Medicine Flashcards

1
Q

Hypertension

A

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)

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2
Q

Peripheral Artery Disease

A

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

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3
Q

Atherosclerosis

A

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.

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4
Q

Coronary Artery Disease

A

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.

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5
Q

Myocardial Infarction

A

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

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6
Q

Acute Coronary Syndrome

A

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.

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7
Q

Angina

A

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.

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8
Q

Congestive Heart Failure

A

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

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9
Q

Aortic Stenosis

A

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

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10
Q

Endocarditis

A

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.

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11
Q

Atrial Fibrillation

A

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

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12
Q

Transfusion Associated Circulatory Overload

A

a common transfusion reaction in which pulmonary edema develops primarily due to volume excess or circulatory overload

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13
Q

Cor Pulmonale

A

Is right-sided heart failure caused by pulmonary hypertension

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14
Q

Cardiomyopathy

A

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

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15
Q

Asthma

A

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,

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16
Q

COPD

A

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%

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17
Q

Bronchitis

A

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

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18
Q

Emphysema

A

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.

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19
Q

Restrictive Lung Disease

A

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

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20
Q

Sleep Apnea

A

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.

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21
Q

Cystic Fibrosis

A

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

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22
Q

Acute Respiratory Distress Syndrome

A

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.

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23
Q

Pneumonia

A

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

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24
Q

Transfusion-related acute lung injury

A

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.

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25
Q

Negative Pressure Pulmonary Edema

A

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.

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26
Q

Pulmonary Embolism

A

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

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27
Q

Pulmonary Hypertension

A

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

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28
Q

Pneumothorax

A

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.

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29
Q

Tuberculosis

A

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.

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30
Q

Obesity

A

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)

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31
Q

Diabetes

A

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

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32
Q

Grave’s Disease

A

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

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33
Q

Hashimoto’s Thyroiditis

A

Is a chronic lymphocytic thyroiditis resulting in hypothyroidism

Levothyroxine-hyroid hormones exert their physiologic actions through control of DNA transcription and protein synthesis

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34
Q

Cushing’s Disease

A

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.

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35
Q

Addison’s Disease

A

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

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36
Q

Anemia

A

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

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37
Q

Polycythemia vera

A

Is a hematologic disorder characterized by an increase in red blood cells, measured by hematocrit over 55%

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38
Q

Sickle Cell Anemia

A

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

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39
Q

Sickle Cell Crisis

A

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]

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40
Q

Von Willebrand’s Disease

A

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

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41
Q

Hemophilia A

A

Is a coagulopathy due to X-linked genetic deficiency of factor 8

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42
Q

Hemophilia B

A

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)

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43
Q

Disseminated intravascular coagulation

A

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.

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44
Q

Heparin induced thrombocytopenia

A

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

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45
Q

Thalassemia

A

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

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46
Q

Hypercoagulability

A

Factor 5 Leiden disorder, Protein C deficiency, Antithrombin-3 deficiency, pregnancy.

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47
Q

G6PD Deficiency

A

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.

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48
Q

Cerebral Palsy

A

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.

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49
Q

Epilepsy

A

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,

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50
Q

Spinal Cord Injury

A

Is an injury of the spine causing sympathetic/parasympathetic dysfunction along with motor and sensory deficits

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51
Q

Amyotrophic Lateral Sclerosis

A

Is a neurologic disorder characterized by terminal peripheral neurodegeneration leading to a lack of motor function

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52
Q

Syncope

A

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

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53
Q

Alzheimer’s

A

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®):

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54
Q

Parkinson’s

A

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.

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55
Q

Multiple Sclerosis

A

Is a neurologic disorder characterized by inflammation and demyelination of the central nervous system [with recurrent relapse]

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56
Q

Cerebrovascular Accident

A

Vascular ischemia or hemorrhage of the brain leading to neurological deficits

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57
Q

TIA

A

a transient episode of neurologic dysfunction due to the focal brain, spinal cord, or retinal ischemia, without acute infarction or tissue injury

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58
Q

Migraine

A

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)

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59
Q

Rheumatoid Arthritis

A

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

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60
Q

Juvenile Arthritis

A

Is a disorder characterized by joint inflammation and stiffness for greater than six weeks in children under the age of 16

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61
Q

Systemic Lupus Erythematosus

A

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

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62
Q

Myasthenia Gravis

A

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

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63
Q

Scaroidosis

A

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.

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64
Q

Human Immunodeficiency Virus

A

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

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65
Q

Acquired Immunodeficiency Syndrome

A

Is an HIV infection with a CD4 count below 200 or the occurrence of HIV-associated diseases

66
Q

Granulomatosis with polyangiitis (Wegners)

A

Is an autoimmune disorder characterized by the formation of granulomas and inflammation of vessels [most commonly affecting URT, lungs, and kidneys]

67
Q

Type 1 Hypersensitivity

A

Is an IgE mediated anaphylactic response to an antigen due to release of histamine from mast cells and basophils

Anaphylaxis, hay fever, eczema, asthma, food allergies,

68
Q

Type 2 Hypersensitivity

A

Hypersensitivity reaction characterized by IgG or IgM directed complement attack against cell surface antigens

Acute transfusion reaction, good pasteur syndrome, hemalytic disease of newborn

69
Q

Type 3 Hypersensitivity

A

Hypersensitivity reaction characterized by IgG or IgM antigen/antibody complex deposition

Rheumatoid, SLE

70
Q

Type 4 Hypersensitivity

A

Hypersensitivity reaction characterized by a delayed, cell-mediated T-cell attack on allergens

Contact dermatitis, graft rejection, tubercillin reaction

71
Q

Gastroesophageal Reflux

A

Is a gastrointestinal disease characterized by reflux of acidic gastric contents to the esophagus

GERD is caused by multiple different mechanisms that can be intrinsic, structural, or both,

Medical therapy is comprised of antacids antisecretory agents like histamine (H2) receptor antagonists (H2RAs) or PPI therapy and prokinetic agents. Currently, there are two US Food and Drug Administration (FDA) approved H2RAs (famotidine and cimetidine) available in the US and are available over-the-counter. The other commonly used H2RA known as ranitidine has been recalled as a potential health hazard or safety risk due to an unexpected impurity in the active ingredient. The less commonly known prescription-only H2RA nizatidine has also been recalled as well due to similar concerns. In the US, there are six PPIs that are currently available, of which three (omeprazole, lansoprazole, and esomeprazole) are available over-the-counter, and the remaining three (pantoprazole, dexlansoprazole, and rabeprazole) are prescription-only medications.

72
Q

Hepatitis

A

A gastrointestinal disease characterized by inflammation of the liver caused by alcoholism or infection
A Fecal-oral; B - DNA Virus; C - RNA Virus; D - Dependent on B,
MASH – Metabolic dysfunction-associated steatohepatitis (non-EtOH)

Other causes include acetaminophen toxicty either intentional or not. Antiepileptics, antibiotics, or anti TB meds.

Patients with serious liver dieases are at increased risk for perioperative morbidity, and decompensated liver disease is associated with an extremely high perioperative mortality. Patients with suspected or known liver diease should have measurement of liver enzyme levels as well as tests of hepatic synthetic function performed prior to surgery. Elective surgery in patients with acute viral or alcoholic hepatitis should be delayed until resolution. In patients with cirrhosis, postoperative complications correlate with the severity of liver dysfunction. Severity assessed with Child-Pugh score. The Model for End-stage Liver Disease (MELD) score-based on serum bilirubin and creatinine levels, and the prothrombin time expressed as the INR. Less than 10 predicts low risk, greater than 16 indicates high risk. The VOCAL Penn score can also be used. When surgery is elective, controlling ascites, encephalopathy, and coagulopathy preoperatively is prudent.

73
Q

Cirrhosis

A

A component of end stage liver disease characterized by fibrosis of the liver

74
Q

Chron Disease

A

A chronic autoimmune disease with patchy transmural inflammation of the entire GI tract

75
Q

Ulcerative Colitis

A

A chronic autoimmune disease with diffuse and continuous mucosal inflammation of the colon

76
Q

Pseudomembranous Colitis

A

A superinfection of clostridium difficile due to recent antibiotic usage

The recent IDSA/SHEA update suggests fidaxomicin preferentially over vancomycin for initial CDI,3 and new ESCMID guidelines concur with this recommendation, with vancomycin being acceptable for a first episode and metronidazole only if other agents are unavailable.4 The older ASID guidelines still recommend metronidazole for a first episode of non-severe CD

77
Q

Diverticulitis

A

An intestinal disease characterized by inflammatory outpouchings of the colon

78
Q

Marfan Syndrome

A

Is an autosomal dominant connective tissue disorder of fibrillin [which can result in cardiac issues such as aortic dilation and mitral regurgitation]

79
Q

Ehlers Danlos Syndrome (Hypermobile)

A

A connective tissue disorder characterized by elastic skin, hypermobility, bleeding tendency, possible aortic fragility, POTS

80
Q

Duchenne Muscular Dystrophy

A

An X-linked recessive disorder characterized by a mutation in dystrophin leading to progressive loss of skeletal muscle function

81
Q

Papillon Lefevre Syndrome

A

An autosomal recessive disorder characterized by a deficiency in cathepsin C, leading to precocious periodontitis and loss of teeth

82
Q

Guillen Barre Syndrome

A

An autoimmune disorder characterized by rapid-onset muscle weakness caused by an immune mediated attack on the peripheral nervous system.

83
Q

Ectodermal Dysplasia

A

Is a heritable condition characterized by abnormalities in two or more ectodermal structures such as hair and teeth.

84
Q

Tetanus

A

Is a bacterial infection of Clostridium tetani characterized by muscle spasms

85
Q

Depression

A

A psychiatric disorder characterized by loss of interest, guilt, sleep disturbances, energy loss lasting for longer than 2 weeks

Major depression, Persistent depressive disorder (also called dysthymia or dysthymic disorder), Perinatal depression, Seasonal affective disorder, Depression with symptoms of psychosis

Selective serotonin reuptake inhibitors/SSRIs (Citalopram (Celexa), Escitalopram (Lexapro), Fluoxetine (Prozac), Sertraline (Zoloft), Paroxetine (Paxil)- inhibition of serotonin reuptake increases serotonin concentration, which causes a downregulation of 5HT1A receptors

Serotonin–norepinephrine reuptake inhibitor/SNRIs-Venlafaxine (Effexor), Duloxetine (Cymbalta), Milnacipran (Savella)- SNRIs (serotonin and norepinephrine reuptake inhibitors. Inhibition of presynaptic neuronal uptake of 5-HT (serotonin) and norepinephrine following release from the synaptic cleft

Tricyclic Antidepressants/TCAs- Amiltriptyline (Elavil), Nortriptyline (Aventyl) Amoxapine, Desipramine, Doxepin,exert their effects by modulating around 5 distinct neurotransmitter pathways. These medications function by inhibiting serotonin and norepinephrine reuptake within the presynaptic terminals, resulting in elevated concentrations of these neurotransmitters within the synaptic cleft. The increased levels of norepinephrine and serotonin in the synapse can contribute to the antidepressant effect. In addition, the neurotransmitters act as competitive antagonists on postsynaptic cholinergic (alpha-1 and alpha-2), muscarinic, and histamine receptors (H1)

Monoamine oxidase inhibitor/MAO inhibitors- Phenelzine (Nardil), Selegiline (Emsam), Tranlcypromine-Monoamine oxidase inhibitors (MAOIs) work by inhibiting the activity of monoamine oxidase, an enzyme involved in removing the neurotransmitters norepinephrine, serotonin and dopamine from the brain

Trazodone (Desyrel)-s a serotonin and histamine antagonist that inhibits reuptake and subsensitizes adrenoreceptors

Bupropion (Wellbutrin)-The mechanism of action of bupropion in the treatment of depression and for other indications is unclear. However, it is thought to be related to the fact that bupropion is a norepinephrine–dopamine reuptake inhibitor (NDRI) and antagonist of several nicotinic acetylcholine receptors.

Mirtazapine (remeron)-is in a group of tetracyclic antidepressants (TeCA). Mirtazapine inhibits the central presynaptic alpha-2-adrenergic receptors, which causes an increased release of serotonin and norepinephrine.

Of particular importance is the potential for local anaesthetic solutions containing epinephrine to cause hypertensive crises in patients receiving TCAs and MAOIs. Meperidine can precipitate a serotonergic crisis in patients taking MAOI as it too interrupts presynaptic uptake of serotonin. It should therefore be avoided in patients known to be on an MAOI. The most important anaesthetic consideration for patients taking MAOIs relate to the profound pressor effect that may be seen after administration of both indirectly and directly acting sympathomimetics. There are a number of interactions with implications for the anaesthetist. Probably, the most important is the risk of precipitating a serotonin syndrome when tramadol or meperidine is given in conjunction with an SSRI. The serotonin syndrome features hyper-reflexia, agitation, and hyperthermia. SSRIs (particularly fluoxetine) may interfere with the metabolism of codeine to morphine by inhibiting CYP2D6. This means that patients given codeine may not receive adequate analgesia.1 There is an increased risk of bleeding in patients taking non-steroidal anti-inflammatory drugs (NSAIDs) or warfarin with an SSRI due to their interference with platelet function.
n addition to the desired therapeutic effects, TCAs may cause sedation and reduce the seizure threshold. Anti-cholinergic side-effects may be problematic for the patient and may also be potentiated by the administration of other anti-cholinergic agents. The cardiovascular side-effects may be significant, particularly in overdose. These include widening of the QRS complexes and QT prolongation. Concerns regarding arrhythmias precipitated by halothane in patients on TCAs are probably less of a problem now that other inhalation agents are used more commonly. Postural hypotension may be significant in the elderly population and is due to α-receptor block. The combination of TCAs and tramadol can result in seizures and precipitate a serotonergic crisis.
One of the most significant interactions for the anaesthetist to be aware of is the potentiation of the effect of indirectly acting sympathomimetics (e.g. ephedrine and metaraminol) by TCAs. These should be avoided if possible and directly acting sympathomimetics used cautiously to prevent hypertensive crises.
Abrupt withdrawal of TCAs should be avoided because of the risk of mainly cholinergic symptoms

86
Q

Bipolar

A

A psychiatric spectrum disorder characterized by alternating episodes of mania and depression

Valproic Acid (for manic events)-inhibition of glycogen synthase kinase and activation of extracellular signal-regulated kinase

Lithium- unknown mechanism

First-generation antipsychotics are dopamine receptor antagonists (DRA) and are known as typical antipsychotics. They include phenothiazines (trifluoperazine, perphenazine, prochlorperazine, acetophenazine, triflupromazine, mesoridazine), butyrophenones (haloperidol), thioxanthenes (thiothixene, chlorprothixene), dibenzoxazepines (loxapine), dihydroindoles (molindone), and diphenylbutylpiperidines (pimozide).[1][2][3]

Second-generation antipsychotics are serotonin-dopamine antagonists and are also known as atypical antipsychotics. The Food and Drug Administration (FDA) has approved 12 atypical antipsychotics as of the year 2016. They are risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole, paliperidone, asenapine, lurasidone, iloperidone, cariprazine, brexpiprazole, and clozapine.[4]

Neuroleptic malignant syndrome (NMS) is a life-threatening emergency associated with the use of antipsychotic agents. Both typical and atypical APDs have been implicated, though it is more commonly seen with formerly called neuroleptic agents such as haloperidol and fluphenazine. The most important risk factor is a prior history of NMS. NMS is characterized by the presence of mental status changes, rigidity, fever, and dysautonomia.

Non-steroidal anti-inflammatory drugs can increase lithium levels on average by 10–25% [44]. Further, stimulation of urine production with thiazide diuretics should be avoided as it can reduce renal clearance of lithium [44].

Perioperatively, an electrocardiogram should be closely monitored as sinus node dysfunction, atrioventricular block, T-wave changes, hypotension, and ventricular irritability can occur with toxicity. In addition, train-of-four neuromonitoring is important, as lithium can prolong neuromuscular blockade [43]. Due to lithium-blocking brainstem release of norepinephrine, epinephrine, and dopamine, there is a reduction of MAC requirements

87
Q

Schizophrenia

A

A psychiatric disorder characterized by psychosis and hallucinations

Antipsychotics

88
Q

Obsessive Compulsive Disorder

A

A psychiatric disorder characterized by repeated unwanted, uncontrollable thoughts or actions

89
Q

Anxiety Disorder

A

A psychiatric disorder characterized by inappropriate reaction to innocuous stimulus impeding daily function

Antidepressants, SSRIs and SNRIs in particular, are considered first-line therapies for GAD and PD

Benzodiazepines are not more effective than antidepressants for treating anxiety disorders and should not be used as first-line therapy.13,37

Generalized Anxiety Disorder. SSRIs and SNRIs are the mainstay of pharmacotherapy for GAD.12 A recent meta-analysis found that escitalopram (Lexapro), duloxetine (Cymbalta), venlafaxine, and pregabalin (Lyrica) appear to be most effective and well tolerated

Pregabalin (Lyrica) -Pregabalin is structurally similar to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). However, pregabalin does not directly bind to GABA-A or GABA-B receptors

90
Q

Anorexia

A

A psychiatric disorder characterized by body dysmorphia leading to abstaining from adequate caloric intake

91
Q

Bulimia

A

A psychiatric disorder characterized by bingeing, purging that affects nutritional status

92
Q

ADHD

A

A behavioral disorder characterized by inattention, impulsivity, and hyperactivity

Amphetamine, the active ingredient of Adderall, works primarily by increasing the activity of the neurotransmitters dopamine and norepinephrine

methylphenidate- act as a norepinephrine and dopamine reuptake inhibitor (NDRI)

lisdexamfetamine
dexamfetamine - Once administered, lisdexamfetamine is converted to its active metabolite, dextroamphetamine, which is taken up by the brain. Dextroamphetamine blocks the reuptake of norepinephrine and dopamine into the presynaptic neuron and increases the release of these monoamines into the extraneuronal space.

atomoxetine-selective inhibition of presynaptic norepinephrine reuptake in the prefrontal cortex

93
Q

Autism

A

A behavioral disorder characterized by spectrum of symptoms affecting social interaction

Kanner’s Syndrome. …
Asperger’s Syndrome. …
Rett Syndrome. …
Childhood Disintegrative Disorder (CDD) …
Pervasive Development Disorder Not Otherwise Specified (PDD-NOS)

94
Q

Delirium tremens

A

Are late-manifesting, severe alcohol withdrawal symptoms such as shaking, confusion, and hallucinations

patients with chronic heavy alcohol use, because of neuro-adaptation, there is a down regulation of Gamma-Amino Butyric Acid (GABA) and up-regulation of the glutamate (NMDA receptor) neurotransmission

Clinical Institute Withdrawal Assessment for Alcohol (CIWA-A) scale, particularly the 10 item revised version, known as CIWA-Ar

First line- Benzodiazapam

Alternatives:
Haloperidol, a first-generation typical antipsychotic, is commonly used worldwide to block dopamine D2 receptors in the brain and exert its antipsychotic action.
Phenobarbital-acts on GABAA receptors, increasing synaptic inhibition.

95
Q

Gestational Diabetes

A

a condition in which a woman develops high blood sugar levels during pregnancy

ACOG and ADA recommend the following target levels to reduce risk of macrosomia
Fasting or preprandial blood glucose values < 95 mg/dL
Postprandial blood glucose values < 140 mg/dL at 1 hour and < 120 mg/dL at 2 hours

Treatment: Insulin

96
Q

Gestational Hypertension

A

a condition in which a woman develops high blood pressure levels during pregnancy

Threshold 140/90 for treatment

Methyldopa first line. Labetalol or nifedipine.

No ACE or ARBS in any trimester

97
Q

Preeclampsia

A

A condition that affects pregnant women characterized by new onset hypertension and proteinuria

Blood pressure of greater than 140 sys or 90 dia after 20 weeks gestation.

Proteinuria of greater than 0.3g in 24hrs

Can have variation of severe features with bp 160/110, kidney injury, vision changes.

98
Q

Eclampsia

A

A condition that affects pregnant women characterized by new onset hypertension, proteinuria, as well as seizures

IV magnesium sulfate for seizures
Labetalol, Nifedipine, Hydralazine for HTN
Delivery

99
Q

HELLP

A

Is a complication of pregnancy associated with preeclampsia characterized by hemolysis, elevated liver enzymes, low platelets

high morbidity, immediate delivery if unstable

100
Q

Fibromyalgia

A

condition defined by the presence of chronic widespread pain, fatigue, waking unrefreshed, cognitive symptoms, lower abdominal pain or cramps, and depression

101
Q

Leukemia

A

Is a cancer of white blood cell lineage in bone marrow

102
Q

Lymphoma

A

Is a cancer of white blood cell lineage in the lymphatic system or elsewhere outside bone marrow

103
Q

Multiple myeloma

A

A plasma cell malignancy characterized by production of monoclonal immunoglobulin

In bone marrow, leads to bony destruction (lesions, fractures), hypercalcemia

Protein electrophoresis detects monoclonal protein

Serum and urine M protein

Bence Jones proteins, urine test, detects light chains, Kappa and lambda)

104
Q

Chronic Kidney Disease

A

Permanent renal insufficiency that develops over month to years resulting in damage to the renal system and decreased function

CKD Pt management
Consult nephrologist to optimize, control co-morbities and normalize as best as possible

Dialysis: undergo day before surgery, if they have shunt, stay away from that arm

Increased bleeding risk to due uremic bleeding and PLT dysfunction
Local hemostatic measures in surg
Renal dosing adjustments
Propofol unaffected, benzo metabolites prolonged, small to moderate doses of fentanyl are safe, lidocaine is safe, careful with fluids
Theoretically compound A with Sevo
If needed, Atracurium and Cis-atracurium are better (Hoffman degradation)

  1. GFR> 90 Slight damage with normal or increased filtration
  2. Mild decrease in FNC 60-89
  3. Moderate decrease in FNC 30-59
  4. Sever decrease in FNC 15-29
  5. Kidney failure/ESRD <15
105
Q

End Stage Renal Disease

A

Chronic kidney disease that has progressed to a GFR less than 15

Desflurane and isoflurane are metabolised to a minimal extent and there are no concerns regarding their use in CKD.

Neuromuscular blocking agents Atracurium is the neuromuscular blocking agent (NMBA) of choice in patients with CKD. Its metabolism is unique. Atracurium undergoes ester hydrolysis and Hofmann degradation, both of which are independent of renal function. Cisatracurium can also be used in patients with CKD. It is predominantly eliminated by Hofmann degradation. Its clearance is reduced by 13% in CKD, and its terminal elimination half-life is increased by 4.2 min. Up to a third of rocuronium is excreted renally in a 24-h period. Its clearance is reduced by 39% in CKD therefore prolonging time to recovery. The effects of rocuronium become less predictable in renal failure. Pancuronium has reduced clearance and a prolonged half-life in those with CKD and so is best avoided.

Suxamethonium should be avoided because of the risk of exacerbating pre-existing hyperkalaemia.

Sugammadex has been used successfully in clinical research to reverse blockade from aminosteroid NMBAs in patients with severe renal impairment. The sugammadex–rocuronium complex can persist in vivo for up to 7 days. The rocuronium–sugammadex complex is very stable and can be cleared by high-flow dialysis.25

Opioid analgesics Opioids have no direct nephrotoxic effects. They do have an antidiuretic effect, which may manifest clinically as urinary retention.
The metabolite responsible for the potent analgesic, sedative and respiratory depressant effects of morphine is morphine-6-glucuronide. Its elimination is dependent on renal function, and its half-life is prolonged from 2 to 27 h in patients with CKD. Therefore, an appropriate dose reduction should be considered. Remifentanil is not dependent on renal function for its elimination. Both oxycodone and its metabolites accumulate in patients with CKD with a related prolongation in elimination half-life of 2.3–3.9 h. This may necessitate a dose reduction and an increase in dose interval. Tramadol is 30% excreted unchanged in the urine. It may be epileptogenic in the context of uraemia because of the lowered seizure threshold. The elimination half-lives of codeine and dihydrocodeine are significantly prolonged, and these drugs should therefore be used with caution.

Coagulation abnormalities must be borne in mind and might pose a contraindication to spinal or epidural anaesthesia.

Irrespective of the technique and drugs used, it is essential to maintain normovolaemia and renal perfusion pressure. Blood pressure targets should be individualised for the patient using preoperative baseline readings as an estimate.

Careful fluid balance extends to the postoperative period. Patients may require dialysis. Patients with CKD are vulnerable to the sedative effects of opioids amongst other drugs and can take longer to emerge from anaesthesia with more prolonged residual drowsiness. They may therefore require an extended period of supplemental oxygen therapy and continuous oxygen saturation monitoring.

106
Q

Secondary hyperparathyroidism

A

Hyperparathyroidism caused by disease outside parathyroid gland, most often CKD and failure to convert Vitamin D to its active form

Management of SHPT targets abnormal phosphocalcic metabolism. Maintaining the serum calcium and phosphorus levels within the normal range along with control of PTH and vitamin D levels is the key in management of secondary hyperparathyroidism.

Primary hyperparathyroidism is the most frequent cause of hypercalcemia in ambulatory patients. The condition is most common in postmenopausal women, although it can occur in persons of all ages, including pregnant women. If symptoms are present, they are attributable to hypercalcemia and may include weakness, easy fatigability, anorexia, or anxiety. However, most persons have no symptoms, and primary hyperparathyroidism usually is diagnosed after an elevated serum calcium level is found incidentally on multiphasic chemistry panel testing. Persistent hypercalcemia and an elevated serum parathyroid hormone level are the diagnostic criteria for primary hyperparathyroidism. Other causes of hypercalcemia are rare, and usually are associated with low (or sometimes normal) parathyroid hormone levels. Malignancy is the most frequent cause of hypercalcemia in hospitalized patients. Parathyroidectomy is the definitive treatment for primary hyperparathyroidism.

107
Q

Goldenhar (Oculo-auriculo-vertebral spectrum) disorder

A

Goldenhar syndrome (GS), also known as oculoauriculovertebral dysplasia or hemifacial microsomia has a wide range of clinical manifestations, including craniofacial, vertebral , cardiac, renal, and central nervous system anomalies1. The typical presentation of GS includes epibulbar dermoids, microtia, mandibular hypoplasia, and vertebral anomalies8,10-11. The classic facial aspect of GS patients, described as hemifacial microsomia, and the other anomalies of this syndrome are probably caused by development defects of the first and second brachial archs12. The causes for these developmental defects seem to be heterogeneous2.

GS is a condition with a prevalence ranging from 1:3,500 to 1:7,000 live births, and a male-female ratio of 3:24. Although most cases are sporadic, familial occurrences have been observed8. Oral manifestations of GS are clearly heterogeneous, and range from malocclusion to a more complex phenotype with complete absence of the mandibular ramus and temporomandibular joint (TMJ)3,13. Different forms of cleft lip and palate and decreased palatal width are frequently found in GS patients4.

108
Q

Hemifacial Mircosomia

A

Hemifacial microsomia (HFM), also known as unilateral otomandibular dysostosis or lateral facial dysplasia, is an asymmetrical, congenital malformation of the 1st and 2nd branchial arches and the second most common craniofacial anomaly after cleft lip and palate.[1] Patients present with unilateral hypoplasia of the ear, facial skeleton (maxilla, mandibular, zygoma, and temporal bones), and surrounding soft tissue.[2][3] HFM and Goldenhar syndrome are considered variants under the same clinical continuum of disorders termed the oculoauriculovertebral spectrum (OAVS), with Goldenhar syndrome encompassing HFM phenotypes along with epibulbar dermoid and vertebral anomalies.[1][4]

109
Q

Treacher Collins

A

Treacher Collins syndrome is a severe congenital disorder of craniofacial development characterized by numerous developmental anomalies that are restricted to the head and neck (Figure 2). Hypoplasia of the facial bones, particularly the mandible (78% of cases) and zygomatic complex (81%), is an extremely common feature of TCS. Hypoplasia of the facial bones may result in dental malocclusion, with anterior open bite a common finding. The teeth may be widely spaced, malpositioned or reduced in number. In a large proportion of cases, the palate is high, arched and occasionally cleft (28%) and in severe cases, the zygomatic arches may be completely absent (Poswillo, 1975). Ophthalmic abnormalities include downward slanting of the palpebral fissures (89%) with notching of the lower eyelids (69%) and a paucity of lid lashes medial to the defect (69%) (Figure 2). Other clinical features of TCS include alterations in the shape, size and position of the external ears, which are frequently associated with atresia of the external auditory canals and anomalies of the middle ear ossicles. Radiographic analysis of the middle ears of TCS patients has revealed irregular or absent auditory ossicles with fusion between rudiments of the malleus and incus, partial absence of the stapes and oval window, or even complete absence of the middle ear and epitympanic space.10 Consequently, bilateral conductive hearing loss is common in TCS patients, whereas mixed or sensorineural hearing loss is rare.

110
Q

Cleidocranial dysplasia

A

Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia that represents a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities), to mild CCD, to isolated dental anomalies without other skeletal features. Individuals with classic CCD spectrum disorder typically have abnormally large, wide-open fontanelles at birth that may remain open throughout life. Clavicular hypoplasia can result in narrow, sloping shoulders that can be opposed at the midline. Moderate short stature may be observed, with most affected individuals being shorter than their unaffected sibs. Dental anomalies may include delayed eruption of secondary dentition, failure to shed the primary teeth, and supernumerary teeth. Individuals with CCD spectrum disorder are at increased risk of developing recurrent sinus infections, recurrent ear infections leading to conductive hearing loss, and upper airway obstruction. Intelligence is typically normal.

111
Q

Gardner

A

is an autosomal dominant disease characterized by the presence of familial adenomatous polyposis (FAP) as well as extraintestinal manifestations such as osteomas, dental anomalies, epidermoid cysts and ocular abnormalities.

112
Q

Nevoid Basal Cell Carcinoma Syndrome (Gorlin)

A

is an infrequent multisystemic disease that is inherited in a autosomal dominant way, which shows the high level of penetrance and variable expressiveness.[1–3] NBCCS characterized mainly by the presence of multiple odontogenic keratocysts (75%), basal cell carcinoma (50-97%), bifid ribs (40%), palmar and planter pits (60-90%) and ectopic calcification of the falx cerebri (37-79%)

113
Q

Pierre Robin

A

classically described as a triad of micrognathia, glossoptosis, and airway obstruction. Infants frequently present at birth with a hypoplastic mandible and difficulty breathing. The smaller mandible displaces the tongue posteriorly, resulting in obstruction of the airway. Typically, a wide U-shaped cleft palate is also associated with this phenomenon.

114
Q

Crouzon

A

is a genetically inherited syndrome characterized by craniosynostosis (premature fusion of coronal sutures) resulting in the skull and facial deformities. The syndrome was first described in 1912 by French physician Octave Crouzon when he identified both a mother and daughter with what was originally called “craniofacial dysostosis.” He described a triad of skull deformities, facial anomalies, and proptosis.

115
Q

Noonan

A

disorder characterized by postnatally reduced growth, distinctive facial dysmorphic features, congenital heart defects (CHD), hypertrophic cardiomyopathy (HCM), skeletal anomalies, and webbing of the neck. Other relatively common features are bleeding diathesis, ectodermal anomalies, lymphatic dysplasias, cryptorchidism, and cognitive deficits

Noonan syndrome is associated with increased ERK-activity induced by RAS activation and, therefore, RANKL up-regulation may lead to development of multiple central giant cell lesions

116
Q

Strickler Syndrome

A

Stickler syndrome is a connective tissue disorder that can include ocular findings of myopia, cataract, and retinal detachment; hearing loss that is both conductive and sensorineural; midfacial underdevelopment and cleft palate (either alone or as part of the Pierre Robin sequence); and early-onset degenerative joint disease.

Medialization of the internal carotid artery

117
Q

Trisomy 21

A

a developmental disorder characterized by distinct physical characteristics manifesting in facial, cardiac, and skeletal features.

Physical traits – include upslanting palpebral fissures, flat nasal bridge and midface, decreased muscle tone (hypotonia), wider space between first and second toe (“sandal gap”), nystagmus, brachycephaly, incurving of the fifth finger (clinodactyly), narrow palate, overfolded helix of the ear (especially with a small ear), short-appearing neck with redundant skin on the back of the neck, broad and short hands and feet, and single transverse crease in the palm of the hand.

Airway management can be difficult as a result of macroglossia, macrognathia, and a narrow hypopharynx. Macroglossia and pharyngeal muscle hypotonia tend to cause upper airway obstruction. The nares and the trachea may be smaller than in normal children. There is also an increased incidence of subglottic stenosis. Disordered breathing during sleep, including upper airway obstruction and obstructive sleep apnea, is seen in 30%-60% of children with Down syndrome. These patients are at risk for congenital cardiac disease (mostly endocardial cushion defects, but also mitral valve abnormalities recognized at a later age). Pulmonary hypertension can result from cardiac disease or chronic obstructive sleep apnea. Patients with Down syndrome have an increased incidence of duodenal atresia, Hirschsprung’s disease, hypothyroidism, and leukemia. They are also at increased risk for atlantoaxial instability. The American Academy of Pediatrics recommends getting an anteroposterior/lateral x-ray of the neck once between the ages of 3 and 5 years old. One should inquire about it, but it is not required prior to the patient’s receiving general anesthesia. It is not a perfect screening tool, and we should always consider these patients at risk and use precautions when manipulating their cervical spines. To screen for pain or abnormal movement in an uncooperative patient, you can use keys, a light, a toy, or something else interesting that they will want to follow with their eyes and move it around them. Also, parents may describe regression in certain milestones, even regression in toilet training, or less tolerance for walking. These kinds of symptoms should prompt a neurologic evaluation. Ensure that you have a recent cardiovascular evaluation, and evaluate for any residual defects or pulmonary hypertension.

Remember that the degree of intellectual impairment varies widely in patients with trisomy 21.

ANESTHETIC MANAGEMENT
Expect obstruction or difficult mask ventilation because of a small mouth, large tongue, and large tonsils, but intubation is generally easy.

Consider moderate continuous positive airway pressure with jaw thrust during mask induction to prevent pharyngeal airway collapse.

Avoid manipulating the cervical spine during direct laryngoscopy.

These patients can present with profound bradycardia upon induction with sevoflurane, presumably because of a predominant parasympathetic response or abnormal sympathetic response.

118
Q

Serotonin Syndrome

A

Is a group of symptoms that may occur with use of serotonergic medications, usually presenting with high blood pressure and tachycardia without fever

Serotonin syndrome

Precipitated by serotonergic drugs -

Classic triad: AMS, autonomic hyperactivity, and neuromuscular abnormalities.
-Mild: hypertension, ↑HR, diaphoresis, tremor, myoclonus, mydriasis, hyperreflexia.
-Moderate: mild features plus hyperthermia, hyperactive bowel sounds, agitation, and hypervigilance.
-Severe cases: above features plus worsening hyperthermia, muscle rigidity, and delirium

-Discontinuation of serotonergic drugs.
-Mild: benzodiazepines, IV fluids
-Moderate: telemetry, serotonin antagonist (cyproheptadine).
-Severe cases: ICU admission with sedation, paralysis, and intubation.

119
Q

Neuroleptic Malignant Syndrome

A

Is a late-presenting, life-threatening reaction that can occur in response to antipsychotic (neuroleptic) medications characterized by high fever, confusion, “lead pipe” muscle rigidity

Neuroleptic Malignant Syndrome Anti-dopaminergic drugs (e.g., antipsychotics, metoclopramide)
Abrupt cessation of dopaminergic drugs (Levodopa)

-Muscle rigidity, hyperthermia, ↑CK, myoglobinuria, ↑HR, diaphoresis, ↑secretions, tremor, AMS, urinary incontinence.
-chorea, akinesia, opisthotonos, trismus, blepharospasm, and oculogyric crisis -

Tx:
Discontinue offending agent (or restarting drug if dopaminergic drug withdrawal)
-Aggressive hydration if ↑CK
-If severe, bromocriptine or dantrolene.
-Cool patient

120
Q

Thyroid Storm

A
121
Q

Myxedema Coma

A

Is a decompensated form of hypothyroidism, usually first manifesting as altered mental status and low body temperature

Patients most commonly present for emergency services with altered mental status and hypothermia, below 35.5°C (95.9° F). The lower the body temperature, the worst is the prognosis.[45] The absence of mild diastolic hypertension in severely hypothyroid patients is a warning sign of impending myxedema coma

Prompt initiation of thyroid hormone therapy is of paramount importance when myxedema coma is highly suspected, even before having thyroid hormone results back (even though results usually come back quickly in most clinical institutions).[59] A delay could increase the mortality and morbidity of the patient.[60] Hydrocortisone is recommended to be administered prior to thyroid hormone therapy, especially if the patient is hypotensive to avoid adrenal crises; suggestions are that levothyroxine will increase cortisol metabolism, and hypothyroidism may mask an underlying adrenal insufficiency. Treat hypothermia and respiratory failure with ventilation

122
Q

Methemoglobinemia

A

Is a condition of elevated methemoglobin in the blood that can precipitate seizures and heart arrhythmias

The main findings are cyanosis, pallor, fatigue, weakness, headache, central nervous system depression, metabolic acidosis, seizures, dysrhythmias, coma, and death.

When treatment with methylene blue is ineffective or not recommended, additional options may include ascorbic acid, exchange transfusion, hyperbaric oxygen therapy.[18][19] High-dose ascorbic acid (vitamin C), up to 10 g/dose intravenously, can be considered to treat methemoglobin

123
Q

Adrenal Crisis

A

Is a life-threatening complication of adrenal insufficiency most commonly manifesting hypovolemic shock

The most prevalent clinical manifestations of adrenal crises include weakness, severe fatigue, unintentional weight loss, nausea, vomiting, abdominal pain, reduced appetite, back or limb pain, dizziness, somnolence, confusion, and loss of consciousness

ACTH: High ACTH levels with low cortisol and aldosterone indicate primary adrenal insufficiency, whereas low ACTH levels with low cortisol suggest secondary or tertiary adrenal insufficiency.

The recommended treatment regimen includes administering an initial dose of 100 mg of hydrocortisone through intravenous or intramuscular (IV/IM) bolus injection. This is followed by administering an additional 200 mg of hydrocortisone as IM or IV over the next 24 hours, with a dosage of 50 mg every 6 hours or as a continuous infusion.[5]

The suggested treatment approach for hypoglycemia is administering either 1 L of normal saline or 5% dextrose in 1 L of normal saline, followed by maintenance fluids.

124
Q

Status Epilepticus

A

Is a neurologic condition characterized by a single seizure lasting more than five minutes, or two or more seizures within the same five-minute period without a return to normal.

Initial management is airway maintenance and 50% dextrose if hypoglycemia is responsible. 10mg midazolam IM. Fosphenytoin and phenobarbital administraction

125
Q

Status Asthmaticus

A

extreme form of asthma exacerbation that is poorly responsive to standard therapeutic measures characterized by hypoxemia, hypercarbia, and secondary respiratory failure.

126
Q

Myasthenia Crisis

A

Is a complication of myasthenia gravis that can lead to respiratory failure

Myasthenic crisis is a life-threatening exacerbation of myasthenia gravis that is defined as worsening of myasthenic weakness requiring intubation or noninvasive ventilation [1]. While the respiratory failure is due to weakness of respiratory muscles, severe bulbar (oropharyngeal) muscle weakness often accompanies the respiratory muscle weakness, or may be the predominant feature in some patients. When this results in upper airway obstruction or severe dysphagia with aspiration, intubation and mechanical ventilation are necessary.

Symptomatic acute treatment:

◦ pyridostigmine (Mestinon®) p.o. 3-6x60mg, max. 540 mg/d or
◦ pyridostigmine iv. (equivalent: orally:parenterally ~ 30:1)

▪ 360 mg/d p.o. equals to 12 mg/d i.v., max. 24 mg/d
▪ bolus 1–3 mg followed by 0.5–1 mg/h

◦ alternatively:

▪ neostigmine iv. (equivalent:: orally:parenterally = ~ 80:1)

▪ 360 mg/d Pyridostigmine p.o. = 4.5 mg/d neostigmine i.v.
▪ starting dose 6–12 mg/24 h, adjust 0.2–0.8 mg/h, bolus of 0.5 mg possible

◦ atropine 0.5–1 mg s. c. oder iv. against side effects (bronchial secretion)

◦ consider “drug-holiday” when intubated and not breathing spontaneously

Effects of causal acute therapy can be observed after a few days usually (see Table 4). Indication for each regime depends on whether there is a crisis or an exacerbation and on complications.

◦ plasma exchange (PLEX) or immunoadsorption (IA)
▪ first-line therapy of crisis

127
Q

Chlolinergic Crisis

A

Is an overstimulation at the level of the neuromuscular junction due to an excess of acetylcholine, which can lead to flaccid paralysis

Cholinergic crisis

Excessive use of AChEI (pyridostigmine, neostigmine), organophosphate poisoning

-Muscarinic receptor stimulation: salivation, ↓HR, lacrimation, urinary frequency/urgency, diarrhea, GI cramping, emesis, and miosis.
-Cholinergic receptor stimulation: muscle fasciculations, weakness, respiratory muscle weakness, ↑HR, ↑BP.
-CNS stimulation: seizures, coma, ataxia, slurred speech, agitation.

-Discontinue offending agent.
-Secure airway if GCS < 8, excess secretions, respiratory muscle weakness
-Atropine to reverse muscarinic effects.
-Pralidoxime if organophosphate poisoning

128
Q

Alcohol Withdrawal Syndrome

A

Is a set of symptoms that follow cessation or reduction in alcohol use after a period of excessive use

The revised Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) scale is a validated 10-item assessment tool that can be used to quantify the severity of alcohol withdrawal syndrome,

Chlordiazepoxide (Librium), 50 to 100 mg
Diazepam (Valium), 10 to 20 mg
Lorazepam (Ativan), 2 to 4 mg

129
Q

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

A

Is a condition characterized by an inappropriate release of antidiuretic hormone

from the pituitary gland or nonpituitary sources or its continued action on vasopressin receptors

The choice of treatment depends essentially upon the severity of symptoms at presentation. A mild but rapid fall in sodium levels can cause severe symptoms like delirium, confusion, and seizures, while chronic but significant hyponatremia (less than 125 mEq/L) may produce mild or no symptoms. So, in patients with mild to moderate symptoms, the mainstay of the treatment is the restriction of oral water intake with the goal of less than 800 mL/day. If hyponatremia is persistent, sodium chloride in the form of oral salt tablets or intravenous saline can be given. Loop diuretics such as furosemide (20 mg twice daily) can also be added to salt tablets as it helps decrease the urine concentration and thereby increase water excretion, particularly among the patients whose urine osmolality is much higher than serum osmolality (greater than 500 mOsm/kg)

130
Q

Diabetes Insipidus

A

Is a condition related to vasopressin characterized by polydipsia and polyuria that can be either central, nephrogenic, dipsogenic, or gestational

Diabetes insipidus is a rare but treatable chronic condition caused by the lack of the posterior pituitary hormone vasopressin (AVP, also known as anti-diuretic hormone) resulting in uncontrolled diuresis. It is treated with desmopressin (DDAVP, a synthetic AVP analogue) which reduces diuresis.

Treating patients with diabetes insipidus
Diabetes insipidus is treated with demopressin/DDAVP in the following doses:

oral or sublingual - 100-200µg (0.1-0.2mg)
intranasal spray - 10=20µg
IM or IV injection - 1-2µg
Please note, in patients with decompensated diabetes insipidus fluid replacement should be the primary treatment with the aim of reducing hypernatraemia and 1-2ug IV or IM DDAVP administered with close attention paid to the clinical and biochemical response to prevent over-rapid overcorrection of hypernatraemia

131
Q

POTS- Postural Orthostatic Tachycardia Syndrome

A

Is a condition of orthostatic intolerance that causes increased heart rate and other symptoms

132
Q

Sepsis

A

The 2016 recommendations define sepsis as life-threatening organ dysfunction due to a dysregulated host response to infection. Septic shock is defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities substantially increase mortality. To facilitate sepsis diagnosis, the task force identified clinical criteria that physicians can use in their offices, emergency departments, and hospital wards to quickly evaluate patients for sepsis. The quick SOFA (qSOFA) consists of these three simple tests that clinicians can conduct at the bedside to identify patients at risk for sepsis: Alteration in mental status, Decrease in systolic blood pressure to less than 100 mm Hg,Respiratory rate greater than 22 breaths/min. If a patient has at least two positive components of the qSOFA, the patient should be examined for organ failure. Septic shock differs from sepsis in that the complications are more severe and the risk of patient death is greater. The task force identified two new clinical criteria that clinicians should use in diagnosing patients with septic shock: 1 Persisting hypotension requiring vasopressors to maintain mean arterial pressure at or above 65 mm Hg and 2. Blood lactate level greater than 2 mmol/L despite adequate volume resuscitation

133
Q

Sudden Cardiac Death

A

Unexpected nontraumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms

Most common causative rhythm is ventricular fibrillation. 70% attributable to underlying CHD. In young patients causes (long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, Brugada syndrome, HCM, arrhythmogenic RV cardiomyopathy, dilated cardiomyopathy)

134
Q

Hypertensive Emergency

A

Hypertensive emergencies are defined as severe elevations in BP (>180/120 mm Hg) associated with evidence of new or worsening target organ damage

For adults without a compelling condition, SBP should be reduced by no more than 25% within the first hour; then, if stable, to 160/100 mm Hg within the next 2 to 6 hours; and then cautiously to normal during the following 24 to 48 hours.

135
Q

Pickwickian Syndrome

A

Obesity-hypoventilation syndrome, awake alveolar hypoventilation appears to result from a combination of blunted ventilatory drive and increased mechanical load.

136
Q

Covid

A

is a highly contagious infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

137
Q

Hyperlipidemia

A

encompasses various genetic and acquired disorders that describe elevated lipid levels within the body

Lipids typically include cholesterol levels, lipoproteins, chylomicrons, VLDL, LDL, apolipoproteins, and HDL.

Patients with a high risk of ASCVD (>7.5% 10-year risk) should receive statin therapy for primary prevention:

Statin therapy should be initiated for secondary prevention in patients with known ASCVD, absent any contraindication:

Tx: Statins (Hydroxymethylglutaryl-Coenzyme A Reductase Inhibitor- inhibit the rate-limiting enzyme in the formation of cholesterol. High intensity: Atorvastatin, rouvastatin. Moderate: Simvastatin, pravastation.

138
Q

Hyperchloesterolemia

A

increased levels of cholesterol in the blood

139
Q

DiGeorge Syndrome

A

ls known as 22q11.2 deletion syndrome, is a syndrome caused by a microdeletion on the long arm of chromosome 22.[7] While the symptoms can vary, they often include congenital heart problems, specific facial features, frequent infections, developmental delay, intellectual disability and cleft palate.[7] Associated conditions include kidney problems, schizophrenia, hearing loss and autoimmune disorders such as rheumatoid arthritis or Graves’ disease.[7][8]

140
Q

Hypothyroidism

A

Hypothyroidism: weakness, cold intolerance, weight gain. MCC Hashimoto’s (low T3, T4, high TSH), txt replacement (levothyroxine)

141
Q

Hyperthyroidism

A

is a set of disorders that involve excess synthesis and secretion of thyroid hormones by the thyroid gland.

Symptoms include unexpected weight loss, rapid or irregular heartbeat, sweating, and irritability, although the elderly often experience no symptoms.

Toxic Multinodular Goiter-autonomous hyperfunctioning thyroid nodules (Plummers Disease) Iodine deficient regions

Thyroiditis-thyroid inflammation with release of stored hormone.

Medication induced- Amiodarone, Iodine induced, Tyrokinase inhibitors.

142
Q

Tetralogy of Fallot

A

VSD, Concentric RVH, RV outflow obstruction due to infundibular stenosis, dilated aorta (half of patients overrides the septum). If ASD its pentalogy of Fallot.

143
Q

Cardiac Transplant

A

MC indication: non-ischemic cardiomyopathy

Heavily immunosuppressed
Resting HR of 90-100

Transplanted heart is denervated, no symp/parasymp inputs, DOES NOT respond to indirect-acting meds (neostigmine, glycol, atropine)
Ephedrine is decreased
Norepi, Epi, B Blockers work

Residual atrial tissue from the original heart, uncommon but does happen, can cause a double P wave on EKG

Full medical W/U with their team

144
Q

Chest Radiograph Algorithm

A

Chest radiograph assessment using ABCDEFGHI
Last revised by Daniel J Bell on 16 Jun 2021
Citation, DOI, disclosures and article data
ABCDEFGHI can be used to guide a systematic interpretation of chest x-rays.

Assessment of quality / Airway
The quality of the image can be assessed using the mnemonic PIER:

position: is this a supine AP file? PA? Lateral?
inspiration: count the posterior ribs. You should see 10 to 11 ribs with a good inspiratory effect
exposure: well-exposed films have good lung detail and an outline of the spinal column
rotation: the space between the medial clavicle and the margin of the adjacent vertebrae should be roughly equal to each other; look for indwelling lines or objects
Bones and soft tissues
Scan the bones for symmetry, fractures, osteoporosis, and lesions. Evaluate the soft tissues for foreign bodies, swelling, and subcutaneous air.

Cardiac
Evaluate the heart size: the heart should be <50% of the chest diameter on PA films and <60% on AP films. Check for the heart shape, calcifications, and prosthetic valves.

Diaphragm
Check the hemidiaphragms for position (the right is commonly slightly higher than the left due to the liver) and shape (may be flattened bilaterally in chronic asthma or emphysema, or unilaterally in case of tension pneumothorax or foreign body aspiration). Look below the diaphragm for free gas.

Effusions / Extrathoracic soft tissue
Pleural effusions may be large and obvious or small and subtle. Always check the costophrenic angles for sharpness (blunted angles may indicate small effusions). Check the lateral film for small posterior effusions (more sensitive for small effusions).

Fields, fissures and foreign bodies
Check lungs for infiltrates (interstitial vs. alveolar), masses, consolidation (+/- air bronchograms), pneumothoraces, and vascular markings. Vessels should taper and should be almost invisible at the lung periphery.

Evaluate the major and minor fissures for thickening, fluid or change in position.

Check the position of foreign bodies e.g. ETT, NGT, pacemaker leads, central venous lines etc. Comment on previous surgery e.g. cholecystectomy clips, sternotomy wires.

Great vessels / gastric bubble
Check aortic size and shape and the outlines of pulmonary vessels. The aortic knob should be clearly seen. The gastric bubble should be seen clearly and not displaced.

Hila and mediastinum
Evaluate the hila for lymphadenopathy, calcifications, and masses. The left hilum is normally higher than the right. Check for widening of the mediastinum (which may indicate aortic dissection in the appropriate clinical setting) and tracheal deviation (which may indicate a mass effect, e.g. from large goiter, or tension pneumothorax). In children, be careful not to mistake the thymus for a mass!

Impression
In most cases, an impression is worthwhile as it not only forces you to synthesize all the findings together but acts as a double check.

145
Q

Acute kidney injury

A

A sudden and reversible reduction in kidney function
There is no clear definition of AKI: KDIGO (Kidney Disease: Improving Global Outcomes) criteria is MC used
Increase in serum creatinine by 0.3mg/dL or more (26.5micromoles/L or more)within 48 hours
Increase in serum creatinine to 1.5 times or more baseline within the prior seven days
Urine volume less than 0.5mL/kg/hfor at least 6 hours
Causes: Pre-renal, Renal, Post renal
BUN/Cr ratio can aid in loose correlation to identify where problem is
Greater than 20:1 (BUN/Cr) = pre-renal
10-20:1 = renal (and sometimes post-renal)
Less than 10:1 = post-renal
Long list of causes for each, gets deep into work up mixed with electrolytes, FeNA, recommend making a note and looking into more on your own
Hydrate and monitor, older rec include NAC

146
Q

Diabetic Keto Acidosis

A

Usually Type 1

Diabetic Ketoacidosis (DKA)
Glucose >250 mg/dL
All the extra sugar causes Polyuria/Polydipsia/Polyphagia, weight loss, blurry vision, nausea/vomiting, Kussmaul breathing
Dehydration (6-8 L often)
Often an inciting event - Illness/infection, alcohol
Ketosis/Acidosis: break down fatty acids for energy (results in acetone fruity breath)
+ Urine Ketones and B Hydroxybutyrate
Normal or Pseudo hyperkalemia, but its actually low

Note: can have DKA in type 2, TXT: rehydrate with LR, start insulin and K+ replenishment, correct other electrolyte abnormalities

147
Q

HHS

A

Hyperglycemic hyperosmolar state (HHS)
Glucose >600 mg/dL
Polyuria/Polydipsia
Dehydration – greater water deficit (8-10 L often)
Blurry vision
Polyphagia
Nausea/Vomiting
Inciting event - Illness/infection, alcohol

TX: Fluid replacement and insulin

148
Q

Osteoporosis

A

bone disease that develops when bone mineral density and bone mass decreases, or when the structure and strength of bone changes

149
Q

Gout

A

disease in which defective metabolism of uric acid causes arthritis

allopurinol-xanthine oxidase inhibitor

150
Q

Malignant Hyperthermia

A

Malignant Hyperthermia

Autosomal dominant inheritance.

Triggered by succinylcholine and volatile anesthetics.

Hyperthermia, muscle rigidity, ↑CK, myoglobinuria, ↑HR, ↑CO2 production, tachypnea, sympathetic nervous system overactivation (tachyarrhythmias and ↑BP).

-Discontinue offending agents.
-Hyperventilation with 100% O2
-Immediate administration of dantrolene.
-Cool patient if fever
-Treat acidosis and electrolyte abnormalities.

151
Q

Pregnancy Drugs

A

Perform procedures if needed in second trimester (1st risks problems with organogesis, 3rd risks inducing a preterm deliver, -use safe drugs
Classes
A: adequate and well-controlled studies demonstrate no risk in 1st trimester and other trimesters
B: animal studies show no risks or animal have but human have shown to be safe, and there are benefits to use
C: animal studies show adverse effects and no human studies, or no studies at all
D: Routine evidence of fetal risk, in certain situation drug may still be used
X: Fetal Abnormalities

Class B: penicillin (amoxicillin and augmentin), erythromycin, clindamycin, cephalosporins, metronidazole, acetaminophen, oxycodone, morphine, fentanyl, hydrocodone, lido, prilocaine
Class C: codeine, aspirin, articaine, Marcaine,
Class D: benzos, do not use
Nitrous is not-rated, do not use
NSAIDs as of early 2021 are NEVER use, besides ductal issues have been shown now to cause hydramnios.
Goal for preg pts is to reduce pain and anxiety.
OR: consult OB, consider intraop fetal monitoring

152
Q

Pregnancy Physiology

A

1st trimester is weeks 0-14, 2nd is 14-27, 3rd is 28-40

Organogenesis is weeks 3-14, extremely sensitive to exogenous insults

CO increases about 30-50%, 20-30% increase in HR, and 20-50% increase in stroke volume, blood volume increase 20-50%, increase in RBCs, decreased SVR, lowered oxygen reserve with increased consumption, displacement of the diaphragm, 20% decrease in FRC

Increased coag factors except 11 and 13, increased fibrin and hematocrit, reduction in protein S activity and resistance to protein C, gravid uterus causes endothelial damage, (makes them all Virchow Triad positive)

In chair, position pts in left lateral decubitus to prevent compression of IVC

Data shows that in the first 16 weeks acute exposure of 0.6 Gy had risks of growth restriction, mental retardation, etc. Diagnostic tests that deliver less than 0.05 Gy are not believed to be teratogenic.

100 Sieverts = 1 Gray, Pano = (approx.) 20 microsieverts = 0.0002 gray

During preg, when intubating, increased friability of upper airway which can lead to lots of bleeding, rate of failed intubations is about 10 fold higher

153
Q

Hyponatremia

A

Sodium: Normal 135* mEq/L to 145* mEq/L
Hyponatremia: often asymp, acute and chronic types, s/s lethargy, confusion, AMS, seizures, deep work up including figuring out if hypotonic, isotonic, hypertonic, looking as FeNA and Uosm (probably too deep for this exam)
Problems that happen slowly should be corrected slowly (respect corrected rates or you may kill them)
Beware central pontine myelinolysis (also called osmotic demyelination syndrome). Correct hyponat. too fast, brain cannot adjust the lytes to keep up, cells swell and explode. 1-14 days after correction, acute encephalopathy develops, seizures, coma, death
Severe symptomatic hypoNa (seizures, AMS): 3% NaCl bolus (100mL up to 3x over 10min until symp resolve or Na+ 4-6 mEq/L)
Severe asymptomatic hypoNa (Na<120): Goal Na+ 6 mEq/L in first 24h. 3% NaCl with rate based on Sodium Correction Rate, usually 15-30mL/hr. Stop 3% NaCl when Na>125 or if correcting too fast

154
Q

Hypernatremia

A

Etiologies: impaired access to free water or impaired thirst, decreased urinary concentrating ability, or diabetes insipidus ( decreased production or efficacy of ADH)
S/S: thirst, weakness, nausea, loss of appetite, with severe (generally over 160) seizures, coma, death
Deeper (Calculate free water deficit, WU, hypervolemic, euvolemic and hypovolemic types)
If you correct it too fast, (theoretically) can cause uncal herniation of the brain and death

155
Q

Potassium

A

Normal Values: 3.5-5.5* mEq/L, main intracellular cation, 98% intracellular
K+ excretion is regulated at the distal nephron, Na+ absorption leads to K+ secretion in the kidney (mechanism of aldosterone)
Transcellular shifts most common cause of changes in K+
This means things like acid/base shifts, insulin issues like DKA, etc., affect the measured K levels. However, these are not always true, the K might just be hiding intracellularly, so the cause of it does matter in the treatment
Obviously, this is predicated on having functional kidneys…without those and for folks on hemodialysis this all goes out the window

156
Q

Hypokalemia

A

<3.5

Signs and symptoms: usually with K+ < 2.5: cramps, ileus, weakness (LEs > trunk/UEs > respiratory muscle paralysis)
ECG: flat T waves, ST dep, U waves (small deflection after the T wave), increased QT, atrial or ventricular ectopy, VT, VF (esp if K+ <3, susceptible pts, or on digoxin
Can be lab artifact (pseudo-hypokalemia): WBC >100  WBC absorb K if sample sits out (check K on ABG+)
Lack of intake, redistribution, renal loss, extra renal loss…many many things can cause

157
Q

Hyperkalemia

A

Hyperkalemia= K> 5.1 mEq/L

Paresthesias, paralysis, confusion, respiratory failure, dysrhythmias, muscle cramps
Note: Any electrolyte abnormality can cause cardiac arrhythmias, which can be benign or fatal. Some are more predisposed to this than others, and K+ is one of these

Evaluate your patient NOW
Repeat Potassium, stat-hemolysis rule out, check a CBC, whole blood more reliable than serum K
EKG*
Review PMH, Medications, renal function, examine patient, and evaluate volume status
Treat is K+ is over 6.5, EKG changes present, or pt is symptomatic
Stabilize, Redistribute, Eliminate
STEP 1: PROTECT THE CORE (aka heart)
Want to give calcium to stabilize the cardiac membrane
Step 2: Give meds to move K around
Step 3: Give more meds to eliminate it from the body
Note: Sux intube dose raises K by 0.5

158
Q

Chloride and Bicarb

A

Chloride
The major extracellular anion in our body (kind of the opposite of sodium)
101-111 mEq/L normal range
Significance:
Evaluation of fluid, electrolyte, and acid-base status, osmotic pressure, body water distribution

Bicarb (HCO3)
Normal 20-34 mEq/L
Extracellular buffer
Both of these are integral part of acid/base

159
Q

Renal

A

Renal function is measured by the glomerular filtration rate
Estimated using Cockcroft-Gault formula (do not need to memorize), newer formulas include CKD-EPI formula
eCCr = (140 – Age) x Mass (kg) x [0.85 if female] / 72 x [Serum Creatinine (mg/dL)]
MC measured using creatinine clearance; by product of muscle metabolism, almost exclusively filtered and not resorbed , hence good indicator of FNC
Serum Cr is .5-1.3. NOT linear interp. Cr of 2 is 50% decrease in GFR, very much depends on pt baseline to interpret

160
Q

Renal Pearls

A

Angiotensin II receptor blockers (ARBS) competitively antagonize angiotensin receptor type 1 (AT1), block vasoconstriction, sodium retention, reduces production/secretion of aldosterone and reduces secretion of vasopressin
Vasopressin and aldosterone both hit the distal convoluted tubule and collecting ducts
Related topics,
SIADH (too much vasopressin),
Diabetes Insipidus (opposite of SIADH; lack of ADH, damage to hypothalamic tract, kidneys do not respond to it, and pregnancy)
Conn’s Syndrome

161
Q

CT with contrast protocol in kidney disease

A

Verify that iodinated contrast material is necessary. If an alternative test is likely to provide an accurate and reliable diagnosis, we proceed without administering contrast material. (See ‘Verify that contrast material is necessary’ below.)

●Among euvolemic and hypovolemic inpatients, and emergency department patients whose clinical course permits it, we administer intravenous isotonic saline. Hypervolemic patients and patients receiving dialysis in general are not given volume expansion. There are no established dosing, duration, or injection rate recommendations for how the saline should be administered. Commonly used regimens are presented below. (See ‘Inpatients and those in the emergency department’ below.)

In high-risk outpatients, we prefer volume expansion with intravenous isotonic saline, if feasible, similar to our approach among inpatients. However, outpatients are sometimes given oral hydration [41]. There are no established dosing or timing recommendations for how the oral hydration should be administered. Some encourage patient-directed oral hydration before and after the scan (eg, total one to two liters). (See ‘Outpatients’ below.)

●Use low- or iso-osmolar contrast agents. Use of these agents is standard for all diagnostic imaging examinations. (See “Prevention of contrast-associated acute kidney injury related to angiography”, section on ‘Dose and type of contrast agent’.)

●If a patient at high risk for contrast-induced AKI (CI-AKI) is taking a metformin-containing medication, it should be discontinued for a minimum of 48 hours after the procedure and, if AKI develops, not reinstated until the kidney function has improved. In addition, metformin should generally be avoided in patients with estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2. (See ‘Withdrawal of metformin and nephrotoxic drugs in high-risk patients’ below.)

If a patient is taking noncritical nephrotoxic medications, these should generally be withheld for 48 hours after administration of contrast material at the discretion of the ordering clinician and, if AKI develops, not resumed until the kidney function has improved.

For patients who are not at high risk for AKI after contrast-enhanced CT, we verify the need for contrast material; however, we do not prescribe prophylactic measures, do not withdraw nephrotoxic medications, and do not suspend metformin.