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OMFS Medicine > Medicine > Flashcards

Medicine Flashcards

1
Q

Moderate Sedation

A

drug-induced depression of consciousness
during which patients respond purposefully
to verbal commands, either alone or
accompanied by light tactile stimulation.
No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually
maintained.

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2
Q

Deep Sedation

A

drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully following repeated or painful stimulation. The ability to independently maintain
ventilatory function may be impaired.
Patients may require assistance in maintaining a patent airway, and spontaneous ventilation may
be inadequate. Cardiovascular function is usually maintained.

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3
Q

General Anesthesia

A

drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. The ability to maintain ventilation function is often impaired. Patients often require assistance in
maintaining a patent airway, and positive pressure ventilation may be required because of depressed spontaneous ventilation or drug induced depression of neuromuscular function. Cardiovascular function may be impaired.

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4
Q

Airway Assessment

A
  • Dental exam (Teeth, tongue, tonsils- Brodsky)
  • Maximal Incisal Opening (40mm)
  • Mallampati Classification
  • Mandibular protrusion
  • Upper lip bite test
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5
Q

Mallampati Classification

A

Predicts difficulty of intubation
Patient seated upright, NHP, with tongue protruded w/o phonation
1: Soft palate, uvula, tonsillar pillars, fauces visable
2: Superior 2/3 of uvula, and soft palate
3. 1/3 of uvula and soft palate
4. Soft palate not visible
5. BMI
6. Neck Circumference (17in)

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6
Q

Upper lip bite test

A

Grade 1- Fully covers upper lip
Grade 2- Partially covers the upper lip
Grade 3- Cannot reach the upper lip

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7
Q

BMI

A

BMI = weight Kg/height m2
Underweight: <18.5
Normal: 18.5-24.9
Overweight: 25-29.9
Obese: 30-39.9
Morbid Obesity- >40

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8
Q

MET

A

Metabolid equivalent of tasks
1 Met = O2 consumption of 70kg 40yo male at rest.
<4 Met = Shopping, slow walking
>4 Met = Housework, climbing stairs, cycling

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9
Q

ASA

A

American Society of Anesthesiology Classification
1: Healthy patient
2: Mild systemic disease w/o limitations
3: Severe systemic disease w/limited activity but not incapacitating
4: Severe systemic disease that is constant threat to life
5: Moribund patient who is not expected to survive w/o operation
6: Organ donor
E: Emergency Surgery

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10
Q

NPO

A

Clear liquids- 2 hours
Breast milk- 4 hours
Infant formula- 6 hours
Non-human mild- 6 hours
Solids (Light meals)- 6 hours
Heavy- 8 hours

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11
Q

Difficult Bag Mask

A

Facial Hair
Edentulism
>55yoa
Snoring
MIO

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12
Q

Cricothyrotomy

A

1: Extend the head and neck, identify and immobilize the cricothyroid membrane.
2: Make a horizontal incision through the skin and cricothyroid membrane
3. Use a tracheal hook to apply caudal and outward traction on the cricoid cartilage and remove the blade
4. Insert ETT (6.0 ETT or 4 Shiley)
5. Ventilate with low pressure
6. Confirm pulmonary ventilation
Convert to tracheostomy w/72 hours (subglottic stenosis)

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13
Q

Pediatric airway

A

1-10yo: Uncuffed tube= (age/4)+4
No cricothyroidtomy less than 12 you
- Large tongue
- Large occiput
- Infant are nose breathers
- Collapsible trachea
- Large tonsils/adenoids
- Larynx is higher and anterior
- Floppy posterior epiglottis
- Cricoid ring is narrowest point
- Short trachea
- HR dependent
- Horizontal ribs and less accessory muscles

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14
Q

Propofol

A

2,6-diisoprophylphenol 1%
intravenous sedative hypnotic used for induction and maintenance of anesthesia
- MOI: GABP potentiation causing depressed reticular activating system
- Soybean oil, glycerol, egg lecithin, EDTA or sodium bisulfite
- Metabolized by liver, excreted by kidney
- Direct myocardial suppression
- Profound respiratory depressant
- Adult dose: 1-2.5mg/kg
- Peds dose: 2.5-3.5mg/kg

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15
Q

Ketamine

A

Lipid-soluble derivative of phencyclidine causing dissociative anesthesia. Separates the thalamus and limbic system placing patient in cataleptic state.
- N-methyl-D-aspartate NMDA receptor antagonist
- Metabolized in liver, some active metabolites, excerpted in kidneys
- indirectly central mediated sympathetic stim
- Pschomimetic effects- salivation, LS
- 0.2-0.5mg/kg sedation
- 3-5mg/kg IM

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16
Q

Midazolam

A

1,4 Benzodiazepine sedative hypnotic
- MOI: GABA potentiation
- metabolized by liver, excreted by kidneys
- Slight cardiopulmonary depressant
- 0.1mg/kg IV Adults

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17
Q

Flumazenil

A

Benzodiazepine receptor ligand with high affinity that is a competitive antagonist with benzos.
- Initial dose: 0.2mg IV 15s
- Repeat dose: 0.2mg every minute
- Max: 1mg

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18
Q

Fentanyl (Sublimaze)

A

Narcotic agonist-analgesics of opiate receptors (mu) that inhibit ascending pain pathways.
- Metabolized by liver, excreted by kidneys
- Analgesia and sedation
- Increased nausea and vomiting
- Depresses ventilation and bradycardia
- 2mc/kg IV

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19
Q

Naloxone

A

Competitive opioid receptor antagonist at the mu receptor
- Adult dose: 0.4 to 2mg IV (2-3min 10mg)
- Pediatric dose: 0.01mg/kg upto 0.1mg/kg

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20
Q

Succinylcholine

A

Depolarizing noncompetitive agent at the cholinergic receptor
- Muscle pain, anaphylaxis, and MH
- Pretreat with atropine
- Pseudocholinesterase deficiency
- 0.3-1mg/kg IV Intubation
- 20mg IV laryngospasm
- Contraindicated in muscular dystrophy

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21
Q

Rocuronium

A

Non-depolarizing muscle relaxant at the cholinergic receptor
- Dose: 0.6-1.2mg Kg RSI
- Reversal by sugammadex (Cyclodextrin)

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22
Q

Hepatitides

A

Chronic B/C
Inflammatory mediated active hepatocellular damage and necrosis with lobular inflammatory response
Hep B: DNA virus with insidious onset
Four phases
Immune tolerant
Immune clearance
inactive HBsAg carrier
Reactivated chronic Hep B
Vertical transmission mother to fetus, percutaneous and sexual
Vaccine- Hep B immunoglobulin
Heb C: RNA virus that progresses to chronic liver disease
Percutaneous
Chronic state develops liver cirrhosis and hepatocellular carcinoma
- Harvoni: antivirals and interferons

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23
Q

Alchololic liver disease

A

Excessive alcohol intake leading to fatty liver disease, hepatitis and cirrhosis
- 5 drinks per day for 10 year
Pathophysiology- inflammation leading to parenchyma necrosis.
Treatment:
- Alcohol cessation
- Folic acid, thiamine, and zinc nutritional support

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24
Q

NASH, NAFLD

A

Nonalcoholic fatty liver disease
-metabolic syndrome
- DM2
- TPN
- Hx of gastric bypass

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25
Q

Cirrhosis

A

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

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26
Q

Liver disease anesthesia

A

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
-

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27
Q

Hypertension

A

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

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28
Q

amlodipine

A

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

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29
Q

lisinopril

A

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

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30
Q

Losartan

A

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

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31
Q

Metoprolol

A

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

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32
Q

Hydrochlorothiazide

A

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

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33
Q

Hydralazine

A

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

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34
Q

Clonidine

A

A2 adrenergic agonist that lead to decrease NE release

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35
Q

Anesthesia for hypertension

A
  • 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)
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36
Q

Congestive Heart Failure

A

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)

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37
Q

Atrial Fibrillation

A
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38
Q

Cricothyrotomy set

A

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

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39
Q

Cricothyrotomy technique

A
  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
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40
Q

Jet oxygen needle cricothyroidtomy

A
  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.
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41
Q

Atherosclerosis

A

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

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42
Q

Ischemic Heart disease

A

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

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43
Q

Stable Angina

A

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

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44
Q

ACS

A

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

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45
Q

Unstable Angina

A

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

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46
Q

NSTEMI

A

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).

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47
Q

STEMI

A

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

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48
Q

Tx of IHD

A

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

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49
Q

Tx of MI

A

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)

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50
Q

Isosorbide mononitrate

A

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

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51
Q

Clopidogrel, prasugrel

A

Reversible ADP receptor inhibitor, decrease ADP activation of platelet aggregation

52
Q

Atorvastatin

A

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

53
Q

Anesthesia management of IHD

A
  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
54
Q

Mitral Regurgitaion

A

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

55
Q

Mitral Valve Prolapse

A

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

56
Q

Aortic Stenosis

A

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.

57
Q

Aortic Regurgitaiton

A

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

58
Q

Anesthesia for valve dx

A

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

59
Q

Heart Transplant

A

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,

60
Q

Theories of tooth impaction

A

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

61
Q

Pell and Gregory vs winters

A

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

62
Q

Indications for third molar removal

A

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

63
Q

Third molar exam

A

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:

64
Q

Roods Criteria (7 signs)

A

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

65
Q

Third molar technique

A

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.

66
Q

Gelfoam

A

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

67
Q

Avitene

A

Microfibrillar bovine collagen aggregates platelets and form blood clot matrix

68
Q

Surgicel

A

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

69
Q

Thombin

A

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

70
Q

Floseal

A

gelatin granules and human thrombin

71
Q

Tanin

A

Vasoconstrictor

72
Q

Aminocaproic acid

A

Stabilizes clot by inhibiting plasmin

73
Q

Tranexamic acid 5% mouth rinse

A

Antifibrinolytic, inhibits conversion of plasminogen to plasmin

74
Q

Tooth displaced in sinus

A
  1. Suction out sinus
  2. Iodoform gauze
  3. Ask patient to blow nose
  4. Antral lavage
  5. Caldwell luc (>3mm with infection)
75
Q

Flap Monitoring

A

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

76
Q

Aspiration of Foreign body

A

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

77
Q

Emesis under anesthesia

A
  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
78
Q

Laryngospasm treatment

A
  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
79
Q

Laryngospasm

A

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.

80
Q

Bronchospasm

A

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.

81
Q

Bronchospasm treatment

A
  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
82
Q

Malignant hyperthermia

A

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.

83
Q

Signs of MH

A
  1. Hypercarbia (>55 hg)
  2. Tachycardia
  3. Tachypnea
  4. Massester muscle rigidity
  5. ECG changes
  6. Hyperthermia
84
Q

Sequelae of MH

A

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

85
Q

Differential diagnosis of MH

A
  1. MH
  2. Sepsis
  3. Stimulants
  4. Thyroid storm
  5. Serotonin syndrome
  6. Neurolepic malignant syndrome
  7. Pheochromocytoma
86
Q

Malignant Hyperthermia txt

A
  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
87
Q

Differential for CP

A

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

88
Q

Hypertension treatment

A

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

89
Q

Hypertensive Crisis

A

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

90
Q

Hypoglycemia

A

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

91
Q

Preop management of DM

A
  • 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
92
Q

Glucagon

A

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

93
Q

%50 Dextrose

A

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

94
Q

Anaphylaxsis

A

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)

95
Q

anaphylaxis treatment
with respiratory or cardiovascular symptoms

A
  1. Recognition
  2. Stop drug drip if present
  3. Activate EMS
  4. IV fluids NS 500ml/hr
  5. Oxygen 2L/min NS
  6. 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
  7. 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
  8. Albuterol
  9. IV diphenhydramine (H1 blocker) 50mg (12-64 yoa), or 25mg (>65, or <12yoa) IV 2-5min
  10. Dexamethasone 10mg
96
Q

Anaphylaxis treatment with only skin symptoms

A
  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
97
Q

Alzheimer Disease

A

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

98
Q

Parkinson Disease

A

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

99
Q

Multiple Sclerosis

A

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

100
Q

Stroke (CVA)

A

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)

101
Q

Seizure

A

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)

102
Q

How to Judge level of sedation

A

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

103
Q

Guelde’s stages of general anesthesia

A

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

104
Q

Nobel Active Series

A

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

105
Q

NobelZygoma 0 degree

A

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

106
Q

Nobel multiunit abutments

A

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

107
Q

Nobel multiunit abutments

A

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

108
Q

Myasthenia Gravis

A

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.

109
Q

Myesthenic crisis vs cholinergic crisis

A

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)

110
Q

Sympathetic opthalmopelgia

A

Why you do an enucleation
Bilateral granulmatomus uveitis

111
Q

Pathophysioogy of diabetes

A

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

112
Q

Complications of diabetes

A

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.

113
Q

Diabetes and nephropathy

A
  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
114
Q

Types of lung cancer

A
  1. Small cell
  2. Non-small cell
  3. Adenocarcinoma
  4. Squamous cell carcinoma
  5. Large cell carcinoma
  6. Carcinoid
115
Q

Transfusion reactions

A

-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)

116
Q

Pierre Robin Sequence

A
  1. Micrognathia
  2. Glossoptosis
  3. U shape cleft palate
    Can be part of syndrome
    Txt- Prone sleeping
    Upright feeding
    Glossopexy
    DO
117
Q

Cleft lip and palate

A

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

118
Q

High quality CPR

A
  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
119
Q

Peds defibrillator dose

A

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

120
Q

Peds epi dose

A

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

121
Q

Amiodarone peds dose

A

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

122
Q

Peds lidocaine dose MI

A

1mg/kg

123
Q

Magnesium for peds (Torsades de pointed)

A

50mg/kg IV/IO
Max 2g

124
Q

ADHD

A

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

125
Q

Erythema Multiform

A

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

126
Q

Gout

A

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

127
Q

Hemostasis

A
  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

OMFS Medicine (3 decks)

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