Medicine Flashcards

Question

Cirrhosis

Answer 1

Many etiologies that lead to hepatic inflammation and fibrosis leading to liver cirrhosis and liver failure. Patients are no longer able to synthesize coagulation factors and metabolize toxins. - Fibrosis leads to intrahepatic blood flow resistance: portal hypertension (gastroesophageal varices, ascites, hypersplenism) - Third spacing fluid in peritoneal cavity - Hepatorenal syndrome Treatment: - Avoid ETOH - Calorie rich diet - HAV, HBV, pneumococcal, influenza vaccines - Ascites/edem: spironolactone and furosemide -TIPS -Hepatic encephalopathy: Lactulose to decrease systemic ammonia levels

Answer 2

Discussion with hepatologist MELD- 90 day mortality - Sodium - INR - Bilirubin - Creatinine Child-Pugh (CTP)- 2 year mortality - Albumin - Bilirubin - PT/INR - Ascites - Hepatic encephalopathy A,B,C A and B can be surgical candidates with pre-op optimization of encephalopathy and coagulopathy C- NO go Assess - O2 saturation: hepatopulmonary syndrome - CBC: anemia, leukopenia, thrombocytopenia - LFT: Albumin, PT/INR, biliary system dysfunction (Hepatic transaminases and bilirubin) - FFP, factor VIIA, or Vitamin K - Intranasal desmopressin (increase in Vfw, Factor 8 and plasminogen activator -CBC, Coagulation studies, CMP - Serum albumin, prealbumin, triglycerides and nutrition consult - Limited LA especially bupivicaine - Midazolam is prolonged -

Answer 3

Persistently elevated arterial blood pressure of 130/80 or higher in adults. - Diagnosis: 2 elevated reading of at least 130/80mmHg on 2 visits - Normotension: <120/80 - Elevated: 120-129/80 - Stage 1: 130-139/80-89 - Stage 2: 140-149/90 Essential HTN no identifiable cause - Decreased vascular response to vasodilation - Renal defect leading to retention of salt - Increase in sympathetic tone - Increased angiotensin II and renin secretion Risk factors: - Obesity - Smoking - Age - Diabetes - OSA - Family history - Males Secondary hypertension - Pheochromocytoma - Renal artery stenosis - Coarctation of the aorta - Pregnancy - Hyperaldosteronism End Organ damage: - Left ventricular hypertrophy - Ischemic heart disease - CHF - Renal insufficency - CVA - Retinopathy - PVD

Answer 4

CCB- decrease influx of calcium ions leading to vasodilation (amlodipine, felodipine, dilitzem, verapamil)

Answer 5

ACE inhibitors- block conversion of angiotensin I to II. AII is vasoconstrictor and aldosterone release. (lisinopril, enalapril)

Answer 6

Angiotensin II receptor blockers decrease the actions of AII leading to vasodilation and decrease aldosterone secretion (losartan, valsartan)

Answer 7

B-Blockers block b-adrenergic receptor response leading to decreased myocardial contractility, renin production, and relaxation of smooth muscles.

Answer 8

Thiazid diuretics block reabsorption of NACL in the distal convoluted tubule leading to contracted intravascular volume (HCTZ, chlorthalidone)

Answer 9

Vasodilator decreasing vascular smooth muscle tone (sodium nitroprusside, hydrazine)

Answer 10

A2 adrenergic agonist that lead to decrease NE release

Answer 11

- Labs to r/o end organ damage: BUN, creatinine, EKG, CBC - Limit epi 0.4mg Epinephine - Anxiolysis - Avoid ketamine - EMS for 180/120 with EOD: Myocardial ischemia, bradycardia, hypertension encephalopathy, dyspnea, CP, confusion, headache, seizures, PE)

Answer 12

Reduction of ventricular filling or ejection of blood to the systemic circulation. It is by definition a failure to meet the systemic demands of circulation. Non-ischemic vs ischemic Symptoms: dyspnea, fatigue, orthopnea, paroxysmal nocturnal dyspnea, edema, chest pain and palpitations. Findings: Increased BNP, JVD, S3 gallop, extermity edema, hepatojugular reflex HFwPEF >60% ejection fraction HFwREF<40% ejection fraction Treatments: Beta blockers Spironolactone Thiazide diuretics Ace Inhibitors NY HF Classification 1: symptoms with more than normal activity 2 symptoms with normal activity 3 symptoms with minimal activity 4: symptoms at rest Workup- EKG, CXR (pulmonary edema), Echo (wall function, EF and valvular dx)

Answer 13

No. 11 Scalpel Bougie Tracheal hook Curved Hemostat / Trousseau Dialator 6.0 cuffed endotracheal tube 4,6 Shirley 10ml syringe

Answer 14

1. Palpate the Cricothyroid membrane and stabilize the thyroid cartilage 2. Horizontal incision through skin, subq and membrane 3. Tracheal hook to elevate cricoid cartilage 4. Insert 6.0 endotracheal tube, confirm placement by affirming ETcO2, listen to breath sounds and absence of gastric sounds

Answer 15

1. 16-18g in kids 2. 14-16g in adults 15L/min and cut hole in the side of the oxygen tube, apply oxygen for 1s or 5s. 30-45minutes of oxygenation. Limited by co2 accumulation and glottis obstruction.

Answer 16

Harding of the arteries due to lipid accumulation within the arterial wall. Causes: Genetics HLD- LDLs Smoking: Oxidation of LDL, endothelial damage and platelet adhesiveness HTN: Damages endothelium leading increase permeability to lipoproteins DM- glycoslation of lipoproteins Estrogen- Increases HDL, lowers LDL Patho: Damage to endothelium, lipoproteins into intima along with leukocytes. Macrophages take up LDL to form foam cells, from smooth muscle cells ECM add bulk and form bulky cap that can rupture to ACS Risks: Embolization of plaque, weakening of vessel forms aneurysm, PVD, Renal artery stenosis, MI

Answer 17

Stenotic coronary arteries leading to myocardial oxygen supply/demand imbalance. Myocardial oxygen demand determined by wall stress, HR and contractility.

Answer 18

Transient chest pain due to fixed atherosclerosis plaque leading to oxygen supply/demand imbalance. Symptoms: CP, dyspnea on exertion, Levine's sign, appear at 70% stenosis. Workup- EKG (st depression or T wave inversion), stress testing, Echocardiogram (wall function, EF and valve function), coronary angiography

Answer 19

Acute Coronary Syndrome Disease process with continuum secondary to ruptured atherosclerosis plaque causing coronary thrombus - Unstable angina - Non-St segment elevation MI - ST segment elevation MI

Answer 20

Partially occlusive coronary thrombus, relieved by rest with ischemic changes of EKG w/o elevated cardiac enzymes

Answer 21

Non- ST segment elevation MI Partially occlusive coronary thrombus causing subendocardial infarction. CP, nausea, dyspnea, diaphoresis. EKG ST depression or T wave inversion. Elevated troponin and CK-MB (Short term early marker).

Answer 22

ST segment elevation MI Occlusive thrombus with transmural defect. CP, nausea, dyspnea, diaphoresis. EKG St elevation and serum biomarkers

Answer 23

Nitrates- Venodialation- decrease after load and dilates coronary arteries B-blocker, CCB- decrease O2 demand PCI- Ballon tipped catheter, DES- more thrombogenic (Anti-platelet drug), prevents epitelialzation CABG- Coronary artery bypass grafting, multi vessel disease

Answer 24

M- Morphine O- Oxygen N- Nitrates (0.4mg nitroglycerin, unto three doses)- coronary artery dilation A- Aspirin (325mg non-enteric coated)- depletes platelet aggregation B-blockers- Decrease 02 demand Hospital transfer (PCI or fibrinolytic)

Answer 25

Causes venodialation which decreases preload (wall stress) and dilates coronary arteries.

Answer 26

Reversible ADP receptor inhibitor, decrease ADP activation of platelet aggregation

Answer 27

HMG Coa reductase inhibitor that decreases circulating LDL, decreases atheroma formation

Answer 28

1. Assess METs 2. Anxiolysis 3. Supplemetal 02 4. Profound analgesia 5. Avoid hypotension 6. Avoid sympathomimetic drugs (Ketamine) 7. Limited cardiovascular depressants (Propofol) 8. Cardiologist risk stratification 9. EKG monitor 10. HR/Bp w/n 20% of baseline

Answer 29

Left sided back flow through the mitral valve due to increase valve orifice during systole. Increased left atrial pressure, decrease SV. Can lead to pulmonary congestion, LV hypertrophy, afib. Acute disease can lead to pulmonary edema and cariogenic shock. Symptoms: Initially asymptomatic, progressive disease- dyspnea on exertion, fatigue, orthopnea, cough, palpitations, holosystolic blowing murmur and fib. Workup: EKG, CXR, Echo Txt: ACEi, B blockers, pacing or valve replacement

Answer 30

Prolapse of valve leaflets into the atrium during systole. Risk factors include Marfan's dx, Ehlers-Danlos, RHD, SLE. Can result in cerebral embolic events, IE, sudden death. Symptoms: Dyspnea, fatigue, anxiety, orthostatic hypotension, mid systolic click, dysrhythmias Workup: EKG, MRI, Echo Txt: B Blockers, SSRIs, mitral valve repair

Answer 31

Decrease aortic valve area leading to decreased CO and increase left ventricular pressures. Risks- Congenitial unicuspid or bicuspid valve, HLD, smoking, RHD, endocarditis, Notch 1 gene. Symptoms develop as heart starts to decompensate, cardiac demand outstrips supply. Symptoms: Dyspnea, fatigue, syncope, angina, sudden death, left sided heart failure, crescendo-decrescendo systolic murmur Workup: EKG (afib and LV hyper), CXR, echo Txt: Asymptomatic- blood pressure and HLD control, Symptomatic- Valve replacement (SAVR- Open, TAVR- Transcatheter) Bioprosthetic- 3-6M of anticoagulation Mechanical- lifelong anticoagulation, warfarin, antiplatlet therapy as well.

Answer 32

Backflow across the aortic valve during diastole, leaflet abnormalities from IE, RHD, cancer drugs. Marfan's ED, RA, AK, psoriatic arthritis. Pressure overload and decreased CO. Decrescendo high-pitched murmur

Answer 33

Cardiologist consultation Be aware of anticoagulation Risk of infective endocarditis Mitral stenosis- Avoid excess fluid, avoid ketamine, decrease afterload Mitral Regurgitation- Normal to elevated HR, avoid HTN Aortic stenosis- No hypotension, NSR, avoid ket/prop Aortic regurgitation- Keep HR up, normotensive

Answer 34

Lifelong immune suppression Tacrolimus- Nephrotoxic,neurotoxic Mycophenolate- Leukopenia Rapamycin- Myelosuppression Cyclosporine- Gingiva hyperplasia, hyperkalemia Prednisone- Corticosteroid Physiologic changes: Cardia denervation- No parasympathetic tone (Resting HR 90-100BPM), sympathetic response by catecholamines (Slow) Mush use direct acting drugs- Catecholamines, bblobkers, are effective Management: Look for fluid overload, peripheral edema, CXR, Echo, EKG, Renal function,

Answer 35

Differential growth of roots Arch length discrepancies Ectopic position Late mineralization Less attrition

Answer 36

Radiographic classification of third molar impaction: ABC: Compared to occlusal plane of 2nd molar 123: Compared to anterior ramus boarder Winters: Degree of impaction Mesioangular Vertical Horizontal Distoangular Inverted

Answer 37

Pericoronitis Orthdontic reasons Orthognathic sx Caries Pain Pathology Fracture Overlying prothesis Periodontal disease

Answer 38

General: Distress or anxiety TMJ: Clicking, popping, or pain MIO: Mandible position: TMD: Mandibular protrusion: Neck size and mobility: Dental: Tongue size and position: Mallampati: Brodsky:

Answer 39

Darkening of root Deflection of the root Narrowing of the root Bifid root apex Diversion of canal Narrowing of canal Interruption of white line

Answer 40

I will administer local anesthetic with vasoconstrictor as b/l IAN and buccal block, PSA, GPNB. #15 blade used to make sulcular incision at the distal aspect of the second molar a distobuccal release is created. FTMP flap laid. A fissure burr with copious irrigation used to make a buccal trough and partially section the tooth. Sectioning completed with elevators. The individual sections are removed with forceps. The socket is curvetted of debris and follicle. A bone file is then used to smooth the osteotomy. Site is irrigated with saline and the flap is re-appoximated with 3-0 CGS.

Answer 41

Gelatin made from purified porcine skin forms a blood clot matrix - Can form granuloma

Answer 42

Microfibrillar bovine collagen aggregates platelets and form blood clot matrix

Answer 43

Oxidized regenerated methyl cellulose binds platelets, is bacteriostatic and precipitates fibrin - low ph is neurotoxic

Answer 44

Activated bovine prothrombin activates factor IIa. Serine protease converting fibrinogen to fibrin. Promotes clot formation

Answer 45

gelatin granules and human thrombin

Answer 46

Vasoconstrictor

Answer 47

Stabilizes clot by inhibiting plasmin

Answer 48

Antifibrinolytic, inhibits conversion of plasminogen to plasmin

Answer 49

1. Suction out sinus 2. Iodoform gauze 3. Ask patient to blow nose 4. Antral lavage 5. Caldwell luc (>3mm with infection)

Answer 50

Arterial occlusion/venous congestion Flap Color (pale/cyanotic) Capillary refill (sluggish/brisk) Tissue turgor (decreased/increased) Temperature (cool/cool) Pinprick test (scant dark blood/rapid bleeding) Doppler signals

Answer 51

Heimleich maneuver Deepen anesthesia and attempt to remove with Magill forceps. Cord pressure. If no respiratory distress, assume ingested. Abdominal and CXR to confirm position and clearance

Answer 52

1. If emesis is observed and aspiration suspected than activate EMS 2. Place patient in Trendelenberg position and right lateral (Right bronchus and right fungus of stomach) 3. Suction out the oral contents 4. Apply 100% O2, watch for respiratory distress. 5. Look for possible bronchospasm or laryngospasm 6. Consider intubation, EMS transfer

Answer 53

1. Pack off surgical sites and suction out the oral contents with Yankauer. 2. Reposition the patient, chin tilt and jaw thrust, tongue protraction 3. No breathing than apply PPV via BVM 4. No break than deepen the anesthetic with hypnotic agent (Propofol) 5. No break than administer succinylcholine 0.1mg/kg to break spasm 6. No break than administer succinylcholine 1-2mg/kg and atropine 0.5mg (IM suc is 4mg/kg) or rocuronium 0.6 to 1.2mg/kg 7. Intubate the patient or manually ventilate

Answer 54

Protective mechanism of larynx muscles causing adduction of the vocal cords. It is caused by upper airway stimulation from saliva, blood, aspirate or solid material entering the trachea. Can be partial (high pitched stridor) or complete with no sounds.

Answer 55

Reflex bronchiolar smooth muscle constriction and increase in mucous production. Can be centrally or locally mediated by airway irritant. Risk factors include asthma, analphylaxsis, aspiration, recent URI, exposure to airway irritants (Smoking, allergens or weather changes), GERD. Symptoms include wheezing and increased airway resistance.

Answer 56

1. Hypoxia, wheezing or respiratory distress than delivery 100% O2 and activate EMS 2. If awake albuterol via face mask (Mild) 3. Epinephrine 0.3-0.5mg subq 1:1000 4. Suspect anaphylactic- Epi 10-20ug IV 5. If worsening hypoxia- deepen the anesthetic and intubate 6. Albuterol via ET tube 7. Be prepared for hypertension and arrhythmias 8. In awake patient monitor for respiratory distress and intubate to maintain oxygenation and ventilation as muscle tire.1s

Answer 57

Autosomal dominant mutation of the ryanodine receptor 1 gene that causes a hyper metabolic state upon exposure to inhalation anesthetics and depolarizing muscle relaxants. Sustained release of calcium from the sarcoplasic reticulum.

Answer 58

1. Hypercarbia (>55 hg) 2. Tachycardia 3. Tachypnea 4. Massester muscle rigidity 5. ECG changes 6. Hyperthermia

Answer 59

Hyperkalemia Cardiac arrhythmias Metabolic acidosis Myoglobinuria Acute renal failure Coagulapathy (DIC)

Answer 60

1. MH 2. Sepsis 3. Stimulants 4. Thyroid storm 5. Serotonin syndrome 6. Neurolepic malignant syndrome 7. Pheochromocytoma

Answer 61

1. Notify EMS and call MH hotline 2. D/c triggering substance and hyperventilate with 100% O2 3. IV Dantrolene 2.5mg/kg, every 5 mins (max is 10mg/kg) 4. Sodium Bicarbonate 1 mEq/Kg 5. Cooling with cold saline, gastric lavage and ice application 6. Blood gas determine metabolic acidosis 7. Correct hyperkalemia >5.9 8. IV push insulin with 50% dextrose 9. Calcium chloride for wide QRS 10. Monitor (UOP, temp, blood gas, BMP, CK, coags

Answer 62

Cardiac- ACS, stable angina, aortic dissection, pericarditis Pulmonary- PE, pneumothorax GI- GERD, esophageal spasm, gastritis Musculoskeletal- costochondritis Psychiatric- Anxiety

Answer 63

Esmolol - b1 selective b blocker 1mg/kg over 30s, then 150ug/kg/min and increase by 50ug (max 300ug/kg/min) Labetalol- a1,b1,b2 blocker 20mg over 2 mins, repeat every 10ming (max 300mg) Hydralazine- Vasodilator (Relex tachycardia) 10-20mg every 2 to 4 hours

Answer 64

End organ symptoms - Chest pain - Headaches - Visual disturbances - Altered mental status - ECG changes

Answer 65

BS <50mg/dl adults BS <40mg/dl Peds Increased sympathetic response, neuroglycopenia - Diaphoresis - Tremors - Anxiety - Increased BP - tachycardia and palpitations - irritability - Confusion - weakness - drowsiness - Seizures - Coma

Answer 66

- Speak with PCP - Half nighttime glargine (Long acting) - Hold sulfonylureas and NPH morning of - Preop BS between 100 to 200mg/dl - <150mg/dl use 5% Dextrose in water (D5W) - >150mg use NS No IV access then Oral glucose, or IM glucagon 0.5 to 1mg IM/SC If BS falls <70mg/dl then give 15g of IV glucose (10ml of 50% dextrose), 1ml of 50% dextrose will raise BS by 2mg/dl

Answer 67

Stimulate glyconeolysis Glycogen to glucose in liver 0.5 to 1mg/dl IM/SC

Answer 68

Essentially IV Glucose 30ml of %50 dextrose = 15g glucose 1ml of %50 raises BS by 2mg/dl Given 30ml

Answer 69

Acute, potentially fatal, multi-organ system event caused by sudden degranulation of mediators from mast cells and basophils. Immunoglobulin E (IgE) and IgE independent (anaphylactoid) forms (no clinical difference). -Mediators Histamine Leukotrienes Kinins Platlete activating factor -Symptoms: Vasodilation Bronchoconstriction Airway edema and mucous production Vascular permeability -Usually two systems (Skin and airway most common) Findings: - Uticaria - Puritis - angioedema - bronchospasm and stridor (Laryngel edema) - cardiovascular collapse (distributive shock) - Hypotension, CP, syncope Triggers - Antibiotics (b-lactam) - propofol (Egg/soy) - NSAIDs - Local anesthetics (metabisulfite preservative)

Answer 70

1. Recognition 2. Stop drug drip if present 3. Activate EMS 3. IV fluids NS 500ml/hr 4. Oxygen 2L/min NS 5. Epinephrine (B2 and a1 activity) - Bronchodilate and vasoconstrictor - Prompt and liberal use - 0.2 to 0.5mg 1:1,000 in thigh - Peds 0.01mg/kg and repeat every 3 mins 6. IV Epi (1mg in 1000ml) at 1ml/min titrate to blood pressure or IV bolus 0.3 to 0.5mg of 1:10,000 epi 100ug/ml 7. Albuterol 8. IV diphenhydramine (H1 blocker) 50mg (12-64 yoa), or 25mg (>65, or <12yoa) IV 2-5min 9. Dexamethasone 10mg

Answer 71

1. Stop drug drip 2. Monitor for respiratory or cardiovascular 3. NS 500ml/hr 4. Diphenhydramine (h1 blocker) 50mg (12-64yoa), or 25mg (<12 and >65yoa) 5. Dexamethasone 10mg

Answer 72

Chronic neurodegenerative disease characterized by progressive congnitive impairment as well as memory loss, apraxia, aphasia and agnosia. Caused by decreased acetylcholine, extracellular amyloid deposits and tau protein abnormalities with consequent neurofibrillary tangles. Patient are typically managed on cholinesterase inhibitors. Manament: - Maintain patience and reorient the patient as needed - Have family or caregivers present to help - Reduced medication dosing - avoid anticholinergics (No atropine, chlorpromazine) glycopyrollate OK as it does not cross BBB

Answer 73

Chronic neurodegenerative disease characterized by extrapyramidal motor system activity and unopposed stimulation by acetylcholine. Cause it loss of dopaminergic fibers in the basal ganglia. Patient present with skeletal muscle tremor, lead pipe rigidity, bradykinesia, instability. Patients are managed on dopamine agonists like levodopa. Management: - Continue llevadora - Avoid antidopaminergic drugs (metoclopramide) - No ketamine as increased sympathetic response - Excessive salivation

Answer 74

CNS disorder of demyelination, thought to be autoimmune. Symptoms depend on location of lesions but can include sensory disturbances, motor weakness or vision changes. Patterns of progression include Relapsing-remitting, primary progressive, secondary progressive, progressive relapsing. Patients are typically managed steroids to manage progression. Management: - Defer elective surgery during relapse - Consent must speak of potential for triggering relapse - Demyelinated fibers are sensitive to temperature increases

Answer 75

Sudden neurological deficit from ischemia or hemorrhage. Risk factors include HTN, DM, obesity, HLD, contraceptive use and smoking. Hypertension is primary risk factor. Warning signs include unilateral numbness, confusion, loss of balance, unilateral vision loss and severe headache. Management: - Medical emergency - Ischemic stroke- IV tissue thromboplastin activator, normalize BP, normothermia, antithrombotic therapy and DVT prophylaxis, no oral intake and maintain normoglycemia - Hemorrhagic stroke- Reverse and cease anticoagulants, target MAP to normalize ICP, decrease ICP HOB elevated and hyperventilation, no oral intake, DVT prophylaxis Office management: - ASA II: Stroke >6M ago and no deficit - ASA III: Stroke >6M ago and minor deficit - ASA IV: Stroke <6M or major deficit - Consider consult with PCP - Avoid hypertension, avoid hypotension, monitor VS, stress reduction (Anxiolytics, analgesics)

Answer 76

Paroxysmal alteration in neurological activity caused by synchronous, rhythmic depolarization of brain cortical neurons. Can be epileptic (Partial or generalized). Generalized or simple (NLOC), non convulsive or convulsive. Multiple causes include overdose, discontinuation or anti-epileptic meds, ETOH withdraw, electrolyte abnormalities, fever, neoplasms or idiopathic. Managed on anti epileptic meds including pregabalin, lamotrigine, topiramate and levetiracetam. Management: -Hospital management for: Recent or questionable seizure hx, hx of status epileptics, drug changes, or vagal NS - Limit lidocaine as OD - Flumazenil can induce seizure, ketamine at sedation doses raised the threshold, propofol raises the threshold - Maintain normoglycemia - Status: Seizure lasting >5min (Benzos or propofol)

Answer 77

Response to name Light- Slow but appropriate Medium- Possible response to verbal stimuli Deep- No response to verbal stimuli GA- No response to verbal stimuli Response to pain Light/moderate- Expected response Deep- Delayed or no response to pain GA- No response to pain Lash reflex

Answer 78

Stage 1- Analgeisa to amnesia: Beginning to LOC Stage 2- Excitation: LOC to autonomic breathing, lash reflex is lost but others remain (Coughing, vommiting), regular to irregular beathing (breath holding) Stage 3- Onset of autonomic breathing to cessation of breathing Stage 4- Cessation of breathing to death

Answer 79

Endosseous threaded implant Material - Pure grade 4 titanium Surface- TiUnite (Thick oxidized titanium TiO2) Lengths- 8.5,10,11.5,13,15,18mm Widths- 3.0,3.5,4.3,5.0,5.5 Platforms- 3.0, NP, RP, WP Insertion torque of 35ncm, angulations up to 45% Coverscrew is titanium alloy (Titanium, aluminum and vanadium) Drills: -1.5 -2.0 -2.4/2.8 -2.8/3.2 -3.2/3.6 -3.8/4.2 -4.2/4.6 -4.2/5.0 Never exceed 70ncm or 45ncm for 3.0

Answer 80

Straight walled external hex end osseous threaded implant Material- Pure grade 4 titanium Surface- TiUnite (Thick oxidized titanium) Lengths- 30-50mm Widths- 4.4mm Drills (Round burr, 2.9,3.5,4.0,4.4 twist drills) 20:1 handpiece max 2,000 RPM Ideal 35-40nCM Multi-unit abutments- 45/60

Answer 81

Straight-35ncm 17/30- 15ncm 45/60- 35ncm 1.5,2.5,3.5,4.5mm heights

Answer 82

Straight-35ncm 17/30- 15ncm 45/60- 35ncm 1.5,2.5,3.5,4.5mm heights

Answer 83

Progressive muscle weakness caused by autoimmune type II, Bcells target nicotine ACH receptors on the muscle endplate and block transduction. Also, activated complement destroys the end plate receptors. Patients complain of muscle weakness with use, diplopia and ptosis. Bimodal patient distribution- young women 20-30 and old men 60-70 Txt- Acetylcholinesterase inhibitors (neostigmine and physostigmine) Chronic corticosteroids And Thymus gland removal (block h-t cells) Crisis- muscles of respiration Anesthesia- resistant to depolarizing muscle relaxants, very sensitive to NDMA. Use smaller doses of medications and prefer short acting med.

Answer 84

Tension test: MC- Patient not taking meds, stess or infection. Severe lack of ACH causes muscle weakness and respiratory distress. - mysriasis, high BP and HR, urinary incontinence. CC- Overdose on meds Severe muscle weakness from over activation,l and respiratory distress. - low BP, Low HR, miosis and SLUDGE Tensilon test- edrophonium (antipseudochlineesterase inhib) Makes CC worse- negative Treatment- atropine, hold other meds Makes MC better- positive Treatment (neostigmine)

Answer 85

Why you do an enucleation Bilateral granulmatomus uveitis

Answer 86

Reduced insulin production and reduced cellular insulin sensitivity leads to hyperglycemia.

Answer 87

Micro vascular: Retinopathy Neuropathy Nephropathy Macrovascular: Neuro vascular changes Coronary vascular changes Peripheral vascular changes Path- increased atherosclerosis, and vessel inflammation from reactive oxygen species creation.

Answer 88

1. Hypertension increases afferent arteriole pressure 2. Activation of RAS due to hyperglycemia leads to efferent construction Both cause mesangial expansion (inflammation ROS and damage to the glomerulus and permeability 3. Due to efferent arteriole constriction, lack of blood flow to the kidney causing ischemia

Answer 89

1. Small cell 2. Non-small cell 3. Adenocarcinoma 4. Squamous cell carcinoma 5. Large cell carcinoma 6. Carcinoid

Answer 90

-Anaphylactic- IgE mediated type 1 hypersensitivity (mast cells and basophills) Anaphylactic shock -Acute hemolytic transfusion reaction- type II hypersensitive due to ABO mismatch leading to plasma cell production of antibodies- fever, dyspnea, cough, tachypnea, jaundice, proteinuria and AKI (w/in 24 hours) - Delayed hemolytic transfusion reaction- type II hypersensitivity to RH factor Mild symptoms- fever and jaundice - TRALI- transfusion related acute lung injury: two hit model 1. Pulmonary lymphocytes and leukocytes are primed due to stressors 2. Transfusion causes antigen Quick pulmonary edema and hypotension - TACO transfusion associated cardiovascular overload (In CHF and CKD patients)

Answer 91

1. Micrognathia 2. Glossoptosis 3. U shape cleft palate Can be part of syndrome Txt- Prone sleeping Upright feeding Glossopexy DO

Answer 92

Failure of fusion of median nasal process and maxillary processes around week 7 More common in boys, left side 1:1000 Rule of 10s form primary lip (10lbs, 10 weeks, 10mg hgb) Cleft palate at 6 to 12 M VPI and pharyngeal flap at 5yoa Alveolar cleft at 7-9, 2/3 canine development. Cleft Orthognathic

Answer 93

1. Push hard 1/3 of chest diameter at 100-120BPM and allow complete chest recoil 2. Minimize interruptions 3. Avoid excessive ventilation 4. Rotate compressor every 2 min 5. 15:2 compression to ventilation

Answer 94

1st- 2J/kg 2nd- 4J/kg 3rd- 10J/kg

Answer 95

0.01mg/kg 1:10,000 IV/IO 0.1mg/kg 1:1,000 ET

Answer 96

5mg/kg IV/IO (Max 300mg) May repeat 2nd dose

Answer 97

50mg/kg IV/IO Max 2g

Answer 98

Attention deficit hyperactivity disorder Neuro developmental disorder that starts between 6-12 - inattentive (lack of attention) - hyperactivity and impulsiveness Environmental and genetics factors- exact cause unknown Dopamine and norepinephrine- lower amounts might contribute Txt- Behavioral psychotherapy- time management and behavioral skills Stimulants- increase NTs - amphetamines - slow release of dopamine vs fast in illicit - dexteoamohetamine: adderal - methylphenidate: Ritalin Can have increase serotonin due to stimulants and this Serotonin syndrome

Answer 99

Type 4 hypersensitivity from activated T cells against basal cells - targetoid lesions :erythema with central necrosis - Intra and sub epithelial vessicles Minor- due to prior infection Starts with lesions on palms and soles that spreads to chest, no mucosal involvement Major- 2 or more moucosal sites (skin, oral and eyes. Painful ulcerations, hemorrhagagoc crusting of the lips - preceding mycoplasma or herpes simple viral infection preceding (type 1 oral herpes most common) or from antibiotics or anticonvulsants Steven Johnson and TEN- due to drugs not infections: More severe and more sites Txt- IV rehydration Treat infection Stop meds Steroids Largely self limiting Acyclovir can help with recurrent herpes

Answer 100

Inflammatory disease caused by urate crystals deposits (hyperuricimeia) - hyperuric acids - Uric acids from breakdown of purines - risk factors are increased production of purines (males, older, obesity, ETOH, shellfish and red meat) or genes - CKD or dehydration can lead to uricemia - 1st metatarsal joint- podagra (big toe on fire), can last days - tophi- chronic gout (gouty kidney stone) DG- joint aspiration to detect urate crystals TX- NSAIDS, colchicine Allopurinol- xanthine reduxtase

Answer 101

1. Primary hemostasis- primary plug 2. Secondary hemostasis- clotting factors to form fibrin plug Thrombotics- fibrinolytics Fibribolysis- plasminogen to plasmin via TPA tissue plasminogen activator Protease to cut fibrin TPA vs streptokinase Increase PT and PTT, platlet time remains the same Treat- MIs, DVT, PE and ischemia strokes 12hrs for MI 3-4 for stroke