Internal-Medicine-Exam-Notes.pdf

Internal Medicine Respirology (11) Pulmonary Embolism Cause: DVT (most common), fat embolism, septic embolism, air embolism, factor V Leiden etc. Risks: immoboliz...

Internal Medicine Respirology (11) Pulmonary Embolism Cause: DVT (most common), fat embolism, septic embolism, air embolism, factor V Leiden etc. Risks: immobolization/stasis, hyper coagulable, endothelial cell damage, increasing age, death from R heart failure Virchow’s Triad: Presentation: acute onset dyspnea, pleuritic CP, cough, hemoptysis, high RR, loud P2 + sys murmur on insp, ↑ JVP Trauma to a vessel wall Diagnostic algorithm: Hypercoagulation) o Wells Criteria: Venous stasis o Normal CXR but hypoxic and no other obvious explanation o ECG → sinus tachycardia (most common finding), T1 inversion, RV (RAD, RVH) strain or RBBB, S1-Q3-T3 if massive PE o Cancer patient/recently hospitalized and new chest pain and dyspnea not otherwise explained Investigations: ex. post-surgery with SOB and tachycardia = get a CTPA o Low PTP → D-dimer can rule out PE, if positive get a CTPA o High PTP → CTPA, venous duplex US, V/Q scan (rules in if high clinical suspicion, if inconclusive need leg doppler US) Treatment: o Anticoagulation – Dalteparin 200 units/kg SC daily, unfractionated heparin (if diminished renal function, need to monitor) o IV thrombolytic therapy (MASSIVE PE ie. SBP < 90 & no CI) – tPA (100 mg alteplase IV) + surgical embolectomy Thromboprophylaxis: 5000 units dalteparin Pulmonary Function Tests How to Differentiate between Asthma, COPD, and IPF: Obstructive Lung Disease: asthma, COPD, CF, bronchiolitis, bronchiectasis o Flow-volume shows reduced peak expiratory flow + scooping o Air trapping and hyperinflation o FEV1/FVC – reduced < 70% (severity indicated by FEV1) o TLC and RV – increased (> 120%) or normal o DLCO – anything depending on disease state (low = emphysema) Restrictive Lung Disease: ILD, pleural disease, chest wall disease, neuromuscular disease o Flow-volume curve is blunted and not scooped o Decreased lung compliance and volumes o FEV1/FVC – normal or increased (reduced FVC) o TLC – reduced < 80% o RV – any o DLCO – reduced (parenchymal ie. ILD, IPF) or normal Obstructive Lung Disease Asthma Chronic airway inflammation Often seen in children, recover as adolescents, and then relapses as adults Dx in Kids: Presents with cough + sputum, wheezing, and/or SOB (exertional) in response to triggers (exertion or exposures) Airflow obstruction Variable airflow obstruction that is usually reversible spontaneously or with treatment Reversible obstruction No alternative diagnosis A. Diagnosis: o Clinical history → symptoms, triggers, risk factors o Objective evidence of reversible airflow obstruction: ▪ ≥ 20% ↑ in PEFR OR ≥ 12-15% ↑ in FEV1 with bronchodilators OR ≥ 20% ↑ with systemic steroids ▪ Bronchoprovocation test (methylcholine challenge) → look for a 10% drop in FEV1 on exposure B. Management: o Patient Education → explain disease and medications/how to use o Assessment of severity + control: ▪ Severity determined by symptom frequency and duration, airflow limitation, and medications ▪ Assessment of control: o Trigger avoidance or control → smoke, pets, dust, etc. o Medication plan → short acting β2 agonists (SABA) initially then + ICS (budesonide, beclomethasone) ▪ If insufficient control can add/increase ICS and add a LABA or combined LABA/ICS (formeterol/budesonide) C. Exacerbations: o Determine/resolve the underlying cause → irritants, allergens, tobacco, infection, medication error o SABA + oral systemic steroids → prednisone for 5 days o Emergency → oxygen, oral steroids, ipratroprium bromide (SAMA), MgSO4 , consider adrenalin o Discharge → ICS maintenance therapy at discharge COPD: Chronic, preventable, and irreversible disease characterized by airflow limitation and air trapping → persistent respiratory symptoms Hyperinflation/barrel chested and gas trapping pushes the diaphragm down leading to SOB Presents with chronic bronchitis (smokers cough) + SOB Infections and irritants can cause exacerbations (see increased sputum, worsening cough, and fever) A. Diagnosis: o CXR shows hyperinflation, hyper lucent (dark) lung markings = emphysema, and flattening of the diaphragm o Post bronchodilator spirometry in smokers > 40 with dyspnea, cough, or frequent RTIs → confirmed if FEV1 < 80% & FEV1/FVC < 0.70 B. Management: o Lifestyle changes o Stop smoking (slows rate of decline in lung function) o Annual influenza vaccine & pneumococcal vaccine q5-10yrs o Triple therapy → LABA, LAMA, ICS (added for moderate-severe disease or frequent exacerbations) o Pulmonary rehabilitation, home oxygen, and surgery C. Exacerbations: o Worsening of 2 of dyspnea, sputum purulence, or sputum production leading to increased use of medications o Usually due to infections (streptococcus pneumonia is the most common organism), can also be allergens, irritants, CHF, PE, MI o Management: ABCs + oxygen, increase SABA + SAMA/Atrovent (Ipratropium bromide) dose, oral corticosteroids, and antibiotics ▪ Puffers → ventolin (MDI + spacer), ipratropium bromide (MDI + spacer) BOTH q4h + q1h prn ▪ Steroids → prednisone 40-50 mg PO daily x 5 days ▪ Antibiotics → ceftriaxone and azithromycin (+ pip/tazo if pseudomonas risk) → if criteria for antibiotics are met o Hypercapnia (CO2 retainer ie. CO2 > 50 + ph > 7.35) → keep O2 between 88-92% with BiPAP Restrictive Lung Disease Idiopathic Pulmonary Fibrosis: Diffuse parenchymal lung disease with progressive scarring of lung tissue and impairment of lung function and gas exchange Distortion and destruction of alveoli and microvasculature Decreased TLC, VC, and DLCO but normal FEV1/FVC ratio Can see pulmonary HTN and cor pulmonale with advanced disease A. Investigations: o CXR – decreased lung volumes, reticular/nodular pattern, honeycombing, hilar/mediastinal adenopathy o PFTs – decreased volumes, normal/increased FEV1/FVC, decreased DLCO B. Management: o Acute exacerbations – prednisone and antibiotics/diuretics if needed o Ongoing – anti fibrotic therapy (pirfenidone, nintedanib) Pulmonary Hypertension Mean pulmonary arterial pressure > 20 mmHg with a PVR > 3 wood units measured by right heart catheterization All types can be treated with oxygen, exercise, anticoagulation, and diuretics (if signs of RV failure, or fluid retention) Presentation: ex. scleroderma, prominent S2, pitting edema, elevated JVP o Progressive shortness of breath o Signs of fluid overload (edema, elevated JVP) o Systolic ejection murmur on the LL sternal border on inspiration A. Pulmonary arterial HTN (PAH): o Managed with CCB, prostanoids, endothelia receptor antagonists, PDE5 inhibitors o Lung transplant for refractory patients B. Pulmonary HTN from left heart disease: o Due to heat failure or left sided heart disease o Treat underlying heart disease C. Pulmonary HTN from lung disease/hypoxia: o From obstructive diseases (COPD, ILD, IPF) o Correct underlying disease o Treat hypoxia D. Chronic thromboembolic pulmonary HTN: o Due to PE or other obstructions o Managed with anticoagulation, pulmonary thrombo-endarterectomy E. Pulmonary HTN with unknown cause: o Treat the cause Pleural Effusions Transudative: usually bilateral not unilateral, can be from CHF, cirrhosis, kidney damage, pulmonary embolism Exudative: bilateral or unilateral, due to increased capillary permeability or lymphatic dysfunction ie. infection, malignancy, inflammation, trauma, drugs Presentation: often asymptomatic, can have dyspnea, pleuritic chest pain, shoulder pain, and tracheal deviation Investigations: CXR (can see > 200 mL fluid, blunting of the costophrenic angle, dense opacification Treatment: thoracentesis (also diagnostic) remove fluid and order serum LDH (UL ~ 240), glucose, and protein for comparison Pulmonary Nodules Benign features: smooth border, calcification (diffuse, central, laminated, popcorn, bulls-eye), solid, < 1 mo. doubling time or > 1 year, < 5 mm Malignant Risk factors: o Patient – older age, smoker, emphysema o Nodule – larger, spiculated (abnormal shape), upper lobe predominate o Family history of lung cancer o Density – semisolid or ground glass Clubbing Causes: lung cancer, TB, endocarditis, IBD, IPF, NOT COPD o Pulmonary – lung CA, bronchiectasis, pulmonary fibrosis, abscess, CF, TB, empyema, AV fistula/malformation o Cardiac – cyanotic congenital heart disease, endocarditis o GI – inflammatory bowel disease, celiac, cirrhosis, neoplasm o Endocrine – Graves’ disease o Other – malignancy, primary hypertrophic osteoarthropathy Presentation: shamroth sign, hyponechial angle > 180, bulbar distal phalynx, spongy nail bed DOAC Contraindications: GFR < 30 Esophageal varicies Active bleed Pregnancy INR > 1.5 or liver disease 72 hours since a major surgery with bleeding risk  Cardiology (7) ECGs  Recognize: atrial fibrillation and pericarditis o Atrial Fibrillation: ▪ Narrow complex irregular SVT = arise from sinus, atria, or AV node ▪ Irregularly irregular rhythm with fibrillatory waves between narrow QRS complexes rather than P waves (no P waves) due to the multiple waves in the atrium ▪ Can reach up to 600 bpm (> 350 bpm) ▪ Causes: HTN, acute MI, hyperthyroidism, alcohol, valve disease, and enlarged artria ▪ Consequences: thrombus and stroke risk due to blood stasis = all valvular Afib needs anticogulation ▪ Treatment: rate, rhythm, and anticoagulation Anticoagulation (if 1+ CHADS2): warfarin (vitamin K agonist, needs INR monitoring) or DOAC (dabagitran, apixaban) o Warfarin should be used if valvular AF (mechanical or rheumatic) o CKD: warfarin NOT DOACs since warfarin is not excreted by the kidney Anti-Pt (if CAD or PAD): ASA + clopdigrel Rate-control: beta blockers, BBCs, digoxin targeting rate < 100, < 110 if CHF Rhythm-control: antiarrhythmics (amiodarone, flecainide) or DC cardioversion (need 3 weeks of rate control + anticoagulation before cardioversion if > 48 hours o Pericarditis: ▪ Presentation (2 + of): pleuritic chest pain, friction rub, pericardial effusion, ECG (ST elevation + PR depression) ▪ Chest pain is worse on inspiration, pain improved by sitting forward + tachycardia ▪ Concave up ST elevation and PR depression in most leads (reversed in aVR + V1) for the first 1-2 weeks (stage 1) ▪ After 2-3 weeks ST segments normalize and T waves become flat (stage 2) and then inverted (stage 3) ▪ Labs: Inflammatory markers (CRP), CT/MRI inflammation, troponin (if myocardial involvement) ▪ Causes: infections (mainly viral), immunologic (SLE, RA), uraemia (renal failure), post-MI/Dressler’s syndrome, trauma, and after cardiac surgery (post pericardiotomy syndrome) ▪ Treatment: NSAIDs for 1-2 weeks (prn until pain/ CRP resolves) and colchicine x3 months ▪ If post MI use ASA not NSAIDs ▪ Do not provide thrombolytics o Myocardial Infarction: ▪ Septal (LAD): V1, V2 show ST elevation ▪ Anterior (LAD): V1-V4 show ST elevation ▪ Inferior (RCA): II, III, aVF show ST elevation ▪ Lateral (LCx): I, aVL, V5, V6 show ST elevation ▪ Posterior (RCA): V7-9 show ST elevations + R-waves in V1 and V2 ▪ PAILS: ie. posterior ST elevation causes reciprocal depression in anterior leads ▪ Never give nitroglycerine if a STEMI with inferior ST suggestive of RV infarction, or if PDE5 d/t risk of bradycardia Endocarditis Valvular infection (most commonly staph aureus acutely and strep viridins subacutely) Features: arrhythmia, cardioembolism, valve involvement o FROM JANE: Fever, Roth spots, Osler nodes, Murmur, Janeway lesions, Anemia, Nail bed hemorrhage/hematoma, Emboli o Anorexia/weight loss, fatigue, malaise, dyspnea, tachycardia, peripheral and pulmonary septic emboli, clubbing  Criteria: Duke criteria (2M OR 1M+3m OR 5m) Major Criteria Minor Criteria 1. Blood culture positive for an organism that commonly causes 1. Predisposing lesion or IV drug use infective endocarditis 2. Temperature > 38 C 2. Echocardiographic evidence of infection 3. Vascular phenomena Vegetation →on the valve, valve supporting apparatus, 4. Immunological phenomena regurgitant jets, or prosthetic material 5. Bacteriological phenomena (ex. blood culture New dehiscence of a prosthetic valve (wound rupture along the positive for microorganisms that only sometimes surgical incision) cause endocarditis) Abscess New valvular regurgitation ★ Initial transthoracic study will detect most episodes of endocarditis but TTE echocardiography improves visualization and may show small vegetations not seen★ Diagnosis: o Transthoracic Echo (TTE) → if non-diagnostic TTE or complications suspected then do TEE (considered gold standard for diagnosis) o Serial blood cultures → most important Treatment: 4-6 weeks of penicillinV o Empiric antibiotics (IV vancomycin + ceftriaxone) IF valve placed within 1 year tx with IV vancomycin, rifampin, and gentamicin o Cardiovascular support → diuretics, vasodilators, and inotropes Orthostatic Hypotension Criteria: taken after standing for 2 minutes from a seated position o Fall in sBP > 20 mmHg OR Supine HR elevation o Fall in dBP > 10 mmHg = hypovolemia Medications: too many blood pressure medications can be the cause o Alpha-blockers, antihypertensives, beta blockers, diuretics, nitrates, tricyclic antidepressants, SSRIs, antipsychotics Hypertension Routine Labs: CBC, lytes, BUN/Cr, Glu, EKG, Urinalysis, serum cholesterol/TGs, ambulatory BP monitor Treatment: ABCD o Healthy behaviours – quit smoking, low fat and sodium, caloric restriction, increase activity, relaxation, moderation of alcohol intake o Pharmacotherapy – ACEi/ARB, beta blocker, CCB, diuretic ▪ Thiazide diuretics (first line) ie. hydrochlorozide, followed by any other class (beta blockers, ACEI, ARB, or long-acting CCB) ▪ DM & CKD & LVH ACEI/ARBs are first line as they provide some renal protection (aldosterone antagonists CI in CKD) ▪ Angina/post MI and a.fib, beta-blockers are first line as they decrease cardiac demand for oxygen ▪ In CFH diuretics are used for congestion and beta-blockers for ↑ HR ▪ In PAD CCB used as they can delay athesclerosis ▪ ACEI, ARBs, and direct renin inhibitors are contraindicated in pregnancy o Treatment Targets: Pulmonary Edema Consider precipitating factors → arrhythmia, rapid A.fib, acute severe HTN, valvular disease (MR), cardiac ischemia Volume overloaded, can see Kerley B lines on CXR Management: LMNOP o Lasix (furosemide) 40 mg IV or at least 2 times higher than home dose ▪ Once > 1.5 Kg weight change (or > 5L UO) decrease dose 25-50% ▪ If < 0.5 Kg weight change (or < 3L UO) increase by 50% + can add metolazone (thiazide diuretic) 1.25-5 mg 1-7x/week o Morphine for pain control o Nitropatch (vasodilators) if BP allows: 0.4-0.8 mg/hr transdermal patch o Oxygen, maintain O2sat > 92% o Positive airway pressure mask  o Position → CPAP or BiPAP Monitoring: o Follow daily electrolytes (hypokalemia with diuretics), Urea, Cr o Salt restrict ( 2g < day), fluid restrict if hyponatremia ( < 1 L / day) o Echo to assess structure of heart → if reduced EF need good long-term medications once acute pulmonary edema resolves (BB, ACE-I, spironolactone) Heart Failure Triad: dyspnea, edema, fatigue [L-sided see pulmonary edema, R-sided see peripheral congestion] Workup: ECG, CXR, TTE, and BNP > 400; consider stress testing or coronary angiography if signs of myocardial ischemia o Systolic (EF < 55%): ischemic heart disease, myocarditis, infiltrative disease, HTN, HIV, CTD, peripartum cardiomyopathy o Diastolic (EF> 55%): ischemic heart disease, HTN, hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy Triggers: infection, ischemia, anemia, arrhythmia, medication, ethanol Kussmaul’s Sign: CXR: increased interstitial markings, jerky B lines, pleural effusions Increase in JVP on Treatment: quadruple therapy for HFrEF inspiration o ACEI/ARB or ARNI → need a 36 hour washout after an ACEI before stating ARNI Seen in restrictive o Beta blocker → NYHA class 4 need to be stable before initiating a beta blocker cardiomyopathy and o Spironolactone (MRA) constrictive pericarditis o SGLT2 inhibitor → need eGFR > 25 o Digoxin (inotropes) → for symptomatic control, doesn’t reduce mortality o Fluid restriction + Na restriction (< 2 g/day) if pulmonary edema o Oxygen to keep saturation > 92% o Diuretics SADMANS Sulfonureas ACEI/ARBs Diuretics/Direct renin inhibitors Metformin/MRAs Angiotensin neprilysin inhibitors (ARNI): entresto (sacubitril/valsartan) NSAIDs SGLT2 inhibitors Acute MI Chest Pain: retrosternal, exertional/stress related and relieved with rest or nitroglycerin + SOB, diaphoresis, N/V Investigations: serial troponin I + CK (q8hr x3), myoglobin, CBC, lytes, BUN/Cr, ABG, CXR ECG: o STEMI: ST elevation or new BBB and peaked T waves (invert 6-12 hours in) then permanent Q-waves → complete occlusion o NSTEMI: ST depression and T-wave inversions → partial occlusion Treatment: Thrombolytics CI: o ABCs and 2 IVs Pericarditis o MONA: morphine, oxygen, nitroglycerin (not if inferior MI), ASA Aortic dissection o Immediate: ASA + ticagrelor/clopdigrel, anticoagulation (heparin), beta blocker (if tachy) Hemorrhagic stroke o STEMI: reperfusion (thrombolytic ie. tPA or PCI within 2 hours!) o NSTEMI: anticoagulation (heparin infusion), anti-platelet (ASA + clopdigrel), + ACEI, BB then revascularization → never thrombolysis Long-term Management: o Antiplatelets → ASA + one of clopdigrel, ticagrelor, or prasugrel  o Anticoagulatiion → LMwH or UFH o ACEIs o Beta blocker or CCB as an alternative o Aldosterone system inhibitor (spironolactone) → used if already on an ACEI and BB o Statin Pneumonia Presentation: productive cough, high-grade fever, SOB + CXR infiltrates Vitals: febrile, HR>100, RR>28 Exam findings: dyspnea, crackles, bronchial breath sounds + decreased breath sounds, egophony, wheezes, increased tactile fremitus Pathogens: S. pneumoniae (#1), H. influenzae, C. pneumoniae, viral, atypical (legionella, chlymidia, mycoplasma) Assessment: o CURB65: confusion, uremia, RR>30, sBP 65 → score > 2 need to admit o Investigations: CBC, lytes, ABG, CXR, sputum C+S, blood C+S Inpatient Treatment: o Non-ICU: beta-lactam (cefotaxime, CTX) + macrolide (azithromycin, erythromycin) OR levofloxacin ▪ Ex. levofloxacin OR cefotaxime+Azithromycin 7-10 days o ICU: beta-lactam (cefotaxime, CTX) + macrolide OR beta-lactam + levofloxacin o MRSA: vancomycin or linezolid o Pseudomonas: pip-tazo or cefepime or meropenem o IV fluid and oxygen (sat > 92%) o If COPD → ipratropium (LAMA) 4-6 puffs q4h PRN, Salbutamol 2 puff q2h PRN Outpatient treatment: amoxicillin 1g TID OR doxycycline 100mg BID o If comorbidities → amox-clav OR cephalosporin + macrolide OR cefuroxime Chest X-Rays CHF (pulmonary Edema): o Enlarged cardiac shilouette > 0.5 (also see this in slow accumulating fluid in tamponade) o Vascular redistribution/cephalization → prominent vasculature near the heart o Interstitial edema → Kerley B lines, peribronchial cuffing; pleural effusions; alveolar edema o In CHF hydrostatic pressure increases this causes fluid in the interstitium and can result in pleural effusions or a pulmonary edema (would see fluid/opacity in base on lung) Tamponade (Back’s Triad): Small quiet heart Hypotension Elevated JVP Pulsus Paradoxus = drop in SBP > 10 mmHg on inspiration Pleural edema: blunted costophrenic angle (best seen on lateral) Pneumonia: will see air bronchograms and consolidation (L lobar pneumonia = right image) Geriatrics (2) Delirium Definition: acute and possibly reversible disturbance in cognition, attention, or LOC Likely if 1+2 are present and either 3 or 4 is: o Inattention (ask serial 7s, months backwards) o Acute onset and fluctuating course o Disorganized thinking o LOC alterations Ddx: dementia, delirium, depression o Dementia should not really have a fluctuating course o Individuals with dementia tend to have increased symptoms at nighttime, called “sun downing” – regular occurrence at night Workup: o Drugs/medications – benzodiazepines (clonazepam), furosemide, TCAs, hypoclorothiazide, opioids, gravol, and Benadryl are most common (others ie. atropine, beta blockers, digoxin etc.) o Infection, infarction, inflammation – CBC, urinalysis, cultures, CXR, ECG/troponin o Metabolic – lytes, B12, TSH, LFTs, toxicology screen o Environmental – no windows, isolation, lost glasses/hearing aids, restraints o Structural – neurologic exam, CT head o Pee/Poop/Pain – urinary retention, constipatiion, pain Prevention: optimize vision/hearing, mobilization, nutrition/hydration, sleep + wakefulness, avoid bladder catheterization, limit medications  Management: o Antipsychotics – haloperidol (1mg BID po prn), loxapine, quetiapine, risperidone, olanzapine (less common since very anticholinergic) ▪ Haloperidol (Haldol) is considered first line for agitation, higher doses not used due to risk of extrapyramidal symptoms ▪ Trazadone and melatonin are also used in some cases ▪ Do NOT use bezodaizepines o Important to monitor for QT prolongation (seen with any antipsychotic especially IV haloperidol) Falls Intrinsic factors: o Age-related changes – musculoskeletal (arthritis, muscle weakness), sensory (visual, proprioceptive, vestibular), cognitive (depression, dementia, delirium, anxiety), cardiovascular (CAD, arrhythmia, MI, low BP), neurologic (stroke, decreased LOC, gait disturbances/ataxia), and metabolic (glucose, electrolytes) o Orthostatic/syncopal o Acute illness, exacerbation of chronic illness Extrinsic factors: o Environmental (e.g. home layout, slippery surfaces, overcrowding, new environments) o Side effects of medications, polypharmacy (>4 medications), and substance misuse (e.g. alcohol misuse) o Situational eg. rushing to the toilet, walking while distracted Physical Exam: orthostatic vitals, visual acuity, cardiac exam Inestigations: CBC, lytes, BUN/Cr, glucose, Ca, TSH, B12, cardiac enzymes, urinalysis, ECG, DEXA (if 65+) Pharmacology Drug Sensitivity: Increased sensitivity to warfarin, sedatives, antipsychotics, anti-Cho., digoxin, and narcotics Medications to STOP on Admission: o SGLT2 inhibitors – euglycaemic DKA risk o ACEI/ARBS – ramipril (AKI) o Metformin o Blood thinners – DOACs = need to be cautious o Most other medications are safe ie. beta blockers AKI drugs to hold: AND = ACEI/ARBs, NSAIDs, diuretics Dementia Management: o ChEIs – donepezil, galantamine, rivastigmine (avoid if conduction defects, bradycardia, or unexplained syncope) o NMDA RA – memantine o In frontotemporal dementia there is no role for ChEI; instead trazodone and SSRIs are used for behaviours Gastroenterology (6) Acute Cholecystitis Risk factors (Fs): forty +, fate, fertile, female, DM, dyslipidemia, hispanic/indigenous Types: cholesterol (high in bile), black (hemolysis – calcium bilirubinate), brown (bacterial/parasitic infection) Acalculous: seen in sepsis, shock, CHF, trauma, ESRD = jaundice, fever, RqU pain, leukocytosis Diagnosis: US or CT abdomen Management: o Supportive – IV fluid, pain control, antiemetics, abx (ceftriaxone + metronidazole, pip-tazo) o Surgical – cholecystectomy GI Bleeding Lower GI bleed: Presentation: HR >99, SBP drop > 20, melena or bright red blood, pallor Diagnosis: o Labs – CBC, lytes, urea, Cr, type/cross-match, PTT, INR, AST, ALT, ALP, bilirubin, albumin o Microbiology – stool C&S o Endoscopy – colonoscopy, gastroscopy o Special imaging – Tc-99 RBC scan for obscure bleed, angiography, or capsule enteroscopy Management: o Resuscitation – 2 large bore IVs, ABCs (NS/RL and oxygen), pRBCs (Hb < 70) o Hold – antihypertensives, diuretics, NSAIDs o Colonoscopy – once stable and bowel is prepared o Surgery – for exsanguinating LGIB Upper GI bleed: Presentation: HR > 99, SBP drop > 20, melena, coffee ground emesis, pallor Diagnosis: o Labs – CBC, lytes, urea, Cr, type/cross-match, PTT, INR, AST, ALT, ALP, bilirubin, albumin  o Imaging – CXR, AXR , EGD Management: o Resuscitation – 2 large bore IVs, ABCs (NS/RL and oxygen), pRBCs o Hold – antihypertensives, diuretics, NSAIDs o Pantoprazole – 80 mg IV bolus + 8 mg/hr IV infusion OR 40 mg BID o Octreotide – 50 mg IV bolus + 50 mg/hr for up to 5 days o Antibiotics (3rd generation cephalosporin ie. 1g ceftriaxone x7 days) as prophylaxis o FFP, PCC, and vitamin K Treatment of underlying cause: o PUD – EDG with hemoclips and epinephrine injection then 3 days of IV PPIs o Varicies – banding + beta blocker ie. nadolol or propanolol o Mallory-Weiss Tear – oral PPI 2-4 weeks + anti-emetics o H.pylori (PAMC) – PPI BID, amoxicillin 1g PO BID, metronidazole 250-500 mg PO BID, clarithromycin 500 mg PO BID × 14 days Non-Variceal Bleeding: Variceal Bleeding: Pantoloc 80 mg IV bolus + 8 mg/hr IV infusion Pantoloc 80 mg IV bolus + 8 mg/hr IV infusion Keeps gastric pH elevated > 4 (inactivates pepsin which Octreotide 50 mcg IV bolus + 50 mcg/hr IV infusion is important since it breaks down clots) Somatostatin analogue = ↓ portal pressure More alkaline environment is preferred for platelets Antibiotics: Cephalosporin or fluoroquinolone (prophylaxis) Decreases acid induced damage to the ulcer Interventional: Endoscopic variceal band ligation (EVBL), Endoscopic Treatment balloon tamponade, TIPS, surgical shunt (↓ portal pressure) Liver Abnormalities Acute Liver Failure: Criteria: acute liver failure with encephalopathy + impaired synthetic function (INR > 1.5) Complications (SCREAM): Diagnosis: Sepsis/SBP o Labs – CBC, type & screen, peripheral smear, AST, ALT, ALP, bilirubin, albumin, INR, extended lytes, Coagulopathy/Cancer urea, Cr, glucose, HAV IgM and IgG, HBsAg, HBsAb, HBcIgM, anti-HCV and HCV RNA, lactate, ABG Renal failure o Imaging – US/CT/MR abdomen, echocardiogram Encephalopathy Management: Ascites/Varicies o Acute – ABCs, O2, IV hydration Metabolic changes o Elevated ICP (cerebral edema) – phenytoin, dexamethasone, mannitol, barbituates (hypoglycaemia, lyte abnormalities, acidosis) o Hepatic Encephalopathy – lactulose 30g PO BID-TID, then rifaximin o HSV infection – Acyclovir 5-10 mg/Kg IV q8h o Autoimmune Hepatitis – prednisone 40-60 mg/day + azithroprine 50-100 mg/day o Wilson Disease – plasma exchange, liver transplant o Acetaminophen Toxicity – N-acetylcysteine 150 mg/kg IV over 1h, then 50 mg/kg over 4h, then 100 mg/kg over 16h) ▪ King’s Criteria: ph < 7.3 or grade 3+ encephalopathy, Cr > 300, and INR > 6.5 Alcoholic Liver Disease/Alcoholic Hepatitis: Liver Enzymes Diagnosis: AST:ALT > 2:1 (elevated GGT, ALP, bilirubin) AST > ALT = alcoholic liver disease, Fatty liver, cirrhosis Treatment: AST/ALT 1000s = viral hepatitis, drugs/toxins, o Abstinence autoimmune, ischemia, Budd-Chiari o Nutrition – folate/thiamine AST/ALT = Hepatocellular o Prednisone/prednisolone – for moderate-severe alcoholic hepatitis o Alcoholic Liver Cirrhosis + melena – suspicious for varicies (#1 cause of bleeding in liver patients is varicies): ▪ Upper endoscopy ▪ Octreotide – 50 mcg IV bolus + 50 mcg/hr IV infusion ▪ Pantoloc – 80 mg IV bolus + 8 mg/hr IV infusion ▪ Ceftriaxone – 1g ceftriaxone x7 days Ascites: Diagnosis: o Fluid wave test – best positive predictor (90% specific) = #1 test o Shifting dullness – most sensitive Management: o Treat slowly – ↓Na+ intake to 2 g/day, fluid restriction – < 1.5 L/day o Diuretics – spironolactone, furosemide o Large volume paracentesis (LVP) with IV albumin of > 5 L at a time o TIPS (transcutaneous intrahepatic shunt (TIPS) if high risk of HE Acute Pancreatitis Complications: o Sepsis Causes (BAD HITS): o Calcium = hypocalcemia Biliary obstruction Alcohol/Anatomic o Abdominal = necrotizing pancreatitis, hemorrhage, abscess, fistula, thrombosis Drugs (thiazides, furosemide) o Respiratory failure, aspiration pneumonia, renal failure Hypercalcemia, Diagnosis: hypertriglyceridemia (> 10 mmol/L) o Labs – CBC, lytes, urea, Cr, glucose, AST, ALT, ALP, bilirubin, INR, LDH, lipase, amylase, Ca, Infection/Ideopathic/Inherited albumin, fasting lipid profile Trauma o Imaging – US abdo, CT abdo (+ contrast for necrotic pancreatitis) Surgery o ERCP – diagnostic and therapeutic to relieve obstruction (pancreatitis is a complication of ERCP) Management: IV hydration, antiemetics, abx (meropenem or imipenem), nurtitional suport Hyperlipidemia Investigations: o Labs – lipid profile (HDL, LDL, Tis), glucose, HbA1c, Cr, TSH, ALP, urine albumin:Cr + ApoB Framingham Risk: (high LGs) < 10% risk: tx if LDLc > 5 mmol/L o Screening begins at age 40 every 2 years 10-19% risk: tx if LDLc > 3.5 to Management: HDLc > 4.3 o Diet – more F&V ❤ 20% + risk: tx always o Statins – ie. atorvastatin, rosuvastatin lower LDL (target 1.8 mmol/L or 50% reduction if low risk) o Other – ezetimibe and bile acid sequestrates (lower LDL) o Fibrates & omega-3 FA – lower triglycerides Rheumatology (2) Osteomyelitis Osteomyelitis is an infection of the bone Can occur due to hematogenous seeding (common) or non- hematogenous seeding: Infectious Organism: S. aureus is the major bacterium involved Diagnosis: o MRI – most sensitive o Tagged WBC – good test to do for reinfection or if a chronic process o Blood – CBC, CRP, blood culture Management: o Antibiotics – ceftriaxone 2g IV q 24h + vancomycin for 6 wks o Surgery or debridement Monoarthritis Acute Monoarthritis: a single joint inflamed for less than 6 weeks Causes: 1. Septic arthritis (infection) → S. aureus 2. Acute gout → needle shaped uric acid crystals, negatively bi-refringent 3. Acute pseudogout → rhomboid shaped calcium pryophosphate, intracellular, positively bi-refringent crystals 4. Rare → reactive arthritis, psoriatic arthritis What should you do to investigate? o Aspirate the joint (take a small sample of fluid from the joint) → if the joint is red, aspirate it! o Send the fluid for the 3 Cs: i. Cell count → when > 2000 think inflammatory ii. Culture → take 24-48 hours iii. Crystals → takes a couple of hours (look for gout or pseudogout crystals) iv. Gram stain Acute Gout An acute inflammatory arthritis caused by uric acid crystal deposition in the joint Usually affects a single joint in the lower extremity → first metatarsophalangeal (MTP) joint (i.e. the big toe) is affected in 50% of cases Diagnosis: o Needle shaped and negatively birefringent monosodium urate crystals o CBC: elevated WBC, receive thrombocytosis o Elevated uric acid → may be falsely low during an attack  o Joint X-ray → soft tissue swelling, normal joint space, erosions Treatment: o Intra-articular corticosteroids injected into the affected joint o Oral NSAIDs or COXIBs → indomethacin 50 mg PO TID o Oral colchicine (older non-NSAID anti-inflammatory) → 0.6 mg PO q8h o Oral prednisone (particularly if the gout is in multiple joints) → 30 mg PO OD x 2 days, then reduce by 5 mg every 2 days o Allopurinol → need prophylaxis with an NSAID/Colchicine ▪ DO NOT start during an acute attack as it can worsen the attack Polyarthritis Osteoarthritis: Rheumatoid Arthritis: CTD Associated: Seronegative: Most commonly symmetric, Most commonly asymmetric Less symmetrical than RA: Axial involvement: affecting smaller joints first: oligoarthritis affecting: − Symmetrical − Rarely affects wrists, MCP − Small joints of hands and feet − Symmetrical − Can involve spine (axial), joints, and ankles − Sparing of DIP joints − Small joints of hands and feet sacroiliac joints, and DIP of − Affects CMC, PIP, and DIP − More chronic, insidious onset − Sparing of DIP joints hands joints of the hands − Similar to rheumatoid arthritis − More chronic, insidious onset − More chronic insidious onset − Chronic onset − Features of other diseases ie. lupus Nephrology (3) Acid-Base Abnormalities Metabolic Acidosis: GOLDMARK (HAGMA): Low Bicarb, 1:1 compensation regardless of chronicity NAGMA: Glycols (ethylene glycol) Differential diagnosis: AG > 12 or AG normal HCl gain Oxoproline (tylenol byproduct) Anion Gap: Na - Cl - HCO3 ~ 8-12 HCO3 loss (renal ie. RTA 1/2/4, Lactate (tx = flumethanazol, IHD) Osmolar Gap: 2Na + glucose + BUN diarrhea) DKA (euglycaemic if on SGLT2) o Measured serum - calculated = 10 HCO3 ↓ production Methanol/metformin o Elevated + ethyl glycol, methanol, ketoacidosis (DM, Pancreatitis ASA alcohol), lactic acidoses, sepsis, renal failure Renal failure Ketones (starvation, alcohol) Delta-Delta: ΔAG/ΔHCO3 = (12 – AG)/(24 – HCO3): o If ΔAG >> ΔHCO3 there is also a metabolic alkalosis Management: ABCs, oxygen, IV fluids NaHCO3 1-2 IV amp if pH < 7.0 Metabolic Alkalosis: High Bicarb, 1:0.5 compensation regardless of chronicity Ddx: Investigations: Aldosterone (↑ aldosterone = hypokalemia), renin HCO3 gain = HCO3, aceetate, citrate Management: ABCs, oxygen, IV fluids H loss = vomiting, NG suction o Treat underlying cause = replace K + fluids if volume sensitive, if volume Fluid loss = skin, urine, vommitting, hypokalemia Aldosterone mediated = high renin, or aldosterone insensitive give spironolactone, amiloride Respiratory Acidosis: High CO2, 10:1 acute, 10:3 chronic Retaining CO2 = hypoventilation, COPD (CO2 retainer) Ddx: CNS injury, OSA Management: ABCs, oxygen, IV fluids, non-invasive intubation Respiratory Alkalosis: Low CO2, 10:2 acute, 10:5 chronic Hypererventillation Ddx: hypoxia, pneumonia, sepsis, liver failure Management: ABCs, oxygen, IV fluids, sedation Sodium Abnormalities Hyponatremia: o Na < 133, seizure risk if < 120 o Headaches, N/V, restlessness, disorientation, seizures o Pseudohyponatremia → Hyperglycemia causes high osmolarity and causes water to exit cells : ▪ Correct Na by 1 mmol/L for every 3-4 increase in plasma [glucose] above normal o True hyponatremia → inadequate water excreted, inappropriately elevated AHD (SIADH); 2 common presentations: ▪ With excess AHD (SIADH) there is excess water absorbed into the blood and concentrated urine (high urine osmolality) but not hypovolemic so there is no reabsorption of Na via RAAS so urine sodium is higher = high urine osmolality and urine Na ▪ If hypovolemic there is low urine sodium since RAAS is activated and Na is absorbed into the blood + K is excreted in urine + high urine osmolality from high ADH (low water excretion in urine) = high urine os and low urine Na o Investigations → urine electrolytes, urine osmolality o Treatment → SAIDH = fluid restriction < 1 L/day o Treatment → hypovolemia = IV NS 75-125 cc/hr ▪ If on a thiazide diuretic, it is likely the culprit and should permanently be stopped ▪ Should not correct sodium more than 8 meq/24 hours (risk of osmotic demyelination + permanent brain damage, more common in alcoholics) → FOLLOW ELECTROLYTES CLOSELY (Q4-6 HRS BLOOD WORK) Hypernatremia: o Na > 144 mmol/L → draws water out of cells so they shrink and dysfunction o Altered mental status, twitching, seizures, and coma o Diabetes insipidus → pass lots of dilute urine: ▪ Central DI – inadequate ADH production ▪ Nephrogenic DI – inadequate renal response to ADH ▪ Dipsogenic DI – disorder of thirst, not associated with hypernatremia o Management: ▪ D5W → up to 300-350 mL/hr ▪ Correct slowly ~ 0.5 mmol/hr or maximum 10 mmol/day → can get cerebral edema if too rapid Potassium Abnormalities K is the major intracellular cation Normal [K] in the ECF is low at 3.5 – 5.0 mmol/L (tightly regulated), normal ICF [K] is 150 mmol/L Because K handling occurs in the collecting duct adjacent to H in the α-intercalated cells, we often get K and acid-base disorders together 1) Hyperkalemia: o Hyperkalemia Emergency → K+ > 6.5 mmol/L OR (ensure not falsely elevated if sample is hemolyzed)  o Cardiac arrhythmias / Muscle weakness or paralysis → peaked T waves (more than 2/3 the QRS), wide QRS o Management (order in powerchart): ▪ IV Calcium Gluconate 1000 mg infusion → stabilize cardiac membrane ▪ IV insulin 10 units with 1 amp of D50W → shift potassium intracellularly (sugar prevents hypoglycemia) ▪ Ventolin 10 mg Nebules → shift potassium ▪ Kayexylate 30- 60 g po x 1 → exchange Na for K in gut (binds K in the gut for excretion) ▪ IV sodium bicarbonate infusion (3 amp of sodium bicarb/1 L D5W and run at 150-200 cc/hr) in patients with severe metabolic acidosis (pH < 7.1) and low bicarbonate levels ▪ IV Lasix in volume overloaded patients OR fluids if hypovolemic ▪ Dialysis in refractory hyperkalemia despite above levels 2) Hypokalemia: o K+ < 3.5 mmol/L o Decreased intake o Increased output → metabolic alkalosis (diuretics, vomiting), metabolic acidosis (GI loss), ↑ aldosterone (metabolic alkalosis + HTN) o Shift → insulin, beta agonists, and aldosterone shift it into cells o Management: ▪ Oral K → if given IV should be < 40 mmol/hr ▪ KCl → an increase of 0.1 in the blood requires 10 mmol/L Dialysis Indications Acidosis: medically intractable acidosis Electrolytes: intractable hyperkalemia Intoxications: toxic alcohols (methanol, ethylene glycol), ASA Overload: fluid overload (persistent) Uremia: pericarditis, encephalopathy Renal Failure Pre-Renal: due to fluid loss o IV fluid replacement o May need dialysis for a short period if one of the AEIOU indications Renal: o Vascular → emboli, microangiopathic hemolytic anemia (TTP, HUS, scleroderma), vasculitis o Tubular → ATN, intra-tubular obstruction o Interstitial → AIN, NSAIDs, PPIs, diuretics, pyelonephritis o Glomerular → nephrotic , nephritic [anti-GBM, immune complex (SLE, HCV, HBV, HIV)] Post-Renal: o Urethra → stricture, stenosis o Prostate → BPH, prostatitis, cancer o Bladder → cancer, stones, clots, neurogenic o Ureters → cancer, stones, clots, pregnancy CKD Ddx: renovascular disease, diabetes, glomerulonephritis, MM, nephrotoxins, polycystic kidney disease Management: lipid control, ACEI, limit protein 0.8-1.0 g/Kg/day, SGLT2 if GFR > 30 Endocrinology (2) Diabetes Mellitus ABCDES of Diabetes Care: ★ABCDEFG★ ASA/ACEI: ACEI/ARB beneficial for microalbuminuria BP < 130/80 Cholesterol < 2/CVD screening Diabetic control < 7% or 6.5% Exercise/Eye exams Fat reduction Get going to quit smoking Hyperglycaemic Emergencies (DKA/HHS): DKA (diabetic ketoacidosis) HHS (hyperosmolar hyperglycaemic state) Insulin deficiency → hyperglycaemia → urinary loss of water & lytes → volume depletion & electrolyte deficiency & hyperosmolarity Hyperosmolar Hyperglycemic State: Diabetic Ketoacidosis: ▪ Caused by partial/relative insulin deficiency (may need insulin to tx) ▪ Caused by absolute insulin deficiency = excess counter ▪ More commonly seen in T2DM regulatory hormone/glucagon production (need insulin to tx) ▪ Marked hyperglycaemia, acidosis unusual ▪ More commonly seen in T1DM ▪ Onset is generally gradual ▪ pH < 7.3, bicarb < 15, AG > 12 ▪ Results in: ▪ Onset is usually sudden o Blood glucose > 30 mmol/L ▪ Results in: o Glucosuria, osmotic diuresis, severe dehydration, loss of electrolytes o Blood glucose > 15 mmol/L = polyuria, polydipsia o Very high serum osmolality > 320 (due ↑ BG + severe dehydration) o Lethary o Beware hypokalemia o Ketonemia, urine ketones, high anion gap acidosis o Minimal or no ketoacid accumulation (trace urine ketones) o Beware hypokalemia ▪ Significant water deficit (9L), ECVF contraction ▪ 6L water deficit (deplete volume status), ECVF contraction ▪ Often significantly decreased LOC ▪ Consciousness usually intact (depends on level of acidosis) ▪ Can cause neurological complications → seizures and stroke due to ▪ Abdo pain, nausea, vomiting, Kussmaul’s breathing excessive serum osmolality ▪ Mortality rate < 5%, 5-15% in the community (most common ▪ Mortality rate = 15% (due to neurological complications) cause of death in children with T1DM) Initial 24 hours: DKA: Volume – IV fluids Management: Electrolytes – IV potassium o IV Insulin infusion at 0.1 U/kg/hr → decrease rate once sugars improve. Transition to s/c insulin Acidosis – IV insulin, when to add ONLY once anion gap normal and patient ready to eat glucose to IV, HCO3 Next few days: ▪ No insulin until 3.3 K (give K first then insulin) Transition to SC insulin and PO diet o IV Normal saline → initially 250-500 cc/hr, decrease rate once more stable Discharge planning ▪ Add D5W once BG < 15 o KCl to IVF if K+ < 5.0 mmol/L Monitoring: o Accucheck q1hr o Electrolytes q2-4hr Look for cause: missed insulin, infection, ischemia, intoxication, drugs, pregnant In Patient Diabetes: Never hold long-acting insulin in a type 1 diabetic → RISK DKA For most non critically ill patients on insulin, pre-meal BG targets should be 5.0 to 8.0 mmol/L with random BG values 3 weeks → stress dose during illnesses or surgical procedures Minimal stress – routine dental work, skin biopsy = NO CHANGE Minor stress – flu, local anesthetic = 2-3x DOSE UNTIL WELL Moderate stress – orthopedic surgery, abdo surgery = 25 mg IV q8h x3 HYDROCORTISONE High stress – major trauma, septic shock, cardiac surgery = 50 mg IV q8h x3 HYDROCORTISONE then 25 mg IV q8h x3 until recovered Adrenal Conditions (CRH → ACTH → cortisol) Cortisol – actions oppose those of insulin: 1) Increases serum glucose and amino acids 2) Increases lipid and bone catabolism 3) Enhances electrolyte and water balance through actions on mineralocorticoid receptors: o Increases Na reabsorption at the distal tubule (water retention, ECF expansion) o Increases K excretion, H excretion (hypokalemia, alkalosis) 4) Suppresses the immune system Aldosterone: Involved in pressure-volume regulation in the kidney RAAS is activated in response to low BP and stimulates the adrenal cortex to produce aldosterone Action in the kidney = activation of MR: i. Increases epithelial sodium transporter (ENaC) transcription ii. Increases transcription of genes (structural/regulatory proteins) which activate current Na transporters Adrenal Hormone Overproduction: ↑ cortisol production = Cushing’s syndrome: o Diagnosis: 1) Two positive screening tests required for diagnosis: i. 24 hour urine collection → increased daily cortisol production ii. 1 mg dexamethasone suppression test → lack of cortisol suppressibility (best) iii. Evening/midnight salivary cortisol tests → lack of diurnal rhythm 2) Determine if it’s ACTH dependent or independent → is only cortisol elevated (ACTH independent) or is ACTH elevated as well o Causes: 1) Iatrogenic → high dose of steroid medications (#1 cause)  2) ↑ cortisol + ↓ CRH + ↓ ACTH = adrenal cortex is independently overproducing cortisol = adrenal cortical adenoma, carcinoma, or hyperplasia 3) ↑ cortisol + ↑ ACTH = there is too much ACTH being produced = pituitary adenoma, ectopic ACTH producing tumour ↑ aldosterone production = Conn syndrome (primary hyperaldosteronism): o Uncontrolled, persistent overproduction of aldosterone by the adrenal gland o Clinical Presentation: ▪ Hypertension and hypokalemia (often but not always together) o Diagnosis: ▪ Screening test = plasma aldosterone/renin ratio (ARR) Elevated ratio (> 900) indicates aldosterone production is no longer renin dependent ▪ Confirmation test = confirmation of lack of aldosterone suppressibility: i. Fludrocortisone → aldosterone-like effect, should suppress RAAS ii. High salt test → normally will decrease aldosterone iii. Stimulation test → furosemide + salt restriction should increase renin, renin remains low in hyperaldosteronism o Causes: ▪ adrenal hyperplasia, adenoma, secondary hyperaldosteronism – due to renal artery stenosis or primary hypertension o Treatment is spironolactone (to improve BP and K to prepare the patient for surgery) then surgical removal of the adenoma ↑ catecholamine production = Pheochromocytoma: o Rare tumours that produce too much adrenaline, usually in the adrenal medulla but can also arise anywhere along the sympathetic ganglia o Clinical Presentation: ▪ Spell-related (usually lasts 20 min to 1 hour) → bursts of adrenaline: Classic triad = headache, palpitations (tachycardia), sweating (pallor) Anxiety, diaphoresis, dyspnea, nausea, ↑BP, vomitting, cold hands o Diagnosis: ▪ Screening = urinary fractionated metanephrines (24 hr urine collection) or fractionated plasma free metanephrines o Treatment: ▪ Surgery after adequate preparation → pre-treatment = alpha blockage (always before beta blockade!!!!) + beta blockade Adrenal Hormone Insufficiency: Causes: o Primary adrenal insufficiency: ▪ Inability of adrenal cortex to synthesize/secrete glucocorticoids and mineralocorticoids ie. Addison’s disease (autoimmune), CAH, hypothyroidism, pernicious anemia, damage due to genetic defects, or infections (ex. TB, most common in developing countries) o Secondary adrenal insufficiency: ▪ Impaired adrenal stimulation from abnormal ACTH and/or CRH from the pituitary or hypothalamus ▪ Will have a cortisol deficiency but not an aldosterone deficiency as CRH/ACTH don’t regulate aldosterone ▪ Causes = pituitary adenoma, Sheehan’s syndrome o Critical illness-related adrenal insufficiency: ▪ Inadequate cortisol production to meet increased metabolic demand in a critically ill patient ie. severe sepsis/shock Signs and Symptoms: CHRONIC ADRENAL INSUFFICIENCY: ADRENAL CRISIS ADDISONS): Symptoms: Signs: ▪ Dehydration, hypotension, shock ▪ Weakness, tiredness, fatigue ▪ Weight loss ▪ Nausea, vomiting ▪ Anorexia ▪ Hyperpigmentation ▪ History weight loss, anorexia ▪ Gastrointestinal symptoms: ▪ Hypotension (< 110 mmHg systolic) ▪ Abdominal pain (acute) o Nausea & vomiting ▪ Vitiligo – due to autoimmune attack ▪ Unexplained fever/hypoglycemia o Constipation on the melanocytes ▪ Na ↓ o Abdominal pain ▪ Auricular calcifications ▪ K ↑ (peaked T waves on ECG) o Diarrhea ▪ Ca ↑ ▪ Salt cravings ▪ Renal insufficiency ▪ Postural dizziness ▪ Eosinophilia ▪ Muscle or joint paint ▪ Hyperpigmentation/vitiligo ▪ Other auto-immune features Diagnosis: 1) Lab findings: ▪ Electrolyte disturbances: ↓ Na, ↑ K, ↑ Ca ▪ Azotemia (renal failure) ▪ Anemia ▪ Eosinophilia 2) Morning Serum Cortisol Levels: ▪ Ruled out if > 500 nmol/L, diagnostic if < 80 nmol/L ↑ ACTH = primary adrenal insufficiency (ACTH differentiates between primary and secondary) ↓ ACTH = secondary  3) Cosyntropin (ACTH) Stimulation Test: ▪ Cosyntropin is synthetic ACTH, measure the cortisol response of adrenal glands to an injection of cosyntropin ▪ Increase over 500 = normal (rules out primary adrenal insufficiency) Management: Acute Adrenal Insufficiency (Adrenal Crisis): Chronic Adrenal Insufficiency: ! Primary = hydrocortisone + udrocortisone ▪ ABCs + get electrolytes and glucose measures ▪ Replacement therapy as maintenance: ! Secondary = hydrocortisone only ▪ IV fluids o Hydrocortisone or prednisone replaces cortisol ▪ Hydrocortisone 100 mg IV (don’t need fludrocortisone o Fludrocortisone replaces aldosterone, not required if 2 since high dose hydrocortisone will stimulate the MRs) insufficiency ▪ Search for underlying cause and treat accordingly ▪ Stress dosing (increased hydrocortisone dose needed) Infectious Diseases (5) COVID-19 Infection Clinical manifestations: o Initial Presentation – cough, myalgia, headache, + diarrhea, sore throat, smell/taste abnormalities, maculopapular/morbilliform eruptions ▪ Pneumonia is the most common serious manifestation = fever, cough, dyspnea, and bilateral infiltrates on CXR ▪ ARDS, arrhythmia, VTE, and encephalopathy seen in severe cases ▪ Dyspnea often seen 1 week after other symptoms o Incubation Period – 14 days, symptoms appear within 4-5 days of presentation Investigations: o Labs – lymphopenia, elevated aminotransaminase, elevated LDH, elevated inflammatory markers (ferritin, CRP, ESR) o CXR – consolidation, ground-glass opacities = often bilateral, have a peripheral distribution, and involve the lower lobes Management: o Dexamethasone – 6 mg daily x10 days in severely ill patients needed ventilation = MOST HELPFUL o Remdesivir/Paxlovid – 100 mg x5 days, can reduce time to recovery and the need for mechanical ventilation Meningitis Presentation: 95% of cases have 2/3: 1. Fever 2. Altered mental status 3. Nuchal rigidity o Young children – irritability, convulsions, meningococcal rash (non-blanching) Causative Organisms: In Children and Adults: In Neonates: 1. Strep pneumoniae (pneumococcus) 1. E. coli 2. Neisseria meningitidis (meningococcus) 2. Group B Streptococci Investigations: o Vitals – RR > 22, systolic < 100 → concerning for sepsis o Toxicology screen + blood culture o Serum glucose → for comparison to CSF glucose, ratio of CSF:serum < 0.6 is abnormal o CT head before LP if 60+, IC, CNS + seizure history, signs of decreased consciousness or focal CNS findings!! o Lumbar puncture → 4 tubes (cell count, protein levels, CSF glucose/gram stain/culture, cell count) Normal CSF: Acute Pyogenic (Bacterial) Meningitis: Aseptic Meningitis (Viral): Opening pressure: < 20 cm ↑ < 20cm or moderately ↑ Complications: Appearance: Clear Clear, cloudy, or purulent Clear/bloody Systemic ie. sepsis ↑↑↑ ↑ Stroke 0-5 (x 106/L) WBC: (500-50,000 x 106/L) (> 5 x 106/L) Seizure lymphocytes High neutrophils → esp. PMNs Moderately elevated lymphocytes Increased ICP Protein: 250-450 mg/L ↑↑↑ (500-10,000 mg/ml) Normal or ↑ (< 1000mg/ml) Brain abscess Glucose: 2.2-4.4 mmol/L Reduced Normal or mildly reduced Pneumonia/ARDS Glucose ratio: 0.6 < 0.4 Normal Gram Stain: Negative Usually, positive result + RBC lysis Negative fl  Management: Cephalosporin (ceftriaxone) o Dexamethasone IV – q6h x 4 days (stop if not bacterial meningitis) = before or with first abx dose o Antibiotics ASAP – ceftriaxone + vancomycin + ampicillin (IC, listeria, age > 65) Vancomycin Aseptic/viral meningitis: won’t look as sick, can often be managed as an outpatient (no confusion/seizures) Dexamethasone o Fever, headache, neck stiffness, mild meningeal signs, photophobia, rash Ampicillin if IC o Analgesia, anti-inflammatories (NSAIDs), rehydration, rest (consider HIV testing) HSV Encephalitis: wo o Focal seizures, fever, confusion, impaired memory, aphasia, focal deficits, headache, mild meningeal signs, photophobia, rash o IV acyclovir – 10 mg/Kg/dose q8h x2-3 weeks Urinary Tract Infections A. Uncomplicated: o Dx if 2+ of: i. Dysuria (pain or burning with voids) Pathogens (KEEEPPSS): ii. Frequency (small and frequent, incomplete voiding) 1. Klebsiella iii.Urgency 2. E. coli (#1 ~ 80% of UTIs caused by E. o Usually treated 3 days (or 5-7 with nitrofurantoin) coli) B. Complicated: 3. Enterococcus o Same symptoms as uncomplicated but additional factors 4. Enterobacter (citrobacter) o Male, pregnant, structural abnormality, obstruction, renal insufficiency etc. 5. Proteus C. Pyelonephritis: 6. Pseudomonus o Spread to ureters and kidneys 7. Staph saprophyticus (“honeymoon cystitis”) o Fever > 38 C, chills, flank pain, CVA tenderness, nausea + vomiting 8. Staph aureus (rare) Investigations: Labs: CBC, lytes, Cr/urea, urinalysis Microbiology: urine culture + screen: o Culture if > 39.4 C, endocarditis suspicion, or indwelling catheter OR 2+ of > 38.3, WBC > 18, Cr > 177, chills, vomiting, > 65, SBP < 90 Imaging: US Treatment: A. Asymptomatic Bacteriuria: o Positive urinalysis or culture but no symptoms o Only treat if pregnant or pending GU procedure → amoxicillin or nitrofurantoin B. Uncomplicated UTI: o Treat with nitrofurantoin for 5-7 days or fosfomycin 3 g for 1 day o C&S if < 2 symptoms, hospitalized, past UTI caused by atypical pathogens, quinolone/cephalosporin use in past 6 months, travel hx. C. Complicated UTI: o Send for C&S Antibiotics: o Treat with cefixime, amox-clav, ciprofloxacin, or TMP/SMX for 7-10 days Septra (TMP/SMX) (out patient) D. Pyyelonephritis: Macrobid (Nitrofurantoin) (out patient) o IV ceftriaxone, if ESBL carbapenem (meropenem), if pseudomonas pip-tazo Amoxicillin (outpatient) E. Pediatric UTI: Fosfomycin (ESBL E. coli) o Send for C&S Ceftriaxone Cefixime o Infants < 1 month → hospitalize + IV abx Aminoglycosides (nephro + ototoxicity) o Infants >1 month and children with fever → cefixime or ceftriaxone for 10 days o Children without fever → cefixime for 3 days Sexually Transmitted Infections Gonorrhoea: ceftriaxone + azithromycin/doxycycline Chlymidia: doxycycline OR azithromycin Pelvis Inflammatory Disease: ceftriaxone + azithromycin/doxycycline OR levofloxacin Trichomoniasis: metronidazole Bacterial Vaginosis: metronidazole or clindamycin IF pregnant or symptomatic Syphillis: penicillin Soft Tissue Infections = S. aureus (GP cocci clusters) , GAS (GP cocci chain) Cellulitis (deep): o Mild = cephalexin o Severe = cefazolin (Keflex) or cloxicillin or IV ceftriaxone o MRSA = vancomycin, daptomycin, TMP/SMX, or doxycycline Erysipelas (superficial): o Mild = penicillin or amoxicillin o Severe = cefazolin or IV ceftriaxone Necrotizing Fasciitis:  o Empiric Pip-Tazo + clindamycin + Vancomycin (MRSA risk) o IVIG if significant hypotension in GAS DM foot infection: Pip-Tazo OR ceftriaxone-flagyl + vancomycin & get an X-ray (r/o bone involvement) Intra-Abdominal Infections In Patient: o Ceftriaxone + Flagyl o IV pip-tazo o Ciprofloxicin + Flagyl o Aminoglycoside (gentamycin) + flagyl Out Patient: o Amoxicillin-Clavulinate C. dificile collitis: PO vancomycin 125 mg x 10 days Pneumonia & Viruses Community acquired: o Ceftriaxone + azithromycin o Amox-clav o Levofloxacin o Pip-Tazo (if thinking pseudomonas) Atypicals: MCL (mycoplasma, legionella, chlymidia) + have no cell wall or are intracellular o Azithromycin and Levofloxacin used for coverage HSV: acyclovir, valcyclovir, famciclovir Influenza: oseltamivir (tamiflu) COVID: remdesivir or paxlovid + dexamethasone (anti-inflammatory) Broad Covering Abx Ceftriaxone-Flagyl: broad spectrum, no pseudomonas coverage Amoxicillin- Clavulin: broad spectrum, no pseudomonas coverage Pip-Tazo: broad spectrum, includes pseudomonas coverage (can also use mero/imipenem for pseudomonas coverage) o Bad CNS penetration o High risk of AKI along with vancomycin o Covers pseudomonas while ceftriaxone-flagyl doesn’t ESBL: fosfomycin, carbapenem Sepsis Septic Arthritis: o Staph aureus is the most common organism ie. fall on knee and get septic arthritis = S. aureus is the most likely causative organism o In a patient that is very sick (ex. shock) the most likely infective cause is sepsis: ▪ Start IV fluids Remove central line if ▪ Give broad spectrum antibiotics ie. ceftriaxone + vancomycin – more important than cultures evidence of bacteremia ▪ Consider vasopressors if BP is dropping fast o Do NOT give prednisone for a joint that is possibly septic ex. RA patient with red/hot joint don’t inject Hematology (3) Anemia Microcytic Anemia: < 80 o TAILS – thalassemia, anemia of chronic disease, iron deficiency, lead poisoing, sideroblastic ▪ With low iron see ↑TIBC→↓Hb→↓MCV ▪ In thalasemia there is ↑Fe→↓TIBC + narrow RDW o Management – transfusion and treat underlying cause Normocytic Anemia: 80-100 o Acute blood loss o ↓ Production – BM supprerssion, MM, drugs, anemia of chronic disease, decreased EPO (renal failure) o ↑ Destruction – splenomegaly, immune (autoimmune = warm/cold), non-immune (spherocytosis, G6PD, sickle cell anemia, MAHA, toxins, infections) ▪ Coombs for immune (DAT +) – anti-IgG and anti-C3, tx with prednisone + rituximab; can be due to CLL o Management – transfusion + EPO if anemia of CKD Macrocytic Anemia: > 100 o BALDRAT – B12/folate, alcohol, liver disease, drugs (MTX, azathioprine), reticulocytosis, aplastic anemia/MDS, ↓TSH o Management – transfusion (slower rate in pernicious anemia) + treat underlying cause Warfarin INR Management: o INR < 10 – hold warfarin dose + oral vitK o INR > 10 – hold warfarin + IV vitK + FFP/PCC o Bleeding – hold warfarin + IV vitK + FFP/PCC Blood Group Compatibilities Emergency Medicine (3) Cardiac Catheterization Cardiac Catheterization Indications: Right heart (Swan-Ganz Catheter) Left heart Pulmonary artery HTN LV function assessment Volume status (unknown or unexplained) in shock Valvular disorder assessment – determine need for surgery Cardiogenic shock (pericardial tamponade, acute valvular CAD (assess extent and severity) + investigate when confusing disease) clinical features or CP of unknown origin Severe underlying Cardiopulmonary disease (CHD, LR Myocardial disorder assessment – determine need for surgery shunt, valvular disease) + undergoing surgery Confirm/compliment non-invasive studies PCI Indications: o Large MI (esp. anterior marked ST elevation) o Cardiogenic shock o Contraindication to thrombolysis o Rescue PCI for thrombolytic failure in a STEMI: ▪ Ongoing/unresolving ischemic pain ▪ Persistent ST elevation (>50% peak) o Medical refractory angina o High risk NSTEMI Stroke Management Acute Thrombotic Stroke: o ABCs, oxygen, and IV fluids o Thrombolytics – IV alteplase o Start ASA daily o Avoid rapid/excessive BP lowering – risk of ischemia in acute setting o Do not routinely treat BP unless SBP > 220 or DBP > 120 – reduce BP by 15% over 24 hours  Acute Hemorrhagic Stroke: o ABCs, oxygen, IV fluid o BP reduction targeting SBP 140-180 – IV labetalol if a hypertensive crisis o Reverse anticoagulation Shock Definition: A state in which blood flow is inadequate to meet cellular metabolic requirements in the tissues of the body A transition between life and death Signs of Tissue Hypoperfusion: Ill appearance or altered mental status Tachycardia ★ Shock first effects Tachypnea the mitochondria ★ Hypotension → presence is NOT required Dusky or mottled skin Delayed capillary refill Low urine output → < 1 mL/Kg/hr (not part of initial assessment) Pathophysiology of Shock Elevated lactate level (not part of initial assessment) Classification of Shock (Hinshaw & Cox): Hypovolemic = not enough fluid volume ie. reservoir depletion Cardiogenic = problem with the heart means the pump is failing and not producing enough cardiac output ie. pump failure Obstructive = something extrinsic to the heart is impairing cardiac output ie. flow obstruction (pump or pipes) Distributive = “the tank is too big and maybe leaky too” ie. vasodilation, pumps are too large + leaky Principles of Shock: Distributive = sepsis → ↓ perfusion from ↓ SVR; maldistribution of blood flow (microvascular issue) Cardiogenic, hypovolemic, obstructive = ↓ perfusion from inadequate CO ** BP may be maintained despite inadequate tissue perfusion Treatment: Initial management: o ABCs – circulation, airway, breathing o Apply 100% O2 by non-rebreather face mask o Monitor o 2 large bore IVs (< 18 G), 1L bolus of normal saline or RL ~ 15-30 min o Blood work (CBC, lytes, Cr, BUN, glucose, VBG + lactate, 2x blood cultures) o Antibiotics Life support: preload (fluid) + afterload (pressors) + contractility (inotropes) o Cardiovascular – vasopressors (NE), inotropes (E) o Pulmonary – mechanical ventilation, prone positioning, lung protective ventilation o Renal – dialysis, CRRT o Neurologic – sedation, delerium medication Sepsis management: o Source control o Administer 30 cc/kg ~ 2-3 L of RL o Empiric antibiotics – IV pip-tazo or IV ceftriaxone Toxicology Methanol & Ethylene Glycol Overdose: o Lethal dose of metabolites (formate, glycolate, glyoxylate, oxalate) is ~ 1 g/Kg o Features – anion and osmolar GAP, Kussmaul breathing, altered LOC, seizure, hypotension o Tx: ▪ Supportive – NG suction, NaHCO3 (if metabolic acidosis) ▪ Cofactor therapy – folic acid, thiamine, pyridoxine ▪ Hemodialysis for confirmed intoxication Alcohol Withdrawal: o Diazepam o Folic acid 1 mg oral o Multivitamin 1 tab oral o Thiamine 100 mg oral Ethylene Glycol and Methanol: Possible sources: Methanol: Ethylene Glycol: − Windshield washer fluid − Engine coolant − Model airplane fuel antifreeze (cars) − Solid cooking fuel − Perfumes − Adulterant in denatured alcohol − Gas-line antifreeze (commercial vehicles) Pathophysiology: o Alcohols are metabolized by alcohol dehydrogenase and toxic alcohols are then further metabolized by aldehyde dehydrogenase o This creates acid metabolites that are toxic to the body: ▪ Methanol → formic acid → end organ toxicity + AGMA ▪ Ethylene glycol → oxalic acid and glycolic acid → end organ toxicity + AGMA Symptoms: Methanol: Ethylene Glycol: − Inebriation − Inebriation − Metabolic acidosis − Metabolic acidosis − Ocular symptoms: − Acute kidney injury (calcium oxalate crystal o Blurry vision precipitation) o “Snowfield” vision − Cerebral edema o Blindness (blindness) − Hypocalcemia (rare) − Bilateral basal ganglia lesions (Parkinsonism) ★ Renal toxin ★ ★ Ocular and basal ganglia toxin ★ Investigations: Gap Depends on Metabolic Process: o Anion gap o Early = most product is in the alcohol form o Blood gas ▪ High osmolar gap + Low anion gap o Osmolality o Late = most has been metabolized into the acid form o BUN/Cr ▪ Low osmolar gap + High anion gap o Electrolytes o Normal osmolar gap can’t rule out toxic alcohols BUT a o Lactate low gap can basically confirm it o Toxic alcohol screen o Ethanol level Need to keep in mind time from ingestion when interpreting anion gap and osmolar gap  Management: o ABCs o Alcohol dehydrogenase blocking → want to prevent further metabolism of the parent alcohol by blocking ADH: i. Fomepizole → drug most commonly used in North America as it has a very high affinity for ADH ii. Ethanol → has a higher affinity for ADH than methanol and ethylene glycol but is hard to dose and causes other complications like inebriation and hypoglycemia o Hemodialysis → if there has already been significant metabolism of the parent alcohol o Call poison control