BARKELY ACUTE NURSE PRACTITIONER EXAMS TEST BANK WITH ACTUAL CORRECT QUESTIONS AND VERIF, Exams of Nursing

Download BARKELY ACUTE NURSE PRACTITIONER EXAMS TEST BANK WITH ACTUAL CORRECT QUESTIONS AND VERIF and more Exams Nursing in PDF only on Docsity! 1 | P a g e BARKELY ACUTE NURSE PRACTITIONER EXAMS TEST BANK WITH ACTUAL CORRECT QUESTIONS AND VERIFIED DETAILED RATIONALES ANSWERS LATEST UPDATE ALREADY GRADED A+ Prophylactic treatment for migraine headaches includes the use of: A. amitriptyline. B. ergot derivative. C. naproxen sodium. D. clonidine. A Antiepileptic drugs useful for preventing migraine headaches include all of the following except: A. divalproex. B. valproate. C. lamotrigine. D. topiramate. C In tension-type headache, which of the following is true? A. Photophobia is seldom reported. B. The pain is typically described as "pressing" in quality. C. The headache is usually unilateral. D. Physical activity usually makes the discomfort worse. B The mechanism of action of triptans is as a(n): A. selective serotonin receptor agonist. B. dopamine antagonist. C. vasoconstrictor. D. inhibitor of leukotriene synthesis. A The use of neuroleptics such as prochlorperazine (Compazine) and promethazine (Phenergan) in migraine therapy should be limited to less than three times per week because of their: A. addictive potential. 2 | P a g e B. extrapyramidal movement risk. C. ability to cause rebound headache. D. sedative effect. B With appropriately prescribed headache prophylactic therapy, the patient should be informed to expect: A. virtual resolution of headaches. B. no fewer but less severe headaches. C. approximately 50% reduction in the number of headaches. D. that lifelong therapy is advised. C A 48-year-old woman presents with a monthly 4-day premenstrual migraine headache, poorly responsive to triptans and analgesics, and accompanied by vasomotor symptoms (hot flashes). The clinician considers pre- scribing all of the following except: A. continuous monophasic oral contraceptive. B. phasic combined oral contraceptive with a 7-day-per-month withdrawal period. C. low-dose estrogen patch use during the premenstrual week. D. triptan prophylaxis. B A first-line prophylactic treatment option for the prevention of tension-type headache is: A. nortriptyline. B. verapamil. C. carbamazepine. D. valproate. A A 47-year-old woman experiences occasional migraine with aura and reports partial relief with zolmitriptan. You decide to add which of the following to augment the pain control by the triptan? A. lamotrigine B. gabapentin C. naproxen sodium D. magnesium C A 68-year-old man presents with new onset of headaches. He describes the pain as bilateral frontal to occipital and most severe when he arises in the morn- ing and when coughing. He feels much better by mid- afternoon. The history is most consistent with headache caused by: ICP Systemic corticosteroid therapy would be most appropriate in treating: A. tension-type headache. B. migraines occurring on a weekly basis. 5 | P a g e • Subjective numbness or tingling • Headache causing awakening from sleep • Headache worse with Valsalva maneuver • Accelerating, new-onset headache • Abnormal neurological examination • Increasing age • More likely nonacute finding such as old infarct, atrophy For HA, unlikely to correlate with abnormal neuroimaging; neuroimaging unlikely to yield helpful clinical information • Neurological examination normal • Long-standing history of similar headache • "Worst headache of my life" HA imaging Consensus-based principles • Testing should be avoided if it would not lead to a change in management • Not recommended if individual no more likely than general population to have significant abnormality • Testing not normally recommended as population policy, although may make sense at individual level (e.g., with patient or provider fear) CT scan vs MRI for HA where does the aura in migraines come from and about migraine with aura The aura is a recurrent neurological symptom that arises from the cerebral cortex or brainstem. 20% of migraine sufferers have aura Typically, the aura develops over 5 to 20 minutes, lasts less than 1 hour, and is accompanied or followed by migraine. Patients who have migraines with aura do not have more severe headaches than patients with-out aura, but the former patients are more likely to be offered a fuller range of therapies. 6 | P a g e Patients without aura may be misdiagnosed as having tension-type headaches and are often not offered headache therapies specifically suited for migraines, such as the triptans. Abortive HA tx acetaminophen; NSAIDs; and combi- nation products such as butalbital with acetaminophen, and acetaminophen, aspirin, and caffeine. when are cluster HA most common middle aged men esp with etoh and tobacco suicide HA cluster tx for cluster HA Treatment includes reduction of triggers, such as tobacco and alcohol use, and initiation of prophylactic therapy and appropriate abortive therapy (triptans, high-dose NSAIDs, and high-flow oxygen). Potential Lifestyle, Health Status or Medication Triggers Influencing the Onset or Severity of Migraine Symptoms: Menses, ovulation, or pregnancy Birth control/hormone replacement (progesterone) therapy Illness of virtually any kind, whether acute or chronic Intense or strenuous activity/exercise Sleeping too much/too little/jet lag Fasting/missing meals Bright or flickering lights Excessive or repetitive noises Odors/fragrances/tobacco smoke Weather/seasonal changes High altitudes Medications Stress/stress letdown Potential Dietary Triggers Influencing the Onset or Severity of Migraine Symptoms: Sour cream Ripened cheeses (cheddar, Stilton, Brie, Camembert) Sausage, bologna, salami, pepperoni, summer sausage, hot dogs Pizza 7 | P a g e Chicken liver, pâté Herring (pickled or dried) Any pickled, fermented, or marinated food Monosodium glutamate (MSG) (soy sauce, meat tenderizers, seasoned salt) Freshly baked yeast products, sourdough bread Chocolate Nuts or nut butters Broad beans, lima beans, fava beans, snow peas Onions Figs, raisins, papayas, avocados, red plums Citrus fruits Bananas Caffeinated beverages (tea, coffee, cola) Alcoholic beverages (wine, beer, whiskey) Aspartame/phenylalanine-containing foods or beverages Oral products for migraines 30min- 1 hr to kick in best suited from slow onset and minimum GI issues use ASAP least expensive and facilitates patient self care Injectable migraine relief Imitrex (sumatriptan and dihydroergotamine (DHE) rapid onset (15-30 min) good if GI upset assoc sx Sumatriptan is self injected DHE is IV along with hydration expensive some of the ergot and triptan are available as nasal spray and with similar tolerance can use analgesic or antiemetic for pain control or GI upset as well Triptans for HA usually just for migraines Selective serotonin receptor agonist inc uptake 10 | P a g e Brudzinski sign one of the clinical signs of meningitis (PE Neck) A positive sign of meningitis, in which there is an involuntary flexion of the arm, hip, and knee when the patient's neck is passively flexed. Of the following, which is the least likely bacterial source to cause meningitis? A. colonization of the skin B. colonization of the nose and throat C. extension of acute otitis media D. extension of bacterial rhinosinusitis A When evaluating the person who has bacterial meningi- tis, the NP expects to find cerebrospinal fluid (CSF) results of: A. low protein. B. predominance of lymphocytes. C. glucose at about 30% of serum levels. D. low opening pressure. C Physical examination findings in papilledema include: A. arteriovenous nicking. B. macular hyperpigmentation. C. optic disk bulging. D. pupillary constriction. C Which of the following organisms is a gram-negative diplococcus? A. Streptococcus pneumoniae B. Neisseria meningitidis C. Staphylococcus aureus D. Haemophilus influenzae B Do I need to know these? Which of the following signs and symptoms most likely suggests meningitis cause by N. meningitidis? A. a purpura or a petechial rash B. absence of fever C. development of encephalitis D. absence of nuchal rigidity 11 | P a g e A During an outbreak of meningococcal meningitis, all of the following can be used as chemoprophylaxis Single dose Ceftriaxone Multiple doses Rifampin Single dose MCV4 ceftriaxone Rocephin Third−generation cephalosporin: active against resistant bacteria including gonococci, H influenzae, and other gram−negative organisms. Crosses the blood−brain barrier rifampin TB Antimicrobial: inhibitor of DNA−dependent RNA polymerase used in drug regimens for tuberculosis and the meningococcal carrier state. Tox: hepatic dysfunction, induction of liver drug−metabolizing enzymes (drug interactions), flu−like syndrome with intermittent dosing Meningitis infection of meninges, CSF, and ventricles can be bacterial, viral, fungal etc most common cause is encephalitis, which can cause flu like sx, fever, HA, confusion, sz, sensory or motor impairment Bacterial meningitis Classic Triad: fever, HA, nuchal ridgidity CSF findings: ■ Low glucose, PMN predominance Kernig and Brudzinski signs indicate A 25-year-old female presents to her primary care provider reporting fever, headache, nuchal rigidity, and decreased consciousness. She was previously treated for sinusitis. Which of the following is the most likely diagnosis? An acute inflammation of the meningeal tissues surrounding the brain and the spinal cord; specifically, 12 | P a g e the arachnoid mater and the CSF; diagnosed by increased CSF presssure, increased WBCs, increased proteins, and decreased glucose viral meningitis elevated WBC, predominantly lympocytes, normal CSF protein, normal CSF glucose, negative gram stain. similar symptoms as bacterial just not as severe and less risk for mortality encephalitis inflammation of the brain Need imaging, CT/MRI LP Multiple Sclerosis A chronic disease of the central nervous system marked by damage to the myelin sheath. Plaques occur in the brain and spinal cord causing tremor, weakness, incoordination, paresthesia, and disturbances in vision and speech Sx occur acutely, worsen over a few days, can last weeks, followed by period of partial to full resolution Descending weakness, Charcot's sign (intention tremor, nystagmus, scanning speech) MS risk factors affects 15 to 50 years of age, women more than men, genetic factor, viruses such as epstein-barr, white with European dissent,thyroid disease, DM1, inflammatory bowel disease, high risk areas after puberty. MS diagnosis MRI scans, CSF analysis MS treatment MS treatment generally falls into three categories: therapy for relapses, long-term disease-modifying medications, and symptomatic management. interferon beta-1b to attenuate disease progression MS classification relapsing-remitting is 85% of pts primary progressive where they do not fully resolve 15 | P a g e AKA temporal arteritis autoimmune vasculitis most common in patients 50 to 85 years old; average age at onset is 70 years. systemic disease affecting medium-sized and large-sized vessels also causes inflammation of the temporal artery Inflammation and swelling of the arteries causes decreased blood flow and its associated symptoms. The swelling normally affects just part of an artery with sections of normal artery in between. Extracranial branches of the carotid artery are often involved; this often results in a tender or nodular, pulseless vessel, usually the temporal artery, accompanied by a severe unilateral headache. On examination, the temporal artery is occasionally normal, however. temporal artery granulomatous vasculitis; ipsilateral blindness (ophthalmic artery) can cause vision loss secondary to vasculitic occlusion and involves the arteries to the optic disk Giant cell arteritis risk factors older female of northern european descent giant cell arteritis diagnosis and tx biopsy of temporal artery Don't wait for biposy start high dose Prednisone right away. giant cell arteritis concomitant diseases acute pancreatitis. psoriatic arthritis. reactive arthritis. ulcer loss of epidermis and dermis ex: pressure sore 16 | P a g e atrophy loss of skin markings and full skin thickness ex: Area treated excessively with higher potency corticosteroids fissure narrow linear crack into epidermis, exposing dermis ex: split lip, athletes foot reticular netlike cluster ex: multiple skin conditions wheal circumscribed area of skin edema ex: hive 17 | P a g e pustule vesicle-like lesion with purulent content ex: impetigo, acne patch flat discoloration greater than 1 cm in diameter example is vitiligo plaque raised lesion, larger than 1 cm, may be same or different color from the surrounding skin ex: psoriasis macule flat discoloration less than 1 cm in diameter example is a freckle confluent or coalescent 20 | P a g e marks produced by scratching ex: Seen in areas of pruritic skin diseases erosion Partial focal loss of epidermis; heals without scarring ex: Area exposed after bullous lesion opens scale raised flaking lesion ex: dandruff, psoriasis dermatomal along a neurocutaneous dermatome ex: herpes zoster linear in streaks ex: poison ivy how much grams of topical ointment 21 | P a g e 2 g for hands, face, head, genitals (28g BID/1wk) 3g for arms, ant or post trunk (42g BID/1wk) 6g for 1 leg (84g BID 1 wk) 30-60g for entire body (420-840g BID 1 wk) greatest place of absorption for topical agent face type of topical agent with maximal absorption ointment not gel, lotion, or cream the less viscous, the less absorbed corticosteroids often used to treat inflammatory and allergic derm disorders mech of action includes immunosuppression and inflammatory properties potency is based on vasoconstrictive activity the most potent steroids, like beclomethasone, have much more vasoconstrictive action hydrocortisone is the least strong low potency topical corticosteroids Hydrocortisone (0.5%, 1%, 2.5%) Fluocinolone acetonide 0.01% (Synalar) Triamcinolone acetonide 0.025% (Aristocort) Fluocinolone acetonide 0.025% (Synalar) Hydrocortisone butyrate 0.1% Hydrocortisone valerate 0.2% (Westcort) Triamcinolone acetonide 0.1% midrange potency topical corticosteroids Betamethasone dipropionate, augmented, 0.05% (Diprolene AF cream) Mometasone furoate 0.1% (Elocon ointment) 22 | P a g e high potency topical corticosteroids Fluocinolone acetonide 0.2% (Synalar-HP) Desoximetasone 0.25% (Topicort) Fluocinonide 0.05% (Lidex) Super high potency topical corticosteroids Betamethasone dipropionate, augmented, 0.05% (Diprolene gel, ointment) Clobetasol propionate 0.05% (Temovate) Halobetasol propionate 0.05% (Ultravate 0.05%) histamine A chemical released by the body during an inflammatory response that causes the blood vessels to dilate antihistamine works by blocking histamine-1 receptor sites How are systemic antihistamines divided into groups standard or first generation ex: Benadryl or Chlor-Trimeton newer or 2nd gen ex: Loratidine (Claritin), Clarinex, Cetirizine (Zyrtec), Allegra, Xyzal 1st gen antihistamine examples and mech of action and AE standard or first generation ex: Benadryl or Chlor-Trimeton 1st gen cross BBB and cause sedation and should be taken with caution. anticholinergic activity can dry secretions, cause visual changes and urinary retention, which is bad for older men with BPH older adults using can have negative cognitive effects 2nd gen antihistamine examples and mech of action and AE newer or 2nd gen ex: Loratidine (Claritin), Clarinex, Cetirizine (Zyrtec), Allegra, Xyzal 25 | P a g e Health promotion and disease prevention. obtaining health hx. interview tech and analyzation. eval s/sx, PE with synth findings. know normal and abnormal. Lab and dx testing- ordering and performing to support and dx. never do a test that doesnt fit. EBP- plan of care based on, guidelines. Assume resources are available to be cost effective EBP. Plan of care and follow up Legal and ethical- malpractice, confident, patient advocacy and competency (some more than others cultural comp, principles of epi healthcare econ and mgmt what do you need to practice RN license, national NP cert, NP license, state rx authority, fed DEA authority, cred with agency and insurance companies clinicL decision making process ADPIE Assessment- subjective-health hx HPI, objective- PE, available diagnostic results Diagnosis- analyze assessment data to determine working dx, keep in mind common dxs Plan- plan of care and prescribe intervention to attain expected outcome Implementation Evaluate- post diagnosis. eval of pts attainment of tx goals and keeping in mind need to adjust cranial nerves olfactory, optic, oculomotor, trochlear, trigeminal, abducens, facial, vestibulocochlear, glossopharyngeal, vagus, accessory, hypoglossal heart anatomy orthopnea= heart failure most of the time 26 | P a g e holosystolic takes all of systole and is the same all of systole VSD, tricuspid regurgitation, mitral regurgitation look at exam content outline question stem: First ABC, airway, breathing, circulation what is the priority question stem: initially assess b4 dx then plan, then intervene, then evaluate response to care. ADPIE question stem: most appropriate EBP guides the choice of dx, intervention etc oxyhemoglobin dissociation curve the relationship between hemoglobin saturation and PO2 is shown by ____ curve Relationship between available oxygen and amount of oxygen carried by hemoglobin. low Sa02 is a late sign in asthma flare post menopause risk factor cardiovascular evidence hierarchy primary prevention -addresses the needs of healthy clients to promote health and prevent disease with specific precaution secondary prevention 27 | P a g e -focuses on early identification of individuals or communities experiencing illness, providing treatment, and conducting activities that are geared to prevent worsening health statu tertiary prevention -aims to prevent the long-term consequences of a chronic illness or disability and to support optimal functionin stridor upper airway obstruction active immunity A form of acquired immunity in which the body produces its own antibodies against disease-causing antigens. passive immunity An individual does not produce his or her own antibodies, but rather receives them directly from another source, such as mother to infant through breast milk onset is within hours but duration is limited, 9 mo or so when delay immunization mod-severe illness with or without fever if youre thinking of admitting to hosp or ED IZ to avoid with hx of anaphylactic reaction to neomycin IPV, MMR, varicella IZ to avoid with hx of anaphylactic reaction to Streptomycin, polymyxin B, neomycin IPV, smallpox IZ to avoid with hx of anaphylactic reaction to bakers yeast Hep B IZ to avoid with hx of anaphylactic reaction to gelatin, neomycin varicella zoster IZ to avoid with hx of anaphylactic reaction to gelatin MMR anaphylaxis a severe response to an allergen in which the symptoms develop quickly, and without help, the patient can die within a few minutes. 30 | P a g e premature destruction (hemolytic anemima) short RBC lifespan <90 Hemogram evaluation in anemia need CBC with RBC indicies dont need CBC w/diff look at HCT, Hb, RBC values should be proportionally decreased Normal H&H ratio=1:3 ex: 10g/dl=30%, 12g/dl=36% Exception: HCT artificially elevated with major dehydration. Normally HCT is circulating blood dependent, Hb is not RBC size Wintrobe's classification of anemia by evaluation of MCV Microcytic: small cell with MCV<80 fL Normocytic 80-96 Macrocytic= MCV>96 key to knowing and interpreting RBC Hb content reflected by MCH (mean cell hemoglobin) Hb is source of cells color (chromic) Hb is 90% of RBC volume Normochromic: normal color=MCHC=31-37 Hypochromic=pale=MCHC<31 RDW RBC distribution width index of variation in RBC size 31 | P a g e NL=11.5-15% ABN: >15% indicating that new cells differ in size early lab indicator of an evolving microcytic or macrocytic anemia As MCV decreases As MCV increases RDW increases RDW increases high RDW =new cells differ in size from old cells reticulocyte % NL response to anemia is inc RTC healthy=1-2% NL response to anemia is>2% (reticulocytosis) cytosis went up normocytic normochromic anemia MCV=80-96 NL RDW NL MCHC most common etiology=acute blood loss or ACD is there a way to practice identifying anemias over and over by looking at labs and patient hx? microcytic hypochromic anemia with elevated RDW what anemia and what is next step? IDA next step: Ferritin for estimate of iron stores small and pale cells always go together Microcytic, hypochromic anemia with NL RDW DX and next step 32 | P a g e Alpha or beta thalassemia minor (trait) Alpha at risk: Asia and africa (AAA) Beta at risk: Africa, Mediterranean, Middle East (BAMME) small pale cells that are all around the same size but lots of them (inc RBC) next step: Hb electrophoresis Macrocytic, normochromic, with elevated RDW DX and next step Pernicious anemia (most common), dietary induced (B12, folate) (uncommon) MCHC is NL because Iron has nothing to do with it Next step: test B12 and folate Pernicious is generally a much lower H&H Drug induced macrocytosis usually without anemia common etiologies Etiology: Carbamazepine, AZT, Valproic Acid, Phenytoin, alcohol reversable when stop med but not always possible intervention in anemia treat the underlying cause if severe or chronic consider multiple causes replace the micronutrients like Fe or vitamins EPO or Procrit: helpful in severe anemia, especially if renal failure (check GFR if needed) most common anemia in childhood, preggo, reproductive years, elderly IDAx3 elderly: ACD so we will see a lot of IDA questions most important source of body's iron supply 35 | P a g e comorbidites immunocompromise ABRS ABX tx 1st and 2nd line Amox-Clavulanate 500mg/125mg PO TID or 875mg/125 mg PO BID (better cuz Augmentin tough on stomach) (Amox for DRSP, Clav inhibit beta lactamase) 2nd Amox-Clavu 2000mg/125mg PO BID or Doxy 100mg PO BID or 200mg POD (Doxy is inexpensive, thats why here, but has DRSP risk) (also preg risk cat D) If beta lactam allergy Doxy (no DRSP so we should use this if no risk) Levoflox (flouroquinolone) (DRSP coverage) Moxiflox (flouroquinolone) (DRSP coverage) CYP 450 drug drug interaction substrate: utilizes a specific enzymatic pathway Viagra, statins, effexor, xanax etc 50% of Rx meds CYP450 3A4 substrate Inhibitor: block specific enzymatic pathway and keeps substrate from exiting Ex: erythro, clarithro, so if you use with 3A4, can inc substrate levels and poss toxicity so simvastatin and erythro is a bad combo risk for Rhabdo Inducer: pushes substrate out exit pathway leads to reduce substrate Ex: St Johns Wort, so with 3A4 can reduce therapeutic effect of the 3A4 Bad mix with select antiretrovirals (HIV drugs), oral contraceptives, cyclosporine (organ rejection) allergic rhinitis is like.. 36 | P a g e asthma in the head inflammatory IGE mediated environmental risks are similar allergic rhinitis 1st line tx allergen avoidance and environmental control allergic rhinitis tx (control sx) intranasal corticosteroids flonase triamcinolone LTRA not first line montelukast Mech of action: inflammatory mediator prevention allergic rhinitis (relieve sx) claritin, zyrtec intranasal antihistamine ocular antihistamine-olopatadine slow growing painless oral lesion squamous cell carcinoma? biopsy, CT on neck syphilitic chancre Firm painless ulcer that develops internally and often is undetected aphthous stomatitis inflammation of the mouth with small, painful ulcers puff out your cheeks CN 7 shrug your shoulders CN 11 37 | P a g e stick out your tongue CN 12 initial response to Bells Palsy with no other sx or hx initiate a course of oral corticosteroids lubricating eyedrops maybe biting cheek when to test for visual acuity any comprehensive PE on adult or child anyone with an eye complaint red eye, painful eye, new onset vision change refer to opthamology eye referral triad red eye, painful eye, new onset vision change refer to opthamology myopia Nearsightedness presbyopia Impairment of vision due to old age retinal arteries vs veins thick vs narrow arteries always narrower glaucoma too much pressure in eyeball deeply cupped optic disk NL optic disk NL because of balance between intraocular pressure and intracranial pressure papilledema too much pressure in the brain etiology- peripheral vision loss untreated open angle vlaucoma etiology- need for increased illumination 40 | P a g e Where is the oldest lesion and when did it occur? Where is the newest lesion and when did it occur? allows for assessment of evolution primary skin lesion from disease process itself not altered by outside manipulation, treatment, natural course of disease ex: vesicle secondary lesions altered by outside manipulation, treatment, natural course of disease ex: crust because develops when vesicle ruptures molluscum contagiosum Smooth wax like round (dome shaped) papules 5 mm size. Central umbilication with white plug impetigo bacterial skin infection characterized by isolated pustules that become crusted and rupture vitiligo a skin condition resulting from the destruction of the melanocytes due to unknown causes autoimmune 41 | P a g e psoriasis vulgaris What is the most common variant of psoriasis? Knees and tips of elbow Auspitz sign when someone scrapes one of the scales and it starts to bleed 2nd degree burn a burn involving the epidermis and the dermis; characterised by erythema, hyperesthesia, and visitations (blisters) thrombocytopenia low platelet count What is the most common: Cause of abnormal bleeding? meningococcal meningitis Inflammation of the meningeal coverings of the brain and spinal cord that can be highly contagious; isolate pt for 24 h after starting antibiotics blueberry muffin rash Description of rash characteristic of congenital rubella. A 17 year old female patient presents to your office with her mom. The patient complains of irritated and inflamed skin on her ear lobes. The patient reports that she recently had her ears pierced and has started wearing earring for the first time. What condition do these findings suggest? nickel allergy chicken pox vs shingles shingles is mostly >50 or hx of varicella Have to have had chicken pox 42 | P a g e cant give another person zoster but person with zoster can give non immune person chicken pox zoster not systemic normally varicella start trunk and move to limbs zoster complications postherpetic neuralgia, opthamalogic involvement, superimposed bacterial infection postherpetic neuralgia Postherpetic neuralgia is a nerve pain due to damage caused by the varicella zoster virus. varicella treatment acyclovir early 24-48 hrs and in high risk for underlying problems can help minimize severity avoid aspirin due to Reyes and NSAID due to necrotizing fascitis Reyes syndrome life threatening swelling of brain and liver, most often affecting children and teens. linked to aspirin use. hx of febrile viral illness(chickenpox, influenza) and aspirin Zoster tx acyclovir early analgesia tx itch systemic and local zostavax age recommended > 60 years old actinic keratosis scaly plaque precursor to Squamous cell carcinoma, and is in mostly sun exposed areas actinic keratosis treatment 5FU cream (topical chemo) and use liquid nitrogen basal cell carcinoma vs Squamous cell carcinoma BCC- more common, sun exposed, de novo, papule nodule w/out central erosion, pearly waxy. Tissue destruction risk but low metastatic risk 45 | P a g e Caused by toxin-producing strain of S. aureus, begins as red macules that progress to bullous (fluid- filled) eruptions on an erythematous base; after rupture, a clear, thin, varnish-like coating forms over denuded area; can be mistaken for cigarette burns often requires systemic antimicrobial erysipelas Streptococcus pyogenes Symptoms include edema, redness, fever, pain, lymphadenopathy, can progress to septicemia and local necrosis of skin need systemic antimicrobial cellulitis Inflammation of subcutaneous, loose connective tissue; skin infection likely cause by Strep Pyo, Staph Aur, MRSA require systemic antimicrobial nonpururlent vs pururlent brown recluse spider bite Lives in dark, undisturbed areas, violin mark on back, Mild stinging, fatty areas become necrotic in hours, "blue-gray" bullae, can cause hemolytic anemia, DIC, death. Tx: Ice, elevation, abx, ASA anaphylaxis is likely with one of these 3 conditions skin and or mucosa AND either respiratory compromise OR BP or end organ dysfunction 46 | P a g e age to start flu vax 6 mo LAIV precaution <2 >49 2-17 and receiving aspirin hx severe allergic reaction preggo immunocompromised 2-4 with asthma or wheezing episode in the last 12 mo influenza antiviral med in the last 18 hrs health belief model Developed in 1974, one of the oldest social cognition models. Whether a person will choose to engage in healthy behaviors in order to reduce or prevent chance of disease and death. Happens when they think something bad's gonna happen to them if they don't stop. tap water temperature <120 degrees 5 min at 120 =3rd degree burn 3rd degree burn a burn involving all layers of the skin; characterized by the destruction of the epidermis and dermis, with damage or destruction of subcutaneous tissue. vaccines by 6 months Hep B at birth RV DTAP Hib PCV IPV IIV (flu shot) vaccines by 1 yr same as 6 mo MMR VAR Hep A stages of change precontemplation, contemplation, preparation, action, maintenance 47 | P a g e 5 A's Successful intervention based upon willingness to quit Ask (ask and document every visit) Advise (urge to quit) Assess (are they willing to) Assist (counseling and pharmacotherapy) Arrange (follow up contact preferably within a week) 3 top killers in adults in US Heart Disease, cancer, Chronic lower respiratory diseases leading sites for new cancer cases Male: prostate and lung Female Breast and lung leading cancer deaths Male: lung, prostate Female: Lung, Breast colorectal screen FOBT >50 annual Sigmoidoscopy at 50 every 5 yrs (colon if pos) Colonoscopy every 10 yrs after 50 low dose CT for smokers 55-74yo >30yr Pack hx <15 yrs since quit breast cancer screen Mammography q2Y starting at age 50 (USPSTF) or 40 (ACOG) cervical cancer screen 21-29 - PAP every 3 years, 30-65 PAP every 3 years or PAP + HPV testing every 5 years normal MCV 80-96 hematocrit (f) 37-47% ; (m) 42-52 % hemoglobin 50 | P a g e inflammation of the outer ear Eardrops: cipro; acetic acid drops might be effective in mild episodes; antibiotics with steroid otic drops are the treatment of choice. Symptoms should be improved in 7 days but can take up to 2 weeks. ABX: cipro exudative pharyngitis first line Penicillin Alt: erythromycin Non purulent (cellulitis/erysipelas/impetigo) tx plan moderate- IV Rx Mild- more often in primary care Penicillin VK Cephalexin Dicloxacillin Clindamycin Purulent (Abscess/carbuncle/furuncle) tx plan moderate- I&D C&S empiric Rx- Bactrim or Doxy If results of C&S- MRSA- Bactrim MSSA- Doxy or cephalexin Mild- I&D 1st degree burn a burn involving only the epidermis; characterised by erythema (redness) and hyperethesia (excessive sensation) tx: cold compress, lotion or ointment, tylenol or ibu second degree burn treatment Cool, wrap sterile gauze loosely around burn, watch for infection, use sunscreen on area for a year burn blister tx 51 | P a g e leave intact when possible debride larger with thin walls that prevent movement of a joint or likely to rupture burn basic tx topical agent and dressing- Bacitracin etc, duoderm etc pain control- 30 min befored dressing promote healing- hydrate, teach clean technique prevent infxn and desiccation desiccation drying out rocky mountain spotted fever disease transmitted by American dog tick Caused by Rickettsia rickettsii Sx: rash on palms and soles (migrating to wrists, ankles, then trunk), HA, fever. Endemic to East Coast (in spite of its name). how to think about thyroid know patho and think conceptually thyroid produces 2 hormones t4 and t3 what do t4 and t3 do act as cellular energy release catalysts and influence the function and health of every cell in the body so think about that happens when there is too much or too little with the hormones in hypothyroidism, what happens to the skin? thick dry in hypothyroidism, what happens to the reflexes? hung up patellar reflex, slow arc out, slow arc back, overall hyporeflexia hung up, knee tapped goes out slowly but comes back even slower in hypothyroidism, what happens to the mentation cant make sense, thoughts too slow in hypothyroidism, what happens to the weight 52 | P a g e small gain 5-10lbs, largely fluid in hypothyroidism, what happens to the stool pattern constipation in hypothyroidism, what happens to the menstrual menorrhagia in hypothyroidism, what happens to the heat/cold tolerance easily cold 3 common hypothyroid etilogies hashimoto post-radioactive iodine tx select meds hashimoto thyroiditis hypothyroid autoimmune Most common cause of goiter and primary hypothyroidism in adults in developed countries. Autoimmune disorder with circulating antithyroid antibody. post-radioactive iodine tx causes hypothyroid S/P graves disease tx, thyroid cancer tx meds that cause hypothyroid lithium, amiodarone, interferon etc lithium Mood Stabilizer Bipolar Disorder amiodarone Antiarrhythmic interferon 55 | P a g e dont need endo mostly tx with levothyroxine calculate body weight adult need more than older, but kids need most mcg/kg/d need to inc with preggo by at least 33% for all check TSH after at least 8 wks of tx levothyroxine bioidentical hormone Synthroid low TSH (<0.15) FT4=79 so high hyperthyroid hyperthyroid intervention Beta blocker to counteract tachycardia, tremor Usually tx together with ENDO Antithyroid med: Propylthiouracil (PTU) Radioactive Iodine with end result of thyroid ablation or hypothyroid TSH inc (8.9) FT4: NL subclinical hypothyroid AACE recc tx with TSH >5 if: has goiter problems that affect infertility, preggo etc malignancy likelyhood of thyroid nodule unlikely 5% most consistent findings with malignant thyroid nodule 56 | P a g e Hx of head and neck irradiation >4cm Firm nontender on palpation nonmobile persistent nontender lymphadenopathy dysphonia hemptysis dysphonia difficulty producing speech sounds, usually due to hoarseness eval of thyroid nodule TSH, US to determine location and characteristics TSH low? Thyroid scan- Hot? ablation or Sg not hot? biopsy TSH ok? Biopsy primary hyperparathyroidism etiology inc PTH Etiology: overactivity of 1+ of 4 parathyroid glands, by enlargement (hyperplasia), adenoma (benign), or malignant tumor PTH parathyroid hormone Appropriate body calcium levels too much=hypercalcemia Primary hyperparathyroid clinical presentation moans, groans, stones, and bones with psychic overtones low E, poor concentration, memory, depression, osteoporosis, insomnia, GERD, dec libido, hair loss, bone and joint aches. Kidney stones, HTN, arrythmia, AFIB, liver, ABN protein Primary hyperparathyroid clinical Diagnosis By elevated serum Ca confirm elevated PTH 57 | P a g e Test 24h Urine calcium to determine severity get consultation Primary hyperparathyroid intervention Sg to remove problematic gland (95% cure) Cinacalcet- Tx if pt also has CKD or PTH Cancer consider HRT or something to prevent bone loss Secondary hyperparathyroidism etiology Result of another condition that lowers Ca and therefore causes the Parathyroid to overproduce PTH Etiology: Severe Ca or Vit D deficiency, CKD Secondary hyperparathyroidism clinical presentation similar to primary moans, groans, stones, and bones with psychic overtones Secondary hyperparathyroidism diagnosis find elevated serum and PTH presence of severe renal dysfunction often on dialysis Secondary hyperparathyroidism intervention Vit D analogues and calcimimetics Sg only if med fails Ensure Ca and Vit D intake screening thyroid reccomendations all over the place >35 every 5 yrs >60 >50 primary HA not assoc with other diZ likely interplay of genetic, developmental, or environ factors 60 | P a g e posture tinted lens HA analgesics NSAID, tylenol etc best taken at onset HA analgesic education limit 2 tx days per wk to avoid rebound use with triptan to enhance relief Migraine specific meds Triptans Ergot derivatives take an onset Migraine specific meds education caution preggo and CVD, HTN Prophylactic meds for migraine HA BB Tricyclics (triptyline) Antiepileptic nutrition supplements: variety Lithium (spec for cluster) dont use CCB Prophylactic meds for migraine HA indication for use use of any product 3x/wk 2+ migraines per month with debilitating sx 3+ days poor sx relief from abortive tx rescue therapy for HA 61 | P a g e opioids, antiemetics, short course systemic corticosteroids use when standard is ineffective when is referral to specialist necessary for HA beyond scope need dx supported or clarified (ex: RA, lupus) complex health prob ongoing (CVD) fails to respond to standard EBP when neuroimaging with HA secondary HA HA MRI vs CT MRI expensive 4x more CT without contrast is cheapest for acute bleed CT with contrast for Tumor/abscess MRI- better for soft tissue so tumor, lesions giant cell arteritis presentation Present with new headache (unilateral or bilateral); scalp pain and temporal tenderness; and jaw claudication. giant cell arteritis initial response and confirm erythrocyte sedimentation rate confirm with biopsy systemic corticosteroid use is rf for duodenal or gastric ulcer gastric duodenal would be H pylori Giant cell arteritis etiology 62 | P a g e Autoimmune vasculitis affects medium and large vessels and temporal artery inflammation and swelling leads to dec blood floe and assoc sx 50-85yo Giant cell arteritis diagnosis inc CRP and ESR definitive dx with biopsy Giant cell arteritis intervention aim to reduce pain and minimize risk of blind high dose systemic corticosteroid f/u with careful reduce dose and continued for 6 mo-2 yrs Aspirin for stroke risk PPI for GI protection Bisphosphonate for bone protection meds to minimize risk of long term systemic corticosteroid Aspirin for stroke risk PPI for GI protection Bisphosphonate for bone protection DX of GERD typical sx of heartburn and regurgitation just H&P, dont need scope etc when endoscopy with GERD in presence of alarming findings dysphagia, odynophagia, involuntary wt loss, hematemesis, melena, chest pain, choking screen pts with high risk for complications H pylori and GERD no indicated no connection 65 | P a g e A 44 year old alcoholic male presents with severe epigastric pain that began shortly after a heavy bout of alcoholic intake, and reached maximum intensity over a period of two hours. The pain is constant, radiates straight through to the back and is accompanied by nausea, vomiting and retching. He had a similar episode two years ago, for which he required hospitalization. acute pancreatitis if the gut cant work well like no bowel sounds, gut distended hospital loose stool Q= lower GI diverticulitis Infected or inflamed pouch (diverticulum) in the colon. Common in older persons; Low-fiber diet and constipation are risk factors. diverticulitis tx oral ABX: Cipro or metronidazole What type of PUD is classically described by the onset of burning epigastric pain 1 to 3 hours after eating that is relieved by food? duodenal ulcer Duodenal ulcer treatment might need upper endocscopy fecal H.Pylori test antibiotic therapy (metronidazole, tetracycline, amoxicillin or clarithromycin) with proton pump inhbitor NSAIDs causes heartburn and small amount of red blood: erosive gastritis erosive gastritis tx PPI tenesmus straining, especially ineffectual and painful straining at stool or in urination Route of transmission Hep A fecal oral 66 | P a g e Route of transmission Hep B Blood, body fluids Route of transmission Hep C Blood, body fluids Immunization available? Hep A, B, C Yes, Yes, No Post exposure prophylaxis available? Hep A, B, C Hep A: Yes and immunize close contacts Hep B: Yes and immunize close contacts Hep C: No Next step if positive for infxn Hep A LFT notify pub health Tx: supportive care liver transplant an option in failure sometimes but rare Next step if positive for infxn Hep B LFT screen for coinfection HepA,C,HIV,STI Immunize HAV is req refer to expert consult Next step if positive for infxn Hep C LFT and coinfxn test and refer sequelae Hep A none, survive or die but low mortality rate sequelae Hep B chronic Hep B hepatocellular carcinoma hep failure 67 | P a g e sequelae Hep C Chronic Hep C hepatocellular carcinoma hep failure Acute disease marker Hep A HAV IgM (M=miserable) Elevated hep enz 10x+ Chronic disease marker Hep A none as it doesnt exist Hx of Hep A marker Anti HAV enzyme normal Acute disease marker Hep B HBV core IGM ab= earliest marker to become pos post HBV exposure HBsAg=Always Growing surrogate marker for HBV HBeAg=Notes a time when HBV is Extra contagious, Extra growing Elevated hep enz 10x+ Chronic disease marker Hep B patient without sx NL or slight elev enz HBsAg (Always Growing)=on board or vax Hep B Hx IZ marker HBsAb and norm enz Acute disease marker Hep C Anti-HCV present HCV viral RNA elev hep enz Chronic disease marker Hep C Anti-HCV present 70 | P a g e or Macrolide+beta lactam common PE findings in pneumonia consolidation pleural inflammation (pleurisy) consolidation PE findings pneumonia dullness to percussion -dense tissue when percussed sounds dull (Dense=Dull) Inc Tactile Fremitus -inc with inc tissue density Bronchial or tubular breath sounds, often with late inspiratory crackles tht do not clear with cough Pleural inflammation PE findings pneumonia (late finding with PE but less common) patient report of sharp, localized pain, worse with deep breath, movement, cough Audible pleural friction rub, from movement of inflamed pleura layers -sound similar to stepping on fresh snow clarithromycin and CYP dont do it, it inhibits basically dont Rx, unless H.Pylori and even then make sure you know their med list most common pathogen in acute bronchitis Respiratory Virus 90% acute bronchitis 71 | P a g e an inflammation of the lower respiratory tract without underlying airway disease if they had COPD, it would be COPD exacerbation acute bronchitis tx they dont need ABX most likely often given ABX they want to stop coughing consider mucarinic antag bronchodilator (ipratropium) also could use albuterol or short course oral stroid (prenidsone 40 3-5d) but this would be for protracted problematic cough Pref- prednisone, gets rid of inflammation in airways and thats what is causing the cough ipratropium Atrovent Muscarinic antagonist used in asthma less likely but still poss bacterial cause of acute bronchitis. ex: M&C pneumo B. Pertussis( keep in back of mind if other cases related etc) bacteria is 10% of all consider macrolide or tetracycline asthma common chronic disorder of the airway that is complex and characterized by variable and recurring sx, airflow obstruction, bronchial hyperresponsiveness, and underlying inflammation asthma sx recurrent cough wheeze SOB and/or Chest tight occur or worsen at night, with exercise, viral resp infxns, aeroallergens, pulm irritants 72 | P a g e Is it asthma? sx consistent airflow obstruction that is at least partially reversible consider dx and perform spirometry if any of these indicators are present what test do we need to make dx of asthma spirometry peak flow is for monitoring (in practice it is used for dx all the time) airflow obstruction that is at least partially reversible what is monitor by FEV inc from baseline inc in FEV1 of at least 12% from baseline post SABA goal of asthma therapy reduce impairment reduce risk optimize health and function Asthma assessment classify severity at initial visit control in follow up visits identify precipitating and exacerbating factors and comorbidities identify pts high risk for exacerbate and death reg assess pt and family education and skills incl meds and technique preferred asthma visit frequency well control- 3-6 mo not well- 2-6 wks asthma tx SABA as acute reliever persistent=inhaled corticosteroid preferred 75 | P a g e well controlled asthma sx <_2d/wk awaken <_2x/mo normal activity ok SABA <_2d/wk FEV>80% air trapping in COPD and asthma sx hyperresonance dec tactile fremitus wheeze(expir first) low diaphragm inc AP diameter all this: COPD consistent presence, Asthma only during exacerbation what if partial response to albuterol there is airway inflammation COPD preventable and treatable dz with some significant extrapulmonary effects that may contribute to its severity in individual patient. its pulmonary component is characterized by airflow limitation that is not fully reversible most common sx of COPD chronic cough, chronic sputum prod, activity intolerance, sx usually progress over time most common RF COPD occupation, smoking, pollution, fam hx, age highest risk for exacerbate COPD and death 2+ exacerbations in the last yr FEV1 <50% and/or 76 | P a g e hospitalization for COPD in last yr goal of COPD tx reduce sx reduce risk assess COPD deg of airflow limitation spirometry for Dx FEV1:FVC<.70 post bronchodilator confirms persistent airflow limitation/COPD determine severity by FEV1 Alpha-1 Antitrypsin def screen Alpha-1 Antitrypsin def screen use if COPD develops in pts of european ancestry under 45 yrs or strong fam hx of COPD Gold 3 severe COPD FEV1/FVC 30-50% predicted Gold 2 very severe COPD FEV1/FVC <30% predicted therapeutic goals for COPD non med smoking cessation phys active flu and pneumo vax pulmonary rehab COPD relief of bronchospasm Rx SABA or SAMA (ipratroprium bromide) usually PRN COPD protracted duration bronchodilation Rx LABA (salmeterol) not PRN COPD protracted duration bronchodilation that minimizes risk of COPD exacerbation 77 | P a g e LAMA tiotroprium bromide not PRN COPD anti inflammatory to minimize exacerbation ICS COPD bronchodilator maybe add on theophylline as add on COPD add on for exacerbation PDE-4 inhibitor roflumilast not great but used bad AE Group1-2 <1_ exacerbation/yr COPD group A- low risk less sx SAMA or SABA Group B- low risk but more sx LAMA or LABA Gold 3-4 2+ exacerbation/yr COPD group C- high risk/less sx ICS+LABA or LAMA group D- high risk/more sx ICS+LABA or LAMA can use both (or) together but only if alone not working how often use home 02 greater than 15 hrs/day tx COPD exacerbation inc SABA PRN add on LABA or LAMA if not on 80 | P a g e Hx: sensation of ear full or pressure itch otalgia conductive hearing loss no fever or otorrhea Findings: -Air fluid level visible, often with air bubbles -Opaque yellow or blue color -Cone of light and bony landmarks diminished or absent -TM mobility with pneumatic otoscopy limited Tx: underlying cause like allergic rhinitis. Usually resolves 1-3 wks without intervention Acute otitis media Hx, findings, Tx Hx: -Sensation of ear fullness, pressure and otalgia. -Conductive hearing loss. -Fever common Findings: -TM redness, bulging -Cone of light and bony landmarks absent -TM mobility with pneumatic otoscopy absent -Otorrhea possible with TM rupture Tx: -Analgesia, antimicrobial therapy typically given. However, high rate of spontaneous resolution without antimicrobial treatment Anterior Uveitis (Iritis) clinical presentation Keratic precipitates in cornea Posterior synechiae in iris pupil constricted, nonreactive, irreg shape perilimbal injection (ciliary flush) Anterior Uveitis (Iritis) Intervention 81 | P a g e refer opthamology acute tx with topical or systemic steroid and cycloplegics tx etiology as it is often accompanied by autoimmune dz cycloplegics Anticholinergic agents that paralyze accommodation of the iris of the eye angle closure glaucoma clinical presentation slit lamp eval: corneal edema synechiae irreg pupil shape or segmental iris atrophy cornea and scleral injection ciliary flush angle closure glaucoma intervention refer Acute intervention to block aqueous production, reduce vitreous volume, facilitate aqueous outflow with acetazolamide (Diamox), topical beta blocker and pilocarpine crohn vs UC location crohn: mouth to anus UC: colon only IBD basic intestinal ulceration, inflammation, detectable microscope or macroscope IBS basic altered GI motility and visceral hyperalgesia microscopic inflammation, altered gut flora IBS sx 82 | P a g e absence rectal bleed, fever, wt loss, elev CRP, ESR broad diff dx IBD sx rectal bleed, diarrhea, fever, wt loss, lab evidence of inflammation- inc CRP or ESR leukocytosis esp during flares IBS intervention lifestyle mod- diet, fiber, fluid, exercise meds: indicated by sx antidiarrhea, promotility, select ABX, probiotics IBD intervention lifestyle mod- diet, fiber, fluid, exercise (less sure of fix) antiinflammatory med- aminosalicylates, steroid as indicated immune modulators if no response to antiinflammatory Sg and monitor malignancy outpatient tx diverticulitis when organism primary and alternative tx for mild (only) and need ABX for G- anaerobic and aerobic Enterobacteriaceae Pseudomonas aeruginosa Bacteroides enterococci Primary: metronidazole+bactrim cipro or levoflox Alternative: augmentin or moxif first line for H Pylori PPI, clarithro and Amox for NON Penecillin allergy 85 | P a g e 1-2% Thiazolidinedione mech of action insulin sensitizer fasting and post prandial min hypo risk Thiazolidinedione risk Edema (esp when used with insulin or SU) can exacerbate HF (avoid) long term maybe bladder CA risk Sulfonylurea (SU) example glipizide glyburide glimepiride cheap $4 Sulfonylurea (SU) expected a1c 1-2% when use Sulfonylurea (SU) often in addition to metformin when second med is needed insulins sensitize with metformin inc availability with SU Sulfonylurea (SU) mech of action inc insulin release from pancreatic beta cells fasting and postprandial Sulfonylurea (SU) risk hypo risk esp in elders or impair renal beta cell fail after many yrs and older adults and not as good with severe hyperG Sulfonylurea (SU) when to give 86 | P a g e SU pushes out insulin all the time so can give nocturnal fasting and 4-6h after meal Dipeptidyl peptidase-4 (DPP-4) inhibitor example sitagliptin (januvia) saxagliptin linagliptin alogliptin (DPP-4) inhibitor A1c drop 0.6-1.4% (DPP-4) inhibitor mech of action inc insulin release mostly post prandial (DPP-4) inhibitor risk low hypo risk (DPP-4) inhibitor when to use as add on with metformin and SU expensive GLP-1 Agonist example exenatide (byetta) liraglutide albiglutide GLP-1 Agonist A1c expected 1-2% GLP-1 Agonist how use injection only GLP-1 Agonist mech of action inc insulin release postprandial slows gastric emptying so wt loss and appetite suppression GLP-1 Agonist risk 87 | P a g e low hypo risk N/V (r/t slow gastric emptying) rare pancreatitis do not use with gastroparesis, renal or pancreatic impair Sodium Glucose cotransporter-2 (SGLT2) example canagliflozin dapagliflozin (SGLT2) expected a1c drop 0.7-1% (SGLT2) mech of action lower plasma glu levels by inc glu excreted in urine mostly postprandial (SGLT2) risk hypo risk genital mycotic infxn UTI inc urination mod wt loss discontinue with renal impair (cant offload sugar) inc risk DKA tx DM2 monotherapy start with metformin Tx DM2 dual therapy if A1C goal not receive after 3 mo monotherapy Next: SU (low cost) or Next: TZD (younger and nocomorbidity) 90 | P a g e ABCDEFG for DM Aspirin BP Cholesterol and Creatinine Diet Exercise and Eye exam Foot exam Goals metabolic syndrome large waistline hypercholesterolemia Low HDL High BP High glucose BP= HRxSVxPR HRxSV= CO target organs for HTN brain, cardiovascular system, kidney, eye creatinine rise and kidney function late marker hypertensive retinopathy narrow branches HTN retinopathy grades 1 and 2 1=long poorly controlled HTN, reversible if tx HTN. narrow terminal branches 2=same but with more local constriction but still no vision changes HTN retinopathy grades 3 and 4 3=DBP>110, now add striate hemorrhages and soft exudates and potential for vision change, permanent 4=DBP>130, papilledema and vision change and permanent this is an EMERGENCY by the way 91 | P a g e most potent lifestyle mod for HTN wt loss 5-20mmHg per 10kg wt loss then DASH (8-14mmHg) then sodium then physical activity then ETOH >60yo HTN goal general 150/90 <60yo HTN goal general 140/90 black normal HTN 1st line Thiazide and CCB alone or in combo HTN drug ramp up try to get 1st line to 1/2 -3/4 most mg then add give what you have a month to work at least HTN with CKD 1st line ACEI or ARB HTN at 4th titration or add on BB HTN with DM 1st line same as normal without DM except 140/90 goal no matter age thiazide diuretics example HCTZ chlorthalidone thiazide diuretics MOA 92 | P a g e low volume sodium depletion that leads to PVR reduction so BV=HRxSVx PVR (dec) thiazide diuretics risk try not to go over 12.5/day monitor Na and K and Mg calcium sparing (so good for osteo risk) not as good with renal ACEI and ARB example lisinopril enalapril Losartan ACEI ARB MOA minimize angiotensin II effect potent vasoconstrictor that also stimulates adrenal catecholamine release does this by minimizing AGII production (ACEI) or blocking its action (ARB) so BP=HRxSVxPVR (dec) ACEI ARB risk adjust dose in renal insuff do not use for bilateral renal artery stenosis modest hyperkalemia risk ACEI cough- can use ARB alternative ACEI- angioedema (less with ARB) preg cat D CCB example 2 subclasses Dihydropyridine: Amlodipine 95 | P a g e high- lowers LDL >50% mod-lowers LDL 30-50% who shouldnt be on high intensity statin impaired renal over 75 bec highest risk for rabdo ASCVD definition peripheral vascular disease carotid artery disease cerebrovascular disease aortic disease high intensity statin ex LDL reduce >50% atorvastatin rosuvastatin long half life more bioavailability mod intensity statin example LDL dec 1/3+ ator rosu also simvastatin pravastatin lovastatin low intensity statin example LDL dec 1/4+ prava lova HMG-CoA reductase inhibitor example statins 96 | P a g e HMG-CoA reductase inhibitor effect LDL dec 18-55% HDL inc 5-15% TG dec 7-30% HMG-CoA reductase inhibitor risk and edu check hepatic enzyme prior for baseline DM2 risk inc slightly with high intensity statin no grapefruit juice AE: rhabdo, myositis Bile acid resins example Cholestyramine Bile acid resins effect sit in the gut and soak up bile acid and lower LDL Bile acid resins risk and edu nonsystemic AE: GI, constipation, dec absorption of other drugs so take separately selective cholesterol absorption inhibitor example ezetimibe selective cholesterol absorption inhibitor effect modest LDL reduce well tolerated selective cholesterol absorption inhibitor risk and edu minimal TG effect well tolerated most often Rx with another agent like statin Niacin why? effect boost HDL lower TG Niacin AE 97 | P a g e flushing, hyperglycemia, hyperuricemia, upper GI contraindicate- liver Dz, gout, peptic ulcer Fibric Acid derivative effect and example gemfibrozil, fenofibrate HDL and TG Fibric acid AE dyspepsia, gallstone, myopathy, rhabdo CI: renal or hepatic Dz Fish oil effect at 4g TG dec 20-30% Fish oil AE inc risk of bleed r/t antiplatelet 3 RF for secondary hypertriglyceridemia untreated hypothyroid poor controlled DM excessive ETOH Stage A HF example and definition at high risk for HF but w/out structural Dz or Sx Pt with HTN, athero, DM, obesity, metabolic or Pr using cardiotoxins or Fam hx of cardiomyopathy Stage A HF tx Goal: heart health lifestyle prevent coronary Dz prevent LV structural abnorm ACE/ARB for vascular Dz or DM statins if appropriate Stage B HF example and definition