Abc's Of Em

Front 1

Predictors of difficult Bag-valve Mask Ventilation

Back 1

BOOTS
B = Beard
O = Obese
O = Older
T = Toothless
S = Snores / Stridor

Front 2

What is the Mallampati score? What are the 4 classes?

Back 2

Mallampati score is used to predict the ease of intubation.

Class I: Soft palate, entire uvula
Class II: Soft palate, body and base of uvula
Class III: Soft palate, only base of uvula visible.
Class IV: Only hard palate visible

I and II are relatively easy. III and IV predict difficult intubation.

Front 3

Features that predict difficult intubation?

Back 3

MAP
M = Mallampati class and measurements
A = Atlantooccipital neck extension (normal = 35 degrees or more)
P = Pathological conditions (e.g. tumour, hematoma, trauma, etc.)

Front 4

Reasons for intubation?

Back 4

4 P's
1. Patency - to obtain and maintain a patent airway in the face of obstruction.

2. Positive-pressure ventilation - to correct deficient oxygenation and/or ventilation.

3. Protection - to protect the airway from aspiration

4. Predicted deterioration

Front 5

What is rapid sequence intubation?

Back 5

Rapid sequence intubation is defined as the simultaneous administration of a powerful sedative (induction) agent and a paralytic agent to facilitate intubation and decrease the risk of aspiration.

Front 6

Basic steps to rapid sequence intubation

Back 6

6 P's

1. Preparation – prepare all equipment, personnel, and medications

2. Pre-oxygenation – patient breathing 100% oxygen for 3-5 minutes

3. Pretreatment – pretreatment with medications such as atropine in children

4. Paralysis with induction – administration of a sedative agent (e.g. ketamine, propofol, etomidate) followed rapidly by the administration of a muscle relaxant (e.g. succinylcholine or rocuronium)

5. Place the tube with proof – intubate the patient, and confirm tube placement with end-tidal capnometry

6. Post-intubation management – chest x-ray, analgesia and sedation, further resuscitation

Front 7

Describe proper sniffing position for laryngoscopy

Back 7

Head angled back, neck forward. External auditory meatus and sternal notch should be in same horizontal plane.

Front 8

Describe the "BURP" technique

Back 8

BURP technique – refers to application of 'backward, upward, rightward pressure' on the larynx to facilitate visualization of the cords during laryngoscopy.

Front 9

Describe how a bougie can be used in endotracheal intubation

Back 9

Bougie is a long, thin, flexible device inserted under the epiglottis during laryngoscopy. As it enters the trachea, clicks are felt as the bougie passes over tracheal rings, and it STOPS when it reaches a mainstem bronchus. If esophageal, no clicks are felt and the bougie advances into stomach. Once in trachea, advance ET tube over bougie.

Front 10

Life threatening causes of dyspnea

Back 10

"Breathing Poorly Can Cause Alot of Tension"
-Pulmonary Embolus
-Pulmonary Edema (CHF)
-Acute exacerbation of COPD
-Acute severe Asthma
-Tension pnuemothorax

Front 11

Anatomical approach to dyspnea

Back 11

Bronchi and bronchioles - Asthma, COPD, Bronchiectasis
Lung Parenchyma - filling or blocking of alveoli eg. pus (infection), fluid (edema), blood, gastric contents (aspiration)
Vasculature/Blood - emboli, metabolic (acidosis, thyroid), anemia
Pleural Space - air (penumothorax), blood (hemothorax), fluid (pleural effusion), pus (empyema)
Chest wall and diaphragm - trauma, neurogenic Causes (GBS, Myasthenia Crisis and ALS)
Cardiac - MI, cardiac Tamponade, valvular and congenital

Front 12

Investigations to order in a patient with dyspnea

Back 12

CBC- looking for evidence of infection or severe
anemia
Electrolytes- looking for evidence of anion gap
acidosis
Cardiac Enzymes- in patients with risk factors for
ischemia
D-dimer- frequently used to rule out the diagnosis
of pulmonary embolism
CXR- visualizes many forms of lung pathology
Blood Gas - to assess oxygenation and ventilation

Front 13

What information does arterial and venous blood gas provide

Back 13

ABG - alveolar oxygenation (pO2), ventilation (pCO2), the acid-base status of the patient, and whether the respiratory condition is acute or chronic.
VBG - provides a close approximation of pH, CO2 and bicarbonate to the ABG.

Front 14

Define acute respiratory failure

Back 14

Hypoxia (pO2 < 50 mmHg) with or without associated hypercapnia (pCO2 > 45 mmHg).

Front 15

Describe the 2 types of respiratory failure

Back 15

Type I: respiratory failure without pCO2 retention. This is characterized by marked V/Q mismatch and intrapulmonary shunting. Examples include diffuse pneumonia, pulmonary edema, ARDS.
Type II: respiratory failure with pCO2 retention. This involves V/Q mismatch and inadequate alveolar ventilation. There are two categories of this type of respiratory failure:
A. Patients with intrinsically normal lungs but with inadequate ventilation due to disorders of respiratory control (e.g. overdose, trauma, CNS disease), neuromuscular abnormalities (e.g. muscular dystrophy, Guillain-Barre, myasthenia), and chest wall trauma.
B. Patients with intrinsic lung disease with V/Q mismatch and alveolar hypoventilation. Respiratory failure is precipitated by additional clinical insult, usually infection, which worsens the underlying disease. Examples include COPD, asthma, cystic fibrosis.

Front 16

List options for oxygen therapy

Back 16

Nasal prongs - 2-6L per min, FiO2 of 25-40%
Face mask - 6-10L per min, FiO2 50-60%
Oxygen reservoir mask - 10+L per min, FiO2 90%
Bag valve mask device - FiO2 100%, manually supplement patients respiratory effort
CPAP/BiPAP

Front 17

Define shock

Back 17

Shock is defined as an abnormality of the circulatory system causing inadequate tissue perfusion which, if not corrected, will result in cell death

Front 18

Signs and symptoms of shock

Back 18

Altered mental status - agitated (early) -> obtunded (late)
Tachycardia
Hypotension - insensitive marker, BP will not drop until blood loss in excess of 30% or 1.5L
Orthostatic vitals
Respiratory rate - in response to sympathetic tone and metabolic acidosis
Skin - cool and pale, cyanosis
Heart sounds - muffled in tamponade
JVP - low (hypovolemia, sepsis), high (left ventricular failure, right heart problem)

Front 19

Estimated BP based on palpation of radial, femoral, and carotid pulse

Back 19

Radial - 80 mmHg
Femoral - 70 mmHg
Carotid - 60 mmHg

Front 20

Describe capillary blanch test

Back 20

Capillary Blanch Test - a positive test occurs when a compressed nail bed takes >2 seconds to
pink up and is said to occur when there is acute blood loss in excess of 15% of total blood volume.

Front 21

Describe classes of hemorrhagic shock

Back 21

Class I - blood loss < 750 mL, pulse < 100, BP normal, RR 14-20, replace with crystalloid
Class II - blood loss 750-1500 mL, pulse > 100, BP normal, RR 20-30, replace with crystalloid
Class III - blood loss 1500-2000 mL, pulse > 120, BP decreased, RR 30-40, crystalloid + blood
Class IV - blood loss > 2000 mL, pulse > 140, BP decreased, RR >35, crystalloid + blood

Front 22

Describe the use of U/S in investigating shock

Back 22

ED ultrasound can rapidly detect intraabdominal hemorrhage, hyovolemia (IVC filling), pericardial tamponade, or RV dysfunction (PE).

Front 23

Describe general management of shock

Back 23

ABC's
O2 monitor
Cardiac monitor
IV access + type and cross match
Serum lactate
Folley catheter - urine output

Front 24

Describe the 3:1 rule in shock

Back 24

You generally need to replace 3x the amount of blood lost to restore BP to the normal value

Front 25

Describe management of anaphylactic shock

Back 25

Epinephrine (IM; IV if cardiovascular collapse) Intravenous crystalloid
Antihistamines (H1 and H2 blockers)
Corticosteroids
Wheezing: Nebulized beta2 agonists
Stridor: Nebulized epinephrine

Front 26

Describe management of cardiogenic shock

Back 26

Inotropes
Intra-aortic balloon pump
Emergency angioplasty

Front 27

Describe management of tension pneumothorax

Back 27

Needle thoracostomy followed by chest tube

Front 28

Describe management of septic shock

Back 28

Intravenous crystalloid
Antibiotics
Goal directed therapy in the ED decreases mortality in sepsis:
-urine output >0.5 mL/kg/h
-CVP 8 to12 mm Hg
-MAP 65 to 90 mm Hg
-ScvO2 >70%
Definitive therapy (drainage of closed space infections, sugery).

Front 29

Describe management of cardiac tamponade

Back 29

Intravenous crystalloid
Pericardiocentesis

Front 30

Describe management of PE

Back 30

Intravenous crystalloid
Inotropes
Thrombolysis or surgery

Front 31

Etiology of coma

Back 31

"TIPS AEIOU"
Trauma/Temperature
Infection (CNS or other)
Poisoning/Psychiatric
Space-occupying lesions/Stroke
Alcohol/Acidosis
Epilepsy (nonconvulsive status epilepticus, post-ictal state)/Endocrine
Insulin (hypoglycemia, hyperglycemia)
Oxygen (hypoxia)
Uremia

Front 32

Universal antidotes to give in a coma

Back 32

"DON'T"
Dextrose: one ampule D50W if low blood sugar
Naloxone: 0.4 – 2mg IV or IM if opiate use is suspected, (often lower initial doses are used)
Thiamine: 100mg IV if history of alcohol abuse or malnourished
Note: Flumazenil (a benzodiazepine antagonist) is not indicated in the treatment of an undiagnosed coma patient

Front 33

Describe a focused neurologic exam in coma patients

Back 33

GCS
Examine head and neck for contusions, lacerations, or signs of trauma (battle sign, racoon eyes, hemotympanium)
Flex neck for meningismus
Check pupils for reaction and symmetry (pupils are typically spared in metabolic and toxic syndromes)
Extraocular movements (have patient follow a finger if awake enough, Doll‘s eye maneuver if no trauma)
Check fundi for papilledema (late sign of increase ICP)
Motor, sensory, reflexes

Front 34

What do focal neurologic findings mean in a coma patient

Back 34

With rare exceptions, focal findings means a structural lesion. In particular, a dilated pupil on one side with weakness of the contralateral limbs indicates an expanding mass lesion on the side of the larger pupil. This occurs when the mass lesion is supratentorial and pushes or herniates the uncus of the temporal lobe through the tentorium (called coning). The oculomotor nerve, which runs adjacent to this, is compressed causing paralysis of the constrictor mechanism of the ipsilateral pupil.

Front 35

Describe the glasgow coma scale

Back 35

EYE OPENING - (4) spontaneous (3) to voice (2) to pain (1) none
VERBAL RESPONSE - (5) appropriate/oriented, (4) confused/disoriented (3) syllables, (2) grunts, (1) none
MOTOR RESPONSE - (6) spontaneous, obeys commands (5) localizes pain, (4) withdraws to pain, (3) decorticate flexion, (2) decerebrate extension, (1) none

Front 36

Define syncope

Back 36

Syncope is defined as a transient, self-limited loss of consciousness with an inability to maintain postural tone, followed by spontaneous recovery.

Front 37

Best diagnostic test in syncope

Back 37

12 lead ECG

Front 38

Etiology of syncope

Back 38

1/4 Cardiovascular - arrythmia, MI, sick sinus syndrome, AS, pacemaker malfunction, PE
1/4 Noncardiovasular - situational (eg. cough, defication), orthostatic (anemia, decreased volume, drugs, autonomic insufficiency), vasovagal
1/2 Unknown -

Front 39

Important points on syncope Hx

Back 39

Presyncope activity, position, and symptoms
Duration of warning (longer = vasovagal)
Duration of loss of consciousness
Post syncopal symptoms
Medications
Family Hx (Heart Dz and unexplained death)

Front 40

Physical exam in syncope

Back 40

Orthostatic BP
CVS exam (listen for aortic stenosis)
CNS exam
Stool for occult blood

Front 41

Describe the San Francisco syncope rule for risk stratification in syncope

Back 41

1. History of CHF
2. Low Hematocrit
3. Abnormal ECG
4. History of Dyspnea
5. Systolic BP < 90 at triage.
Any of these present and the patient is not in the low risk group. Admit these patients for observation along with older patients with sudden onset and those with cardiac etiology.

Front 42

ECG findings in PE

Back 42

1. Sinus tachycardia
2. S1Q3T3: S wave in Lead 1, Q wave in lead 3, inverted T in lead
3. Inverted T waves in the precordial leads
4. RBBB indicating heart strain in large PE
5. Clockwise rotation with persistent S wave in V6, implies rotation of the heart secondary to right ventricular
dilatation

Front 43

% breakdown of headache etiology

Back 43

50% have tension headaches
10% migraines
30% benign nonspecific headaches
8% a headache emanating from a potentially serious cause. Less than 1% will have a life threatening reason for their headache such as a subarachnoid hemorrhage.

Front 44

Pathophysiology of migraine

Back 44

Migraine headaches are believed to result from changes in the reactivity of blood vessels inside and outside of the skull.

Front 45

Triggers for migraine

Back 45

Alcohol [especially red wine], cheeses, chocolate, caffeine, MSG, stress, change in sleep patterns, oral contraceptives, certain phases of menstrual cycle, changes in weather

Front 46

Describe the International Headache Society Diagnostic Criteria for Common Migraine

Back 46

A: At least 2 of the following:
1. Moderate or severe intensity
2. Pulsating quality
3. Unilateral location
4. Inhibits or prohibits daily activities
B: At least 1 of the following symptoms:
1. Nausea or vomiting
2. Phonophobia and photophobia
C: Attacks have occurred:
At least 5 times, AND Lasting 4-72 h each

Front 47

List all migraine therapy options in the ED

Back 47

1. Tylenol, ASA, NSAIDs
2. Neuroleptics - chlorpromazine, haloperidol
3. Dopamine antagonists – metoclopramide (maxeran), prochlorperazine (stemetil)
4. Vasoactive medications – ergotamine (DHE),
sumatriptan

Front 48

Common migraine therapy

Back 48

5-10 mg prochlorperazine, repeated once in 30-60 minutes if needed, with the addition of an intravenous NSAID such as ketorolac

Front 49

Life threatening causes of head ache

Back 49

1. Subarachnoid Hemorrhage
2. Temporal Arteritis
3. Hypertensive Encephalopathy
4. Pseudotumour Cerebri
5. Carbon Monoxide Poisoning
6. Tumour
7. Meningitis/Encephalitis
8. Pre-eclampsia
9. Cervical Artery Dissection
10. Cerebral Venous Thrombosis
11. Acute angle closure glaucoma

Front 50

Clinical features of subarachnoid headache

Back 50

-Sudden onset
-Often occurs with exertion (exercise, intercourse)
-Usually severe (worst headache of my life)
-Most severe at onset
-Frequently associated with nausea and vomiting
-Look for: pupillary changes, meningismus,
altered level of consciousness, focal deficits (NB: Initially may have normal neurological examination)

Front 51

Diagnostic tests in suspected SAH

Back 51

CT scan - perform in 6 hours window for 100% sensitivity, sensitivity decreases with time
If a patient with a suspected SAH has a normal CT scan and is beyond the 6 hour window, then a LP must be performed to look for blood in the CSF (sensitivity 100% up to 14 days)

Front 52

Causes of raised ICP

Back 52

Tumour
Brain Abscess
Intracerebral hemorrhage

Front 53

Features of raised ICP

Back 53

-Worsening of the headache when supine or bending down; frequently worse in the a.m.
-Neurological symptoms and focal findings including cranial nerve abnormalities
-Subtle, gradual changes in mood, cognition, behaviour, memory
-Absence of vomiting and photophobia

Front 54

Features of meningitis

Back 54

-Gradual onset of headache over hours to days
-Fever
-Altered level of consciousness
-Evidence of a focus of infection (intra or extra-
cranial)
-Meningismus

Front 55

When can LP safely be performed in suspected meningitis

Back 55

LP may safely be performed without CT scanning in patients with normal mental status, no focal neurologic signs, and no papilledema.

Front 56

When should antibiotics be started in suspected meningitis

Back 56

Antibiotics should be administered before obtaining a CT scan or awaiting LP results; standard of care is to administer antibiotics within one hour of suspecting the diagnosis of meningitis.

Front 57

Clinical features of temporal arteritis

Back 57

-Middle-aged to elderly
-Gradual onset of headache over days
-May have visual changes (but not universal)
-Localized headache and tenderness in the
temporal region

Front 58

Red flag features on history in headache

Back 58

-Sudden onset
-Most severe headache, or unlike previous
headaches
-New onset of headache at age 50 or older
-Associated neurological symptoms

Front 59

Red flag features on physical exam in headache

Back 59

-Pupillary changes
-Altered level of consciousness
-Abnormal vital signs, especially temperature
-Meningeal irritation
-Focal neurologic signs

Front 60

Differentiate somatic vs visceral pain

Back 60

Somatic pain - precisely located, sharp, piercing, arises from dermal pain fibres that enter the spinal cord at a single level
Visceral pain - poorly localized, less distinct, dull, aching, pressure, arises from internal organ pain fibres that enter the spinal cord at multiple levels (T1-T6 for organs of the thorax or upper abdomen)

Front 61

Big 5 acute life threatening causes of chest pain

Back 61

1. Myocardial Infarction
2. Pulmonary Embolism
3. Aortic Dissection
4. Tension Pneumothorax
5. Esophageal Rupture

Front 62

DDx for chest pain

Back 62

CV: MI*, aortic dissection*, cardiac tamponade*, pericarditis, myocarditis, endocarditis, arrhythmias
Resp: PE*, tension pneumothorax*, infections (pneumonia, bronchitis) 
GI: esophageal rupture*, pancreatitis, biliary colic, GERD,
esophageal spasm
MSK: costochondritis, rib fractures
Psych: panic attack (diagnosis of exclusion) 
Other: shingles

Front 63

History in patients with chest pain

Back 63

Characteristics of pain - OPQRST
Hx of trauma
Medications (including cocaine)
Cardiac risk factors
PE risk factors
Past and present significant illnesses, medications, allergies, drugs, smoking and alcohol use.

Front 64

Placement of chest tube in pneumothorax

Back 64

Thoracostomy with placement of one or more chest tubes, usually inserted in the 4th of 5th costal interspace at the anterior or mid axillary line

Front 65

Landmark for needle decompression in tension pneumothorax

Back 65

Needle decompression is performed at the 2nd intercostal space at the midclavicular line

Front 66

Can reproducible chest pain be used to rule out MI

Back 66

Reproducible chest wall pain is seen in up to 15% of MI. Tenderness on forceful palpation does not rule out an ACS.

Front 67

Life threatening causes of abdominal pain

Back 67

Intra-abdominal
-Ischemic bowel (middle age to elderly)
-Abdominal aortic aneurysm; dissection, leakage,
rupture (middle age to elderly)
-Hepatic or splenic injury (blunt trauma)
-Perforated viscus
-Acute pancreatitis
-Intestinal obstruction
Extra-abdominal
-Ectopic pregnancy (female of child bearing age)
-Myocardial infarction

Front 68

DDx for abdominal pain (intra-abdominal)

Back 68

Peritoneal inflammation -
Obstruction of hollow viscus - intestine, biliary tree, ureter
Vascular disorder - bowle ischemia, AAA

Front 69

DDx for abdominal pain (extra-abdominal)

Back 69

Abdominal wall - contusions, hematoma, muscle strain, trauma
Pelvic - ectopic pregnancy, salpingitis, torsion/rupture of ovarian cyst, testicular torsion
Intrathoracic - myocardial infarction, pneumonia, pulmonary embolus, esophageal disease
Metabolic - DKA, sickle cell crisis
Neurogenic - preeruptive phase of herpes zoster, spinal disc disease

Front 70

Describe how location can provide clues towards the diagnosis of abdominal pain

Back 70

-diverticulitis - left lower quadrant
-appendicitis - periumbilical, then right lower
quadrant
-cholelithiasis, cholecystitis - right upper quadrant
-pancreatitis - epigastric, periumbilical

Front 71

Descibe symptoms that suggest peritonitis

Back 71

Pain increased with coughing, driving over bumps
in the road

Front 72

Which test is more specific for pancreatitis, amylase or lipase

Back 72

Lipase

Front 73

Tests to order in abdominal pain

Back 73

CBC + dif
Urinalysis
Serum lipase/amylase
bHCG
Electrolytes, creatinine, urea are important in
patients with vomiting and diarrhea
Alkaline phosphatase and bilirubin may be
elevated with cholecystitis and obstructive biliary
tract disease
ECG

Front 74

Indications for CT in abdominal pain

Back 74

-trauma
-suspected ruptured or leaking aortic aneurysm
-pancreatitis
-urolithiasis, renal colic (non-contrast)
-diverticulitis
-appendicitis

Front 75

Most Common Causes of surgical abdomen in the Elderly

Back 75

1. Cholecystitis
2. Bowel Obstruction
3. Appendicitis

Front 76

Spinal causes of back pain

Back 76

1. Cauda Equina & Spinal Cord Compression (cancer spinal metastasis, central disc herniation)
2. Osteomyelitis - infection of bone or bone marrow
3. Transverse Myelitis - inflammation of spinal cord

Front 77

Vascular causes of back pain

Back 77

1. Aortic dissection
2. Rupturing abdominal aortic aneurysm
3. Pulmonary embolism
4. Myocardial infarction
5. Retroperitoneal bleed

Front 78

Red flags in back pain

Back 78

1. Constitutional symptoms including fever (cancer, epidural abscess, osteomyelitis)
2. IV drug use (epidural abscess, osteomyelitis) 
3. Immunocompromised status including
corticosteroid use (epidural abscess,
osteomyelitis)
4. Pain worse at night (cancer)
5. Urinary retention or incontinence; or fecal
incontinence (cauda equina)
6. History of cancer (spinal metastasis)
7. Spinous process tenderness (spinal causes as
above)
8. Saddle‘ parasthesia or anesthesia (cauda equina
syndrome)
10. Neurologic deficit 
11. Anticoagulant use or bleeding disorder (epidural
hematoma)

Front 79

Cancer most likely to metastasize to the spine

Back 79

Prostate, lung and breast

Front 80

Treatment of cauda equina and spinal cord compression in the ED

Back 80

1. IV opioids
2. IV dexamethasone, especially if cord compression
from tumour is suspected
3. Neurosurgery consult

Front 81

What tests can be done before MRI in patients suspected of spinal cord compression or cauda equina syndrome

Back 81

Post void residual volume. If > 200 mL spinal cord compression is more likely. If less than 100 mL spinal cord compression is less likely.

Front 82

Define chronic pain

Back 82

Chronic pain is defined as pain that persists for 6 months or more or pain that lasts beyond the expected point of resolution of tissue damage.

Front 83

What is the annual risk of bleeding if NSAIDs are used continuously? 2 month risk?

Back 83

NSAIDS used continuously have an annual 4 percent risk of gastrointestinal perforations, ulcers or bleeds.
Taking an NSAID for two months or more carries a one in five risk of an endoscopically proven ulcer and a one in one hundred and fifty risk of a bleeding ulcer.

Front 84

What IV NSAIDs are available in Canada?

Back 84

The lone intravenous NSAID available in Canada is ketorolac (Toradol). Ketorolac is effective for pain due to fractures, inflammatory conditions, renal colic, migraine headaches and sickle cell pain. The dosage of ketorolac is 30-60 mg/dose IM.

Front 85

Describe metabolities and excretion of morphine

Back 85

Morphine-6-glucuronide (M6G) is the active metabolite of morphine, while morphine-3- glucuronide (M3G) may be responsible for neurotoxic adverse effects such as hyperalgesia and myoclonus. Both metabolites are excreted by the kidney. Both metabolites accumulate with higher doses, renal impairment, oral route of administration and increasing age.

Front 86

Dose of morphine and hydromorphone

Back 86

For rapid control of acute pain, titrate morphine by intermittent IV bolus doses at 2-3 mg every 5 minutes as needed with no limitation on the number of bolus doses given. Hydromorphone may be administered at a dosage of 0.25-0.5 mg IV q 5 minutes as needed or 1-2 mg IV q3-4 h prn

Front 87

Dose of Fentanyl

Back 87

0.5μg/kg q5-10 mins until the patient is comfortable.

Front 88

Advantages of Fentanyl over morphine

Back 88

No active metabolites
No histamine release or nausea
Can be used in patients with morphine allergy

Front 89

What anti-nausea medications can be paired with morphine

Back 89

1. dimenhydrinate (Gravol®) 25-50 mg IV or 50 mg
IM q4h PRN
2. ondansetron (Zofran®) 8 mg or 0.15 mg/kg IV
3. prochlorperazine (Stemetil®) 10 mg IV or by
suppository, or 10-20 mg IM q8h PRN

Front 90

Downside of codeine

Back 90

For codeine to be effective it must be metabolized to morphine. Six to ten percent of individuals are unable to metabolize codeine and are thus unable to derive analgesic benefit from the drug.

Front 91

Formulation of Percocet

Back 91

Acetominophen + oxycodone

Front 92

Describe how opioid doses change in the elderly

Back 92

Sensitivity of the elderly brain to fentanyl is increased by 50%. The dosage of morphine and fentanyl may be 2-4 fold times lower in that age group.

Front 93

Describe pain management in osteoporotic vertebral compression fractures

Back 93

Calcitonin has been shown to relieve pain associated with osteoporotic vertebral compression fractures. The recommended dosage is 200 IU per day IM or 400 IU per day by nasal spray (1x 200 IU spray per nostril).

Front 94

How effective is reperfusion therapy in decreasing mortality in MI

Back 94

Reperfusion therapy (pharmacological or mechanical) decreases mortality by 25 to 50 %, and improves left ventricular function

Front 95

Symptoms of acute MI

Back 95

-crushing retrosternal chest pain
-radiation of pain to arm or jaw (right arm more specific)
-diaphoresis
-nausea/vomiting
-dyspnea

Front 96

Common presentation of MI in the elderly

Back 96

Presentation in the elderly is often without pain and diaphoresis, but with an increased frequency of neurological symptoms such as syncope, stroke, acute confusion, and weakness as the presenting complaint.

Front 97

Describe the Killip classification of hemodynamic status in MI

Back 97

Killip l: well perfused, chest clear
Killip ll: some pulmonary congestion (orthopnea, crackles)
Killip lll: pulmonary edema (severe shortness of breath, crackles above scapulae)
Killip lV: poor perfusion, cardiogenic shock

Front 98

ECG findings in acute MI

Back 98

-increase in R wave voltage, usually in the precordial leads (early)
-hyperacute T waves, usually in the precordial leads and over 10mm (early)
-ST segment elevation (early)
-Q waves (hours later)

Front 99

Describe how ECG findings can help localize the area of infarction

Back 99

II, III, AVF - inferior
V1-V3 - anteroseptal
1, AVL, V4 –V6 - lateral
V1-V6 - anterolateral
V8,V9 - posterior

Front 100

Causes of ST elevation

Back 100

-pericarditis
-hyperkalemia
-LV aneurysm
-LBBB
-LVH
-hypothermia.

Front 101

Why is chest x-ray performed in patients with suspected MI

Back 101

R/O aortic dissection - look for a widened mediastinum and a pleural effusion

Front 102

How long after the onset of symptoms will patients with MI have a rise in troponin

Back 102

Troponin will not be positive for at least 2 to 6 hours. Serial troponin must be done 6-9 hours after arrival.
Troponin peaks at 12-24 hours after infarction.

Front 103

Causes of elevated troponin

Back 103

MI
Renal failure
Sepsis

Front 104

Describe complications of acute MI

Back 104

-Arrhythmias
-Conduction disturbances - AV blocks
-LV pump failure - cardiogenic shock, assess
Killip status
-Mechanical defects - cardiac rupture, VSD, papillary muscle dysfunction
-Thromboembolism - can be prevented with heparin
-Pericarditis - occurs 5-7 days following an acute MI

Front 105

How effective is aspirin in decreasing mortality in MI

Back 105

2-4 baby aspirin chewed decreased mortality up to 21%

Front 106

Describe caution that must be taken in inferior MI

Back 106

Right ventricular infarctions occur in approximately 1/3 of all inferior MI's, suggesting more proximal occlusions of their right coronary artery. Right ventricular (RV) ischemia results in decreased RV stroke volume, impairing filling of the left ventricle. Cardiac output is reduced, and systemic BP drops. It is therefore critically important to avoid drugs that result in venodilatation if the patient might have RV infarction. These patients are preload dependent, and drugs such as NTG may precipitate dramatic hypotension. Suspect RV infarction on all patients with inferior MI's. Do right-sided precordial leads (specifically V4R) looking for ST elevation.

Front 107

What is the time window for performing thrombolysis in acute MI

Back 107

Ideally the first hour or two after the onset of symptoms. Thrombolytic therapy may be beneficial up to 12 hours after symptom onset, early therapy achieves maximal myocardial salvage and helps preserve left ventricular function.

Front 108

Indications and mechanism of action for thrombolytics in MI

Back 108

Thrombolytics activate plasminogen to lyse clot.
They are indicated for all acute infarcts with ST elevation >1mm in two contiguous leads
They are not indicated if the ECG is normal or shows ST segment depression.

Front 109

Contraindications to thrombolytic therapy

Back 109

-recent major surgery or any active internal bleeding
-history of hemorrhagic strokes, or any recent stroke
-severe uncontrolled hypertension
-known intracranial neoplasm, AVM, or aneurysm
-suspected aortic dissection

Front 110

Describe treatment recommendations regarding reperfusion therapy in STEMI

Back 110

1. Patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 minutes
2. Patients presenting to a hospital without PCI capability and who cannot be transferred to a PCI centre and undergo PCI within 90 minutes of first medical contact should be treated with fibrinolytic therapy within 30 minutes of hospital presentation.

Front 111

At what point should heparin be given to patients with STEMI

Back 111

Following thrombolytics, heparin is indicated to prevent rethrombosis. It should be initiated immediately following the thrombolytic.

Front 112

Advantages of LMWH over unfractionated heparin

Back 112

-more predictable anticoagulant effect
-no need for PTT monitoring
-lower rates of thrombocytopenia
-better bioavailability

Front 113

At what point should clopidogrel be given to patients with STEMI

Back 113

Dose for patients 75 and under: 300 mg as adjunctive therapy to TNK; 600 mg as adjunctive therapy to PCI.
The earlier the clopidogrel is given the better.

Front 114

Describe the pathophysiology of heart failure

Back 114

-cardiac output decreases, reflex arterial vasoconstriction redistributes blood flow so that the brain and heart remain well perfused
-drop in renal blood flow activates the renin- angiotensin-aldosterone system, causing increased sodium and fluid retention
-decreased cardiac output also results in an increase in left atrial and left ventricle filling pressures, which is in turn reflected in elevated pulmonary capillary pressures
-elevated pressure causes pulmonary edema.

Front 115

How do you differentiate systolic from diastolic dysfunction in CHF

Back 115

Systolic - low cardiac output, ejection fraction <40%, dilated LV, poor contractility, fatigue, lethargy, hypotension
Diastolic - impaired ventricular compliance, ejection fraction >40%, backward failure, dyspnea, peripheral edema, ascites,

Front 116

Causes of congestive heart failure

Back 116

-Coronary artery disease
-Hypertension
-Valvular heart disease
-Cardiomyopathy (dilated, hypertrophic,
restrictive)
-Pericardial disease
-Metabolic disorders (e.g. hypothyroidism) 
-Viral myocarditis
-Toxins

Front 117

Precipitants of acute CHF

Back 117

Cardiac - infarction, tachy/bradyarrhythmias, mechanical complications of acute MI
Drugs - beta-blocker, CCB, NSAIDs, steroids
Dietary - increased Na
High output - anemia, infection, pregnancy, hyperthyroidism
Other - iatrogenic fluid overload, renal failure, hypertensive crisis, drug/alcohol

Front 118

Symptoms of congestive heart failure

Back 118

-Dyspnea
-Orthopnea, paroxysmal nocturnal dyspnea
-Cough, wheezing
-Fatigue, generalized weakness
-Edema of lower limbs, increased abdominal girth

Front 119

Physical exam findings in congestive heart failure

Back 119

-Tachypnea, tachycardia, hypertension or hypotension, hypoxia
-Crackles, wheezes
-S3, S4
-Jugular venous distension, hepatojugular reflux
-Hepatomegaly
-Dependent edema
-Weak peripheral pulses, cool extremities, i.e.
hypoperfusion

Front 120

Chest x-ray findings in acute congestive heart failure

Back 120

-cardiomegaly
-increase in prominence of upper lung fields (pulmonary vascular redistribution)
-interstitial edema and obliteration of vasculature structures
-kerley B lines (1-2 cm lines perpendicular to the pleura and continuous with it, representing edematous septal lines)
-pleural effusions (usually absent in acute pulmonary edema)

Front 121

Investigations to be done in CHF

Back 121

-CXR
-ECG
-troponin
-BNP
-renal function
-electrolytes (hyponatremia)

Front 122

Treatment of acute congestive heart failure

Back 122

-Nitroglycerin 0.4 mg sublingual q 5 min. (if sBP >
100) +/- Nitrodur 0.4 - 0.8 mg/hr topical
-Furosemide 40 - 100 mg IV (if sBP > 100), if no response double dose
-CPAP or BiPAP if hypoxic on 100% O2
-if sBP <90 and no shock give dobutamine (milrinone if taking beta-blocker), if sings of shock give dopamine

Front 123

DDx for PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia

Back 123

H's and T's
Hypovolemia
H+ (acidosis)
Hypothermia
Hypo/Hyperkalemia
Hypoxia

Tension pneumothorax
Toxins
Tamponade cardiac
Thrombosis cardiac
Thrombosis pulmonary

Front 124

Describe drug therapy during cardiac arrest

Back 124

epinephrine IV 1 mg every 3-5 minutes
amiodarone IV 300 mg bolus

Front 125

What should be done for narrow complex tachycardia that is symptomatic but stable

Back 125

Synchronized cardioversion
OR
Adenosine 6 mg rapid IV push

Front 126

What antiarrhythmics should be used in stable wide-QRS tachycardia.

Back 126

procainamide
amiodarone
sotalol

Front 127

Treatment of persistant symptomatic bradycardia

Back 127

Atropine
Dopamine
Epinephrine

Front 128

Describe the stanford classification of aortic dissection

Back 128

Stanford type A dissections involve the ascending aorta, where type B dissections are more distal. Type A dissections are more common and are associated with increased mortality.

Front 129

Risk factors for aortic dissection

Back 129

-Male
-Elderly (>65 years)
-History of hypertension
-Pregnancy
-Family or personal history of aneurysm or dissection
-Connective tissue disease (Marfan‘s, or Ehlers-
Danlos syndromes)
-Cocaine use
-Congenital bicuspid aortic valve

Front 130

History and physical in aortic dissection

Back 130

History: sudden onset chest pain felt maximally at onset, hypertension, chest pain + syncope, abdominal pain, or ischemic symptoms to lower extremitiy
Physical: aortic regurgitation murmor, pulse differential between carotid, radial and femoral

Front 131

Chest x-ray findings in aortic dissection

Back 131

-left pleural effusion
-wide mediastinum
-aortic calcification >5mm from the outside of the expanded aortic contour

Front 132

Management of aortic dissection

Back 132

-analgesia
-blood pressure control - labetolol titrated to target BP of 120/80 and sodium nitroprusside adjuvant
-Stafford type A - surgical management
-Stafford type B - medical management

Front 133

Risk factors for AAA

Back 133

-Hypertension
-Age greater than 50
-Male
-Peripheral vascular disease and/or coronary
artery disease
-Family history of aneurysm
-Smoking
-Diabetes
-Connective tissue disease

Front 134

History in AAA

Back 134

-sudden onset abdominal, back, or flank pain
-syncope (due to transient hypotension)
-unexplained hypotension

Front 135

Physical exam in AAA

Back 135

-palpable aorta (majority infrarenal, palpable just above aorta)
-diminished femoral pulses
-signs of distal micro-embolism "blue toe syndrome"

Front 136

Investigations in AAA

Back 136

-ED ultrasound - AAA if > 3cm, can not determine if ruptured because most ruptures are retroperitoneal
-CT scan

Front 137

Classic history in arterial occlusion

Back 137

6 P's
-Parasthesia
-Pain
-Pallor
-Pulselessness
-Poikilothermia (cool to touch)
-Paralysis

Front 138

Virchow's triad.

Back 138

-venous stasis
-injury to the vessel wall
-hypercoagulable state

Front 139

Risk factors for venous thrombosis

Back 139

"THROMBOSIS"
T - Trauma, travel
H - Hypercoagulable, hormone replacement
R - Recreational drugs (IV drugs)
O - Old (age > 60)
M - Malignancy
B - Birth control pill
O - Obesity, obstetrics
S - Surgery, smoking
I - Immobilization
S - Sickness (CHF/MI, nephrotic syndrome, IBD, vasculitis)

Front 140

Classic features of DVT

Back 140

-pain
-redness
-swelling
-warmth
-tenderness

Front 141

Investigations in suspected DVT

Back 141

-doppler ultrasound (gold standard), if neg. but moderate/high risk proceed to d-dimer or repeat U/S in 7 days. If neg and neg d-dimer DVT is ruled out.
-computed tomographic venography

Front 142

Management of PE or proven DVT

Back 142

-early ambulation
-analgesia
-LMWH (eg. enoxaprin) or fondaparinux. Continued until warfarin is therapeutic for 2 days
-warfarin (started at same time as LMWH and continued for 3 months if known cause, 6 months if unknown etiology)
-if massive PE thrombolytics can be used

Front 143

Classic triad of PE

Back 143

-Pleuritic chest pain
-Hemoptysis
-Dyspnea

Front 144

Well's Criteria

Back 144

Clinical signs of DVT - 3.0
Alternative diagnosis less likely than PE - 3.0
Heart rate > 100 - 1.5
Immobilization or surgery within 4 weeks - 1.5
Previous DVT/PE - 1.5
Hemoptysis - 1.0
Malignancy (ongoing treatment/palliative) - 1.0

Front 145

What is the PERC rule? How is it applied?

Back 145

Pulmonary Embolism Rule-Out Criteria (‘PERC’ Rule)
1. age < 50
2. heart rate < 100
3. oxygen saturation of > 94% on room air
4. no previous history of DVT or PE
5. no recent surgery
6. no hemoptysis
7. no estrogen use
8. no clinical signs of DVT
No objective testing needed if all criteria met and patient has <15% chance of having a PE (low risk/<2 points Well's criteria).

Front 146

DDx for SOB and wheezing

Back 146

Asthma, COPD, CHF, upper airway obstruction, pneumonia, ACS, and PE

Front 147

Define pulsus paradoxus. Which diseases is it a sign of?

Back 147

Abnormally large decrease in sBP during inspiration >10 mmHg.
Cardiac tamponade, pericarditis, chronic sleep apnea, COPD, asthma.

Front 148

Investigations in asthma and COPD

Back 148

-peak expiratory flow rate – helps determine severity and guide therapy
-consider CXR
-consider ECG/cardiac workup
-ABG if deteriorating (pCO2 level indicates
severity and fatigue)

Front 149

Treatment of acute asthma

Back 149

1. Oxygen - titrated to at least 92%
2. Salbutamol (Ventolin)
3. Ipratropium (Atrovent)
4. Steroids (Prednisone 40-60mg PO)
5. Magnesium sulfate - 2g IV over 20 mins
6. Assisted ventilation

Front 150

Which patients are safe to discharge home following an asthma attack

Back 150

FEV1 > 60% predicted - generally safe to discharge
FEV1 40-60% predicted - discharge possible based on risk factors for recurrance
FEV1 <40% - admit

Front 151

Discharge instructions following asthma attack

Back 151

-SABA (salbutamol) 2- 4 puffs q4h, then prn once symptoms controlled and return if use required more than q1-2h
-Oral corticosteroids for patients with moderate to severe attack - prednisone 30-60 mg/day for 7-14 days (no need to taper)
ICS – Beclomethasone or Budesonide (500-1000 ug/d) or continue inhaled steroid (if patient already on inhaled steroid)

Front 152

Symptoms of COPD exacerbation

Back 152

-Dyspnea
-Cough
-Sputum production

Front 153

Investigations in acute exacerbation of COPD

Back 153

CXR, ECG, ABG, CBC, and routine biochemistry
Spirometry is not useful in managing acute exacerbations

Front 154

Treatment of COPD exacerbation

Back 154

-O2 - saturation targeted at 88-92%, PaO2 60-65 mmHg
-Inhaled B2 agonist (Salbutamol) – 2.5-5 mg via nebulizer q15min x3 prn
+/- anticholinergic (Ipratropium) – 500ug via nebulizer q15min x3 prn
-prednisone 50 mg OD
-antibiotics if all 3 symptoms, 2 if sputum present (Levoquin)
-CPAP or BiPAP

Front 155

Common causes of upper GI bleeding

Back 155

75% PUD, gastric erosions, and verices
1. Peptic Ulcer Disease - H.pylori or
NSAIDS
2. Varices (esophageal or gastric)
3. Mallory-Weiss tears
4. Gastritis
5. Esophagitis

Front 156

Define esophagitis. What are the causes?

Back 156

Inflammation of the esophagus producing symptoms of nausea and heartburn.
Causes - infectious (fungal, viral), reflux esophagitis, chemical or pill, eosinophilic esophagitis

Front 157

Common causes of lower GI bleeding

Back 157

80% diverticulosis and angiodysplasia
1. Diverticulosis
2. Angiodysplasia (dilated tortuous submucosal
vessels)
3. Neoplasm
4. Inflammatory bowel disease
5. Anorectal disease (proctitis,hemorrhoids,
fissures)

Front 158

Common causes of LGIB in children less than 2

Back 158

Meckel's diverticulum
Intussiception

Front 159

Presentation of chronic GI bleed

Back 159

Anemia, chest pain, shortness of breath, or fatigue

Front 160

History in GI bleed

Back 160

-symptoms or risks for GI bleeding
-protracted wretching or vomiting
-features of malignancy
-previous GI bleeds and their cause
-presence of liver disease or alcohol use
-surgical history (AAA repair or peptic ulcer
surgery)
-medication review (especially anticoagulants
such as coumadin, ASA, clopidogrel (Plavix), dabigatran (Pradax), NSAIDS)

Front 161

Investigations in suspected GI bleed

Back 161

-CBC
-PTT/INR
-group + screen (consider cross and type)
-BUN/Cr ( BUN/creatinine ratio > 10:1 is suggestive of UGIB) -LFT

Front 162

Management of GI bleed

Back 162

-2 large bore IV's
-Type and cross match blood. Transfuse young, healthy people if still unstable after 2 L NS or HgB < 70. Transfuse elderly if HgB < 100.
-If INR > 1.5 give FFP + vit K or prothrombin complex concentrate (octaplex) + vit K
-PPI for suspected UGIB - pantoloc 80 mg IV
-Octreotide (sandostatin) or vasopressin for esophageal
vadrices
-Endoscopy or colonscopy

Front 163

What % of strokes are ischemic vs hemorrhagic

Back 163

Ischemic 80%
Hemorrhagic 20%

Front 164

Define TIA

Back 164

A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction

Front 165

Symptoms of a stroke

Back 165

-abrupt onset, focal symptoms.
-arm, leg, or face numbness or weakness
-speech disturbance or difficulty understanding speech
-vision disturbance, especially in one eye
-severe headache
-vertigo

Front 166

Feature that make stroke less likely

Back 166

-decreased level of consciousness
-gradual onset
-fluctuating signs
-fever
-no focal signs

Front 167

Blood pressure guidelines in stroke

Back 167

Only lower if BP >220/120 or > 185/110 if using tPA.
Do not treat too aggressively as it may lead to under perfusion of the punumbra.

Front 168

Management of stroke

Back 168

-tPA (alteplase) if ischemic and within 4.5 hours
-ASA, Plavix, Aggrenox as soon as hemorrhagic stroke ruled out

Front 169

Exclusion criteria for receiving tPA in ischemic stroke

Back 169

-History of intracranial hemorrhage at any time
-Serious head trauma in past 3 months
-Major surgery in the past 2 weeks
-Non-compressible arterial puncture in past 7 days
-INR > 1.7, or platelets <100,000
-Blood glucose <2.7 or >22.2

Front 170

Describe the ABCD2 score. What is it used for?

Back 170

Estimates risk of stroke after TIA. Admit patients with a score of 5 or 6.
Age > 60 (1)
Blood pressure > 140/90 (1)
Clinical feature - unilateral weakness (2), speech deficit (1), other (0)
Duration of symptoms - > 59 min. (2), 10-59 (1), <10 (0)
Diabetes (1)

Front 171

Describe the CHADS2-Vasc score. What is it used for?

Back 171

CHADS2 score estimates stroke risk in patients with AFIB
CHF (1)
HTN (1)
Age >75 (2), 65-74 (1)
Diabetes (1)
Stroke or TIA previously (2)
Sex (female) (1)
Vascular disease - MI or peripheral arterial disease (1)

Front 172

How should the CHADS2-Vasc be interpretted.

Back 172

If score 0, patients should receive daily ASA
If score 1, patients may receive either warfarin or dabigatran or ASA
If score 2 or greater, patients should receive either warfarin or dabigatran

Front 173

Define seizure

Back 173

A seizure is a clinical manifestation of abnormal neurologic function caused by aberrant electrical firing of neurons in the brain.

Front 174

Define status epilepticus

Back 174

Continuous or intermittent seizure activity for more than 5 minutes without regaining consciousness

Front 175

Etiology of status epilepticus

Back 175

Withdrawal - anticonvulsants, EtOH, benzo, barbituates
Toxins - anticholingerics, sympathomimetics, ASA, lithium, lidocaine, isonazid
Structural - brain tumor, ICH, stroke
Cerebral injury - infection, trauma, hypoxia
Metabolic - hypoglycemia, hypo/hypernatremia, hypocalcemia, lactic acidosis, uremia
Ecclampsia

Front 176

Investigations in status epilepticus

Back 176

-Immediate bedside glucose level
-CBC, electrolytes, anticonvulsant drug levels,
venous blood gas, calcium, Mg, ETOH level,
serum salicylates, urine toxicology screen
-ECG, LP, CT head and other imaging must be deferred until seizure activity has stopped

Front 177

Treatment of status epilepticus

Back 177

-Lorazepam: 2-4mg IV q2min, up to 0.1 mg/kg IV, maximum 8–10 mg
-If seizure fails to resolve in 5-10 minutes start a second IV and give Phenytoin 20 mg/kg IV administered at a rate of 25-50 mg/min (may repeat 10mg/kg dose once to total dose 30 mg/kg) *must be run in separate IV line
-Phenobarbital 20 mg/kg IV at 50 mg/min
-Propofol: 2-5 mg/kg IV loading dose and then 2-
10 mg/kg/hr

Front 178

Blood tests to differentiate pseudoseizure from status epilepticus

Back 178

Patients with SE will develop a transient physiologic leucocytosis, elevation of serum lactate and prolactin levels. These markers will not be elevated in patients with pseudoseizures.

Front 179

Most common side effects of benzodiazapens

Back 179

Respiratory depression and confusion

Front 180

Management of agitated patient

Back 180

lorazepam (Ativan) 0.5-2 mg PO
haloperidol (Haldol) 2-10 mg IM, can be given with lorazepam in same syringe

Front 181

Definition of diabetic ketoacidosis

Back 181

DKA is characterized by the triad of hyperglycemia, ketosis, and acidosis.
One of the more widely accepted criteria of DKA is serum Glucose > 16, pH <7.30, and Bicarbonate <18.

Front 182

What causes the acidosis in DKA

Back 182

As blood glucose rises, the renal glucose threshold is reached and glucose is excreted into the urine, leading to an osmotic diuresis. This diuresis in turn, leads to losses of glucose, electrolytes, and water, potentially causing dehydration, poor tissue perfusion and lactic acid production.

Front 183

Causes of DKA

Back 183

1. Lack of insulin (initial presentation of diabetes, non compliance, under dosing)
2. Infection
3. Myocardial infarction
4. Pulmonary embolism
5. Stroke
6. Pancreatitis
7. Substance abuse
8. Medications (steroids)
9. Trauma
10. Surgery

Front 184

Typical presentation of DKA

Back 184

Polydipsia, polyuria
Nausea, vomiting, abdominal pain
Signs of decreased volume - tachycardia, hypotension, tachypnea, flat JVP, poor skin turgor

Front 185

Investigations in DKA and HHS

Back 185

CBC, electrolytes, creatinine
Glucose, serum and urine ketones, serum osmolality
Liver function tests, amylase, calcium, magnesium, phosphate, troponin and an EKG and a blood gas.

Front 186

Difference in pH of venous and arterial blood gas

Back 186

Venous blood gas pH levels are approx. 0.03 units lower than ABG pH levels

Front 187

Treatment of DKA and HHS

Back 187

1. Fluid resuscitation
2. Glucose control with Insulin
3. Correction of potassium
Long form:
1. Fluids - total body water loss is estimated at 5-8L or 100mL/kg in a typical adult male with DKA. Generally speaking, half of the fluid deficit should be replaced in the first 8 hours while the remainder is infused over the next 16 hours. When the serum glucose falls to approximately 16 mmol/L, the intravenous fluid should be changed to a dextrose containing solution
2. Insulin - can not be given in K is < 3.3 mmol/L. Give 0.1 U/kg/hr of insulin IV. Goal is to lower the blood glucose by 3-5 mmol/L per hour. Measure glucose ever 30-60 minutes. Once glucose falls below 14 mmol/L switch to subcutaneous insulin.
3. Potassium - f the K is between 3.3-5.0mmol/L, administer 20-30 mmol/L of KCl with each liter of fluid. If the K is > 5.0, no K is given and it should be rechecked in 2 hours. If the K is <3.3, hold the insulin and give 40 mmol/L KCL in the 1st hr and then 20-30 mmol/L in an effort to keep the K between 4-5.

Front 188

Describe psuedohyponatremia as it relates to DKA

Back 188

Pseudohyponatremia - for every increase in serum glucose by 10 mmol/L (above normal ~ 6 mmol/L), the true serum sodium is actually about 3 mmol/L higher than the measured value.

Front 189

Define hyperosmolar hyperglycemia state (HHS)

Back 189

HHS is seen predominantly in type 2 diabetics and is generally defined by the presence of: serum glucose > 33.3 mmol/L, pH>7.3, bicarbonate >15, anion gap <12, serum osmolality >320 mOsm/kg, and the absence of serum ketones.

Front 190

What is the key distinguishing feature between DKA and HHS

Back 190

The key distinguishing feature between HHS and DKA is the absence of serum ketones.

Front 191

Whipple's triad of hypoglycemia

Back 191

1. Low plasma glucose
2. Symptoms suggestive of hypoglycemia
3. Prompt resolution of symptoms with administration of glucose.

Front 192

Causes of hypoglycemia

Back 192

Excessive insulin use, alcohol intoxication, sepsis, liver disease, or the use of oral anti-hyperglycemics (i.e. sulfonylureas)

Front 193

Symptoms of hypoglycemia

Back 193

Autonomic - diaphoresis, nausea, hunger, tachycardia and palpitations.
Neuroglycopenic - headaches, confusion, seizures, and coma.

Front 194

Treatment of hypoglycemia in the ED

Back 194

IV D50 (dextrose 50%) at 1g per kg, typically starting with 1 ampoule (50g).

Front 195

Area affected by anterior and posterior epistaxis

Back 195

Anterior epistaxis (90%) - Kiesselbach‘s plexus (Little‘s area) on the anterior-inferior nasal septum.
Posterior epistaxis - posterior branch of the sphenopalatine artery (Woodruff's area).

Front 196

Treatment of anterior epistaxis

Back 196

1. Compress the soft, cartilaginous part of the nose for 10-15 minutes.
2. Place an anterior pack with lidocaine + epi on soaked pledgets. To be removed in 48-72 hours.
3. Give anti-Staph antibiotics (cloxacillin or cephalexin) to prevent sinusitis or TSS if placing anterior packing.

Front 197

Which of the complications of group A Strep can be prevented with antiobiotic therapy

Back 197

Antibiotics prevent acute rheumatic fever but not post-strep glomerulonephritis

Front 198

Signs and symptoms of epiglottitis

Back 198

-prodrome of typical URTI
-severe sore throat, dysphagia, odynophagia and muffled voice
-tenderness to palpation of the hyoid bone and the larynx
-thumb print sign on lateral x-ray

Front 199

Treatment of epiglottitis

Back 199

1. Airway management involving ENT, ICU or anaesthesia
2. ceftriaxone 1 g IV

Front 200

When should you consider epiglottitis

Back 200

Consider epiglottitis when the patient has a severe
sore throat or looks toxic, and the pharyngeal
exam is unimpressive

Front 201

Describe the Centor criteria for Strep pharyngitis

Back 201

1. Presence of fever >38 C
2. Tonsillar exudates
3. Swollen anterior cervical lymph nodes
4. Absence of cough

Front 202

Most common orbital bone fractured
How is diagnosis confirmed

Back 202

Infraorbital bone
Diagnosis confirmed with x-ray (facial view) and confirmed with CT

Front 203

Which lacerations around the eye should be referred to an opthomalogist

Back 203

Lacerations through the tarsal plate or the lacrimal apparatus and lacerations that involve the lid margin.

Front 204

How can corneal abrasions be detected

Back 204

Fluorescein stain and cobalt blue filter

Front 205

Symptoms of corneal abrasion

Back 205

Painful red eye, foreign body sensation and mild photophobia.

Front 206

Treatment of corneal abrasion

Back 206

-topical antibiotics (such as polymyxin B/trimethoprim drops or fusithalmic ointment)
-pain relief with either topical NSAID drops (like diclofenac or ketorolac) or oral narcotics.
-do not use tetracaine drops or eye patch

Front 207

Define hyphema. What is the initial treatment?

Back 207

Blood in the anterior chamber. Usually see a blood layer inferiorly.
Treatment involves protecting the eye with an eye shield and referral to an ophthalmologist. They will be followed on a daily basis until resolution to detect complications such as secondary glaucoma, corneal staining, or secondary rebleeding.

Front 208

Signs and symptoms of post traumatic glacoma

Back 208

-Intense eye pain or headache, nausea and vomiting, mild photophobia, and decreased vision.
-fixed mid-dilated pupil, injected conjunctiva, a cloudy cornea, decreased visual acuity, and an increase in intraocular pressure (usually >40)

Front 209

When should retinal detachment be suspected

Back 209

If the patient complains of new floaters and flashes of light or a visual deficit often described as a curtain falling over the visual field of the affected eye.

Front 210

Treatment of acute angle glaucoma

Back 210

1. Topical pilocarpine
2. Topical timolol
3. I V acetozolamide
4. IV mannitol
5. Laser iridotomy.

Front 211

Typical presentation of optic neuritis. What is it associated with?

Back 211

Young women between the ages of 20-40 who present with a decrease in their vision as well as retroocular pain and pain with eye movement.
Optic neuritis is the presenting complaint in 50% of cases of MS

Front 212

Causes of painless vision loss

Back 212

-retinal detachment
-central retinal artery or vein occlusion
-amaurosis fugax (TIA of retinal artery)
-occipital stroke

Front 213

What percent of patients with nephrolithiasis have microscopic or gross hematuria?

Back 213

70-90%

Front 214

What causes falsely elevated serum

Back 214

Hemolysis of sample
or
Severe thrombocytosis or leukocytosis.

Front 215

Most common causes of hyperkalemia

Back 215

Renal failure (missed dialysis)
Medications (ACEi, NSAIDs, K sparing diuretics, succinylcholine, digoxin)
Acute acidosis
Cell death (trauma, burns, crush injuries)
Increased K intake (supplements)

Front 216

Presentation of hyperkalemia

Back 216

Generally nonspecific or asymptomatic
Muscle weakness, cramps, or occasionally focal neurologic signs

Front 217

ECG changes in hyperkalemia

Back 217

1. Tall peaked T waves and ST segment depression (approx. 5.5mEq/L)
2. Loss of P waves
3. Widening of the QRS complex, prolongation of the PR interval
4. Sine wave pattern
5. Asystole or ventricular fibrillation

Front 218

Management of hyperkalemia

Back 218

Mnemonic: C BIG K Die - CaCl, beta agonist, bicarb, insulin/glucose, kayexalate, diuretic and dialysis

1. Protect the heart: Calcium chloride IV. This is indicated if there is evidence of QRS widening or patient is hypotensive.
2. Decrease serum K: 1-2amps D50W + Insulin 10 units (approx. 1mEq decrease). Beta agonist, salbutamol via continuous nebulization. Bicarbonate if acidotic or fluids if dehydrated.
3. Excrete K: kayexalate, diuretic (if kidney function), dialysis

Front 219

Criteria for systemic inflammatory response syndrome (SIRS)

Back 219

More than 2 of:
>38 C or < 36 C
Pulse >90 beats/min
RR >20 breaths/min (or PaCO2<30mmHg)
WBC >12 x 10*9 cells/l or < 4 x 10*9 cells/l or
>10% bands

Front 220

Define sepsis, severe sepsis, and septic shock

Back 220

Sepsis - SIRS in response to an infection
Severe Sepsis - sepsis and signs of organ dysfunction (e.g. acute lung injury, coagulopathy, altered mental status, renal failure, decreased urine output, liver failure, lactic acidosis etc.)
Septic Shock – severe sepsis and hypotension (sBP<90) unresponsive to IV crystalloid fluid bolus.

Front 221

Treatment of septic shock

Back 221

1. ABC's monitors, lines, IV's
2. IV fluids - 20-40 mL/kg over 15-30 mins and 500 mL's every 15-30 minutes. Some patients may require 6-8 L's to achieve MAP and CVP targets.
3. Antibiotics - piperacillin-tazobactam 4.5 g IV with vancomycin 1g IV if MRSA is suspected and azithromycin 500mg IV if pneumonia is suspected
4. Surgical intervention or removal of old lines/catheters
5. Early goal directed therapy
6. Others: steroids (IV hydrocortisone), intubation, sedation, paralysis

Front 222

Describe early goal directed therapy for severe sepsis and septic shock

Back 222

1. CVP is measured through a central line (internal jugular or subclavian) and a target of 8- 12 mmHg is achieved through frequent fluid boluses.
2. MAP of 65-90 mmHg is achieved by giving vasopressors (dopamine or norepinephrine).
3. Central venous oxygen saturation of >70% by giving packed red blood cells to achieve a hemoglobin of 90 and dobutamine is given for its inotropic effect

Front 223

Define anaphylaxis

Back 223

Anaphylaxis is a severe allergic reaction to any stimulus, (usually) having sudden onset and generally lasting less than 24 hours, involving one or more body systems and producing one or more symptoms

Front 224

Signs and symptoms of anaphylaxis

Back 224

Urticaria, angioedema (88%)
Upper airway edema (56%)
Dyspnea, wheeze (47%)
Dizziness, syncope, hypotension (33%)
Nausea, vomiting, diarrhea, cramping, abdominal pain (30%)

Front 225

Pathophysiology

Back 225

IgE-mediated allergic phenomenon. Allergic anaphylaxis requires prior exposure and sensitization to an allergen. When a recognized allergen binds IgE on the surface of mast cells and plasma basophils, causing them to degranulate and release histamine and other bioactive mediators.

Front 226

What causes hives and angioedema?

Back 226

Histamine causes increased capillary permeability and vasodilation. In the skin, this leads to urticaria. In subcutaneous tissue, this causes angioedema.

Front 227

Management of anaphylaxis

Back 227

1. ABC's - including intubation or surgical airway
2. 100% O2 via nonrebreather mask
3. epinephrine 0.3–0.5 mg IM (0.01 mg/kg in children) of 1:1000
4. Inhaled beta agonist
5. 1-2 L cyrstalloid if hypotensive
6. H1 receptor blocker dyphenhydramine 50 mg IV (1mg/kg) and an H2 receptor blocker such as ranitidine 50mg (1 mg/kg) IV should both be given.
7. Steroids to reduce second phase reaction - Methylpredinsone 1 mg/kg IV

Front 228

How should anaphylaxis be treated in patients on a beta blocker?

Back 228

Try epi first. If unsuccessful give glucagon 1 mg IV, in repeat doses every 5 minutes (max 10 doses). If bolus administration is successful, a glucagon infusion should be started at 1–5 mg/hr.

Front 229

Dose of epinephrine to give in anaphylaxis reaction

Back 229

Epinephrine 0.01 mg/kg IM (1:1000)
or
0.5 mg IM (1:1000)

Front 230

Medications that can cause serotonin syndrome

Back 230

Antidepressants: SSRI, SNRI, MAOI, lithium
Antibiotic: linezolid (MAOI activity)
Stimulants: cocaine, amphetamine, ecstasy
Migraines: sumatriptans
Opiods: meperidine, dextromethorphan, tramadol
Herbal remedies: St. John‘s Wort

Front 231

Triad of serotonin syndrome

Back 231

1. Altered mental status (confusion, agitation, coma)
2. Autonomic nervous system dysfunction (fever,
shivering, sweating, diarrhea, tachycardia, tachypnea, high or low BP)
3. Neuromuscular abnormalities (ataxia, hyperreflexia, myoclonus, tremor, rigidity, akathisia)

Front 232

Medications causing QT prolongation

Back 232

amiodarone
procainamide
haloperidol
fluorquinolones
macrolides
fluconazole

Front 233

Define menorrhagia/hypermenorrhea and metrorrhagia

Back 233

Menorrheagia - menses >7 days or >80mL, or <21 day recurrence
Metrorrhagia - irregular vaginal bleeding outside the normal cycle

Front 234

Life threatening causes of vaginal bleeding

Back 234

Ectopic pregnancy
Abruptio placentae
Placenta previa
Uterine rupture
Post-partum hemorrhage
Post partum or post procedural endometritis 
Trauma

Front 235

Causes of vaginal bleeding in prepubertal females

Back 235

Vaginitis (10%)
Precocious puberty (21%)
GU tumors (10%)
Vulvar pathology (8%)
Trauma (including sexual abuse) (8%).

Front 236

Describe the prevalence of first trimester vaginal bleeding. What is the risk of abortion

Back 236

Up to 40% of women have cramping and spotting during the first 20 weeks of gestation. Half of these women (20%) undergo first trimester abortion and 60% of those are related to chromosomal abnormalities. Bleeding and expulsion of uterine contents usually starts a week after the death of the fetus.

Front 237

Treatment of incomplete abortion under 12 weeks

Back 237

Misoprostol can be given for incomplete abortion (success rate of 66-93%).

Front 238

What bHCG level must be achieved before an intrauterine pregnancy can be seen on transvaginal U/S

Back 238

At levels of 500-1500 IU/L, an intrauterine sac should be seen on trans-vaginal ultrasound

Front 239

Management of ectopic pregnancy

Back 239

Methotrexate - if stable, able to follow up, bHCG level < 5000 mIU/L, and no fetal cardiac activity
Surgical

Front 240

Causes of vaginal bleeding in 3rd trimester

Back 240

Placenta previa, abruptio placentae, and uterine rupture.

Front 241

Causes of postpartum hemorrhage

Back 241

Uterine atony
Uterine rupture
Lacerations/tears
Retained placental tissue
Uterine inversion
Coagulopathy

Front 242

Definition of gestational hypertension

Back 242

Systolic BP >140mmHg or diastolic BP >90 developing after the 20th week of gestation
No proteinuria
BP returns to normal within 12 weeks post-partum

Front 243

Definition of preeclampsia

Back 243

Systolic BP >140mmHg or diastolic BP >90 after
20 weeks gestation
Proteinuria >300mg/24hr (>1+ dipstick is
suggestive)

Front 244

Definition of eclampsia

Back 244

Grand mal seizures that cannot be attributed to other causes in women with preeclampsia

Front 245

Describe HELLP syndrome

Back 245

-Hemolysis, elevated liver enzymes, low platelets
-Decreased organ perfusion secondary to
vasospasm and endothelial activation in pre-eclamptic
-May also result in bleeding, pulmonary edema,
renal insufficiency, infection, CNS morbidity

Front 246

Treatment of severe preeclampsia and eclampsia

Back 246

-Treat severe preeclampsia with IV magnesium sulfate (4-6g loading then 2g/hour to maintain levels 4.8-8.4 mg/dL) to prevent seizures. Also used to prevent recurrent seizures.
-Antihypertensives: Hydralazine 5mg doses in 15 minute intervals when diastolic BP >105mmHg or systolic >160 until diastolic 90-100 mmHg or IV Labetolol 20 mg IV followed by repeat doses every 10 minutes, maximum dose 300mg.
-Fluid: 60-125 cc/hr maximum even if oliguric to avoid pulmonary and cerebral edema.

Front 247

Describe an approach to hematuria in the ED

Back 247

Painful - obstruction, stone, UTI, trauma
Painless - urinary tract cancer (renal, bladder, ureter), anticoagulation, BPH

Front 248

History in patients with renal colic

Back 248

-Renal colic typically presents as sudden onset of unilateral flank pain that radiates anteriorly and inferiorly toward the groin.
-Patients are commonly described as writhing in pain, and are often unable to find a comfortable position to relieve their symptoms.
-Patients with renal colic often have nausea and/or vomiting.

Front 249

Physical exam findings in patients with renal colic

Back 249

-Mild tachycardia or hypertension due to pain
-The main and often only physical exam finding in renal colic is unilateral CVA tenderness. In general, there should not be any significant anterior abdominal tenderness.

Front 250

DDx of renal colic

Back 250

AAA - renal colic is rare in elderely, r/o AAA in all patients over 50
Aortic dissection
Renal artery thrombosis
Appendicitis
Pyelonephritis
Ectopic pregnancy

Front 251

Investigations in renal colic

Back 251

-urine dipstick reveals microscopic hematuria, no white blood cells, and no nitrites
-noncontrast CT for elderly, 1st presentation, and uncertain diagnosis

Front 252

Treatment of renal colic

Back 252

-Pain management with morphine + Naproxen (po) or Toradol (IV)
-alpha-blocker such as Tamsulosin (Flomax) 0.4mg once daily for 7-10 days
-Fluids

Front 253

Prognosis of stone passage in renal colic

Back 253

If the stone is 4 mm or smaller, they will eventually be passed 90% of the time.
Stones 5-7 mm have a 50% chance of passing spontaneously.
Stones larger than 7mm are unlikely to pass spontaneously, and should be referred for consideration of lithotripsy.

Front 254

Most common causes of paediatric cardiac arrest

Back 254

1. Underlying respiratory abnormality (most common)
2. Circulatory failure from hypovolemia (loss of fluid or blood, sepsis)

Front 255

Differences and considerations in pediatric vs. adult airway

Back 255

-large tongue relative to oral cavity

-higher and more anterior larynx (c3-c4 vs c5-c6)

-long floppy epiglottis

-subglottic area is the narrowest portion of the infant larynx

-large head leads to flexed neck

Front 256

Estimated size of endotracheal tube needed in children based on age group

Back 256

-infants to 1 year = 3.5 ETT uncuffed

-1–2 yrs=4.0 uncuffed ETT

-child > 2 yr. = (Age/4) + 4 uncuffed ETT

-child >2 yr = (age/4) + 3.5 cuffed ETT

-internal diameter of ETT = size of the child's little
finger

Front 257

When should oropharyngeal airway be used over nasopharyngeal airway in children

Back 257

An oropharyngeal airway can only be used in an unresponsive child without a gag reflex.

Nasopharyngeal airways are generally better tolerated, but should not be used if there is suspicion of skull base trauma in order to avoid potential infection or penetration of the anterior cranial fossa with insertion.

Front 258

How to verify endotracheal tube placement following intubation

Back 258

-Bilateral chest movement, listen for equal breath sounds over both lung fields

-Listen for gastric insufflation over stomach

-Check exhaled CO2 (end-tidal CO2)

-Check oxygen saturation if perfusing rhythm

-If uncertain, direct laryngoscopy

-Chest X-ray in hospital setting

Front 259

Things to consider if patient deteriorates following intubation

Back 259

DOPE

Displacement of tube
Obstruction of tube
Pneumothorax
Equipment failure

Front 260

Normal respiratory rate based on age

Back 260

Infant 30-60

Toddle 24-40

Preschooler 22-34

School Age 18-34

Adolescent 12-16

Front 261

Hypotension by age in children

Back 261

Team neonates (0-28 days) <60 mm Hg

Infants (1-12 mo) <70 mm Hg

Children (>1 yrs) <70+ 2 x age mm Hg

Children (>10 yrs) <90 mm Hg

Front 262

Normal heart rate for age

Back 262

Infant 100-160
Toddle 90-145
Preschooler 80-140
School age 70-120
Adolescent 60-100

Front 263

When should chest compressions/CPR be initiated on a child

Back 263

-no pulse palpable

-heart rate is <60 bpm and there is evidence of poor systemic perfusion

Front 264

Rate of breaths to compressions in pediatric CPR with and without advanced airway

Back 264

No advanced airway, 1 rescuer - 30:2

No advanced airway, 2 rescuer - 15:2

Advanced airway - compressions uninterupted, 8-10 breaths/min

Front 265

Size of fluid bolus in pediatric patient in shock

When to give blood if acute hemorrahge cause of shock?

Back 265

10-20mL/kg NS

Blood replacement is indicated in children with severe acute hemorrhage if a child remains in shock after 40 -60 mL/kg of crystalloid

Front 266

Drug of choice in pediatric cardiac arrest

Mechanism of action?

Back 266

Epinephrine

Has both alpha and beta adrenergic properties but the alpha adrenergic mediated vasocontriction is most important, acting to restore diastolic pressure

Front 267

Complications of sodium bicarbonate administration during CPR

Back 267

Excessive bicarbonate may impair tissue oxygen delivery (shifts O2 dissociation curve), cause hypokalemia, hypocalcemia, hypernatremia, hyperosmolality, decrease ventricular fibrillation threshold, and impair cardiac function

Front 268

Effects of atropine

When would it be used in CPR

Back 268

Competitive antagonist of the muscarinic acetylcholine receptor (acetylcholine being main neurotransmitter used by the parasympathetic system)

Used to treat symptomatic bradycardia and vagally mediated bradycardia that can occur with intubation attempts

Front 269

Effect of dopamine

When would it be used during CPR

Back 269

Dopamine is an endogenous catecholamine with complex cardiovascular effects. In higher doses it stimulates beta receptors and alpha adrenergic vasoconstriction

Used for the treatment of circulatory shock following resuscitation, or when shock is unresponsive to fluid administration

Front 270

Effect of adenosine

When would it be used in CPR

Back 270

Causes a temporary atrioventricular (AV) nodal
conduction block and interrupts reentry circuits that involve the AV node

Used for treatment of supraventricular tachycardia

Front 271

Treatment of nonshockable rhythm (asystole/PEA) arrest in children

Back 271

1. Continue CPR
2. Second rescuer obtains vascular access and
delivers epinephrine 0.01 mg/kg (0.1 mL/kg of 1:10,000 solution) while CPR continues; repeat dose every 3 – 5 minutes
3. Check rhythm every 2 minutes with minimal interruptions in chest compressions
4. Search for reversible causes (H's and T's)

Front 272

Causes of asystole and PEA arrest

Back 272

H's and T's

Hypothermia, Hypoxia, Hydrogen ion (acidosis), Hypoglycemia, Hypovolemia

Tension Pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (pulmonary and coronary)

Front 273

When is defibrillation with AED or manual defibrillator indicated

Back 273

ventricular fibrillation

pulseless ventricular tachycardia.

Front 274

Treatment of SVT in infants and children

Back 274

-If hemodynamically stable, begin with vagal maneuvers (e.g. ice to face in an infant without occluding airway, blowing through narrow straw in older child)

-If unsuccessful, adenosine is the drug of choice

-If hemodynamically unstable, then consider synchronized cardioversion (0.5 to 1 J/kg; increase to 2J/kg for subsequent attempts)

Front 275

Treatment of asthma exacerbation in children

Back 275

Salbutamol - 4-8 puffs q20min
Ipratropium bromide - 4-8 puffs q20min up to 3 hrs
Prednisone 2 mg/kg
MgSO4 - 40 mg/kg IV

Front 276

Discharge therapy for patients with asthma exacerbation

Back 276

-Salbutamol 4–8 puffs/dose q4h prn via MDI and spacer (with a mask < 6 years, with a mouthpiece 7 years or older) for 24-48 hours, then 2 puffs qid prn x 1 week.
-Prednisone 1mg/kg daily x 4-5 days orally. No tapering necessary.
-Fluticasone 50 mcg bid for 4-8 weeks after discharge
-Mandatory follow up at 24-48 hours
-Return if increased work of breathing requiring
bronchodilators <q4h.

Front 277

Classic history for croup

Back 277

-6-36 months of age
-barking cough
-hoarse voice
-inspiratory stridor +/- respiratory distress

Front 278

Management of croup

Back 278

-Dexamethasone 0.6 mg/kg po once (all patients)
-Nebulized epinephrine 1:1000 (2.5 - 5 ml) in severe respiratory distress

Front 279

Define lethargy

Back 279

Lethargy - a level of consciousness characterized by poor or absent eye contact; or the failure of a child to recognize parents; or failure to interact with persons or objects in the environment.

Front 280

Workout required for fever without a focus 0-1 months of age

Treatment?

Back 280

CBC
Urinalysis
Blood, urine, LP cultures
+/- chest x-ray

Hospitalization + ampicillin and gentamicin for all

Front 281

Workup required for fever without a focus in infant 1-3 mo of age

Back 281

Lethargic - full septic workup + hospitalization + Abx

High risk rochester criteria - full spetic workup + hosptialization + Abx

Low risk rochester criteria - CBC, urinalysis, blood and urine culture + discharge w/o Abx + 24 hr followup

Front 282

What must be ruled out for all infants with bilious vomititng

Back 282

Malrotation with volvulus

Front 283

Classic history for patients with intussuception

Back 283

-3-12 mo old male

-intermittent colicky abdominal pain

-abdominal distension

-bilious vomiting

-blood per rectum /currant jelly stools (late sign)

Front 284

Management of mild and moderate dehydration with oral rehydration

Back 284

Pedialyte

Mild: 20 mL/kg 1st hour, 10 mL/kg thereafter, 10 mL/kg per bowel movement

Moderate: 20 mL/kg 1st hour, 20 mL/kg thereafter, 10mL/kg per bowel movement

Front 285

When should a culture be taken of taken from the bite site following an animal or human bite

Back 285

Only culture when there is clinical evidence of a wound infection (e.g. progressive erythema, purulent discharge, signs of sepsis)

Front 286

Management of mammal bites

Back 286

1. Copious irrigation - 18 - 20 gauge angiocath on a 20 cc syringe will provide adequate irrigation pressure for most wounds. Do not open or widen the puncture wound for irrigation

2. Debride - decreases infection in crushed and devitalized tissues.

3. +/- suture - if low risk of infection (good vascular supply like face), do not suture if high risk of infection. Option for delayed repair after 3-5 days of antibiotic Rx.

Front 287

High risk criteria for mammal bite (wound factors)

Back 287

- puncture wounds or crush injuries
- wounds greater than 12 hours old
- hand or foot wounds
- wounds near joints

Front 288

High risk criteria for mammal bite (patient factors)

Back 288

- immunocompromised patient: diabetes, splenectomy, chronic alcoholism, AIDS, on immunosuppressive meds
- patient age greater than 50 years
- prosthetic joints or valves

Front 289

Rate of infecton from mammal bites

Back 289

Dog 10-30%

Cat 10-50%

Human 50%

Front 290

Antibiotic choice for mammal bites

Back 290

1st line - amoxacillin-clavulanic acid (Clavulin)

2nd line - 2nd generation cephalosporins
(e.g. cefuroxime, cefaclor, or cefoxitin iv)

Front 291

Likely cause of infection following dog or cat bite that becomes infected within 24 hours

Back 291

Pasteurella multocida

causative organism in up to 80% of cat bite
infections and up to 50% of dog bite infections

propensity to cause metastatic infections:
septicemia, osteomyelitis, tenosynovitis,
meningitis

Front 292

Describe postexposure immunoprophylaxis following high risk animal bite

Back 292

Persons not previously immunized:

- Passive immunization with Rabies Immune
Globulin (RIG): 20 IU/kg-

- Active immunization with rabies vaccine (e.g.
HDCV): 5 injections of 1 ml IM over 28 days,
given on days 0, 3, 7, 14, and 28

Front 293

Goal temperature in patients with heat stroke

Back 293

rectal temp. < 39.5 C

Front 294

Which electrolytes must be monitored during heat stoke

Back 294

K (hyperkalemia) and Mg

Front 295

Describe the classifiation of burns

Back 295

Superficial (first degree) involves epidermis only i.e. sunburn

Superficial partial thickness (second degree) extends to epidermis and superficial dermis, blister formation occurs and the burns are very painful.

Deep partial thickness (second degree) involves hair follicles, sebaceous glands. Skin is blistered and exposed dermis is pale white to yellow in colour. Sensation is absent.

Full thickness burns (third degree) involve the epidermis and all dermal layers. The skin is pale, insensate and charred or leathery. Surgical treatment is required, spontaneous healing does not occur.

Fourth degree burns extend through skin to all underlying layers e.g. fat, muscle, and bone. Amputation or reconstruction is often required.

Front 296

Describe how to estimate total body surface area burned in adults

Back 296

Rule of 9's for Adults: 9% for each arm, 18% for each leg, 9% for head,18% for front torso, 18% for back torso.

Front 297

Describe how to estimate total body surface area burned in children

Back 297

Rule of 9's for Children: 9% for each arm, 14% for each leg, 18% for head, 18% for front torso, 18% for back torso.

Front 298

Describe fluid requirements in burn patients

Back 298

Fluid Requirements = TBSA burned(%) x Wt (kg) x 4mL

Given for burns equal or larger than 20% BSA, partial thickness or greater. Use ringers lactate. Given over 24 hrs, 1/2 in first 8 hrs.

Front 299

Half life of carbon monoxide in blood

Describe treatment

Back 299

room air, 240-320 minutes
100% O2, 90 minutes
hyperbaric oxygen, 20 minutes

Give high flow O2 for all. Transfer to a hyperbaric chamber is indicated in those with levels >25

Front 300

Describe basic wound care in burn patients

Back 300

Burns are covered with a gauze dressing and polysporin ointment for superficial partial thickness and flamazine (silver sulphadiazine) for deep partial thickness burns (except on the face)

Front 301

What antibiotics and immunizations are indicated for burn patients

Back 301

No role for prophylactic antibiotics.

Tetanus should be updated.

Front 302

Which patients need to be transfered to a specialized burn center

Back 302

- Partial thickness or full thickness burns > 10% ages <10 or >50
- Partial thickness or full thickness burns > 20% in all others
- Partial-thickness and full-thickness burns involving the face, hands, feet, genitalia, or perineum or overlying major joints
- Full-thickness burns greater than 5% BSA in any age group

Front 303

Complications following electircal injury/burn

Back 303

Cardiac dysrhythmias: occurs at time of injury asytole or ventricular fibrillation, will not develop in the ED

Deep muscle injury/necrosis

Rhabdomyolysis

Compartment syndrome

Front 304

Characteristics of acidic and alkali chemical burns

Back 304

Acids cause coagulation necrosis and formation of a leathery eschar.

Alkalis cause liquifaction necrosis and deeper burns.

Front 305

Treatment for chemical burns

Back 305

Aggressive irrigation is the main treatment for chemical burns. pH paper is used to determine the presence of additional chemical, ideally applied 10-15 minutes after irrigation is stopped.

Front 306

Define hypothermia

Back 306

Hypothermia is defined as a core body temperature of less than 35.0 C

Front 307

Most accurate site for noninvasive temperature reading

Back 307

Esophageal temperature

Front 308

At what temperature does the body cease to shiver

Back 308

30-32 C

Front 309

ECG changes in hypothermia

Back 309

J waves (Osborn wave)

Front 310

At what temp are hypothermic patients at risk of developing arrythmia's

What is the typical progression

Back 310

Patients are at risk for arrhythmias at temperatures <30°C

Sinus bradycardia -> atrial fibrillation -> ventricular fibrillation -> asystole

Front 311

Pathophysiology of frost bite

Back 311

Frostbite occurs when tissue temperature drops below 0 ̊C. The tissue is damaged by both the freeze-thaw insult and subsequent progressive dermal ischemia.

Front 312

Treatment of frostbite

Back 312

Immerse 40-42 ̊C water bath, until the part feels pliable and distal erythema is noted, usually requires 10-30 minutes of immersion

Ibuprofen 400 mg q12h to inhibit thromboxane A production by injured tissue

Benzyl penicillin 600 mg every 6 hours

Front 313

In hypothermic patients, below what temperature should you use active core rewarming

Back 313

<32 C

Front 314

Pathophysiology of drowning

Back 314

Lung damage and hypoxemia leading to hypoxic encephalopathy

Aspiration of fluid leads to:
- loss of surfactant causing atelectasis
- injury to the alveolar-capillary membrane leading
to interstitial and alveolar edema (can lead to secondary drowning)
- obstruction of small airways by water and
particulate matter
- bronchospasm
- +/- chemical injury if stomach contents aspirated

Front 315

List universal antidotes

Back 315

O2, glucose, thiamine, naloxone

Front 316

Mnemonic for anticholinergic toxidrome

Back 316

Blind as a bat, dry as a bone, red as a beet, mad as a hatter, and hot as a hare

Front 317

Define toxidrome

Back 317

A toxidrome is a constellation of clinical signs and symptoms associated with a particular class of substances.

Front 318

Manifestations of anticholinergic toxidrome

Back 318

Hyperthermia
Dilated pupils
Dry skin & mucous membranes Agitation
Hallucinations
Seizures
Tachycardia
Urinary retention
Ileus

Front 319

Etiology of anticholinergic toxidrome

Back 319

Antihistamines
Atropine & belladonna
Diphenhydramine
Tricyclic antidepressants

Front 320

Manifestations of cholinergic toxidrome

Back 320

Salivation, Seizures
Lacrimation
Urinary incontinence
Diarrhea, Diaphoresis
Bronchospasm, Bradycardia
Emesis, Excitation

Front 321

Etiology of cholinergic toxidrome

Back 321

Carbamates
Nerve gases
Organophosphates

Front 322

Manifestations of sympathomimetic toxidrome

Back 322

Hyperthermia
Mydriasis
Diaphoresis
Tachycardia
Hypertension
Excitation
Seizures

Front 323

Etilology of the sympathominetic toxidrome

Back 323

Amphetamines ASA
Cocaine
LSD
PCP
Theophyllines
Sedative & alcohol withdrawal

Front 324

Manifestations of narcotic/sedative toxidrome

Back 324

CNS depression
Respiratory depression
Hypotension
Miosis +/-

Front 325

Etiology of narcotic/sedative toxidrome

Back 325

Barbituates, Benzodiazepines
Ethanol
GHB
Opioids
Other sedatives

Front 326

Describe 3-3-2-1 rule for predicting difficult intubation

Back 326

3-3-2-1

3 finger mouth opening

3 fingers from hyoid to chin

2 fingers from thyroid cartilage notch to floor of mandible

1 finger lower jaw anterior subluxation

Front 327

Formula for anion gap

Normal value?

Back 327

Anion Gap = Na+ - (HCO3- + Cl-)

Normal AG < 10 mmol/L

Front 328

Formula for osmolar gap and calculated osmolality

Normal value

Back 328

Osmolal Gap = (Measured – Calculated) Osmolality

Calculated Osmolality = 2[Na+ ] + BUN + Glucose + 1.25 X Ethanol

Normal Osmolal Gap should range from -14 to +10 mosmoles/L

Front 329

DDx of increased anion gap

Back 329

Methanol
Uremia
Diabetic Ketoacidosis, Alcoholic Ketoacidosis, Starvation Ketoacidosis
Phenformin, Paraldehyde
Iron, INH
Lactic acidosis
Ethylene Glycol
Salicylate

Bonus: Carbon Monoxide, Cyanide, Toluene

Front 330

DDx of increased osmolar gap

Back 330

Ethylene Glycol
Isopropyl Alcohol
Glycerol
Mannitol
Methanol
Sorbitol

Front 331

In which poisoned patients should activated charcoal be considerered

Back 331

Patients who present within one hour of their gastrointestinal exposure to a toxin.

Consider in: Carbamazepine, Phenobarb,
Quinine, Theophylline

Front 332

In which toxins can elimination be enhanced with urine alkalinization

Back 332

Chlorpropamide
Methotrexate
Phenobarb
Salicylates

Front 333

In which toxins should hemodialysis be considered to enhance elimination

Back 333

ASA
Ethylene Glycol
Lithium
Methanol
Valproate

Front 334

Antidote for acetaminophen overdose

Back 334

N-acteylcysteine

Front 335

Antidote for beta blocker overdose

Back 335

High dose insulin

Front 336

Antidote for carbon monoxide poisoning

Back 336

High dose O2 +/- hyperbaric O2 therapy

Front 337

Antidote for digoxin overdose

Back 337

Digoxin FAB fragments

Front 338

Antidote for ethylene glycol and methanol poisoning

Back 338

Fomepizole or Ethanol

Front 339

Antidote for hydrofluoric acid poisoning

Back 339

Calcium

Front 340

Antidote for isoniazid overdose

Back 340

Pyridoxime

Front 341

Antidote for opioid overdose

Back 341

Naloxone

Front 342

Antidote for organophosphates poisoning

Back 342

Atropine plus pralidoxime

Front 343

Antidote for sodium channel blocker overdose

Back 343

NaHCO3

Front 344

Antidote for sulfonylurea poisoning

Back 344

Octreotide

Front 345

Mechanism of action of alcohol

Back 345

Depressing the excitatory neurotransmitter glutamate

Increases the inhibitory activity of GABA and glycine

Front 346

Features of alcohol intoxication

Back 346

Slurred speech, nystagmus, slowed responses to verbal, visual or physical stimuli and decreased motor coordination/control

Front 347

How long must intoxicated patients be held in the ED

Back 347

Until:

awake and oriented with a Glasgow Coma Scale (GCS) of 15

able to respond appropriately to questions

able to ambulate normally

Front 348

Treatment to prevent Wernicke‘s encephalopathy

Time before resolution of symptoms?

Back 348

Thiamine 100 mg po, IM or IV daily

Ocular signs may be reversed in as little as 1-6 hours. Ataxia and confusion may improve over days to months.

Front 349

Over what time period can alcohol withdrawal occur following discontinuation of alcohol

Back 349

Up to 7 days later

Front 350

Symptoms of alcohol withdrawal

Back 350

Tachycardia, hypertension,elevated temperature

Agitation, tremor, diaphoresis

Nausea, vomiting

Seizures

Front 351

Symptoms of delirium tremons

Back 351

Hallucinations, delirium and confusion

Profound autonomic dysfunction: hyperthermia, tachycardia, hypertension, and seizures

Front 352

Time period when patients are most likely to have a seizure during alcohol withdrawal

Back 352

12-48 hours

Front 353

Triad of Wernicke's enchaphalopathy

Back 353

oculomotor abnormalities (nystagmus, lateral gaze palsies or disconjugate gaze)

cerebellar dysfunction

global confusion

Front 354

Characteristic of isopropyl alcohol intoxication

Back 354

- ketosis but NO acidosis
- normal blood glucose
- clinical features similar to those of ethanol poisoning but of longer duration
- fruity odor of acetone or smell of rubbing alcohol on the breath

Front 355

Products containing methanol

Back 355

windshield washer fluid

varnishes

antifreeze

improperly fermented EtOH

Front 356

Products containing isopropyl alcohol

Back 356

rubbing alcohol

skin and hair care products

hand sanitizer

industrial solvents.

Front 357

Features of methanol poisoning

Back 357

• CNS depression
• Visual disturbances and blindness
• Abdominal pain
• Marked anion gap-type metabolic acidosis
• Osmolar gap
• Possible renal failure

Front 358

Criteria for hemodialysis in patients with methanol poisoning

Back 358

- Visual or CNS disturbances
- Ingestion of more than 30 ml of methanol
- Severe metabolic acidosis
- Renal failure
- Elevated methanol level > 15

Front 359

Features of ethylene glycol poisoning

Back 359

- signs of intoxication yet no ethanol smell on the breath
- anion gap-type acidosis
- osmolar gap
- calcium oxalate crystalluria
- renal failure

Front 360

If unable to intubate after a paralytic is given during RSI what are the options

Back 360

Bag valve mask ventilation

Surgical airway

Front 361

Cricothyrotomy technique

Back 361

An incision is made through the cricothyroid membrane (i.e. below the thyroid cartilage).

A cricothyrotomy kit may be used which uses the Seldinger technique (introducer needle > guidewire > tracheostomy tube).

Front 362

Differentiate tracheostomy vs cricothyrotomy

Back 362

A tracheostomy (done just superior to the suprasternal notch) involves dissecting through superficial vessels, a cricothyrotomy avoids these vessels.

Front 363

Decribe the ABCDE's of trauma

Back 363

Airway - Is the airway patent? Have patient talk

Breathing - Auscultate lung fields. Look for equal rising of chest. Rule out tension pneumothorax.

Circulation

Disability - brief neurologic assessment (AVPU - Alert, voice, pain, unresponsive) or GCS

Front 364

DDx for shock

Back 364

S – septic

S – spinal (i.e. neurogenic) – may result from high spinal with loss of sympathetic trunk, these patient present with a low BP and a low HR

H – hypovolemic – usually hemorrhagic in trauma

O – obstructive – may occur from tension pneumothorax, PE, or pericardial tamponade

C – cardiogenic

K – anaphylac(K)tic

Front 365

Components of the FAST exam

Back 365

Lt flank (Spleen) - free fluid in the spleno-renal space

Rt flank (Liver) - free fluid in Morrison‘s pouch

Pelvis

Subxypohoid - pericardial effusion

Front 366

When should blood products be given in trauma

Back 366

If patient remains hypotensive following 2 L NS

Front 367

What needs to be examined in a trauma patient during the log roll

Back 367

1. Inspection for penetrating injuries, contusion, lacerations

2. Palpation for T and L spine tenderness

3. Rectal exam to assess for a high riding prostate (a contraindication to foley insertion), gross blood (indicative of bowel injury)

Front 368

What does FAST stand for?

Back 368

Focused Assessment with Sonography for Trauma

Front 369

What are the components of the 'Disability' assessment in a trauma patient

Back 369

Patients LOC - 'AVPU' - Alert, responds to Verbal, responds to Pain, Unresponsive

Pupils

Moving all four limbs

Front 370

Basic investigations for all polytrauma patients

Back 370

CXR

FAST

AP Pelivs

Front 371

What does the 'E' component of ABDCE's of trauma include

Back 371

Expose patient including back (log roll)

Enviroment - keep patient warm and dry

Front 372

Describe the secondary survey in trauma

Back 372

H & N - pupils equal and reactive, gross abnormality in visual acuity, facial bones (swelling, deformity, laceration), scalp, tympanic membranes, c-spine tenderness

Chest -

Abdomen - peritonitis, distension, FAST

DRE - lower GI bleed, tone, prostate

Extremeties

Neuro - GCS, motor or sensory defecites

Front 373

Layers of the meninges

Back 373

Pia (innermost)

Arachnoid

Dura (outermost)

Front 374

Normal ICP

Define cerebral perfusion pressure

Back 374

10-15 mm Hg

CPP = MAP - ICP

Front 375

Signs of basilar skull fracture

Back 375

Hemotympanum

Blood in ear canal

Rhinorrhea

Racoon eyes

Battle sign

Front 376

Describe eye component of GCS

Back 376

4 - open spontaneously

3 - to verbal command

2 - to pain

1 - no response

Front 377

Describe the verbal component of GCS

Back 377

5 - Alert and oriented

4 - Disoriented

3 - Incomprehensible

2 - Moans and sounds

1- None

Front 378

Describe the motor component of GCS

Back 378

6 - Moving spontaneously

5 - Localizes pain

4 - Withdraws from pain

3 - Decroticate posturing ( flexion of upper, extension of lower)

2 - Decerebrate posturing (extension of upper and lower)

1 - Done

Front 379

Describe the classification of head injuries

Back 379

Mild - GCS 14-15

Moderate - GCS 9 - 13

Severe - GCS 3 - 8

Front 380

Describe the CT head rule

Back 380

CT head is required for minor head injuries (GCS 13-15) with 1 of the following:

1. GCS < 15 at 2 hrs post injury

2. Suspected open or depressed skull fracture

3. Signs of basal skull fracture

4. Vomiting >/= 2 episodes

5. Age >/= 65Sn 98%, Sp 50% for dectecting clincally important HI

6. Amnesia before impact >/= 30 min

7. Dangerous mechanism

Front 381

Define concussion

Back 381

Type of minor head injury after a direct or indirect blow to the head characterized by transient change in cognitive or neurologic function

Front 382

Describe special considerations for intubation in patients with a head injury

Back 382

1. Consider premedication to prevent raising ICP with lidocaine (1.5-2 mg/kg IV push) to attenuate cough reflex and vecuronium (0.01 mg/kg IV) defasicullating dose

2. Induction with etomidate, midazolam (0.1-0.3 mg/kg), or propofol (1-2 mg/kg IV)

Front 383

Treatment of increased ICP

Back 383

1. Elevate head of bed

2. Provide sedation and analgesia

3. Mannitol 0.25-1 g/kg IV

4. Neuromuscular blockade

5. Mild hyperventilation PaCO2 30-35 mm Hg

Front 384

How does hyperventilation decrease ICP

Back 384

Hyperventilation reduces PaCO2 which temporarily reduces the ICP by cerebral vasoconstriction and subsequent reduction of cerebral blood flow.

The aim of hyperventilation is to reach an arterial PCO2 of 30-35 mm Hg (avoid PaCO2 < 25 as it can cause ischemia due to severe vasoconstriction).

Hyperventilation should be avoided during the first 24 hours after injury when cerebral blood flow is often critically reduced.

Front 385

Describe the approach to the interpretation of c-spine x-rays

Back 385

ABC'S approach

A - alingment - follow anterior and posterior contour lines. Translation of 1 vertebra over another > 3.5 mm is significant.

B - bone - follow boney contours looking for breaks in the cortex.

C - cartilage - disc spaces of equal length. Pre-dental space < 3mm

S - soft tissue - retropharyngeal space measures less than 7mm at C2 and 21mm at C7

Bonus - odontoid view, lateral mass of C1 & C2 should align.

Front 386

Describe canadian c-spine rules

Back 386

1. High risk factors that warrant radiography - Age >65, dangerous mechanism, paresthesia in extremity

2. Any low risk factors that allow safe assessment of ROM - simple rear end collision, sitting position, ambulatory, delayed onset neck pain, absence of midline c-spine tenderness

3. If no high risk + 1 or more low risk then assess ROM, if can rotate >45 degress left and right then no radiography.

Front 387

Describe considerations in nasal fracture

Back 387

- x-ray rarely needed

- final alignment needs to wait 2-3 weeks for swelling to subside and a plastic surgeon can make an assessment

- inspect nasal septum for hematoma. Submucosal collection of blood (septal hematoma) should be drained to avoid ischemic depression in septum

Front 388

Describe LeFort Classification of midface fractures

Back 388

leFort I - extends down through maxilla to either side of the mouth and the upper teeth and bones will be mobile.

leFort II - extends through (or just inferior to) the infraorbital rim and the nasal aperture and upper teeth will move as a unit separate from the cheekbones (zygoma)

leFort III - extends across through the orbits or just above them and the entire midface (including the zygomas) will be mobile

Front 389

Treatment of tooth fracture in ED (removed from socket)

Back 389

a. Rinse socket with NS

b. If the patient has the tooth, sterilize it with

chlorhexidine, or hydrogen peroxide (5 second rinse in any of these). Cleanse the tooth immediately with sterile NS. Place tooth in socket. Secure with bone wax.

c. If tooth cannot be replaced or if patient asks for advice about storage, have the tooth preserved in milk.

d. refer to dentistry

Front 390

Treatment of chipped tooth in ED

Back 390

See if the residual tooth is loose and

splint if necessary with bone wax or skin glue.

Classify tooth fracture according to Ellis

Classification

If the fracture is Ellis 3 or 4 (Pulp exposed),

consider covering the tooth with bone wax for

pain relief.

Refer patient to dentistry for definitive care

and follow-up

Front 391

Describe Ellis classification of tooth fracture

Back 391

Ellis 1 - through enamil

Ellis 2 - through dentin + enamil

Ellis 3 - through pulp + dentin + enamil

Front 392

When should fractures of the mandible be suspected?

Back 392

irregular bite (malocclusion)

misalignment in the jaw

point tenderness of the bone

loose teeth

strong pain when biting down on a tongue depressor you forcefully try to remove from the mouth

intraoral bleeding

Front 393

Describe approach to describing fractures

Back 393

Open vs. closed

Neurovascular status: intact vs. compromised

Which bone(s) is/are broken

Location the fracture: i.e., proximal humerus; metacarpal head

Type of fracture: i.e. oblique vs. transverse; simple vs. comminuted)

Alignment of fragments: Angulation, Displacement, Shortening

Front 394

Features of compartment syndrome

Back 394

Pain out of proportion

Parasthesia

Pallor

Pulselessness

Paralysis.

Front 395

What nerve is at risk in an anterior shoulder dislocation

Back 395

Axiallary nerve - supplies sensation to lateral shoulder and motor to the deltoid

Front 396

X-ray finding in anterior shoulder dislocation

Back 396

Lateral view shows the humeral head sitting anterior to the glenoid

Front 397

Describe Ottawa Ankle Rules

Back 397

An ankle X-ray is required if:

A foot X-ray is required if:

1. Boney tenderness at base of navicular or base of 5th metatarsal

2. Inability to weight bear both immediately AND in the ED

Boney tenderness at posterior aspect of distal 6cm of medial or lateral malleolus

inability to bear weight both immediately AND in the ED

Front 398

Describe a Colle's fracture

Back 398

Extraarticular fracture of the distal radius due to FOOSH

Front 399

Which two parameters are of importance in deciding which colle‘s fractures require reduction?

Back 399

Volar tilt - at least neutral, anatomic 20 degrees volar tilt

Radial length - at least as long as the ulna

Front 400

Maximum dose of lidocaine with and without epi

Back 400

Without epi 3-5 mg/kg

With epi 5-7 mg/kg

Front 401

Signs and symptoms of lidocaine toxicity

Back 401

Dizziness

Perioral numbness

Seizures

Cardiovascular collapse

Front 402

Describe the difference between primary, secondary, and delayed closure. When would you use each?

Back 402

Primary closure refers to closure immediately after the injury

Secondary closure involves leaving the wound open and allowing it to close over time. This option is used for wounds that present late, or are otherwise at increased risk of infection

Delayed - leave open for 4-5 days when close if no signs of infection

Front 403

List common absorbable and nonabsorbable sutures

Back 403

Nonabsorbable - Ethilon (nylon), Prolene

Absorbable - vicryl

Front 404

List basic rules for selecting suture size

Back 404

Facial wounds are closed with 5-0 or 6-0

Hands 4-0 and 5-0

Feet, and other limb wounds with 4-0

Trunk wounds or wounds under high tension (joints, gaping) with 3-0 or 4-0

Front 405

Wounds characteristics that increase the risk of tetanus

Back 405

Delayed presentation

Deep wound

Gross contamination

Ischemia, infection

Crush or puncture injuries.

Front 406

List conversion factor from codeine, morphine, oxycodone, and hydromorphone

Back 406

Codeine - 100

Morphine - 10

Oxycodone - 5

Hydromorphone - 2