis ○ Fragile bones → fractures ○ Scoliosis ○ Vertigo and heart problems ● Lab analysis ○ People with Paget's disease of bone often have raised levels of ALP alkaline phosphatase ● Treatment ○ Osteoporosis medications Module 9: Muscles and Ligaments Sprain/Strain (4 questions) ● Sprains = stretch or tear of ligaments ○ Ligaments join bone to bone ○ Stretch or tear → unstable joint ● CLASS ACT ○ Inflammatory s/s ○ Pain r/t tissue injury ○ Heat and redness r/t inflammation ■ Inflammation → blood vessels dilate → heat and color to surface ○ Swelling r/t bleeding and inflammation ■ Inflammation → blood vessels dilate → plasma fluid moves from intra capillary to interstitial ○ Bruising r/t ruptured capillaries ● History ○ Trauma: inversion injury of ankle ● Physical associated s/s ○ Redness, swelling, heat, and bruising ○ Joint instability r/t degree of ligament injury ■ Complete ligament tear → most instability ● Diagnosis ○ History and physical exam (ROM) ● Treatment ○ Rest ○ Ice ○ Compression ○ Elevation ○ NSAIDs ○ Goal: patient verbalizes a comfort at a level of 3 on scale of 1-10 ● Compartment syndrome ○ A wrap or boot that is too tight ○ An ankle that is swelling inside the “container” ● Knee ligament injury ○ Diagnose and treat with arthroscopy ○ ACL Tear (anterior cruciate ligament) ■ Injury occurs when bones of the leg twist in opposite direction under full body weight ■ Popping sensation ■ Pain and swelling ■ Drawer sign: anterior movement of tibia indicative of ACL tear ■ Diagnosis confirmed with MRI ■ Treatment: arthroscopy, hamstring graft ○ Sprain but not tear ■ Control pain and swelling ■ Rest knee ■ Functional brace ○ Meniscal tear ■ Arthroscopy Carpal Tunnel (6 questions) ● Etiologies ○ Congenital predisposition ■ Smaller than normal carpal tunnel (decrease size) → increased pressure → compression of median nerve → thumb, index finger, long finger, and lateral ring finger ○ Contributing factors ■ Repetitive injury ● Cumulative trauma injury ● Work stress ■ Abnormal wrist alignment ■ Wrist sprain or fracture ● Swelling ■ Rheumatoid arthritis ● Synovial tissue swelling → pressure on median nerve ■ Fluid retention during pregnancy ■ Idiopathic ■ Hypothyroid and diabetes ● Implications ○ Ulnar nerve passes over the ligament → little finger and medial ring are unaffected ● Signs and symptoms ○ Compression or compartment syndrome: 6 p’s ■ Paresthesia ■ Paralysis ■ Pain ● CLASS ACT ○ Location: numbness/pain follows distribution of median nerve thumb, index finger, long finger, and lateral ring finger ○ History: repetitive wrist injury and RA ○ Physical: little and medial ring finger are unaffected ● Diagnosis ○ Nerve conduction study ○ Expect that conduction through the median nerve is slow, nerve is compressed ● Treatment ○ Positioning to open up the carpal tunnel with a splint ○ Cortisone injections to decrease inflammation and build up fluid ○ Modify activity ○ Physical therapy ○ Surgery to make compartment or container bigger ■ Cutting transverse carpal ligament ■ Similar to fasciotomy in orthopedic compartment syndrome ● Prevention ○ Prevent wrist trauma ○ Position and job r/t issue Duchene’s Muscular Dystrophy (3 questions) ● Inheritance pattern ○ X linked recessive ○ When mom is a carrier → 25% girl carrier 25% boy affected ○ A carrier can be symptomatic if defective x takes over and expressed itself ● S/S ○ Around ages 3-4 ○ Lordosis ○ Enlarged calves ○ Progressive muscle weakness ■ Normal muscle is being replaced with fat and connective tissue ● Diagnosis ○ Suspected when … ■ Waddled walk ■ Tip toe walk ■ Delayed onset of walking ■ Difficulty performing standing jump ■ Gower’s sign: difficulty getting up from floor (use hands) ○ Mutated dystrophin → skeletal muscle irregularities ○ Labs: elevated creatine kinase mm (CKmm) ■ Muscle breakdown → increased CKmm ○ Electromyography: weakness r/t breakdown in muscles rather than problems with nerves (healthy nerve, diseased muscle) ○ Definitive diagnosis: muscle biopsy ■ Hypercontracted, necrotic, and degenerated fibers ● Cause of death ○ Respiratory failure ■ Muscle atrophy → ineffective respirations → failure Myasthenia Gravis (2 questions) ● Patho ○ Condition of failure of self recognition (autoimmunity) ○ The immune system produces antibodies that block muscle receptor sites → block from acetylcholine → muscles relieve fewer nerve signals → muscular weakness ○ Nerve signals muscle contraction by releasing the neurotransmitter acetylcholine ○ It is possible the thymus gland may trigger the development of the autoantibodies ● Signs and symptoms ○ Muscle weakness ○ Eyelid drooping = ptosis ○ Blurred or double vision ○ Impaired speech ○ Difficulty swallowing ○ SOB, tube breathing ○ Changes in facial expression ● Activity weakness, rest relief ○ Activity → more acetylcholine is needed to promote muscle contraction → receptors need to receive more acetylcholine ○ With less receptors available → less impulses pass muscle → complain of muscle weakness ○ Rest → fewer receptors are need to transit impulses → increased acetylcholine → increased energy and strength Module 10: Cerebrovascular TIA (3 questions) ● Transient Ischemic Attack = angina of the brain ○ Brief episode of neurological dysfunction caused by local brain or retinal ischemia with clinical symptoms typically lasting less than 1 hour and without evidence of acute infarction (no cell death) ○ Tissues are ischemic ○ Cellular changes are reversible ● Ischemia ● ● ● ● ○ Temporary and reversible ○ Localized area of reduced blood and oxygen flow ○ S/S depends on the cells and tissues deprives of blood and oxygen Presenting signs and symptoms eFAST ○ Eyes: deviated, sudden or temporary loss of all/partial vision ○ Face: sudden numbness/weakness especially on 1 side of body ○ Arm: sudden arm/leg numbness/weakness especially on 1 side of body ○ Speech: slurred, difficulty speaking, difficulty understanding what is said ○ Time: time to call 911 “time is brain” Rationale for short term S/S ○ Symptoms last < 60 min because 1. TPA lyses clots 2. Blood rerouted or 3. Occlusion incomplete ○ Clots are lysed quickly ■ Plasminogen activator (tPA) ● tPA → plasminogen to plasmin → fibrinolysis ○ Blood vessels in the area dilate to allow blood to perfuse tissue or blood is reroute around the obstruction ○ Vessel occlusion is incomplete Risk factors ○ Same as atherosclerosis ■ Narrowing of lumen of vessel → slow moving blood tends to clot ■ Narrows the lumen by intimal thickening, plaque formation, or thrombus (clot formation) ○ Smoking ○ High LDL ○ Hypertension ○ High triglycerides ○ Obesity and visceral fat ○ Inactivity ○ T2 DM ○ Hx of atrial fibrillation Etiology ○ Dysrhythmia ■ Atria quiver does not contract → blood is static in atria → static blood clots → embolism breaks away from thrombus in L atrium → L ventricle → aortic valves → aortic arch → carotid artery → brain → TIA ■ L atrium → mitral valve → left ventricle → aortic valve → aortic arch → right brachiocephalic artery → left common carotid → carotid arteries → cerebral circulation ○ Hypotension ■ Episodes of hypotension → decreased perfusion through narrow blood vessels → risk for ischemia, thrombus → TIA ■ Orthostatic hypotension and TIA is great concern in person who already has atherosclerosis, cerebrovascular disease, previous TIA, or previous brain attack ● Physical exam ○ Carotid bruit ■ Sound blood makes when it passes through a narrow opening ■ R/t plaque and intimal thickening ○ Ultrasound ■ Determine severity of vessel narrowing ○ Diagnosis = CT angiography ● Treatment ○ Reperfuse ○ Prevent stroke/brain attack ○ IV tPA ○ Anticoagulants (antiplatelets) ○ Angioplasty and stenting ■ Open up carotid artery ○ Endarterectomy ■ Physical removal of plaque from carotid artery ○ MERCI Retrieval ■ Mechanical clot removal in cerebral ischemia ● Risk factor modification ○ BP less than 140/90 then 150/90 at age 80+ ○ A1c normal at < 5.7% ■ 7% for DM pt ○ LDL less than 100 mg/dL ■ Or less than 70 if atherosclerosis pt Brain attack (hemorrhagic/ischemic) (18 questions) ● Prolonged ischemia, ischemic brain attack ● Necrosis or cell death … loss of tissue ● Brain attack is to brain what heart attack is to the heart ● Leading cause of mortality and morbidity in the US ● Incidence ○ Increases with age (men at younger age more often than women) ○ African americans have increased risk ● Risk factors ● ● ● ● ○ Risks for atherosclerosis: smoking, obesity, HTN, sedentary lifestyle, high LDL, high triglycerides ○ Risks for metabolic syndrome: ⅗ criteria ■ Waist ≥ 40 inch men and ≥35 inch women ■ High triglycerides ■ Low HDL ■ Hypertension ■ Fasting BS ≥ 100 Presenting S/S ○ Same as TIA ○ EFAST ○ S/S can vary depending on tissues affected ○ Motor deficits: contralateral = symptoms on opposite side ○ Dysarthria: slurred speech CN 12 ○ Facial droop: CN 7 ○ Ataxia: cerebellum ○ Fluent aphasia: Wernicke’s area ■ Clear speech with impaired meaning, poor understanding ○ Broca’s aphasia: Broca’s area ■ Affect speaking and writing; comprehension intact ○ Hemianopia: loss of ½ visual field in both eyes; brain attack occurs in optic tract ○ Dysphagia: difficulty swallowing; brainstem damage ■ CN 5, 7, 9, 10, 11, 12 ■ → aspiration ■ Look for coughing and choking ○ Left hemispheric brain attack: right hemiparesis, Broca’s, Wernike’s, dysphagia ○ Right hemispheric brian attack: left hemiparesis, left visual field deficit, dysphagia ○ LOC issues ■ Ischemia and necrosis → inflammation → swelling → increased ICP → decrease blood supply and further decreased blood and oxygen to brain → deteriorating LOC Etiology ○ Ischemic: artery blockage (80% of all brain attacks) ○ Hemorrhagic: bleeding into brain tissue Diagnosis ○ MRI shows identifiable ischemia and necrosis in brian ○ Ischemic penumbra: area of cells that are at risk but salvageable with reperfusion Treatment ○ Irreversible but the ischemic penumbra is reversible ○ ○ ○ ○ Goal is to reperfuse and save tissue tPA within 3 hours of onset of symptoms Door to needle: reperfuse within 60 minutes Angioplasty and stenting: save ischemic tissue ■ Open up artery ○ Endarterectomy ■ Physical removal of plaque ○ MERCI ■ Mechanical clot removal ● Prevention ○ Anticoagulant therapy ■ Aspirin ■ Antiplatelet ○ Treat other conditions such as atrial fibrillation ○ Slow down progression of atherosclerosis with lifestyle modifications ● Hemorrhagic Brain Attack ○ Excessive flow of blood occuring in tissues of the brain ○ Problem: blood vessel bursts → spilling of blood into tissues of the brain ○ Increase BP → rigid vascular container cannot give → increased pressure in blood vessels with limited gibe → container brustes ■ Atherosclerosis, plaque, calcium deposits → rigid vascular containers ○ Symptoms ■ Blood = volume ■ Increased volume in cranial cavity → increased pressure → compressed blood vessel → ischemia ■ Creates pull → more plasma leaves blood vessels and enters tissue space → increased volume → increased pressure → compression of blood supply → more ischemia and worsening S/S ■ Signs and symptoms evolve over time ■ Cells slowly dying ■ Cell death → inflammation ■ Inflammation → fluid shifts from inside arteries to outside → increase size of brain → increase volume in cranial cavity → increase pursue → compression of blood vessels → more tissue → ischemia → necrosis ○ High mortality rate ■ Impaired perfusion → increase amount of tissue lost ■ Increase ICP ■ Blood in cranial cavity → increase pressure ■ Ischemia → inflammation → more pressure → more tissue lost ■ Pressure on the brain stem → brain death ○ Etiologies ■ Hypertension (atherosclerosis → burst in blood vessel ) ■ Advancing age ○ Diagnosis ■ CT scan or MRI ○ Treatment ■ If brain attack is r/t bleeding into tissue you DO NOT give anticoagulants ■ Supportive: Airway, Breathing, Circulation ■ Anticonvulsants ■ Antihypertensive ■ Osmotic diuretics to pull fluid out of brain ■ If aneurysm → clip or coil to stop source of bleeding MI (1 question) ● Prolonged ischemia → Necrosis or cell death … loss of tissue ● Brain attack (stroke) is to the brain what heart attack (MI) is to the heart ● Leading cause of mortality and morbidity in the US Brain Herniation (1 question) ● Brain herniation occurs when something inside the skull produces pressure that moves brain tissues ● Result of brain swelling or bleeding from a head injury, stroke, or brain tumor ● Side effect of tumors in the brain, including: Metastatic brain tumor Module 11: Memory and Cognition Basic Confusion (3 questions) ● Confusion: person experiences altered levels of consciousness disoriented to time, place or person … a disturbed mental state ● Confusion is reversible and solved by correcting the situation ● Dementia is more permanent and irreversible ● ALL dementia has confusion but NOT ALL confusion is dementia ● Acute Confusion Related to .. . ○ Hypothyroidism (high TSH, low T3 and T4) ○ Side effects of medication ○ Heart failure – decrease oxygen to brain ○ MI ○ Depression ○ Dehydration and electrolyte imbalance ○ Alcohol abuse ○ Infections in elderly ■ Increase WBC, + chest x-ray, urinalysis nitrite or LE+ ○ Anemia ■ Low H/H ○ Renal failure ■ Increase creatinine ■ Reduced GFR ○ Liver disease ■ Increased liver enzymes ○ Malnutrition ○ Intracranial pathos ■ MRI or CAT scan →brain tumor ● Chronic confusion (Dementia) ○ Impairment of short and long term memory; deficits in abstract thinking, impaired judgment and other high cortical function or personality changes; interferes significantly with work or social activities ○ 60% Alzheimer’s ○ 15% LBD ○ 5% Vascular (atherosclerosis) Lewy Body Dementia (1 question) ● Progressive brain disorder ● Neuron has trouble processing alpha-synuclein protein fragments ● Lewy bodies build up in the brain tissue ● Decrease in acetylcholine ● Problems in area of the brian that regulates behavior, cognition, and movement ● Result of misfolded proteins that collect in cytoplasm of neurons → destroy neuron → decreased acetylcholine and dopamine → weaken communication → dementia ● Can exist as single disease (LDB affecting cerebral cortex) ● Can be a component of Alzheimer’s (decrease acetylcholine) or Parkinson’s (decreased dopamine) Alzheimer’s Disease (8 questions) ● Memory issues ○ Forget whole experiences ○ Rarely remember things later ○ Gradually unable to follow written or spoken erection and make choices ○ Often get lost in familiar places ● Risk factors ○ Advances age ● ● ● ● ○ Genetic defect on chromosome 19 ■ Apoe4 gene mutation Patho ○ Disease of plaques and tangles ○ Plaques: amyloid precursor protein on the surface of brain cells → if snipped by enzyme beta secretase in the wrong place → plaques in extracellular spaces ○ Tangles: abnormal tau → microtubule disintegrate → neuron apoptosis → terminal axon disintegrate → does not produce acetylcholine → no neuron communication ■ With abnormal tau cells cannot nourish themselves, lessen ability to produce and release acetylcholine, liability to make synapses (synapses help us make sense of our world) ○ Starts in the hippocampus (memory) ■ Frontal lobe = judgment and problem solving ■ Limbic system = emotions ○ As neuron dies → decrease size of brain → cerebral atrophy ○ A person may have significant plaques and tangles in the brain but still be cognitively intact ○ Inability for nerves to talk to each other and eventually undergo apoptosis and die Diagnosis ○ Exclude all other etiologies ○ Physical exam ○ Mini mental status exam ○ MRI or CT scan: cerebral atrophy r/t loss of neurons → ventricle enlargement and hydrocephalus r/t loss of brain tissue ○ PET scan: areas that light up = use of glucose ○ Pattern of cognitive decline in absence of other explanations ○ Definitive diagnosis = autopsy Treatment ○ Cholinesterase inhibitors → increase acetylcholine at synapse → improve memory ○ Glutamate regulator → reduce glutamate (common excitatory NT that promotes learning and storing new information) → slow apoptosis ■ In AD: increased glutamate → neurotoxic → apoptosis Interventions ○ Heart healthy life choices to control BP and atherosclerosis ○ Quality sleep ○ Move your body for 30 min at day ○ Eat well ○ Be social ○ Try new things ● Down Syndrome ○ By age 40 down syndrome patients brain has high levels of plaques and tangles ● Fatal complications ○ Aspiration pneumonia ○ Sepsis from decubitus ulcer ○ Recurrent UTI ○ Immune suppression ○ Cardiac arrest (brainstem affected by AD) Vascular Cognitive Impairment (2 questions) ● VCI is a decline in thinking skills caused by the conditions that block or reduced arterial blood flow to the brain depriving the brian cells of oxygen and other nutrients ● Etiologies ○ Atherosclerosis: plaque and intimal thickening → clot formation ● Early symptoms ○ Memory loss ● Risk factors ○ Same as atherosclerosis: smoking, high LDL, high triglycerides, obesity, HTN ○ Previous brain attack ○ Atrial fibrillation ■ Left atrial thrombus → embolus in L ventricle→ brain ● Diagnosis ○ Rule out other etiologies for impaired cognition (acute confusion) ○ MRI shows multiple small cerebral infarctions called lacunar infarctions ■ Subcortical= below cerebral cortex Huntington’s Disease (2 questions) ● CAG repeats more than normal → neuron degeneration ● Etiology ○ Detect through genetic screening ○ Autosomal dominant ● Signs and symptoms ○ Fatal ○ Breakdown of nerve cells in the brain ○ Deterioration of physical ability and mental capability r/t basal ganglia effects ○ Onset between 35 and 50 years old ○ Chorea movements = sudden, unintended and uncontrollable jerky muscle movements → impaired gait and balance (clumsy walking)