S01E06: High Yield Internal Medicine Review (Part One and Two)

Here you will find the show transcripts and cited resources used for the HY IM Podcast Episode (part one) and the rapid review (part two). To jump to the Rapid Review questions, click here.

Hello and Welcome to PASPAC Podcast, Your Audio Passport from Physician Assistant Student to Certified – and beyond – with your host, Rebecca Harrell, MPA, PA-C.

Today, our destination is a high yield review of Internal Medicine based on the EOR topic blueprint

Please sit, back, relax, and let’s get to it

Hey Everyone, It’s Becca

As you know, we’ll be doing an overview of the highest yield IM topics today, going in descending order of the covered content on the EOR topic blueprint, starting with Cardiovascular Disorders which makes up a whopping 20% of the EOR.

CARDIOVASCULAR

Your 55 year old patient arrives to the ER due to onset of chest pain while working in his garage ~25 minutes ago. He has his fist clenched over his sternum and is speaking through clenched teeth. He has a history of stable angina and is currently prescribed daily beta blockers and SL Nitro PRN, but for the first time, his nitroglycerin is not providing him any relief. He denies any substance use. EKG shows T wave depression in leads II, III, and AVF. What should be done to establish a definitive diagnosis in this patient?

Coronary Catheterization with Angiogram

• This will provide a definitive diagnosis of UA vs. NSTEMI, which should be suspected in any patient with chest pain unrelieved with nitroglycerin in the setting of a history of CAD.

  • The only difference between UA and NSTEMI presentation is elevation of cardiac enzymes in NSTEMI, but given our patient is presenting within 25 minutes of onset, cardiac enzymes at this time will likely be nondiagnostic, though valuable so still initiate serial testing.

• His EKG does not meet criteria for an Acute STEMI, but ST Depression with persistent chest pain are both considered a high-risk factors for ACS.

• Remember your steps prior to obtaining your definitive diagnosis.

  • For example, patient should have been given High Dose Aspirin, 3 doses of SL Nitro 0.4 mg q5 minutes (unless contraindications exist, like use of PDE-5 Inhibitor within 24 hours or signs of right ventricular infarct), already have IV access established with lab work sent off, including serial cardiac biomarkers, plus initiation of oxygen therapy and possibly IV Morphine for severe pain.

• Assuming all of this has been started when brought in by EMS, and EKG shows concerning features, antiplatelet and anticoagulation therapy should be considered and give PO Beta Blocker (ex. Metoprolol Tartrate) if no signs of heart failure, bradycardia, hemodynamic compromise, or reactive airway disease.

  • If the patient was hypertensive, you could switch to IV Metoprolol instead.

• Because our patient has evidence of possible right ventricular infarct, given changes to leads II, III, and aVF – we would want to forgo the IV Nitroglycerin.

  • However, in general, Afterload reducers like IV Nitroglycerin and Loop Diuretics should be given if Left Heart Failure, is present.

• You can assume our patient is stable for now, given lack of unstable features in the stem, but if hemodynamic compromise existed you would want to remember your ABCs and get them into an emergent cath for diagnostic angiography with consideration for PCI if determined it is needed during the Cath.

• For high-risk patients undergoing Cath with or without PCI, you can consider adding GPIIb/IIIa Inhibitor before angiography.

• Additionally, start patient on a High Intensity Statin, if not already on.

• Cardiac Catheterization with Angiogram will provide a definitive diagnosis with the option of performing PCI if need for a stent is identified given the blockage.

• In low risk patients who present with angina and low probability of ongoing ischemia by evidence of relief of chest pain with normal serial troponins, consider non-cardiac causes or, if high risk of cardiac disease given age, presentation, and additional risk factors consider obtaining a noninvasive cardiac evaluation, such as a NST, prior to discharging.

• Remember, if patients has STEMI or evidence of infarction, they should be discharged with an ACE Inhibitor, which are proven to decrease LVH and remodeling, improving ejection fraction.

Your 17 year old patient is brought in via EMS after fainting during a football game. He is stable now and states he thinks he might have just been dehydrated but did feel shortness of breath and dizziness before he passed out. Physical exam reveals a loud S4 and harsh crescendo-decrescendo murmur over the apex and left lower sternal border. EKG reveals prominent Q Waves and deeply inverted T waves. What is the initial management of suspected diagnosis?

Initiation of Negative Ionotropic Agents, such as a cardio-selective Beta-Blocker, like Metoprolol, or Non-Dihydropyridine CCBs, like Verapamil should be initiated in patients with Hypertrophic Cardiomyopathy (HCMO).

• These agents both decrease contractility and slow down the heart rate, two huge contributors to outflow obstruction if elevated.

  • Drugs that decrease the preload, like nitrates, diuretics, ACE-I and ARBs, should be avoided and Digoxin is contraindicated due to its positive ionotropic action.

  • In all patients presenting with syncope or sudden cardiac arrest, an implanted cardio defibrillator should be strongly considered. All patients with HCMO need to be advised to avoid strenuous exercise and dehydration.

• HCMO is an Autosomal Dominant genetic condition and is the most common cause of sudden cardiac death in young athletes, so typically stems will present with an athlete who either faints or experiences dyspnea on exertion during their practice or a game.

• While most other cardiomyopathies present with systolic dysfunction, HCMO is a diastolic dysfunction.

  • This can be remembered with visualizing the thickened ventricle that is so thick and heavy, it cannot stretch easily, leading to decrease in preload – which is a diastolic (filling) problem. Considering the left ventricle is so big and "muscle-y", the systolic function is intact because it typically has no problem forcing the blood out, but instead, it’s problem is allowing for actual problem filling.

• Additionally, HCMO will have an asymmetrical interventricular septum, leading to that characteristic murmur that will decrease with increased preload (aka flattening the septum out) and increases with decreased preload (aka septum isn’t flattened and obstructs the outflow).

What Dynamic maneuvers increase preload vs. decrease preload?

Valsalva and standing will decrease preload – which increases sound of HCMO murmur

Leg Raise & Squatting will increase preload – which decreases sound of HCMO murmur

• HCMO also commonly presents with S4 gallop, which is also called an atrial gallop, and occurs right before S1 while the atria is trying to squeeze blood which is vibrating against a non-compliant LV.

  • Other signs include JV pulse with prominent “A” wave.

• As with other structural heart conditions, cardiac echo, is diagnostic – showing LVH with thickened septum and diastolic dysfunction.

How does paroxysmal SVT appear on an EKG and what are the different treatment options?

SVT will appear as a narrow QRS tachycardia which often has no identifiable P wave, or possibly a delayed and inverted P wave. There will be no dropped or extra beats and the rhythm will appear regular, but fast

• The most common cause of SVT is AV Nodal Reentrant Tachycardia, which is when there is reentrant conduction circulating within the AV node itself.

  • The P wave, which is a result from the SA node receiving an impulse that leads to atrial depolarization, will either be buried within the QRS due to the initial impulse coming from the AV node, or inverted after the QRS, due to the delayed atrial contraction from an electrical conduction traveling backwards from the AV node to the SA node, leading to the inversion of the P wave.

• The patient will either present stable or unstable, and this will determine your treatment options.

  • Signs of instability include impending or current hemodynamic compromise – so always look at the vitals given – or even just altered mental status.

• If the patient is stable and asymptomatic, the initial treatment is Vagal Maneuver, in which the patient should be instructed to bear down in order to increase their intrathoracic pressure.

• If the patient is stable and symptomatic OR the vagal maneuver was unsuccessful, the treatment of choice is Adenosine 6mg Rapid Bolus IV push which will lead to a transient inhibition of AV node conduction.

  • Advise the patient they will likely feel sick or even a feeling of impending doom for a few seconds during this time.

  • If the 6mg bolus does not correct the SVT, you may go up to 12mg followed by another 6mg.

  • In over 80% of cases, this will terminate the SVT.

  • Patients can also be given IV Diltiazem and Metoprolol to control rate and decrease AV nodal conduction if Adenosine does not control rhythm and they are still stable.

• If the patient is unstable, always remember “unstable gets the cable” which means electricity.

  • Because this is a regular rhythm with an identifiable QRS, you should always choose synchronized cardioversion, because the machine will be able to identify and synchronize to deliver the shock timing with the QRS.

  • FYI Any time a patient has an irregular rhythm with unidentifiable QRS, such as in VF or pulseless VT, you would choose defibrillation which is a form of unsynchronized cardioversion.

What underlying cause of paroxysmal SVT would you suspect if the patient has prior EKGs showing shortened PR intervals and wide, upsloping QRS waves?

Wolf-Parkinson-White, suspect this given the description or presence of Delta Waves.

• In the case of Wolff-Parkinson-White Syndrome, which is not an SVT in and of itself, but places the patient at risk of SVT through an accessory pathway, not the AV node. This accessory pathway is named the Bundle of Kent .

  • If a reentrant tachycardia occurs, can either be orthodromic, in which the conduction begins at the AV node and travels through the accessory pathway, leading to a narrow complex tachycardia; or it can be Antidromic, which will result in a widened QRS due to conduction starting at the pathway which “pre-excites the ventricles” and then travels to the AV node.

• Immediate treatment is similar to SVT which is stable gets vagal and/or adenosine and then a 3rd line AV nodal blocking agent if adenosine is ineffective, like IV Verapamil as long as the complex is narrow.

  • AV Nodal blockers are contraindicated in wide complex antidromic SVTs. As always, if a patient is unstable, they need immediate cardioversion.

• The definitive treatment of WPW includes catheter ablation of the accessory pathway, or even surgical ablation if needed.

Your patient is a 56 year old postmenopausal female with PMHx of Generalized Anxiety Disorder and social history notable for recent death of her wife presents with acute substernal chest pain and shortness of breath. EKG reveals a STEMI in the anterior precordial leads but in the cath lab, there is no angiographic evidence of any obstruction or acute plaque rupture. What should be suspected as the cause of this patient’s presentation?

Stress Cardiomyopathy aka Takotsubo Cardiomyopathy

• This will present with TRANSIET regional systolic dysfunction and can mimic an acute STEMI, both in clinical signs and symptoms AND on EKG with elevated troponin.

  • However, the key here is that there will be no evidence of CAD once evaluating in the Cath Lab.

• This condition has also been known as “Broken Heart Syndrome” and is classically seen after a major physical or psychological stressor, such as the death of a loved one as we see in our stem.

• In Stress CMO, there will be regional wall motion abnormalities that can even extend beyond a territory perfused by a specific coronary artery.

  • The pathogenesis is poorly understood, but proposed mechanisms include excess of catecholamines, microvascular dysfunction, or even coronary artery spasm.

• Because Stress CMO is generally transient, treatment is usually supportive and conservative.

  • However, some patients can develop shock or heart failure which require intensive therapy, following standing HF guidelines after stabilization.

  • Occasionally, there may be need for mechanical circulatory support like with a percutaneous flow-device.

• Since there is a risk of intraventricular thrombus in patients with systolic dysfunction and wall motion abnormalities, consider echo to evaluate for thrombus and initiation of anticoagulation if a thrombus is seen.

What are the common medications used as lipid lowering therapy and what are some high yield adverse effects or contraindication associated with them?

Statins (1st line) – Rhabdomyolysis, Increased LFTs, Potentiates Warfarin, Pregnancy Category X

ADDITIONAL:

• Ezetimibe (only non-statin that has proven to prevent CVD A/E when combined w Statin) – Increases LFTs

• PCKS9 Inhibitors (Alirocumab, Evolocumab) – Injection site reactions

• Fibric Acid Derivatives (Fenofibrate) – Can decrease Cyclosporine, Gemfibrozil can increase Warfarin effects

• Nicotinic Acid (Niacin) – Flushing, HA, Warmth, Pruritus, Acanthosis Nigricans

• Bile Acid Sequestrants (Cholestyramine, Colestipol, Colesevelam) - Bloating and Cramping, increased LFTS, can also impair absorption of fat soluble vitamin and medications like Amiodarone, Digoxin, Warfarin, Levothyroxine, Beta-Blockers, and Thiazides

• Neomycin – Nephrotoxicity and Ototoxicity – I remember this by relating the prefix NeO with N standing for Nephrotoxic and O standing for Ototoxic.

Your patient is a 27 year old who arrives to the ER due to new onset of exercise intolerance and excessive fatigue. He denies any history of substance use and is not taking any medications. He states he is generally healthy but had a small cold last week that resolved on its own. Physical exam is notable for a new summation gallop and EKG reveals non-specific ST changes in the setting of tachycardia. His cardiac enzymes are elevated and cardiac cath reveals no CAD. What would provide definitive diagnosis for your top differential?

Endomyocardial Biopsy provides definitive diagnosis of Myocarditis; however, this is generally not done due to its low sensitivity and high risk of complications.

• Myocarditis is due to cardiac cell necrosis secondary to inflammation of the myocardium and can be caused by seemingly everything, but is most commonly secondary to a Viral Infection, like Coxsackie B Virus.

  • Other causes of myocarditis include parasites like T. Cruzi aka Chagas Disease, Bacterial causes like Lyme Disease; Autoimmune conditions like SLE and Kawasaki, Systemic Inflammatory Disorders, Vaccines, or even Idiopathic.

• EKG findings can really vary from “saddle shaped” ST elevation to non-specific changes to dysrhythmias and HB.

  • So, you should really have a high index of suspicion for this in a patient with history of viral illness and new EKG changes or even pericarditis, with cardiac injury evidenced by elevated enzymes, and a normal cardiac cath or MRI.

• Physical findings may present with unexplained sinus tachycardia out of proportion to fever or new onset dyspnea and excessive fatigue which later escalates to heart failure and risk for sudden cardiac death.

  • A summation gallop is a high yield finding for myocardial disease and is the result of both an S3 and S4.

  • Pulses will also typically be weak and there may be a pericardial friction rub is pericarditis is also present.

• In patients with a suspected viral cause, therapy is supportive, and heart failure therapy should be initiated as needed. Also consider antidysrhythmic or the need for immunosuppressants or IVIG if suspecting autoimmune etiology.

  • Of course, bacterial and parasitic etiologies can be treated with antibiotics and antiparasitics, respectfully.

• If suspecting myocarditis is secondary to a drug toxicity, you should stop the drug and give Corticosteroids.

Your patient is a 21 year old male with PMHx notable for Marfan Syndrome who presents for annual follow up. Cardiac Auscultation reveals a late systolic murmur proceeded by a mid-systolic click best heard at the apex. The intensity of the murmur increases with standing and decreases with squatting. What diagnosis do you most suspect?

Mitral Valve Prolapse

• Most cases are asymptomatic, and because the patient is presenting for an annual follow up with no chief concerns otherwise mentioned – we can assume he is asymptomatic as well.

  • If the prolapse is severe, symptoms may be evidenced by palpitations, dyspnea, fatigue, and non-exertional chest pain.

• The murmur is unique in that it will increase with decreased preload (aka standing) and decrease with increased preload (aka squatting), as is also seen in Hypertrophic Cardiomyopathy.

  • The other valvular murmurs are opposite, so most others will present with decreased intensity with decreased preload and increased intensity with increased preload. MVP and HCMO dare to be different – and different is always high yield.

• Like all valvular disorders or structural heart disease, the diagnostic test of choice is echocardiogram, specifically transesophageal echocardiogram.

• In severe cases of MVP that are symptomatic or at risk of progressing to Mitral Valve Regurgitation, you can repair the valve percutaneously or with surgery.

  • If Mitral Valve Regurgitation develops, which should be suspected with a new blowing systolic murmur at the apex and radiating to the left axilla OR, if acute, leads to harsh mid-systolic murmur radiating to base and leading to acute left sided heart failure then the treatment is with afterload reduction agents like nitrates, beta-blockers, CCBs, or ACE Inhibitors +/- Anticoagulation if Afib develops or TEE visualizes a thrombus.

  • Valve replacement should be done in patients that are surgical candidates with clinically significant disease, such as acute MR or MR leading to heart failure or severe symptoms.

Your 15 year old female patient presents with new onset joint pain that seems to affect different large joints each day and development a widespread nonpruritic rash that spares her face and of painless, firm, nodules overlying her lower extremities. Physical exam reveals she has temperature of 100.4 F and auscultation overlying the apex reveals a new blowing systolic murmur that radiates toward her left axilla. Her past medical history is unremarkable aside from a sore throat a couple weeks ago that her mom states went away on its own. How should your treat suspected diagnosis at this time?

IM PCN G Benzathine every 21-28 days for at least 10 years or until age 40

• This patient most likely has Acute Rheumatic Fever secondary to an untreated Strep Infection.

  • You should also suspect if she had presented the same way but with a past medical history notable for scarlet fever or even impetigo.

• Acute Rheumatic Fever is diagnosed based on the Jones Criteria – Which requires evidence of a Streptococcal Infection via Anti-Streptolysin O or other Strep Antibodies, positive strep throat culture, positive rapid antigen test, or recent scarlet fever.

  • In addition to evidence of a current or prior strep infection in initial acute rheumatic fever, you need either two major criteria OR one major and two minor criteria:

    • I remember the Major Criteria by the mnemonic JONES where J = Joints aka Arthritis, O is shaped like a heart to represent Carditis, N is for nodules, E for Erythema Marginatum and S stands for Sydenham’s Chorea (also known as “St. Vitus Dance”, which results in abrupt purposeless movements)

    • Minor Jones Criteria include arthralgias, fever, elevated inflammatory markers CRP or ESR and prolonged PRI on ECG.

• Treatment of Rheumatic Fever essentially depends on presence of cardiac involvement

  • Standard of care includes PCN + NSAIDs and then monitoring CRP for continued decrease even after anti-inflammatories are discontinued

  • Specifically, the duration of treatment with PCN depends on the following

    • If valvular heart disease is present – they’ll need monthly IM PCN for 10 years or until age 40 (whichever is longer)

    • If Carditis is present, but NO valvular disease – you’ll do monthly IM PCN for 10 years or until age 21 (whichever is longer)

    • If the heart is not involved in the course of the Acute Rheumatic Fever, then you’ll give monthly IM PCN for 5 years or until 21, again – whichever is longer.

    • Alternatives to IM PCN include PO PCN V BID or Azithromycin 250mg PO daily if allergic to PCN.

    • If valves are damaged enough, surgery for valve replacement or repair may be warranted.

Ok, we will cover a whole bunch more cardio high yield at the end during the rapid review, but for now lets move onto Pulmonology, which makes up 15% of the EOR

PULMONOLOGY

Your patient is a 66 year old male with longstanding history of COPD who presents to your clinic due to increased sputum production that has a particularly foul odor. Additionally, he is reporting chest pain that is worse with inspiration. Physical exam reveals crackles and wheezing overlying the inferior lung fields bilaterally. Vitals are largely normal aside from slight fever and O2 sat of 90%. What is the gold standard for diagnosing top differential?

CT of the Chest is considered gold standard for diagnosis of Bronchiectasis, which is secondary to permanently dilated or destructed bronchial walls due to chronic inflammation and infection.

• While the most common cause of Bronchiectasis is Cystic Fibrosis, you should also suspect this in any patient with longstanding pulmonary inflammation or recurrent pulmonary infections, like COPD, with increased purulent and foul-smelling sputum.

• Most commonly, Bronchiectasis is due to viruses like Adenovirus and Influenza, but can also be bacterial with common causes including Strep pneumoniae and Pseudomonas.

• Differentiate this from pneumonia, which will more commonly present with a specified area of consolidation unilaterally.

  • Another way to differentiate from Pneumonia is via imaging. Specifically, CXR in Bronchiectasis will be unique due to the appearance of linear “tram track” lung markings from the thickened bronchial walls and “plate-like” atelectasis, secondary to scarring.

• The mainstay of treatment includes treating the underlying infection, typically with aggressive antibiotic therapy

• Additional treatment includes Chest Physiotherapy, Indomethacin and Bronchodilators, Supplemental Oxygen and underlying diseases as warranted.

• Lung Transplant is definitive

Your 40 year old male patient with BMI 51 is admitted to the hospital due to new onset of dyspnea on exertion and LE swelling. Physical reveals JVD and hepatojugular reflex with palpation of enlarged liver. He denies any past medical history, but his wife mentions she’s been trying to get him to go for a health check up due to his horrible snoring which she states can sometimes abruptly stop and it seems he isn’t breathing at all. Vitals reveal he is afebrile, BP 140/88 with respiratory rate of 10. ABG reveals a PCO2 of 48. Assuming he is stable, what is the first line therapy for the suspected diagnosis?

Weight loss & Positive Airway Pressure, in patients with Obesity Hypoventilation Syndrome plus OSA, Nocturnal CPAP should be initiation or BiPAP if CPAP fails or they also have hypoventilation during sleep. Adjuvant supplemental oxygen is required if they have severe hypoventilation and still cannot reach their ventilation goals

• Obesity Hypoventilation Syndrome (previously known as Pickwickian Syndrome) is secondary to hypercapnia in the alveoli during wakefulness that is not attributable to anything except for obesity.

  • Typically, they will have Obstructive Sleep Apnea on presentation, but late stages may present with Cor Pulmonale (aka Right Heart Failure), like in our patient.

• ABG will represent pattern of chronic hypoventilation, which results in primary respiratory acidosis (due to increased CO2 retention) with FULL metabolic compensation, due to the chronic nature

  • So, in addition to the pCO2 being over 45, Bicarb will also be elevated which may result in a normal pH overall.

• To diagnose OHS, you should rule out differentials including hypothyroidism, electrolyte disturbances, COPD, interstitial lung disease, and external factors like drugs and alcohol.

Your 60 year old male patient is admitted to the hospital due to new onset dyspnea and cough in the setting of an abnormal chest x-ray showing eggshell calcifications that are mostly in the upper lung fields. FEVI/FVC ratio is 82%. History reveals he is retired but was formerly working as a sandblaster for many years. What is your top differential?

Silicosis which is a restrictive lung disease that is under the overall umbrella Pneumoconiosis diseases secondary to inhalation of particulate matter, like Silica.

• Typically stems will differentiate the type of Pneumoconiosis based on the patient’s occupational history leading to exposure of the causative agent

• For example:

  • Silica exposure is associated with Sandblasting and Coalmining

  • Asbestos exposure is associated with Shipbuilding, Construction, and Roofing

• The 3 most common causes of pneumoconiosis in the US include Silicosis, Asbestosis, and Anthracosis (also know as Coal Worker’s Pneumoconiosis secondary to Coal Dust)

• In addition to occupational exposure, the various forms of pneumoconiosis appear differently on CXR

  • Silicosis is classically described, as in our stem, with eggshell calcifications in the upper lung fields

  • Asbestosis is classically described as pleural plaques in the lower lobes

  • The best way I have found to remember this is by thinking things from the base affect the roof and things form the roof affects the base.

    • Therefore, asbestosis exposure from roofing construction affects the base of the lungs, and silicosis and/or coal exposure from the base (aka earth) affects the roof of the lungs aka upper lobes.

• You may also be given histology in the stem or answer choices, revealing asbestos bodies which look like transparent skinny fibers surrounded by iron and protein coating.

• Management is supportive, including removing or minimizing exposures and smoking cessation.

  • There is some evidence that corticosteroids help with alveolar inflammation in Silicosis.

• Complications of pneumoconiosis is Bronchogenic Carcinoma – remember the most common lung cancer overall is Adenocarcinoma – which is true in Pneumoconiosis malignancy as well.

  • Try not to get confused between the most common diseases in a category (ex. Most common lung cancer in patients with history of Asbestosis) vs the most common risk factors or etiologies behind a certain diseases (Ex. MC Risk Factor of Malignant Mesothelioma.)

  • To explain more, the most common cause of Lung Cancer overall is Adenocarcinoma, regardless of risk factors, which is why the stem will usually present someone without a smoking history – because, while cigarette smoking is the most common risk factor for developing lung cancer – this risk factor in stems is usually used to point you toward a diagnosis that is more commonly seen in patients with that risk factor, whereas adenocarcinoma occurs in nonsmokers as well.

  • However, if you take a less common cause of lung cancer, like Squamous Cell Carcinoma, this is more likely to present in patients with a history of smoking, so that risk factor will be part of the stem.

    • So it isn’t necessarily that smokers only get SCC, but more so that SCC will most commonly occur in someone with a history of smoking.

    • Same with Small Cell Carcinoma, which is even less common than SCC, but is almost exclusively seen in smokers and also the most aggressive form of lung cancer overall.

You are consulted regarding a possible medical admission from the ER. The patient is a 45 year old patient with relatively unremarkable past medical history who has a sudden on set of cough, fatigue, and fever. She assumed she caught the flu from her preschooler, but her symptoms have been worsening and she feels she is having increased difficulty breathing. Physical reveals rales overlying the right lower lobe with associated egophony, increased tactile fremitus, and dullness to percussion. This is which is visualized as a lobular consolidation on CXR. Her vitals are within normal limits aside from a low grade fever and labs reveal BUN is 12 mg/dL. What do you decide regarding her possible admission?

Using the common algorithm CURB-65 to determine admission need for community acquired pneumonia, this patient currently does not warrant inpatient treatment at this time.

• CURB-65 is a mnemonic standing for Confusion, Urea (aka BUN > 19 mg/dL or >7mmol), Respiratory Rate (>30), BP (≤ 90/ 60), and 65+ years old. Each of the CURB-65 components are each given a score of 1.

  • Adults who have a CURB-65 score of 0, like our patient does, without any comorbidities can be high dose Amoxicillin plus a macrolide, like azithromycin, or doxycycline for outpatient treatment with emergency precaution education and appropriate follow up with PCP.

    • If our patient had the same presentation but had comorbidities or recent antibiotic use, we would want to give Augmentin PLUS a macrolide, like Azithromycin, or Doxycycline.

    • If a patient has a hx of PCN Anaphylaxis, you can use monotherapy Respiratory FQ, but this is avoided as much as possible to curb growing resistance.

  • Those with CURB-65 Scores of 2 have a higher 30-day mortality rate than those with CURB-65 scores of 0-1 and they should be considered for admission.

    • If they are really compliant and have an established PCP, you could consider close outpatient management, but most patients with this score will probably need to be admitted.

  • CURB-65 score of 3-5 indicate a 22% 30-day mortality risk and these patients definitely need to be admitted.

    • Inpatient treatments for CAP include a beta-lactam, like Ceftriaxone or Unasyn (Amp-Sul) PLUS a macrolide, like Azithromycin.

    • If there is concern for Pseudomonas you should initiate anti-pseudomonal beta-lactams, like Pip-Tazo aka Zosyn PLUS a FQ like Ciprofloxacin or Levofloxacin.

  • If there is any suspicion for MRSA, regardless of severity, you need to add Vancomycin or Linezolid.

• Prior to initiating antibiotics inpatient, you should be getting at least 2 cultures and a sputum gram stain.

  • You can start empiric treatment while waiting for results of the culture and sensitivities and up or downgrade antibiotics depending on what the C&S shows.

• Remember, overall, the most common cause of CAP is Strep pneumoniae so all of the coverages will be things that give good gram negative coverage and work well with penetrating the respiratory membranes, such as antipneumococcal beta-lactams, macrolides, and respiratory fluoroquinolones.

• Another scoring system that is used for admission consideration to be aware of, especially during clinicals or working in IM, is PSI which is the Pneumonia Severity Index.

Your patient is a 55 year old male who is generally good health but is a current smoker with a 30 Pack Year History. What screening recommendation do you recommend at this time, given his risk factors?

Annual Low Dose Helical CT Scan is recommended by the ACS for everyone 55-80 years old, in good health, with 30+ PYH and is either currently smoking or has quit within the past 15 years.

• The USPSTF has similar recs but instead recommends LDCT for patients 20 PYH who are current smokers or have quit within the past 15 years.

• If there is suspicion of lung cancer, then you would move onto diagnostic measures – so you would not choose a LDCT as a diagnostic modality– but should consider initial CXR with CT Scanning and confirmatory biopsy.

  • Remember, screening mechanisms are sensitive and meant to be for low risk patients to rule out illness, while diagnostic mechanisms are more specific and meant to rule in a diagnosis in patient with a suspected illness, like a biopsy.

Your patient is a 35 year old woman with new onset and progressive fatigue and weight loss. For the past few weeks, she’s had a cough, low grade fever, and joint pain. Physical exam reveals violaceous raised plaques around her cheeks, nose, and eyes, which she says have been present for a long time. Her labs are notable for elevated ESR, hypercalcemia, and elevated serum ACE. You order a CXR which reveals bilateral hilar adenopathy. Based on your top differential, what do you suspect histology would show following a biopsy of her skin lesions?

Non-Caseating Granulomas

• This patient has a clinical presentation and diagnostics supporting a diagnosis of Sarcoidosis.

  • In a patient with Sarcoidosis affecting the lungs, Endobronchial Lung Biopsy is definitive, but biopsy can be performed on the most accessible lesion affected, which in this case, is the patient’s cutaneous sarcoid involvement, which is termed Lupus Pernio.

• Initial test of choice in patients with suspected Sarcoidosis includes CXR and next is High Res CT if CXR has findings concerning for Pulmonary Sarcoid, like the bilateral perihilar adenopathy we see in our patient.

• An elevated serum ACE is also concerning for Sarcoidosis and can be a high yield lab finding on your stems.

  • Hypercalcemia is also commonly elevated due to the uncontrolled synthesis of Calcitriol, which is the active Vitamin D metabolite, and ESR is typically elevated given the inflammatory nature of this disease process.

• The treatment of choice in patients with Pulmonary Sarcoidosis is Systemic Corticosteroids and consideration for Methotrexate or other Immunosuppressants if patient is non-responsive to steroids.

Okay, that was a good amount of Pulmonary and we will hit on even more later in our rapid review. For now, lets keep it moving with GI/Nutrition which accounts for 12% of the EOR

GI/Nutrition

Your patient is a 33 year old female with PMHx GERD who presents to your clinic due to continued dysphagia despite PPI therapy. Physical exam reveals a thin patient with conjunctival pallor, a smooth red tongue, and cheilosis. You consult GI for an upper endoscopy, and they report during the procedure they visualized a thin mucosal membrane encroaching over the lumen of her mid-upper esophagus. What diagnosis do you suspect?

Plummer-Vinson Syndrome

• This syndrome, while rare, is high yield given its unique triad of Iron-Deficiency Anemia, Dysphagia, and Esophageal Webbing.

  • Other findings in PVS include glossitis and angular cheilitis, as our patient had, with other possible findings associated with IDA like conjunctival pallor and koilonychia.

• These patients may require esophageal dilation if there is significant obstruction of the lumen, but in mild cases, replenishing the iron may resolve the dysphagia.

• An esophageal web is similar to an esophageal ring, however a web is much thinner and eccentric, while a ring is concentric (aka encircling the lumen) and is typically between 2-5mm

• The most common cause of an esophageal stricture overall is long-standing GERD leading to scarring and narrowing of the esophagus from stomach acid.

• The most common cause of an esophageal RING is a Schatzki Ring, thought to be secondary to GERD and nearly always associated with a Hiatal Hernia.

  • Schatzki are in the lower esophagus and typically presents classically with progressive dysphagia with acute food impaction after “wolfing down a mean”, awarding it the nickname “Steakhouse Syndrome”. Though, occasionally these can be associated with Eosinophilic Esophagitis (EoE)

    • Of note, The much higher yield to know regarding EoE is the trachealization or felinization of the esophagus giving rise to the classic appearance of a ribbed esophagus with multiple concentric rings and linear furrowing.

• History is important when considering differentials of dysphagia. For example, had the patient described a progressive dysphagia of both solids to liquids, we would probably be thinking about Achalasia, which is a motility disorder causing tightening of the LES that leads to the classic bird-beak tapering on barium swallow.

• Whatever the cause of dysphagia, the diagnosis will be made by upper endoscopy. Barium swallow may be done initially, but again, diagnosis is done by actually visualizing on endoscopy.

Your patient is a 60 year old female who presents with colicky abdominal pain, bloating, and a few episodes of bilious vomiting. She denies any past medical history, but records show surgical history of cholecystectomy years ago, and you note the scar from the procedure on physical exam. She denies any diarrhea, and states she actually hasn’t been able to pass a bowel movement at all for the past few days. Physical reveals high-pitched, hyperactive bowel sounds diffusely over the abdomen with tympanic percussion and no rebound tenderness. You order a KUB series, which reveals distended loops of bowel and air-fluid levels present and no visualization of colonic gas. What do you suspect is the underlying cause of your top differential?

Adhesions

• Small bowel obstruction in adults is most commonly associated with post-operative adhesions (aka mechanical obstruction) and should be suspected in any patient with history of abdominopelvic surgery with new onset abdominal pain, obstipation, high pitched hyperactive bowel sounds which may progress to hypoactive bowel sounds the later they present, and abdominal radiograph showing evidence of dilated bowel with air-fluid levels and little to no gas in the colon.

  • In kids, the most common cause of SBO is intussusception which would present with the classic symptoms of currant jelly stools, sausage shaped mass in abdomen, and intermittent knees-to-chest position with a pained cry.

• Had the patient presented with similar symptoms but more gradual with more indolent abdominal pain on-off, less frequent vomiting, fever, and tachycardia and dilation of the large intestine – with or without history of prior abdominal surgery – the stem is likely wanting you to consider a large bowel obstruction, which is most commonly at the Sigmoid Colon and secondary to neoplasms but can also be from fecal impaction or diverticulitis.

• Treatment for small and large bowel obstruction is making the patient NPO, administering IV fluids, and initiating decompression via NGT, pain management, and surgery if mechanical obstruction is the suspected cause.

• At any time, if there is free air seen on a radiograph, such as seeing what looks like visualization of a “right sided gastric bubble” on a radiograph, indicates emergent surgery due to the apparent perforation.

You are called to consult on a patient is a 36 year old male with history of Cirrhosis who presents with rapidly increasing ascites. Additionally, you note about a 30 lb weight loss from when he last presented the ER a few years ago when he was originally diagnosed with Cirrhosis. Aspiration of the ascites reveals sanguineous fluid and labs reveal an increased AFP level. He has never had a prophylactic ultrasound of his liver, but based on his current presentation, which diagnosis do you suspect at this time?

Hepatocellular Carcinoma

• The most common cause of hepatocellular carcinoma is Cirrhosis, of nearly any etiology, but most commonly secondary to chronic infection with Hepatitis B or C.

  • A less common etiology, yet high yield for exams, is Hereditary Hemochromatosis (build-up of Iron) and Wilson’s Disease (which is a build-up of Copper).

• Ultrasound screening q6-12 months is commonly recommended in patients with Cirrhosis with or without HCV and chronic HBV even in the absence of Cirrhosis.

  • If a lesion is found to be > 1 cm then you should evaluate with a CT or MRI to diagnose HCC if radiologic hallmarks are noted, such as having a “washout” with a hypoenhanced appearance on imaging with a contrast enhanced capsule.

    • If you don’t visualize any hallmarks on CT or MRI, you would then need to acquire biopsy for definitive diagnosis.

• Alpha-Fetoprotein (AFP) is the most commonly used serum marker for hepatocellular carcinoma and elevated levels in a high-risk patient, as seen in our stem, should raise suspicion of this diagnosis.

• The mainstay of treatment for hepatocellular carcinoma is surgical resection since many of these patients are not eligible for transplant due to underlying disease or tumor burden, however if there is only one small tumor or only a few very small tumors isolated to the liver– you could consider transplant.

• Remember, while hepatocellular carcinoma is the most common cause of primary hepatic malignancy, the most common malignancy overall affecting the liver is from metastatic disease, most commonly originating from the GI Tract.

Your patient is a 22 year old male who arrives to the ED for recurrent hematochezia and abdominal cramping. After consulting GI who performs a colonoscopy, they report visualization of continuous mucosal inflammation starting from the rectum and progressing proximally. What are some high yield extraintestinal manifestations associated with your suspected diagnosis?

Primary Sclerosing Cholangitis and Ankylosing Spondylitis

• Other extraintestinal manifestations of ulcerative colitis include Pyoderma Gangrenosum, Erythema Nodosum, Sacroiliitis, Arthritis, Liver Disease, and Renal Stones.

• Primary Sclerosing Cholangitis is considered the most serious liver disease associated with IBD and can progress to Cirrhosis or even hepatobiliary cancer.

  • I recommend creating a comparison chart between Ulcerative Colitis and Crohn’s Disease to distinguish their unique characteristics

    • We will briefly touch on some in our IM rapid review, but I recommend taking the time to really sort these two out so you have an easy time differentiating between them on exams.

Lets shift to Ortho and Rheumatology, which also make up 12% of the IM EOR

ORTHO/RHEUM

Your patient is a 40 year old male admitted to your service due to new onset fatigue and fever in the setting of progressive joint and muscle pain as well as significant weight loss secondary to sitophobia. On physical exam, you note painful and violaceous plaques on his lower extremities surrounded by livedo reticularis. Additionally, you note unilateral foot drop when observing his gait. Vitals reveal temp of 100.4 F, BP 180/98, HR 88, and RR 16. Labs are notable for elevated creatine, ESR, and CRP. ANCA is negative. Mesenteric and Renal angiography shows microaneurysms in the small arteries and “beading :in the medium arteries. Biopsy confirms your suspected diagnosis, which is what disorder?

Polyarteritis Nodosa

• This is a systemic necrotizing vasculitis which will affect both small and medium ARTERIES (not veins or venules).

• It is most commonly idiopathic and the most common organ affected is the Kidneys which can lead to HTN and renal failure.

  • Of note, patients are typically middle aged males that may have a history of Hepatitis B or C.

• High yield findings in Polyarteritis Nodosa includes “starburst livedo” which is considered pathognomonic and described in our stem as painful violate plaques surrounded by livedo reticularis.

  • One of the most common findings is mononeuropathy, like wrist or foot drop.

  • Finally, these patients also classically present with signs and symptoms of mesenteric ischemia, as our patient has with his sitophobia aka fear of eating secondary to triggering abdominal pain.

• Separating the vasculitis by organs of involvement is commonly helpful to differentiate.

  • For example, Goodpasture Syndrome, which is a small vessel vasculitide is typically presented with a combination of pulmonary and renal symptoms.

  • Granulomatosis with Polyangiitis, another small vessel vasculitis, also can present with pulmonary and renal symptoms, but also has an HEENT component with sinusitis.

  • Then you have your medium vessel vasculitides, including polyarteritis nodosa, but also Behcet Disease which classically affects the mouth, genitals, and eyes.

  • Higher yield large vessel vasculitides to know, which most of you probably already have at least heard of, is Giant Cell Arteritis which can lead to the classic symptoms of jaw claudication, temporal artery tenderness, and transient to permanent blindness.

• All of the vasculitides are pretty much treated the same way, plus or minus some differences.

  • But if you ever have to guess – choose Prednisone. If Prednisone isn’t an option, choose Cyclophosphamide.

    • Obviously, it’s not necessarily as easy as that, but if you’re in a rut and are asked the treatment of a vasculitide and have no idea, best bet is to choose Prednisone.

Bonus FYI: Don’t confuse polyarteritis nodosa with Polymyalgia Rheumatica which is typically seen in women over 50 with painful morning stiffness in shoulders and hip girdle and commonly associated with Giant Cell aka Temporal Arteritis (also don’t confuse with Polymyositis, which presents with MUSCLE pain, not joint pain, and commonly as proximal muscle WEAKNESS, most commonly quad femoris, not stiffness like seen in polymyalgia rheumatica).

Your patient is a 27 year old male that is admitted due to progressive dysphagia, fatigue, and generalized weakness and stiff joints. Physical sign shows tightened skin around his fingers with pitting at the tips and labs are positive for Anti-topoisomerase I. What diagnosis do you most suspect?

Systemic/ Diffuse Scleroderma

• He has signs and symptoms of scleroderma and the antibody, anti-topoisomerase I, suggests the diffuse disease

  • If only had CREST syndrome, or limited scleroderma, which is seen with positive Anti-Centromere antibody and holds a better prognosis

• Scleroderma is an autoimmune disease that leads to excess production and deposition of collagen and vascular damage.

  • Diffuse Scleroderma can affect nearly any organ, but most notably the kidneys and lungs, in addition to the skin and GIT as seen in CREST syndrome.

• Treatment for scleroderma depends on if managing acute presentation or specific organ/system involved.

• The most common cause of death from Scleroderma is pulmonary disease

We’ll tackle more HY Ortho/Rheum in our Rapid Review, for now lets move onto Endocrine, which makes up 8% of the EOR

ENDOCRINE

Your patient is an 8 year old female with no PMHx who presents to the ER with intense nausea and fatigue. Her weight has dropped according to her parents she appears pale and drowsy. When questioning the patient symptoms, she says she feels really tired and thirsty all the time now and her mom states she noticed she’s been constantly using the bathroom, even waking up frequently in the night to pee, and she’s worried she may have a UTI. Physical reveals dry mucus membranes, decreased skin turgor, and a sweet smell to her breath. Her vital reveals she is afebrile with HR 115, BP 100/72, RR 26 with deep expirations and inhalations. What do you suspect labs will show?

Given the likely diagnosis of Diabetic Ketoacidosis in a patient with undiagnosed Diabetes Type I you should suspect labs will show

• Hyperglycemia with Blood Glucose > 200

• High Anion Gap Metabolic Acidosis

• Abnormal Serum Sodium, ranging from (mc) hyponatremia 2/2 increased plasma osmolarity, but can be mildly hypernatremia 2/2 osmotic diuresis from glucosuria leading to water loss > sodium loss

• Total body serum potassium deficit that and appear normal due to redistribution, which is why regardless of initial potassium levels, potassium replacement and careful monitoring should be occurring when giving insulin and fluids to correct the DKA.

• Normal to high serum phosphate secondary to cellular shifting from an overall depletion 2/2 phosphaturia from osmotic diuresis; when DKA is treated, this typically levels out as the transcellular shift is reversed

• (+) Urine or Blood Ketones, elevated BUN and occasionally Creatinine secondary to hypovolemia/ dehydration with a subsequent AKI

• The name of the game with DKA is Dehydration, which needs to be corrected with FLUIDS to resolve. Dehydration leading to DKA can be due to many etiologies, but most commonly is secondary to an underlying infection.

• Treatment of DKA includes large volume fluids inpatient and IV Insulin with monitoring of potassium and repletion as warranted.

  • You need to continue giving insulin as you close the gap and usually will need to add dextrose to the IVF to keep them from bottoming out while closing the gap with insulin.

  • Rehydration and reduction of osmolality needs to be monitored and not performed too rapidly or you risk cerebral edema.

Your patient is a 52 year old woman who presents with fatigue, irritability, and muscle spasms, perioral paresthesias. History reveals she had recent thyroidectomy. Physical reveals carpopedal spasm when progressively squeezing blood pressure cuff and tapping her facial nerve results in uncontrolled contraction of her ipsilateral facial muscles. What do you suspect labs to show?

Low PTH, Low Ionized Calcium, High Phosphorus

• This patient has evidence of Primary Hypoparathyroidism which is MC Iatrogenic secondary to surgical resection of some or all of the thyroid.

• Patients may have other symptoms like a hoarse voice (bronchospasms), personality changes, seizures, hyperactive deep tendon reflexes, etc.

• EKG may reveal QT prolongation (“low calcium = slow to get from Q and T”) which runs the risk of Torsades and death

• The high yield signs for hypocalcemia include Chvostek Sign (inducing facial spasm) and Trousseau Sign (inducing carpopedal spasm)

• Ionized calcium is the most active form of calcium so this will be low secondary to the low PTH from the, likely resected, loss of parathyroid production

• Treatment for primary hypoparathyroidism is with immediate replacement of calcium and vitamin D.

  • If the patient has tetany, you need to ensure their airway is secure and give IV Calcium Gluconate.

• The patient should be started on Long Term Recombinant PTH

Your patient has a history of bipolar disorder that has been well controlled on Lithium therapy. However, when they come in for a follow up visit they share they have been having difficulty getting anything done because they’ve suddenly been urinating a large volume, very frequently, and are always thirsty. Given suspected diagnosis, what do you suspect urine osmolality with be after restriction of water and vasopressin challenge?

No change in urine osmolality

• This patient likely has Nephrogenic Diabetes Insipidus, which most commonly caused by Chronic Lithium Use.

  • In Nephrogenic Diabetes Insipidus, the ADH secreted by the posterior pituitary has little to no effect on the kidney, thus the message to concentrate urine to preserve intravascular fluids is blunted, leading to a large volume of diluted urine.

• Because the Kidneys are resistant to ADH, giving Desmopressin – which is an analog of ADH – will not have any effect on concentrating the urine.

  • Restricting water will also have no effect on concentrating urine, ruling out primary or psychogenic polydipsia.

• In NDI, patients will have increased serum osmolality due to their total volume depletion, which can lead to subsequent raise in intravascular sodium and protein.

  • This is why, sodium and protein restriction is part of the pearls of treatment in addition to hydrochlorothiazide, which in a patient with a low-solute diet, can relive polydipsia and induction of a mild volume depletion which can induce proximal sodium and water reabsorption.

    • Consider adding a potassium sparing diuretic, especially in patients with reversible Lithium nephrotoxicity.

  • Additionally, indomethacin, an NSAID, can improve NDI due to the inhibition of renal prostaglandin synthesis which antagonizes ADH.

• Central DI, which is more common than NDI, and is most commonly idiopathic or secondary to tumors involving the hypothalamic-pituitary region.

  • In cases of CDI you want to consider pituitary imaging to rule out a mass lesion if there is no obvious cause.

For the sake of time, lets keep it rolling and move onto Neurology that makes up 8% of the EOR

NEUROLOGY

Your patient arrives to the clinic for evaluation of her progressive bilateral tremor in her hands that worsens when she’s trying to write or use her phone. She states she has noticed it for a few years and thinks it has been getting progressively worse. History reveals she only consumes about 1-2 beers/week but she has noticed an improvement in her tremors during that time. Physical reveals symmetrical fine tremor in her upper extremities that is worse when she closes her eyes and is asked to hold a piece of paper. Assuming she has the most common movement disorder, which medication should you initiate?

Propranolol long term or episodic Primidone or Propranolol.

• Propranolol, a NS beta blocker, is considered first line for Essential tremor, which is the most common movement disorder and leads to a “working tremor” in which it is more noticeable with activity.

• Differentiate this with the tremor in Parkinsonism which gets worse with rest and is commonly described as a unilateral “pill-rolling” tremor initially.

Your patient is a 25 year old female with unremarkable PMHx who presents to the ER due to a bilateral, non-pulsating, headache that feels like it is “squeezing” her head in all directions. She denies any nausea, vomiting, photophobia, or other vison changes. She says this isn’t the first time this has happened. In fact, she reports at least 10 episodes lasting ~30 minutes each in the past couple years when she started her new fast-paced and stressful job. What do you suspect is this patient’s diagnosis?

Tension HA

• Tension HAs are the most common headache in the general population and are most commonly caused by stress and will not be aggravated by everyday activity.

  • There may be associated neck muscle tenderness and the pain will be in a constricting band-like pattern involving the frontalis all the way around to occipitalis.

• No other alarming features will be present in these patients and diagnosis can be made clinically without any diagnostic studies if the patient is otherwise healthy and tension-type HA presents classically without ANY neurological symptoms.

• Treatment is with Acetaminophen or NSAIDs and you can consider TCAs as preventative treatment if the patient cannot decrease stressors and has impaired functioning/quality of life.

Your patient is a 49 year old male that is brought into the ER by his wife due to his new onset nausea, vomiting, and weakness. He states he thinks this is just due to a migraine he has had for a while that feels like its progressively worsening – especially when sitting up in the morning after a night of sleep or when coughing/sneezing or bending down to pick something up. Head CT with contrast reveals an intracranial mass. Which primary malignancy suspected in this patient is both most common and has the poorest prognosis?

Glioblastoma – Grade IV Astrocytoma

• This is a type of Glial primary brain tumor, termed Glioma. The most common grade of Astrocytoma in Adults is Grade 4, termed Glioblastoma, which unfortunately carries the poorest prognosis.

• In children, the most common primary malignant tumor is a Medulloblastoma, but overall the most common CNS tumor children is Astrocytoma which is often benign.

  • So be sure to read the stem carefully for if they’re asking about most common primary CNS malignant tumor or mc primary CNS tumor over.

• Speaking to that, in Adults, when considering causes for an intracranial tumors, remember the most common intracranial malignancies in adults overall are NOT primary, but instead are secondary to mets from origin sites of possible primary lung, breast, kidney, colorectal malignancies or even melanoma.

• Suspect a brain tumor or intracranial mass in anyone presenting with a constant and progressive headache that is worse during activities leading to increased intracranial pressure and nausea/vomiting.

• FYI Another high yield intracranial malignancy to remember is Retinoblastoma, which is a malignancy of the retina

  • Will typically present in a stem in a child < 3 years with leukocoria (absence of red-light reflex)

Your patient is a 12 year old male A&Ox4 who was admitted to your service in the early fall after he presented to the ER with a headache and fever and was found to have nuchal rigidity. When reviewing the results of his CSF analysis, you note a slight elevation in lymphocytes, normal protein, and normal glucose. What do you suspect as the causative agent to his suspected diagnosis?

Enterovirus

• The most common cause of meningitis is viral, most commonly Enterovirus and will present in a patient in the late summer or fall with the classic triad of HA, fever, and nuchal rigidity with NO change in mental status (remember, AMS = Encephalitis).

• Nuchal rigidity is usually described by the presence of Kernig Sign (knee extension leading to neck pain/bending neck) or Brudzinski (bending neck results in leg raise)

• In patients with viral meningitis, CSF is typically unremarkable but may have lymphocytes

  • If Bacterial Meningitis was the cause, CSF would show increased protein and decreased glucose in addition to the leukocytosis and increased opening pressure.

    • Think of this as the bacteria in the CSF eating up all the glucose leading to a depletion.

• The MCC Bacterial Meningitis overall is S. Pneumoniae but suspect N. Meningitidis if a patient appears with a petechial rash in the setting of meningitis.

  • In a neonate with bacterial meningitis, you should suspect E. Coli as the cause – which I remember as E. Coli coming from fecal matter which the neonate may encounter during delivery

• In immunocompromised patients, like AIDs patients, consider fungal cause – like Cryptococcus Meningitis which can be diagnosed on India Ink Staining.

• The treatment of viral meningitis is supportive, but any time HSV is suspected, which is the most common cause of Encephalitis, give IV Acyclovir.

• Patients with bacterial meningitis should be treated with empiric broad spectrum antibiotics and dexamethasone and their household and close contacts should be started on Rifampin.

Your patient is a 62 year old female who has been admitted due to new onset apraxia and impairment in executive function. Her kids say she has been increasingly irritable and has been having progressive short term memory loss for the past few years. You consult psychiatry who report she does not have evidence of depression or delirium but had an abnormal clock drawing test when they performed and MMSE. What do you suspect is the pathology leading to her current condition?

Neurofibrillary tangles and amyloid beta-peptide plaque deposition

• This leads to Alzheimer Disease which is the most common cause of dementia

• The most common initial symptom is impaired short term memory, but patients can also present with personality changes, sleep disturbances, and apraxia.

• Diagnosis can be made clinically, but if histology is performed, you will likely see the neurofibrillary tangles with amyloid plaques.

• Imaging may also reveal enlarged ventricles with extreme shrinkage of the cerebral cortex and hippocampus.

• Treatment for Alzheimer Disease is with Cholinesterase Inhibitors, like Donepezil, Rivastigmine, or Galantamine and NMDA Blockers like Memantine, which is neuroprotective

We’ll cover more neuro later, but lets begin our last heavy hitter that has its own dedicated section before our rapid review, Urology/Renal which also makes up 8% of the EOR

UROLOGY/RENAL

Your patient arrives to the ER with marked dehydration secondary to a diarrheal illness. ABG shows pH 7.34, Bicarb of 18, pCO2 of 35, and Anion gap of 12. What acid-base abnormality does she exhibit?

Non-Anion Gap Metabolic Acidosis

• The most common cause of Metabolic Acidosis is severe and/or persistent diarrhea.

• ABG will show a metabolic acidosis due to resulting loss of bicarb which leads to acidity. You may also have compensatory decrease in pCO2 due to the rapid respiratory compromise seen in metabolic acid-base conditions.

  • Typically, in respiratory causes of acid-base disorders, the compensation is much slower due to the time it takes to alter the bicarb or H+ enough to cause a compensatory change.

• I remember the lab values quickly with the mnemonic ROME = Respiratory Opposite, Metabolic Equal – to remind me that in Respiratory acid-base disorders the pCO2 direction will be opposite of the pH direction - for example, in Respiratory Acidosis – the pH will be low (acidotic) and the pCO2 is high (> 45) vs. what our patient has, Metabolic Acidosis, where we look to the bicarb after looking at the pH and determine both of these are LOW – so they “equally decline” vs. a metabolic alkalosis where both the pH and bicarb would be elevated as opposed to Respiratory Alkalosis (remember RO or ROME =Respiratory Opposite) where you’d see an elevated pH but have a decline in pCO2

• Anion Gap is determined by the formula Sodium + (Chloride + Bicarb). It is normal if it is under ~ 14.

• Separate Anion Gap MA from Non-Anion Gap MA with the mnemonic MUDPILES – which stands for Methanol, Uremia, DKA, Propylene Glycol, Isoniazid Intoxication, Lactic Acidosis, Ethanol/Ethylene Glycol, and Salicylates

• Non-AG MA can be remembered with the mnemonic HARDASS which stands for Hyperalimentation, Addison’s Disease, Renal Tubular Acidosis, Diarrhea, Acetazolamide, Spironolactone, and Saline Infusion

Your patient is a 55 year old current smoker who presents with hematuria without any endorsement of dysuria. You discover he has a good amount of weight since his last visit, but he states it just “fell off” without him even trying. Given his current presentation, what diagnostic test should you order?

Cystoscopy

• Direct visualization of bladder and ability to biopsy due to suspected diagnosis of Bladder Cancer

• Could also consider UA with cytology initially and/or CT Urography or Abdominopelvis.

• The most common type of bladder cancer in the US is Transitional Cell Carcinoma

• The most important risk factor for bladder cancer is SMOKING, but other identified risk factors that may be in the stem include infection from Schistosoma or occupational exposures

• Suspect bladder cancer in any patient with PAINLESS hematuria, especially in the setting of weight loss and risk factors. Advanced stages may present with LEE and bone pain 2/2 mets.

Your are consulted in the ED for a possible admission of a 41 year old male that presented with sudden and severe flank pain that radiates to his groin and has already vomited several times. Despite NSAIDs, he continues to have pain that makes him unable to lie still. He reports recent blood in his urine and results for the Non-Contrast Helical Abdominopelvic CT are pending, but the bedside renal ultrasound shows ipsilateral mild hydronephrosis. What do you suspect is causing this patient’s current condition?

Acute Ureteral Obstruction 2/2 Nephrolithiasis (aka renal calculi) that has likely gotten lodged in his Ureterovesical Junction

• Most common type of stone is Calcium Oxalate

• Suspect this condition in any patient that has unilateral flank pain radiating to groin and cannot sit still during an exam due to severe pain.

• Dehydration is the enemy of a patient with Nephrolithiasis so IVF restoration is needed, especially if vomiting, and opioids and NSAIDs can be used for the pain

• Alpha blockers and even CCBS are useful in relaxing the smooth muscles enough to allow for stone passage

• However, if a stone is > 8 mm, it is unlikely to pass on its own and will require urgent referral to a urologist for likely surgical intervention

Okay, that was a LOT and there are still 3 topics left to cover on this EOR - including Critical Care, Hematology, and Infectious disease - which make up a smaller percentage of the EOR - therefore, we will be covering these in our high yield IM Rapid Review on a separate episode for the sake of time.

Be sure to check that episode out for even more high yield pearls from the topics we've already hit on as well as a good mix of those leftover topics.

Don't forget to like, subscribe, comment, review - do all the things to get this out there to help others on their PA Journey.

Check out the website for the list of sources used in todays episode as well as the transcript. Also be sure to follow on Instagram @paspac_passport for near daily questions, quizzes on the story, and so much more. Thanks again for tuning in -

And as always, safe travels.

PART TWO: RAPID REVIEW

Okay lets hit up our rapid review where we will cover a lot more HY throughout the topics we discussed in part one plus and a good mix of the remaining, less involved, topics on the Blueprint which are Critical Care, Hematology, and Infectious Disease which make up 7%, 5%, and 5% of your EOR respectively.

RAPID REVIEW

1. What is the definitive treatment of a patient presenting with acute, unilateral painful vision loss found to have an ipsilateral cloudy cornea, fixed mid-dilated pupil, and IOP 48?

a. Iridotomy

b. Dx = Acute Closed Angle Glaucoma (gold standard dx = Gonioscopy)

c. Initial tx = topical beta blockers, alpha-agonists, carbonic anhydrase inhibitors, and miotics – as pupil dilation can exacerbate the closure.

2. Which causative organism for pneumonia should be suspected in a patient with both respiratory symptoms and diarrhea in someone who works with air conditioning units?

a. Legionella

b. Also associated with hyponatremia and fever is typically pretty high

3. Which autosomal Dominant neurodegenerative disorder results from trinucleotide repeat of cytosine-adenine-guanine on chromosome 4P leading to uncontrolled and seemingly random hyperkinetic movements, hypotonia, and eventual cognitive decline?

a. Huntington Disease

4. What is the most common cause of non-ischemic cardiomyopathy?

a. Dilated CMO

5. What diagnosis should you suspect in a patient with ascending paralysis that began after a diarrheal illness and CSF showing elevated protein with a normal white count?

a. Guillain-Barre Syndrome

b. Suspect in a patient with history of recent immunization or GI bug (mc Campylobacter jejuni from eating uncooked poultry) who resents with ascending paralysis and/or evidence of albuminocytologic dissociation which is seen when CSF protein is elevated in the setting of normal WBC.

c. Ddx pattern of paralysis by GBS = Ground to Brain (ascending) vs. MG = Mind to Ground (descending)

6. What should be done in respiratory distress of an asthmatic patient with impending respiratory failure?

a. RSI (rapid sequence initiation) – Use Ketamine to decrease risk of hypotension and increase bronchodilation while also causing dissociative anesthesia prior to intubation.

7. What is visualized on upper endoscopy in a patient with HSV Esophagitis?

a. Shallow, punched out lesions

b. Differentiate with Candida Esophagitis, which appears as yellow-white plaques and CMV Esophagitis which is described as “volcanic lesions” that are large and solitary ulcers or erosions

8. What is the first line treatment for acute Hypertensive Crisis in Pheochromocytoma?

a. Phentolamine then Sodium Nitroprusside +/- Nicardipine

b. Patients need to be on Phenoxybenzamine (alpha blocker) prior to surgical resection of the adrenal medullary neoplasm. After alpha blockade, you can start beta blockers but do NOT start before alpha blockade or you can cause unopposed alpha leading to a worsened or new hypertensive crisis.

9. How would you definitively diagnosis hypervolemia and hypovolemia?

a. Swan-Ganz Catheter (pulmonary artery catheter) which measures CVP

10. What is the gold standard for diagnosing a Pulmonary Embolism?

a. CT Pulmonary Angiography

b. If patient Is pregnant, choose VQ Scan

c. D-Dimer should only be used in screening to rule out a low-risk patient, if you have any suspicion of PE you need to get a CTPA

11. What is the most common immune mediated inflammatory demyelinating disease of the CNS?

a. Multiple Sclerosis

b. Suspect in a patient with relapsing-remitting neurologic symptoms and MRI imaging of brain and spine showing areas of demyelination, such as Dawson’s Fingers, which are periventricular plaques

12. What is the difference between Cushing Disease and Cushing Syndrome?

a. Cushing SYNDROME is a collection of signs and symptoms from increased cortisol without indication of an actual etiology

b. Cushing DISEASE is specifically referring to increased cortisol secondary to ATCH excess, which is most commonly from a pituitary adenoma

13. Stroke affecting which artery can lead to symptoms of Broca Aphasia and contralateral upper extremity weakness?

a. Middle Cerebral Artery

14. What autoimmune disease is associated with keratoconjunctivitis sicca, xerostomia, and parotitis?

a. Sjogren’s Syndrome – idiopathic autoimmunity attacking salivary and lacrimal glands. Diagnose can be made with Anti-Ro (SSA) & La (SSB) Antibodies and positive Schirmer test

15. Where do most prostate cancers originate from?

a. Peripheral Zone of the prostate

b. Suspect in a patient with asymmetric enlargement or nodule on DRE with elevated PSA and diagnose with TRUS guided Needle Core biopsy

16. What determines who develops Acromegaly vs. Gigantism in patients with GHRH excess?

a. Age of onset

b. If the growth hormone excess begins in childhood, before the closure of the epiphysis, patients with develop Gigantism, referring to their excessive height

c. If the growth hormone excess begins in adulthood, after epiphyseal closure, the soft tissues will grow and bones will develop abnormally leading to the classic presentation of “shoes becoming too small, hands enlarging, and jaw, nose, and tongue growth with protruding brow

17. What splenic differentials can lead to Acute Abdomen?

a. Splenic Rupture (ex. EBV infection)

b. Splenic Infarct (ex. Sickle Cell, Afib)

18. What complication can occur if correction of hyponatremia occurs too quickly?

a. Osmotic Demyelination Syndrome aka Central Pontine Myelinolysis (aka “Locked-In” Syndrome)

b. “High to low, brain will blow; low to high brain will die” – for differentiating correcting hypernatremia too quickly leading to cerebral edema and correction of hyponatremia too quickly leading to ODS.

19. What is the most common type of Insulinoma?

a. Adenoma of Islets of Langerhans (90% benign, but lead to acute hypoglycemia)

20. What is the most common cause of MINOR hemoptysis

a. Acute Bronchitis – typically 2/2 viral infection and presents with cough > 5 days up to 3 weeks +/- fever and rhinorrhea

21. What is the most common cause of Acute Kidney Injury?

a. Prerenal – dehydration/hypovolemia

b. MC Infectious cause acute glomerulonephritis = Post-Streptococcal (suspect with RBC casts and proteinuria in patient with history of recent strep infection and new onset hematuria)

22. What should be suspected in a patient who presents with tachycardia, hyperpyrexia, tremor and agitation that has physical findings of a goiter?

a. Thyroid Storm

b. Life-Threatening Thyrotoxicosis

23. What should be suspected in a patient with chronic alcohol use who has longstanding steatorrhea, newly diagnosed diabetes, and KUB showing epigastric quadrant calcifications?

a. Chronic Pancreatitis (MCC = Excessive longstanding ETOH consumption, vs. Acute which is MCC 2/2 Gallstones > ETOH)

b. Pancreatic calcifications can be seen on XR

c. May or may not present with an acute on chronic exacerbation

24. What is the most common site affected by Crohn’s Disease

a. Terminal Ilium

b. Distribution can be anywhere from “mouth to anus” and can skip around to different portions of the GIT, hence the term “skip lesions”

25. What physical maneuver can determine if a patient in coma has an intact brainstem?

a. Oculocephalic Test (“Doll’s Eyes” Maneuver) – only if c-spine uninjured

b. If patient is breathing on their own, brainstem is also likely intact

c. If pupils are responsive, midbrain is intact

26. What is contraindicated during work up of suspected acute bacterial prostatitis?

a. Massaging of the prostate

b. Can lead to sepsis

27. Which type of dementia is most associated with extreme personality changes of disinhibition preceding memory changes, such as making sexual references to strangers or seemingly saying the first thing that comes to their mind, regardless of inappropriateness?

a. Frontotemporal Lobar Degeneration

28. What should be suspected in a patient with koilonychia, ice cravings, and pallor?

a. Iron Deficiency Anemia – MCC of Microcytic Anemia (decreased MCV)

29. What type of renal disease is associated with Muddy Casts

a. Acute Tubular Necrosis

30. Which drug is considered the cornerstone therapy of Rheumatoid Arthritis?

a. Methotrexate – this can be effective as monotherapy in many patients

b. Adjuvant therapies can include Hydroxychloroquine, Sulfasalazine, NSAIDs, and Biologics like Recombinant Interleukin 1 Blockers and TNF-alpha Blockers

31. What diagnosis should be suspected in a patient with hyperkeratotic hands and presence of heliotrope rash and erythema of the upper chest?

a. Dermatomyositis

b. This is a type of inflammatory and degenerative skin & muscle disease that is associated with malignancy and has high yield findings including heliotrope rash, Gottron papules, and (+) shawl sign (erythema over the neck/upper body as if covered by a shawl)

32. What gives a patient a definitive diagnosis of Sickle Cell Anemia?

a. Hemoglobin Electrophoresis showing + HgbS (if Hb SA, then trait only)

33. Which forms of Viral Hepatitis have vaccinations?

a. Hepatitis A and Hepatitis B

34. Which medication used for Erectile Dysfunction can lead to blue color discoloration?

a. Sildenafil, a PDE-5 Inhibitor

b. Secondary to cross reaction of PDE-6 inhibitor in the retina that has a role in color vision

35. Which autoantibody is associated with Primary Biliary Cholangitis?

a. Antimitochondrial Antibody

36. When should children be screened for hyperlipidemia?

a. All children 9-11, before puberty, and again after puberty around 17-21

37. What is the time goal for receiving a PCI after an EKG reveals a STEMI?

a. Under 90 Minutes

38. What should be suspected in a male > 50 years old with 30 Pack Year History who has nonproductive cough and honeycombing on CT scan?

a. Idiopathic Pulmonary Fibrosis – this is a type of fibrosing interstitial pneumonia caused by damage and improper repair of the epithelial cells leading to changes to the lung parenchyma visualized on High Res CT Scan.

39. What is the most common infectious cause of Reactive Arthritis aka Reiter’s Syndrome?

a. Chlamydia most common, less commonly caused by Gonorrhea

b. Also seen with GI infections like Shigella, Salmonella, Campylobacter and Yersinia

c. Remember this by symptoms illustrating the rhyme “Can’t Pee, Can’t See, Can’t Climb a Tree” which indicate conjunctivitis or uveitis, urethritis, and arthritis

40. What is the most common genetic bleeding disorder?

a. Von Willebrand Disease (Autosomal Dominant)

b. Don’t confuse with Factor V Leiden which is the most common clotting disorder

41. Which small vessel vasculitis should be considered in a cANCA + patient with chronic sinusitis, new onset cough with CXR showing pulmonary infiltrates, and hematuria secondary to nephritis?

a. Granulomatosis with polyangiitis

b. Lung biopsy confirms diagnosis, treat with prednisone or cyclophosphamide

42. Which foods are considered triggers for GERD and should be avoided in GERD patients?

a. Caffeine, ETOH, Chocolate, and acidic foods like tomato sauce

43. Which form of IBD should be suspected in a patient with serology (+) for ASCA, aka anti-saccharomyces cerevisiae antibodies?

a. Crohn’s Disease

44. What is the best prognostic factor for a patient with pancreatitis?

a. Leukocyte Count

b. Ranson’s Criteria and APACHE II Scoring system are both used to determine prognosis.

45. Which large vessel vasculitis affects the aorta and major branches leading to arm claudication and ischemia in the fingers?

a. Takayasu Arteritis – diagnose with aortic arch arteriogram and treat with prednisone

46. What diagnosis is caused by inhibition of ADAMTS13 leading to uncleaved Von Willebrand Factor?

a. Thrombotic Thrombocytopenic Purpuric

47. What is a high yield dermatologic presentation of Celiac Disease?

a. Dermatitis Herpetiformis – appears as pruritic vesicular rash over knees, elbows, and occasionally over the buttocks.

48. How does Pericarditis classically appear on EKG?

a. Diffuse (global) ST Segment Elevation

49. Which malignancy is associated with painless lymphadenopathy with biopsy showing evidence of B cell proliferation with bilobed nuclei on histology?

a. Hodgkin’s Disease Lymphoma

b. Reed-Sternberg Cells

50. What serology findings indicate active Hepatitis B infection?

a. Positive HBsAg – indicating you have an active surface antigen present and if HBeAg is positive , either in acute or chronic infection, the virus is actively replicating and there is a high viral burden present.

51. What might you see on x-ray imaging of a joint that has a buildup of rod shaped, negatively birefringent crystals within the synovial fluid?

a. Small, punched out lesions

b. This question describes Gout.

c. Pseudogout should be suspected had the crystals been rhomboid shaped positively birefringent which can show fine, linear calcifications in cartilage on x-ray

52. What retinal findings on fundoscopy is associated with Hypertension?

a. AV Nicking (compression and outward bulging of small venule at the area it is crossed by higher pressure arteriole), suggesting Hypertensive Retinopathy

b. Other fundoscopy findings in hypertensive retinopathy include Silver Wiring or even retinal hemorrhages suggesting a retinal vascular occlusion.

c. Fundoscopic signs of malignant hypertension include optic nerve pallor or edema, Cotton Wool Spots, and Flame Hemorrhages

53. What does CREST syndrome stand for?

a. Calcinosis, Raynaud’s Phenomenon, Esophageal Dysmotility, Sclerodactyly, Telangiectasia

b. This is a limited form of Scleroderma

54. What is the most common cause of Community Acquired Pneumonia?

a. Streptococcus pneumonia

b. In patient’s with Cystic Fibrosis, the most common cause is P. Aeruginosa

55. What collection of systems/symptoms are associated with Multiple Myeloma?

a. CRAB = Calcium Elevated, Renal Failure, Anemia, Bone Lesions

b. Lead to bones, stones, groans, moans, fatigue, bone & back pain.

56. Which type of IBD is associated with fistula formation?

a. Crohn’s Disease

b. Remember Crohn’s is transmural which means deep ulcerations can form and in addition to chronic inflammation, fistulas may be present.

57. What is the treatment of a patient with Whooping Cough?

a. Whooping cough aka Pertussis is bacterial, caused by Bordetella pertussis

b. Treat with Macrolide (ex. Azithromycin) +/- supportive steroids or SABA

58. When should prophylactic Fluconazole be started in a patient with AIDS and why?

a. CD4 Count < 100

b. Prophylaxis from Cryptococcus

59. In which ways do external hemorrhoids and internal hemorrhoids present differently?

a. External – painful, no bleeding – may be thrombosed, appearing swollen and purple or bluish.

b. Internal – no pain, bright red bleeding

c. Dentate line separates external from internal (above = internal, below = external)

60. What is the most sensitive cardiac marker and when does it appear?

a. Troponin I

b. First appears within 2-4 hours, peaks 12-24 hours, and lasts for 7-10 days

61. What is considered first line therapy for patients with Cardiovascular Disease?

a. Statins – ex. Rosuvastatin and Atorvastatin, as long as no contraindications exist

b. Don’t forget high yield adverse effects of Stains, such as increased LFTs, Rhabdomyolysis, and potential to increase Warfarin. Also Statins are Contraindicated in Pregnancy with a Category X classification.

62. What is considered curative in Ulcerative Colitis?

a. Colectomy

b. Differentiate from Crohn’s Disease in which surgery is NOT curative.

63. What is the most common benign primary tumor of the liver?

a. Hemangioma

64. What is the most common cause of viral Myocarditis?

a. Coxsackie B which most commonly result in a dilated cardiomyopathy 2/2 myocarditis

65. Which esophageal cancer is more common in the upper esophagus vs. lower esophagus?

a. Squamous Cell Carcinoma secondary to epithelial dysplasia (which is also MCC esophageal cancer globally) and MC associated with smoking and etoh use vs. distal esophagus which is Adenocarcinoma (MCC in US) and MC results from uncontrolled GERD/Barrett’s Esophagus leading to intestinal metaplasia.

b. Remember this because the upper esophagus is closer to the skin which is made up of squamous epithelium. Then as you move distally, you have more glandular cells that secrete mucus and digestive juices, leading to adenocarcinoma.

66. What organism is responsible for “walking pneumonia”, is cold agglutinin (+) and associated with bullous myringitis?

a. Mycoplasma pneumoniae, this is the most common atypical cause of pneumonia

b. Suspect this in a young patient who has pneumonia with very minimal symptoms or presenting with bullous myringitis

67. What are some dermatologic signs of high cholesterol?

a. Cutaneous Xanthoma like Tendinous Xanthomas, Tuberous Xanthomas, Verruciform Xanthomas (2/2 subcutaneous cholesterol deposits)

b. Also remember Plane Xanthomas which are commonly on the eyelids, which is termed Xanthelasma

68. What diagnosis should be suspected in a patient with a painless ulcer on the genitals with subsequent rash involving palms and soles?

a. Syphilis

b. Chancre is primary stage and rash indicates secondary stage

c. Gummas and neurocognitive deficits represent tertiary stage

69. What is the first line treatment for pediatric patients with RMSF?

a. Doxycycline, even in children, despite adverse effects of dental staining and hepatotoxicity

b. This is due to the high risk of morbidity and mortality leading to benefits of doxy outweighing the risks

70. What labs indicate a primary adrenal insufficiency, such as Addison’s Disease?

a. Little or no increase in Cortisol following administration of ACTH Analog, Cosyntropin, during the High Dose Cosyntropin Stimulation Test

b. In primary adrenal insufficiency, both cortisone and aldosterone is decreased despite the elevation of ACTH (and elevated CRH which subsequently stimulates MSH -> hyperpigmentation aka tanned appearance)

c. Hyperkalemia, Hyponatremia are commonly seen due to the low aldosterone causing sodium excretion and potassium reabsorption along with low fasting glucose, since cortisol stimulates glucogenesis

d. Hypotension is seen secondary to the fluid loss from sodium excretion (where salt goes, water goes)

71. What is the most common cause of MASSIVE lower GI bleeding?

a. Diverticular Disease, remember it is Diverticulosis when no inflammation or infection is present and Diverticulitis when signs/symptoms of inflammation or infection is present and you’ll likely see radiographic evidence of fat stranding and bowel wall thickening on Abdominopelvic CT.

b. Don’t forget diverticulitis is a contraindication for barium enema and colonoscopy due to risk of perforation

72. What diagnosis should you suspect in a patient with rice water diarrhea and extreme fluid losses secondary to ingestion of contaminated water?

a. Cholera – Vibrio Cholerae

73. What might an EKG show in a patient with pulmonary hypertension?

a. RV Hypertrophy noted by presence of RAD, R wave/S wave ratio > 1:1 in V1, RBBB, +/- “Tee-Pee” P-Waves in lead II, which are large amplitude P waves, 2/2 RAE. I remember by TeePee with P standing for “P Pulmonale”)

74. What is the difference between Osler Nodes and Janeway Lesions?

a. Both are associated with signs of Infective Endocarditis

b. Osler Nodes are painful nodules on the pads of fingers and toes – (“Osler’s Ouch”)

c. Janeway Lesions are non-tender erythematous macular lesions seen on the palms and soles (“Gentle Jane”)

75. What EKG changes are seen in a Lateral Wall Infarction?

a. ST Elevation in leads I, aVL, and V5-6 (lateral leads) with reciprocal ST depression in inferior leads (II, III, AVF).

b. Lateral Wall Infarction is most commonly secondary to blockage of Left Circumflex Artery.

76. When should Cholangitis be suspected?

a. Patient with Charcot’s Triad (Fever, RUQ Pain, Jaundice) or Reynold’s Pentad (Charcot’s + Shock features, aka AMS & Hypotension)

b. Goal standard for diagnosis is ERCP, but start with bedside ultrasound for your gallbladder differentials

77. What is the most common cause of Congestive Heart Failure?

a. Ischemic Heart Disease

78. Which part of the myocardium is infarcted in STEMI?

a. Transmural infarction, which means it involves the full thickness of the myocardium.

b. NSTEMI is a subendocardial infarction

79. What results of fasting insulin and c-peptide levels suggest T2DM?

a. High Fasting Insulin

b. Elevated C-Peptide Level

c. High Insulin with Low C-Peptide level indicates external insulin administration

80. What is the Levine Sign?

a. Sign seen in ACS when patient with chest pain is holding a clenched fist over their chest and talking through clenched teeth

81. What is the most common valve site for Native Valve Endocarditis?

a. Mitral Valve

b. If the patient has history of IVDU, mc site is Tricuspid Valve

c. MCC Endocarditis is S. Aureus

d. Mitral Valve is also the most common valve affected in Rheumatic Heart Disease

82. What are the signs and symptoms of Restrictive CMO?

a. This will present as Right Heart Failure, aka systemic fluid overload

b. The most common cause of this is amyloidosis, with close 2nd being Sarcoidosis

83. What is the MOA of the lipid lowering therapy, Cholestyramine?

a. Bile Acid Sequestrant

b. Lowers cholesterol due to inhibition of bile acid reabsorption from the intestines, which leads liver needing to pull more LDL from the plasma in order to reestablish hepatic cholesterol which is converted into Bile Acid.

84. What are Roth Spots?

a. Hemorrhagic Retinal Lesions, associated with Infective Endocarditis

85. Which type of pneumonia is a patient with HIV and CD4 score < 200 at risk for?

a. Pneumocystis jiroveci (PJP)

86. What is the Dawn Phenomenon in patients with DM1?

a. Euglycemic until ~2-8am, then will become hyperglycemia

b. 2/2 Decreased insulin sensitivity at night and surge of couter-regulatory hormones when fasting (aka asleep)

87. What is the Carcinoid Syndrome triad?

a. FDR = Flushing, Diarrhea, and Right Sided Heart Defects

b. Most commonly will lead to Tricuspid Regurgitation, resulting in Holosystolic murmur at the left sternal border.

88. What is the most common cause of Pericarditis

a. Idiopathic

b. When etiology is identified, the most common cause is Coxsackie Virus

89. What genetic condition places a patient at risk for COPD presenting in a non-smoker at a young age?

a. Alpha-1 Antitrypsin Deficiency

b. MCC of COPD overall is Smoking

90. How is DM Type II Diagnosed?

a. 2 Random Glucose > 200; OR

b. 2 Fasting Glucose > 126; OR

c. A1c > 6.5%

91. Which type of Viral Hepatitis is spread via fecal-oral transmission?

a. A and E – I remember this by the word “AtE” where A and E stand for the subtypes and the word “ate” to remind myself its from “eating” fecal matter. Another good way to remember this I’ve heard before is “the vowels are from the bowels” since A and E are the only vowel subtypes.

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65. https://www.picmonic.com/learn/normal-gap-metabolic-acidosis_259(referral link https://www.picmonic.com/viphookup/PASPACPASSPORTLIK22 for 20% off subscription)

66. https://www.uptodate.com/contents/treatment-of-male-sexual-dysfunction?search=erectile%20dysfunction%20treatment&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H19736880

67.