Geriactric EOR 2 PDF

Valve Disorders and Murmurs Aortic Stenosis Mitral Stenosis Narrowing of the aortic valve, leading to obstructed blood flow from Narrowing of the mitral valve orifice...

Valve Disorders and Murmurs Aortic Stenosis Mitral Stenosis Narrowing of the aortic valve, leading to obstructed blood flow from Narrowing of the mitral valve orifice, impeding blood flow from the left atrium to the left ventricle to the aorta → fixed cardiac output, increased the left ventricle afterload, LVH and eventually LV failure MCC is rheumatic heart disease MCCs → calcific degeneration, congenital bicuspid valve, rheumatic S/S: heart disease ○ Dyspnea, fatigue, orthopnea, hemoptysis S/S: ○ Diastolic, low pitched decrescendo rumbling murmur with opening ○ Triad of symptoms: angina, syncope, dyspnea on exertion snap heard best at the apex (mitral area) often with loud S1 ○ Harsh, high pitched, “diamond shaped”, ejection Heart best with patient in left lateral decubitus position crescendo-decrescendo midsystolic murmur best heard at ○ Can lead to atrial fibrillation due to atrial enlargement and increased right upper sternal border that radiates to the carotid pressure → increased risk of thromboembolism and stroke Increased intensity: sitting while leaning forward, Dx: increased venous return (squatting, supine, leg ○ Echo is diagnostic, shows thickened immoble mitral valve leaflets and raise, expiration, decreased afterload (amyl nitrate) decreased mitral valve area Decreased intensity: decreased venous return ○ Chest x ray shows left atrial enlargement and pulmonary congestion (valsalva, standing), inspiration, increased afterload Tx: (handgrip) ○ Diuretics and sodium restriction for symptoms relief (edema and volume ○ Delayed and diminished carotid pulses (pulsus parvus et overload) tardus) ○ Anticoagulation for afib Dx: ○ Percutaneous balloon mitral valvotomy for mitral valve replacement for ○ Echo is test of choice; shows valve area, pressure gradient severe cases and left ventricular hypertrophy Mitral regurgitation ○ ECG may show left ventricular hypertrophy and strain Mitral valve does not close properly, leading to the backflow of blood from left pattern ventricle into the left atrium Tx: MCCs → mitral valve prolapse, rheumatic heart disease, ischemic heart disease and ○ Valve replacement surgery (surgical or transcatheter aortic infective endocarditis valve replacement, TAVR) for symptomatic pts or severe S/S: Mechanical: prolonged durability but ○ Heart failure symptoms: dyspnea, fatigue, orthopnea, palpitations thrombogenic, need long term anticoagulant ○ Blowing holosystolic murmur at apex with split S2 that radiates to the therapy left axilla Bioprosthetic: less durable but minimally ○ May be accompanied by S3 thrombogenic (for pts who can't be on Dx: anticoagulant) ○ Echo diagnostic, mitral valve dysfunction, left atrial enlargement and ○ Avoid strenuous activities/venodilators (nitrates)/negative increased left ventricular end-diastolic volume isotopes (Ca channel blockers, beta blockers) in severe AS ○ Chest x ray shows cardiomegaly and pulmonary congestion Aortic Regurgitation ○ ECG shows left atrial enlargement and LVH Diastolic backflow of blood from the aorta into the left ventricle due to Tx: an incompetent aortic valve ○ ACE-I, diuretics, beta blockers for symptom relief and afterload reduction MCCs → rheumatic heart disease, endocarditis, bicuspid aortic valve, ○ Surgical intervention for severe and symptomatic pts (repair preferred aortic root dilation (marfans) over replacement)  S/S: Mitral Valve Prolapse ○ Dyspnea, fatigue, palpitations, angina Mitral valve leaflets bulge into the left atrium during systole ○ Soft, high pitched, blowing, diastolic, decrescendo murmur MC valvular heart disorder in US best heard song the left sternal border at the 3rd intercostal S/S: space on the left (Erb's point) ○ Often asymptomatic but may present with palpitations, chest pain Loudest with patient sitting, leaning forward after dyspnea or syncope exhaling, squatting and hand grip ○ Midysytolic ejection click followed by late systolic murmur best heart ○ Austin Flint Murmur → rumbling diastolic murmur best at the apex heard at the apex of the heart that is associated with severe Longer and louder while standing and valsalva aortic regurgitation ○ Symptoms may worsen with dehydration or reduced blood volume, ○ Bounding pulses and widened pulse pressure due to which increases the click and murmur intensity increased stroke volume ○ Associated with marfan syndrome, ehlers danlos syndrome and other ○ De Musset sign (head bobbing) and Quincke’s sign (nail bed connective tissue disorders pulsations) Dx: ○ Water hammer pulse → swift upstroke and rapid fall of the ○ Echo is diagnostic, shows prolapse/displacement of the mitral leaflets radial pulse accentuated with wrist elevation and possible mitral regurgitation ○ Corrigan's pulse → referring specifically to the carotid artery Tx: ○ Hill;s sign → popliteal artery systolic pressure greater than ○ Asymptomatic → no tx, reassurance brachial artery by 60 mmHg (most sensitive) ○ Beta blockers for symptomatic relief of chest pain and palpitations Dx: ○ Surgical repair or replacement for severe ○ Echo is diagnostic, showing regurgitant jet and left ventricular dilation ○ Chest x ray shows cardiomegaly and pulmonary edema ○ ECG may show LVH Tx: ○ Afterload reduction improves forward flow → ACE-I or ARBs ○ Surgical valve replacement for acute severe AR, symptomatic pts and those with significant left ventricular dysfunction HTN, hyperlipidemia, orthostatic Orthostatic hypotension hypotension An excessive fall in BP when an upright position is assumed Definition → drop of > 20 mmHg systolic, > 10 mmHg diastolic, or both within two to five minutes of quiet standing (after 5 min period of supine rest) Causes → dehydration, medications (diuretics, antihypertensives), autonomic dysfunction and aging S/S: ○ Dizziness, lightheadedness, blurred vision, fainting upon standing Tx: ○ Address underlying cause – discontinuing ot adjusting medications, increasing fluid and salt intake, and using compression stockings ○ Medications like fludrocortisone or midodrine may be used for patients with persistent symptoms despite lifestyle meds ○ Pt education on slow position changes and avoiding prolonged standing ot sudden movements Essential hypertension Primary htn is defined as a resting systolic BP > 130 or diastolic BP > 80 on at least two readings on at least two separate visits with no identifiable cause  MCC → idiopathic ACC/AHA classification of BP: ○ Normal → < 120/80 mmHg ○ Elevated → 120-129 mmHg and < 80 mmHg ○ Stage 1 → 130-139 mmHg or 80-89 mmHg ○ Stage 2 → >140 mmHg or > 90 mmHg ○ Hypertensive criteria → systolic over 180 and/or diastolic over 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage Complications: ○ Cardiovascular → CAD, heart failure, MI, LVH, aortic dissection, aortic aneurysm, peripheral vascular disease ○ Neurologic → TIA, stroke, ruptured aneurysm=s, encephalopathy ○ Nephropathy → renal stenosis and sclerosis, htn is the second MCC of end stage renal disease in the US (behind DM) ○ Optic → retinal hemorrhage, blindness, retinopathy Workup → 12 lead ECG (LVH), fundoscopy (retinopathy), creatinine, cholesterol, urine albumin to creatinine ratio Tx: ○ Newly diagnosed htn → lifestyle modification ( wt loss, 30 min exercise a day, DASH diet (increased fruits and veg, lower sat fat and salt), decrease alcohol intake ○ Blood pressure target is 180 or diastolic > 120) WITHOUT target organ damage Tx: ○ Acute complications are unlikely, so immediate BP reduction is NOT required; pts should be started on a 2-drug oral combination and close evaluation (with an evaluation of treatment efficacy) should be continued on an outpatient basis ○ Clonidine (alpha 2 agonist) or captopril (ACEI) Hypertensive emergency Severe hypertension (SBP >180 and/or DBP > 120) WITH signs of damage to target organs → retinal hemorrhages, papilledema, encephalopathy, acute and subacute kidney injury, intracranial hemorrhage, aortic dissection, pulmonary edema, unstable angina or MI Tx: ○ BP must be reduced within 1 hr by approximately 10 to 20 percent to prevent the progression of end organ damage or death and a further 5 to 15% over the next 23 hours ○ This often results in a target blood pressure of 1 mm in > 2 contiguous leads on ECG and evidence of myocardial necrosis (cardiac markers in blood; troponin I or troponin T and elevated CK) ECG: ○ ST elevation → acute ischemia ○ T wave depression → myocardial injury ○ Q wave → infarct S/S: ○ Pain in substernal region of the chest that radiates to the left arm, SOB, and diaphoresis Patho → plaque rupture with the adhesion of platelets and platelet aggregation Location: ○ Lateral (I, aVL, V5, V6): left circumflex Anterior: I, aVL, V2-V6 (LAnteriorD) ○ Anterior (V2-V4): left anterior descending Inferior: II, III, aVF (RCA) ○ Septal (V1, V2): left anterior descending Lateral: I, aVL, V5-V6 (Circumflex) Posterior: ST DEPRESSION V1-V3  ○ Anterolateral (V4, V5, V6): left main ○ Posterior (V1, V2, ST depression): right coronary artery ○ Inferior (II, III, aVF): right coronary artery Serial cardiac enzymes: ○ Troponins → most specific test, appears 4-8 hours, peaks at 12-24 hours, and lasts for 7-10 days ○ Myoglobin → elevates in 1-4 hours ○ CK-MB → appears at 4-6 hours, peaks at 12-24 hours, and lasts for 3-4 days Tx: MONA-B ○ Beta blockers ○ NTG – nitrates CI in inferior wall MI/right sided MI are fluid dependent – if we decrease venous return (vasodilation) we are making the condition worse ○ Aspirin ○ Heparin ○ ACEI ○ Reperfusion: PCI gold standard within 90 minutes of onset Thrombolytic therapy done if no access to cath lab or surgery is CI → SPA, streptokinase CI for fibrinolytic use in STEMI: ○ Prior intracranial hemorrhage ○ Known structural cerebral vascular lesion ○ Known malignant intracranial neoplasm ○ Ischemic stroke within 3 months ○ Suspected aortic dissection ○ Active bleeding or bleeding diathesis Upon discharge: ○ ACEI decrease LVH and remodeling to allow for a greater ejection fraction Angina Stable Angina (Angina Pectoris) Unstable Angina Chest discomfort due to myocardial ischemia as a result of a fixed Characterized by ischemic symptoms suggestive of ACS, negative biomarkers epicardial coronary artery obstruction (troponin and CK-MB), and with or without ECG changes indicative of ischemia (ST A complication of coronary artery disease usually due to depression or new T wave inversion) atherosclerosis Patho → plaque rupture → MCC is plaque rupture of a previous nonsevere lesion RF → Diabetes mellitus, smoking, hyperlipidemia, htn, male, >45y/o , with subsequent thrombus formation that leads to coronary artery stenosis that is family hx not fully occlusive (no myocardial cell death) S/S: S/S: ○ Chest pain or discomfort → substernal, poorly localized, ○ Angina at rest, lasting longer than 20-30 minutes exertional, short in duration (4mm) Tx: ○ Uncomplicated → metronidazole and cipro OR levofloxacin for 7 days + CLD outpatient ○ Abscess: 3-4 cm: CT guided percutaneous drainage ○ Surgery: if refractory to medication, perforation, recurrence, strictures Criteria for admission: ○ Complicated diverticulitis ○ Uncomplicated with fever, sepsis, immunosuppression, increased age or unable to tolerate oral intake Colon Cancer Most colon and rectal cancers are adenocarcinomas that arise from adenomatous polyps Epidemiology → CRC ia the 3rd MC non skin cancer in the US after lung cancer in both men and women, 8% of cancer related death in the US RF → age, personal or family hx, hereditary forms of CRC, IBD, abdominal radiation, AA, diet and lifestyle, smoking ○ Familial adenomatous polyps – genetic mutation of APC gene, up to several thousand polys, almost all develop CRC by 45 ○ Gardner syndrome ○ Turcot syndrome ○ Lynch syndrome (hereditary nonpolyposis CRC – autosomal dominant, loss of function in DNA mismatch repair genes ○ Peutz-Jehgers syndrome – autosomal dominant, hamartomatous polyps, mucocutaneous hyperpigmentation (lips, oral mucosa, hands) and risk of breast and pancreatic cancer Protective factors → physical activity, aspirin, NSAID  S/S: ○ Painless rectal bleeding and change in bowel habits in a patient 45-80 y/o ○ Unexplained iron deficiency anemia and/or abdominal pain ○ Large bowel obstruction → CRC is the MCC of LBO in adults ○ Right sided → chronic occult bleeding (iron deficiency anemia, positive guaiac), diarrhea ○ Left sided → bowel obstruction, changes in stool diameter, change in bowel habits Dx: ○ Colonoscopy with biopsy is the diagnostic test of choice ○ Barium enema shows apple core lesion ○ Carcinoembryonic antigen: CEA is the MC monitored tumor marker Polyps: ○ More likely to be malignant: sessile, >1cm, villous ○ Less likely to be malignant: pedunculated, 40, caucasian, male sex. Schistosomiasis Occupational exposure to dyes, leather and rubber (beautician and auto workers) Medications: Cyclophosphamide, Pioglitazone Long-term indwelling catheter use and infected bladder stones (squamous cell carcinoma) Clinical Manifestations: Hematuria: most common presentation ○ Intermittent, gross, painless and present throughout micturition (may be microscopic) Irritative voiding symptoms: dysuria (second most common symptom), urgency and frequency Diagnosis: Urinalysis with microscopy and cultures: rule out benign causes ○ Unexplained hematuria may represent urothelial cancer in individuals over the age 35 until proven otherwise Workup for Bladder cancer: ○ Initial evaluation with cystoscopy, renal function testing and upper urinary tract imaging (CT urography preferred) Cystoscopy with biopsy criterion standard for diagnosis and staging of bladder cancer and management of bladder cancer Imaging of GU tract: this is part of the initial evaluation for bladder cancer, as imaging of the upper urinary tract will determine the location and extent of tumor as well as detect sites of multifocal disease ○ CT urography with contrast is preferred to assess local extent of thee disease Urine cytology: cytology is commonly used as an adjunct to cystoscopy to detect carcinoma in situ (CIS) and upper-tract malignancies Management:  Localized or superficial: transurethral resection of bladder tumor (electrocautery) is the mainstay of therapy + follow up every 3 months for non-muscle invasive disease Muscle-invasive: radical cystectomy with urinary diversion is the first-line for muscle invasive bladder cancer ○ Neoadjunctive cisplatin-based chemotherapy followed by radical cystectomy improves survival and is the standard of care Metastatic disease: platinum-based chemotherapy: MVAC (methotrexate, vinblastine, doxorubicin and cisplatin), dose =-dense MVAC or gemcitabine plus cisplatin ○ If not eligible for chemotherapy immunotherapy is an option Recurrent: Intravesical BCG vaccine (Bacillus Calmette-Guerin) if electrocautery is unsuccessful but do NOT use BCG if immunosuppressed or gross hematuria is present (can cause sepsis) DM treatment and complications Diabetes Mellitus Type 1 Diabetes Mellitus: Insulin deficiency due to pancreatic beta cell destruction (pancreas is no longer making insulin) These patients require exogenous insulin Onset is typically before age 30 and is NOT associated with obesity Etios: Type 1A: autoimmune in origin Type 1B: non-autoimmune beta cell destruction Clinical Manifestation: Hyperglycemia without acidosis: polyuria, polydipsia, polyphagia Weight loss. Lethargy Diabetic Ketoacidosis: hyperglycemic hyperosmolar syndrome Associated with somogyi phenomenon and dawn phenomenon Treatment: Dietary control +insulin (all type 1 will need insulin) ○ A1C goal < 7 - check every 3 months ○ Basal insulin (such as Glargine) with once or twice daily long-acting or intermediate-acting insulin or continuous subcutaneous insulin via a pump ○ Pre Meal bolus of short (regular) or rapid-acting insulin (such as Humalog) – dose based on FSBs before a meal, size, and composition of the meal, and anticipated activity levels ○ Glucose monitoring 4-7 times daily – before meals, mid-morning, mid-afternoon, before bedtime, and occasionally at 3 am Daily aspirin prevention; men over 50 and women over 60 with one CVD risk factor Blood pressure management with ACE inhibitors or ARBs ○ Thiazide-like diuretic like chlorthalidone ○ Dihydropyridine CCB (amlodipine) Cholesterol management with statins for ages 40-75 ○ Type 2 DIabetes Mellitus: Combination of insulin insensitivity (resistance) and relative impairment of insulin secretion ○ Patients are producing insulin but have resistance Anti-Hyperglycemic Agents Mechanism Of Action Side Effects/Caution Biguanides: Metformin Decreases hepatic glucose production and Can cause lactic acidosis increases peripheral glucose uptake needs to be stopped 24 hours before contrast decreases intestinal glucose absorption and and resumed 48 hours after with monitoring increases insulin sensitivity (these are reasons for creatinine, stop if creatinine is > 1.5 it leads to weight loss) Not given in patients with renal impairment First line PO medication used to control type w/ Cr>1.5 or hepatic patients 2 and decrease triglycerides GI complaints are common Macrocytic anemia (low B12) Metallic taste Sulfonylureas: Stimulates pancreatic beta-cell insulin release Causes hypoglycemia First gen: Tolbutamide, Chlorpropamide (insulin secretagogue- non glucose weight gain Second gen: Glyburide (Glynase), Glipizide (Glucotrol, dependent) GI upset if taken c food, dermatitis Glucotrol XL), Glimepiride (Amaryl): 2nd generation: less S/E (so are preferred), Disulfiram reaction, sulfa allergy shorter half lives Cardiac dysrhythmias CP450 inducer (drug-drug interactions) Meglitinides: Stimulates pancreatic beta-cell insulin release Hypoglycemia (less than sulfonylureas) Repaglinide (Prandin) and Nateglinide (Starlix (insulin secretagogue) Weight gain α-Glucosidase inhibitors: Acarbose (Precose) and Glyset Delays intestinal glucose absorption (inhibits May cause increased LFTs and hepatitis, (Miglitol) pancreatic alpha amylase and intestinal diarrhea, flatulence a-glucosidase hydrolase Caution in patients with gastroparesis, Does NOT affect insulin secretion inflammatory bowel disease, on bile acid resins Thiazolidinediones: Pioglitazone (Actos) and increases insulin sensitivity in peripheral Can cause fluid retention and edema (CHF), Rosiglitazone (Avandia) receptor site adipose and muscle has no effect hepatotoxicity bladder cancer fractures on pancreatic beta cells Cardiovascular toxicity with Avandia or Rosiglitazone GLP(glucagon-like peptide)-1 Agonists: Lowers blood sugar by mimicking incretin - Hypoglycemia Exenatide (Trulicity, Byetta) causes increase in insulin secretion and Pancreatitis decreased glucagon secretion and delays Caution for gastroparesis pt gastric emptying No weight gain DDP-4 Inhibitors: Dipeptidyl peptidase inhibition - inhibits pancreatitis  Sitagliptin (Januvia) degradation of GLP-1 so more circulating renal failure GLP-1 GI symptoms SGLT2 Inhibitor: SGLT2 inhibition lowers renal glucose hypoglycemia Aka Sodium- Glucose Transport threshold, which results in increased urinary urinary tract infections Canagliflozin (Invokana or Sulisent) glucose excretion Thirst Dapagliflozin Nasua Abdominal pain Diabetic neuropathy Diabetic Neuropathy- A complication of Diabetes Mellitus Symmetric Polyneuropathy ○ Most common type of diabetic neuropathy ○ Progressive distal sensory loss in a “stocking-glove” pattern, involving the distal lower extremities at first then progressing to the hands Loss of vibratory, proprioception, light touch and temperature Can lead to foot ulcer formation ○ Decreased ankle reflexes, gait abnormalities and motor dysfunction can occur Autonomic: ○ Orthostatic (postural) hypotension ○ Gastroparesis (occurs after many years) ○ Enteropathy (constipation or diarrhea) Cranial Mononeuropathy: ○ Most common to affect extraocular muscles CN 3 (oculomotor): diplopia and ptosis with sparing of the pupils CN 6 abducens CN 4 trochlear CN 7 (facial) palsies Peripheral Mononeuropathy: ○ Median neuropathy most common: Carpal tunnel syndrome, ulnar neuropathy Management: Optimal glucose control First-line pharmacotherapy options for painful diabetic neuropathy includes ○ 1. Serotonin-norepinephrine reuptake inhibitors (Duloxetine> Venlafaxine) ○ 2. Tricyclic antidepressants (Amitriptyline, Desipramine, Nortriptyline) ○ 3. Gabapentinoid antiseizure medications (Pregabalin Gabapentin Second lineL topical agents (Capsaicin cream and Lidocaine patches), alpha-lipoic acid or neuromodulation (transcutaneous electrical nerve stimulation) Screening: After initial screening all diabetics should be screened annually by examining sensory function in the feet and assessing ankle reflexes Neuro/Psych MMSE Drugs associated with changes in mental status Dementia Dementia screening tests Delirium Internal & external causes / medications that precipitate delirium Depression Alzheimer's disease Parkinson's disease TIA/CVA Herpes zoster ophthalmicus Bell’s palsy MMSE Mini-Mental Status Exam (MMSE) ( source: bates textbook) Bedside screening test for cognitive dysfunction or dementia ○ MMSE has the best sensitivity and specificity over 86% for dementia Provides quantitative measure of cognitive impairment Consist of 5 components: ○ Appearance and behavior ○ Speech and language ○ Mood ○ Thoughts and perceptions ○ Cognitive function, including memory, attention, information and vocabulary, calculations, abstract thinking and constructional ability Scoring: can earn a total of 30 points ○ A score of less than 25= suggestive of impairment ○ A score of less than 20- definite impairment Example exam questions: ○ Orientation to time: Ask “what is the date?” ○ Registration: “listen carefully. I am going to say three words. You say them back after I stop…” ○ Naming: “What is this?” (point to common items like a pen) ○ Reading: “Please read this and do what it says” The following is from McCulloch neuro lecture: Mini-Mental Status exam is the first step of the neurological examination  Drugs associated with changes in The DSM-5 substance-related and addictive disorders encompass 10 separate classes of drugs with subcategories including intoxication and withdrawal. mental status Alcohol S/S: ○ Withdrawal: increased CNS activity tremors, anxiety, irritable, palpitations, diaphoresis, alcohol hallucinations, seizures or withdrawal delirium (delirium tremens) Caffeine Symptoms include restlessness, nervousness, excitement, insomnia, flushed face, diuresis, and gastrointestinal complaints, which can occur with low doses (e.g., 200mg) in vulnerable individuals such as children, the elderly, or individuals who have not been exposed to caffeine previously. Cannabis s/s ○ Intoxication: euphoria, giddiness, anxiety, intense sensory experiences, fear, depression or psychosis ○ Withdrawal: irritability, insomnia, depression, restlessness, diaphoresis, diarrhea and twitching Hallucinogens (with separate categories for phencyclidine [or similarly acting arylcyclohexylamines] and other hallucinogens) Phencyclidine (PCP) ○ Is a dissociative anesthetic and hallucinogenic drug that is a NMDA glutamate receptor antagonist (aka angel dust) ○ s/s of intoxication: agitation, rage, bizarre and violent behavior, hallucinations, delusions of physical prowess, diminished perception of pain LSD ○ Intoxication: visual hallucinations and synesthesias (e.g., seeing sound as color), marked anxiety or depression, delusions, pupillary dilation ○ Withdrawal: largely no withdrawal because it does not affect dopamine, flashbacks can occur years later Inhalants Intoxication: depends on the dose of inhalant sniffed. ○ For mild to moderate doses: the following are noted: euphoria, slurring of speech, confused state, and auditory and visual hallucinations. ○ For high doses: cardiopulmonary failure, liver problems, kidney problems, and bone marrow suppression.  ○ Withdrawal: not well characterized, no treatment Opioids S/S: ○ Intoxication: Euphoria and sedation; pupillary constriction, comatose state and respiratory depression, CNS depression Sedatives, Hypnotics, and anxiolytics Benzodiazepines ○ Patient with CNS depression and a history of anxiety or panic disorder ○ On the physical exam, she is hypotensive with a respiratory rate of 4/min. ○ Anxiolytics are medications such as benzodiazepines used for the treatment of anxiety disorders. They have additive effects with alcohol and tend to have a cumulative effect if doses are repeated indiscriminately. ○ Intoxication: respiratory depression, hypotension, amnesia, ataxia, stupor/somnolence, coma, death ○ Withdrawal: rebound anxiety, seizures (life-threatening) and tremor-most commonly found in short-acting benzos such as alprazolam Barbiturates ○ Patient will present as a 35-year-old female who arrives at the ED with impaired memory, poor concentration, and extreme drowsiness. Pupils are not dilated on the exam and the patient is minimally responsive. Of greatest concern is the patient’s respiratory rate of 5/min. ○ Intoxication: respiratory/CNS depression - can be fatal. Does not have a depression "ceiling" in contrast to benzodiazepines. ○ Withdrawal: anxiety, seizures, delirium, similar to alcohol, life-threatening cardiovascular collapse. Stimulants (amphetamine-type substances, cocaine, and other stimulants) cocaine S/S ○ Intoxication: CNS stimulations (elevated euphoric mood, psychomotor agitation, paranoia, pressured speech, ams) can progress to respiratory depression or cardiovascular arrhythmia ○ Withdrawal: irritability, post-intox depression, hypersomnia, disorientation, constricted pupils, suicide ideation Tobacco Smoking is the most important modifiable risk factor in the US for preventable pulmonary, cardiac and cancer deaths and the leading cause of preventable death S/S: ○ Toxicity: CNS stimulation, restlessness, anxiety, insomnia and increase in gastrointestinal motility ○ Withdrawal: anxiety, mental discomfort Dementia and dementia screening Dementia aka Major/mild neurocognitive disorders tests Neurocognitive disorders (NCDs) are described as those with significant (major) or moderate (mild) impairment of cognition or memory that represents a marked q Dementia aka Major/mild deterioration from a previous level of function neurocognitive disorders know Etios: 6 causes of reversible neurocognitive disorder: specific ○ NCD secondary to an infection of the CNS (neurosyphilis) types ○ NCD secondary to metabolic and nutritional causes (vitamin B12 deficiency) ○ NCD secondary to inflammatory causes (vasculitis involving cerebral blood vessels) ○ NCD caused by a structural defect impinging on the brain (a subdural hematoma or tumor) ○ Normal pressure hydrocephalus (NPH) ○ Endocrine-related NCD (hypothyroidism) Types of major and mild Neurocognitive Disorders: Alzheimer's Disease: is a lack of acetylcholine and the most common type of dementia American Academy of Neurology (AAN) recommends screening for: depression, vitamin B12 deficiency, hypothyroidism, and medication side effects. Screening for syphilis is not recommended unless the patient has known risk factors. Structural neuroimaging with noncontrast CT or MRI should also be considered, but such testing is not required for diagnosis. Several screening tools are available to help diagnose dementia. The Mini-Mental State Examination had been the gold standard, but trademark restrictions now limit its use. The Montreal Cognitive Assessment (MoCA) includes a measure of executive function, but it also has been recently trademarked.  ○ Risk factors: disease of older age like 65+, genetics, family hx ○ S/S: short-term memory loss that progresses to long term memory loss and cognitive deficits ○ Physical Exam: Abnormal clock drawing test ○ Definitive diagnosis on autopsy Loss of brain cells, beta-amyloid plaques and neurofibrillary tangles ○ Treatment: Anticholinesterase drugs (Tacrine, Donepezil) Vascular Disease: associated with arteriosclerotic small vessel disease ○ This is any dementia that is primarily caused by cerebrovascular disease or impaired cerebral blood flow or in which cerebrovascular disease or impaired cerebral blood flow is a contributing causative factor ○ Risk factor: #1 is Hypertension ○ S/S: sudden decline in functions with stepwise progression of symptoms ○ Treatment/prevention: control blood pressure Substance/Medication induced: Related to medication or non-prescription drug use Lewy body disease: progressive dementia characterized by the diffuse presence of Lewy bodies (abnormal neuronal protein deposits) in comparison to parkinson disease, where the Lewy bodies are localized ○ s/s: Parkinsonian symptoms (bradykinesia, rest tremor, rigidity and gait disorder), REM sleep behavior disorder Gradual, progressive decline in cognitive abilities Hallucinations and delusions, gait difficulties, and falls Frontotemporal Dementia (Pick’s DIsease): localized brain degeneration of the frontotemporal lobes ○ Histology shows pick bodies (round or oval aggregates of Tau protein) seen on silver-staining of the cortex ○ s/s: Personality changes precede memory changes, Language difficulties, personality changes, and behavioral disturbances Diagnosis: of dementias: History + examinations + Mini-mental Status Exam or Montreal COgnitive Assessment ○ If these findings are not conclusive then begin neuropsychological testing Screen for B12 deficiency, hypothyroidism, routine CBC and liver function test Neuroimaging with noncontrast magnetic resonance imaging MRI or CT in initial evaluation of all patients with dementia Screening Test: Mini-Mental Status Exam (MMSE) ( source: bates textbook) Bedside screening test for cognitive dysfunction or dementia ○ MMSE has the best sensitivity and specificity over 86% for dementia Provides quantitative measure of cognitive impairment Consist of 5 components: ○ Appearance and behavior ○ Speech and language ○ Mood ○ Thoughts and perceptions ○ Cognitive function, including memory, attention, information and vocabulary, calculations, abstract thinking and constructional ability Scoring: can earn a total of 30 points ○ A score of less than 25= suggestive of impairment ○ A score of less than 20- definite impairment The following is from McCulloch neuro lecture: Mini-Mental Status exam is the first step of the neurological examination:  Delirium → internal and external Delirium causes/medications that Acute, abrupt transient confused state due to an identifiable cause precipitate delirium Has a rapid onset, is short term and reversible Etios: medical condition, substance, intoxication or withdrawal, or medication side effect causing temporary altered mental status How to differentiate depression ○ Common in hospitalized elderly patients, is often caused by drugs, dehydration, and infections (eg, UTI) but can have many other causes and delirium ? Patients with ○ Examples: Sepsis, sundowning, ETOH withdrawal, opiate withdrawal, sunstroke delirium may present as agitated, Risk factors: advanced age, severe illness, polypharmacy, uaw of psychoactive medications, sensory impairment, depression and alcohol use disorder psychotic, somnolent, or ○ Medications that are likely to increase the risk of delirium include withdrawn (these are the tough sedative/hypnotics ones to recognize). Dementia is Anticholinergics more chronic in nature with an Opioids insidious onset. Dementia Benzodiazepine progresses over time and usually H1 and H2 antihistamines cannot be reversed. Often delirium Clinical Manifestations: is treatable or reversible if the ○ Primary deficit in attention rather than memory underlying medical condition is ○ Confusion Assessment Method: Requires acute onset and fluctuating course, inattention or disorganized thinking or altered level of consciousness identified and treated. Patients ○ Clinician must review patients medications because polypharmacy is a major cause with dementia usually have intact Diagnosis: attention, whereas patients with ○ Considered in elderly patients who present with impaired memory or attention delirium have markedly impaired Can be recognized through History taken from family members, caregivers, and friends and mental status examination attention. Patients with dementia ○ Lab test: CBC (to rule out underlying infection in the elderly), BUN, UA, ECG, CT or MRI have “poverty of thought,” which Diagnosis criteria: implies decreased content of their ○ Disturbed level of consciousness, such as a decreased attention span or lack of environmental awareness thoughts. Patients with delirium ○ Cognitive change, such as a memory deficit, disorientation, or language disturbance, possibly also including visual illusions or hallucination may have a rich content in their ○ Rapid onset within hours or days with a fluctuating course thoughts, but the thoughts are ○ Evidence of a causal physical condition disordered. Patients with Treatment: dementia are at higher risk for ○ Tx the cause and supportive care developing delirium, but dementia ○ Sedation when necessary is not a pre-requisite for delirium ○ Patients with delirium of unknown causes should be admitted for an expedited workup Depression Depression: Primarily serotonin neurotransmitter others include norepinephrine (NE) and dopamine (DA) females>males Depression is seen in the elderly man age group upon retiring ○ S/S: will persist for longer than 2 months Diminished interest or pleasure in hobbies/activities Significant weight loss or gain Insomnia or hypersomnia Psychomotor agitation or retardation Fatigue or loss of energy Feelings of worthlessness Diminished ability to think or concentrate; indecisiveness Recurrent thoughts of death, suicidal ideation, suicide attempt or specific plan for suicide Diagnostic test: ○ Need to rule out thyroid involvement TSH (hypothyroidism) ○ Need to rule out Addison’s, Cushing’s Treatment: ○ Psychotherapy ○ 1st line medication: SSRI including FLuoxetine (Prozac), paroxetine (paxil), sertraline (Zoloft), flucoxamine (Luvox), citalopram (Celexa), and escitalopram (Lexapro) If no effect after 4 weeks switch to another SSRI ○ Second line: SNRI like Duloxetine, Venlafaxine or Bupropion ○ Tricyclic antidepressants, Tetracyclics, MAO inhibitors ○ Electroconvulsive therapy ○ See the patient within 2–4 weeks of starting medication and every 2 weeks until improvement, then monthly to monitor medication changes Depressive Disorder Types Summary: Major depressive disorder: a mood disorder in which a person experiences (in the absence of drugs or medical condition) two or more weeks of significantly depressed moods, feelings of worthlessness and diminished interest or pleasure in most activities Persistent Depressive disorder (dysthymia): mood disorder involving persistently depressed mood, with low self-esteem, withdrawal, pessimism or despair, present for at least 2 years with no absence of symptoms for more than 2 months Premenstrual dysphoric disorder: a disorder marked by repeated episodes of significant depression and related symptoms during the week before menstruation Suicidal/homicidal behaviors: mood disturbances, somatic complaints, feeling hopelessness, worthlessness, helplessness Other forms include: ○ Psychotic major depression: characterized by paranoia & delusions. It is more commonly seen in pts over 50 years old. Pts typically have high suspicions or hallucinations ○ Major depression with atypical features: characterized by fatigue, hypersomnia, excessive eating & reactive mood ○ Melancholic major depression : lack of interest and vegetative symptoms are severe ○ Major depression with seasonal onset: A form of major depression that occurs seasonally mostly in the fall and winter months. It is characterized by lethargy, excessive carb craving, hypersomnia and excessive eating. ○ Postpartum depression Alzheimers Alzheimer Dementia is a lack of acetylcholine and the most common type of dementia ○ Usually a disease of older age 65+, associated with poor memory and difficulty learning ○ Is a neurodegenerative disease Risk factors: increasing age, genetics, family history Patho: Unknown but there are 3 hypothesis: ○ 1. Amyloid-hypothesis: extracellular amyloid-beta protein deposition (senile plaques in the brain are neurotoxic ○ 2. Tau hypothesis: neurofibrillary tangles (intracellular aggregations of tau protein an insoluble cytoskeleton microtubule element) are neurotoxic ○ 3. Cholinergic hypothesis: acetylcholine deficiency leads to memory, language and visuospatial changes Clinical Manifestations: ○ Short-term memory loss. Progresses to long-term memory loss and cognitive defects (disorientation, behavioral and personality changes, language difficulties, loss of motor skills) Diagnosis: ○ Dx of rule out Work up of MRI of brain, CBC, renal and liver tests, VDRL or RPR to rule out syphilis, B12, and thyroid function studies MRI is the preferred neuroimaging test: expect to see cortex atrophy Management: ○ Acetylcholinesterase inhibitors: Donepezil, Rivastigmine, Galantamine Used to improve memory function and symptom relief but does NOT slow down alzheimer progression ○ NMDA Antagonist: Memantine- can be adjective or used as monotherapy Used when Mini-Mental Status Exam (MMSE)≤18 * Parkinsons Parkinsons Neurodegenerative movement disorder due to decreased dopamine resulting from idiopathic loss of dopaminergic neurons in the striatum and substantia nigra and the presence of Lewy bodies ○ Low dopamine and high ACh Onset of symptoms are most common among the 45-65 age groups Patho: decreased dopamine leads to imbalance of dopamine and acetylcholine, resulting in improper movement due to failure of acetylcholine inhibition in the basal ganglia (acetylcholine is an excitatory CNS neurotransmitter, dopamine is inhibitory) Pathologic hallmark of PD seen on post-mortem histology of eosinophilic cytoplasmic inclusions (lewy bodies) amd loss of pigment cells seen in the substantia nigra Clinical Manifestations: Think TRAP: tremor, rigidity, akinesia, postural instability Dementia is found in 50% as a late finding and many develop depression Motor triad (cardinal motor symptoms): Resting tremor, bradykinesia and muscle rigidity Resting tremor: often the first symptom ○ Pill rolling: resting tremor of the hand ○ Tremor is worse at rest, emotional stress excitement and walking ○ Tremor improves with voluntary activity, intentional movement and sleep Typically the tremor disappears with action of the involved limb and reemerges with maintained posture ○ Confined to one limb or side for years before it becomes generalized Bradykinesia: slowness of voluntary movement and decreased automatic movements  ○ Lack of swinging of the arms while walking and shuffling gait Rigidity: sustained increased resistance to passive movement; cogwheel rigidity (ratchety pattern of resistance and relaxation as the examiner moves the limb through its full range of motion) ○ Festination= increasing speed while walking ○ Freezing: inability to initiate stepping Postural Instability: stems from the rigidity; including a flexed (stooped) posture and loss of postural reflexes ○ Is a sign of advanced disease Nonmotor symptoms: include the loss of smell (anosmia), mood disorders, constipation, excess salivation or drooling (sialorrhea) and sleep dysfunction Physical Exam: Normal deep tendon reflex, NO MUSCLE WEAKNESS Face involvement: relatively immobile face (fixed facial expressions), widened palpebral fissure ○ Myerdon’s sign: tapping the bridge of the nose repetitively causes a sustained blink Decreased blinking and seborrhea of the skin is common Postural Instability: a late finding ○ Pull test: stand behind the patient and pilling the shoulders causes the patient to fall or take steps backwards Management: Discontinue drugs that may induce parkinsonian symptoms ○ Haldol and Risperidone (Psychotropic medications) and Metoclopramide (antiemetic) No cure. The goal of medical treatment is to delay disease progression and relieve symptoms by increasing dopamine signaling (done so with an increase of levodopa which crosses the BBB) ○ Levodopa-Carbidopa: most effective treatment Levodopa: converted to dopamine once it crosses the BBB Carbidopa: reduced amount of levodopa needed by reducing peripheral conversion of levodopa into dopamine, reducing adverse effects of levodopa ○ Dopamine agonist (Bromocriptine, Pramipexole, Ropinirole) May be used as initial treatment Stimulate dopamine receptor, increasing dopamine levels Less motor adverse effects but NOT as effective as levodopa Can be used as first line agents in younger patients under 65 to delay the use of levodopa ○ Anticholinergics (Trihexyphenidyl, Benztropine) Blocks excitatory effects of acetylcholine Monotherapy in younger pts under 70 with tremors ○ Amantadine: increases dopamine. MAO-B inhibitors (Selegiline, Rasagiline) ○ COMT inhibitors (Entacapone, Tolcapone): given with levodo[a to prevent dopamine breakdown outside of CNS so more enters the BBB ○ Deep pain stimulation: is extremely effective for rigidity and tremors in select patients ○ Physical therapy can be beneficial TIA/CVA 1. TIA/CVA TIA: Transient Ischemic Attack Is an immediate obstruction to the vessel that resolves in 24 hours Transient acute episode of ischemia neurologic deficits caused by focal brain, spinal cord or retinal ischemia without acute infarction , lasting less than 24 hours (usually under 1-2 hours) TIA patients are increased stroke risk Risk Factors: Hypertension Cardiovascular Types: 1. Embomic: Atrial fibrillation, left ventricular thrombus, heart failure, endocarditis, atrial septal defects ○ Atrial fibrillation occurs when there are multiple irritable atrial foci fire at fast rates, three is an increased risk of atrial thrombus formation that can lead to cerebral or systemic embolization 2. Large artery (low flow): ischemia due to atherosclerosis and atherothrombosis 3. Lacunar: penetrating small vessels Clinical Manifestations: Neurologic deficits last less than 24 hours (this depends on which artery is involved) ○ Duration is typically few minutes with complete resolution within one hour Amaurosis fugax: transient monocular vision loss ○ Described as “temporary shade down one eye” or as seeinging darker ○ Is an occlusion or stenosis of the internal carotid artery or retinal artery or ophthalmic artery circulation and will lead to hypoperfusion of ocular that last for seconds to 30 minutes Physical Examination: carotid bruits may be heard ○ While auscultating the carotid it is possible to hear turbulent flow due to atherosclerotic plaques causing stenosis Diagnosis: Requires results from neuroimaging, neurovascular imaging and tests to rule out cardioembolic sources ○ Neuroimaging: CT scan is performed initially to rule out hemorrhage but MRI is more sensitive ○ Neurovascular imaging: CT or MRA (MR angiography), carotid doppler US, transcranial doppler US MRA is the definitive test for identifying stenosis and emboli and preferred test to evaluate the vessels in the neck Carotid Doppler US: helps find source Transcrainial doppler US: Rules out obstructive lesion in large artery supplying affected regions ○ Conventional Angiography: definitive diagnosis (invasive) ○ Ancillary testing: rule out cardioembolic source (with ECG, telemetry or echocardiogram) Rule out metabolic ot hematologic cause of neurologic symptoms cbc HIV and syphilis Management: Patients should be placed in the supine position to increase perfusion, avoid lowering blood pressure unless blood pressure is greater than 220/120 mmHg. ○ Intense risk factor management ○ Side note: Thrombolytics are contraindicated in TIA treatment Noncardiogenic: antiplatelet therapy + risk score assessment  ○ Dual antiplatelet therapy: Aspirin and Clopidogrel, followed by Aspirin only substantially reduces risk of future TIA or strokes for high risk (risk score ≥4) and is started while evaluating the ischemic mechanism Another combo: Aspirin + extended-release Dipyridamole ○ Aspirin monotherapy: Aspirin (162-325 mg/day) a;one for low risk TIA (Risk score under 4) ○ Long term: reduce modifiable risk factors (like DM, hyperlipidemia, hypertension control, smoking cessation, weight reduction and regular exercise), statin therapy regardless of LDL levels For long term care we want to work on anything that can attribute to the build up of plaques or impact the heart's blood supply ○ Revascularization: Carotid endarterectomy recommended ig internal carotid artery stenosis 50=99% with a life expectancy of 5+ years + aspirin Endovascular intervention and stenting is only performed if life expectancy is 5+ years Cardiogenic (Nonvalvular Atrial Fibrillation): treat with oral-anticoagulant ○ Oral anticoagulation: Warfarin or a direct oral anticoagulant (Dabigatran, Rivaroxaban, Apoxaban, Edoxaban) ABCD2 SCORE ASSESSMENT IN TIA: The risk of stroke after a TIA is greatly increased and the risk is highest during the immediate days following the TIA. THis assessment will aid in predicting the risk of stroke within the 3-90 days after a TIA. The following factors are one point each: ○ Age greater than 60 ○ Blood Pressure over 140/90 ○ Clinical symptoms (one point for slurred speech OR 2 points for unilateral weakness) ○ Duration (one point if last longer than 10 mins or two points for over 60 mins) ○ Diabetes Reading the ABCD2 score: ○ 0-3 points= 3.1% 90 day stroke risk ○ 4-5 points= 9.8% 90 day stroke risk ○ 6-7 points= 17.8% 90 day stroke risk Quick TIA Highlights: Transient episode of neurologic dysfunction caused by ischemia without acute infarction Amaurosis fugax Antiplatelet treatment (aspirin) CVA Cerebrovascular Accident 5th most common cause of death in US and most common cause of chronic severe disability Major differential from bell’s palsy: PATIENT IS ABLE TO WRINKLE FOREHEAD Risk Factors: #1 hypertension, hypercholesterolemia, diabetes, atrial fibrillation, carotid artery disease and cigarette smoking Nonmodifiable risk factorsL increasing age, family history, male sex General Clinical Manifestations of Strokes: Begin abruptly or upon awakening Correlate with the area of the brain that is supp;oed by the affected vessel  History and Physical exam reveal hemiparesis or hemisensory deficit Symptoms must be present on only one side ○ Symptoms will be contralateral (thee side of the symptoms are opposite to the stroke) ○ Example: right side symptoms= left side stroke Diagnosis: Noncontrast CT scanning is the most common form of neuroimaging Transcranial doppler ultrasound: can evaluate proximal vascular anatomy Echocardiography to rule out suspicion of cardiogenic embolism Types: (specific) There are two basic stroke types 1. Ischemic strokes (80%) and 2.Intracranial hemorrhages (20%) 1. Ischemic Stroke: acute onset of neurologic deficits due to death of brain tissue from ischemia ○ Etios: i. Thrombotic: caused by a blood clot forming in the blood vessels supplying the brain ii. Embolic : caused by a blood clot or plaque debris that develops elsewhere in the body and then travels to one of the blood vessels in the brain through the bloodstream Occur abruptly and without warning ○ Diagnosis: i. Initial test: finger stick BGL, O2 saturation and noncontrast CT CT head without contrast is the best initial test to rule out hemorrhagic stroke a. CT may be normal in the first 6-24 hours b. MRI is more accurate to dx stroke ii. Neurovascular imaging: CT or MRA, Carotid doppler ultrasound, transcranial US iii. Ancillary testing: rule out cardioembolic source with ECG or echocardiogram and cardiac monitoring ○ Treatment: i. Imminent management: within 3 hours of symptoms onset: Alteplase (thrombolytic aka TPA) if no contraindication Mechanical thrombectomy can be performed within 24 hours of symptom onset of large artery occlusion in the anterior circulation (this has less risk than TPA) If over 3-4.5 hours of symptom onset: conservation (Aspirin and long term management) Blood pressure should only be lowered ig blood pressure is 185/119 and thrombolytics are going to be used or if blood pressure is over 220/120 Neurologic exams every 15 minutes during infusions then every hour for the next 6 hours then and until 24 hours after treatment ii. Longterm (outpatient) management: Antip;atelet therapy: Aspirin therapy should not be initiated until 24 hours after thee time of thrombolytic therapy (if patient was already on aspirin prior to stroke switch to Clopidogrel) Initiate Statin therapy 2. Hemorrhagic Stroke: ○ Secondary to hypertension  ○ 2 categories: intra-axial and extra axial i. Extra axial: hemorrhages that occur outside the brain tissue Includes: epidural hematoma, subdural hematoma and subarachnoid hemorrhage ii. Intra-axial: intracerebral hemorrhage: hemorrhages that occur inside the brain tissue Includes intracerebral hemorrhage ○ Etios: weakened vessels that ruptures and bleeds into the surrounding brain, compressing the surrounding brain tissue i. Most common weakened blood vessels are aneurysms and arteriovenous malformations (AVM) ○ Diagnosis: CT confirms bleed ○ Treatment: i. For epidural hematoma and intracranial give IV mannitol if ICP is increased ii. Subarachnoid hemorrhage also may need to regulate the bp with nicardipine, nimodipine or labetalol iii. Hematoma evacuation Herpes zoster ophthalmicus Herpes Zoster Ophthalmicus Potentially sight-threatening disorder that is a variant of reactivation, Varicella zoster (shingles) Pathophysiology: After initial infection varicella zoster virus becomes latent in the dorsal root ganglia or trigeminal ganglia. It can then reactivate and involve the ophthalmic division of the trigeminal (cranial nerve V). Clinical Manifestations: Prodrome: ○ Herpes Zoster Ophthalmicus (HZO) begins with a prodrome of headache, malaise and fever. Unilateral pain or hypesthesia(a loss or decrease in sensation, or numbness, in a part of the body) in the affected eye, forehead and top of the head may precede or follow the prodrome. Vesicular rash: grouped vesicles on an erythematous base of the face Ocular involvement: with the onset of the rash, hyperemic (an excess of blood) conjunctivitis, uveitis, episcleritis and keratitis may occur. Acute keratitis typically involves the epithelial, stromal or endothelial layers of the cornea and may lead to vision loss Physical Exam: Hutchinson sign: Vesicular lesions on the tip of the nose, inner corner of the eye and root and side of the nose indicate involvement of the trigeminal nerve and correlate highly with eye involvement ○ Lesions in this area of the face significant involvement of the nasociliary branch of the trigeminal nerve (CN5) which also innervates the globe Slit lamp examination: dendritic (branching) uptake of fluorescein if keratoconjunctivitis is present Diagnosis: Clinical diagnosis Polymerase chain reaction viral DNA analysis via PCR has the highest yield when testing is needed (it is 95% sensitive) ○ Is performed on fluid from blisters, skin scrapings and non-skin samples, such as BAL fluid or CSF Management: Immediately ophthalmologist referral, analgesics for severe pain, Atropine and antivirals (Acyclovir, Valacyclovir or Famciclovir) The use of glucocorticoids should be made by the ophthalmologist IV Acyclovir in immunocompromised or in cases requiring hospitalization for sight-threatening cases Bell's palsy Bell’s Palsy Idiopathic, unilateral CN VII/ facial nerve palsy leading to hemifacial weakness and paralysis due to inflammation or compression ○ Is a lower motor neuron disorder Etios: Idiopathic Possible cause: reactivation of the Herpes Simplex Virus (HSV) type 1 DNA in the geniculate ganglion may be responsible for most cases Patho: Inflammation or damage to lower motor neurons ○ A peripheral lesion affects the nerve fibers from both hemispheres, casing complete hemifacial paralysis Risk Factors: Diabetes Mellitus, pregnancy (especially in the third trimester), post URI, dental nerve block Clinical Manifestations: Prodrome: Sudden onset of ipsilateral hyperacusis (ear pain) 24-48 hours followed by weakness Unilateral facial weakness or paralysis (forehead included) ○ Patient is unable to lift the affected eyebrow, wrinkle forehead, smile, loss of nasolabial fold, drooping of the corner of the mouth, biting inner cheek, eye irritation (decreased lacrimation and inability to fully close eyelid) ○ Bell Phenomenon: eye on the affected side moves laterally and superiorly when eye closure is attempted ○ Weakness and paralysis only affects the face Sensory dysfunction: taste disturbance involving the anterior ⅔ of the tongue Diagnosis: Diagnosis of exclusion Management: No treatment is required as over 85% of cases resolve within 1 month ○ Supportive care: artificial tears, eye patches to sleep in or massage of weakened muscles Prednisone: start within the first 72 hours of symptom onset ○ Reduces recovery time and increases the likelihood of complete recuperation at 9-12 months In severe cases Acyclovir in combination with glucocorticoids can improve symptoms and recovery times Advanced Care Planning: Hospice care Skilled nursing care Inpatient rehabilitation Palliative care Hospice care (source: current) Hospice In the united states hospice is a type of palliative care service that is available to patients with prognosis of 6 months or less (a criterion for eligibility under the medicare hospice benefit) and addresses the needs of the dying Focuses on their comfort while not attempting either to prolong their life or to hasten their death Emphasizes individualized attention for patients and family members while using an interdisciplinary approach including nurses, social workers, chaplains, physicians and personal care attendants on the team Hospice care is less often provided in medical facilities and more often provided in the patients home as hospice staff will visit to provide support  Patients engage in hospice care often near the very end of life, once they have decided they no longer wish to pursue curative treatments Often appropriate for patients with end-stage dementia Medicare hospice benefit includes coverage for: ○ Medications related to symptom management ○ Social work visits ○ Home health aide services ○ Room and board for a patient living in a nursing home criteria for hospice enrollment by The National Hospice and Palliative Care Organization (NHPCO): three components: ○ (1) demonstrating severity of dementia (e.g., an inability to walk or dress or bathe without assistance, urinary/fecal incontinence, or inability to speak six different intelligible words per day) ○ (2) evidence of a severe comorbid condition within the past 6 months (e.g., aspiration pneumonia, pyelonephritis, sepsis, stage ≥3 decubitus ulcer, or fever despite antibiotics) ○ (3) inability to maintain fluid/caloric intake (by demonstrating weight loss >10% in 6 months or albumin