Medicine Flashcards
Hypertension
A pathologic dysregulation of the homeostatic mechanisms that control blood pressure.
Essential (no identifiable cause) and secondary
Best understood pathways of hypertension include overactivation of the sympathetic nervous system and renin-angiotension-aldosterone systems, blunting of the pressure-natriuresis relationship, variation in cardiac or renal development. Secondary causes include Cushing syndrome, Thyroid disease, Pheochromocytoma, Polycystic Kidney disease, renal artery stenosis, various medications, OSA, etc
Most recent: JNC 8 (2014), ACC/AHA update 2017
Normal: <120/<80
Elevated: 120-129/<80
HTN Stage 1: 130-139 or 80-89
HTN Stage 2: 140 + or 90+
HTN Urgency: >180/120 no signs of end-organ dysfunction (prompt referral)
HTN Emergency: same but with end-organ dysfunction
Symptoms: Largely asymptomatic. May have a headache, Hypertensive emergency- encephalopathy (headache, somnolence, vomiting, AMS)
Pharmacological Treatment: ACC/AHA if over 140/90 and low risk, if 130/80 and high risk. No consensus but 120-130/80 reasonable for controlled range
Meds:
Angiotensin-Converting Enzyme Inhibitors: Commonly used as initial medication. Mode of action is inhibition of the RAAS, but also inhibit bradykinin degradation, and can reduce sympathetic nervous system activity. Young white patients. Agents of choice in with Type 1 diabetics with proteninuria or evidence of kidney dysfunction. Dry cough, angioedema, fetal effects, sometimes hyperkalemia. Ramipril, Lisinopril, Quinapril
Angiotensin II Receptors: May improve cardiovascular outcomes in HF and diabetic nephropathy. Can cause hyperkalemia. Losartan, Valsartan, Telmisartan
Renin Inhibitors; Renin inhibitor, binds the proteolytic site of renin, preventing cleavage of angiotensinogen. Aliskiren drug name
Calcium Channel Blockers: Peripheral vasodilation with less reflex tachycardia and fluid retention than other vasodialators. May be preferable in black and elderly. Protective factor against strokes. Ie Diltiazem, cardizem, verapamil, amlodipine, nifedipine. Amlodipine and nifedipine are dihydropyridine. Side effects headache, peripheral edema, bradycardia. CA blockers negative iontropes and only amlodipine can be used safely in severe HF.
Diuretics: decrease plasma volume initially but long term reduction of peripheral vascular resistance. Loop diuretics used in patients with kidney dysfunction. More potent in Blacks, older, obese persons than beta blockers or ACE inhibitors. Thiazides can cause hyponatremia. Hypokalemia uncommon but can happen. Loser Mag Increase uric acid, glucose, and CA. S
Thiazides-chlorthalidone, HCTZ Loop-Furosemide, Bumetanide,
Aldosterone Receptor Blockers: Spironolactone. Spironolactone can cause hyperkalemia, metabolic acidosis, gynecomastia.
Beta Blockers: Decrease heart rate and cardiac output. Also decrease renin release. neutralize the reflex tachycardia caused by vasodialators. Cardioprotective in patients with angina pectoris, previous MI, sinus tachycardia, and stable HF. Differ in pharmacologic properties between cardiac beta-1- receptors and whether they block the beta-2-receptors in the bronchi and vasculature. However all are nonselective at high doses. Metoprolol reduces mortality and morbidity in patients with stable and reduced EF. Typically not first line agents, except in active CAD. Side effects-exacerbate bronchospasm, sinus node dysfunction, and AV conduction depression. Carvedilol and nebivolol maintain cardiac output and may reduce peripheral resistance by cocomitant alpha blockade. Beta blockers used cautiously in patients with diabetes since they can mask hypoglycemia and inhibit glucoenogenesis. Beta blockers not used in cocaine users will unopposed vasoconstrictor alpha adrenergic activation. Beta-1 selective-Atenolol, Metoprolol, Bisoprolol. Carveilol and propanolol non selective.
Alpha Antagonists- Prazosin, terazosin- block postsynaptic alpha-receptors, relax smooth muscle, and lower peripheral vascular resistance. Can have marked hypotension after first administration.
Central Sympatholytic Action- Methyldopa, clonidine, guanfacine lower blood pressure by stimulating alpha adrenergic receptors in the CNS thus reducing efferent peripheral sympathetic outflow. Side effects include sedation, fatigue, dry mouth, and rebound hypertension. Methyldopa can cause hepatitis.
Arteriolar Dilators-Hydralazine and minoxidil. Relax vascular smooth muscle and produce peripheral vasodilation. Can have reflex tachycardia and increase myocardial contractility.
Initial titration: Ace/arb or ccb or thiazide. 2nd Ace/Arb plus CCB or Thiazide. 3rd ACE/Arb plus CCB plus Thiazide
55yrs or greater and blacks 1st line CCB or diuretic then ARB or ACE or vasodilating beta, then aldosterone receptor blocker if resistant. All others Ace or Arb or CCB or diuretic, 2nd vasodilating beta-blocker
Stage 2 require medical evaluation and risk stratification prior to surgery (ABOMS anesthesia guide)
Peripheral Artery Disease
Is a vascular disorder characterized by an abnormal narrowing of the peripheral vasculature secondary to blockage or spasm
ABI ankle-brachial index: below .9 normal
Statin therapy, Antiplatelet Therapy, Peripheral Vasodilators
Atherosclerosis
Is a vascular disorder characterized by an abnormal thickening or hardening of the arteries due to plaque accumulation caused by HLD and inflammation.
Atherosclerosis is initiated by endothelium activation and, followed by a cascade of events (accumulation of lipids, fibrous elements, and calcification), triggers the vessel narrowing and activation of inflammatory pathways.
Coronary Artery Disease
Is a cardiac disorder characterized by accumulation of plaques that could lead to hypoperfusion of the myocardium [relative to demand]
Statins remain first line therapy for lipid lowering in patients with CCD. Several adjunctive therapies (eg, ezetimibe, PCSK9 [proprotein convertase subtilisin/kexin type 9] inhibitors, inclisiran, bempedoic acid) may be used in select populations
Diagnosis with ECG, Echo, Stress test, Cardiac MRI
Ezetimibe inhibits the absorption of cholesterol from the small intestine and decreases the amount of cholesterol normally available to liver cells.
Myocardial Infarction
Infarct of myocardium secondary to hypoperfusion of coronary arterial system.
MONA IS CHANGING
Nitrates (nitroglycerine 0.3-0.6 mg SL q5 mins x 3 max), Aspirin (325mg chew), consider Beta Blockers but be careful with nitrates and BB if hypotensive. Can also give more oral nitro if hypertensive
Oxygen only if sating 90 or less or concerns for hypoxemia
2014 AHA guidelines rec morphine, more and more lit is showing increased 30-day MACE with this due to concerns that opioid interacts and inhibits P2Y12 inhibitor, though evidence is still controversial. Only use if pain is refractory, can also use small dose(s) fentanyl, some meta-analyses showed equivocal with morphine
Percutaneous coronary intervention: balloon-tipped catheter maneuvered to stenotic artery and stent placed (bare metal vs drug eluting, drug eluting slow rate of local neointimal hyperplasia)
Bare metal rarely used currently, 2nd or 3rd generation DES, Long-term DAPT recommended (Aspirin + a Platelet P2Y12 Receptor Blocker like Clopidogrel 75mg daily), continue for 12 months, re-assess, then continue for 18 months (at least)
ACC/AHA “Door-to-Balloon” Time <90 Minutes
Previous stent: Defer non-emergent noncardiac surgery for at least 6 months regardless of stent type
For most patients continue DAPT as opposed to stopping it prior to surgery (conversation with managing doctor based on RISK)
CABG preferred for multivessel disease vs PCI
Acute Coronary Syndrome
A range of conditions associated with suddenly reduced blood flow to the heart
Unstable Angina: symptoms not relieved by rest
NSTEMI: EKG can show ST depression or T wave inversion
STEMI: ST segment elevation
NSTEMI and STEMI have elevated troponins (Trop I is best, vs trop T)
Troponin I binds to actin. Specific to cardiac. Over 0.04ng/ML abnormal.
Angina
Reversible hypoperfusion of coronary artery system leading to chest pain
Usually due to artherosclerosis. Coronary vasospasm may occur.
Stable: Typically occurs at exertion and is improved with rest.
Symptoms: Sensation of tightness, burning, pressing, choking, aching, indigestion, discomfort.
Usually lasts under 3 minutes if precipitated by exertion. After angler or large meals can last 15-20 minutes.
ECG is often normal. Characteristic horizontal or downsloping ST segment depression that reverses after the ischemia.
Stress test, myocardial stress imaging.
Pain not responding to three tablets or lasting more than 20 mins may represent evolving infarction.
Dosage 0.3, 0.4, or .6mg.
nitroglycerin converts to nitric oxide (NO) in the body. NO then activates the enzyme guanylyl cyclase, which converts guanosine triphosphate (GTP) to guanosine 3’,5’-monophosphate (cGMP) in vascular smooth muscle and other tissues
Beta-blockers should be considered for first-line therapy in most patients with chronic stable angina.
Ranolazine- Myocardial ischemia exerts effects on adenosine triphosphate flux, leading to a decrease in the energy available for contraction and relaxation of the heart muscle. inhibits sodium and potassium ion channel currents.
Prinzmetal Angina- coronary vasconstriction with chest pain that occurs without the usual precipitating factors and is associated with ST segment elevation.
Congestive Heart Failure
A condition characterized by the inability of the heart to pump enough blood to meet the metabolic demands of the tissues
New York Heart Association Classification
Class 1: Heart disease with no symptoms or limitations of physical activity
Class 2: No symp at rest, slight limitations with ordinary activity
Class 3: Marked limitation of activity with minimal exertion
Class 4: Symptoms at rest. Severe limitation of activity
S3: Ventricular Gallop, can be a sign of HFrEF, can be normal
S4: Atrial Gallop, can be a sign of HFpEF, almost always pathologic
Largely a clinical diagnosis
Work Up: Exam may have edema, JVD, hepatomegaly, S3/S4, consider EKG, echo, CXR, labs
B-type natriuretic peptide (BNP): initially identified in the brain (hence originally called brain NP), but primarily released from the ventricles
TX: diuretics, B blockers, etc
Aortic Stenosis
Is a cardiac valvular disorder characterized by restricted blood flow through the aorta [leading to dyspnea, angina, syncope]
Echo for diagnosis
Tx: TAVR, SAVR, TAVI
Endocarditis
Is a cardiac disorder characterized by inflammation of the internal lining of the heart
IV drug use Staphylococcus aureus
Native valve Viridans streptococci, S aureus, enterococci
Prosthetic valve Staphylococcus epidermidis, S aureus
Culture negative HACEK organism (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella corrodens,
Kingella), Candida, Aspergillus
Duke criteria for diagnosis
* Definite IE: 2 major; 1 major and 3 minor; 5 minor
* Possible IE: 1 major and 1 minor; 3 minor
Major criteria
* Positive blood culture
* Echocardiogram with evidence of
endocardial involvement
Minor Criteria
* Predisposition to IE (IV drug use, indwelling catheter, diabetes)
* Fever
* Vascular phenomena (Janeway lesions, arterial emboli, intracranial hemorrhage, splinter hemorrhage)
* Microbiologic evidence
* Immunologic phenomena (Osler nodes, Roth spots)
Treatment
* Native valve endocarditis: Vancomycin and gentamicin
* Prosthetic valve endocarditis: Vancomycin, rifampin, and gentamicin
* Culture positive: Treat organism
ADA Prophylaxis
The current infective endocarditis/valvular heart disease guidelines7, 8, 10 state that use of preventive antibiotics before certain dental procedures is reasonable for patients with:
-prosthetic cardiac valves, including transcatheter-implanted prostheses and homografts;
-prosthetic material used for cardiac valve repair, such as annuloplasty rings and chords;
-a history of infective endocarditis;
-a cardiac transplant with valve regurgitation due to a structurally abnormal valve;
-the following congenital (present from birth) heart disease:
unrepaired cyanotic congenital heart disease, including palliative shunts and conduits
any repaired congenital heart defect with residual shunts or valvular regurgitation at the site of or adjacent to the site of a prosthetic patch or a prosthetic device
a According to limited data, infective endocarditis appears to be more common in heart transplant recipients than in the general population; the risk of infective endocarditis is highest in the first 6 months after transplant because of endothelial disruption, high-intensity immunosuppressive therapy, frequent central venous catheter access, and frequent endomyocardial biopsies.9
b Except for the conditions listed above, antibiotic prophylaxis is no longer recommended for any other form of congenital heart disease.
Pediatric Patients
Congenital heart disease can indicate that prescription of prophylactic antibiotics may be appropriate for children. It is important to note, however, that when antibiotic prophylaxis is called for due to congenital heart concerns, they should only be considered when the patient has:
Cyanotic congenital heart disease (birth defects with oxygen levels lower than normal), that has not been fully repaired, including children who have had a surgical shunts and conduits.
A congenital heart defect that’s been completely repaired with prosthetic material or a device for the first six months after the repair procedure.
Repaired congenital heart disease with residual defects, such as persisting leaks or abnormal flow at or adjacent to a prosthetic patch or prosthetic device.
Atrial Fibrillation
Abnormal electric foci in the atrium leading to irregularly irregular rhythm
10% of people over 65 have A Fib
Rate or Rhythm control (strategies are equal, AFFIRM Trial, RACE Trial) BUT newer evidence is STARTING to show that rhythm controlled is better (it used to be really done mostly in symptomatic people) East Afnet 4 Trial https://www.nejm.org/doi/full/10.1056/NEJMoa2019422
Necessitates anticoagulation strong consideration
Chads 2 Vasc, Hasbled for anticogulation
RVR- rapid ventricular rate; treatment is beta-blockers (esmolol, propranolol, metoprolol) calcium channel blockers (diltiazem and verapmil). If unstable cardioversion indicated.
Anticoagulation with dabigatran, rivaroxaban, apixaban.
Long time antiarrhythmic medications include sotalol, flecainide, propafenone, dronedarone
Transfusion Associated Circulatory Overload
a common transfusion reaction in which pulmonary edema develops primarily due to volume excess or circulatory overload
Cor Pulmonale
Is right-sided heart failure caused by pulmonary hypertension
Cardiomyopathy
Cardiomyopathy is a disease process affecting the myocardium that impairs the heart’s ability to pump or fill
Leads to retention of blood in the cardiopulmonary circuit, hence CHF are possible in all CMs
BEST diagnostic test is echocardiography
4 types
Hypertrophic Cardiomyopathy (non-obstructive type): MCC is HTN, thickened walls, reduced space for blood
Hypertrophic Obstructive Cardiomyopathy: Similar to above but with obstruction of outflow by interventricular septum blocking blood flowing out of the aorta. Genetic (AD). Common cause of young athletes dying
Dilated Cardiomyopathy: Opposite from above, can FILL but can cannot pump, MCCs are MI, alcoholism
Restrictive Cardiomyopathy: A little different, problems with filling and pumping, Rigidity of the myocardium, have histologic damage, infiltration, MCC is sarcoidosis, also can be amyloidosis, hemochromatosis, scleroderma, malignancy often from mets
Asthma
A chronic reactive respiratory disease characterized by a variable levels of obstructive pattern lung disorder with bronchiolar inflammation and hyperresponsiveness
Pathogenesis: Airway inflammatory cell infiltration with eosinophils, neutrophils, and lymphocytes, goblet cell hyperplasia, mucus plugging of the small airways, bronchial smooth muscle hypertrophy, airway edema, mast cell activation.
Symptoms: Episodic wheezing, shortness of breath, chest tightness, and cough.
ABG: Increased PaCo2 and respiratory acidosis may indicate impending respiratory failure.
Pulmonary Function Testing: Either a spirometry or peak expiratory flow measurement. Airflow obstruction is indicated by a reduced FEV1/FVC ratio generally below 0.7. FEV1 is forced expiratory volume in 1 second. FVC forced vital capacity. Significant reversible was previously 12% with short acting bronchodilator. Now 10% based on 2022 guidelines.
Bronchoprovocation testing: Inhaled histamine or methacholine may be useful when asthma is suspected despite non diagnostic spirometry. Not recommended if FEV1 is less than 65% of predicted. A positive test is defined as a fall in the FEV1 of 20% or more.
Methacholine is a non-selective muscarinic receptoragonistthat acts directly on airway smooth muscle receptors to induce bronchoconstriction.
Step 1: SABA as needed
Step 2: Low dose ICS daily and SABA or concomitant ICS and SABA
Step 3: Combination low-dose ICS plus formoterol daily
Step 4: Combination medium-dose ICS-formoterol daily
Step 5: Medium high dose IC-LABA plus LAMA and SABA as needed
Inhaled Corticosteroids: Beclomethasone dipropionate, fluticasone propionate, flunisolide, triamcinolone acetonide
Beta-adrenergic agonists: All asthmatics have access to SABA. Short-Acting Beta-2-Agonists- Albuterol, Levalbuterol. Long acting Beta-2-Agonists-Formoterol, Salmeterol.
Systemic Corticosteroids:
Anticholinergics: Reverse vagally mediate bronchospasm but not allergen or exercise-induced bronchospasm. They may decrease mucous gland hypersecretion. Short acting or long acting muscarinic antagonists. Ipratropium bromide is a SAMA.
Leukotriene modifiers: Zileuton is a 5-lipoxygenase inhibitor that decreases leukotriene production. Montelukast and Zafirlukast are cysteinyl leukotriene receptor antagonists.
Monoclonal antibody agents-Omalizumab recombinant antibody that bind IgE. IL-5 antagonist-reslizumab, mepolizumab, benralizumab.
Phosphodiesterase Inhibitor- Theophylline mild bronchodilation. Anti-inflammatory and inmmunomudulatory, enhances mucociliary clearance.
Mediator Inhibitors- Cromolyn sodium and nedocromil.
Systemic Corticosteroids: Methylprednisolone, Prednisolone,
COPD
Irreversible obstructive pattern lung disorder characterized by either bronchitis and/or emphysema
Risk Factors: MCC is smoking, resp infecs, occupational exposure, alpha-1 antitrypsin deficiency
Hypercarbia and hypoxemia: triggers to breath…they live in hypercarbic state, so hypoxemia is their trigger
Stage 1: Mild FEV1/FVC < 70%, FEV1 > 80%
Stage 2: FEV1/FVC <70%, 50% FEV1 <80
Stage 3: FEV1/FVC <70%, 30% FEV< 50% predicted
Stage 4: FEV1/FVC <70%, <30% predicted FEV1 <50%
Stage 3-4 are ASA 4.
Keep 02 between 90-94%
Bronchitis
Is a respiratory disease characterized by chronic cough and mucus production greater than 3 months for 2 consecutive years
Major complaint is chronic cough, productive of mucopurulent sputum, with frequent, exacerbations due to chest infections. Dyspnea is usually mild, Patients are typically over weight and cyanotic is common. Chest is noisy, with rhonchi invariably present, wheezes are common.
Increased perfusion to low V/Q
Emphysema
Is a respiratory disease characterized by destruction of alveoli
“Pink Puffer”
Major compliant of dyspnea, cough is rare, with scant clear, mucoid sputum. Thin with recent weight loss. Evidence of of accessory muscle use. Chest is quite.
CXR: shows hyperinflation with flattened diaphragms. Vascular markings are diminished, particularly at the apices
Increased ventilation to high V/Q areas, high dead space ventilation.
Restrictive Lung Disease
A disorder characterized by a decrease in the total volume of air that the lungs are able to hold, is often due to a decrease in the elasticity of the lungs themselves or caused by a problem related to the expansion of the chest wall during inhalation.
Idiopathic pulmonary fibrosis (IPF)
Non-specific interstitial pneumonia (NSIP)
Cryptogenic organizing pneumonia (COP)
Sarcoidosis
Acute interstitial pneumonia (AIP)
Inorganic dust exposure such as silicosis, asbestosis, talc, pneumoconiosis, berylliosis, hard metal fibrosis, coal worker’s pneumoconiosis, chemical worker’s lung
Sleep Apnea
Is a central or obstructive cessation of breathing during sleep
Upper airway obstruction during sleep occurs when loss of normal pharyngeal muscle tone allows the pharynx to collapse passively during inspiration.
Reported daytime somnolence, morning sluggishness, headaches, day time fatigue, cognitive impairment, recent weight gain, impotence.
May have arterial hypertension, erythrocytosis.
Polysomnography includes electroencephalography, electrooculography, electromyography, ECG electrocardiogram, pulse oximetry, and measurement of respiratory effort and airflow.
Cystic Fibrosis
Is a condition characterized by a genetic mutation of the cystic fibrosis transmembrane conductance regulator protein (CFTR) causing exocrine impairment/thickening. Patient can develop an obstructive pattern.
Recurrent airway infections with H. Influenzae, P aeruginosa, S aureus
Extrapulmonary disease: Sinus, GI recurrent pancreatitis, meconium illeus, genitourinary problems.
Diagnosis: Sweat chloride concentration > 60mEq/L on two occasions, or presence of two disease causing mutations.
Treatment: CTFR modulators include medications that modify trafficking, folding, or function. Ivacaftor (increases time the CFTR channel remains open), Lumacaftor, tezacaftor, elexacaftor (improving CFTR protein folding and cell-surface trafficking). Recombinant human deoxyribonuclease (rhDNase, dornase alpha) cleaves extracellular DNA in sputum, decreasing sputum viscosity.
Antibiotics: Short time or Long time Azithromycin
Vaccination against Pneumococcal and coronavirus
Acute Respiratory Distress Syndrome
Is a diffuse, inflammatory lung injury leading to respiratory failure
CXR: New, bilateral radiographic pulmonary opacities not explained by pleural effusion, atelectasis, or nodules
The Berlin criteria used for the diagnosis of ARDS in adults.3 These criteria are based on timing of symptom onset (within one week of known clinical insult or new or worsening respiratory symptoms); bilateral opacities on chest imaging that are not fully explained by effusions, lobar or lung collapse, or nodules; the likely source of pulmonary edema (respiratory failure not fully explained by cardiac failure or fluid overload); and oxygenation as measured by the ratio of partial pressure of arterial oxygen (Pao2) to fraction of inspired oxygen (Fio2). ARDS is classified as mild, moderate, or severe based on the following criteria:
Mild: 200 mm Hg < Pao2/Fio2 ratio ≤ 300 mm Hg with positive end-expiratory pressure (PEEP) or continuous positive airway pressure ≥ 5 cm H2O.
Moderate: 100 mm Hg < Pao2/Fio2 ratio ≤ 200 mm Hg with PEEP ≥ 5 cm H2O.
Severe: Pao2/Fio2 ratio ≤ 100 mm Hg with PEEP ≥ 5 cm H2O.
Pneumonia
Is a pulmonary infection leading to inflammatory response at the alveolar level
Community acquired pneumonia, nosocomial pneumonia (hospital acquired pneumonia or ventilator associated pneumonia
CXR or CT chest
Transfusion-related acute lung injury
Transfusion-related acute lung injury caused by massive transfusion [which mimics ARDS in causing respiratory failure]
Lab test for antileukocyte, anti-HLA, or anti-neutrophil
Stop the transfusion, supportive measures to improve oxygenation, low tidal volume.
Negative Pressure Pulmonary Edema
or postobstructive pulmonary edema is a well-described cause of acute respiratory failure that occurs after intense inspiratory effort against an obstructed airway, usually from upper airway infection, tumor, or laryngospasm.
Pulmonary Embolism
Complete or partial blockage of pulmonary arterial vasculature leading to ventilation-perfusion mismatch (V/Q)
Common sources: lower extremity venous system, mural thrombus from A Fib, fat embolism from long bones
Signs: Dyspnea, chest pain, hemoptysis, tachypnea, cyanosis, JVD, diminished breath sounds
D-dimer less than 500ng/mL
CXR: Westermark-A prominent central pulmonary artery with local oligemia or pleural-based areas of increased opacity that represent intraparenchymal hemorrhage (Hampton hump).
Helical CT-PA
Wells Criteria: look up. PERC for low risk patients
Treatment: Anticoagulation impedes additional thrombus formation, allowing endogenous fibrinolytic mechanisms to lyse existing clot.
Streptokinase, recombinant tissue plasminogen activator rt-PA, Thrombolectomy or pulmonary embolectomy.
Inferior vena cava filters if contraindications to anticoagulation.
Virchows Triad Stasis, Endothelial damage, Hypercoagulability
Pulmonary Hypertension
Pathologic elevation in pulmonary arterial pressure. Can develop into right sided heart failure.
5 groups.
Treatment: Nitric oxide pathway: Phosphodiesterase inhibitors (sildenafil), Endothelin pathway: Endothelin receptor antagonist (bosentan, ambrisentan) and Prostacyclin pathway: Prostacylin analogs (Epoprostenol, Treprostinil)
Normal is 20mm Hg
Pneumothorax
Accumulation of air in the pleural space due to trauma, idiopathic, or spontaneous.
Tension pneumothorax: Positive-pressure of air in the pleural space exceeding alveolar and venous pressures throughout the respiratory cycle; resulting in compression of lung and decreased venous return.
Signs: Chest pain, dyspnea, cough
CXR: Lucency without lung markings between the chest wall and lung, and visualization of the visceral pleura.
Stable, spontaneous may be observe. Needle decompression. Chest tube.
Tuberculosis
Is a mycobacterial infection resulting in granulomatous formations mainly in the lungs
Symptoms: Fatigue, weight loss, fever, night sweats, and productive cough
CXR: pulmonary opacities, including nodular or cavitating
Acid-Fast bacilli on smear of sputum, rapid molecular testing positive,
4,6,9 month regimen, new evidence of 4 month treatment regimen as appropriate.
4 month: 8 weeks of daily treatment with rifapentine, moxifloxacin, isoniazid, and pyrazinamide, followed by 9 weeks of daily rifapentine, moxifloxacin, and isoniazid.
Obesity
Abnormally high amount of adipose tissue compared with lean muscle mass with an excess body weight >20% over the predicated ideal body weight
BMI=kg/m2
Class 1 – BMI 30-35; Class 2 – BMI 35-40; Class 3 – BMI >40
Body Mass index: kgs / height (m2)
Review effects on all systems in the body
Pediatric: BMI (used for 2+ years as best measure for adiposity)
Management: Know which drugs are based on ideal body weight vs total
What is your plan to establish IV access in a difficult venipuncture?
BP cuff appropriate size
Decreased FRC –> more preoxygenation
BMI 30-40 = ASA 2, >40 = ASA 3 (ASA last amended in 2020, does not take into account other comorbidities)
Diabetes
Is a metabolic disorder characterized by insulin resistance or decreased insulin production leading to hyperglycemia.
How to diagnose: >126 fasting BG, HbA1c - 6.5% (pre- is 5.7), 200 random BG
Type 1 (10%) or type 2 (90%), Duration of disease, complications of diabetes (eye, kidney, nerve), Recent episodes of DKA, HHS, or severe hypoglycemia, History of coronary disease or stroke
Evaluate HBA1C: The HBA1C test looks at how much hemoglobin is glycosylated. HbA1 has two alpha and two beta chains and makes up about 98% of our hemoglobin, the other two percent being HbA2 and a small amount of HbF or fetal hemoglobin. The c added onto the HbA1 means it is glycosylated.
Measures last 1-3 months. The more recent time interval, the last 6 weeks before the test, are more weighted than the prior 6 weeks. There is an average chart that correlates the % of HBA1c to blood sugar, for example an HBA1C of 6 corresponds to an average blood sugar of 126, whereas an HBA1c of 9 correlates to an average blood sugar of 212. Normal, 5.7 of below. 5.7-6.4 is prediabetic or high risk of DM, and 6.5 or higher is indicative of DM.
DM 1: autoimmune destruction of pancreatic Beta cells
DM2: Insulin resistance and relative lack of insulin (fat)
The “Polys”
Polyuria
Polydipsia
Polyphagia
Blurry vision
Fatigue
Weight loss
Recurrent urinary tract infections
Dysuria
In the absence of symptoms, must have TWO positive tests on same or different days
Separate criteria for pre-diabetes
TXTs:
Lifestyle modifications, Oral hypoglycemics, Injectable hypoglycemics, Insulin: Injectable or continuous pump
Rapid-acting insulins include lispro (Humalog), aspart
(Novalog) and glulisine (Aprida) . They have an onset of five to 15 minutes, peaks of one to two hours and durations of four to six hours . Short-acting or regular insulins (Humulin R and Novolin R) have an onset of 30 to 60 minutes, peaks of two to three hours and durations of six to eight hours . Intermediate insulins include NPH or Lente (Humulin N and Novolin N) and have an onset of two hours, peaks of 12 hours and durations of 24 hours . Long-acting insulins include Ultralente (Humulin), glargine (Lantus) and detemir (Levemir) with onsets of six to eight hours, peaks of 16 to 24 hours and durations of 36 hours . Combination insulin preparations also are available with NPH/Regular ratios of 70/30 and 50/50 .
Type 2 DM is treated with weight loss and exercise as well
as oral or injectable medications . The classes of medications
used today are:
1 . Sulfonylureas: glyburide (DiaBeta, Glynase PresTab,
Euglucon), gliclazide (Diamicron), glimepiride (Amyryl)
2 . Meglitinides: repaglinide (Prandin), nateglinide (Starlix)
3 . Biguanides: metformin (Glucophage, Glumetza,
Fortamet, Riomet)
4 . α-Glucosidase inhibitors: acarbose (Precose, Glucobay), miglitol (Glyset)
5 . Thiazolidinediones: rosiglitazone (Avandia),
pioglitazone (Actos), Sodium-glucose co-transporter 2
(SGLT-2) inhibitors: dapagliflozin (Farxiga), canagliflozin
(Invokana)
6 . Dipeptidyl peptidase-4 (DPP-4) inhibitors: sitagliptin
(Januvia), saxagliptin (Onglyza)
7 . Glucagon-like peptide-1 (GLP-1) receptor agonist:
liraglutide (Saxenda, Victoza), exenatide (Byetta
Prefilled Pen), dulaglutide (Trulicity Pen, Trulicity)
The hypoglycemic agents sulfonylureas and meglitinides
increase the release of insulin to decrease blood glucose
levels . The biguanides reduce hepatic glucose production in the presence of insulin, increase anaerobic glycolysis, increase glucose uptake and use by muscles, and decrease intestinal glucose absorption . The α-glucosidase inhibitors break down disaccharides and complex carbohydrates by competitive inhibition of the α-glucosidase enzyme in the proximal intestinal wall, delaying carbohydrate absorption . They do not cause hypoglycemia in a fasting patient .
Thiazolidinediones reduce insulin resistance and improve
the peripheral action of insulin by increasing the uptake
and use of glucose by peripheral tissues and reducing
hepatic glucose production . SGLT-2 inhibitors reduce renal reabsorption of glucose, thereby increasing urinary glucose excretion . DPP-4 inhibitors increase insulin secretion, decrease gastric emptying and decrease blood glucose . GLP-1 receptor agonists slow gastric emptying, suppress pancreatic glucagon secretion and stimulate insulin secretion in response to hyperglycemia
A major surgical and anesthetic concern in the diabetic
patient is the difficulty maintaining a balance between
insulin and the counterregulatory hormones . Insulin lowers blood glucose levels by glucose uptake in the muscle and fat cells, decreasing gluconeogenesis and glycogenolysis in the liver . Counterregulatory hormones – such as epinephrine, glucagon, cortisol and growth hormone – can increase blood glucose levels by stimulating gluconeogenesis and glycogenolysis in the liver, increase lipolysis and ketogenesis, and inhibit glucose uptake in the muscle and adipose cells of
the body . Other concerns include poor wound healing secondary to inflammatory response inhibition, decrease in macrophage infiltration, angiogenesis, fibroplasias, collagen accumulation and collagen maturation . They also have decreased phagocyte capabilities of the polymorphonuclear leukocytes, decreased chemotaxis and decreased migration . Increased plasminogen activator inhibitor concentrations and abnormal platelet function also are seen . Patients with poorly controlled DM have increased postoperative infections due to these effects . Patients with DM also can have a higher risk of aspiration due to delayed gastric emptying
Peri-op
Consider additional work up with EKG and labs (BMP, HbA1C), pre and post op finger stick to check levels
Morning procedures are preferred for insulin-dependent diabetics
↓ bedtime long-acting insulin dose, if morning procedure basal insulin dose can be cut in half. (short and rapid acting held morning of), if basal is taken in the morning, can reduce dose by 25 to 50%. For ultra long-lasting insulin, consult endocrine.
Do not administer rapid-acting insulin on morning of procedure
Consider IV dextrose if longer procedure or unable to eat afterwards
Pumps: consult endocrinology, NEVER STOP THE PUMP
In general, may hold all orals EXCEPT for SGLT-2 inhibitors for which the current recommendation is 24 hours, drugs that end in -liflozin like canagliflozin
Higher risk for infections due to impaired white blood cells from the glycosylation.
Be careful with steroids.
GLP-1 agonists (about 8 drugs currently on the market), Glucagon-Like-Peptide 1 receptor agonists
Semaglutide aka Ozempic
Jan 2023, “For adolescents with refractory obesity who opt for pharmacologic therapy, we suggest subcutaneous semaglutide rather than other agents (Grade 2C),
Evidence is developing, ASA and AAOMS among others have appointed task forces to come up with recommendations
Problem is it delays gastric emptying increasing risk of aspiration
Currently (SEP 23) rec from ASA is for patients on DAILY dosing, hold day of, for WEEKLY dosing, hold a week prior, all irrespective of type of surgery or indication
Consider IV dextrose if longer procedure or unable to eat afterwards. D50 is dextrose 50%, and the most appropriate to use for severe hypoglycemia. In a crash cart, this often comes as a 50 cc syringe, or in a hospital setting, a 50 ml bag, with a concentration of 0.5g/ml, which equates to 25 grams of dextrose. It is given over 1-5 minutes IV. Generally, 1 gram of dextrose raises blood sugar by 4-6, so giving 25 grams raises it by about 100-150. This effect is short lived, about 30 minutes or so.
Can also do D5W added to fluids like LR or NS
Grave’s Disease
Is a hyperthyroid autoimmune disease stimulating increase secretion of T3/T4
Most common cause of hyperthyroidism. Palpable goiter ocassionally with bruit, ophthalmopathy concerns.
Thyroid stimulating immunoglovulins or antibodies bind TSH receptors.
Treatment:
Propanolol,
Thiourea drugs (methimazole or Propulthiouracil )PTU)) methimazole’s mechanism of action is its potent inhibition of thyroperoxidase (TPO), an enzyme crucial for thyroid hormone synthesis
Iodinated Contrast agents- Iopodate sodium, Iopanoic acid
Radioactive Iodine
Surgery when Euthyroid
Hashimoto’s Thyroiditis
Is a chronic lymphocytic thyroiditis resulting in hypothyroidism
Levothyroxine-hyroid hormones exert their physiologic actions through control of DNA transcription and protein synthesis
Cushing’s Disease
Is an endocrine disorder of excess cortisol, endogenous, or exogenous steroids
Caused by supraphysiologic dose of steriods, benign ACTH pituitary adenoma, neoplasms.
Central obesity, muscle wasting, hirsutims, purple striae.
Osteoporsis, hypertension, poor wound healing, hyperglycemia, leukocytosis, lymphocytopenia, hypokalemia.
Addison’s Disease
Is an endocrine disorder characterized by insufficient glucocorticoids and mineralocorticoids usually due to destruction of adrenal gland or insufficient ACTH secretion
Weakness, vomiting, diarrhea, abdominal pain, amenorrhea
Increased skin pigmentation
Hypovoemic hypotension, hyponatremia, hyperkalemia, hypoglycemia, eosinophilla
Anemia
Anemia is a reduction in hemoglobin (Hb) or hematocrit (HCT) or RBC count.
It is a presentation of an underlying condition and can be subdivided into macrocytic, microcytic, or normocytic. Patients with anemia typically present with vague symptoms such as lethargy, weakness, and tiredness. Severe anemia may present with syncope, shortness of breath, and reduced exercise tolerance.
Erythropoietin (EPO), which is made in the kidney, is the major stimulator of red blood cell (RBC) production
The etiology of anemia depends on whether the anemia is hypoproliferative (i.e., corrected reticulocyte count <2%) or hyperproliferative (i.e., corrected reticulocyte count >2%).
Hypoproliferative anemias are further divided by the mean corpuscular volume into microcytic anemia (MCV<80 fl), normocytic anemia (MCV 80-100 fl), and macrocytic anemia (MCV>100 fl).
1) Hypoproliferative Microcytic Anemia (MCV<80 fl)
Iron deficiency anemia [1]
Anemia of chronic disease (AOCD)
Sideroblastic anemia [2] (may be associated with an elevated MCV as well, resulting in a dimorphic cell population)
Thalassemia
Lead poisoning
2) Hypoproliferative Normocytic Anemia (MCV 80-100 fL)
Anemia of chronic disease (AOCD)
Renal failure
Aplastic anemia
Pure red cell aplasia
Myelofibrosis or myelophthisic processes
Multiple myeloma
Macrocytic anemia can be caused by either a hypoproliferative disorder, hemolysis, or both. Thus, it is important to calculate the corrected reticulocyte count when evaluating a patient with macrocytic anemia. In hypoproliferative macrocytic anemia, the corrected reticulocyte count is <2%, and the MCV is greater than 100 fl. But, if the reticulocyte count is > 2%, hemolytic anemia should be considered.
3) Hypoproliferative Macrocytic Anemia (MCV>100 fL)
-Alcohol
-Liver disease
-Hypothyroidism
-Folate and Vitamin B12 deficiency [3]
-Myelodysplastic syndrome (MDS)
Refractory anemia (RA)
Refractory anemia with ringed sideroblasts (RA-RS)
Refractory anemia with excess blasts (RA-EB)
Refractory anemia with excess blasts in transformation
Chronic myelomonocytic leukemia (CMML)
-Drug-induced
Diuretics
Chemotherapeutic agents
Hypoglycemic agents
Antiretroviral agents
Antimicrobials
Anticonvulsants
4) Hemolytic anemia. Hemolytic anemia (HA) is divided into extravascular and intravascular causes.
Extravascular hemolysis: red cells are prematurely removed from the circulation by the liver and spleen. This accounts for a majority of cases of HA
Hemoglobinopathies (sickle cell, thalassemias)
Enzyemopathies (G6PD deficiency, pyruvate kinase deficiency)
Membrane defects (hereditary spherocytosis, hereditary elliptocytosis)
Drug-induced
Intravascular hemolysis: red cells lyse within the circulation, and is less common.
PNH
AIHA
Transfusion reactions
MAHA
DIC
Infections
Snake bites/venom
Polycythemia vera
Is a hematologic disorder characterized by an increase in red blood cells, measured by hematocrit over 55%
Sickle Cell Anemia
An autosomal recessive disorder where a point mutation (Valine for Glutamic acid) causes sickling of RBCs and hemolysis
Questions similar to asthma WU; hospitalizations, treatments, what causes crises for you, etc
TXT: Hydroxyurea increases HbF which prevents sickling, bone marrow transplant
Peri-op: keep every as normal as possible and control pain well, deviations can cause a crisis
Normothermia, euvolemia, well oxygenated, control pain
Sickle Cell Crisis
Is a term used to describe several acute conditions of sickle cell anemia, most commonly describing a painful, vaso-occlusive crisis. [Can also be splenic sequestration crisis, hemolytic crisis, aplastic crisis]
Von Willebrand’s Disease
Is a coagulopathy due to reduced quantity or quality of von Willebrand’s factor, which is responsible for stabilizing platelet adhesion.
vWF mediates PLT adhesion, adhesion to endothelium, and prevents degradation of Factor 8
Inherited phenotypic forms of Von Willebrand disease are:
Type 1: This is an autosomal dominant disease (AD, incomplete penetrance approximately 60%) and is caused by a partial quantitative deficiency of von Willebrand factor.
Type 2: This is an autosomal dominant disease caused by several qualitative defects in von Willebrand factor. It has four subtypes (2A-AD or AR, 2B-AD, 2N-AR, 2M-AD). 2A is the most common variant.
Type 3: This is an autosomal recessive disease (AR) and is caused by a complete quantitative defect. The von Willebrand factor levels are not detectable, and the severe bleeding disorder characterizes this variant.
Normal PT and PTT, ristocetin cofactor assay and vWF assay
Often a DDAVP trial is done by heme team to assess response
Type 1: partial quantitative def (MC). DDAVP, 0.3 mcg/kg IV or 150 mcg spray to each nostril, 20 mins before procedure
Type 2: Qual def (2A, 2B, 2N, 2M), cannot give DDAVP to 2B, will induce hypercoag state
Type 3: total quan def
Cryoprecipitate (8, 9, vWF, fibrinogen) can help in all types
Humate-P = (vWF, 8) concentrate
Hemophilia A
Is a coagulopathy due to X-linked genetic deficiency of factor 8
Hemophilia B
Is a coagulopathy due to X-linked genetic deficiency of factor 9
PTT prolonged (intrinsic pathway), normal PT
Classified based on severity
Mild: Factor lvls over 5% but below normal
Moderate: Factor lvls 1-5%, infrequent spontaneous bleeding, prolonged bleeding from surgery
Severe: Less than 1%, multiple spon bleeds per year
TXT: Recomb Factor 8 or 9, goal of 80-100% normal lvls pre-op and maintain at 50% for 1-2 weeks to allow for healing. Infuse 20 min before surgery
DDAVP helps as well (causes release of Factor 8 a vWF from endothelial cells)
Disseminated intravascular coagulation
Is a systemic, intravascular activation of the clotting cascade which can lead to microvascular thrombi in various organs
Supportive treatments may include:
Plasma transfusions to replace blood clotting factors if a large amount of bleeding is occurring.
Blood thinner medicine (heparin) to prevent blood clotting if a large amount of clotting is occurring.
Heparin induced thrombocytopenia
Is a complication caused by heparin that causes decreased platelets in the blood
Heparin induced thrombocytopenia (HIT) is an immune‐mediated event that can have severe life‐ and limb‐threatening complications.
Despite thrombocytopenia, bleeding is rare; rather, HIT is strongly associated with thromboembolic complications.
When a diagnosis of HIT is suspected immediate cessation of all forms of heparin, including unfractionated heparin (UFH), low molecular weight heparin (LMWH) and heparin flushes, is imperative.
Treatment of HIT should be initiated based on clinical suspicion and must never be delayed pending laboratory confirmation of HIT.
A direct thrombin inhibitor, such as lepirudin, danaparoid or argatroban, is considered the agent of choice for treatment of HIT.
Warfarin should not be used until the platelet count has recovered
Thalassemia
Is a hemoglobinopathy with absent Alpha/Beta globulin leading to microcytic anemia
Mild thalassemia (Hb: 6 to 10g/dl):
Signs and symptoms are generally mild with thalassemia minor and little if any, treatment is needed. Occasionally, patients may need a blood transfusion, particularly after surgery, following childbirth, or to help manage thalassemia complications.
Moderate to severe thalassemia (Hb less than 5 to 6g/dl):
Frequent blood transfusions: More severe forms of thalassemia often require regular blood transfusions, possibly every few weeks. The goal is to maintain Hb at around 9 to 10 mg/dl to give the patients a sense of well being and also to keep a check on erythropoiesis and suppress extramedullary hematopoiesis. To limit transfusion-related complications, washed, packed red blood cells (RBCs) at approximately 8 to 15 mL cells per kilogram (kg) of body weight over 1 to 2 hours are recommended.
Chelation therapy: Due to chronic transfusions, iron starts to get deposited in various organs of the body. Iron chelators (deferasirox, deferoxamine, deferiprone) are given concomitantly to remove extra iron from the body.
Stem cell transplant: Stem cell transplant, (bone marrow transplant), is a potential option in selected cases, such as children born with severe thalassemia. It can eliminate the need for lifelong blood transfusions.
Gene therapy
Genome editing techniques
Splenectomy
Hypercoagulability
Factor 5 Leiden disorder, Protein C deficiency, Antithrombin-3 deficiency, pregnancy.
G6PD Deficiency
Is an X-linked recessive disorder characterized by enzymatic deficiency of glucose-6-phosphate dehydrogenase. This deficiency leads to RBC breakdown which ultimately limits the patient’s ability to respond to oxidative stress.
Antimalarial medicines such as quinine.
Aspirin (high doses)
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Quinidine.
Sulfa drugs.
Antibiotics such as quinolones, nitrofurantoin.
Cerebral Palsy
Is a non-progressive, motor disorder characterized by spasticity, dyskinesia, and ataxia
Therapies
Drug Treatments
Oral medications such as diazepam, baclofen, dantrolene sodium, and tizanidine are usually used as the first line of treatment to relax stiff, contracted, or overactive muscles.
Botulinum toxin (BT-A), injected locally into muscles, has become a standard treatment for overactive muscles in children with spastic CP.
Intrathecal baclofen therapy uses an implantable pump to deliver baclofen, a muscle relaxant, into the fluid surrounding the spinal cord. Baclofen decreases the excitability of nerve cells in the spinal cord, which then reduces muscle spasticity throughout the body.
Baclofen is an agonist for gamma-aminobutyric acid (GABA)B receptors on pre- and postsynaptic neurons in the central nervous system (CNS) and peripheral nervous system.
Epilepsy
Is a neurologic disorder characterized by abnormal electrical activity causing at least 2 unprovoked seizures more than 24hrs apart
Seizure-transient disturbance of cerebral function due to an abnormal paryoxysmal neuronal discharge in the brain.
Focal Onset, Generalized Onset, Combined general and focal.
Focal- Restricted to one cerebral hemisphere.
Meds:
Brivaracetam-act by binding to the ubiquitous synaptic vesicle glycoprotein 2A (SV2A), like levetiracetam, but with 20-fold greater affinity.
Carbamazepine-binds preferentially to voltage-gated sodium channels in their inactive conformation
Lamotrgine-acts by inhibiting sodium currents by selective binding to the inactive sodium channel, suppressing the release of the excitatory amino acid, glutamate.
Levetiracetam (Keppra)- The exact mechanism through which levetiracetam exerts its anti-epileptic effects is unclear
Phenobarbital-increases the amount of time chloride channels are open, consequently depressing the central nervous system. This action occurs by acting on GABA-A receptor subunits.
Topiramate- an anticonvulsant medication that blocks sodium channels and enhances the activity of gamma-aminobutyric acid (GABA)
Clonazepam (klonopin) long acting benzo
Valproic Acid-Proposed mechanisms include affecting GABA levels, blocking voltage-gated sodium channels, inhibiting histone deacetylases, and increasing LEF1
Cannabidiol-CBD has been shown to act as a negative allosteric modulator of the cannabinoid CB1 receptor,
Spinal Cord Injury
Is an injury of the spine causing sympathetic/parasympathetic dysfunction along with motor and sensory deficits
Amyotrophic Lateral Sclerosis
Is a neurologic disorder characterized by terminal peripheral neurodegeneration leading to a lack of motor function
Syncope
Transient loss of consciousness and postural tone from vasodepressor or cardiogenic causes with prompt recovery without resuscitative measures
Vasovagal- Most frequent normally initiated by pain, stress, or claustrophobia that is characterized by a excessive vagal tone or impaired reflex control of the peripheral circulation
Orthostatic-
Nausea, diaphoresis, tachycardia, pallor
ECG recommended for all patients requiring a syncope work up. May require EP testing.
Midodrine- alpha-agonist that can increase peripheral vasoconstriction
Alzheimer’s
Is a neurologic disorder characterized by progressive loss of cognitive ability due to accumulation of plaques
The cholinesterase inhibitors most commonly prescribed are:
Donepezil (Aricept®):
Rivastigmine (Exelon®):
Galantamine (Razadyne®):
Glutamate regulators
Memantine (Namenda®):
Parkinson’s
Is a neurologic disorder characterized by progressive loss of dopaminergic neurons manifesting with tremors and rigidity
Amantadine- is poorly understood.[19] Amantadine is a weak antagonist of the NMDA-type glutamate receptor, increases dopamine release, and blocks dopamine reuptake
Levodopa- Levodopa converts to dopamine in both the CNS and periphery
Dopamine Agonists (Pramiexole, ropinirole) act directly on dopamine receptors
Selective MAO inhibitors (rasagiline). MAOs=Monoamine oxidase inhibitors (MAOIs) are a class of drugs that work by inhibiting the activity of the enzyme monoamine oxidase (MAO), which is responsible for breaking down neurotransmitters such as serotonin, dopamine, and norepinephrine
COMT-Catecholamine O methyltransferase inhibitors reduce the metabolism of levodopa to 3-O-methyldopa leading to more sustained plasma levels.
Multiple Sclerosis
Is a neurologic disorder characterized by inflammation and demyelination of the central nervous system [with recurrent relapse]
Cerebrovascular Accident
Vascular ischemia or hemorrhage of the brain leading to neurological deficits
TIA
a transient episode of neurologic dysfunction due to the focal brain, spinal cord, or retinal ischemia, without acute infarction or tissue injury
Migraine
Is a neurologic disorder characterized by headaches with or without aura [with photophobia, sonophobia]
Triptans such as almotriptan, eletriptan (Relpax), frovatriptan (Frova), naratriptan (Amerge), rizatriptan (Maxalt, Maxalt-MLT), sumatriptan (Imitrex), zolmitriptan (Zomig)- serotonin 5-HT1B and 5-HT1D receptors in blood vessels (causing their constriction) and nerve endings in the brain, and subsequent inhibition of pro-inflammatory neuropeptide release, including CGRP and substance P.
Ergots such as dihydroergotamine nasal (Migranal, Trudhesa), or ergotamine tartrate (Ergomar)-activating 5-HT 1D receptors located on intracranial blood vessels, leading to vasoconstriction, which correlates with the relief of migraine headache1
Calcitonin gene-related peptide antagonists (gepants) such as oral ubrogepant (Ubrelvy), rimegepant (Nurtec ODT) or intranasal zavegepant (Zavzpret)- small-molecule calcitonin gene-related peptide receptor antagonist
Ditans such as lasmiditan (Reyvow)
TCAntidepressants: amitriptyline (Elavil), or nortriptyline (Aventyl, Pamelor)-function by inhibiting serotonin and norepinephrine reuptake within the presynaptic terminals, resulting in elevated concentrations of these neurotransmitters within the synaptic cleft
CGRP inhibitors used to block the calcitonin gene-related peptide: atogepant (Qulipta), eptinezumab (Vyepti), erenumab (Aimovig), fremanezumab (Ajovy), galcanezumab (Emgality), and rimegepant (Nurtec ODT – helps treat and prevent migraines)
Rheumatoid Arthritis
systemic autoimmune disease characterized by inflammatory arthritis and extra-articular involvement
Cotricosteroids-Blocking the action of inflammatory mediators (transrepression) and inducing anti-inflammatory mediators (transactivation) to mediate anti-inflammatory effects.
Suppressing delayed hypersensitivity reactions by direct action on T-lymphocytes to mediate immunosuppressive effects.
Inhibiting genes responsible for expression of cyclooxygenase-2, inducible nitric oxide synthase, and pro-inflammatory cytokines, including tumor necrosis factor alpha and various interleukins.
Disease-modifying antirheumatic drug- Methotrexate- antimetabolite of the antifolate type. inhibition of enzymes involved in purine metabolism, leading to accumulation of adenosine; inhibition of T cell activation and suppression of intercellular adhesion molecule expression by T cells;
NSAIDs, which can affect the kidney function and increase the risk of toxicity2
Certain antibiotics, which can interfere with the metabolism or clearance of methotrexate
Juvenile Arthritis
Is a disorder characterized by joint inflammation and stiffness for greater than six weeks in children under the age of 16
Systemic Lupus Erythematosus
Is a disorder characterized by chronic inflammation due to autoantibody production responsible for multisystem tissue damage
Antinuclear antibody Lab
Hydroxychloroquine- rashes or joint treatment. alkalinizing lysosomatropic drug that accumulates in lysosomes where it inhibits some important functions by increasing the pH.
Mycophenolate mofetil-The active metabolite of mycophenolate, mycophenolic acid, prevents T-cell and B-cell proliferation and the production of cytotoxic T-cells and antibodies
Cyclophosphamide-Cyclophosphamide is an alkylating agent that is used as chemotherapy and to suppress the immune system
Azathioprine- metabolism are thiouric acid (38%) and various methylated and hydroxylated purines, which are excreted via the urine. Mechanism of action. Azathioprine inhibits purine synthesis. Purines are needed to produce DNA and RNA
Myasthenia Gravis
is an autoimmune disorder affecting the postsynaptic “motor end plate” nicotinic acetylcholine receptor causing weakness and rapid fatigue of skeletal muscles
Anticholinesterase- Neostigmine or pyridostigmine
Scaroidosis
Is a multisystem granulomatous disorder of unknown etiology characterized by non-caseating granulomas
May involve skin, eyes, peripheral nerves, liver, kidney, heart.
Malaise, fever, dyspnea, iritis, lupus pernio.
CXR: Typically bilateral hilar lymphadenopathy.
Biopsy needed
Treatment: Corticosteroids, Immunosuppressive therapy to include methotrexate, azathiprine, infliximab.
Human Immunodeficiency Virus
Is an infection with the HIV retrovirus leading to immunocompromise via CD4 T-helper cells
If a patient is taking ART and has an HIV viral load <200 copies/mL and a CD4 count >200 cells/mm3, the clinician should proceed with the surgical plan as with a patient who does not have HIV
CYP3A4
There is increased potential for drug-drug interactions in patients taking ART due to cytochrome P450 interactions with PIs, NNRTIs, and regimens boosted with ritonavir or cobicistat. Increased levels of fe
