final blue print

o post tussive emesis o rib fractures o carotic artery dissection o seizure pneumonia and encephalopathy o spreads respiratory secretions  ANY ONE PREGNANT GETS A TDAP Haemoephilus Influenza Type B  Causes respiratory disease processes and MENINGITIS o Mengingitis o Otitis media o Periorbital cellulitis Hepatitis A- least concerning hepatitis. Sourced from contaminated water and under cooked food  Fecal oral spread  Causes diarrhea and high liver enzymes, jaundice  Does not manifest into chronic problem  Has two vaccines Hepatitis B- has 3 vaccines. Virus affects the hepatocytes causing low grade chronic hepatitis and hepatocellular cancer.  If mom has hepatitis b while pregnant give hep b shot and hep b immunoglobulins  All babies get hep b when they are born. Birth is bloody.  Phases o Prodromal- starting to get sick. Malaise, anorexia, nausa o Icteric- clay colored stools jaundize elevated liver enzymes o Convalescence phase- for months malaise and fatigue  Spread by contaminated blood, semen, vaginal secretion, saliva  Don’t give if allergy to baker’s yeast Human papillomavirus- original vaccine protected against only 4  Gardasil 9 covers 9 different strains of HPV that cause precancer  Can do 2 doses before 14  If after 14 do 3 doses  Contraindications is allergy to bakers yeast and pregnancy  Virus must be present for cancer to develop Measles, Mumps, and Rubella : rash that progresses to pneumonia Measles- affects nasopharyngeal epithelium and spreads to lymph nodes  Immune suppression gives bacterial and viral infection  Spreads by respiratory droplets  KOPLIK SPOTS- white lesions with moist red background Mumps- affects the nasopharyngeal epithelium and spreads to regional lymph nodes  Replicates leads to plasma viremia  Enlarged parotid glands, fever, malaise, uri, and rash  Spreads through respiratory droplet or direct contact with saliva  Salivary glands, pancreas, ovaries, testes affected Rubella- infection in the nasopharyngeal epithelium and spread to lymph nodes to respiratory tract, skin, body fluids, and in pregnant women the placenta  Causes vasculitis affecting organ development

 The last two numbers tell you the level  The first three numbers tell you outpatient, inpatient, longterm care  Established patient  99213- lower acuity may or may not receive a Rx  99214- 3 chronic conditions, 2 new problems with a rx or diagnostic point of care testing  99215-worsening condition especially with neurological sx ascending level of care. In outpatient sent to er.  Established patient  You have more information embedded in the pt  This is paid less than 99205 because they are established  CPT Coding is the things you do  In house treatment and point of care testing can be billed  Ekg  Oxygen  Nebulizer  Rsv test  Ua  ICD10 is the diagnosis writing Rx as a NP  Look at prescription template that is saved in pharmacology NEURO migraine HA- vascular headache primary headache- the problem is the headache with or without aura  Without aura is more disabling than with aura  Without aura lasts 4-72 hours  Without aura has two of the following o Unilateral location o Pulsating quality o Moderate to severe intensity o Aggravated by routine physical activity  During headache has one of: o Nausea o Vomiting o Photophobia o Phonophobia  Atleast 5 of the above reaches criteria Chronic migraine is on that occurs about every 15 days for atleast 3 months trigeminal thalamic pain circuit  unilateral dull throbbing headache  classic is with aura common is without aura o aura is preceded or accompanied with a set of self limited sensory symptoms

Treatment  Management of seizures for the pt to return to a normal life style  Antiepileptic drugs and anticonvulsants o Comanage with neurology o Check their med levels  Precipitants o Metabolic electrolyte imbalance o Stimulant intoxication o Alcohol withdrawal o Sleep deprivation o Hormonal variations o Antiepileptic medication reduction or inadequate AED tx o Fever or systemic infection o Closed head injury o Low blood sugar Antiepileptic drugs Seizure/epilepsy type Pharmacokinetic profile, efficacy, adverse effects, cost, interactions Monotherapy Alternatives Ketogenic diet can assist in having less seizures Status epilepticus- seizure for more than 30 minutes  Two or more seizures spanning this period without full recovery between seizures  Medical emergency  Goal stop seizures asap  Emergent tx with benzodiazepine, phenytoin, and barbituates SKIN- LOOK UP THE IMAGES  care, prophylaxis, common organisms physical exam is whole body skin exam, palpitation of rash, dermoscopy or woods lamp Fungi: Candidiasis- thrush, vaginal, balanitis, intertriginous, paroychia, subungual Dermatophytoses- tinea capitis, tinea corporis, tinea cruris, tinea pedis, tinea versicolor Onychomycosis- Infection: impetigo, follicuolitis, furuncles & carbuncles, cellulitis (erysipelas, necrotizing, periorbital cellulitis  erysipelas is like cellulitis, but it is very flat and red  Periorbital cellulitis needs to be sent to peds in the ER and given systemic antibiotics. If it involves the eye you need a short route to ophthalmology to Viral conditions Warts and Herpes Simplex  can be on the feet and fingers

Ulcer- skin defect that goes to the dermis or deeper. Usually can do a culture. Check blood sugar and how long the area has been there. Abscess/ Furuncle/Carbuncle  Etiology is S aureus (MSSA, MRSA) Gram positive  Sterile abscess can form with foreign body like o Splinter o Infection site  Treated by incision and drainage o Packing if needed or tunneling o Culture and sensitivity o Systemic antibiotics  Choice depends on the degree of abscess, location, resistance by strain, and comorbidiites Abscess- acute or chronic localized inflammation with collection of pus in tissue. One big area. Treated with Incision and draining . anesthetize the area. Furuncle- acute, deep seated, red, hot, tender nodule evolves from staphyloccoal folliculitis. Carbuncle- deeper infection composed of interconnecting abscesses usually arising in several contiguous hair follicles. Like a bunch of furuncle together and they are channels of furuncles. Broad spectrum antibiotic and referral to derm Think about tetanus shot for breaks in the skin FACE/HEAD  Face cosmetically apparent  Eyes never use adhesives refer to optho  Nose common area for roasacea  Lips angular chelitis can be anemia Cheeks/face-acne Upper extremity  Check for motor and sensory testing of the peripheral nerves  Tinea ungiuum is under the nails  Eczema  Contact dermatitis  Ring tourniquet syndrome- traumatic injury and there may be excessive swelling in the skin. Lower extremity  Check for tendon injury  Motor function  Hair tourniquet- hair gets wrapped around the toe of the infant. Take all the clothes off to look at the skin. The baby will be crying but it can be hair on the finger. Soft tissue foreign bodies- may need ultrasound and xray. HEENT & PULM AOM - acute otitis media (middle ear)  Ear drops do not help the patient.  When you are doing prescriptions you have to give a higher dose of most drugs to concentrate the med in the middle ear canal

 Cefdinir 14mf/kg bid x 10 days  Azithromycine 12mg/kg daily x 5 days (gram +)  Adults amoxicillin or high dose azithromycin  Supportive tx  Saline gargle  Increase fluids  Tylenol or motrin  Complications (our goal is to avoid this)  Scarlet fever  Rheumatic fever  Gomerularnephritis  Strep A infection Tx  Penicillin is first line  Amoxicillin  If penicillin allergy do erythromycin  Cephalosporines (Keflex) and macrolide (azithromycin) Sinusitis History Facial pain Headache Fever chills Teeth pain Nasal discharge Body aches Cough Symptoms often follow URI and worsen within 7-10 days Physical Exam  Fever  Nasal discharge  Tenderness over maxillary/frontal sinus- press hard o The ethmoid and sphenoid sinus can be ocular pain  Dull illuminations over cavity  Posterior oropharyngeal drainage Bacterial sinusitis  Symptoms 7-10 days  Nasal discharge with/without cough in the PM  Frontal/maxillary pressure with the headache  May have dental discomfort  Know what bacteria you are treated and If not be hesitant to right rx.  If the pt does not have severe sx, persistent sx, or high risk pt doesn’t need antibiotics o High risk  Pneumonia  Copd  Cystic fibrosis

o Severe persistent asthma  Some degree of sx all the time  Limited in activity  Nighttime sx 7 days a week  Pef <60%  STEP 1 SABA prn+ICS prn o Albuterol metered dose inhaler is 2 puffs q 4-6 hours o Nebulizer dose is 2.5mg/dose o Dose may need repeated x 2 after 5-10minutes o Use spacer  Spacers are prescribed separately o Adverse effects tachycardia and palpitations, CnS excitation, headaches  Selective beta 2 agonist is levalbuterol- albuterol has been removed from this so it gives less side effects of tachycardia and excitement.  SABA has instruction of deep breath, hold it for 10 seconds, breathe it out, repeat  Rule of Twos- asthma needs controlled when o Use of inhaler is more than 2 times a week o Symptoms are more than 2 times a week o Night attacks more than 2 times a week o Need oral steroids more than 2 times a year o 1 metered dose inhaler should last one year  STEP 2 SABA and low dose inhaled corticosteroids o Asmanex (mometasone) 440mcg 2 inhalations bid o Alvesdo (ciclesonide) 80mcg 2 inhalations bid o Beclomethasone 40/80mcg 2 puffs bid o Budenoside (Pulmicort) inhaler is 90/180 mcg 2 inhalations bid. Neb 0.5mg (qd or bid) o Fluticasone 44mcg/110mcg 2 puffs bid o Alternative singulair (montelukast to block leukotrienes  12 mo-2 years 4mg granules  3-5 yo 4mg chewable  6-14 yo 5mg  Adult up to 10mg  Step 3 low dose ICS with LABA o Salmeterol (serevent) o Formoterol (foradil)  Last 12 hours  Can’t be used alone  Must be used with ICS  Adviar (fluticasone + serevent) -age 4 and older  Symicort (budenoside+formoterol-age 12 and older  Step 4 medium dose ICS and laba o Advair 250/50 o Symbicort 160/4.5  Step 5 high dose ICS + LABA

 Comorbidities of atopic dermatitis or eczema, asthma  Aeroallergen driven so avoid what it is that you are allergic to  If avoiding does not work get testing with allergist  History-  Nasal congestion  Rhinorrhea  Pruritis of nose, eyes, ears  Sneezing  Itching watery eyes  Chapped lips mouth breathing  Fatigue malaise  Headache  Physical exam  Pale boggy nasal mucousa  Rhinorrhea with clear discharge  Dark circles under the eyes  Post nasal mucosa discharge  Treatment- antihistamines and intranasal corticosteroids are first line  Loratadine (Claritin)  Desloratadine (clarinex)  Fexofenadine (Allegra)  Cetirizine (Zyrtec)  Flonase daily  Nasonex daily  Zatidor or patanoleye drops for allergic conjunctivitis  Oral antihistamine, nasal steroid or antihistamine, eye drops  Education is to wash hair at night, avoid allergen, follow up with allergist for testing and eval of immunotherapy CARDIAC risk for CVA- Diabetes, hypercholesteremia, hypertension, obesity, smoking history Left Ventricular Hypertrophy and ECGs (EKGs) From long standing untreated hypertension. Big r in the qrs. In a 12 lead ECG Limb leads  R wave in lead I and S in lead III greater than 25mm  R wave in aVL greater than 11mm  R wave in avf greater than 20mm  S wave in avr greater than 14mm Precardial leads  R wave in V4, V5, V6 greater than 26mm  R wave in V5 or V6 plus swave in V1 greater than 35mm  Largest r wave plus largest swave in precardial leads are greater than 45 Nonvoltage criteria  Increased r wave time greater than 50ms in leads V5 or V6  ST segment depression and twave inversion in the left sided leads- left ventricular strain pattern

ECG 1- Look at the rate 2- Look at the pwaves. Is there a pwave for every qrs 3- Look at the axis 4- Look at the pr interval should be .12-0.1. this could be a block 5- Length is .06-.1 seconds. Wide can happen if medication or cardiac conduction issue. Can indicate bundle branch block 6- Look at st segment for repolarization. Should be a flat line HLD: guidelines for low vs. moderate vs. high intensity statins Goal should be :  Decrease central obesity below 35-40 inches  Fasting triglycerides to be greater than 150mg  HDL to be greater r than 40-50  Blood pressure to be less than 130/85  Fasting glucose to be less than 100 Order cbc, lipid, hbga1c, bp , tsh, t3, and t4 Risk to develop cardiovascular disease  Goal is to o Decrease LDL- gives risk to cvd o Decrease TG- gives risk to cvd o Increase HDL- cardioprotective

o  Medications o Statins low, medium, and high dose  Medium is for someone that we need to lower cholesterol 30-50%  Low dose is for someone that is at risk  High dose is for someone that needs to lower cholesterol greater than 50%  o No longer niacin o Omega 3 o Take statins at night because cholesterol is produced at night  Diet and lifestyle o Quit alcohol o Increase activity o Increase vegetables

o Decrease sugar and fat HTN: meds, nonpharmacy measures, pt education Behavioral changes: quit smoking, reducing weight, healthy diet, exercise, address emotional triggers, stress reduction, decrease alcohol intake Teach pt how to monitor bp at home: bp log book, lifestyle changes Best way to take bp is sitting in a chair with feet on the ground, make sure they are calm, check it twice. Cuff has to fit appropriately  Imbalance in the vasodilator and vasoconstrictor agents  Goal is to identify and treat early  Factors of o Genetics o Lifestyle o Age  Goal is to prevent end organ damage.  Normal bp less than 120/80 o Elevated is 120-129/ less than 80 o Stage 1 htn is 130-139/ 80-89 o Stage 2 is 140 or higher over 90 and higher  Medications o Table 35.1 o Thiazide diuretic- first line medication o Ace inhibitors- starts in stage 2 for combo therapy. Don’t give in pregnant . consider side effect of cough o Arbs- don’t give if pregnant o Betablockers- watch for bradycardia or pt that have bradycardia o Calcium channel blocker- for African Amercians PSYCH Major depressive disorder Pathophysiology- dyregulation of biogenic amines, norepinephrine and sertotonin changes, decreased prolactin tsh, lh, and testosterone, increased adrenal size, genetic basis Stinking thinking is what is addressed in cognitive therapy to combat negative thinking patterns Differential disorders- thyroid disorders, sleep disorder, unrecognized bipolar, neurological, medications, substance use, adrenal functioning, anemia Pharmacological causes- narcotics, self medicating, cardiac and htn drugs (central acting antihypertensives, beta blockers, sedative and hypnotics, benzodiazepines, steroids, hormones, stimulants, and appetite suppressants, neurological agents, antineoplastic drugs Rule out other med causes through : H&P, CBC, CMP, Thyroid studies, RPR  Major Depressive disorder- someone with severe depression and 5 or more of the symptoms present during a same 2 week period and represents a change from previous function and has 1 of the symptoms of depressed mood or loss of pleasure. Stinking thinking  depressed mood most of the day

 diminished interest  weight change  insomnia or hypersomnia  psychomotor agitation or retardation  fatigue  feeling of worthlessness  diminished concentration or indecisiveness  recurrent suicidal ideation with or without a plan o have they previously attempted o always ask are you at risk for suicide do you have a plan It can not be a mixed episode. It cannot be depression with mania. Unipolar of only depression. It is not caused by a medical condition or bereavement. Mania is excessive spending, excessive eating, reckless behavior  most have first episode before 40 yo  untreat episode last 6-13 months  over 20 years have a mean number of episodes of 5-6  chronic with relapses  positive prognosis is mild episodes, short hospital stays, stable family function, social function for 5 years prior to depression  Negative progrnosis is co occurring dysthymia, substance abuse, anxiety , more than one episode, male gender  Treat with SSRI o Takes 6-8 weeks for affect o A range of how much to give  Fluoxetine ranges 10-80  Lexapro 10mg narrow therapeutic window  Zoloft for pregnant mothers and breastfeeding mothers o Combination of psychotherapy and meds for 6-12 months and then consider taper o If it does not improve consult psychiatrist o Electroconvulsive therapy  Black box warnings for antidepressant have increased risk of suicide for under 24 years old do not give more than 7 days work of medication. Collaboration with psychology is needed.  First line is SSRI, SNRI, NDRI o SSRIs  From more relaxing to more activating levels  Fluvoxamine 100mg  Citalopram 20mg  Escitalopram 10mg  Paroxetine 20mg  Sertraline 50mg  Fluoxetine 20mg o SNRI  Venlafaxine start 37.5mg goal 75-375mg  Venlafaxine xr start 37.5-75mg goal 75-225mg

 Desvenlafaxine start 50mg goal 50-100mg  Duloxetine- start60mg goal 60-120mg  Levomillnacipran start 20mg goal 40-120mg  Do not use augmentation and ancillary therapy  Consider how to get the pt off the medication  SSRI have the benefit of low and slow for dosing and titration. Do a slow taper for atleast 1-2 months to get them off the ssri.  SNRI have the benefit of Cymbalta being used for chronic pain. Venlafaxine depression anxiety and panic disorder. o Side effects are risk of htn, discontinuation syndrome, drug drug interaction, mild anticholinergic affect  NDRI is buproprion but do not use because it is the third box to the left o No sexual side effects o Risk of seizures. o Helps to stop smoking  New antidepressants o Serotonin agonist and reuptake blocker  Vilazodone  Vortioxetine o SNRI  Levomilnacipran 20-40mg o If pt does not respond to those meds  Try antidepressant 2 nd line  Block reuptake of serotonin and norepinephrine  Acknowledge possible side effect of anticholinergic, narrow angle glaucoma, weight gain, worsening bundle branch block o MAOI are barely used due to  Food high in tyramine  Antihypertensive crisis Nonpharmalogical- Can be treated with nonpharmacological treatment like cognitive behavior therapy knowing what we think affect how we think and do and what we do. Can be treated with group therapy Dysthymia Low low mood and function- sx for atleast 2 years. Baseline is just generally depressed but can still function. Sx of :  Poor appetite or over eating  Insomnia hypersomnia  Low energy fatigue  Low self esteem  Poor concentration  Feelings of hopelessness  most have first episode before 40 yo

 untreat episode last 6-13 months  over 20 years have a mean number of episodes of 5-6  chronic with relapses  positive prognosis is mild episodes, short hospital stays, stable family function, social function for 5 years prior to depression  Negative progrnosis is co occurring dysthymia, substance abuse, anxiety , more than one episode, male gender  Treat with SSRI o Takes 6-8 weeks for affect o A range of how much to give  Fluoxetine ranges 10-80  Lexapro 10mg narrow therapeutic window  Zoloft for pregnant mothers and breastfeeding mothers o Combination of psychotherapy and meds for 6-12 months and then consider taper o If it does not improve consult psychiatrist o Electroconvulsive therapy Adhd 5 % prevalence in children and can continue into adulthood. 50% are diagnosed by age4. Sx present by age 3 and present before 7 for diagnosis More prevalent in men Must have childhood onset to diagnose with ADHD Cause is not completely known, genetic factors, developmental factors, neurochemical factors, neurophysiological factors, and psychosocial factors. Problems with attention starting in adulthood can be undiagnosed depression or anxiety Differential diagnosis:  Normal age development  Anxiety  Depression  Learning disability o Reading disorder o Math disorder o Written disorder  Conduct disorder Characteristics  Persistent pattern  Inattention and impulsivity motor hyperactivity  Interferes with social, school, work Special subtypes  Predominantly (more in adults)  Hyperactive impulsive  Combined Tests  Vanderbilt rating scale- teacher and the parent fills it out and brings it back

 Connors parent and teaching rating  Pediatric symptom checklist  Assess adults for anxiety, depression, substance abuse, and refer to neuropsychologist if they think they have ADHD Look at personal history:  Family history  Academic performance underachievement  Behavior in unstructured environment  Medications  Functioning  Poor job performance or frequent job change  Chronic stress from failures  Order labs o Serum lead levels o Ferritin o thyroid If an adult thinks they have ADHD they need to be screened for depression or anxiety disorder, screen for substance abuse and refer them to neuropsychology Tx pharmacological is stimulants like Adderall. Nonpharmalogical is a magazine called ADDITUDE  organizational skills  time management  CBT therapy  Minimize distractions Early diagnosis with prescriptions have better outcome Stimulants schedule II  2 categories methylphenidate and amphetamines  More than 80% response rate  Block reuptake of dopamine and norepinephrine at presynaptic neuron  Release catecholamines  Inhibit monoamine oxidase  Reduce inattention and impulsivity  SE: insomnia, weight loss/anorexia, irritability headaches, and abd pain, and tics o Children can fall off the growth curve Be careful with pt self diagnosed and knows what med they want Consider pretreatment drug screen and intermittent drug screens Consider drug diversion and income potential Highschool and college students can abuse Follow up is :  Monitor clinical progress  Consider baseline and yearly ekg with family hx of cardiac problems  Use standardized rating scale to track progress  Monitor growth and development  Monitor for psychiatric comorbidities. GAD Need to have generalized treatment plan.

Substances can induce anxiety or withdrawal can cause anxiety. Diet is a mix of fat carbohydrates fiber and protein and if they are not having it balanced it can create anxiety. Caused with a stimulus Etiology and biology: Learning theory  Learned through identification and imitation of anxiety patterns in parents and care givers  Associated with a naturally frightening stimulus  Disorders involve faulty distorted or counterproductive pattern of cognitive therapy Biological theory:  Catecholamines increased  Increased norepinephrine metabolites  Decreased REM latency  Decreased levels of GABA  Serotonin decrease increased dopaminergic activity Usually has a stimulus or trigger Antihypertensives and sedative-hypnotics can cause anxiety in withdrawal. GAD—course is chronic. With theime secondary depression can develop if GAD is not treated. Correlated with depression pervasive for 6 months or more. Have symptoms of cardiac and respiratory problems basically panic attack. Pervasive and difficult to control. Order blood chemistry, ecg, and thyroid function Treatment- Therapy CBT, psychoanalysis, group therapy family therapy Pharmacotherapy- do not use benzodiazipines as first line treatment. Long term ssri, beta blockers for social anxiety with performance. Benzodiazepines are alprazolam and diazepam Education- avoid alcohol and stimulants and symptom recognition Follow up monthly assess severity of anxiety assess suicidal risk 1 st line treatment is therapy and ssri and snri. Buspar has to be dosed bid for it to be effective. Buspirone is a serotonin 1A partial agonist is 5-20mg tid or 15-30mg bid  Works better results with benzo naïve pts and takes a few weeks to work  Do not dose prn  Not a narcotic CAGE questionnaire Stands for Cutdown, annoyed, guilty, and eye opener Ask the pt how many times have you had more than x amount of drinks in the past year. X is 4 for women and 5 for men. Anything more than one drink is a positive for alcohol use disorder. CAGE Questions are Have you ever felt you should cut down on your drinking? Have people annoyed you by criticizing your drinking?

Have you ever felt bad or guilty about your drinking? Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover (eye-opener)? bipolar disorder- manic depression before beginning treatment for someone that has depression assess for bipolar disorder! Type 1 is variant that goes into mania and depression Type 2- neurophysiological it is like type 1 but it looks more like depression. Hypomania Co-manage with psychiatry because mood stabilizers are needed and need closely managed Epidemiology  Can be seen more in women  Can be genetic  Can be confounding with substance abuse Often mistaken for major depression disorder  Three kinds o Cyclothymia- numerous episodes of depression and hypomania for a period of two years  High and lows but on a similar scale that doesn’t meet criteria for true depressive or hypomanic episodes o Bipolar I disorder- most severe  Full manic episodes at least 1 week in duration  Must have been manic at least one. Must have depressive episodes  Risky behaviors o Spending too much o Sexual rushes o Drug use o Bipolar II disorder- hypomanic episodes of at least 4 days in duration  Episode of hypomania  Has met criteria for depressive and hypomanic episodes but does not cause impairment of function  Sx DIGFAST o Distractibility o Insomnia o Grandiosity o Flight of ideas o Activities o Speech o Thoughtlessness o Then depression symptoms  There is not difference in major depressive disorder episode and bipolar depressed phase episode  Screen with mood disorder questionnaire! Differentials

 Substance abuse  Medication  Cluster b personalitydisorders Order  CBC with diff, platelet, free t4, tsh, rpr, hiv, blood chemistry, urine toxicology o Rule out hiv, rpr to rule out neurosyphilis or neuro complications of hiv  Pregnancy test- can’t use lithium Treatment  Refer for specialty  Explain that untreated mood swings get worse and cycling becomes more rapid o Kindling is cycling becoming more rapid  Tx decreases risk of suicide and decreases disruption to patient lives  Lithium- 300mg tid qid o Do not rapidly stop o Neurotoxicity >2.0 o N/V/D, ataxia, coma, death o Fine tremor and increased urination common o Can cause irreversible renal failure and junctional rhythm o Can’t be used if pregnant  Valproic acid- most frequently prescribed o Effective for rapid cycling o Can dose by wt o Side effects of gi, liver, dyscrasias and sedation o Monitor levels  Carbamazepine (Tegretol) o Rapid cycling o Can cause blood dyscrasias o Check levels  Lamotrigine (Lamictal) o Good for bipolar depression o Watch steven Johnson syndrome  Oxcarbazepine and Topamax are newer medications  Phenytoin phenobarbital don’t use Mental health  characterized by subjective experience of the patient and how well the person is functioning in society  the resources for mental illness can be scarce  the level of functional impairment is key  dsm 5 changed five axis system  mild forms of mental illness the thinking patterns are a problem and cognitive behavioral therapy can help  some pts will not go to therapy for psychiatry or counseling so alternatives need to be found. Medical services should be with mental health care.  Language and approach

o No fault language and non judgmental approach o Convey empathy o Avoid language that is stigmatizing o Instill hope  Develop therapeutic alliance  Take all conditions seriously and not dismiss them because they are psych pts  General approach o Chief complain o Hpi o Full history of psych family personal o Mental status exam o Lab and diagnostic testing  Cbc, tsh, ft4, cmp, ua, head CT, urine drug screen o Hyperthyroidism can seem like anxiety. Hypothyroidism can seem like depression  Psych tests o Phq9 and GDS for depression o GAD for anxiety o Vanderbuilt rating scale for adhd o PTSD o Montreal cognitive assessment for cognitive impairment o Connors paretnt teach rating scale for adhd  DSM5 o Diagnostic classification system o Symptom and distress criteria o Common language for standard criteriz o Removed subtypes of schizophrenia o Removed aspergers/autistic o Includes autism spectrum o APA uses decimals to identify updates and whole numbers for new editions  Where to refer o if they are in crisis or a danger to themselves they should be inpatient o emergent vs non emergent  resolve and crisis for emergent  crisis is for pt that meets involuntary psychiatric hospitalization  not a violation of hippa  wpic for diagnostic evaluation center o pt insurance  commercial insurance has greater access to providers  Medicaid and medicare and limited number of providers due to low reimbursement  When to refer out

o Has more than 2 inpatient psychiatric hospitalization o Unfamiliar with current psych meds o Bipolar variant or thought disorder o Personal history of suicide attempts o Drug and alcohol involvement o Cluster b personality disorder diagnosis- antisocial, narcissistic, histrionic, borderline  Have adaptive mechanisms that make it harder to treat due to their behaviors.  Team approach is the apprach o Do not give SSRI to those in mania for bipolar disorder because it will have them cycle into mania  Voluntary hospitalization (201) o Signs self in to be evaluation o For anyone over 14 with mental health crisis o Younger than 14 admitted by parent or guardian o Pt to agree to 72 hours of notice before leaving if they decide to leave AMA o No time limit  Involuntary hospitalization (302) o Involuntarily committed and tx to not exceed 5 days  Person must be severely mentally disable Screen for suicide by : SADPERSONS  Sex  Age  Depression  Previous attempts  Ethanol abuse  Rational thinking loss  Social support lacking  Organized plan to commit  No spouse  sickentess ENDO Thyroid issues Thyroid is controlled by the pituitary gland and the pituitary gland is where TSH comes from. The thyroid is needed for metabolism and is the engine of the endocrine system. Screen pts for thyroid disorder for hypo or hyper thyroid and metabolic syndrome. TSH is the most helpful screening tool  made the anterior pituitary  negative feed back loop- TSH is trying to turn on the thyroid and it is not getting enough hormone. TSH is screaming please turn on if TSH is low.  low tsh – hyper  high tsh-hypo Free T4 metabolically active is the most helpful for confirmation of dx  40% converted to T3 in periphery and it is more metabolically active than T4

 Insufficient evidence +/- routine thyroid screening in the absence of clinical suspicion. Hypothyroid  easier to manage. We will do labs, physical exam for enlargement and nodules. We replace the thyroid hormone with levothyroxine for 1.6mcg/kg/day and check in 6-8 weeks. US if goiter or nodules. Start low and go slow. Take levothyroxine on the empty stomach. Variability in preparations  Sx is goiter and cretinism  You see an elevated TSH and normal T4.  Feeling slow sluggish constipation and depression  Subclinical hypothyroidism is elevated TSH and normal T4.Tx levothyroxine vs watch and wait. Clinical presentation is nonspecific. Diagnostic reasoning is mildl increased TSH 5.5-15 with a normal T4 level  Check TSH and free T4 every 6 months  If T4 is inadequate the thyroid gland enlarges. Autoimmune hypothyroidism can start and the body recognizes thyroid antigens as foreign. Destructive thyroid inflammation may be due to immune cross reactivity  Sx- early is fatigue, dry skin, slight wt gain, cold intolerance, constipation and heavy mesnes  Later sx is very dry skin, coarse hair, loss of lateral eyebrows, alopecia, hoarseness, wt gain, impaired mental ability, depression, decreased libido hypesomnia  Objective is facial puffiness, dry skin, brittle nails, slow speech, large tongue, thinning hair, enlarged thyroid, bradycardia, lateralized PMI, diminished bowel sounds, constipation, hypotonic, and hyporeflexic  Refer to endocrinology if you think it is anemia, renal failure, elevated ldl and triglycericedes, and antibody titers  Tx for older adult or coronary artery disease it would be 25-50mcg/day. If pt is pregnant increase replacement therapy Hyperthyroid calm the thyroid down. Consult endocrinology. Ultrasound if goiter or nodules. Antithyroid drugs: methimazole and propylthiouracil. Betablockers for sx management. Radioiodine ablative tx and if this is done just give levothyroxine. Heterogeneous group of condition. Excessive secretion and synthesis of thyroidism. Signs and sx from excessive thyroid hormone is  alterations in growth, metabolism, and development  all metabolic activity is increased.f o sweating o diarrhea o tachycardia  Long term o Heart disease o Osteoporosis o Mental illness

o Infertility  Epidemiology and causes o More common in men than women o Peaks 20-40 years old o Spontaneous o Factitious or exogenous if someone is over using thyroid meds o Grave disease most common in U.S. o Most common form happens during pregnancy  Try to control the symptoms and treat with removing and then treating with synthroid  Sx- anxiety, diaphoresis, fatigue, heat intolerance, palpitations, weight lost, diarrhea, tachycardia, exophthalmos, dtrs, thyroid enlarged and nodules  Initial testing o TSH less than 0.35mcIU  Normal is 0.35-3.5 o Usually elevated T4 >12.5 o If T4 normal look at T3 o CBC, LFT  Subsequent testing o Nuclear scintigraphy with radiolabeled iodine o 24 hour radioactive iodine uptake identifies hot and cold spots  Hot and cold spots are increased and decreased thyroid function o Ultrasound of the thyroid o Fine needle biopsy- used for nodules. Pts are usually not satisfied with this  Refer to endocrinology for management for euthyroid goal o Meds- betablockers for faster sx relief. Antithyroid medication is PTU and MMI  Radioactive iodine is the treatment of choice for hyperthyroidism  Surgery subtotal or total thyroidectomy Diabetes Main symptoms are polydipsia, polyphagia, lethargy, stupor, blurred vision, smell of acetone, nausea, vomiting, abdominal pain, kussmaul breathing, polyuria, glycosuria Diabetes Mellitus is a syndrome of:  disordered carbohydrate, fat, and protein metabolism  hyperglycemia resulting from deficits in insulin secretion, action, or a combo Two distinct types of type 1 and type 2, gestational, and insipidus  diabetes insipidus is not related to DM an has excessive urinating and thirst b/c of inadequate output of antidiuretic hormone by the primary or the lack of the normal response by the kidney to ADH Diagnosis of diabetes from ADA is

 fasting glucose of greater than 126  Hba1c greater than 6.5%  2 hour plasma glucose greater than 200 with classic symptoms of hyperglycemia o Random plama glucose gretater than 200 whether fasting or not is diabetes Type 1 - onset in childhood. Loss of beta cells. Can’t produce insulin.  Need insulin  Screening complications begin 5 years after diagnosis  Polyuria and polydipsia  Wt loss- water loss, glycogen, TB depletion, and muscle catabolism Vague symptoms and then they get admitted with DKA Absolute beta cell destruction from genetic risk factor and something environmental like viral illness triggering sudden onset. Most people diagnosed by 30. Tx is insulin shots. We are to mimic insulin production by the pancreas with a basal insulin and then a bolus insulin. Combination of genetic factors with secondary insults and beta cells are destroyed in a autoimmune fashion. Can be due to perinatal intrauterine factors, prenatal factors, postnatal factors. Objective- wt loss, reduced muscle mass, signs of dehydration like poor skin turgor, dry mucous membranes, and diabetic retinopathy The body is trying to get rid of sugar. Insulin puts sugar in the cells or in the fat cells. Sugar just running causes microvascular damage and increased risk of infection Testing- UA, random glucose, A1c, fasting lipid profile, urinalysis, microalbuminuria, thyroid function tests, serum creatinine  A1c- mean plasma glucose concentration over the preceding 2-3 months  Not appropriate for pregnancy or hemoglobinopathies Management:  Team approach  Insulin regimen- try to mimic the pancreas o Do a long acting insulin and then a bolus insulin  Frequent self-monitoring of blood glucose  Medical nutrition therapy  Regular exercise  Periodic assessment of tx goals Goals are maintained glucose, lipid, and bp level, prevent hypoglycemia, control lipi levels, attain reasonable wt, meal planning, exercise without limitation as long as glycemic control is good. 150min a week of aerobic activity with muscle strengthening

DM2:  Most diabetics  Late onset  Insulin resistance increases insulin levels  Occult disease with insidious onset  Start screenings at diagnosis  Obesity is prevalent Risk factors: genetics, age, gestational DM, metabolic disease. If sugar is not managed while pregnant their child is at risk to have a difficult birth and increased size Pathophysiology- ciruculating insulin is insufficient  Insulin resistance  Impaired insulin secretion decline in beta cell function Diagnosis-  Fasting glucose of 8 hours >126  Oral Gtt with results >200mg at 2 hours  Random glucose >200mg with symptoms  HGA1C >6.5% o Can be done in non fasting state o Can repeat to confirm  Refer them to diabetic education  HBA1c under 6 excellent, 7-8 good, 9-14 action needs considered. o Hba1c of a 9 is a mean blood glucose of about 200 o Some drugs can lower hba1c by 1% so if someone a1c is of 15 % you can’t manage on metformin only Pharmalogical treatment- Required when diet and exercise do not fix Should be done with exercise and diet Oral medication is given when 3 months of nutritional therapy and exercise have not work to get fasting plasma <120 and a1c of <7%. Insulin has the greatest change in percentage of a1c. Begin with metformin. Metformin only lowers hba1c by 1% only. Insulin has the largest effect on decreased hbga1c %  Initiation of therapy- 6.5-7.5 is monotherapy metformin

 7.6-9.0 is dual metformin plus o Sulfonylurea o TZD: piolitazone o Glinide:Repaglinide/nataglinide o DPP4 Sitagliptin, saxagliptin, linagliptin o GLP1 antagonist- exenatide/prunlinitide/liraglutide  Greater than 9%- insulin or triple therapy o Metformin plus o DPP4 or GlP1 Plus o Sulfonylureas or glinide plus or TZD Start with biguanides (metformin) for first line therapy  Dosage should be titrated to max dose of 2000mg  Reduces hepatic glucose production and intestinal absorption, insulin sensitizer in periphery  Lowers a1c 1 percent  Not for use in chf or renal impairment  SE hypoglycemia (little) and diarrhea  Stop takin within 48 hours before contrast dye Thiazolidinedione is an alternative to sulfonylureas for those that doe not have HF or bone fracture GLP agonist is an option for those over wt and avoiding hypoglycemia Meglitinide is an option for those that cant take sulfonylurea or prefer to avoid injections Treatment goal is less than 7%  <6.5% for new diagnosis long life expectancy  <8% for longstanding DM advanced complication limited life expectancy  Monitor every 3 months BP goal less than 140/90 Start a statin no specific LDL goal Prediabetes- deleterious progression Concern for end stage organ disease:  Hardening of arteries  Deposition of lipids on the arteries  Renal insufficiency  Loss of nerve sensation  Retinopathy Treatment medications:

Sulfonylurea: squeezes the insulin out of the pancreas  Glipizide, glyburide, glimepiride  Insulin secretagogue can cause hypoglycemia o Reduces hepatic glucose output o Increases peripheral glucose metabolism  Lowers A1C 1-2% o Can lower blood sugar by 20%  Cautions o Wt gain hypoglycemia o Sulfa allergy o Not recommended for use during pregnancy or with elderly o Metabolized in the liver, should be avoided with significant hepatic dysfunction o Lower dose in renal dysfunction Make sure the patient knows how to use their glucometer to be aware of possible hypoglycemia Thiazolidinediones (TZDs)  Pioglitizzone and rosiglitazone  Sensitizes peripheral tissue to insulin  Lowers LDL and increases HDL  Lowers A1c 1-2%  SE edema and wt gain  Contraindicated in CHF and low EF  Can increase bladder CA, limb fractures, and macular edema  Monitor ALT (if >2.5x NL don’t use)  12 weeks for max effect  Removed from market for CV events (Avandia) hepatitis (Rezulin)  May be used with metformin Meglitinides  Repaglinide and natelglinide  Works like sulfonylureas. Don’t ad with sulfonylureas. Decreases by 1%  Short acting so gives with meals o Not used first line because it is more expensive than sulfonylureas are short acting so they must be taken with meals  May be good for people who forget to eat because they take it when they eat  Lowers A1c- 1-1.5%  Insulin secretagogue o Hypoglycemia has major side effect  Not useful to add to sulfonylurea  Monitor creatinine and ALT Alpha Glucosidase Inhibitors

 Acarbose and miglitol  Competitively inhbits enzymes that digest dietary starch and sucrose o Works like metformin o Side effect is GI upset  Given with first mouthful  Helpful for erratic eating schedules  Reduce post prandial glucose by 30-50%  Reduce hgba1c by 0.5-1%  Adverse effects is flatulence and diarrhea o Watch LFT  Don’t use with renal dysfunction Incretin mimetics- super class of itself - incretin is a hormone that tells you body to release insulin after you eat. These help your body lower blood sugar by helping your pancreas to give more insulin, prevent pancreas to give less glucagon, and improve satiety. These drugs help with weight loss. Must have a working pancreas to use  Glucagon like peptide-1 GLP-1 o Exenatide o Liraglutide- once daily o Pramlintide Injection only Stimulates insulin production and inhibits glucagon and slows gastric emptying making the person feel fuller Good adjunct Lowers a1c 1-2% Wt loss and n/v Increased risk of pancreatitis  Glucose dependent insulinotropic polypeptide  Dipeptidyl peptidase 4 inhibitors (DDP-4 inhibitors) o Sitagliptin o Saxagliptin o Vildagliptin Increases incretin levels to increase insulin release and decrease glucagon Lowers a1c 0.6-1.4% Wt neutral Monitor for creatine

Good for combo therapy Don’t use with sulfonylureas SGLT2 Inhibitors- removes sugar and blocks reabsorption of it at the kidney. Extra sugar pushed out in the urine  Dapagliflozin, canalgliflozin, empagliflozin  SGLT2 is expressed in proximal tubule and mediate reabsorption of 90% of filtered glucose load o Block reasbsorption of glucose in the kidney  Urine analysis not useful on these pts .  Modest improvement in hyperglycemia  Decrease wt and bp  Increases hdl  Not for routine use  Third line agent if no control on metformin and sulfonylurea if insulin not an option  Does not cause hypoglycemia  SE: UTI, ketoacidosis, candida vulvovaginitis, poliuria, fungal infections  Work in the distal tubule of the nephron to get rid of excess glucose in the blood. SGLT1 10% reabsorption and SGLT2 90% reabsorption Combo meds- can be cost saving Metformin and glipizide Rosiglitazone and glimepiride Pioglitazone and metformin Metformin and glyburide Rosiglitazone and metformin Pioglitazone and glimepiride Januvia and metformin Prandin and metformin Insulin  Can increase wt but glucose control is needed o Opens up the cells taking in glucose to store as fat or use  Bioavailability changes with site of injection o Faster in abdomen and slower in thighs  Exercise accelerates absorption in thigh  Best combo is long acting basal and rapid acting with meals  Consider starting if hgba1c>9.

Insulin pump- type I diabetics  Associated with carb counting  High pt satisfaction  Good glucose control  Short acting insulin Aspirin- diabetics are at risk for CV complications and stroke  Has bleeding risk  Low dose ASA if ASCVD is >10% and low risk for bleeding o Males over 50 and females over 60 with a risk factor  Risk factors smoking htn, lipidemia, albuminuria, family history o Secondary prevention for diabetics with known DV disease o Protein in the urine they get ace inhibitor and counseling not to smoke All diabetics  Initial diagnosis o Refer to dietician and certified diabetes educator o Goal of tx is to stop chronic complications  Frequency of pt visits depends on o Glucose level control o Changes in therapy o Presence and degree of complications o Once regulated pt should be seen atleast quarterly o FOOT EXAM EVERY VISIT DM Type 2 follow up  Quarterly visit every 3 months  Results of smbg  Symptoms  Problems with adherence to plan  Medication  A1C funduscopic exam Pt education  Definition of type 2 DM, causes of diabetes, and functon of the pancreas and insulin  Regulation of blood glucose o Diet exerercise o Sx of hyper and hypo glycemia o When to contact the doctor o Blood glucose monitoring and urine testing o Medication and insulin administration

 Meal planning  Glucose control, vision exams, foot care, infection prevention, o Refer to opthamology, podiatrist, cardiologist, dentist exam  Fasting lipid panel annually  Foot inspection with shoes and socks off  Diet should be mix of carbs, fats, healthy proteins o Stick with vegetables and water o Fruit for dessert and limit fruit o Match foods to food journal  Send out type I diabetics if we are not getting to goal  Hypglycemia o Adult blood glucose of <55 o Infant <45 o Clinical hypoglycemia is bg low enough to cause signs and symptoms o Fasting  Low blood sugar >5 hours after eating  Blood sugar does not return without glucose o Reactive  Acute symptoms 2-4 hours following carb diet o Induced  Medication and alcohol causing  Most common form o Differentials  GAD  Panic attacks  Hyperventilation  Pheochromocytoms  Drug or alcohol intoxication  TIA/CVA  Psychosis o Evaluate the cause and focus on eating habits, alcohol intake, exercise habits o Initial testing  Obtain blood glucose level when sx  If hypoglycemia and sx related to eating postprandial hypoglcyemia is confirmed  For definite diagnosis patient should have  Documented occurrence  Sx occurring  Evidence that symptoms relived by sugar  Id the particular type of hypoglycemia Action plan for hypoglycemia

 Normalize blood glucose and tx cause  Initial action juice IV bolus D50  Dietary modifications with high protein, low carb, and divide into 6 small meals o Caffeine sugar and alcohol restricted o Consider allergy testing metabolic disease Central obesity in men >40inches Central obesity in women >35 inches Fasting triglycerides >150mg/dL HDL in men <40mg/dl or taking medication for low HDL HDL in women <50mg/dl or taking medication for low HDL Blood pressure >130/>85 mmhg or taking meds for HTN Fasting glucose >100mg/dl or taking meds for hyperglycemia Can all indicate htn, hyperlipidemia, and diabetes Labs to be ordered- vitals, ht, wt, wasit circumference, lipid panel, hemoglobin a1c, ekg, urinalysis, tsh, free t4 level Thyroid issues Thyroid is controlled by the pituitary gland and the pituitary gland is where TSH comes from. The thyroid is needed for metabolism and is the engine of the endocrine system. Screen pts for thyroid disorder for hypo or hyper thyroid and metabolic syndrome. TSH is the most helpful screening tool  made the anterior pituitary  negative feed back loop- TSH is trying to turn on the thyroid and it is not getting enough hormone. TSH is screaming please turn on if TSH is low.  low tsh – hyper  high tsh-hypo Free T4 metabolically active is the most helpful for confirmation of dx  40% converted to T3 in periphery and it is more metabolically active than T4  Insufficient evidence +/- routine thyroid screening in the absence of clinical suspicion. GI GERD Dyspepsia and heart burn Dyspepsia  Epigastric discomfort  Postprandial fullness, early satiety  Anorexia, belching, bloating  Nausea/vomiting  Dysphagia and abdominal burning Heart burn  Extreme pain that is difficult to distinguish from angina  Sometimes radiates to back, arms, or jaw Heart burn-retrosternal burning.

GERD IS THE MOST COMMON CAUSE OF HEARTBURN Causes of GERD  Stomatch and duodenal contents backflow into esophagus and can cause mucosal damage and serious consequences Pathophysiology  Something is happening with the esophageal sphincter that it is not working correctly to prevent reflux. o Can be intra abdominal pressure is increased  Pregnancy  Obesity  Bending over o Hiatal hernia o Gravity o Decreased tone of the Lower esophageal sphincter caused by caffeine, alcohol  Normal squamous epithelium gets replaced by metaplastic columnar epithelium (Barrett’s epithelium) o Tissue is more resistant to acid but it has a higher risk of esophageal cancer Aggravating factors (fun foods)  Reclining after eating  Large meal  Nicotoine  Alcohol  Chocolate  Caffeine  Fatty or spicy food  Heavy lifting  Peppermint and spearmint  Tomato products  Medications o Anticholinergic agents o Calcium channel blockers o Diazepam o Estrogen and progesterone o Beta adrenergic blocking agents o Theophylline Diagnostic Test Empiric trial of acid suppression 4-8 weeks to diagnose gerd  Unless an alarm sx is present  Test for H.Pylori Alarm sx  Black and bloody stool  Chocking  Chronic cough  Dysphagia

 Hetmatemesis  Iron deficiency anemia  Wt loss Test  Ambulatory esophageal ph monitoring- 85% sensitivity/ 95% specificity  Upper endoscopy with biopsy- lacks sensitivity o Test of choice to assess complications for tissue damage  Erosive esophagitis  Stricture  Barrett’s esophagus  Screen with sx greater than 5 years  Risk factors are male, white, over 50, hiatal hernia, increased bmi and obesity  Barium radiology- not super useful Differential diagnosis:  Peptic ulcer disease o Pain is usually relieved by food  Cholelithiasis/cholecystitis o High fat meals o Epigastric or right subcostal pain o Nausea and vomiting  Angina/ MI o Relieved by nitrates o Calcium channel blockers, beta blockers, and nitrates decrease lower esophageal pressure and can produce consistent esophageal reflux Symptoms  Heart burn  Regurgitation  Sour taste in am  Belching  Coughing Objective – may have occult blood in stool or increase in dental caries Management-  Goal is to eliminate sx and reduce complication  Give education on pharmacological interventions  Antacids o If its mild and infrequent o Onset is instant o Duration 20-30 min o Calcium carbonate, magnesium hydoroxide  Tums, rolaids, Maalox, Mylanta o Neutralizes stomach acid to increase ph for short term relief o Magnesium can cause diarrhea o Calcium can cause constipation  H2 blockers

o Use for mild moderate episodes o Onset is 30-45 min o Duration 4-10 hours o Famatodine, ranitidine, cimetidine  Works to bind to h2 receptros and decrease acid secretion  Treat mild to moderate heart burn and can be used prn  Proton pump inhibitors o Use if frequent of atleast 2 days a week o Onset is 2-3 hours several days to completely relieve o Duration is 12-24 hours o Start at low doses and consider reevaluating at 6 weeks  Step wise process o Step 1 for mild sx  Dietary modification  Lifestyle changes  Try antacids o Step 2 for non responders without erosive disease  Lifestyle changes  H2 antagonists  PPI  8-12 weeks therapy o Step 3 severe sx for erosive disease  GI work up endoscopy  High dose h2 anatgonist  Higher dose PPI Adverse effects of PPI  Hypochlorhydria can cause infections and malabsorption of calcium and magnesium  Decrease calcium absorption  Hypomagnesia due to reduced absorption o Get a magnesium level  Cdiff can occur Nonpharmacological tx  Don’t eat before lying down  Elevate head of bed  Reduce portion size  Lose weight Taper PPI if used longer than 6 months Refer to GI if surgery needed Refer to GI if they have not had a colonscopy Nausea and vomiting If nausea vomiting diarrhea think infectious Watch for dehydration Unpleasant sensory experience in the stomach Can be accompanied with diaphoresis, increased salivation, vasovagal sings

Vomitting- can be reflexive Forceful expulsion of gastric contents Reflex response to stimulation of receptor sites in the upper gi tract, inner ear, chemoreceptor trigger zone in the medulla oblongata (CTZ) For nausea and vomiting ask- Onset and duration- association to meals, projectile vomiting Characteristic- odor, color, contents Associated symptoms- nausea, vertigo, tinnitus, headache, diarrhea Symptoms  IV fluids are not preferrable we want them to take it orally  Do they have orthostatic hypotension (dehydration sign)  n/v/d  fever  abdominal pain and cramping  fatigue, mailaise, anorexia, tenesmus Differential diagnosis-  IBS-  IBD- irritable bowel disease  Ischemic bowel disease  Partial bowel onstruction  Pelvic abscess  Pancreatitis  Eating disorder Treatment  Fluids with sodium (Pedialyte or Gatorade)  IV therapy  Possible hospitalization  Antimotility drugs like loperamide o Do not give in febrile dysentery or with bacterial infections  Antibiotics known for bacterial infection  Antiemetics Teach  BRAT- banana rice apples toast  Hand washing  Safe disposal of wast  Travel precaution – safe food choice  Don’t send kids to school Rule out pregnancy- beta hcg if they have ovaries and are of child bearing age Treat underlying cause and provide sx relief with antimetics and dehydration Most common cause is acute gastroenteritis  Viral most common is rotavirus leading cause in kids and norovirus leading in adults and protozoa o Protozoa  Entamoeba histolytica  Crypotsporidum

 Giardia lambia If N/V continues, requires a more in depth work up work through differential diagnosis list Constipation Usually subjective and is a decrease in frequency or increase in difficulty of defacation Common in the western society, elderly, and sedentary  Causes o Lack of fiber o Habitual use of laxative o Not enough water o Irritable bowel syndrome o Change in environment or travel o Medication o Tumors o Hypothyroidism o Diabetes o Hypercalcemia o Pregnancy  History is fecal description and bowel pattern  Physical exam o Occult or frank blood o Abdominal exam  Categories o Simple- low fiber and suppression of defacation o Disordered motility- slowed transit time, IBS, diverticular disease o Secondary constipation- medication, chronic laxative use, immobility, functional, tumor  Meds can be opiates, calcium channel blockers aluminum antacids  Treatment o Increase dietary fiber 25-35 g daily o Exercise o Adequate hydration o Medications  Bulking agents  Psyllium methylcellulose preparations  Stool softeners  Docusate sodium o Action draws water into the stool to the mix with soften stool o Indication constipation to prevent straining with anorectal conditions  Saline laxatives  Magnesium sulfate

 Stimulating laxatives- last line of therapy because it can cause abdominal cramping and cause diarrhea  Bisacodyl, senna, cascara o Senna is 15mg daily only daily doses should be taken at night  Lubricants  Mineral oil Diarrhea Increased frequency or increased fluid in the bowels. This is subjective to the patient Frequent diarrhea can cause hypokalemia and dehydration You want to know duration, triggers, alleviating, and worsening factors.  Osmotic diarrhea o Lactase deficiency o Ingestion of poorly absorbed solutes magnesium sulfate o Small bowel injury  Secretory diarreha o Bacterial entertoxins like cholera and strains of e.coli o Laxative abuse o Bile salt malabsorption o Endocrine tumors o Diarrhea associated with morphological changes  Inflammatory bowel disease  Differential diagnosis o Acute  Abrupt onset and last for more than 1 week  Viral or bacterial gastroenteritis  Dysentery syndrome- amoeba in origin  Drug induced  Laxative induced  Antibiotic induced cdiff  Chronic- last more than 2 weeks or recurs over months or years o Inflammatory bowel disease  Crohn’s disease  Ulcerative colitis  Irritable bowel syndrome  Treatment o Loperamide (Imodium)- binds to intestinal opioid receptors to inhibit peristalsis o Can be used acute or chronic Musculoskeletal: back pain Low back pain  Common complaint  Can be acute or chronic  Can be benign (overuse) or serious (nerve compression, metastatic disease)

 Can be a signal symptom of a serious underlying medical condition or emergency  Red flag: tingling down the leg, less movement worsening pain, paresthesia These pts need to move ASK FOR URINALYSIS MAKE SURE ITS NOT A KIDNEY STONE Differential diagnosis  Musculoskeletal strain  Sciatica  Spinal stenosis  Infection  Pyelonephritis  Prostatitis  Ankylosing spondylitits  Cauda equina syndrome  Cholelithiasis  Herniated disc  Aortic aneurysm  Spondylotlithesis Assessment:  Precipitating event  Active rom  Presence of palpable muscle spasm  Character of pain- numbness tingling radiation or localized  Age of pt  History  Check spinal processes  Strait leg test LBP RED FLAGS  Cancer likely to have bone mets (breast, lung, thyroid, renal prostate)  Urinary or fecal incontinence  Urinary retention  LE motor or sensory loss  Severe pain + lumbar spinal surgery in past 12 months  Pain worsens with laying flat Imaging:  You have to go in order. Very rarely have imaging  Lbp without red flags with suspected degenerative changes/sprain/strain o Try 4 – 6 weeks of tx o If sx improve  Stop imaging o If sx continue  Neuro deficit could need mri  No neuro deficit stop imaging Acute low back pain tx: Goal is to keep them up and moving because they are very sedentary

 Immediate referral for emergent sx  Pt not found to have better outcomes with early imaging  Non surgerical refer to pt  Medications o Nsaids- start with Tylenol and ibuprofens o Muscle relaxants (watch side effects) o Caution with opiates o Antidepressants for neurofibromyalgia o Pain clinic for epidural steroid injections o Referral to ortho neuro surgeon. o Behavioral therapy for referred pain that could be a psychological problem Scoliosis- lateral deviation of the spinal column that may or may not include rotation or deformity of the vertebrae  Classification o Postural scoliosis- small curve that corrects with bending o Structural scoliosis- fixed deformity that does not correct with bending o Congenital scoliosis- caused by disturbances in vertebral development during the 6 th -8 th week of embryologic development o Neuromuscular scoliosis- develops from neuropathic or myopathic diseases o Idiopathic scoliosis- structural spinal curvature for which no causes has been established.  Bending forward is looking for asymmetry in rib cage and shoulders. Screen for in kids Joint pain- hip, knee, arm, should, foot  Precipitating event  Active rom  Presence of palpable muscle spasm  Character of pain-numbness, tingling, radiation or localized  Age of pt history of degenerative arthritis  Red flags: joint specific pain pattern, loss of pulses or function, pain out of proportion, erythema with effusion, systemic symptoms rotator cuff injury  impingement is usually in older pts and involves the supraspinatus or infraspinatus  rotator cuff is usually younger pts with acute onset and pain with muscle movement palpate at the sternoclavicular, acromioclavicular and subacromial areas noting tenderness Differentials  adhesive capsulitis  tendinitis  impingement  fracture  arthritis

Diagnosis  3 signs or 2 signs if you are over 60 years old o Supraspinatus weakness o Weakness in external rotation o Impingement signs  Neer’s supraspinatus is the long head of the biceps tendin  Raising the arm up to the side and to the head o If positive it is pain in the 70-120 degree  Haskins rc muscles long head of biceps tendon Rotator cuff tear test:  arm drop sign is the pt has to abduct the arm to shoulder level and lower it slowly o abduction above 90-120 degrees shows action of the deltoid muscle so they can only go up 90 degress Tet supraspinatus strength (empty can test)  elevate the arm to 90 degress and internally rotate the arms with the thumbs pointing down as if emptying a can. Pt should be able to resist you when you push down on their arms Shoulder pain treatment  physical therapy  nsaid  subacromial corticosteroid injecton  extracorpeal shockwave therapy if tendon is calcified  may require surgical intervention  oral prednisone for frozen shoulder sports physicals preparticipation physical are screening for life threatening conditions ht wt immunization, physical exam, and musculoskeletal exam is needed Red flags are  heart murmurs  inguinal hernia- specifically on male athletes  marfan syndrome- refer to cardiology Refer when appropriate  female athlete triad  musculoskeletal issue  cardiac  ortho presports counseling preparticipation screening that is a standardized form from the state the primary care physician is the best to do this Do musculoskeletal assessment GU  UTI Urinary tract invaded by organism  Acute – sudden and easy to tx with short course of antibiotics

 Chronic – caused by obstruction, antibiotic resistant bacteria, multiple bacteria o Can be asymptomatic  Complicate uti- accompanied by factors that complicate infection Honeymoon cystitis- frequent sexual activity is more likely for UTI ** Predisposing factors  Diabetes  Sexual contact  Urinary obstruction Can have fecal contamination secondary to hygiene, sex, and a short urethra MOST COMMON INFECTION IS E.COLI Spermicides alter vaginal microenvironment Change in ph of the urine grows bacteria and the bacteria irritate the cells in the urethra Candida can the cause as well Sx  Dysuria  Frequency urgency  Nocturia  Hematuria  Low back or suprapubic pain  Urinary incontinence  Cloudy smelly urine or painful urination is not diagnostic of a UTI Test  Urine culture is the gold standard  Sample more than 100,000 organisms plus clinical symptoms  We do not need to treat if it is not symptomatic unless it is someone pregnant  Clean catch is midstream urine sample for urinalysis  Indwelling catheter samples can’t be more than 24 hours old  Sensitivity gives antibiotic narrowing Urinalysis may have  Cloudy appearance alkaline ph hematuria  Elevated nitrities and leukocytes  Urine sediment of rbc, wbc, mucus, bacterial overgrown Nitrites are more specific for bacterial UTI. They are a byproduct of bacterial growth. If a uti only has wbc. The nitrates are very specific for bacterial infection Culture and sensitivity will be done if the uti is not getting better or they have recurrent infections, or you are making sure you need to start antibiotics A LOWER UTI DOES NOT GIVE YOU SIGNS OF SEPSIS (FEVER, CHILLS, WBC CLASTS, FLANT OR COSTOVERTEBRAL TENDERNESS) Differentials  Tumors  Upper uti  Vaginitis  Std  Asymptomatic bacteriuria chronic uti needs to be referred to urology. Avoid treating colonized pt. interstitial cystitis doesn’t get antibiotics

Treatment  Nitrofurantoin (Macrobid)- covers g- and g+ bacteria o Works only in the urinary tract by concentrating in bladder o Do not use in elderly  Trimethoprim-sulfamethoxazole (Bactrim) 3 days for uncomplicated o Use in women o Use in children  Fungal UTI fluconazole 200mg qd 7-14 days  Analgeics pyridium 200mg po tid- turns ears and urine orange o On a dipstick appears as hematuria  Antispasmodics prn  Extend treatment time if it is a man. Atleast 7 days of treatment . LGBTQ PrEP therapy Truvada ( emtricitabine 200mg/tenofovir disoproxil fumarate (TDF) as preexposure prophylaxis to prevent HIV for those at risk Orders: Do a cmp, STI panel, HIV 1 antibody screen, GFR) Taken once a day Hep a, b, and hpb vaccination can be encouraged Vitamin d3 and calcium decrease bone loss caused by Truvada  Labs to do before giving prep o Hiv 1 4 th generation antigen/antibody assay o Hiv 1 RnA quantitation o STI screen o Creatinine o Urinalysis o Hep A o Hep b o Hep C o Pregnancy test o Baseline dexa scan for those with previous anorexia  Every 3 months you do o Hiv 1 4 th generation antigen and assay o Hive 1 rna quantitation o Sti o Serum creatine o Urinalysis o Pregnancy test Patient education  N, V, D, HA, fatigue can go away 4 weeks after starting o Treat with Tylenol  Can cause: o Decreased bone density o Lactic acidosis o Hepatomegaly

o Renal toxicity o Pancreatitis o Osteomalacia  Must take daily to keep concentration of the drug in the body  Mutations can occur if it is not taken each day. HIV can mutate and become resistant to prep if it is not taken routinely PAIN  opioids  substance abuse  prescription drug monitoring Rules of thumb, common sense rules: • Use the lowest effective dose by the simplest route. • Start with the simplest single agent and maximize it’s potential before adding other drugs. • Use scheduled, long-acting pain medications for constant or frequent pain, with prn, short-acting medication available for breakthrough. Treat breakthrough pain with one-third the 12 hours scheduled dose