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Oral Boards Medicine – Flashcards

Anthony Richie

7 July 2022

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Upper Airway Anatomy • Small Nares • Large Tongue • Head Large, Neck Small • Limited Cervical Extension • Adenoids/Tonsils - Largest ages 4-10 • Long, Narrow, Higher Epiglottis • Higher, Funnel Shaped Larynx • Vocal Cords Inclined • Compliant, Shorter Trachea • Cricoid is narrowest portion of airway (adults=cords)

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Pediatric Airway Upper Airway

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Pediatric Airway- lower airway

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Narrower Airway • Diaphragmatic Breathing • Horizontal Ribs • Poorly developed Accessory Muscles • Decreased Alveoli • Decreased FRC - lung size increases rapidly until age 6, then more slowly • Lack of elastin causes collapse of terminal airways to occur earlier, decrease in airway resistance at age 8

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Pediatric intubation

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Technique similar to adults but always use straight blade up to age 5 # Increased vagal tone, prone to bradycardia on intubation # Tube size • Estimate by size of little finger OR • Diameter: (age + 16)/4 i.e 4y.o. = size 5 • Length: (age/2) = 12 i.e. 4y.o. = 14 cm # Avoid hyperextension because it may occlude airway # Bag valve mask - tidal volume 10-15cc/kg

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Pediatric physiology

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Blood pressure mainly dependent on HR (vs adults where controlled by HR, SV, SVR) # Cardiac output needs to be twice as high as adults due to increased metabolic rate and oxygen consumption • Major determinant is Heart rate • Bradycardia leads to sharp decrease in cardiac output and BP # Decreased FRC - one of the reasons they desaturate faster than adults

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Laryngospasm

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Protective reflex to prevent foreign matter from entering the larynx, trachea, or lungs. # Classic signs and symptoms • Increased respiratory effort and increased difficulty exchanging air ♦ Flared nostrils ♦ Tracheal tugging ♦ Paradoxical breathing

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Laryngospasm TX

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100% Oxygen • Suction all blood and foreign material with yankauer suction • Pack surgical site to prevent further bleeding into the hypopharynx • Depress patient's chest and listen for a rush of air to indicate patency • If obstruction persists, break spasm with positive pressure via 100% O2 and full-face mask with good seal (appropriately sized for child vs. adult patient.) • If obstruction persists - Succinylcholine (where is it kept in your office?) ♦ Adults 0.1-0.2mg/kg IV for adults (small dose 10-20mg IV for partial obstruction). Pediatric dose 0.25-0.50mg/kg IV ♦ In a complete spasm where smaller dose fails to break spasm, use 20- 40mg IV ♦ Complications of succinylcholine " Myalgias " Malignant hyperthermia " Hyperkalemic cardiac arrest (in susceptible patients with myopathies) " Masseter muscle spasm in pediatric patients (potential indicator of MH)

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Bronchospasm

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Constriction of the walls of the bronchioles often caused by mast cell degranulation that can occur in response to allergic triggers or physical stimuli (secretions or ETT). Airway diameter decreases due to mucosa thickening and increased production of thick, viscous mucous.

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Broncho spasm Signs and Symptoms

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Signs and symptoms • Wheezing • Diminished breath sounds • Prolonged expiration • Increase airway pressures (in ventilated patients)

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Bronchospasm Predisposing factors

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History of asthma • Recent symptoms of Asthma • Recent respiratory infection: wait several weeks for airway edema to resolve • Anesthetic technique

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Bronchospasm TX

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Treatment • Awake/cooperative patient ♦ Inhaled beta agonist via inhaler of nebulizer ♦ Oxygen • Obtunded/Unconscious patient (without ETT) ♦ 100% Oxygen ♦ Epinephrine (1:1,000) 0.3 to 0.5mg SC [Peds= 0.01mg/kg] ♦ IV Epi can be used (less preferred) 0.1-0.25mg IV (1:10,000) infused slowly ♦ Airway support ♦ Consider corticosteroids ♦ If situation deteriorates -> intubation • Intubated patient ♦ 5-10 puffs of albuterol via ETT

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Emesis and Aspiration

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At risk groups • Pregnant • Diabetics • Anxious • Geriatric • Obese • Smokers • GERD • Hiatal Hernia

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Emesis and Aspiration SIGNs and Symptoms

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Signs/Symptoms - may set-in rapidly • Rales • Dyspnea • Tachycardia • Bronchospasm • Cyanosis • Progressive hypotension

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Emesis and Aspiration TX

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Treatment in emerging patient • Encourage coughing to clear airway • Put chair in Trendelenburg (head down 15 degrees) with patient onto right side • Suction airway - remove any foreign material • 100% oxygen If patient fails to improve and develops signs of severe dyspnea, cyanosis, tachycardia, and hypotension: • Activate EMS • Clear airway again • Intubate and manage bronchospasm with beta agonist • Small volume tracheobronchial lavage • No antibiotics and no steroids

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Post-emergent management of recovered patient

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Observe at least 2 hours in office • Discharge criteria ♦ SpO2 > 94% on room air ♦ No wheezing, shortness of breath and minimal cough • Consider hospital transfer if ♦ Aspiration of particulate matter ♦ Supplemental O2 needed to keep SpO2 in 90's

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Angina

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Most common sign of an acute coronary syndrome (70-80% of affected patients) # Presents due to inadequate coronary blood flow to the myocardium # Pain may have: • Visceral component - dull and poorly localized • Somatic component - sharp with dermatomal distribution • Psychological component - subjective sense of impending doom # Clinical presentations - vary depending on individual differences in neural transmission and perceptions of pain • Classic angina: Dull substernal discomfort/pressure/tightness that may radiate to left arm, neck and/or jaw. Associated shortness of breath Anginal equivalent: No pain or discomfort, but sudden or decompensated ventricular failure (dyspnea) or ventricular arrhythmias. • Atypical chest pain: Pain and discomfort that is localized to the precordial area and has positional, musculoskeletal, or pleuritic features. # Women more likely to show nausea, shortness of breath, dizziness and fatigue as symptoms

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Classifications of Angina

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Stable - poorly localized deep chest pain that is associated with physical exertion and relieved by rest or sublingual nitro • Unstable - Pain with more random pattern of appearance - no physical exertion and unrelieved by rest. • Prinzmetal - cyclic vasospasm of coronary vessels frequently seen in women

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Management of patients with known frequent angina attacks

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Prophylactic Nitroglycerin 0.4mg SL prior to stressful procedure • 100% O2 • Anxiolytics - IV sedation to control stress response • Psychological support - stress reduction

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Treatment of angina event in patient with documented history of frequent attacks

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Terminate procedure • Administer O2 @ 4L via mask or nasal canula • Monitor vitals • Sublingual nitro if SBP >90mmHg • CP >5 minutes -> administer second dose of nitro • IV morphine 1-3mg increments at 5 minute intervals • ASA 160-325mg -> chew • If patient unresponsive to 3 doses of nitro in 10 minutes, assume AMI and activate EMS

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Acute Myocardial Infarction

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Most frequent presentation is sudden onset of severe, prolonged (>15 minutes) substernal chest pain and pressure occurring usually at rest. # Diagnosis - by history, EKG, and cardiac enzymes • 12- lead EKG ♦ S-T segment elevations in leads II, III, and aVF (acute inferior) ♦ Q waves represent scarred heart tissue from prior MI • Cardiac enzymes - proteins from damaged heart tissue found in blood ♦ CK and CK-MB elevated - MB predominant more specific for heart ♦ Troponins (subunits I &T) - most specific and diagnostic if seen in conjunction with EKG findings ♦ Angiogram (cath through femoral artery) " visually identifies narrowed artery " Allows ability of stent or angioplasty for treatment

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Ventricular rhythms frequently observed during acute ischemia and infarctions include:

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PVC, Vtach, Vfib

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Management of AMI

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Remember basics first (same as angina) " EMS " Stop surgery, clear mouth and 100% O2 " Morphine " ASA " Nitroglycerine - take BP first, do not give if hypotensive " Vitals - watch for decompensation (hypotension, hypoxemia, bradycardia, or ventricular dysrhythmia and cardiac arrest)

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Allergic Reactions

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The union of an antigen and antibody causes a reaction that forms or liberates chemical mediators. These mediators exert certain pharmacologic responses that determine the nature and extent of a hypersensitivity or allergic reaction. # Primary effects • Smooth muscle contraction • Dilation and increased permeability of arterioles • Increased glandular secretion # Chemical mediators include: Histamine, slow-reacting substance (lung), eosinophil chemotactic factor, kinins, prostaglandins, and complement. " Manifestations of an allergic response # Cutaneous reaction - most common in drug reactions • Patterns - urticarial, exanthematous, and eczematoid

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Angioedema

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Slight swelling of eyelids and lips • Severe, life-threatening in mouth and upper airway

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Anaphylaxis

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Massive release of chemical mediators • Progressive cardiovascular collapse due to increased capillary permeability refractory to treatment, smooth muscle spasm, and acute pulmonary edema. • Additional pulmonary compromise due to upper airway edema causing obstruction

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Management of allergic reactions # Mild reactions

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urticarial, mild angioedema • Identification and discontinuation of offending agent • 50mg Diphenhydramine IV, IM or PO

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Management of allergic reactions # SEVERE reactions

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Stop administration of any causative agent • ABC's • Support circulation with IV fluids - Adult = rapid infusion of 1L lactated Ringer's • Epinephrine IV 1:10,000 (1mg in 10mL) ♦ Adults: titrate 0.2mg (2mL) to 0.5mg (5ml) to affect every 2-5 minutes ♦ Children: 0.01mg/kg • Epinephrine IM/SC 1:1,000 (1mg/ml) - only if IV route is unavailable ♦ Adults: 0.3 to 0.5mg of a 1:1,000 concentration repeated in 10-20 minute intervals Children: 0.01 mg/kg repeated in 10-20 minute intervals

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Epi via ETT tube Dose

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Administered at twice the IV dose

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Malignant Hyperthermia

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Hypermetabolic crisis due to an inherited muscle disorder that can result in elevated levels of Ca+ in the myoplasm of muscle cells resulting in activation of muscle contraction. In MH crisis, the muscular contraction is sustained and heat, lactic acid, and carbon dioxide are produced. # Liver can't clear lactate and severe metabolic acidosis occurs # Increased CO2 -> tachycardia -> tachypnea

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MH Risks factors

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Personal or family history of MH # Personal or family history of muscle of neuromuscular disorders (Duchene's or Becker's) # History of dark of cola-colored urine following previous anesthesia of exercise

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MH triggering Factors

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Succinylcholine (don't be surprised if laryngospasm case leads to MH) # Volatile anesthetic inhalation agents

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MH safe Agents

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Local anesthetics # Benzodiazepines # Opioids Barbituates # Propofol # Ketamine # Nitrous oxide # Etomadate

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Primary signs and symptoms of impending MH

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Increased EtCO2 (double or triple over 10-20 minutes) # Unexplained tachycardia, tachypnea, or hypercarbia # Generalized muscle rigidity # Hyperthermia (often late) # Respiratory and/or metabolic acidosis. # Cardiac arrest

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Treatment of MH

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Activate EMS and discontinue all volatile inhalation anesthetics substituting 100% O2 # Dantrolene - must be solubilized • Mix 20mg dantrolene, 3g of mannitol and 60mL of sterile water • Administer 1-3 mg/kg bolus rapidly up to 10mg/kg until signs are controlled # Administer bicarbonate in order to correct the metabolic acidosis (1-2mEq/kg) # Active cooling with cold IV saline 15mL/kg every 15 minutes x 3 # Treat hyperkalemia with hyperventilation and IV glucose and insulin. Consider calcium chloride (2-5mg/kg) if hyperkalemia is life threatening. # ICU observation for 24hours because MH may recur. # Continue dantrolene administration 1mg/kg every 4-6 hours.

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Asthma

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A chronic inflammatory disorder of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness and cough particularly at night or in early morning. These symptoms are usually associated with widespread but variable airflow limitation that is at least partially reversible either spontaneously or with treatment.

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Asthma Triad of Symptoms

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Wheeze (high-pitched upon expiration) # Cough - may be dry of productive (mucoid or pale yellow sputum) # Shortness of breath or difficulty breathing

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Asthma Triggers

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Exercise - 5-15 minutes after brief exertion # Cold air # Exposure to allergens (dust, mold, pollen)

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Asthma Physical FIndings

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Tachypnea # Tachycardia # Prolonged expiratory phase (decreased I:E ratio) # Pulsus paradoxus (>12mmHg fall in SBP during inspiration) # Nasal Polyps

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Classification of Asthma

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Intermittent • Symptoms 2 or fewer days per week • No interference of normal activity • FEV1 between exacerbations are normal range # Mild Persistent • Symptoms more than 2x weekly • Minor interference with normal activity • FEV1 within normal range # Moderate Persistent • Daily symptoms and need for short acting beta agonist • Some limitation of normal activity • FEV1 60-80% of predicted # Severe Persistent • Symptoms throughout the day • Extreme limitation of normal activity • Nocturnal wakening nightly • FEV1<60% of predicted

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Asthma Perioperative management

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Peak Flow rate (PEFR) # Reduce exposure to triggers # Prophylactic use of bronchodilator

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Asthma Drugs to Treat

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Short -acting beta-2-selective adrenergic agonist # Low dose inhaled glucocorticoid # Alternatives - Leukotiene receptor agonists, theophylline, and cromoglycates

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Diabetes Mellitus

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# Type I (IDDM): juvenile onset, insulin/diet controlled • polyuria, polydipsia, polyphagia, polyphagia, wt. loss, and incontinence # Type II (NIDDM): adult onset, oral hypoglcemics/diet • slight wt loss or gain, nocturnal awakenings to void # Secondary diabetes: gestational, steroids, tumor, or pancreatic resection

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DM Pathology

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# Increased plasma glucose stimulates insulin release • Insulin is produced by beta cells islets of Langerhans in the pancreas and provides glucose and AA transfer to muscle, fat, liver, tissues (not brain or renal cortex) • Type 1 - shows failure to produce insulin • Type II - Insulin resistance and sometimes combined with a relative insulin deficiency

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Diagnosis of DM

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Fasting blood sugar = >120 on 2 or more occasions • Glucose challenge: >200 sustained with a check at 2 hours • HbA1C: >7; provides insight into mean blood glucose over past 2-3 months (assess control - good question to ask of diabetic patients)

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DM TX

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# Insulin preparations • Fast-acting - regular and semilente • Intermediate - NPH and lente • Prolonged - protamine and ultralente • *often asked on boards (hold fast acting forms the AM of surgery, consider ½ dose of prolonged forms the night prior) # Oral hypoglycemics • Metformin (Glucophage) - decreased hepatic gluconeogenesis production and intestinal absorption • Glyburide (sulfonylurea) - stimulates insulin release form beta cells

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Complications of IDDM

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# Hyperglycemia/hypoglycemia # Acidosis # Ketosis # Significant end-organ damage (microvascular disease) - retinopathy, HTN, CAD, gastroparesis # Oral - xerostomia, infection, decreased healing, perio disease, burning mouth # Fungal infections: candida, mucormycosis # Cardiovascular disease - myocardial ischemia/infarction

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DM Surgical Risks Assessment

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Disease control (HgA1c) target is <7 # Medications # Physical exam - signs of end-organ damage # Increased glucose leads to glycosylation of neutrophils with decreased response for impaired immune function and wound healing. # Beware silent MI (seen more commonly in diabetics) " Pre-

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DM PreSurgical recommendation

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NPO 12 hours for IDDM (due to gastroparesis) # Early morning appointments (breakfast only delayed) # Stop oral hypoglycemics on day of surgery # Metformin is contraindicated in situations that risk renal hypoperfusion (hypotensive anesthesia for Maxillary surgery) # Omit short-acting insulin on morning of procedure # Take between ½ - 2/3 total morning dose of intermediate acting glucose # IV fluids D5 (1L contains 50gms of Dextrose)

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DKA

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Hyperglycemia (>500), anion gap metabolic acidosis, and ketonemia • Treatment ♦ IV fluids 0.9% NS (1L over 30 minutes) ♦ Replace K - measure K+ and replace 10-20 meq/hour IV ♦ IV regular insulin (15 units ) then sliding scale ♦ Correct pH with bicarb if <7

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Hypoglycemia (<50 mg/dL) - insulin shock

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Signs/symptoms ♦ fatigue, malaise, trembling, cold sweats, confusion, coma • Treatment ♦ If alert - snack of glucose tabs ♦ If unconscious - " dextrose IV 50% (D50) 1mL/kg IV up to 50mL " OR D5W 10mL/kg IV up to 500mL " OR Glucagon 0.025 0.1 mg/kg IV/IM/SC up to 1 mg

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Hypertension

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Underlying defect is a failure in the regulation of vascular resistance # Sympathetic vasomotor tone # Extracellular fluid and sodium stores # Renin-angiotensin-aldosterone pressor system # Neural reflexes # Decrease vascular elasticity

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TX Diagnosis

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Defined as two BP readings of at least 140/90mmHg separated by 2 minutes on two or more visits

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HTN Classification

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Classification # Normal 160/100

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HTN Causes

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Essential Hypertension - most prevalent (90-95%) • Stress • Smoking • Sedentary lifestyle obesity (85% occur w/ BMI >25) • Alcohol • Aging Secondary Hypertension - results from a clearly identifiable cause • Pheochromocytoma • Cushings's syndrome • Kidney disease • Pre-eclampsia • Coarctation of the aorta

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HTN Preoperative management

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Defer treatment for elective procedures (have in mind your own BP limits that you use - i.e. >180/110) # Optimize patient and ensure they adhere to routine medical management. # Consider pre-operative medical assessment for uncontrolled/untreated hypertensive patients # Patients who are taking chronic antihypertensive medications should continue taking their medication until the time of surgery. The drug can be administered with a sip of water on the morning of surgery and resumed postoperatively as needed. Alternative parenteral agents can be prescribed for patients who are unable to resume oral medications.

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Hypertensive urgency

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When BP >220/120 and no signs or symptoms • Consider immediate physician referral

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Hypertensive crisis

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Anxiety # Pain # Cardiovascular disease # Drug interaction # Full bladder # Hypoxia " Pharmacologic management (in-office) - decrease cardiac output and/or peripheral resistance • Esmolol ♦ A cardioselective B1 receptor blocker with rapid onset and short duration of action ♦ 10-30 mg IV q5minutes ♦ Good choice if tachycardia present ALSO good in Asthmatics

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Labetalol

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♦ An alpha- and ß-adrenergic blocker, given as an intravenous bolus or infusion. ♦ 5-20 mg initially, followed by 20 to 80 mg every 10 minutes to a total dose of 300 mg. Infusion: 0.5 to 2 mg/min.

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Hydralazine

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♦ An arteriolar dilator, given as an intravenous bolus. Initial dose: ♦ 5-10 mg given every 20 to 30 minutes; maximum dose: 20 mg. ♦ Good for pregnant women or if bradycardia present

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If hypertensive crisis activate EMS

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Hospital medical management may include: ♦ Nitroprusside — a rapidly acting arteriolar and venous dilator, given as an intravenous infusion. Initial dose: 0.25 to 0.5 mcg/kg per min; maximum dose: 8 to 10 mcg/kg per min which should be continued for no more than 10 minutes. ♦ Propranolol — a ß-adrenergic blocker, given as an intravenous infusion and then followed by oral therapy. Dose: 1 to 10 mg load, followed by 3 mg/h. ♦ Nitroglycerin — a rapidly acting venous and, to a lesser degree, arteriolar dilator, given as an intravenous infusion. Initial dose: 5 mcg/min; maximum dose: 100 mcg/min. ♦ Nicardipine — a calcium channel blocker, given as an intravenous infusion. Initial dose: 5 mg/h; maximum dose: 15 mg/h.

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Hypotension

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A reduction of arterial blood pressure of 15-20% from baseline " Cardiac symptoms accompanying reduced blood pressure: # Bradycardia (early) or tachycardia (late) # Decreased cardiac output and tissue perfusion " Preoperative Hypotension # Frequent causes

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Hypotension treatment algorithm - in patients demonstrating signs or symptoms of hypo-perfusion

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Patient positioning - supine with legs elevated # 100% O2 # Monitors (BP, pulse-ox, EKG) # Look for specific cause and treat • Anxiety • CV disease - MI? • Drugs • Hypercarbia • Hypoxia # Administer drug to increase cardiac output and/or peripheral resistance • 0.01 mg/kg of atropine (up to 0.5mg if bradycardia) • 5-10mg of ephedrine q5 minutes • 0.1mg phenylephrine q 5 minutes - if tachycardia # Consider reversal # Consider EMS activation

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Von Willibrand Disease

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Factor VIII deficiency and von Willebrand factor deficiency # Most common inherited bleeding disorder (up to 1%) # VWF serves to stabilize platelet adhesion and is produced by endothelial cells and monocytes # Types • Type 1 ♦ Most common type (75%) Partial quantitative deficiency of VWF • Type 2 ♦ Qualitative abnormalities ♦ Four subtypes - 2A, 2B, 2M and 2N • Type 3 ♦ Total deficiency of VWF ♦ Severe disease

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Hemophillia A

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Sex-linked factor VIII deficiency # Clinical manifestations appear when deficiency >80% # Severity • 5% Factor VIII activity = mild disease, but significant bleeding from surgery

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Treatment of Von Willibrands and Hemophillia A

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Mild: DDAVP→ ↑ release vWF (req >5% active factor VIII to release stores) • Desmopressin (synth analog of ADH)→ ↑ stored vWF & VIII from endothelial cells • max effect: 15-20 min/ ½ life 6 hrs (↓ effect w/ ↑ doses b/c limited vWf stored) # Moderate: cryoprecipitate (VIII, XII, vWF + fibrinogen) # Severe: Factor VIII conc (often does not help w/ VWD alone → + cryo) # Post-op: Amicar (inhibits fibrinolysis), 6g PO qid • Note: can give pre-op: 5g IV 30 min before (= loading dose) for hemophilia, bleeding, rebleeds (intracranial aneurysms), GI bleeds

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Hemophilia B (Christmas Disease)

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Factor IX deficiency # Treatment • Mild-Moderate: FFP(factors II, VII, IX, X) • Severe: IV Proplex (contains concentrate factors II, VII, IX, X)

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Sickle Cell Anemia

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Autosomal recessive disorder of change in chemical composition of HgB with valine substitution for glutamic acid # Diagnosis is by Hgb electrophoresis # Sickling (change in shape of RBC's) is exacerbated by dehydration and hypoxia (decreases in O2 concnetration). Amnormal RBS'c lead to: • Vessel damage and associated tissues • Thrombosis/microvascular occlusion • Pain • Ischemic damage to surrounding tissues # Chronic anemia with Hct= 19-24 # Shortened life span of RBCs • Normal = 120 days • Sickle Cell trait = 29 days • Sickle Cell Dz = 17 days Labs • CBC - shows decreased Hgb, increased WBCs and creatinine • Peripheral smear - shows sickle cells • U/A - may show hematuria and casts # Sickle Cell Crisis - increased risk in acidosis, hypoxia, dehydration, and hypercarbia • Hemolytic crisis - breakdown of damaged RBC's • Splenic sequestration - enlargement of spleen due to breakdown of malformed RBCs ♦ Immune compromised to encapsulated organisms (S. pneumo and H influenza) ♦ Abdominal pain (LUQ) ♦ Drop in hemoglobin by at least 2 g/dl ♦ Splenectomy considered

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Aplastic crisis

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decreased production of RBCs from bone marrow due to infection

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Treatments Sickle Cell

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Folic acid - improves RBC turnover • Hydroxyurea - Mainstay to decrease crisis frequency by increasing fetal Hgb • Early treatment of HTN - mild increases in BP show significant increase of stroke • Transfusion therapy - decrease percent of HbS

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Spinal injured patients # Acute transection

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Potential for respiratory insufficiency and increased susceptibility to respiratory infections (seen in both acute and chronic injury) • Exaggerated hyperkalemic response to succinylcholine administration for first 6 months • Orthostatic hypotension - due to lack of regulatory control -> peripheral vasodilation

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Spinal injured patients Chronic transection

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Autonomic hyperreflexia due to sympathetic spinal reflex activity (no inhibition) • Hypertension! (T6 or higher) • Cervical SCI is associate with increased vagal tone • Cardiovascular/hemodynamic instability

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Effects of fractures at different levels

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C4 - loss of spontaneous respiration • C5 - quadriplegia • C6 - Paraplegia • C7 - Flexion, but poor extension • T1 - weak flexion and extension

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Epilepsy - syndrome of 2 or more unprovoked seizures in a lifetime

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Generalized - sudden loss of consciousness ♦ Convulsive - muscle contractions ♦ Myoclonic - contract and relax continuously ♦ Tonic-clonic (grand mal) - LOC, fall to ground, and jerking movements ♦ Absence - brief LOC with miniml activity Partial ♦ Complex - aura followed by impaired awareness ♦ Simple - no LOC, but isolated tonic-clonic activity • Status Epilepticus ♦ Repeated sz activity and impaired arousal for 30 minutes ♦ Treatment " Control airway " O2 " Activate EMS " Diazepam 10mg over 2 minutes every 10 minutes or (more common in office setting) Midazolam 2mg IV then 1mg/min IV (0.05mg/kg, or 0.025mg/kg in children " Glucose check " Glucose and thiamine prn " Monitors and possible respiratory support in postictal period

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Other causes of seizures

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Vasovagal syncope - most common cause in OMS office • Lidocaine overdose • Anesthetic agents that increase electrical activity ♦ Methohexital (Brevital) ♦ Ketamine (Ketalar) ♦ Enflurane.sevoflurane ♦ Flumazenil

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Multiple Sclerosis

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A disease characterized by inflammation, demylination and axon degeneration resulting in various clinical manifestations including: # Optic Neuritis # Internuclear ophthalmoplegia # Sensory symptoms # Pain # Vertigo # Nystagmus # Motor Symptoms # Heat sensitivity # Fatigue # Depression Cognitive dysfunction # Epilepsy Disease Patterns # Relapsing remitting # Secondary Progressive # Primary Progressive # Progressive relapsing " OMFS Considerations # Stress reduction - studies show relapses are more common after stressful events # Temperature management - relapse may be stimulated by overheating # Patients often with history of large steroid doses over prior 6 months necessitating stress-dose steroids # Patients with a history of interferon use should prompt an investigation to rule out thrombocytopenia, neutropenia, or anemia # Pain control issues (pre-existing) may make post-operative management challenging. # Undiagnosed MS - may present as bilateral trigeminal neuralgia -> prompt referral to neurologist

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Myesthenia Gravis

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An autoimmune disorder characterized by weakness and fatigability of skeletal muscles caused by autoantibodies directed against acetylcholine receptors of the neuromuscular junction. " Muscle groups impacted # Ocular muscles • Lid muscles (ptosis) • Extraocular muscles - resulting in binocular diplopia # Bulbar muscles • Masticatory muscle weakness and fatigue • Oropharyngeal weakness - dysarthria and dysaphagia # Facial muscles Patient appears expressionless # Neck and Limbs # Respiratory Muscles • Weakness can lead to respiratory insufficiency • Can lead to "myasthenic crisis" which can occur spontaneously or in response to infections, surgery, medications, or tapering immunosuppression.

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Medications that may unmask or exacerbate MG (partial list relative to OMS)

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Ketamine # Lidocaine # Procaine # Diazepam # Aminoglycosides # Ampicillin # Clindamycin # Neurontin # Methylprednisolone # Prednisone # Botulinum Toxin # Narcotics

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Myastenia Gravis OMFS Considerations

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Respiratory muscle weakness is a major concern. Can be quantified with PFT's # Avoid non-depolarizing muscle relaxants

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ADHD

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A disorder that usually manifests in early childhood with symptoms of hyperactivity, impulsivity and/or inattention " Drugs used to treat # Stimulants • Methylphenidate - blocks dopamine transport (Ritalin, Concerta) • Amphetamine - blocks re-uptake of dopamine and noradrenaline, inhibits MAO # Nonstimulants • Atomoxetine - inhibitor of noradrenaline tansporter (Strattera) " OMFS Concerns # Patient behavior mangment Drug interactions • Methylphenidate may significantly reduce effects of midazolam • Stimulants may decrease MAC • Some sypmpathomemetics may exacerbate increases in heart rate and blood pressure • Long-term stimulant use man result in depleted catecholamine stores and prolonged hypotension # Post-operative nausea and vomiting • Central dopamine is increased by methylphenidate and amphetamines • Methylphenidate exacerbates emetogenic effects of ketamine

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Psychiatric Patient

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Perioperative concerns for patients receiving psychotropic drugs are grouped into the following categories # Drug-drug interactions • Lowered seizure threshold • Altered response to vasoconstrictors • Exaggerated CNS depression • Anticholinergic effects # Drug-disease interactions • Drug induced EKG changes • Hepatic and renal impairment leading to accumulation of parent drug and metabolites # Drug class physiologic effects • Serotonins syndrome • Neuroleptic malignant syndrome

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Depression

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Most antidepressants exert actions by blocking reuptake of norepinephrine, serotonin or both # MAOIs Nonselective inhibition of MAO (A&B) resulting in decreased metabolism of 5HT and catecholamine neurotransmitters • Drug-drug interaction - MAOI + Meperidine -> hyperthermia, BP instability, Szs, and coma

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Tricyclic Antidepressants

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Inhibit norepinephrine and serotonin reuptake to varying degrees • May see exaggerated effects of sympathomimetics (ephedrine, epi, phenylephrine) • Reports of induction of cardiac dysrhythmias • Excessive sedation with narcotics

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SSRIs

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Inhibit serotonin reuptake in CNS • More favorable profile with limited adverse effects (with regard to sedation, orthostasis, and cardiovascular risks) • Serotonin syndrome ♦ Occurs when SSRIs are used in combination with agents that increase serotonin concentrations (MAOIs, tramadol, fentanyl, ondansetron and St. John's Wort) ♦ Symptoms include: confusion, agitation/restlessness, fever, diaphoresis, diarrhea, ataxia, hyperreflexia, myoclonus ♦ Management is supportive " lorazepam 1-2mg slow IV push q30minutes until improvement or extreme sedation " Cyproheptadine 4mg PO q4hours " Methylsergide 2-6mg PO to block serotonin " Propranolol 1-3mg slow IV push

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Bipolar disorder

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a mood disorder characterized by episodes of mania and depression # Medications • Neuroleptics - typical (1st generation) and atypical (2nd generation) ♦ Inhibit dopamine contributing to extrapyramidal effects ♦ Perioperative concerns for hypotension, cardiac conduction effects, sedation, lowered seizure threshold ♦ Neuroleptic Malignant Syndrome (NMS) " potentially fatal " Fever, MS changes, muscle rigidity, respiratory distress and rhabdomyolysis " Progresses over hours to days (not minutes like MH - even though symptoms are similar)

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Lithium

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Mood stabilizer used for prophylaxis and treatment ♦ Lithium toxicity - narrow therapeutic window " Vomiting " Tremors " EKG - inverted and flattened T-waves; widened QRS, heart block " Diuretics should be taken with caution b/c increase in Li levels

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Anticonvulsants - valproate and carbamazepine

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used as mood stabilizers ♦ Valproate effects bleeding time and platelet aggregation ♦ Carbamazepine - sedation, nausea, thrombocytopenia (monitor CBC)

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Drug Addicted patient

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When an individual persists in use of alcohol or other drugs despite problems related to use of the substance, substance dependence may be diagnosed.Compulsive and repetitive use may result in tolerance to the effect of the drug and withdrawal symptoms when use is reduced or stopped. # Addiction - inability to discontinue use despite consequences # Tolerance - increasing dose to gain desired effect " Physical Evaluation # Vitals • Decreased Pulse/BP: Opiod, acute EtOH • Increased Pulse/BP: Stimulants; EtOH or barbiturate withdrawal # Pupils • Miosis - opiods • Mydriasis - hallucinogens and stimulants # Parotid hypertrophy - EtOH # Dental caries (rampant) - stimulants (crystal meth) # Nasal mucositis - Cocaine/inhalants # Cardiac - tachycardia and other dysrhythmia (stimulants)

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Alcoholic

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Increased metabolism of sedation meds due to microsomal enzyme induction # Additive effects of CNS depressants in acute use # Coagulopathies due to decreased liver function - seen in advanced alcoholic hepatitis # Electrolyte disturbance due to dehydration and malnourishment • Hypokalemia • Hypomagnesemia • Hypophosphatemia # ECG anomalies - conduction disturbances • AV Block • Bundle branch block • Prolonged QT interval # Withdrawal concerns (DT's) in in-patients (>24h)

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Opioid addict

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Increased doses required for effect # Consider benzos or ketamine # Patients on agonist/antagonists (Subutex) are able to be sedated with fentanyl, but must refrain from use for 36 hours prior to procedure. # Pain control issues in medically dependent/chronic pain patients • Communicate with pain specialist managing patient. • Be aware of baseline patch doses and days of application when sedating or prescribing post-op meds

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Cocaine abuser

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Anesthetic management is directed toward optimization of cardiopulmonary parameters # Increased risk of cardiac dysrhythmias # Avoid dopaminergic agonists (haloperidol, droperidol and promethazine) which may cause delayed awakening # No treatment within 24 hours of last use # Local anesthetics with AND without vasoconstrictors have additive dysrhythmic effects # Greater incidence of CVA, malignant HTN, and MI

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Stimulant abuser (amphetamines, ephedrine, nicotine, caffeine)

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Chronic users will demonstrate labile BP secondary to catecholamine depletion # Careful use of epinephrine and bupivacaine due to dysrhythmia potential # Avoid ketamine # MDMA causes a missive release of serotonin • Serotonin syndrome - 5-HT receptor hyperstimulation ♦ Hyperthermia ♦ Mental status changes ♦ Autonomic instability ♦ Increased muscle tone rigidity

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Marijuana user

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Few anesthetic considerations # Chronic use may result in reduced pulmonary function # Reactive airway and increased susceptibility to laryngospasm # THC potentiates the respiratory depressive effects of opioids in acute intoxication # May see mild tachycardia and ST and T wave changes

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Duschene's Muscular dystrophy

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x-linked, more common in men " Progressive muscular atrophy " Vertebral & rib contractures→ # Kyphoscoliosis # Restrictive ventilatory defect " Anesthesia concerns: # No depolarizing muscle blockers (→ hyperkalemia) # Can use non-depolarizing steroidal muscle relaxants # ↑ incidence of MH (may be triggered by NDNM blockers, volatile anesthetics) # AVOID volatile anesthetics

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Marfan's Disease

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Autosomal dominant; abnormal chemical makeup of connective tissue # 2° mutations in gene fibrillin-1 which plays an important role as scaffolding for elastic tissue # Disruption of scaffolding causes changes in elastic tissue (aorta, eye, skin) " Overgrowth of long bones of body (→ tall stature & long limbs) " Clinical findings - # skeletal defects - long, lanky frame, spider-like fingers (arachnodactyly), chest abnorm (pectus excavatum or pectus carinatum), scoliosis, joint laxity # facial features - highly arched palate, micrognathia, crowded teeth) # eye problems - nearsightedness, dislocation of lens) Cardiovascular abnormalities- dilatation of base of aorta (aortic root), aortic regurg, MVP, Dissceting aortic aneurysm " Treatment - no curative tx # β blockers: decrease HR, help prevent stress on aorta (discourage athletics/contact sports # annual echo to assess the aortic root # sometimes surgical replacement of aortic root & valve # Consider antibiotic prophylaxis to prevent endocarditis - this is somewhat controversial as it is not specifically recommended in the special cases category of the current AHA guidlines

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Rheumatoid Arthritis

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Chronic systemic inflammatory disorder that affects many tissue and organs, but primarily attacks synovial joints by producing an inflammatory response in the synovium. Pathologic process often leads to destruction of the articular cartilage and ankylosis of the joints. " Other systemic manifestations # Cardiovascular - pericarditis, valve insuff, conduction disturbances # Pulmonary - pleural effusions and pneumonitis # Salivary glands - Sjogren's " Pre-op concerns # NSAIDs - cornerstone of pain management -> platelet dysfunction (may consider holding NSAIDs 10-14 days prior for platelet normalization) # High dose steroids # Potential for cervical instability (C1-C2) - decreased ROM -> consider Cspine films if GA planned # TMJ dysfunction

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Physiology of Pregnancy

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Cardiac output increases 30-40% " Maternal blood volume increases 25-50% # Dilutional anemia RBC mass increases 20% # Optimal hematocrit 30-38% # All coagulation factors are increased except XI and XIII # Overall they are in a hypercoaguable state " Supine hypertension syndrome # Caused by compression on inferior vena cava # Place patient on left lateral side with 5-15 degree tilt " Physiologic changes # Restriction of respiratory function • 50% complain of dyspnea by week 19 • 75% by week 31 # Increased nausea and vomiting • GERD in 70-75% of all pregnant women • Gastric emptying time doubles • Increased aspiration risk # Mucosa in upper airways is edematous # Potential for hypoglycemia increases

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Medications in pregnancy

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Drug risk classification • A: No risk in controlled human studies • B: No risk; Animal studies • C: Teratogenic in animal studies • D: Positive evidence of human fetal risk; benefits may outweigh risks if life-threatening situation • X: Positive evidence of human fetal risk

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Medications in pregnancy Sedation

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Barbituates - Congenital abnormalities reported in animals # Propofol - No reported teratogenesis # Ambien - OK - ideal for anxiolysis # Ketamine - OK - dose not to exceed 1.5mg/kg # Antiemetics - Zofran and promethazine are OK # Muscle relaxants - no teratogenicity # Anticholinergics - meconium ileus # Analgesics • Acetaminophen - drug of choice • Ibuprofen/ASA - risks of peripartum hemorrhage, pulmonary hypertension and fetal closure of ductus arteriosus

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Lactating/Breast Feeding patients

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Lactation accounts for 2-5% of drug elimination # Store milk if sedation planned # Avoid prolonged opioid use # NSAIDs, Morphine, and hydrocodone are OK # Avoid meperidine and oxycodone # Rapidly clearing benzos OK # Avoid long term Benzo use

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Transfusion Reaction

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2° agglutination of blood by Ab in plasma # 1/3000 transfusions 2° clerical error (incompatible blood) # s/s: fever*, ↓ BP, sweats/chills, shock, hives, anaphylaxis/dyspnea, rigors, vomiting, tachypnea, flank, back & extremity pain, occipital HA

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Types:of Transfusion reaction

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1. Acute hemolytic: immune-mediated • severe, potentially fatal complement-mediated intravascular hemolysis • typically→ extravasc sequestration, ↓ survival of transfused RBCs & mild clinical rxns 2. Hemolytic: non-immune-mediated • RBCs are damaged prior to transfusion • hemoglobinemia & hemoglobinuria w/o significant clinical symptoms 3. Nonhemolytic febrile " Ab against Ag on WBCs (transfused granulo/lymphocytes) " fever, chills, rigors (dx of exclusion) " tx: ASA, benadryl 4. Allergic rxns • rash, urticaria, pruritus • IgE-mediated (anaphylactic rxns may be assoc w/ IgA if pts are IgA deficient tx: benadryl 5. Ag contamination • stop transfusion, C&S samples • prevent septic shock/death 6. Delayed transfusion rxns: • ↓ Hct, fever, slight ↑ bilirubin • rarely dramatic & significant hemolysis of AHTR • often unidentified; usually self-limited (usually only destroys transfused cells) • tx: stop transfusion, monitor vitals, start supportive therapy immediately

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Transfusion Reaction Goal of initial therapy:

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achieve & maintain adequate BP & renal perfusion 1. Initial IVF→ 0.9% NS, monitor U/O 2. Consult nephrologist early • if Ø diuretic response w/in ~2-3 h after initial tx may be Acute Tubular Necrosis (ATN), further fluid & diuretics may be contraindicated 3. Initial diuretic therapy • furosemide 40-80 mg (1-2 mg/kg in peds), titrate to effect • maintain urinary flow >100 mL/h during 1st 24hrs 4. Mannitol (osm diuretic) • 20 g IV bolus (100 mL/min 20% soln)→ 10-15 mL/min→ 1000mL 5. Dialysis: anemic & oliguric 6. Monitor for hyperkalemia (2° RBC breakdown) 7. anti-HT meds w/ caution→ dopamine 2-5 μg/kg/min 8. benadryl/steroids may be helpful " AVOID pressor drugs that ↓ renal blood flow " Correct way to administer transfusion: • type & screen crossmatch & check w/ 2nd person • use NS (not LR*) b/c Ca in LR→ coagulation w/ citrate in stored blood→ emboli • blood warmer, milipore filter

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Transfusions:

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Whole blood: PRBC + PRP • PRP: platelets + FFP (II, VII, IX, X, XIII) • FFP: all factors (II, VII, IX, X, XIII) • Cryoprecipitate: insoluble factors in FFP as it thaws (VIII, XII, vWF, fibrinogen)

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Shock # Types

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Hypovolemic→ 2° blood loss 2. Neurogenic→ 2° spinal cord injury 3. Cardiogenic→ 2° cardiac tamponade, MI 4. Septic→ 2° G(-)

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Hypovolemic shock: types I, II, III, IV→ based on % blood loss

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I: 15%→ mild tachy, no BP/P/RR Δ # Tx: none required • II: 15-30%→ tachy, ↑DBP, narrow PP, anxiety/MS Δ, tachypnea # Tx: fluid 3:1 • III: 30-40%→ ↓U/O, ↓SBP, ↓MS, tachycardia, tachypnea # Tx: fluid 3:1 + blood • IV: >40%→ ↑↑HR, ↓↓SBP # Tx: blood + surgery

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Subacute Bacterial Endocarditis (SBE)

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Bacterial infection→ growths on endocardium • usually 2° strep viridans; occurs on damaged valve • if untreated can be fatal w/in 6 wks→ 1 yr • most pts have underlying cardiac disease ( except IVDA & hospital-acquired infections) • 2° Strep viridans, enterococci, other bacteria/fungi • average incubation period: 1-2 wks often develops on abnormal valves after asymptomatic bacteremias from infected gingiva, GI, GU • fever for several days→ 2 wks, nonspecific symptoms (cough, SOB, joint pain, diarrhea, abdominal/flank pain) • ~90 % have murmurs # may be absent in R sided cardiac infections # changing or acute murmur→ only in acute endocarditis

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Osler nodes

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red-purple, slightly raised, tender lumps, often w/ pale center # pain often precedes development by 24 hours # found on fingers &/or toes # can occur any time during course of endocarditis (usually subacute) # last from hours→ several days

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Janeway lesions:

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non-tender, often hemorrhagic # occur mostly on palms/soles; last days to weeks before healing # more common in acute endocarditis (septic microembolism)

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Acute intermittent porphyria

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defects in hemoglobin metabolism " autosomal dominant # excessive secretion of porphyrins & porphyrin precursors # causes: fasting, drugs that ↑activity of hepatic P450 (phenobarb, sulfonamides, estrogens, EtOh), barbiturates, phenytoin, infection " Signs/Symptoms # abdominal pain/constipation # psychiatric symptoms (hysteria) # peripheral neuropathies- mainly motor # Ø rash→ diff from other porphyrias " labs: ↑ levels urinary porphobilinogen→ brown urine or port wine " Tx: ↓ heme synthesis & ↓ prod of porphyrin precursors 1. ↑ doses of glucose (400 g/d) inhibit heme synthesis in mild attacks 2. hematin 4 mg/kg/d x 4 days: severe attacks, if severe neurologic symptoms 3. narcotics (pain), laxatives/stool softeners 4. neurontin: tx of seizures (avoid phenobarbital)

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Midazolam:

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Dose: 0.05 - 0.15 mg/kg IV; titrate slowly to effect (1→ 7 mg); PO dose: 0.5 mg/kg # Compared to diazepam: 3× potency, H2O soluble, ↑ amnesia, slower onset, ↓ pain on injection # H20 soluble: onset→ 3-8 min; upon injection, highly protein bound # Duration: 20-35 min # ↑ lipid solubility: exposure to blood pH Δs structure; crosses BBB early for CNS effects # ½ life→ 2 hrs; shorter duration 2° Ø active metabolites; elim ½ life→ 1-4 hrs # Adverse effects: resp depression, disorient on emergence, n/v, flushing, anxiety, agitation # Withdrawal rxns: depression, insomnia, irritability, sweating, diarrhea, seizure # Reverse with Flumazenil: competitive antagonist of benzo receptor • specific antidote for benzo overdoses • dose: .2mg IV q1min, peak→ 1-3min, duration→ 60-120 minutes (max =1mg) • ½ life: 40-60 min (re-sedation may occur) • adverse effects: n/v, dizziness, sweating, HA, vision Δ, injection pain, agitation (anxiety, nervousness, xerostomia, tremors, palpitations, insomnia, dyspnea, hyperventilation) • significant adverse effects: sz*, acute benzodiazepine withdrawal • Decreased sz threshold by blocking binding of GABA; AVOID in patients w/ sz d/o • Drug interactions: TCA, cocaine, lithium, methyxanthines, isoniazid, propoxyphene, MAOi, bupropion, cyclosporine→ Incresed risk of sz

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Opioids:

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MSO4, codeine, demerol→ release histamine (→ hypotension & vasodilation) # Fentanyl, alfentanil, sufentanil→ ↓ histamine release # mechanism: act on opioid receptors in CNS/peripheral tissues (mu1, mu2, kappa, delta) # onset: initial rapid pharmacologic onset→ via initial rapid crossing of BBB effects: analgesia, ↓ MAC, anti-tussive # ↑ vagal tone, ↓ sympathetic tone # little cardiac depression (except demerol→ ↑ myocardial depression) # 1st pass effect: GI→ portal circulation (extensive hepatic metabolism before entering circulation) seen w/ codeine & hydrocodone # adverse effects: • 1. n/v (2° stim CTZ in medulla) • 2. chest wall rigidity (↑ muscle tone) w/ rapid admin; tx: narcan + succ • 3. Respiratory depression, ↓BP, ↓HR • 4. urinary retention

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Fentanyl:

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↑ lipid solubility; stored in fat/released slowly • faster onset (3-6 min), shorter duration than MSO4 (30-60 min), rapid redistribution • longer elimination ½ life than MSO4 2° larger volume distribution • cardiac stability: more stable than MSO4 • dose: 2 μg/kg IV • Adverse effects: recurrent respiratory depression, chest wall rigidity, cardiac depressant • skeletal muscle static contraction (respiratory muscles included) ♦ Seen after bolus administration (can occur w/ other bolus narcs) ♦ s/s: difficult (+) press ventilation w/ LMA, ventilatory sounds over lungs ♦ Treatment: narc antagonist (Narcan) + succinylcholine 1mg/kg • Drug interaction: diltiazem (↑ effects of fentanyl)

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Naloxone

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Competitive binding at mu receptor ♦ May elicit withdrawal symptom in a heroin addict ♦ Adult dosing: 0.1-0.3μg/kg initially, then→ .25 μg/kg @ 2-5 min intervals ♦ Pediatric dosing: 0.005-.01mg ♦ Complications of rapid doseL n/v, increase BP, increased HR, pulmonary edema ♦ Serious adverse effects: pulmonary edema, cardiovascular instability, HT, v-tach/v-fib, sudden death

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Ketamine:

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5mg/kg IV, 2-4mg/kg IM; (Give w/: .05mg/kg versed, .005mg/kg robinul/glyco) # can also be given PO # NMDA receptor antagonist, opiod agonist (blocks catecholamine re-uptake) # dissociative anesthesia: chemically related to phencyclidine (PCP derivative) # electrophysiologic dissociation: between limbic system & thalamus→ little higher cortical depression # cortical awareness blocked from external stimuli (auditory, visual, painful input) cataleptic state: eyes open, nystagmus, non-communicative, analgesia, amnesia # ↑ lipid solubility: crosses BBB quickly # indications: dissociation, amnesia, analgesia, ↑ ICP, resp tract infection # metabolism: in liver by cytochrome P450 # Benefits: • Bronchodilation- good for asthmatic pts & best induction agent for rapid-sequence intubation during status asthmaticus; protects airway reflexes→ upper airway muscle tone maintained, reflexes intact, ↓ resp depression • No histamine release • intrinsic analgesic & amnestic props • ↑ HR, BP & CO→ good sedative for pts in shock, acts on symp NS→ ↑ circ catechols • only IV induction agent that ↑ sympathetic outflow # adverse effects: unpleasant emergence hallucinations, emesis, muscle hypertonicity, transient stridor, emesis, transient rash, agitation, ↑ recovery time

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Propofol:

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IV sedative-hypnotic w/ amnestic props; rapid & smooth emergence structurally unrelated to other hypnotics (barbiturates, benzos), ↑ activity of GABA # Very lipophilic (oil in water emulsion) # rapid LOC→ rapid redistribution; ½ life: 2-8 min # No histamine release # causes hypotension (20-30% ↓ BP), no change in heart rate or respirations # dose: • preinduction anxiolysis (25 μg/kg/min); • induction (2-2.5mg/kg over 60 sec) → for intubation: does not req muscle relaxant* • GA maintenance: 100-150 μg/kg/min • IV sedation: .5mg/kg + boluses 5-20mg; uniquely titratable # Effects: • 1. sedation: as effective as midaz w/ ↓ time of onset & recovery • 2. hypnotic: synergistic w/ other analgesic/sedatives (barbs, benzos, opioids, ketamine) → poor analgesic*, must use adjunctive analgesic • 3. amnesia • 4. muscle relaxant • 5. anti-convulsant # Advantages: • 1. intrinsic anti-emetic props (unlike ketamine, barbs, etomidate) • 2. rapid recovery & euphoria (→ smooth recovery w/o dysphoria) • 3. protects against bronchospasm (bronchodilation, ↓ intra-op wheezing in asthmatics)

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COPD/Emphysema:

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a chronic inflammatory condition characterized by loss of elasticity of the alveoli which causes obstruction of the airways during exhalation. In emphysema, PMN's allow protease to work unopposed and cause proteolysis of elastin may also be caused by lack of alpha 1 antiprotease patients will maintain oxygenation with emphysema

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COPD exam

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flat diaphragms and enlarged chest wall prolonged expiratory phase hyperinflated lungs on chest xray

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COPD TX

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ipratropium inhalers are the primary therapy for COPD albuterol inhalers are more second line treatment for COPD/emphysema For acute exacerbations treatment is more similar to asthma with the use of beta agonists and may need nebulized drugs rather than just inhalers. Steroids are more helpful for acute exacerbations than for chronic treatment. Consider respiratory infection as a cause of acute exacerbation.

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Pneumothorax:

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usually represents an acute collection of air in the pleural space. Can occur spontaneously or from trauma, may occur with rupture of subpleural cysts or "bleb" ruptures from emphysema. Tension ptx occurs when there is a tear in the pleura that is acting as a check valve allowing air to collect in the pleural space but not letting it escape.

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Pneumothorax signs and symptoms

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Signs/Symptoms: small ones may be asymptomatic tachypnea cyanosis hypotension absent breath sounds over hemithorax Tension ptx: will see tachypnea, loss of chest motion during breathing, hypotension, deviation of heart/aorta on CXR

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Pneumothorax TX

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small ptx may only require monitoring with serial cxr's to ensure it is not enlarging supplemental oxygen can speed resolution by increasing diffusion of the air out of the pleural space in tension ptx a needle decompression may be needed, ultimately a chest tube and hospitalization are needed.

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Cystic Fibrosis:

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a disease process caused by irregular or absent sodium and choride transport across epithelial membaranes leading to thick, viscous secretions. It can affect the lungs, pancreas, intestines, and liver. CF is caused by a mutation in the CFTR gene on chromosome 7 that regulates electrolyte concentration of sweat, digestive fluids, and mucus.

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Cystic Fibrosis Signs/ Symptoms

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poor growth and weight gain thick mucus frequent pulmonary infections (due to decreased mucociliary clearance and thick secretions). Infections usually caused by S. aureus, H. influenza, adn P. aeruginosa. infertility malabsorption (failure of a newborn to pass meconeum may be diagnostic) exocrine function of the pancreas is blocked due to thick secretions

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DX of CF

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usually done with the sweat chloride test. The most commonly used form of testing is the sweat chloride test. The following is a description of this test just for your knowledge: Sweat-testing involves application of a medication that stimulates sweating (pilocarpine). To deliver the medication through the skin, iontophoresis is used to, whereby one electrode is placed onto the applied medication and an electric current is passed to a separate electrode on the skin. The resultant sweat is thencollected on filter paper or in a capillary tube and analyzed for abnormal amounts of sodium and chloride. People with CF have increased amounts of sodium and chloride in their sweat. May also need CXR, lung function tests, Upper GI or small bowel films, CT.

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CF Management

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prophylactic antibiotics for lung infections Dornase (DNA-ase) is a nebulized drug that helps break down thick secretions supplemental enzymes for digestion including vitamins A, D, E, K. percussive lung therapy (to break up secretions)

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Anesthetic Considerations for CF

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be aware of decreased vital capacity and increased residual volume and airway resistance. If intubating ensure that they are very deep to decrease coughing and stimulating mucus secretions. Agressive suctioning to remove secretions Better outcomes with pre and postanesthetic use of bronchodilators, spirometry, and possible antibiotic use.

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Obstructive Sleep Apnea:

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Characterized by repetitive pauses in breathing during sleep, despite the effort to breathe, and is usually associated with a reduction in blood oxygen saturation and likely has severe snoring. Apneas may last greater than 20-30 seconds.

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OSA signs and symtoms

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Signs/Symptoms: daytime sleepiness hypertension headaches mood changes/irritability weight gain obesity retrognathia

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DX of OSA

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most commonly used is the sleep study (involves EEG, EKG, pulse ox, capnography, EOG, EMG). Apneas and hyponeas will be measured and counted to figure the AHI or RDI

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Anesthetic considerations: of OSA

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What are the CPAP/BIPAP settings that the patient uses? the higher they are the worse the apnea and the more likely they are to obstruct and be hard to manage during sedation. Consider the airway relaxation that occurs with sedation/anesthesia and reduce doses as needed. If they have OSA then you know intubation likely to be difficult if needed, recovery is going to be longer and more dangerous due to obstructions. In children look at the tonsils on your exam, if they are large then assume they have apnea. Be prepared to use adjunctive airways to maintain ventilation during procedure if obstructions occur. IF there is any doubt about the severity of OSA or whether they can be managed in an office setting, do the procedure in an OR setting with a secure airway.

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HYPERNATREMIA:

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nearly always caused by loss of total body water in excess of sodium or the retention of sodium. Usually seen in debilitate pt's who can drink enough, very old, very young, or those with altered consciousness. may see HyperNa with low total body Na - this occurs when the pt is loosing both Na and water but loosing more water. HyperNa with normal total body Na - DI is the most common cause of hyperNa and normal total body Na. This is caused by the kidneys not being able to concentrate urine in response to ADH.

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Central DI:

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can be caused by tumors near the hypothalamus, intracranial and spinal surgery, head trauma. Signs are polydipsia, polyuria, and no hyperglycemia. Treat with DDAVP. Nephrogenic DI: the kidney doesn't respond to ADH. Can be seen in chronic renal dz, electrolyte disturbances, drugs can cause it. Diagnose by giving ADH and the kidney will not concentrate urine.

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Hyper NA Signs and Symtoms

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neurologic signs are the most common and thought to be from cellular dehydration. Restlessness, lethargy, hyperreflexia The above can progress to seizure, coma, death Rapid correction of hypernatremia can cause cerebral edema

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Hyper NA TX

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aimed at restoring plasma osmolarity correcting the cause Correct water deficits over 48 hrs with hypotonic solution If Na low, use isotonic solution to correct b/f you give hypotonic solution. HyperNa and increased total body Na should be given loop diuretic and IV D5 Rapid correction of hyperNa can cause seizures, brain edema, possible death. Plasma Na should not be corrected faster than 0.5 mEq/L/hr.

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Anesthesia Considerations Hyper NA

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the problems are more related to the volum deficits. Hypovolemia makes the patient more reactive to vasodilation or cardiac depression by anesthetics Decreased volume of distribution will force dose reductions Postpone elective surgery if above 150 mEq/L

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HYPONATREMIA:

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caused by retention of water through increase in TBW or a loss of sodium in excess of water. This is usually caused by a deficit in urine diluting capacity.

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Hypo NA Classification and Causes

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HypoNa and low total body Na: see loss of both Na and water and can be renal (urine Na > 20mEq/L) or extrarenal (urine Na < 10 mEq/L). extrarenal causes: vomiting, diarrhea, third spacing renal causes: diuretics, mineralocortocoid def, osmotic diuresis, RTA HypoNa and increased total body Na: caused by "edematous" disorders and see increased total body water and Na but water is greater. These causes include CHF, cirrhosis, renal failure, nephrotic syndrome. HypoNa and normal total body Na: seen with glucocorticoid def, hypothyroidism, drugs, and SIADH to dx SIADH other causes must be ruled out and they must not have hypovolemia, edema, or adrenal, renal, or thyroid dz. SIADH can be caused by malignant tumors

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Clinical Signs of Hypo NA

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mild (<125 mEq/L): usually assymptomatic but may have anorexia, nausea and weakness. serious (<120 mEq/L): With progression will see cerebral edema, that causes lethargy, siezures, coma, confusion, and death. slowly developing hypoNa will be less symptomatic due to compensatory loss of intracellular solutes (K, Na, and amino acids) to restore cell volume

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Tx of Hypo NA

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goal is to treat the low Na and the underlying disorder. priamary treatment is isotonic saline for those with low total body Na. water restriction is the treatment for hypoNa and normal to increased total body Na. for acute symptomatic hypoNa must figure the Na deficit and correct to 125 mEq/L. Very rapid correction of Na could result in central pontine myelinosis that could cause permanent neurologic sequelae.Anesthetic considerations: levels of Na > 130 mEq/L are safe for anesthesia, lower concentrations can lead to cerebral edema. Generally if the hypoNa is fairly severe the pt should undergo a work up and the underlying cause be treated.

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HYPOKALEMIA:

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defined as plasma K below 3.5 mEq/L and can be due to intracompartmental shift, increased K loss, or inadequate K intake. intracellular movement of K is caused by insulin therapy, alkalosis, beta 2 agonists, hpyothermia. May also be seen with transfusion b/c the transfused cells loose K and then reabsorb it once they are transfused. increased K losses: almost always renal or gastrointestinal. If from a renal cause most usually from increased mineralocorticoids, or hypoMg, RTA, ketoacidosis, or some drugs. GI losses due to vomiting, NG suctioning, diarrhea, fistulae, laxative abuse

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Hypokalemia Signs

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assymptomatic until it falls below 3 mEq/L. Digoxin will make the heart more sensitive to K changes flat T waves, U waves, prolonged PR interval, and ST depression on EKG skeletal muscle weakness, ileus, muscle cramps, tetany if caused by diuretics you will also see metabolic alkalosis

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TX of Hypokalemia

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monitor with EKG changes. Oral replacement is usually the safest and can give 60-80 mEq/day. IV is usually only used for severely low K or those with EKG changes or weakness. Can only give 8 mEq/hr IV if need to replace faster must use central line and EKG monitoring. Don't give with D5 b/c the insulin secretion can force K intracellular.

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Anesthesia Consideration of HypoKalemia

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can procede with chronically low k of 3 to 3.5 if assymptomatic. If more acute or symptomatic it should be corrected prior to anesthetic. They may be more responsive to neuromuscular blockers if have hypoK - should reduce doses.

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HYPERKALEMIA:

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occurs when serum K is > 5.5 mEq/L. Can be caused by intracellular shift, decresed excretion, or increased intake. Most common cause is hemolysis of RBC's on blood draw. Extracellular mvmt of K is seen with succinylcholine, acidosis, cell lysis, chemotherapy, hemolysis, rhabdomyolisis, massive tissue trauma, hyperosmolality, beta blockers Decresed renal excretion is seen with decresed GFR. May also see hyperK with reduced aldosterone activity

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Clinical Signs of HperKalemia

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Clinical signs: ascending paralysis with levels > 8 mEq/L peaked T waves wide QRS complex long PR interval loss of P wave loss of R wave amplitude ST segment depression Sine wave → Vfib → asystole hypocalcemia, hyponatremia, and acidosis with accentuate cardiac effects of hyperK.

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Tx of HyperKalemia

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Goals are to reverse cardiac effects, skeletal muscle weakness, and restore plasma K to normal levels. calcium: (5-10 mL of 10% Ca gluconate) stablilzes the cardiac membranes glucose and insulin can give lasix if intact kidneys kayexalate will bind up K and eliminate it through a bowel movement Dialysis for severe or refractory K elevations

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Anesthesia Consideration

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correct before surgery if not emergent need for surgery. Monitor the ECG throughout for changes. DO NOT give succinylcholine and avoid K containing IV fluids. Monitor muscle function b/c hyperK can accentuate neuromuscular blockade.

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THYROID:

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T3 adn T4 are made from iodine absorbed from the GI tract. They are both protein bound and stored in the thyroid. Both are made in the gland itself but T3 is more potent and bound, T4 is converted to T3 peripherally. TH increases carb and fat metabolism, maintains metabolic rate, HR and contractillity are also increased by TH.

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Hyperthyroidism:

answer

production of excess TH. May be caused by the following: Grave's disease multinodular goiter TSH secreting tumors and functioning thyroid adenomas overdose of thyroid replacement medications thyroiditis

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Hyperthyroidism Clinical SIgns

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weight loss heat intolerance muscle weakness hyperactive reflexes and nervousness diarrhea fine tremor, exopthalmos may be noted with Graves' disease cardiac signs range from tachycardia to atrial fibrillation to CHF thyroid storm: s/s are hyperpyrexia, tachycardia, hypotension, agitation, delirium, and eventually coma.

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DX of HyperThyrodism

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confirmed by abnormal thyroid function tests with elevations in total serum thyroxine, serum T3 and free T4 elevations. Treatment: usually treated with medical therapy to block TH using propythiouracil or methimizole. Can also block hormone release or block the signs with propanolol (blocks conversion of T4 to T3). May also use radioactive iodine but may cause hypothyroidism. Removal usually reserved for tumors or large goiters.

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Anesthesia Conserns of HyperThyroidism

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delay anesthesia until the symptoms of hyperthyroid are controlled medically. Should have normal thyroid function tests and HR < 85. Intraoperative: ketamine, pancuronium, indirect beta agonists and other sympathetic stimulators should be avoided. these pt's are chronically hypovolemic and may have an exaggerated response to BP fluctuations. Postoperative: must monitor for thyroid storm unless pt's had good control of symptoms prior to surgery. Tx with hydration and cooling, propranolol, propylthiouracil. with thyroidectomy must monitor for reccurent laryngeal nerve damage (can cause hoarsness and partial airway obstruction), hematoma formation, hypoparathyroidism, and pneumothorax.

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Hypothyroidism:

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low TH formation from autoimmune disease, thyroidectomy, radioactive iodine, antithyroid medications, iodine def, or secondary hypothyroidism.

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Hypothyroidism Signs/Symptoms:

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weight gain cold intolerance muscle fatigue lethargy constipation hypoactive reflexes dull facial expression depression HR, contractility, stroke volume, and CO decrease. Cool extremities Myxedema Coma: very low TH and have impaired mentation, hypoventilation, hypothermia, hyponatremia, CHF Treat by replacement of TH and Close monitoring

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Anesthesia Conserns of hypoThyroidism

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should be corrected prior to any surgical procedures. They will have slower gastric emptying and will be more responsive to sedatives. This also means they may have a slower recovery. Ketamine is usually good to give b/c these pts have decreased CO, HR, and are volume depleted

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HYPERPARATHYROIDISM:

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Causes of primary HyperPT are carcinoma, adenoma and hyperplasia of the gland. Secondary hyperPT is a secondary response to diseases that produce low calcium (renal failure, malabsorption). Can also have ectopic production of parathormone by rare tumors outside of the thyroid gland

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Hyper-parathyroidism CLinical

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most are due to hypercalcemia hypertension, ECG changes hypercholoremic metabolic acidosis polyuria, dehydration, polydipsia Renal stones ileus, nausea/vomiting, pancreatitis muscle weakness, osteoporosis delirium

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Anesthesia Consideration of Hyperparathyroidism

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ensure volume status is normal. Can correct Ca with normal saline and furosemide. IV bisphosphonates can decrease Ca levels - these are rarely used though. avoid hypoventilation since acidosis will increase ionized calcium may have prolonged response to paralytics osteoporosis makes vertebral fracture more likely if have severe ostoporosis.

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Heart Failure

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Failure of the heart to effectively pump blood to meet metabolic needs of the body. Manifestations seen are due to inadequate pumping of the associated ventricle and systemic or pulmonary congestion occurs (Systemic=RHF; Pulm congestion=LHF). Cardiac output is reduced in most forms of heart failure. In compensated failure, the arteiovenous concentration of oxygen is adequate at rest, but quickly lapses with exertion Subclassifications of heart failure include: Left-sided (most common type is LV heart failure)àsee pulmonary edema Usually caused from myocardial damage due to CAD. Other causes are valvular dysfunction or arrhythmias Right-sided àsee increased JVP, hepatomegaly, peripheral edema Cor pulmonale: RHF due to long term HTN in pulmonary vasculature COPD SystolicàInability to expel enough blood to meet tissue demands DiastolicàFailure of heart to relax/fill properly Causes include HTN, DAD, Hypertrophic cardiomyopathy

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NY Heart Assoc Functional classifications of Heart Failure

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Class I: symptomatic only with greater-than-normal activity Class II: symptomatic with ordinary activity Class III: symptomatic with minimal activity Class IV: symptomatic at rest

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Treatment of CHF

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Treatment of CHF includes: ACI's, Diuretics, Digoxin Treatment of acute pulm edema: Lasix, Morphine, Nitrates (venodilator), Oxygen, and placing patient in upright position OMFS Considerations Consider CXR to R/o pulm edema (LHF) Palpate lower extremities to evaluate for edema (RHF) Caution with beta-blockers in severe CHF (patient has reduced stroke volume and a decrease in HR can plummet Cardiac Output)

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Atrial Fibrillation

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An arrhythmia in which numerous automaticity foci in the atria discharge causing "quivering" of the atria. Rates can be 350-400/min This is the most common heart arrhythmia

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Afib Causes

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Cardiac Ischemia, MI, CHF, myocarditis, HTN Pulmonary COPD flare, PE Metabolic High catecholamine levelsàstress, thyrotoxicosis Drugs ETOH, cocaine, amphetamines, Theophylline Chronic Causes Older age, HTN, ischemia, Valvular disease

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Tx of Afib

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Acute/urgent cardiovert Stable/Chronic Rate control: CCB/ beta Blocker Anticoagulate (to reduce CVA risk) Cardiovert If 48hr (high stroke risk) anticoagulate 3 wks prior and 4-12 wks after. OMFS Considerations: 7x increased risk of CVA The quivering of the heart allows thrombus formation Consider continuing anticoagulation and extracting teeth in multiple visits

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Bifid aortic valve:

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A congenital defect where there are 2 aortic valves rather than the normal 3. In childhood, problems are rare. With time, the valve becomes stenotic and regurgitation occurs. This leads to aortic hypertrophy Symptoms Baby or child tires easily Chest pain Difficulty breathing Rapid and irregular heartbeat (palpitations) Loss of consciousness (fainting) Pale skin

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Liver disease

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The liver is the largest organ in the body. Functions include synthesis of most essential serum proteins (albumin, coagulation factors), production of bile, the regulation of nutrients (glucose, glycogen, lipids, cholesterol, amino acids), and metabolism/conjugation of lipophilic substances (bilirubin, cations, anions, and drugs). Liver disease: The damage of normal liver tissue resulting in liver injury, inflammation, and necrosis. Often times there are no symptoms (Jaundice, fatigue, RUQ pain etc) until late in the disease process Laboratory testing is useful to establish liver damage (ALT, AST, alk phos, PT)

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Classifications of liver disease:

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Hepatocellular- Hepatitis, alcoholic liver disease Cholestatic (obstructive)- gallstones, malignant obstruction Mixed

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Hepatocellular Disease

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Hepatitis: Swelling and inflammation of the liver and is usually viral in nature (Can progress to Cirrhosis with time) Cirrhosis: Replacement of normal liver tissue with fibrous tissue/scar as a consequence of liver disease

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Hepatitis:

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Subclasses: Hep A: Fecal-oral transmission Hep B Transmission is percutaneous, sexual, or perinatal Sub Class Hep Delta/D Hep C: Transmission is percutaneous more often than sexual Hep D: Requires HBV to occur. This is more severe and progresses to cirrhosis more quickly Hep E: Transmission is fecal-oral; Seen in travelers to SE Asia, Pakistan, India, Mexico, Africa

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OMFS IMPLICATIONS FOR MANAGEMENT OF LIVER DISEASE

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The liver has a remarkable ability to manage a significant amount of damage before serious surgical complications occur. As disease progresses, a reduction in coagulation factors (evidenced by increased PT) becomes important. All coagulation factors except VIII are made exclusively in hepatocytes Consult with internist for high risk patients Liver biopsy is the gold standard to determine amount of liver disease, but is an invasive test

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Dialysis/Renal transplant patient

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The kidneys are the organs which regulate water, Na, K, and nitrogenous waste metabolism/excretion. The most common causes of kidney failure (in order) include:Diabetes mellitus (45%) HTN (28%) Other: glomerulonephritis, polycystic kidney disease, obstructive uropathy

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INDIRECT measurements of renal function:

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BUN Creatinine A measured creatinine clearance can be determined by 24 hr urine collection Direct measurement of GFR: The most accurate way to determine clearance is by injection of a radio-isotope followed by 2 subsequent blood samples to determine GFR (expensive test)

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Accepted criteria for considering dialysis include:

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Uremic syndrome, hyperkalemia, acidosis (uncontrollable with meds), bleeding diathesis, Creatinine clearance of 10 ml/min per 1.73 m^2

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Options for a patient with chronic kidney failure include:

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Peritoneal dialysis Hemodialysis Renal transplant

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Peritoneal dialysis

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1 to 3 L of dextrose-containing fluid is infused into the peritoneal cavity and left for 2 to 4h. Absorption of solutes and water from the body relies on diffusion from the body into the dialysate.

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Hemodialysis:

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The passing of blood across a semipermeable membrane which allows metabolic waste to travel down a concentration gradient into the dialysate. Usually performed 3x/wk Patients on long term hemodialysis have a surgically-created AV fistula established (usually in the antecubital fossa)

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OMFS keys for hemodialysis patients:

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NO BP cuff on the arm with the fistula. Heparin is required to "thin" the blood on the day of dialysis. Perform surgery the morning following dialysis Clotting efficiency is greatly reduced in uremic patients Consider antibiotics for protection of the fistula (especially when recently created) Caution with renally cleared drugs (PCN) May be added in with dialysate by the nephrologist Consult with nephrologist advised

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Kidney transplant

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The transplantation of a donor kidney improves life for the recipient, but requires immunosupression to prevent rejection of the kidney OMFS concerns: Consider consult with nephrologist. Lab testing to determine kidney function (especially when renally-cleared medications are needed) Higher rate of cancer in patients on long-term immune suppressive drugs

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CVA

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A "stroke" occurs when blood flow to the brain is damaged Classifications include: Ischemic Hemorrhagic

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Ischemic stroke subclassifications

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Thrombotic stroke: A clot forms in an artery that is already narrow Embolic: A clot breaks free from another area in the body, then travels to the brain vasculature and occludes the vessel Atrial Fib is one of the more common culprits of an embolic stroke These patients are often on Coumadin (goal INR of 2.0-3.0). Continue Coumadin perioperatively to decrease risk of stroke.

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Hemorrhagic stroke:

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A vessel weakens, then ruptures and causes brain damage, often due to AVM or aneurysm

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Eating disorder - anorexia/bulimia

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Anorexia Nervosa: An eating disorder characterized by the fear of gaining weight Patients become obsessed with calorie intake and self-starvation Clinical characteristics: Mild normochromic, normocytic anemia Leucopenia Dehydration Elevated BUN and Cr Can develop cardiac abnormalities such as prolonged QT

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Bulimia Nervosa:

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Eating disorder in which the patient binge eats, then self-induces vomiting or use of laxatives Features: Erosion of the lingual surfaces of teeth Repeated vomiting à alkalosis Repeated use of laxativesàmild metabolic acidosis Esophageal tears (rare) Some type I diabetics with BN have been known to not take their insulin High risk of DKA/electrolyte abnormalities

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The Dementias

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Dementia results from disorders of cerebral neural circuits. It is the result of the total quantity of neuronal loss + the specific location of the loss. Memory is the most common cognitive ability lost with dementia

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Alzheimer's disease

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The most common cause of dementia AD begins with forgetfulness and progresses. As the disease progresses, delusions and loss of language skills are common. Some patients are aware of their disease process; others are defiant Pathology: Hippocampus, temporal cortex, and lateral septum are affected. Histologically: Neurotic plaques occur in these areas MRI: See reduction in the brain volume in the affected areas

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HIV/AIDS

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HIV is an RNA virus which infects CD4+ T-cells. Once the T cell is infected, reverse transcription of its RNA genome to double-stranded DNA is accomplished by the enzyme reverse transcriptase. The DNA then translocates to the nucleus and ins integrated into host cell chromosomes by the enzyme integrase AIDS: The point at which a HIV-infected individual has a CD4+ T cell count of <200/microLiter The risk of transmission to a surgeon following skin puncture is quite low and is around 0.3%. The risk is slightly higher with hypodermic needle stick. Risk of hepatitis transmission is much higher.

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Systemic Lupus Erythematosus

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SLE: an autoimmune disease in which cells, tissues, and organs are damaged by tissue-binding autoantibodies and immune complexes. Susceptible genes and environmental factors result in abnormal/hypersensitivity responses in T and B lymphocytes. 90% are females of childbearing age. Prevalence is 15-50:100,000. African Americans are the most commonly affected ethnicity. The pathogenic autoantibodies and formation of immune complexes bind to tissues and result in Sequestration and destruction of Ig-coated circulating cells Fixation of complement proteins Release of destructive enzymes into tissues. Disease manifestations: Nephritis: The most serious complication of SLE Evaluate renal function prior to surgery Vascular occlusions Increased risk of TIA, CVA, MI Pulmonary Pleuritis, interstitial inflammation/fibrosis Pericarditis Hematologic Anemia GI N/V, diarrhea Treatment is aimed at: Suppressing the autoimmunity with steroids and cytotoxic drugs.

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Breast cancer

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A hormone-dependent (estrogen) malignancy of epithelial cells ling the ducts or lobules of the breast. 2nd most common cancer in women (Skin ca = #1) F:M ratio is 150:1

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Breast CA tx

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Treatment of cancer with antineoplastic drug(s) in a standardized fashion with the goal of cure, remission, or reduction of size of the tumor. Types of chemotherapy Neoadjuvant chemotherapy: Chemotherapy given as initial treatment (after biopsy confirmation of cancer) in an effort to reduce the magnitude of surgery and/or radiation and to make it more effective Adjuvant chemotherapy: (postoperative treatment) Chemotherapy used after surgical treatment of the tumor, but risk of recurrence exists. Palliative chemotherapy: Chemotherapy used to reduce tumor size and improve patient comfort without the goal of cure. Induction Chemotherapy: The use of chemotherapy as the initial treatment for a cancer that cannot be treated by other means

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Malignant hyperthermia (MH)

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Dantrolene sodium is a postsynaptic muscle relaxant that lessens excitation-contraction coupling in muscle cells. It achieves this by inhibiting Ca2+ ions release from sarcoplasmic reticulum stores by antagonizing ryanodine receptors.[1]

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G6PD deficiency

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X-linked recessive disorder with abnormally low level of glucose 6 phosphate dihydragenase. Leads to RBC hemolysis and eventually anemia. Symptoms: most show no symptoms Jaundice Hemolytic response after certain foods - FAVA beans Drugs can cause hemolysis - anti malaria drugs and sulfa antibiotics Who gets it: middle eastern and Kurdish, artificial protection against Malaria Diagnosis: jaundice and fits the heritage Tests : Emty RBC = Heinz bodies CBC left pt/ptt Will have a very high reticulocyte count - new RBC are being being pumped out Rule out other causes of Jaundice Classificatoin; 1-5 based on severity Treatment : avoidance of foods that cause it : FAVA Beans, Stress Transfusion and splenectomy

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POTS

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Postural Orthostatic Tachycardia Syndrome Autonomic disorder of increase in heart rate of at least 30 bpm on standing without any signifant change in blood pressure. The problem is lack of return of venous blood to the heart Who's gets: sudden abrupt onset in otherwise healthy individuals, maybe autoimmune or after a major surgery Symptoms: flushing redness, nausea ,palpitations, headaches Treatment: Propranolol,increase salt diet, Clonodine

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