Family Medicine Rotation Study Guide PDF

Family Medicine Rotation Study Guide – Updated 2023 **Yellow Highlight = High Yield*** Objective 1: Population Health & Social Influences of Health i. Identify the relationships and linkages between population health, public health, and clinical care Population health is the he...

Family Medicine Rotation Study Guide – Updated 2023 **Yellow Highlight = High Yield*** Objective 1: Population Health & Social Influences of Health i. Identify the relationships and linkages between population health, public health, and clinical care Population health is the health outcomes of group of individuals including the distribution of such outcomes within the group o Is focused on a particular community/subcommunity & seeks effective ways to improve health of community & reducing health inequities among different population groups o Societal issues, attitudes, values, beliefs & behaviors are measured to determine outcomes because they directly influence population health Public health is the science of protecting and improving the health of people & their communities o Is focused on population health as a whole, seeking prevention strategies & identifies causes of health-related problems that can affect the larger population, such as immunization programs o Public policy question town put in place a “sin tax” for tobacco/alcohol products to defer use; what type of intervention is this? Clinical care is based on the medical model & focuses on the individual (diagnosis, treatment, intervention, etc.) o Clinical practice works alongside population and public health to provide the best care to patients o For example, public health agencies establish guidelines ii. Recall the leading and underlying causes of death in the US 2022 CDC Data: o Heart disease, cancer, COVID-19, accidents (unintentional injuries), CVA, chronic lower respiratory diseases, Alzheimer’s, diabetes, chronic liver disease/cirrhosis, chronic kidney disease iii. Identify factors that play a role in disease trends Factors affecting disease trends may include ecological changes (deforestation, famine, climate changes), human behavior (war or conflict, sedentary lifestyle, population migration to urban areas, sexual behavior, IVDU), international travel commerce, technology & industry (globalization of food supplies, organ or tissue transplantation, widespread use of antibiotics), microbial adaptation, breakdown in public health measures (vaccine resistance, inadequate sanitation) o These factors may explain re-emergence of syphilis, TB, measles/mumps in the US, COVID-19 pandemic, etc. iv. Recognize the purpose and progress of the Healthy People 2030 framework o The Healthy People initiative is designed to guide national health promotion and disease prevention efforts to improve the health of the nation. Released by the U.S. Department of Health and Human Services (HHS) every decade since 1980, Healthy People identifies science-based objectives with targets to monitor progress and motivate and focus action. Healthy People has established benchmarks in order to: o Identify nationwide health improvement priorities. o Increase public awareness and understanding of the determinants of health, disease, and disability and the opportunities for progress. o Provide measurable objectives and goals that are applicable at the national, State, and local levels. o Engage multiple sectors to take actions to strengthen policies and improve practices that are driven by the best available evidence and knowledge. o Identify critical research, evaluation, and data collection needs The Healthy People 2030 mission is to promote, strengthen, and evaluate the nation’s efforts to improve the health and well-being of all people. Achieving these broad and ambitious goals requires setting, working toward, and achieving a wide variety of much more specific goals. Healthy People 2030’s overarching goals are to: o Attain healthy, thriving lives and well-being free of preventable disease, disability, injury, and premature death o Eliminate health disparities, achieve health equity, and attain health literacy to improve the health and well-being of all o Create social, physical, and economic environments that promote attaining the full potential for health and well-being for all. o Promote healthy development, healthy behaviors, and well-being across all life stages. o Engage leadership, key constituents, and the public across multiple sectors to act and design policies that improve the health and well-being of all. v. Define health disparities Health disparities are inequities in the quality of health, health care and health outcomes experienced by groups based on social, racial, ethnic, economic, and environmental characteristics vi. Recall and list examples of health disparities in the US Many factors contribute to health disparities, including genetics, access to care, poor quality of care, community features (e.g., inadequate access to healthy foods, poverty, limited personal support systems and violence), environmental conditions (e.g., poor air quality), language barriers and health behaviors. These social, economic, and environmental conditions where people live, learn, work and play are known as social determinants of health. Communities of color, populations with a lower socioeconomic status, rural communities, people with cognitive and physical disabilities and individuals who identify as LGBTQ are often disproportionately exposed to conditions and environments that negatively affect health risks and outcomes and lead to higher rates of health disparities, often due to systemic racism & discrimination. For example, Americans living in rural areas are more likely to die from unintentional injuries, heart disease, cancer, stroke, and chronic lower respiratory disease than their urban counterparts.  vii. Define health equity Health equity is the state in which everyone has a fair and just opportunity to attain their highest level of health & is defined by WHO as, “the absence of unfair and avoidable or remediable differences in health among population groups defined socially, economically, demographically or geographically”. Achieving this requires focused and ongoing societal efforts to address historical and contemporary injustices; overcome economic, social, and other obstacles to health and healthcare; and eliminate preventable health disparities. viii. Relate health equity to health disparities in the US Health disparities & social determinants of health are often 2 of the metrics used for assessing health equity o Achieving health equity requires valuing everyone equally with focused and ongoing societal efforts to address avoidable inequalities, historical and contemporary injustices, and the elimination of health and healthcare disparities. o Achieving health equity also requires addressing social determinants of health and health disparities. It involves acknowledging and addressing racism as a threat to public health and the history of unethical practices in public health that lead to inequitable health outcomes. ix. Define and list examples of the determinants of health Social determinants of health (SDOH) are the nonmedical factors that influence health outcomes. They are the conditions in which people are born, grow, work, live, and age, and the wider set of forces and systems shaping the conditions of daily life. These forces and systems include economic policies and systems, development agendas, social norms, social policies, racism, climate change, and political systems o Education Access & Quality Examples: literacy, vocational training, language, access to loans & higher education o Economic Stability Examples: debt, expenses, insurance & medical bills, job opportunities, income, working conditions, food insecurity, housing insecurity o Social & Community Context Examples: social support & inclusion, nondiscrimination, community engagement o Neighborhood & Built Environment Examples: housing, transportation, parks, walkability, access to grocery store & healthy options, pollution, playgrounds o Healthcare Access & Quality Examples: insurance coverage, availability, access to affordable quality care x. Recognize the influence of social determinants of health on clinical decision-making By incorporating SDOH data into the clinical decision-making process, providers gain a much more comprehensive understanding of the patient’s circumstances. This knowledge allows them to address the root causes of health disparities and tailor interventions that promote better health outcomes. Every individual is influenced by their social context, and recognizing these factors allows healthcare professionals to create interventions that align with patients’ unique needs. For example, understanding a patient’s housing situation can guide recommendations for home modifications or support services already available within the community. Considering socioeconomic constraints can help tailor medication prescriptions and treatment regimens that are feasible for the patient’s circumstances, enhancing adherence, safety, and efficacy. By identifying social risk factors early on, clinical professionals can implement preventive measures and intervene before health conditions worsen. For instance, recognizing food insecurity as a social determinant can prompt referrals to community food programs or nutritional counseling. By addressing these underlying determinants, healthcare providers can help prevent the development of chronic diseases and improve overall population health. Other examples may include access to payment plans or applications for medical bill financial assistance, transportation, office hours (having clinic open past 5pm), etc. xi. Identify the influence of social determinants on health outcomes Per the CDC, SDOH have been shown to have a greater influence on health than either genetic factors or access to healthcare services & numerous studies suggest SODH accounts for 30-55% of health outcomes. For example, poverty is highly correlated with poorer health outcomes and higher risk of premature death o There is a difference of 18 years of life expectancy between high- and low- income countries o In 2016, the majority of the 15 million premature deaths due to non-communicable diseases (NCDs) occurred in low- and middle-income countries o Relative gaps within countries between poorer and richer subgroups for diseases like cancer have increased in all regions across the world o The under-5 mortality rate is more than eight times higher in Africa than the European region. Within countries, improvements in child health between poorest and richest subgroups have been impaired by slower improvements for poorer subgroups. SDOH, including the effects of centuries of racism, are key drivers of health inequities within communities of color. The impact is pervasive and deeply embedded in our society, creating inequities in access to a range of social and economic benefits— such as housing, education, wealth, and employment, putting people at higher risk of poor health. People without access to grocery stores with healthy foods are less likely to have good nutrition, thus increasing their risk of health conditions, like heart disease, diabetes, & obesity, leading to lower life expectancy than people who do have access to healthy food choices o People that are food insecure are 50% more likely to have diabetes, 60% more likely to experience heart failure, & 14% more likely to have hypertension Objective 2: Hypertension Guidelines & Diagnosis The USPSTF recommends screening for hypertension in adults 18 years or older with office blood pressure measurement (OBPM) & recommends obtaining blood pressure measurements outside of the clinical setting for diagnostic confirmation before starting treatment Typically, patients must have at least two elevated measurements, at least 5 minutes apart, one in each arm, on two or more occasions, in order to be accurately diagnosed with HTN. Additionally, patients cannot be diagnosed with HTN if they are in pain or acutely ill. i. Recognize the nationally accepted guidelines for screening, diagnosing, and staging the severity of hypertension using JNC-8 The JNC-8 recommends a goal of 130 mmHg systolic or >80 mmHg diastolic Medication is recommended for primary prevention in adults with a 10-year risk of atherosclerotic CVD >10% and an average BP of >130 mmHg systolic or >80 mmHg diastolic, or if patient has stage 2 HTN regardless of 10-year CV risk. First-line agents include thiazide diuretics, calcium channel blockers, and angiotensin-converting enzyme inhibitors or angiotensin receptor blockers o Initiation of BP-lowering therapy with 2 different first-line agents is recommended for adults with stage 2 HTN and an average BP more than 20/10 mm Hg above their target (avoid simultaneous use of ACEs/ARBs/renin inhibitors). Therapy with a single agent is reasonable in adults with stage 1 hypertension and target BP 45 years old, or younger if additional CHD risk factors o The USPSTF makes no recommendation for or against routine screening for lipid disorders in men aged 20 to 35, or in women aged 20 and older who are not at increased risk for coronary heart disease. Objective 4: Skin Lesions, Skin Cancers, and Skin Biopsy i. Differentiate physical characteristics of seborrheic keratosis from melanoma Seborrheic keratosis = hyperkeratotic lesions of the epidermis o “Stuck on” lesion with discrete border; color variable (white/tan dark brown/black); rough surface, typically 2mm-3cm in size  o Trunk is the most common site, more common with age Dermatoscope is used to differentiate SK from melanoma o Both can be varied dark colors, large, & irregular o SK = rough surface, can have horn cysts (keratin), comedo-like openings, milia-like cysts Treatment of SK = Reassurance (benign lesion, not precancerous) ii. Contrast the physical characteristics & prognosis of seborrheic keratosis & actinic keratosis AK = scaly, pink to flesh colored macules or papules with rough texture o Can transform into SCC (0.1% per lesion per year) Treatment of AK = cryotherapy if limited number of lesions, topical 5-FU if more extension lesions iii. Contrast management of seborrheic keratosis & actinic keratosis See above iv. Recognize the physical characteristics of BCC and the indications for Mohs surgery Most common human malignancy Slow growing, nonhealing sore on sun exposed skin 3 Types: o Nodular (most common) = pink papule/nodule with central depression/ulceration & pearly, rolled borders with overlying telangiectasis +/- pigmentation o Superficial o Sclerosing (morpheaform, infiltrating) Diagnosis: Shave Biopsy Treatment: Electrodesiccation and Curettage (ED&C), topical 5-FU or imiquimod, or excision if nodular subtype (curative) o Mohs surgery indicated when BCC has a more aggressive histologic pattern (sclerosing, morpheaform, or infiltrating), >2cm, poor margins, OR when near vital/cosmetically sensitive structures o Removes tumor by a scalpel in sequential horizontal layers – each tissue sample is frozen, stained, and examined during the procedure to determine if entire lesion has been excised or if tissue remains v. Recognize the physical characteristics of SCC and treatment modalities Pink to flesh-colored papules/nodules with crusting/ulceration o May be keratotic/develop a cutaneous horn o Many are asymptomatic, but can cause bleeding/pain o Most commonly located on the ear, scalp, face, neck, lip, genitalia, or areas of chronic inflammation ▪ Metastasis rates 2-3%, but up to 30-40% when found on ear, lip, genitalia, or areas of chronic inflammation Diagnosis with shave or punch biopsy Treatment options: o Surgical excision: most widely used treatment for cutaneous SCCs ▪ Used for well-defined, 2cm, recurrent lesions, and lesions close to important structures (eyes, nose, mouth) o Topical 5-FU: approved by the FDA for the treatment of AK ▪ Not approved for treatment of Bowen’s disease (SCC in situ) or superficial SCCs, it is widely used in these diseases when other treatment options are impractical & for patients refusing surgical treatment o Cryotherapy: destroys malignant cells by freezing & thawing ▪ Useful for small, well-defined, low-risk invasive SCCs and Bowen’s disease ▪ Does not permit histologic confirmation of the adequacy of treatment margins; thus, a substantial amount of training & experience is required to achieve consistently high cure rates Radiation therapy: option for the initial management of small, well-defined, primary SCCs, especially in older patients and those who are not surgical candidates ▪ Contraindicated in tumors located on the trunk and extremities increased tension & risk of trauma more prone to break down/ulceration due to atrophy & poor vascularization vi. Recognize the physical characteristics of melanoma & risk factors for development Arise from pigment-producing cells (often nevi) o Newly acquired nevi or nevi changing in size, color, symmetry, or pigmentation in a patient >20 years old is a warning sign o Lesion also may bleed/itch/ulcerate/cause pain Types: o Superficial spreading (most common): on trunk or legs o Nodular: solid black, thickness confers worst prognosis o Lentigo maligna: in situ variant on face of elderly patients Risk Factors = fair skin, red/blonde hair, inability to tan/burn easily, freckles, increased childhood sun exposure, >3 blistering childhood sunburns, increased number of moles (nevi) or dysplastic nevi, family history of melanoma, personal history of melanoma, immunosuppression, & older age  Graded with ABCDE criteria (asymmetry, border irregularity, color, diameter, evolution) Diagnose & treat with excisional biopsy vii. Recall the most important prognostic indicator in the treatment of melanoma Breslow depth of tumor invasion/thickness viii. Define the terms that describe the morphology, shape, and pattern of skin lesions Primary skin lesion: Uncomplicated lesion representing initial pathologic change, uninfluenced by secondary alterations such as infection, trauma, or therapy. Secondary skin lesion: A lesion in which a change has occurred as a consequence of progression of disease, scratching, or infection of the primary lesion. Macule: A change in the color of the skin. It is flat, and if you were to close your eyes and run your fingers over the surface of a purely macular lesion, you could not detect it. Size definition varies from < 1 cm to 1 cm in diameter. Papule: A solid, raised lesion that has distinct borders and < 1 cm in diameter. Plaque: A solid, raised, flat-topped lesion > 1 cm in diameter. It is analogous to the geological formation, the plateau. Nodule: A raised, solid lesion and may be in the epidermis, dermis or subcutaneous tissue. Tumor: A solid mass of the skin or subcutaneous tissue; it is larger than a nodule. Vesicle: A raised lesion < 1 cm in diameter and filled with clear fluid. Bulla: A circumscribed, fluid-filled lesion > 1 cm in diameter. Pustule: A circumscribed, elevated lesion that contains pus. Wheal: An area of elevated edema in the upper epidermis. Distribution: Many conditions have typical patterns or affect specific regions: o Psoriasis (extensor surfaces) o Atopic eczema (flexor areas of the extremities) o Erythema mutliforme, secondary syphilis, and eczema (palms and soles) Shape: Oval, round, linear, etc. Arrangement: o Linear: Contact reaction to an exogeneous substance brushing across the skin. o Zosterform: Cutaneous distribution of spinal nerve o Annular: Circular lesion with normal skin in the center: drug eruptions, secondary syphilis, lupus erythematosus o Iris lesions: Type of annular lesion in which an erythematous annular macule or papule develops a second ring or a purplish papule or vesicle in the center (“target” or “bull's eye” lesion). Size: o Squamous cell carcinoma of the skin > 2 cm in diameter: high risk for recurrence and metastasis. o Nevi > 6 mm in diameter tend to be more malignant than the smaller nevi Associated symptoms: itching, pain, or burning sensation. o Itchy: eczema o Pain: herpes simplex or herpes zoster ix. Utilize the ABCDE criteria for the evaluation of hyperpigmented lesions as possible melanoma Asymmetry: Asymmetry in two or more axes Border: Irregular border Color: Two or more colors Diameter: 6mm or larger Enlargement/Evolving: Change in or enlargement of lesion x. Discriminate common biopsy procedures including shave biopsy, punch biopsy, incisional, & excisional biopsies Incisional biopsy: Removing a part of the skin lesion. Punch biopsy: A specific incisional biopsy using a cylindrical dermal biopsy tool for full thickness excision. Disposable punch 2–8 mm. Lesion < 3 mm does not need stitches. Excisional biopsy: Removing the whole lesion with a 2-3 mm margin, depending on the nature of the lesion. o If lesion is larger than 2 cm, excisional biopsy requires a large incision and is not the best option for an initial diagnostic procedure unless there is a strong suspicion of malignant melanoma, in which case it would be the diagnostic method of choice. Shave biopsy: Feasible when the lesion is elevated above the surface. (In certain circumstances, some experts will elevate flatter lesions with lidocaine and obtain a shave biopsy to avoid stitches.) o Never use if have suspicion for melanoma xi. Develop patient education on the importance and methods of prevention of skin cancer Protect against further sun exposure and damage o Stay out of the sun; do not use a sunlamp o When outside, wear clothes made from tightly woven cloth, stay in the shade, wear a wide-brimmed hat. o Remember, clouds do not protect you, and the sun’s rays reflect off water, snow, and white sand. o Use sunscreen with a sun protection factor (SPF) of 15 or more. Put sunscreen everywhere the sun's rays might touch you, including your ears, the back of your neck, and bald areas on your scalp. Put more on every two to three hours and after sweating or swimming. Perform self, skin examinations o Examine your skin every month.  o Stand in front of a full-length mirror and use a hand-held mirror to check every inch of your skin, including the bottoms of your feet. o Have someone help you check the top of your head & use a blow-dryer set on low speed to move hair out of way. o Look for new moles and changes in moles. o See the doctor every six months for a whole-body skin examination or if you see any changes in your moles. o Know the ABCDEs of looking for signs of skin cancer Objective 5: Headaches, Including Migraines i. Distinguish between primary and secondary headaches using history findings Primary headaches include migraine with or without aura, tension, and cluster headaches Secondary headaches are symptoms of organic disease caused by another medical condition o Examples: meningitis (fever + HA), abscess (F + HA + FND), intracranial hemorrhage, brain tumors, pseudotumor cerebri (abrupt onset N/V due to increased ICP, relieved by LP), trigeminal neuralgia, giant cell arteritis, concussions/head or neck trauma, depression, substance abuse/withdrawal, infections, poor sleep, etc. ii. Recall the differential diagnosis associated with headaches Tension headache, migraine headache, cluster headache, medication overuse headache, meningitis, brain tumor, intracranial hemorrhage, traumatic brain injury, concussion, depression, ophthalmic zoster, or glaucoma (older patients) o Brain tumor does not cause pain unless the tumor affects the dura mater (the brain itself does not contain fibers that can detect painful stimuli) ▪ Red flag symptoms include: First headache in a patient >50 years old Abnormal thinking/confusion Abnormal neurologic examination Weight loss or other systemic symptoms o Intracranial hemorrhage is usually associated with recent history of trauma or an acute change in the pattern or severity of headaches ▪ Red flag symptoms include: Findings of first or worse headache of the patient’s life A change in existing headache Hypertension Abnormal neurologic examination History of recent trauma to the head iii. Infer the components of the history of the patient that presents with the complaint of headache Age of onset, location, frequency, duration, intensity, character, associated symptoms, triggering, or ameliorating factors, medications, impact on work/family, psychological symptoms, history of head trauma, previous imaging results, family history iv. Recognize the diagnostic criteria for each of the primary headache types Migraine headaches o Diagnostic criteria for migraine headaches include at least 5 attacks with: ▪ Headache lasting 4-72 hours with at least 2 of the following: Unilateral Pulsating Moderate to Severe (inhibits daily activity) Aggravated by physical activity ▪ And during headache, must have one of the following: Nausea/vomiting Photophobia/phonophobia ▪ If with aura, patient will have associated visual, sensory, motor, or speech impairments (aphasia, hemiparesis, prodrome (heightened sensitivity to light/sounds, lethargy, mood changes) Tension headaches: o Diagnostic criteria for tension headache include at least 10 previous headache episodes with: ▪ Headache for 30 minutes to 7 days with 2 of the following: Pressure/tightening (non-pulsating) Mild to moderate Bilateral Not aggravated by physical activity ▪ With both absent: Nausea/vomiting Photophobia/phonophobia (absent or only 1 present) Cluster headaches: o Diagnostic criteria include at least 5 attacks with: ▪ Severe unilateral or orbital/supraorbital pain lasting 15-180 minutes ▪ With at least 1 of the following ipsilateral signs: Conjunctival injection Lacrimation Nasal congestion Miosis, ptosis  Periorbital edema Forehead/facial sweating Sense of restlessness/agitation ▪ Can occur every other day or up to 8 times daily Medication overuse headache = rebound headache o Typically diffuse, bilateral, almost daily headache, aggravated by mild physical/mental exertion ▪ Present on walking, associated with restlessness, nausea, forgetfulness, depression o More than 15 headaches per month o Associated with regular overuse of an analgesic for >3 months v. Distinguish headaches associated with giant cell arteritis (GCA) versus primary headaches Giant cell arteritis: diffuse bitemporal or unilateral moderate-to-severe headache o Can be throbbing, persists throughout the day & often worsens at night o Associated with systemic symptoms (weight loss, joint pain) and can be aggravated by jaw movement o Can cause BLINDNESS ▪ If suspect, start high dose prednisone ASAP to prevent blindness prior to biopsy o Diagnose with temporal artery biopsy o Treat with steroids (high dose prednisone) vi. Choose the appropriate physical examination techniques for a patient presenting with headache Physical exam includes vital signs, cardiac exam, cervical spine exam, nuchal rigidity (r/o meningitis), ophthalmologic exam (optic fundi, pupils, visual fields), neurologic exam, including cranial nerve exam, cognition, motor function, reflexes, plantar response, coordination, & gait vii. Identify appropriate indications for ordering imaging tests on a patient who presents with headache Per the American Academy of Neurology & the U.S. Headache Consortium guidelines, neuroimaging is recommended only if: o Patient has a migraine with atypical headache patterns or neurologic signs o Patient is at higher risk of a significant abnormality or secondary headache history o Study results would alter the management of the headache o Symptoms that increase the odds of positive neuroimaging results include: ▪ Rapidly increasing frequency of headache ▪ Abrupt onset of severe headache that reaches maximal intensity within seconds or minutes of onset ▪ Marked change in headache pattern (for example: worst headache of life, progressively worsening) ▪ History of poor coordination, focal neurologic signs (papilledema, AMS), fever/rash/stiff neck, and a headache that awakens patient from sleep ▪ Headache that is worsened with use of a Valsalva maneuver, exertion, sexual activity, coughing/sneezing ▪ Persistent headache following head trauma ▪ New onset of headache in a person aged 35 or over ▪ History of cancer or HIV o Lumbar puncture is indicated in presence of meningeal signs (infection), suspicious for SAH, or pseudotumor cerebri viii. Formulate an acute treatment plan for each of the primary headaches Non-pharmacologic o Headache diary: patient keeps daily notes of presence of headache, severity, treatment, & alleviation to help monitor triggers and daily stressors ▪ Physical or environmental stressors may include intense or strenuous exercise, sleep disturbance, menses, ovulation, pregnancy, acute illness, fasting, bright or flickering lights, emotional stress ▪ Medications or substances that can act as triggers may include estrogen (oral contraceptives or HRT), tobacco, caffeine, alcohol, aspartame & phenylalanine (found in diet sodas) ▪ Dietary triggers can include ripened cheeses, cured meats, organ meats, pickled or fermented foods, monosodium glutamate (MSG), yeast-based products, chocolate, legumes & beans, onions, citrus fruits, bananas o Stress reduction with meditation, prayer, or scheduled moments of stillness, relaxation techniques or audio programs, setting limits & boundaries on others’ expectations, moderate regular exercise, 8-9 hours of restful sleep each night Pharmacotherapy o Migraines: ▪ Mild attack: Excedrin (aspirin, caffeine, acetaminophen) ▪ Severe: Triptans (e.g., sumatriptan Imitrex) immediately at onset of symptoms (do not wait >1 hour), ergotamine compounds, aqueous lidocaine nasal spray, antiemetics (chlorpromazine, metoclopramide) ▪ Prophylaxis: identifying & avoiding triggering factors, NSAIDs, B-blockers (propranolol, timolol), calcium channel blockers (verapamil), SSRIs, TCAs (amitriptyline, nortriptyline), anticonvulsants (Depakote, gabapentin, topiramate, cyproheptadine) Do not use opioids or butalbital (barbiturates) to treat migraines except as a last resort o Tension: ▪ Amitriptyline (TCA) is first line, along with short term muscle relaxants if pain extends into shoulder or trapezius muscles o Also, relaxation techniques, physical therapy, stress management ▪ Abortive therapy: NSAIDs & analgesics with caffeine o Cluster ▪ Abortive: 100% O2  ▪ Prophylaxis: valproate, ergotamine, triptans ix. Determine when a patient requires prophylaxis for headaches Prophylactic treatment of migraine headaches is recommended when headaches occur with increasing frequency & there appears to be a potential overuse of acute therapies (such as NSIADs) Preventative treatment recommended for patients who have frequent attacks (4+/month) or when headaches are so severe that acute treatment is no longer completely effective o 6 headache days/month, 4 headache days/month with some impairment, 3 headache days/month with severe impairment or requiring bedrest For cluster headaches, prophylaxis is recommended for headaches that are intense or do not respond to abortive treatment x. Formulate an acute treatment plan for chronic primary headaches See above xi. Recall the typical somatic dysfunctions associated with the primary headache types and their osteopathic treatment (cervicogenic, tension, migraine, cluster) Tension: bilateral, steady pain described as a pressure or tightening sensation, radiating from the forehead to neck & does not worsen with activity o Increased tenderness in the frontal, temporal, suboccipital region at inion (location of greater occipital nerves), masseter, pterygoid, SCM, splenius, & trapezius muscles ▪ Can be associated with tender or trigger points of these regions, cranial somatic dysfunction, cervical somatic dysfunction (esp. OA, C1-3) occipitomastoid compression, sacral/pelvic somatic dysfunction (dural attachment at S2), forward head carriage, thoracic somatic dysfunction (increases sympathetic tone, T2-4), ribs 1-2 inhalation SD, ribs 3-4 exhalation SD o Can use trapezius muscle energy, paraspinal rib raising, cervical stretch/contralateral traction, suboccipital release, MFR of cervical musculature, OA decompression/CV4, cervical counterstain, HVLA if tolerated, etc. Cervicogenic headache presents as unilateral pain that starts in the neck & is referred from bony structures or soft tissues of the neck, usually associated with decreased ROM of the c-spine similar associated SDs & treatments as tension HAs Migraine: unilateral, pulsating/throbbing headache that worsens with daily activities & are associated with nausea/vomiting and photo- and/or phonophobia +/- preceding aura o SD of the upper thoracic spine (increased sympathetic tone vasoconstriction), cranial dysfunction (trigeminal nerve courses through sphenoid bone, sphenosquamous compression can compromise function of middle meningeal artery, SD of the temporal bone can cause reflex dilation of the carotid arteries via the facial nerve, occipitomastoid compression can cause reduced venous drainage), upper cervical somatic dysfunction, myofascial strain patterns within the abdomen/elsewhere in the body, excessive tension around the sacrum & coccyx (dural attachment), rib SD o Can use upper thoracic & rib counterstain or MFR to improve suboccipital tissue texture, CV4, occipital condyle decompression, OA decompression, parietal lift, etc. ▪ Best to perform cranial techniques between attacks & treat cervical indirectly with BLT, counterstain, or gentle MFR to avoid further vagal stimulation Cluster: severe unilateral pain in & around one eye, with associated tearing & redness of the eye, stuffy or runny nose, and/or ipsilateral Horner’s syndrome o Similar SDs as migraines, especially C1-C2 SD & cranial dysfunction (trigeminovascular complex & trigeminal autonomic reflex account for symptoms of cluster headaches) Headaches secondary to organ disease o For example: bilious headache from GB disease ▪ Sympathetic afferents go to T6-9 facilitate dermatome increased muscle tone causing type II dysfunction (T8 frequently SRRR) increased muscle tension cephalad to suboccipital area ▪ Treatment of these regions can improve both organic disease & subsequent symptoms (such as headache) xii. Identify the primary headache and counsel a patient on the appropriate prevention & treatment of the somatic dysfunction associated with the headache See above xiii. Utilize suboccipital release, soft tissue techniques to the cervical paraspinal musculature & cranial techniques to improve the somatic component of the headache Suboccipital release, bilateral cervical stretch & contralateral traction, MFR of the cervical spine (“driving the bus”), CV4, vault hold, decompression of occipital condyles, parietal lift xiv. Develop self-care techniques for patients to use outside the office to help treat headaches See above for non-pharmacologic techniques  Include sleep hygiene, reduction of screen time or blue light glasses, exercise, regular well-balanced meats, reduced caffeine, increased water intake, keeping a headache diary Objective 6: Ophthalmology and the Family Medicine Patient i. Utilize a complete physical exam of the eye, including use of handheld ophthalmoscope to determine causes of ‘Red Eye’ History: o Did irritation occur rapidly or progress slowly? ▪ Rapid hyperemia = foreign body ▪ Slower onset = viral or allergic conjunctivitis or iritis o Description of pain ▪ Superficial irritation = grain of sand sensation ▪ Deeper inflammatory process or penetration = severe, dull pain Physical Exam (examine both eyes for comparison, even if only one eye is affected): o Inspect the palpebral conjunctiva carefully with magnification to determine whether lymphoid hyperplasia (cobblestone appearance) exists ▪ Conjunctival infection = individually visible vessels in conjunctiva branching from sclera towards cornea, vascular dilation, cellular infiltration, & exudation ▪ Ciliary infection = red ring surrounding cornea, individual vessels not clearly visible ▪ Canaliculitis = mildly red eye with slight discharge ▪ Dacyrocystitsis = localized unilateral pain, edema, & erythema over the lacrimal sac at the medial canthus of the eye; +/- purulent discharge from the puncta ▪ Episcleritis = inflammation limited to an isolated patch of the episclera (no diffuse involvement) ▪ Pinguecula or pterygium: triangular band of fibrovascular tissue on either side of the cornea (pinguecula) or may encroach onto the cornea (pterygium) Can become inflamed; often caused by UV damage o The type & quantity of discharge are assessed by pulling down the lower eyelid ▪ The appearance of the punctum should be examined to determine whether pus is coming out of the tear duct o Normally, the cornea is perfectly transparent ▪ Excessive fluid within the stroma of the cornea results in partial opacification that can be observed by direct illumination with a penlight ▪ A diffuse corneal haze can occur with congenital glaucoma & angle-closure glaucoma ▪ After inspection with a penlight under magnification, corneal staining is performed with fluorescein using sterile filter paper strips o Assess pupil size & shape o Assess anterior chamber depth with side illumination with a penlight o If no obvious signs of infection, then the intraocular pressure should be measured with tonometer (usually normal in patients with red eye, except acute angle closure glaucoma) o Assess for preauricular lymph node enlargement (frequent sign of viral conjunctivitis) ii. Assess the need for referral in evaluation of the following conditions: Reduced Vision Pain Photophobia Corneal Staining Corneal edema Unequal pupils Elevated intraocular pressure **All of these conditions require referral to ophthalmologist if present** **Triad of red eye, pain, & loss of vision could mean potentially blinding condition is present** iii. Differentiate symptoms of conjunctivitis to help determine viral, bacterial, versus allergic causes Allergic o Papillary projections & pruritis, typically seasonal with stringy, white discharge bilaterally o Tx: Avoid allergens, topical antihistamine decongestant Viral o Lymphoid follicles on the undersurface of the lid & enlarged tender preauricular nodes; can be associated with URI o Less discharge, more watery (serous, clear) o Self-limited, no specific treatment required but is highly contagious (hand washing is crucial to avoid infection) Bacterial o Most common pathogens include S. pneumonia, H. influenzae, S. aureus, & P. aeruginosa ▪ The most common causes of hyperacute conjunctivitis are N. gonorrhoeae & N. meningitidis o More purulent discharge, more likely to be unilateral o Tx = topical antibiotic drops (erythromycin, bacitracin, tobramycin, ciprofloxacin, other quinolones) ▪ **Assume bacterial etiology is involved if unclear based on history & exam** Topical corticosteroids are CONTRAINDICATED for conjunctivitis due to 4 potentially serious ocular side effects & should only be reserved for patients under the care of an ophthalmologist:  1. Steroids can facilitate penetration of an undetected corneal herpetic infection to the deeper corneal layers & cause corneal perforation 2. Prolonged local use of topical corticosteroids (usually >2 weeks) can cause chronic open-angle glaucoma 3. Prolonged local use of topical corticosteroids can cause cataracts 4. Topical corticosteroids are capable of potentiating the development of fungal corneal ulcers iv. Recall the proper management of styes, chalazions, and blepharitis Blepharitis = inflammation of the eyelids usually involving lid margins o Chronic staphylococcal infection is the most common ▪ Sx: asymptomatic then FB sensation, matting of the lashes, burning, eyelid crusting, discharge, redness o Seborrheic blepharitis ▪ Sx: seborrhea of the scalp, lashes, eyebrows, & ears, characterized by greasy, dandruff-like scales on the eyelashes o Long-term, repeated treatment is required for both conditions ▪ Treatment includes eyelid hygiene, topical antibiotics for staphylococcal blepharitis Stye = acute boil-like lesion with swollen, tender, red eyelid o Treatment is warm compress for 15 minutes 4x/day and topical antibiotics ▪ Systemic antibiotics only indicated if periorbital cellulitis present ▪ Refer to ophthalmology if it does not drain in 2 weeks Chalazion = chronic swelling of the eyelids NOT associated with conjunctivitis o Granulomatous inflammatory reaction that may persist for weeks or months o Rubbery, cystic, and non-tender on palpation o Typically, does not respond to oral or topical antibiotics ▪ If it persists for more than 4-6 weeks, it may require I&D ▪ Recurrent chalazion may be caused by an underlying sebaceous carcinoma, so the lesion should be biopsied & send for pathologic testing v. Identify the common causes of dry eyes and appropriate treatment Eye will typically appear normal; may have decreased tear meniscus at the lower lid margin Corneal epithelium shows varying degrees of fine punctate stippling in the interpalpebral fissure, which stain with rose Bengal or fluorescein if more severely damaged Keratitis sicca = deficiency in tear production o Acquired disorder seen in 5th decade of life, more often in women o Initial symptoms include a foreign body sensation, dryness, and burning, which often worsens as this condition progresses ▪ Can have paradoxical tearing from reflex stimulation of the lacrimal gland ▪ Associated with autoimmune diseases, such as SLE and Sjogren’s o Initial treatment is lubrication with artificial tears and ointments to supplement of replaces the tear film deficit ▪ In moderate or severe cases, an ophthalmologist may need to occlude the eyelid punctum surgically and perform a tarsorrhaphy to protect the corneal surface. Moisture chambers may also be prescribed. Topical antibiotics are required only if secondary infection occurs. ▪ Cyclosporine 0.05% (Restasis) is also useful in addressing inflammatory components of tear film insufficiency when other treatments are insufficient Exposure keratitis = a condition symptomatically similar to keratitis sicca that is caused by incomplete closure of eyelids during blinking or sleep o Seen with bell’s palsy, scarred or mispositioned eyelids, thyroid exophthalmos o Treatment = ophthalmic lubricating solutions/ointments vi. Recall the leading causes of reduced vision in the United States and appropriate screening and treatment for: Cataracts = clouding of the lens of the eye o Screening is performed with at least yearly examination of the eyes & testing of visual acuity o Treatment = surgery with intraocular lens implantation Glaucoma = leading cause of blindness; increased intraocular pressure leading to damage of the optic nerve o Screening done with IOP measurement at least yearly (more frequent if history, risk factors, etc.) o Treatment: ▪ Medications: Prostaglandins (increase aqueous humor outflow; “-prost”) Beta blockers (decrease aqueous humor production; timolol) Alpha-adrenergic agonists (reduce production/increase outflow; apraclonidine) Carbonic anhydrase inhibitors (reduce production; acetazolamide) Cholinergic agents (increase outflow; pilocarpine) ▪ Surgical management: Laser trabeculoplasty (opens up trabecular meshwork) Filtering surgery (opening in sclera to remove part of trabecular meshwork) Drainage tube insertion Electrocautery (removed tissue from trabecular meshwork) Macular Degeneration = damage of the macula (the center of the light-sensitive retina at the back of the eye) o Age-related macular degeneration causes central vision loss o Screening performed with yearly eye examination & testing of visual fields  o There is no cure, but treatment options include laser therapy, anti-VEGF medications to treat neovascularization, or carbonic anhydrase inhibitors ▪ Advanced cases have been treated with macular translocation o Progression can be delayed by multivitamins with beta-carotene (avoid in smokers) & vitamin E Diabetic Retinopathy = most common cause of blindness in Americans aged 20-74 o Target tissue is retinal capillary ▪ Nonproliferative retinopathy: capillaries leak & later become occluded; vision loss only occurs if macula is involved ▪ Proliferative retinopathy: cotton wool spots (white opacities with feathery edges indicative of localized retinal infarct of nerve fiber layer) New blood vessels form due to chronic retinal ischemia vessels form vascularization in vitreous cavity retinal detachment o Screening eye examinations recommended yearly for patients with diabetes to reduce the chance of vision loss ▪ Patients with type 1 diabetes should have their first eye examination 5 years after onset ▪ Patients with type 2 diabetes should have their first eye examination at diagnosis ▪ Patients with diabetes should have a baseline eye examination before becoming pregnant or early in the first trimester ▪ On initiation of ophthalmic screening, all patients with diabetes should have annual dilated fundus examinations by an ophthalmologist or sooner if poor diabetic control or visual symptoms develop o Treatment includes management of diabetics & blood sugar control; however, after proliferative diabetic retinopathy develops, laser photocoagulation is the primary prevention of vessel progression that leads to retinal detachment vii. Differentiate between open-angle and angle-closure glaucoma and when emergent referral is needed Narrow angle (acute closure) o Elevation in IOP when outflow of aqueous humor is suddenly blocked ▪ Can be associated with ocular trauma, intraocular inflammation, intraocular tumors, carotid vascular disease, or certain medications o Symptoms include severely painful red eye, commonly associated with haloes around light, nausea/vomiting ▪ Patients are usually >50 years old complaining of blurred vision & photophobia o Physical Exam: ▪ Pupil may be dilated and/or non-reactive to light ▪ Slit lamp examination reveals corneal edema & injection with a shallow anterior chamber ▪ IOP is elevated (reference range is 100.4, or patients 3-14 years old o 0 points for patients 15-44 years old o -1 point for patients >45 years old Interpretation: o 4: begin empiric treatment, no testing recommended iv. Recognize dysphagia, medication induced esophagitis, & globus hystericus Dysphagia = difficulty swallowing solids or liquids o Motor disorders difficulty with liquids o Mechanical obstruction difficulty with solids & liquids Medication induced esophagitis = retrosternal chest pain exacerbated by swallowing o Common culprits: tetracyclines, KCl, iron, quinidine, aspirin, NSAIDs, bisphosphonates Globus hystericus = constant sensation of lump in the throat, commonly associated with GERD v. Name the elements of an obstructive sleep apnea (OSA) study, the symptoms of OSA, and the chronic illnesses associated with OSA.  OSA study measures the intensity of snoring, presence of apnea/hypoapnea, oxygen saturation, sleep efficiency, & cardiac rhythm, along with a physical exam (looking at body habitus, tonsillar hypertrophy, excess soft palate tissue, size of tongue, nasal obstruction, size of mandible, etc.) o Numeric value of the total apneas/hypoapneas = respiratory distress index (RDI) ▪ RDI 102° F), tachycardia out of proportion to temp, GI dysfunction (N/V, diarrhea, jaundice), and CNS dysfunction (hyperirritability, anxiety, confusion, apathy, coma) ix. Identify the most common cause of hypothyroidism in the United States as well as the role of iodine deficiency in hypothyroidism Most common cause in US is Hashimoto’s Thyroiditis (autoimmune) o Caused by the development of antithyroid antibodies that attack the thyroidal stroma, causing progressive fibrosis of thyroid gland o Anti-TPO Abs and Anti-Thyroglobulin Abs are responsible, with TPO Abs considered the primary cause o Labs = ↑ TSH with ↓ to normal T4 o Treat with T4 replacement (levothyroxine) Most common cause worldwide = inadequate dietary intake of iodone o Iodine deficiency excess thyrotropin production glandular growth & colloid production goiter o Addition of iodine to table salt has made hypothyroidism a rare cause in developed countries Other causes of hypothyroidism include surgery (thyroid surgery), radiation exposure, viral infection, central disease (primary pituitary failure) x. Recognize when to consider biopsies for nodules and cysts of the thyroid gland A nodule that is palpable on examination or >1.0 cm on ultrasound requires further evaluation If a nodule is 5 mm) or presence of cervical adenopathy (all nodules regardless of size) As long as the cyst remains small or is asymptomatic, no intervention is required; however, if the cyst increases in size or becomes symptomatic, it can be drained via FNA xi. Recall the common medications which may affect thyroid function Inhibit T4 synthesis o Iodine, propylthiouracil, methimazole, amiodarone, lithium, cytokines Blocks T4 secretion o Amiodarone, lithium, cytokines Blocks TSH release o Antipsychotics, phenytoin, dopamine, glucocorticoids Compete for site on thyroid hormone transport proteins (can potentially exacerbate thyrotoxic symptoms by releasing additional thyroid hormone into peripheral circulation) o Salicylates, NSAIDs, furosemide, heparin, enoxaparin Inhibit deiodination of T4 → T3: o Dexamethasone, beta blocker, amiodarone, contrast agent Inhibit action at tissue level: o PTU, beta blocker Inhibit uptake of T3 at tissue level: o Benzodiazepines, CCB Affect thyroid hormone clearance time: o Phenytoin, phenobarbital, carbamazepine, rifampin Inhibit GI absorption o Sucralfate, calcium carbonate, aluminum hydroxide, soy, ferrous sulfate xii. Develop patient education on the signs and symptoms of over-treatment of hypothyroidism Signs include symptoms of hyperthyroidism, including tachycardia, tremors, sweating, diarrhea, weight loss, etc. Serum TSH is checked every 4-6 weeks & medication dosage of levothyroxine is adjusted based on sTSH response o Doses of levothyroxine resulting in sTSH > herniated disc ▪ Predisposing factors: 45–60-year-old Caucasian population, no strong relationship between height, weight, body build or physical fitness ▪ Most episodes of low back pain or sciatica resolve spontaneously in first 2 weeks Psychosocial factors: emotional tension, stress, job dissatisfaction, monotony at work, poor relations with coworkers Physical factors: heavy work, lifting, static work postures, bending with twisting, vibration Most common causes of sacroiliac dysfunction: psoas or lumbar somatic dysfunction, short leg syndrome, pelvic side shift, simple traumatic sacral somatic dysfunction, pelvic floor somatic dysfunction, cranial somatic dysfunction, lumbosacral instability, disc protrusion o Risk factors: prolonged sitting (truck driving > desk jobs), deconditioning, sub-optimal lifting and carrying habits, repetitive bending and lifting, spondylolysis, disc-space narrowing, spinal instability, spina bifida occulta, obesity, low education iii. Recall the osteopathic physical examination necessary to differentiate causes for low back pain and differential diagnosis of low back pain Straight leg raise: patient supine with legs straight, leg on symptomatic side is lifted with knee in extension o Tests for lumbar disc herniation, positive test = pain between 30-70 degrees in low back or leg Standing flexion test: patient standing with examiner behind, place thumbs on sacral base and have patient bend forward o Tests for iliosacral dysfunction, positive result = one thumb moves asymmetrically higher Psoas muscle test: patient prone, knee flexed to 90 then lifted off table to assess ROM o Tests for psoas involvement, positive test = asymmetry in ROM or reproducing low back pain symptoms Piriformis test: patient lies on side, lower leg flexed at hip and knee, upper leg straightened off table, stabilize pelvis and push down on upper leg o Tests for piriformis muscle involvement, positive test = pain in buttocks o If pain radiates down leg = sciatic nerve impingement DDX: o Emergent disorders associated with acute paraplegia: spinal cord tumors, epidural abscess, embolus, spinal artery thrombosis, central herniation of nucleus pulposus (cauda equina syndrome) o Axial MSK causes: degenerative disc disease, facet arthritis, sacroiliitis, ankylosing spondylitis, discitis, paraspinal muscular issues, SI dysfunction o Radicular causes: disc prolapse, spinal stenosis o Trauma: lumbar strain, compression fracture o Neoplastic: lymphoma/leukemia, metastatic disease, multiple myeloma, osteosarcoma ▪ Hx of elevated PSA, back pain worse at night, weight loss suspicion for metastatic prostate cancer to spine o Inflammatory: rheumatoid arthritis o Visceral: endometriosis, prostatitis, renal lithiasis o Infection: discitis, herpes zoster, osteomyelitis, pyelonephritis, spinal or epidural abscess m. Vascular: aortic aneurysm o Endocrine: hyperparathyroidism, osteomalacia, osteoporosis, Paget disease iv. Recognize the value of diagnostic testing, and describe routine treatment for low back pain Classification system: nonspecific back pain, radicular pain, red flag associated symptoms dysfunction, reflex causes (viscerosomatic) Treatment: offer information about self-care in addition to a therapeutic course of physical therapy, manual therapy, or acupuncture o Self-care: remaining active, rehab exercises specific to spine and aerobic exercise o Medication: first line = NSIADs, muscle relaxers, IM steroid ▪ Opioids have been shown to improve pain but do not improve function more than other analgesics  In absence of red flags or findings suggestive of systemic disease, imaging/diagnostic testing is not indicated until after 4-6 weeks of conservative treatment o X-rays (AP, Lateral, oblique) – rarely needed in uncomplicated cases of strain, useful is pain persists > 6wks or if something more than strain is suspected, such as a fracture o Indication for MRI: worsening or unremitting neurologic deficit or radiculopathy, progressive major motor weakness, cauda equina compression (sudden bowel/bladder disturbance), suspected systemic disorder, failed 6 weeks of conservative care v. Recognize the clinical signs and symptoms associated with disc herniation syndromes and when to refer for surgical evaluation Disc herniation symptoms: exacerbated with sitting or bending, relief with standing or lying down, increased pain with cough/sneeze, pain radiating down leg and sometimes foot, paresthesia, muscle weakness (may have foot drop) o Lumbar herniations most frequently increase pain with sitting, are more commonly central or paramedian o Compression of nerve root exiting at next lower level (L4-5 herniation compresses L5 root), in contrast a far lateral herniation into the neuroforamina compresses the upper nerve root (L4-5 compresses L4 root) o Surgical evaluation indications include loss of bowel or bladder control, progressive neurologic involvement ▪ Relative: static motor loss, intractable pain causing debilitating functional loss vi. Identify the clinical signs, symptoms, and treatment of lumbar compression fractures, spinal stenosis, and scoliosis Compression fracture: most commonly caused by osteoporosis, often identified incidentally and most commonly are asymptomatic, plain radiographs are test of choice o Most common site of fracture = thoracolumbar junction ▪ Fractures superior to T7 and those occurring in patients with osteoporosis should prompt further workup looking for systemic disease (malignancy, hyperparathyroidism, osteomalacia, TB) ▪ Common mechanism is fall from ladder onto feet, jumping into a pool feet first o Treatment: pain control, prevention of further fractures and disability ▪ Conservative therapy: analgesic meds, bed rest, back braces, physical therapy ▪ Interventional treatment: balloon kyphoplasty, vertebroplasty Spinal stenosis: buttock or lower extremity pain associated with diminished space for neural and vascular structures in spinal canal, pain is relieved by sitting and flexion, worse with extension o Neurogenic claudication in older adults = classic presentation o Conservative treatment: physical therapy, analgesics, lumbosacral braces, manual therapy, weight loss o Interventional treatments: epidural steroid injections, spinal decompression surgery Scoliosis: lateral curvature of spine usually accompanied by rotation, pain is not a common complaint until later in life and occurs at the segments adjacent to the restricted areas o Scoliosis is named according to side of rotation and convexity of curve curve sidebent left and rotated right (concave left/convex right) = right scoliosis o Imaging = scoliosis series (XR) with patient standing & should include entire spine and pelvis ▪ First exposure taken with patient standing normally and weight bearing equally in both upper extremities, used to measure spinal curves ▪ Second and third exposures taken when patient sidebends torso to L and R, used to differentiate structural curves from nonstructural (functional) curves ▪ Fourth radiograph often of hand is taken to evaluate status of epiphyseal fusion in adolescents ▪ Standing lateral lumbosacral spine film required for measurement of sacral angle and pelvic index o Treatment: dependent on age (bone age & mineralization), and curve severity ▪ May include exercise therapy, physical therapy, cranial manipulation in infants, mobilization & stabilization, bracing, or surgery if curve is severe (>50% can impact lung and cardiac function) vii. Recognize the red flags/alarm symptoms for serious causes for low back pain Fever, weight loss, nausea, saddle anesthesia, recent trauma, bowel or bladder incontinence or retention, recent UTIs, neurologic symptoms History of: IV drug use, cancer, immune suppression, chronic steroid use, TB viii. Apply osteopathic physical examination findings to develop appropriate treatment for back pain Complete physical exam with emphasis on regions mentioned in history or that have functional association Vital signs can document presence of fever associated with infection or neoplasm, tachycardia or elevated BP may indicate pain Observation of posture, gait, & skin (spondyloarthropathies can cause dermatologic abnormalities) Measure degree of lordosis/kyphosis, flexion & extension ROM, palpation to determine pain location on flexion and lateral bend, pain location in lower extremities, sensory changes or weakness in lower extremities, special tests, neurologic testing Special tests: straight leg raise (lumbar radiculopathy), bragard test (SLR with dorsiflexion of ankle), Nachlas test (prone knee bending test – done by bending knee until heel reaches ipsilateral buttocks), Slump test (seated patient slumps forward and extends neck, push down on head, extend knee, dorsiflex foot = each progressive maneuver adds more tension causing impingement of dura and spinal cord/nerve roots), Schober test (measures amount of lumbar flexion, make points with horizontal line and have patient bend forward, measure, if distance < 4cm = decreased flexion), hip drop test, Thomas test ix. Apply counterstrain, soft tissue manipulation, myofascial release, muscle energy and HVLA in the setting of lumbosacral back pain Indirect techniques (counterstrain, soft tissue, MFR) better for acute problems, direct techniques as patients tolerate (muscle energy, HVLA) HVLA relatively contraindicated at level of disk herniation, with chronic steroid use, fracture, etc. x. Develop patient education on home exercises and other home treatments for low back pain  Acute low back pain due to psoas syndrome: patient can do stretches at home for psoas, also stay in rest position, ice and some medications can be useful Lumbar compression fractures: exercises that encourage gradual extension of lumbar region and/or a brace that prevents active flexion and maintains slight extension With any back injury it is important for patient to remain active as much as able and to avoid prolonged bed rest Objective 11: Ethics/Medical Legal Considerations i. Recognize patient rights in the regards to confidentiality The Health Insurance Portability and Accountability Act of 1996 (HIPAA) is a federal law that required the creation of national standards to protect sensitive patient health information from being disclosed without the patient’s consent or knowledge. o The patient always has a right to confidentiality unless release of information is agreed to & signed by the patient, the patient is at risk of harming themselves/others, suspected child or elder abuse, some communicable diseases, some situations related to illegal or criminal activity o States differ on their laws regarding confidentiality & minors – as of now, it is permitted for a minor to access sexual health care (birth control access, STI testing, etc.) confidentially without notification of parents ii. Identify indications for public reporting and knowing state by state variations exist Per the CDC, indications for reporting include certain infectious diseases (anthrax, arboviral diseases, babesiosis, botulism, STIs, COVID-19, diphtheria, giardia, hepatitis, HIV, cholera, polio, rabies, small pox, tetanus, TSS, etc.), cancers, & other conditions that are of public health concern (carbon monoxide poisoning, foodborne disease outbreak, lead poisoning, pesticide related injury/illness, silicosis, VRE, etc.) Variations exist for which diseases are reportable, depending on the state you are practicing in iii. Define “capacity” in the setting of patient decision making Capacity is determined by the PHYSICIAN (versus competency is determined in a court of law) In a medical context, capacity refers to the ability to utilize information about an illness and proposed treatment options to make a choice that is congruent with one's own values and preferences iv. Recognize the utility of a Durable Power of Attorney and a Living Will Both a living will and a durable healthcare POA allow you to choose someone you trust to make certain medical choices on your behalf. You must be at least 18 to create either document and you must be of sound mind. That means no one is allowed to coerce you into making a living will or healthcare power of attorney. A living will is limited to deathbed concerns only and is used to declare your desire to not have life-prolonging measures be taken if there's no hope of recovery, for example, in the event of brain death or terminal illness. A durable power of attorney for healthcare, on the other hand, covers all health care decisions, and lasts only as long as you are incapable of making decisions for yourself, for example, if on a ventilator for pneumonia or stroke. However, you can set out specific provisions in the Power of Attorney telling your agent how you would like them to act in regard to deathbed issues. v. Identify principle of informed consent Informed consent is the process in which a health care provider educates a patient about the risks, benefits, and alternatives of a given procedure or intervention. The patient must be competent to make a voluntary decision about whether to undergo the procedure or intervention Informed consent is both an ethical and legal obligation of medical practitioners in the US and originates from the patient's right to direct what happens to their body. Implicit in providing informed consent is an assessment of the patient's understanding, rendering an actual recommendation, and documentation of the process The following are the required elements for documentation of the informed consent discussion: o (1) the nature of the procedure o (2) the risks and benefits and the procedure o (3) reasonable alternatives o (4) risks and benefits of alternatives, o (5) assessment of the patient's understanding of elements 1 through 4. It is the obligation of the provider to make it clear that the patient is participating in the decision-making process and avoid making the patient feel forced to agree to with the provider. The provider must make a recommendation and provide their reasoning for said recommendation. vi. Recognize the legal rights that minors have regarding sexual health As of 2022, all jurisdictions have laws that explicitly allow a minor of a particular age (as defined by each state) to give informed consent to receive STD diagnosis and treatment services. While most states allow minors to give informed consent to contraceptive services, some states have restrictions on certain ages or types of contraception permitted, and some states do not allow minors to consent at all Laws vary by state similarly for access to prenatal care, medical care for a minor’s child, abortion services, and adoption vii. Explain and apply the ethical principle of: Autonomy – the right of a patient to retain control of their body, make their own decisions regarding their body, to respect patients as individuals, and honor their preferences in accepting or not accepting medical care Beneficence – actions to promote the wellbeing of others & acting in the patient’s best interests Non-maleficence – do no harm Fidelity – honesty & integrity, faithfulness to the patient Justice – to treat all persons fairly & equitably, equal distribution of resources  Utility – actions are right if they produce the greatest balance of happiness over unhappiness & the most benefit to the greatest number of people viii. Define the four criteria for negligence: Duty of care – an obligation that one party has toward another party to exercise a reasonable level of care given the circumstances Breach of duty – violation of law or duty, must breach duty in order to be liable Causation – how harm or damages wouldn’t have happened but for the liable party’s actions Damages – actual losses as a direct and proximate result of the liable party’s negligence Objective 12: Cigarette Smoking & Associated Risk i. Relate pathologic basis of smoking and its effect on tissues Smoking increases intravascular oxygen free-radical production and induces diffuse endothelial dysfunction marked reductions in nitric oxide (NO) and tissue plasminogen activator (tPA) Increase oxidative damage to cells and lipoproteins, vasoconstriction, and reduced capacity for fibrinolysis in the setting of plaque rupture and overlying thrombus formations Reduces rates of arterial and venous graft patency in heart and peripheral vasculature Increased serum levels of multiple emerging risk factors, including CRP, fibrinogen, and homocysteine ii. Infer the morbidity and mortality associated with tobacco use in relation to the following disease processes Cancer (especially pulmonary, oral, laryngeal, and bladder neoplasms) Pulmonary disease (especially COPD/emphysema secondary to structural damage to lung parenchyma, pneumonia) Cardiovascular disease (especially atherosclerotic disease, myocardial ischemia, AAA, ED) Alzheimer disease Endocrine diseases (especially diabetes, poor wound healing, osteoporosis, etc.) Skin aging Visual disease Mental health disease **increased risk, morbidity, and mortality from of all conditions listed above** iii. Infer the risks associated with smokeless tobacco and passive tobacco smoke exposure Secondhand smoke increases risk of CAD, CVA, lung disease/cancer, adverse reproductive health effects in women such as low birth weight, increased risk of infections, asthma, SIDS Risk of smokeless tobacco include CAD, CVA, dental disease (cavities, teeth staining, gum disease, bone loss, tooth loss), leukoplakia/oral cancers iv. Infer the pharmacologic effects of the following medications used to assist with smoking cessation Bupropion: inhibits neuronal reuptake of NE, serotonin, & dopamine reduces intensity of withdrawal symptoms in patients trying to quit smoking o CI in patients with seizures or eating disorder Nicotine replacement: controls withdrawal & craving by providing an alternative source of nicotine that can progressively be weaned over weeks to months Varenicline (chantix): nicotinic acetylcholine receptor agonist helps control withdrawal symptoms o AE: N/V, nightmares, vivid dreams ***Which medication should you use if a patient is pregnant??*** o Rakel Textbook and ACOG favor nicotine replacement v. Select the most appropriate medication to assist a patient in smoking cessation based on the patient’s medical history Dependent on patient goals, past medical history, & other comorbidities vi. Develop patient education on community opportunities to help smoking cessation Physician advice to quit smoking provides marginal benefit o Can also establish effective quit smoking groups and other smoking cessation programs locally Interventions combining counseling + education or group strategy + pharmacologic treatment have sustained quit rates of 25-30% o Counseling is most effective when it includes practical problem solving and social support o “Quit lines” deemed ineffective by research Ex-smokers have an average of 8 attempts before they successfully quit vii. Recall the stages of change in respect to the patient’s desire to stop smoking Ask: systematically identify all tobacco users at every visit Advise: strongly urge all tobacco users to quit  Assess: determine willingness to make a quit attempt Assist: aid the patient in quitting – help with quit plan, provide practical counseling, intra-treatment social support, help patient obtain extra-treatment social support, recommend use of approved pharmacotherapy except in special circumstances Arrange: schedule follow up contact Objective 13: Sexually Transmitted Infections i. Describe the guidelines for STI screening and partner notification including HIV Clinical & nonclinical providers can assess a person's behavioral and biologic risks for acquiring or transmitting STIs and HIV, including having sex without condoms, having recent STIs, and having partners recently treated for STIs The federal guidelines recommend clinical and nonclinical providers to offer or make referral for regular screening for multiple STIs, on-site STI treatment when indicated, and risk-reduction interventions tailored to the person's risks Health care providers should encourage persons with a new HIV diagnosis to notify their partners and provide them with referral information for their partners about HIV testing. o Partner notification for exposure to HIV should be confidential o Health care providers can assist in the partner notification process, either directly or by referral to health department partner notification programs. ii. List the causative pathogens of common STI’s See below iii. Describe the symptoms and physical exam findings associated with common STI’s Cervical motion tenderness is indicative of pelvic pathology  Diagnosis Causative Common Symptoms Physical Exam Diagnostic Treatment AEs of Tx Pathogen Findings Labs/Studi (*treat es partner*) Chlamydia Chlamydia Mostly asymptomatic (75- Cervical/vaginal Voided Azithromycin, Rash, trachomatis 90%); Symptomatic men discharge, dysuria, urine doxycycline eosinophilia, GI have penile discharge/ vaginal bleeding, sample, (**treat motility issues urethritis, but can also have abdominal NAATs concomitantly Photosensitivity, epididymitis or reactive tenderness, cervical for gonorrhea**) drug induced arthritis motion tenderness lupus, painful Symptomatic women (PID) swallowing present with watery mucopurulent discharge, dysuria, or lower abdominal pain; 10-20% develop acute salpingitis & PID Gonorrhea Neisseria Vaginal discharge Same as above Same as Ceftriaxone Induration after gonorrhoeae (thin, white, purulent, above (**treat injection, odorous), dysuria, bleeding, concomitantly eosinophilia, lower abdominal pain for chlamydia**) diarrhea, rash Syphilis Treponema Painless chancre lesions Painless chancre w/ Serologic Benzathine N/V, type I pallidum (primary) that can progress to lymphadenopathy testing, Penicillin hypersensitivity diffuse mucocutaneous rash (primary); rash VDRL & preferred in reaction involving the palms & soles with involving palms and RPR w/ non-allergic nontender lymphadenopathy soles and confirmato patients with and condylomata lata condylomata lata ry FTA- early syphilis (secondary) and multiorgan (secondary); ABS, and their recent involvement (tertiary), including gummas, Argyll darkfield (within 90 days) aortic aneurysm, aortic Robertson pupil, microscopy sex partners regurgitation, tabes dorsalis endarteritis (tertiary) Chancroid Haemophilus Extremely painful ulcer with Painful genital ulcer Isolation of Doxycycline Photosensitivity, ducreyi tender lymphadenopathy; and tender inguinal H ducreyi with drainage of GI symptoms, asymptomatic carrier state is lymphadenopathy on special buboes or teeth common in women media; PCR abscesses discoloration in children/pregnan cy Trichomoniasis Trichomonas Abnormal vaginal discharge Abnml vaginal odor Saline wet Metronidazole Disulfiram-like vaginalis (classically described as frothy, and discharge w/ mount; or tinidazole rxn w/ alcohol, green-yellow, & malodorous), elevated pH; standard headache, musty vaginal odor, vulvovaginal strawberry cervix culture; metallic taste itching, dyspareunia, dysuria, whiff test postcoital bleeding HSV Herpes Initial infection can cause Herpetic vesicles Viral Acyclovir, Obstructive simplex systemic symptoms (fever, that can rupture culture, valacyclovir, crystalline virus headache, malaise, myalgia); can and form tender Tzank famcyclovir nephropathy, present with local pain & ulcers smear, PCR acute renal blisters, dysuria, and/or tender failure if not lymphadenopathy adequately hydrated iv. Discuss the steps in the evaluation and initial management of common STI’s See above v. Review the CDC guidelines for treating the following sexually transmitted infections (see above) Chlamydia Gonorrhea Syphilis Chancroid Trichomoniasis HSV vi. Recognize the most common side effects and drug interactions of the antimicrobials used in the treatment of STI’s See above vii. Develop plan for STI prevention Provide condoms, advice abstinence or reduce number of sexual partners, PrEP if high risk for HIV Objective 14: Crystal Arthropathies & Spondyloarthropathies i. Recognize the signs and symptoms of gout Manifests as an acutely painful monoarticular arthritis, possibly becoming chronic after years of progressively more severe & frequent episodes, interspersed with variable symptom-free periods Hyperuricemia is a marker for gout, but each can exist without the other The first MTP joint is involved in 50% of initial acute gouty attacks (podagra) aspiration will show negatively birefringent monosodium urate crystals ii. Recall the most important factors in the development of acute gouty arthritis Manifestations of gout are proportional to the degree and duration of hyperuricemia o Multiple genetic & environmental factors can affect uric acid concentration o Uric acid is derived from purines; therefore, uric acid levels may be increased with a purine-rich diet (eg., the typical American diet, beer, seafood, etc.), as well as from endogenous production of purines Primary hyperuricemia: inborn errors of metabolism, either reduced excretion (90% of patients) or increased production (10%) of uric acid Secondary hyperuricemia: results from diseases or therapies that raise uric acid levels o Myeloproliferative and lymphoproliferative diseases, hemolytic anemia, multiple myeloma, and other malignancies result in overproduction o Renal disease, thiazide diuretics, salicylates, alcohol, nicotinic acid, & chronic lead intoxication (saturnine gout) all cause underexcretion of uric acid o Chemotherapy for hematologic or myeloproliferative disorders can result in gouty nephropathy ▪ Prevention with adequate hydration and allopurinol iii. Identify the causes of secondary gout See above iv. Define the mechanism of action of Allopurinol and use in the prophylaxis of gout Allopurinol is a xanthine oxidase inhibitor that decreases uric acid production, but also produces a more soluble metabolite Used after resolution of gout attack for prophylaxis (do NOT use during an acute attack) v. Recognize the diseases associated with calcium pyrophosphate deposition disease Associated with hyperparathyroidism (increased calcium), hypothyroidism, hypomagnesemia, hypophosphatemia, hemochromatosis, amyloidosis, previous joint injury vi. Formulate an evaluation for a suspected new diagnosis of calcium pyrophosphate deposition disease CBC (Hgb/Hct & WBC), CMP (calcium, magnesium levels, ALP), phosphorus, TSH, iron studies (ferritin, transferrin, serum iron) Confirmation with linear deposition in cartilage on x-ray, (+) ANA and RF, aspiration will show rod-shaped crystals with blunt ends that are positively birefringent vii. Recognize the signs and symptoms of ankylosing spondylitis and the classic radiographic appearance Manifests as vague, somewhat diffuse low back pain, generally felt in the buttocks or sacroiliac area, but also in the lumbar region, more commonly in men ages 15-35 years old o With time, pain becomes more persistent and bilateral o After a period of inactivity (for example, upon awakening in the morning), back stiffness is common & can be relieved with activity or a hot shower/bath o Can also cause sleep disturbances, leading to fatigue, & can be associated with systemic symptoms, such as malaise, low-grade fever, and weight loss Classic radiographic findings of ankylosing spondylitis are the “bamboo spine” due to ossification of the supraspinous ligament o Early radiographic findings include bilateral sacro-iliitis and early axial (lower lumbar spine) ankylosis. Typical X-ray findings are florid spondylitis (Romanus lesions), florid diskitis (Andersson lesions), early axial ankylosis, enthesitis, syndesmophytes and insufficiency fractures viii. Recall the classic triad of reactive arthritis (Reiter syndrome) and the suggested causes Only 1/3 of patients with reactive arthritis will present with the classic triad of urethritis, conjunct