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Special Populations > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

For people age 5-29 years, 3 of the top 5 causes of death are:

A

injury related, namely road traffic injuries, homicide and suicide

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2
Q

Injuries and violence are responsible for an estimated _____% of all years lived with disability.

A

10%

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3
Q

The general approach to evaluation of the acute trauma victim has 3 sequential components:

A
  1. rapid overview
  2. primary survey
  3. secondary survey
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4
Q

The primary survey is designed to do what?

A

to access and treat life-threatening injuries rapidly

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5
Q

What are the leading causes of death in trauma patients:

A

-airway obstruction
-respiratory failure
-hemorrhagic shock
-brain injury

therefore, these are the areas targeted by the primary survery

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6
Q

What is the most frequent cause of asphyxia?

A

airway obstruction
-may result from posteriorly displaced or lacerated pharyngeal soft tissues, hematoma, bleeding, secretions, foreign bodies or displaced bone or cartilage fragments

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7
Q

signs of upper and lower airway obstruction

A

-dyspnea
-hoarseness
-stridor
-dysphonia
-Sq emphysema
-hemoptysis

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8
Q

Initial steps in airway management are:

A

-chin lift
-jaw thrust
-clearing of the oropharyngeal cavity
-placement of an oropharyngeal or nasopharyngeal airway
and in inadequately breathing patients, ventilation with a self-inflating bag

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9
Q

if the initial steps in airway management are inadequate definitive airway management should be achieved by:

A

intubation or cricothyroidotomy

-LMA can be useful in intermediary
-blind passage of nasal tubes should be avoided

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10
Q

What are the most common trauma-related causes of difficult tracheal intubation:

A

-maxillofacial neck
-chest injuries
-cervicofacial burns

-airway assessment should include a rapid examination of the anterior neck for feasibility of access to the cricothyroid membrane

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11
Q

Maxillofacial injury

A

-obstruction by blood, bone, teeth, pharyngeal tissues
-a hematoma or edema in the face, tongue or neck may expand during the first several hours after injury and ultimately occlude the airway
-many isolated facial injuries do not require intubation

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12
Q

Cervical penetrating

A

-escape of air, hemoptysis and coughing
-may intubate through defect

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13
Q

blunt cervical

A

-hoarseness, muffled voice, dyspnea, stridor, dysphagia, odynophagia, cervical pain and tenderness, ecchymosis, subcutaneous emphysema and flattening of the thyroid cartilage
-CT if stable
-thoughtful intubation strategy

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14
Q

thoracic

A

-penetrating can obviously be anywhere
-blunt unjury usually involves the posterior membranous portion of the trachea and the mainstem bronchi, usually within approx 3cm from the carina
-pneumo, pneumomediastinum, SQ emphysema, and continuous airleak from chest tube are the usual signs of this injury
-they occur frequently but are not specific for thoracic airway damage
-in patients intubated without the suspicion of a tracheal injury, difficulty obtaining a seal around the endotracheal tube or the presence on a chest radiograph
-of a large radiolucent area in the trachea corresponding to the cuff suggests a perforated airway

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15
Q

Rapid inspection–primary survey: breathing

A

-cyanosis
-tracheal deviation
-significant chest wounds
-fail chest
-paradoxical chest movement
-asymmetric chest wall excursion
-auscultation of both lungs should be conducted to identify decreased asymmetric lung sounds

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16
Q

Tension Pneumothorax

A

-life-threatening emergency wherein a large air collection in the pleural space comprises respiration and cardiac function

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17
Q

s/s of tension pneumo

A

-cyanosis
-tachypnea
-hypotension
-neck vein distension
-tracheal deviation
-diminished breath sounds on affected side

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18
Q

tx for tension pneumo

A

-needle decompression by insertion of an angio cath in the 2 intercostal space midclavicular line
-followed by chest tube placement

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19
Q

Open pneumothorax

A

-when an injury creates a hole in the chest wall that allows air from the environment to enter the pleural cavity
-similar s/s to tension pneumo
-air that gets entrained though the wound but not able to escape–>tension physiology
-tx three sided dressing and chest tube

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20
Q

Flail chest

A

-may occur when 3 or more ribs are broken in at least 2 places
-arises when these injuries cause a segment of a chest wall to move independently of the rest of the chest wall
-continuity of the chest wall is disrupted and the physiologic action of the ribs is altered. The motion of the flail segment is paradoxical to the rest of the chest. It is paradoxical because the flail segment moves inward while the rest of the chest wall moves outward
-ineffective ventilation because of increased dead space, decreased intrathoracic pressure and increased oxygen demand from injured tissue
-pulmonary contusion in adjacent lung tissue is almost universal with flail chest. Pulmonary contusion impairs gas exchange and decreases compliance. Hypoventilation and atelectasis result from the pain of the injury.

Tx: maintain adequate ventilation, fluid management, pain management and management of the unstable chest wall

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21
Q

What is the most common cause of shock in trauma patients?

A

blood loss-second cause of death

TBI is first

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22
Q

how is blood loss assessed?

A

-level of responsiveness
-obvious hemorrhage
-skin color
-pulse (presence, quality, and rate)

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23
Q

Level of responsiveness can be quickly assesed by _______.

A

AVPU

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24
Q

What is a warning sign of hypovolemia?

A

pale or ashen extremities or facial skin

-rapid, thread pulses in the carotids or femoral arteries are also concern for hypovolemia

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25
Q

In trauma, hypovelemia is addressed by what first

A

addressed first with 1L-2L isotonic solutions but should then be followed by blood products. CRT can be used to assess the adequacy of tissue perfusion.

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26
Q

A CRT > _____sec may indicate poor perfusion.

A

2

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27
Q

Any patient presenting with pale, cold extremities is in ______ until proven otherwise.

A

shock

-with no obvious signs of hemmorhage and when there is hemodynamic compromise a pericardial tamponade must be considered and if suspected, corrected through creation of pericardial window

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28
Q

Class I blood loss

A

Blood loss in %: <15
Pulse: <100
BP normal
Pulse pressure; normal or increased
RR: 14-20
Mental Status: slightly anxious
UOP: >30

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29
Q

Class II blood loss

A

Blood loss in %: 15-30%
Pulse: 100-120
BP: normal
Pulse pressure: decreased
RR: 20-30
Mental Status: mildly anxious
UOP: 20-30

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30
Q

Class III blood loss

A

Blood loss in %=30-40
Pulse: 120-140
BP: decreased
Pulse pressure-decreased
RR: 30-40
Mental Status: anxious, confused
UOP: 5-15

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31
Q

Class Iv blood loss

A

Blood loss in %: >40
Pulse: > 140
BP: greatly decreased
Pulse pressure: dereased
RR: >35
Mental Status: confused, lethargic
UOP: minimal

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32
Q

Primary survey: disability

A

-neurologic status
-a rapid assessment of the patient’s neurologic status is necessary on arrival in the ED
-this is assessed by the patient’s Glasgow coma scale
-if the GCS <8-intubate
-a maximum score of 15 is reassuring and indicates the optimal level of consciousness, whereas a minimum of 3 signifies a deep coma

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33
Q

AVPU

A

A-alert and conscious
V-responds to verbal stimulus
P=responds to painful stimulus
U=unresponsive to any form of stimulus

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34
Q

Management of TBI

A

-hypoxia and hypotension is TERRIBLE for injured brain
-maintain MAP >80mmHg, SpO2> 92%
-goal to maximize CPP
-mannitol/furosemide to decrease ICP
-head elevation
-isotonic/hypertonic fluid resusitation-may be prudent to avoid Lr (no colloids)
temporary hyperventilation (prolonged worsens cerebral ischemia)
-sedation (to decreased CMRO2)

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35
Q

Management of Spinal cord injury

A

-focused neuro assessment
-immobilization until clinical or imaging clearance
-spine is like the brain-hypotension and hypoxia bad
-spinal shock=hypotension from vasodilation and brady cardia from unopposed vagal tone (may require inotropes and vasopressors)
-catecholamine surge can–>pulm edema
-C4 injuries or above likely impair respiration
-loss of gastric sphincter tone–> may increase risk of aspiration
–steroids controversial-generally avoided
-surgical intervention-when able-<72 hrs ideally

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36
Q

Secondary survey

A

indicated in all trauma patients who have had primary survey completed
-purpose is to obtain a detailed history, perform a head to-toe physical exam, reassess all vital signs and obtain pertinent lab and imaging studies to identify injuries and metabolic abnormalities
-these are injuries you may manage later

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37
Q

Anesthetic management of trauma patients

A

-airway management
-manage hemodynamic instability
-lung-protective ventilation
-maintenance of normothermia
-maintenance of adequate cerebral blood flow, oxygenation, and ventilation is prudent to avoid
-prevention of unpleasant experiences during painful interventions

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38
Q

<____MAC if TBI suspected

A

<0.5 MAC
-nitrous avoided

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39
Q

in addition to early surgical control of hemorrhage what other strategies limit ongoing blood loss?

A

-maintenance of a low to normal SBP at 90 mmHg (or <110mmHm in older adults) and/or mean arterial pressure at 50-65mmHg. Once hemostasis has been achieved higher BP values are targeted
-although increasing BP indicated increasing macrocirculatory pressure, microcirculatory flow may still be abn

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40
Q

Current ATLS guidelines recommend no more than _____ of warm 0.9% saline prior to administration of blood components

A

1L

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41
Q

True/false: availability should not rely on full crossmatch in patients with hemorrhagic shock since uncrossmatched blood can be administered until crossmatched blood is available.

A

true

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42
Q

acute coagulopathy after severe traumatic injury has multifactorial etiologies including:

A

-acidosis related to tissue injury and shock
-hypothermia related to exposure and fluid administration
-systemic anticoagulation with activation of protein C and protein S
-hyperfibrinolysis from amplification of tissue plasminogen activator
-platelet dysfunction following platelet activation

-hemodilution due to fluid or component blood product administration
-consumption of clotting factors manifesting as DIC

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43
Q

TXA administration

A

initial 1g IV bolus over 10 minutes with TEG guided determination of further dosing or following by 1g infusion over 8 hours if TEG unavailable
-TXA is part of MTP protocol in most major trauma centers in US and military

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44
Q

ESA in trauma suggests target fibrinogen concentration of?

A

> 150-200mg/dL

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45
Q

Lethal Triad

A
  1. Acidosis
  2. Coagulopathy
  3. Hypothermia
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46
Q

Targets of rescuscitation

A

-SBP>90mmHg
-Hgb 7-10 depending on coexisting disease
-normothermia T36-38C
-INR<1.5
-base deficit <6
-pH >7.2
-normocalcemia (0.5-1g calcium every 2-3 units of product)

-frequent use of TEG and ABG recommended to guide overall rescuscitation transfusion requirements and to correct coagulopathy

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47
Q

Other etiologies of shock

A

-volume, volume, volume
-SCI
-vasoplegic shock
-ischemic myocardial dysfuction causing cardiogenic shock
-tension pneumo
-pericardial tamponade
-increasing intra-abdominal pressure
-vasopressors/inotropes thoughtfully deployed to manage shock refractory to volume resuscitation

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48
Q

REBOA

A

-resuscitative endovascular balloon occlusion of the aorta-in selected patients, resuscitative endovascular balloon occlusion of the aorta is a temporizing measure to support vital organ perfusion , decrease amount of bleeding distal to the occluded site, and provide a window of opportunity for rescuscitation and definitive hemorrhage control

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49
Q

Inflation-Proximal aortic occlusion during REBOA does what?

A

-increases SVR, BP and cardiac afterload thereby increasing cerebral and myocardial perfusion

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50
Q

deflation-Proximal aortic occlusion during REBOA does what?

A

attempted when hemostasis has been achieved or to check for sources of ongoing hemorrhage

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51
Q

deflation of intra-aortic balloon cath may result in:

A

-severe hypotension due to a sudden decrease in SVR, decreased preload due to venodilation,
hypoxia-mediated reactive hyperemia and decreased myoardial contractility due to metabolic (lactic)acidosis. Metabolic acidosis and washout of ischemic muscle tissue may result in hyperkalemia, malignant arrhythmias and cardiac arrest

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52
Q

Lung protective ventilation

A

-lung-protective strategy used during controlled ventilation for patients with trauma and shock
-low tidal volumes 6-8ml/kg predicted body weight
-mild permissive hypercapnia 40-45mmHg unless patient has metabolic acidosis or known or suspected TBI
-maintenance of low plateau pressure < or equal to 30cmH20
-adjustment of FiO2 to maintain O2 sat > or equal to 92%
-initial PEEP at 0 cmH20 until hemodynamic stability and control of hemorrhage and adequate resuscitation has been achieved. Subsequently PEEP may be slowly and incrementally increased to 5-10cmH20 if tolerated without provoking hypotension

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53
Q

goal of protective lung ventilation

A

provide an optimal balance between minimizing lung injury and preventing hemodynamic instability.
in patients with hemorrhagic shock it is particularly important to avoid high levels of PEEP and auto-peep increase intrathoracic pressure and decrease venous return, CO and systemic BP

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54
Q

Pregnant patients and trauma

A

-airway consideration
-LUD
–aggressive volume resuscitation
-in maternal cardiac arrest, C-section is recommended for viable pregnancies >or equal to 23 weeks, if possible no later than 4 minutes following arrest. this facilitates both maternal resuscitation and fetal salvage

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55
Q

Neurogenic shock s/s

A

-hypotension, bradycardia and hypothermia resulting from acute SCI

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56
Q

neurogenic shock occurs with injury above _____ level

A

T6

-seen in 14$ isolated SCI
-up to 8 % major traumas

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57
Q

neurogenic shock most common in:

A

-complete c-spine transection

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58
Q

neurogenic shock less common in:

A

incomplete c-spine/thoracolumbar

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59
Q

in neurogenic shock unopposed vagal tone on heart can lead to :

A

-refractory bradycardia, bradyarrythmias, and heart block

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60
Q

Hemostasis

A

process by which the body maintains the delicate balance btwn bleeding and clotting

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61
Q

procoagulants

A

initiators of coagulation/clot formation

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62
Q

anticoagulant

A

inhibit coagulation/clot formation

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63
Q

fibrinolytic

A

dissolve clots

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64
Q

Tunica Intima

A

-most interior/closest to blood

broken down into:
1. endothelium (synthesizes vWf)
2. subendothelial layer (highly thrombo genic
3. internal elastic lamina

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65
Q

3 layers of vessel wall

A
  1. tunica intima
  2. tunica media
  3. tunica externa (aka adventitia)
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66
Q

Which vessel layer is a smooth muscle layer and thicker in arteries?

A

tunica media

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67
Q

Which layer is connective tissue and provides vessel protection?

A

tunica externa/adventitia

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68
Q

Primary Hemostasis

A

unstable platelet plag
1. adhesion
2. activation
3. aggregation

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69
Q

Secondary Hemostasis

A

stable platelet plug
coagulation cascade:
-intrinsic
-extrinsic
-common

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70
Q

tertiary hemostasis

A

fibrinolytic system

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71
Q

When endothelial lining of blood vessel is disrupted, the vessel contracts to cause a tamponade and decrease blood flow:

A

-autonomic nervous system reflexes
-thromboxane A2
-ADP

then areas adjacent to injury vasodilate
-distributes blood to surrounding organs/tissues
-bring factors and platelet to injured site

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72
Q

Where are platelets formed?

A

in the bone marrow

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73
Q

Do platelets reproduce?

A

no

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74
Q

life span of platelets

A

7-12 days

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75
Q

normal platelet count

A

150,000-300,000/mm3

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76
Q

Which cell roams active until activated by vascular trauma?

A

platelets

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77
Q

they do patch minor vascular injuries that occur in perpetuity (using 7,000 each day)

A

platelets

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78
Q

What do platelets contain?

A

-vWF
-fibrinogen
-fibronectin
-histamine
-epi
-PLT factor 4
–platelet growth facator
-serotonin
-ADP
-ATP
-contains thrombin

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79
Q

Adhesion phase of primary hemostasis

A

-vWF is mobilized from within the endothelial cells and emerges from the endothelial linine
-vWF makes the platelet “sticky” and allows them to adhere to the site of injury
-Glycoprotein Ib receptors emerge from the surface of the platelet
-Gp1b (receptor on platelet) adheres to vWF (on endothelial surface)

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80
Q

Activation phase of primary hemostasis

A
  1. the binding of Gp1b to vWF causes platelet activation
    -platelets dislike structure swells and becomes oval and irregular
    -glycoprotein IIb-IIIa receptor complex project on surface of platelet
  2. The binding of Gp1b to vWF causes platelet degranulation
    -vWF, fibrinogen, fibronectin, histamine, epi, PLT factor 4, platelet growth factor, serotinin, ADP, ATP, Thromboxane A 2, Thrombin
    -some of the mediators released recruit other platelets to site of injury
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81
Q

Aggregation phase of primary hemostasis

A

-GpIIb-IIIa complex links to other activated platelets
-these mediatorys are responsible for platelet aggregation and form a primary unstable clot/unstable platelet plug
- in less threatening injuries, a primary unstable clot may be enough to maintain hemostasis
-in larger injuries, activation of coagulation clotting cascade required for permanent repair to create and stabilize a secondary clot to cease bleeding

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82
Q

Drugs that block GpIIa-IIIb

A

Abciximab
Tirofiban
Eptifibatide

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83
Q

Factor 1

A

fibrinogenf

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84
Q

Factor 1a

A

fibrin

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85
Q

Factor 2

A

prothrombin

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86
Q

Factor 2a

A

thrombin

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87
Q

Factor 3

A

tissue factor or thromboplastin

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88
Q

Factor 4

A

calcium

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89
Q

Factor 5

A

proaccelerin

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90
Q

Factor 7

A

proconvertin

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91
Q

Factor 8

A

Antihemophiliac

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92
Q

Factor 9

A

Christmas

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93
Q

Factor 10

A

Stuart-Prower

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94
Q

Factor 11

A

plasma thromboplastin antecedent

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95
Q

Factor 12

A

Hageman

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96
Q

Factor 13

A

fibrin stabilizing

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97
Q

Prekallikrein

A

Fletcher

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98
Q

Which factors are synthesized in the liver?

A

1
2
5
7
8
9
10
11
12
13

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99
Q

Where is factor 3 synthesized?

A

vascular wall
and extravascular cell membranes
released from traumatized cells

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100
Q

Where is vWF synthesized?

A

endothelial cells

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101
Q

Which factors are Vitamin K dependent?

A

“1972”
10, 9, 7, 2

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102
Q

Action of Prothrombin

A

when active form activated:
1, 5, 7, 13, platelets and protein C

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103
Q

What is a cofactor of factor 7?

A

prothrombin

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104
Q

Action of calcium in clotting cascade?

A

promotes clotting reactions

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105
Q

Which factor is a cofactor of 10 and forms a prothrombinase complex?

A

Factor 5 (proaccelerin)

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106
Q

Which factor activates 9 and 10?

A

Factor 7-proconvertin

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107
Q

Which is a cofactor to 9?

A

factor 8, antihemophiliac

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108
Q

Which factor activates 10?

A

9-christmas

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109
Q

Which activates 2 and forms a prothrombinase complex with 5?

A

Factor 10

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110
Q

Which factor activates 9?

A

Factor 11-plasma thromboplastin antecedent

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111
Q

Which factor activates 11?

A

Factor 12-Hageman

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112
Q

Which cross-links fibrin?

A

Factor 13-fibrin stabilizing

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113
Q

Which aactivates 12, cleaves HMWK?

A

prekallikrein

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114
Q

Which supports activation of prekallikrein, 12, 11?

A

high molecular weight kininogen (HMWK) or contact activation factor

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115
Q

When is the extrinsic pathway activated?

A

when injury occurs outside vessel wall
-organ trauma or crushing injuries

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116
Q

Which factors are part of the extrinsic pathway?

A

3 (tissue factor) and 7 (proconvertin)_

3+7=10

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117
Q

When is the intrinsic factor activated?

A

also contact activation pathway
-occurs with damage to blood vessel themselves
which then activates the common pathway (10)

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118
Q

Which factors are involved in the intrinsic pathway?

A

8
9
11
12
prekallikrein

if you cant buy the intrinsic pathway for $12, you can always purchase it for $11.98

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119
Q

Common pathway

A

starts with Factor 10

1,2, 5, 13

ends with stable secondary plug

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120
Q

Cell-based theory of coagulation

A

new concept that platelets, extrinsic and intrinsic pathways form a very interdependent relationship, not independently

-explains why certain deficiencies fail to cause bleeding despite changes in lab values (such as PT or PTT_

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121
Q

3 phase of the cell-based theory of coagulation

A
  1. initiation
  2. amplification
  3. propagation
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122
Q

initiation

A

-endothelial surface injury which exposes TF (3)
-TF makes the phospholipid surface acidic and less repellent to platelets
-TF down regulates anti-coagulants that reside in the subendothelial layer (ATIII)
-TF activates Factor 7

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123
Q

amplification

A

Factor 9 activates 8, which activates 10 to produce more and more thrombin
-thrombin generation has a positive feedback to activate more clotting factors 5, 8, 9

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124
Q

Propagation

A

-all coagulation factors are actively influencing one another, promoting coagulation and finally activating prothrombin, resulting in large burst of thrombin
-enough thrombin must be present to convert fibrinogen to fibrin to the stable secondary hemostatic plug

-from the burst of thrombin
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125
Q

Fibrinolytic system/tertiary hemostasis

A

counterbalance system that degrades fibrin
-starts with an increase in blood flow that washes away procoagulant mediators

Plasminogen–>plasmin (breaks down fibrin into fibrin degradation products)
Protein C and S (inhibit factor 3, 5, 8)
Antithrombin III (sequesters factors 9, 10,11, 12) which then inhibits thrombin (3)
Thrombin (initially acting as procoagulant), now acts as an anticoagulant and activates other anticoagulant mediators
Tissue factor pathway inhibitor (also calls to stop the fibrinolysis when clot has been digested)

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126
Q

PLT count <150,000

A

thrombocytopenia

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127
Q

Sufficient PLT count for hemostasis

A

> 100,000

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128
Q

high risk surgery platelet count

A

> 100,000

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129
Q

low risk surgery PLT count

A

> 50,000

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130
Q

central line placement PLT count

A

> 20,000

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131
Q

Spontaneous bleeding PLT count

A

<10,000

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132
Q

tests to assess platelet function and anti-platlet therapy

A

verify now and PFA-100

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133
Q

What tests evaluate extrinsic factor (VII) and the common pathway (1, 2, 5, 10)?

A

PT (prothrombin time) and INR (international normalized ratio)
-tests for coumadin/warfarin
-fails to identify specific factor, the existing problem may or may not cause bleeding

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134
Q

Normal PT

A

12 -14 seconds but is reagent dependent

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135
Q

Normal INR

A

0.8-1.2

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136
Q

Therapeutic levels for Warfarin

A

INR 2-3

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137
Q

aPTT evaluates:

A

intrinsic pathway (8, 9, 11, 12)
also evaluates common pathway (1 ,2 ,5 ,10)

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138
Q

normal PTT

A

25-32 secs

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139
Q

Normal ACT

A

70-150

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140
Q

A factor deficiency must be decreased by _____% before evidence of prolonged PT or PTT can be appreciated.

A

30%

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141
Q

What does thrombin time measure?

A

conversion of fibrinogen to fibrin
Factors 1 and 2
assess fibrinogen level and function (dysfibrinogenemia)

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142
Q

Normal Thrombin time

A

15 seconds

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143
Q

Normal fibrinogen

A

> 150
(200-350mg/dl)
can treat with fibrinogen or cryoprecipitate

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144
Q

What does D-dimer measure?

A

specific degradation by-products of fibrinolysis

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145
Q

normal D-dimer

A

<500mg/ml

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146
Q

3 parts of the TEG or ROTEM

A
  1. clot initiation
    R time: clotting factors
  2. Clot strength
    K value: fibrinogen
    Alpha angle: fibrinogen
    MA: platelets
  3. Clot stabilization
    LY-30: antifibrinolytic agents
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147
Q

What measures the time to start forming a clot?

A

R time

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148
Q

Normal R time

A

5-10 miniutes

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149
Q

R time problem with?

A

coagulation factors

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150
Q

Treat R time with

A

FFP

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151
Q

What measures the time until clot reaches a fixed strength?

A

K time

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152
Q

Normal K time values

A

1-3 minutes

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153
Q

K time problem with

A

fibrinogen

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154
Q

treat K time with

A

cryoprecipitate

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155
Q

Alpha angle

A

speed of fibrin accumulation

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156
Q

normal alpha angle

A

53-72 degrees

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157
Q

alpha angle problem with

A

fibrinogen

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158
Q

treat alpha angle with

A

cryo

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159
Q

maximum amplitude

A

highest vertical amplitude of TEG

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160
Q

normal MA

A

50-70mm

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161
Q

MA problem with

A

platelets

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162
Q

treat MA with

A

platelets and/or DDAVP (if normal plt count but max amplitude low so PLT not functioning well)

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163
Q

LY 30

A

percentage of amplitude reduction after 30 minutes after max amplitude
lysis at 30 minutes

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164
Q

normal LY 30

A

0-8%

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165
Q

LY 30 problem with

A

excess fibrinolysis

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166
Q

tx with LY 30

A

TXA and or aminocaproic acid

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167
Q

Antiplatelets

A

stop platelets from sticking together and forming a clot
works by inhibiting primary hemostasis (platelet plug)

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168
Q

ADP antagonists (thienopyridines)

A

Ticlodipine
Clopidogrel
Prasugrel

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169
Q

Anticoagulants

A

work to inhibit coagulation pathway (secondary hemostasis)
4 main categories:
1. FActor Xa inhibitors (Xarelto, Eliquis)
2. Thrombin inhibitors (Pradaxa, dabigatran, argotroban, bival)
3. Coumarin and indandiones (warfarin)
4. Heparins (activates AT III)

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170
Q

Drugs that act on tertiary hemostasis

A
  1. fibrinolytic (thrombolytic)
    -works to activate tertiary hemostasis or fibrinolytic system
    -break down thrombus
    -“clot busters”
    -tpA, streptokinase, urokinase
  2. Antifibrinolytic
    -prevent the breakdown of clots
    -work to inhibit the tertiary/fibrinolytic system
    -allows clots to stay formed and used to prevent bleeding
    -TXA or aminocaproic acid
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171
Q

Apheresis

A

-used forplatelets and plasma components
-blood components separated while a single donor is attached to separate device
-collection component is removed and other components given back to donor

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172
Q

Benefits of apheresis

A

-can remove more of selected component because giving other components back
-transfusion recipients patients have less exposure with single donor

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173
Q

Once FFP is thawed can be transfused within ______ days if kept refrigerated

A

5 days

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174
Q

Cryo average volume

A

15ml per bag, usual dose 4-6 bagsPL

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175
Q

Platelets whole blood derived average volume

A

-50mL per bag, usual dose 4-6 bags

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176
Q

Leukoreduction

A

-process used to filter and remove white blood cells from blood products
-no benefit to recipient but increases risk
-leukored decreases risk of infection (CMV and EBV)
-decreases risk of immunologic transfusion reactions
-decreased risk of febrile nonhemolytic rxn. TRALI and TRIM

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177
Q

CPDA preservative solution

A

improved RBC shelf life to 35 days

Citrate-anticoagulation binding to calcium
Phosphate-buffer
Dextrose and Adenine-to maintain ATP levels and maintain RBC integrite

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178
Q

1 unit of PRBC will increase HGB approx_____g/dL

A

1

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179
Q

pediatric dosing of PRBC

A

3-5ml/kg to increase Hgb by 1

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180
Q

Restrictive goal of PRBC

A

6-10g/DL

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181
Q

Asymptomatic ICU patient hgb level

A

> 7g/DL

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182
Q

CV disease Hgb level

A

> 8d/DK

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183
Q

Physiologic compensation for anemia

A

-increase CO
-sympathetic surge from anemia and hypoxia (increased HR/SV)
-altered microcircualtory blood flow (decreased blood viscosity improves blood flow; nitric oxide released from endothelial cells during hypoxia)
-improved tissue oxygen extraction from Hgb
-right shift of O2 curve, unloading of O2
-anemia causes increased 2,3 DPG, acidosis, and increased CO2

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184
Q

When you are transfusing RBC you are giving the ___________

A

antigens

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185
Q

RBC changes during storage

A

at end of shelf life of additive solutions RBC:
pH=6.5
Plasma K=50mmol/L from RBC leakage and hemolysis
15-20% of RBCs nonviable
-2,3 DPG depleted within the first 2 weeks of storage

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186
Q

RBC transfusion issues

A

-hyperkalemia (contain as much as 7mEq of K)
-hypothermia
-metabolic alkalosis-citric and lactic acid quickly metabolized to bicarb in liver
-citrate binds to calcium causing hypocalcemia (cardiac depression and prolonged QT, acquired coagulopathy)

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187
Q

Which have the highest bacterial infection risk?

A

platelets because stored at higher temps

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188
Q

1 unit of whole blood derived platelets by ________ in average adult

A

6,000

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189
Q

1 unit of apheresis platelets =

A

5-6 units of platelets =pooled platelet pack
increases platelets by approx 25K-60K

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190
Q

Plasma contains all coagulation factors and other proteins found in blood except:

A

5 (only 80%)
8 (only 60%)

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191
Q

use of plasma

A

global or multiple factor deficiences
or when a specific factor concentrate is unavailable

for hemostasis: need 30% of coagulation factors and 100mg/dl of fibrinogen
dose: 10-20m/kg

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192
Q

Plasma takes ______minutes to thaw

A

20-30 minutes

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193
Q

Forms of plasma

A

-FFP, PF24, and thawed plasma used interchangeable
plasma Cryo reduced/cryopoor plasma: plasma without cryo
missing factor 8, 13, vWF and fibrinogen
-suitable for patients with vitamin K deficiency when specific factors or factor concentrated are unavailable

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194
Q

When transfusing plasma you are giving____________

A

the antibodies

195
Q

What is the universal donor of plasma since there are no antibodies?

A

AB

196
Q

O blood type can only receive _______ for plasma

A

O

197
Q

Cryoprecipitate contains:

A

-fibrinogen
-factor 8
-factor 13
-vwF
-fibronectin

198
Q

1 unit cry per 10kg body weight will raise fibrinogen level by ______

A

50mg/gl
usually pooled into 5 units (usually receive 1-2 pools

199
Q

fibrinogen concentrate

A

-derived from plasma with viral inactivation
-stored at room temperature and can be reconstituted for administration

200
Q

Prothrombin complex concentrate 3 contains factors

A

2
9
10

201
Q

Prothrombin complex concentrate 4 contains factors

A

2
7
9
10

202
Q

Recombinant activated FVII (rFVIIa)

A

-factor 7 stimulated thrombin formation
-names: novoseven
-for localized sites of injury that express TF
-not for systemic levels of TF because can lead to systemic activation of thrbomin and thrombosis

203
Q

Recombinant activated FV7 contraindicated in

A

CNS bleeding
huge trauma, bleeding from multiple sites

204
Q

adverse reactions due to blood transfusion is reported to be _____%

A

0.2%
9% of these are severe or life threatening

205
Q

most common cause of adverse blood transfusion reactions

A

clerical error, miscommunication, delay in care and over transfusion

206
Q

All blood donors checked for:

A

-HIV
HepB
-Hep C
-Syphillis
-Human T-cell lymphotropic virus
-West nile

207
Q

Which test significantly shortened the window period between donor infection and viral load is detectable because screens for viral DNA or RNA?

A

nucleic acid Amplification Testing (NAT)

208
Q

Most common type of transfusion reaction?

A

febrile nonhemolytic transfusion reaction

209
Q

Acute reactions

A

within 24 hours

210
Q

Delayed reactions within

A

more than 24 hours

211
Q

Symptoms of Hemolytic transfusion reaction

A

-fever
-chills
-rigors
-chest/back/abd pain
-infusion site pain
-N/V
-dyspnea
-hemoglobinuria
-oliguria/anuria
-diffuse bleeding
-acute kidney failure
-shock
-DIC
-death

212
Q

Treatment of hemolytic transfusion reaction

A

-stop transfusion
-send blood for transfusion reaction workup (positive direct COOMBs test)
-monitor for DIC
-fluids to maintain UOP

213
Q

Hemolytic Transfusion reaction

A

most commonly due to ABO incompatibility
-noncompatible blood causes intravascular hemolysis

214
Q

Febrile nonhemolytic transfusion reaction

A

-most common transfusion reaction
-mild and self limiting
-diagnosis of exclusion
-due to cytokines released by WBC in stored blood products

215
Q

symptoms of Febrile non-hemolytic transfusion reaction

A

-fever >100.4 (38C) and a change of at least 1.8F (1.0C) from pretransfusion level during or within 4 hours of transfusion.
-occasionally fever may be absent with presence of chills and rigor only

216
Q

treatment of febrile non-hemolytic transfusion reaction

A

-stop transfusion
-transfusion reaction work up
-tylenol

217
Q

Symptoms of allergical/anaphylactic reactions

A

-hives
-edema
-pruritis
-angioedema to serious life threatening reactions like anaphylaxis presenting with hypotension and bronchospasm

218
Q

Anaphlyactoid reactions are from ________deficient recipient

A

IgA

219
Q

treatment of allergic rxn

A
  • stop transfusion, transfusion reaction work-op
    -benedryl to epinephrine
220
Q

Alloimmunization

A

-IgG mediated immunity creating antibodies to foreign proteins in allogenic blood.
-concern is on second exposure to foreign proteins
-2-4% in patients who have had a blood transfusion
- concern is patients who require frequent transfusions (up to 35-80%)
-decrease risk with matching RBC beyond ABO blood groups

221
Q

Transfusion related immunomodulation (TRIM)

A

immunosuppressant effect of stored allogenic blood products
-increases incidence of healthcare associated infections
-increases recurrence of malignancies in patients undergoing cancer sx

222
Q

Transfusion associated graft versus host disease

A

-rare but fatal complication
-donor T-cell lymphocytes engraft in recipient and attack host cells they recognize as foreign
-8-10 days after transfusion
-no treatment
-prevention with pathogen inactivation techniques for T-cell destruction

223
Q

Posttransfusion purpura

A

-severe thrombocytopenia
-<25% pretransfusion level or <10,000
-previously pregnant women with platelet alloantibodies
-tx: immunoglobulin or plasmapheresis to remove antibody

224
Q

Transfusion related acute lung injury (TRALI) also called

A

low pressure noncardiogenic pulmonary edema

225
Q

4 criteria for TRALI

A
  1. life-threatening lung injury within 6 hours of transfusion
  2. hypoxemia:O2 saturation or < or equal to 90% on RA; PaO2/Fio@< or equal to 300mmHg
  3. new onset B/L infiltrates on chest x-ray in absence of any other cause of acute lung injury
  4. no evidence of left atrial htn
226
Q

Treatment of TRALI

A

stop transfusion and transfusion reaction owrkup
chest x-ray
respiratory support (Positive airway ventilation and oxygen)

227
Q

1: ____________ transfusions are associated with TRALI but ______% of fatalities.

A

1:10,000
15-20%

228
Q

Transfusion associated circulatory overload (TACO)
(high pressure pulmonary edema)

A

-multiple blood products and fast rate of transfusion
-acute respiratory distress within 6 hours of transfusion

229
Q

Symptoms of TACO

A

-dyspnea, hypoxemia, tachycardia, HTN
-increased CVP
-signs of volume overload
-B/L acute pulmonary edema
-elevation of Beta-natriuretic peptide (BNP)

230
Q

treatment of TACO

A

-stop transfusion and transfusion reaction workup
-chest x-ray
-BNP lab
-diuretics-symptomatic relief with diuretics favor TACO over TRALI

231
Q

Transfusion associated dyspnea (TAD)

A

-mild respiratory symptoms iwthin 24 hours of transfusion -tachypnea, mild hypoxemia, SOB
-diagnosis of exclusion
-slow transfusion rates can mitigate risk

232
Q

Rhesus incompatibility

A

Mom Rh- , Baby Rh + isdangeroous for pregnancy
-ok first time because baby is delivered and mom
-second time antibodies are so small they can cross placenta and attach Rh + baby blood
-baby blood cells are broken down and bilirubin levels
-HDN (Hemolytic disease of newborn)

233
Q

Which sensitizing events in Rh incompatiblity are where blood from mom and baby mix

A

-miscarriage >12 weeks
-abdominal trauma/bleeding during pregnancy
-at birth

234
Q

Prevention of HDN-RhoGam

A

-anti-D immunoglobulins
-works by killing off Rh+ blood before mom can become sensitized and prevent mom from developing her own Anti-D antibodies
-IM injection at any sensitizing event (lasts 13 weeks)
-mom gets injection at 28 weeks in prep for child birth
-at birth, baby cord blood is checked and if Rh +, mom gets another anti-D injection

235
Q

Massive transfusion

A

> / 10 units of RBCs in 24 hours
-replacement of >50% of total blood volume within 3 hours
-transfusion of >4 units of RBCs within 1 hour with expected need for additional transfusions
-loss of one blood volume (70kg pt is appro 5L)
O- blood (especially females of childbearing age )until crossmatch blood is available during trauma
-1:1:1 ratio still controversial
-TXA helpful if given within 3 hours of trauma

236
Q

Complications of MTP

A

-metabolic alkalosis
-citrate toxicity
-hyperkalemia
-hypothermia
TACO

237
Q

Resuscitation goals of Massive transfusion

A

-MAP within range of 60-65mmHg
-hgb level between 7-9 gdL
INR below 1.5
fibrinogen levels within the range of 150-200mg/dL
-plt count above 50,000
-pH between 7.35-7.45
-core temp above 35C

238
Q

What is the most common inherited bleeding disorder?

A

von Willebrand’s disease
-vWF function
facilitates platelet adhesion
-blinds platelets GP ib to subendothelial matrix
-plasma carrier for factor 8 and protects factor 8 from degradation from protein c or s
-elevated aPTT (factor 8 is intrinsic pathway)
-normal PT (extrinsic pathway)

239
Q

Which type of VW disease is DDAVP contraindicated?

A

Type 2B
-qualitative variants with increased affinity for platelet

contraindicated because causes thrombocytopenia

240
Q

Which type of vW disease is DDAVP useful?

A

Type 1
Type IIa: helpful in some
Type IIM: helpful in some

241
Q

Which type of Vw disease is DDAAVP not helpful?

A

Type IIN and Type III,
type IIB

242
Q

Hemophilia primarily affects__________

A

men
are on X gene, X-linked recessive, women can carry gene

243
Q

Most common type of Hemophilia?

A

Hemophilia A (85%)

244
Q

Hemophilia A is due to factor ______deficiency.

A

8

245
Q

Hemophilia B is due to factor ______deficiency.

A

9
14%

246
Q

Hemophilia C is due to factor ______deficiency.

A

11

1%

247
Q

Labs for Hemophilia’s

A

PTT will be prolonged (intrinsic pathway)
then look at specific factor activities and mutation testing of the genes

248
Q

Tx of hemophilias

A

replace missing or nonfunctional clotting factor
if patient has a severe deficiency (absent/very low) the replacement factors can be seen as foreign and antibodies (AKA: inhibitors) form against the factor
-inhibitors can diminish the effectiveness of tx
-bethesda test : detects inhibitors

249
Q

Tx of Hemophilia A

A

Desmopressin (DDAVP)-helpful in mild VIII deficiency because it stimulates release of vWF
Emicizumab (mimics Faactor 8 function)

250
Q

Hemophilia and bleeding

A

-initiate tx immediately, do not delay for testing
-maintain factor level above 50% at all times
-initial dose of 80-100% of factor
-subsequent dosing based on peak and trough levels

251
Q

Hemiarythrosis

A

-give factor early-goal to raise levelabove 50%
-common manifestation of hemophilia
-bleeding into hip presents concern due to greater risk of increased intra-articular pressure and osteonecrosis
-some patients develop a “target” joint

252
Q

Vitamin K deficiency decrease in what faactors?

A

2, 7, 9, 10 protein C and S

253
Q

Vitamin K is absorbed by the small intestine and depends on availability of ___________.

A

bile sales from liver
-liver insufficiency, sterile gut of newborn and oral abx can cause vitamin K deficiency

254
Q

Oral Vitamin K replacement can take _____ hours for full effect

A

24

255
Q

IV Vitamin K can take ______hours for full effect.

A

6-8 hours

256
Q

Protein C and S deficiencies

A

-protein C inactivates F 5a and Factor 8a
-protein S is a cofactor for proper function
-deficiences result in prothrombotic state

257
Q

Factor 5 Leiden Thrombophilia

A

5% of caucasians
-gene mutation that makes factor 5 resistance to the inactivation by protein C
-protein C cannot suppress coagulation due to resistance from factor 5
-high risk for development of DVT

258
Q

Heparin induced thrombocytopenia (HIT)

A

-life threatening complication of exposure to heparin (any form of heparin but most commonly due to UFH)
-mortality rates improved with earlier recognition and interventions >2%
-igG antibodies bind to Heparin PF 4 complexes and activate plts
-thrombocytopenia in HIT caused by consumption of activated platelets

259
Q

Hypercoagulable state in HIT

A
  1. venous thrombi-limb gangrene
  2. arterial thrombi-organ ischemia/infarction
  3. skin necrosis
260
Q

HIT Type I

A

-not clinically significant
-non-immune and caused by direct effect of heparin on platelets
-mild transient platelet drop that occurs within first two days after heparin-platelet count returns to normal even with continued heparin exposure

261
Q

HIT Type II

A

clinically significant
-IgG immune mediated where autoantibodies to platelet factor 4 (PF4) complexed with heparin activate plt
-platelet drop 5-10 days after exposure

262
Q

HIT treatment goals

A

-halt platelet activation
-stop all heparin
-therpeutic dose anticoagulation with non-heparin anticoagulant
DTI: argatroban and bival
-plt count should see improvement in platelet counts w/in 3-4 days heparin discontinuation

263
Q

subacute/subclinical HIT

A

recovered platelet count but still have positive antibodies (would not give heparin)

264
Q

Remote HIT

A

-recovered plt count and negative antibodies

may be able to give heparin

265
Q

Disseminated intravascular coagulation (DIC)

A

potential for causing both thrombosis and hemorrhage
-process of coagulation and fibrinolysis become abnormally activated-consumptive coagulopathy

266
Q

sequence of events DIC

A

-procoagulant exposure
-coagulation
-fibrinolysis
-end organ damage: from decreased perfusion, thrombosis and/or bleeding

267
Q

Acute/decompensated DIC

A

-rapid onset and large amounts of procoagulant substances
-rapid consumption of coagulation factors and platelets that outpace their production
-liver unable to remove FDPs
-at risk for bleeding and consumption coagulopathy

268
Q

labs for acute /decompensated DIC

A

-prolonged Pt/PTT
-low fibrinogen
-elevated d-dimer
-thrombocytopenia

269
Q

Chronic/compensated DIC

A

-continuous or intermittent exposure to smaller amounts of procoagulants
-coagulation factors and platelet production are able to keep up with consumption rate
-live is able to clear FDPs
-thrombosis risk but many patients are asymptomatic

270
Q

Labs in chronic/compensated DIC

A

Normal or mildly prolonged PT/PTT
normal fibrinogen
elevated D-dimer
normal platelets

271
Q

sickle cell disease

A

genetically inherited condition and occurs when obtains two non-HgbA genes (A is normal form of hgb) and at least one HgBS

272
Q

HgBSS

A

2 sickle cell genes (most severe form)
aka sickle cell anemia

273
Q

Beta thalassemia (sickle beta thalassemia)

A

2 types of Beta thalassemia “0” or “+”
HgbS beta 0 thalassemia-more severe
HgbBS beta + thalassemia (milder)

274
Q

HgBS lifespan is ______days

A

7

275
Q

Hgb A lifespan _______days.

A

120 days

276
Q

baseline chronic anemia in SCD around _______

A

8-10g/dL

277
Q

Vasoocclusion in SCD

A

tissue ischemia or infarction-high risk for stroke, TIA, Acute chest pain syndrome
-acute and chronic pain: never withhold or underdose pain meds
-multiorgan failure: life-threatening complication where multiple organs are affected by ischemia and or infarction

278
Q

preop for SCD

A

-recommend preop transfusion for most patients
standard of care for SC anemia and those with Hgb-sBeta 0 undergoing surgery that requires more than 30 minutes
-goal is to raise hgb >10 with simple transfusion
-if starting Hgb >10 then can consider exchange transfusion

279
Q

Indications for Tonsillectomy and Adenoidectomy

A

-chronic or recurrent acute tonsillitis
-peritonsilar abcess
-tonsillar hyperplasia
-obstructive sleep apnea syndrome
-valvular heart disease at risk for endocarditis from recurrent streptococcal infection of tonsils

280
Q

Goal of tonsillar hyperplasia

A

to relieve airway obstruction and increase cross-sectional area of pharynx

281
Q

Patients with ______,______, and _______ can develop cor pulmonale

A

-hypoxemia
-hypercarbia
-increased airway resistance

282
Q

_______ of patients with ECG evidence right ventricular hypertrophy will reveal a chest x-ray consistent with cardiomegaly.

A

1/3C

283
Q

Cor Pulmonale

A

defined as an alteration in the structure and function of the right ventricle (RV) of the heart caused by a primary disorder of the respiratory sysem

284
Q

Pumonary HTN

A

common link between lung dysfunction and the heart

285
Q

Digitalis medicines

A

strengthen the force of heartbeat by increasing the amount of calcium in the heart’s cells

286
Q

Complications of tonsillectomy

A
  1. to prevent emesis
    -suction stomaach
    -ondansetron 0.10-0.15mg/kg
    -dexamethasone 0.5mg/kg
  2. postop hemorrhage (avg EBL: 4ml/kg or 5% blood volume)
  3. Pain (cautery, laser, sharp dissection)
  4. acute postoperative pulmonary edema
287
Q

Where does blood flow to the tonsils arise from?

A

external carotid

287
Q

Blood flow to tonsils arises via the external carotid and its branches:

A

-ascending pharyngeal artery
-facial artery
-dorsal lingual artery
-and palatine branch of maxillary artery

288
Q

Sensory innervation to the palatine tonsils is supplied by the:

A

–glossopharyngeal (tongue control)
-lesser palatine nerves

289
Q

Post-tonsillectomy bleeding

A
290
Q

Is peritonsillar abscess an emergency?

A

yes, emergency surgical intervention

291
Q

Peritonsillar abscess (Quinsy tonsil)

A

-generally in older children and young adults
-fever, pain, and trismus (restricted Jaw rOM)
-surgical drainage, removal and IV antibiotics
-mask ventilation Okay, visualization of vocal cords should not be impaired, as abscess is supraglottic and well above laryngeal inlet
-gentle intubation

292
Q

Ludwig’s angina location

A

submandibular cellulitis out of 2nd and 3rd molars
patient describes “suffocating sensation
-tongue is elevated and displaced with hard firm induration of the floor of the mouth and perioral edema
-trismus=lockjaw
-airway generally secured via nasal fiberoptic or tracheostomy

293
Q

What is ludwigs angina caused by?

A

cellulitis of the floor of the mouth caused by a bacterial infection of the sublingual and submandibular tissues
-can lead to stridor and eventually asphyxia and death
-abx therapy is usually ineffective due to the mixed bacterial flora

294
Q

Ear surgery for myringotomy and tube insertion (BMT)

A

-chronic serous otitis in children can lead to hearing loss
-treatment drainage of middle ear
-mask management/short procedure

current URI status-may perform sx despite URI

295
Q

Intraoperative management of tympanoplasty and mastoidectomy

A

-avoid nitrous oxide!
-hemostasis
-facial nerve identification
-post operative vertigo, N/V-high risk
-positioning (extreme lateral neck turn)

296
Q

What indicates an upper airway obstruction/

A

inspiratory stridor

297
Q

What indicates a lower airway obstruction?

A

expiratory stridor

298
Q

What indicated mid-tracheal lesions?

A

biphasic stridor (inspiratory and expiratory)

299
Q

most common cause of stridor

A

laryngomalacia (soft larynx)
-inherited (tx time)

300
Q

Clinical components of evaluation of patients with stridor

A

-respiratory rate
-chest retractions
-heart rate
-nasal flaring
-wheezing
-LOC
-cyanosis

301
Q

Vast majority of airway foreign bodies occur in children under age _____ with peak incidence occurring between 1 and 2 years of age.

A

3

302
Q

Most common aspirated item in younger children:

A

-peanut
followed by: popcorn, jelly-beans and hot dogs

303
Q

Most common site of AFB

A

main stem bronchus–>right side–>more often than left

304
Q

Classic triad of aspirated foreign body:

A

-wheezing
-cough
-diminished breath sounds

305
Q

what is a good indication of aspiration

A

-coughing
-choking
-cyanosis occuring while eating

306
Q

common radiographic findings of AFB

A

-radiopaque object
-atelectasis
-emphysema (obstructive with mediastinal shift)
-consolidation
-+/- normal x-ray depending on time of injury

307
Q

anesthetic management of AFB

A

+/- premed
-EMLA cream before starting IV
-Full stomach RSI
-consider sevo induction if not at risk for aspiration
-spontaneous ventilation may be preferred but gentle assisted ventilation may be necessary if oxygenation/ventilation is insufficient vs controlled ventilation with muscle relaxants to avoid coughing and bucking during bronch
-if spontaneous ventilation induction, consider 1-2% lidocaine spray for larynx and vocal cords to facilitate fiberoptic bronchoscopy

308
Q

What is the most common procedure for chronic sinusitis

A

functional endoscopic sinus surgery (FESS)

309
Q

Nasal surgery issues

A

optimal visualization of surgical field, bleeding kept to minimum

310
Q

nasal surgery practice

A

vasoconstrictors
elevation of head and modest hypotension (issues systemic absorption of vasoconstrictors

311
Q

Complications of nasal surgery that can lead to death

A

right cribiform plate traumatic defect
anterior cerebral artery injury with frontal lobe damage
-basilar subarachnoid hemorrhage

312
Q

Upper third facial bones

A

facial frontal bones

313
Q

middle third facial bones

A

zygoma
maxilla
nasal bones
orbits

314
Q

lower third facial bones

A

mandible
sympheal area
ramus
body of angle condyl
coronoid process

315
Q

Can oral or nasal intubation be used in Lefort 1 fracture?

A

yes can be accomplished in almost all cases
-often used to correct dental fascial deformities

316
Q

What is contraindicated in Lefort II?

A

nasal intubation

pyramidal
involving the thick upper part of the nasal bone and the thinner part forming the upper margin of the anterior nasal aperture

317
Q

Lefort III airway issues

A

loss of supporting facial structure=difficult intubation, early tracheostomy

318
Q

Lefort III facture

A

-runs parallel to base of the skull, separating the midfacial skeleton from the base of the skull
-basal skull–>CSF rhinorrhea and exposure of ethmoidal sinuses of “air cells” to air to infection

319
Q

What does Laser stand for?

A

Light Amplification Stimulated Emission Radiation

320
Q

Which is the most powerful laser?

A

Nd: YAG

green glasses
uses: tissue debulking trachea, upper bronchus

321
Q

Which laser is used when precision is needed and absorbed by water

A

CO2

322
Q

Which laser is absorbed by Hgb?

A

Argon

-uses: eye, dermatologic

Glasses: orange

323
Q

Uses of CO2 laser

A

oropharynx
vocal cords
plastic surgery
urology
GYN

Clear glasses

324
Q

Safety protocol for surgical lasers

A

-post warning signs outside any OR
-matt finish (black) surgical instruments reduce beam reflection and dispersion
-avoid N2O as it supports combustion
-patient’s eyes should be protected with appropriate colored glasses and/or wet gauze
-use the lowest concentration of oxygen as possible>: FiO2<30%
-lasers should be placed in Standby mode when not in use

325
Q

Safety protocol for surgical lasers

A

-use ETT specifically prepared for use with lasers
-inflate cuff of laser tube with dyed saline so that cuff perforation is readily apparent
-all adjacent tissues should be shielded by wet gauze to prevent damage by reflected beams
-plume should be suctioned and evacuated from the surgical field

326
Q

Estimated frequency (2010) per year of OR fires

A

600 or higher

(550-650 fires occur in the OR every year)
-20/ yr result in serious injury
-1-2 patient deaths annually

327
Q

Ignition sources

A

surgeons
-ESUs
-lasers
-

328
Q

Oxidizer

A

anesthesia providers
-O2, N20

329
Q

Fuel

A

nurses-drapes, prepping agents

330
Q

Common causes of OR fires

A
  1. Oxygen rich environment-involved in 75% of OR fires
  2. Alcohol based prep solutions-involved in 4% of OR fires
  3. Heat (ignition) sources
    -70% electrocautery
    -10% laser
    -remaining 20%: light sources, defibrillators and high-speed burns account for remaining 20% of OR fires
331
Q

Increased risk procedures for airway fires

A

-head, neck and upper chest (above T6-anything above xyphoid process)
-use of an ignition source (electrosurgical, electrocautery devices or laser) in proximity to an oxidizer-enriched (oxygen and nitrous oxide) atmospheres
-laser use during procedures involving the airway

332
Q

The tracheal cuff of the laser tube should be filled:

A

-saline rather than air
-saline in the tracheal cuff should be tinted with methylene blue to act as a marker for cuff puncture by a laser

333
Q

Airway fires and Association with decreased risk

A

-determine if patient is at risk for a surgical fire
-surgical team discusses: the strategy for preventing and managing a surgical fire in a high-risk patient
-minimize the concentration of oxidizer near surgical site
-safely manage ignition sources
-safely manage fuels (drapes, cannulas, hair, gowns)

334
Q

Wait time for hairless skin

A

3 min

335
Q

wait time for hair

A

1 hour

336
Q

wait time for O2 to dissipate

A

1 minute for O2 to dissipate (turn it off) before using an ignition source

337
Q

Airway management of fire steps

A
  1. remove ETT
  2. stop the gas flow
  3. pour water or saline into airway
  4. care for patient
338
Q

Types of head and neck cancer surgery

A

-laryngectomy
-glossectomy
-pharyngectomy
-parotidectomy
-hemimandibulectomy
-radical neck dissection

339
Q

Preoperative considerations for head and neck cancer surgery

A

heavy tobacco and alcohol usage, co-existing disease
-abnormal airway issues, preop radiation, direct laryngoscopy, fiberoptic or elective tracheastomy

340
Q

Monitoring for head and neck cancer surgery

A

-blood loss, co-existing diseases, a-line, CVP (consider location of surgery–>fem line)
-if forearm flap, consider IV lines
-forced air warming
-intraop nerve monitoring (anterior neck operations) preserve SLN, RLN and vagus nerves
-meditronic Xomed NIM ETT

341
Q

Superior laryngeal nerve unilateral nerve injury

A

minimal effect

342
Q

Superior laryngeal nerve bilateral nerve injury

A

hoarseness, tiring of voice

343
Q

Recurrent laryngeal nerve unilateral nerve injury

A

hoarseness

344
Q

Bilateral recurrent nerve injury

A

Acute=stridor, respiratory distress
chronic=aphonia

345
Q

Unilateral vagus nerve injury

A

hoarseness

346
Q

bilateral vagus nerve injury

A

aphonia

347
Q
A
348
Q
A
348
Q

Maintenance of anesthesia for head and neck cancer surgery

A
  1. surgeon may request no NMBs during EENT procedures
  2. moderate controlled hypotension-may be helpful but be mindful of cerebral perfusion (a-line zeroed at external auditory meatus)
  3. microvascular free flap–>issues with vasoconstrictor and vasodilators; avoid excessive diuresis
  4. transfusion decisions (recurrence of cancer rates increase)
  5. manipulation of carotid sinus and stellate ganglion
349
Q

Macula

A

dark mass near center of retina, containing color-sensitive rods and central point of sharpest vision

350
Q

Retina

A

-back of eye is lined with thin layer=retina
-this is where photoreceptors are located
-retina would be the film of camera
-also contains nerves that tell the brain what the photoreceptors are seeing

351
Q

2 types of photoreceptors

A

rod and cones

352
Q

Rods

A

-work at very low levels of light (night vision) only a few bits of light (photons) can active rod
-rods do not help with color vision, this is why at night we see everything in gray scale

353
Q

how many rod cells does the human eye have?

A

100 million

354
Q

cones

A

-require more light for color vision
3 types:
blue
green
red

355
Q

how many cones does the human eye have?

A

6 million

356
Q

Many of the cones are packed into:

A

fovea, a small pit in the back of the eye that helps with sharpness or detail of images

357
Q

requirements for ophthalmic surgery

A

-akinesia
-analgesia
-minimal bleeding
-avoidance or obtundation of oculocardiac reflex
-control of IOP
-awareness of drug interactions
-smooth emergence (avoid coughing, N/V

358
Q

Which pressure has a greater role in IOP?

A

venous pressure>arterial

359
Q

Extraocular factors that will increase IOP

A

-contraction of orbicularis oculi muscle or contraction of other extraocular muscle
blink-10mmHg
forceful lid closure=50mmHg

360
Q

Clinical conditions increasing IOP

A

-hypercarbia
-hypoxia
-airway obstruction
-coughing/straining increases IOP 40mmHg
-vomiting
-overhydration
-retrobulbar hemorrhage
-ETT intubation

361
Q

Oculo-cardiac reflex

A

5 and dime
-bradycardia
-junctional rhyhm or asystole can occur secondary to traction on eye and ocular muscles
Tx: atropine, stope eye manipulation

362
Q

Factors that contibute to Oculo-reflex

A

preoperative anxiety
light GETA
hypoxia
hypercarbia
increased vagal tone due to age or drugs

363
Q

which nerve is the afferent limb of the OCR

A

trigeminal nerve

364
Q

efferent limb of OCR

A

vagus nerve

365
Q

Oculocephalic reflex

A

“doll’s eye”
movement of eye for maintaining forward gaze in response to rotation of the neck in a particular direction

366
Q

which block is conal?

A

retrobulbar

367
Q

which block is extraconal

A

peribulbar

368
Q

IS regional anesthesia okay for open globe?

A

no, relatively contraindicated

369
Q

General anesthesia for open globe

A

aspiration risk and increasing IOP with laryngoscopy (Sch increases 8mmHg for 5-7 minutes)

370
Q

Strategies to prevent increases in IOP for open globe

A
  1. avoid direct pressure on globe-patch eye with fox shield, no retrobulbar or peribulbar inj;careful with face mask techniques
  2. avoid increase in CVP: prevent coughing during induction and intubation; avoid head down position
  3. extubate under deep anesthesia (suction with OGT secondary to full stomach issues)
    4, avoid pharm agents that increase IOP–>phenylephrine and epinephrine (if change in venous pressure will change IOP)
371
Q

What are the anesthetic issues relative to retinal detachment procedures?

A

-sulfurhexafluoride (SF6) is used during retinal detachment repairs to form a bubble in the posterior chamber of the eye that flattens the retina and promotes correct healing
-nitrous oxide issues (35x more soluble than N2 and 117x more soluble than SF^)
-increase bubble volume, increase IOP, decreased retinal blood flow and compromising retinal repair
-SF6 remains the posterior chamber for 5 or more days
-avoid Nitrous oxide for at least 10 days

372
Q

Needle placement for retrobulbar block

A

needle punctures the bulbar fascia and enters the orbital muscle cone

373
Q

needle placement for peribulbar block

A

needle directed parallel and lateral to the bulbar fascia rather than passing through it

374
Q

LA volume for retrobulbar

A

2-4mL

375
Q

Peribbulbar LA volume

A

4-12ml
combo of lidocaine and bupivacaine

376
Q

onset of retrobulbar (intarconal) block

A

2 minutes

377
Q

onset of peribulbar (extraconal) block

A

10-20 minutes

378
Q

advantage of retrobulbar block

A

quick onset

379
Q

limitation of retrobulbar block

A

often requires supplemental cranial nerve (facial-7) block to prevent movement of eyelid

380
Q

advantage of peribulbar block

A

reduce risk of injury to optic nerve, globe perforation and subdural injection

381
Q

limitation of peribulbar block

A

cause swelling of the conjunctiva which may disrupt the surgical field

382
Q

minor complication of ophthalmic anesthesia

A

-corneal abrasion
-bruising
-subconjunctival hemorrhage
-chemosis (conjunctival swelling)
-transient diplopia

383
Q

symptoms of brainstem anesthesia

A

-contralateral amaurosis (partial or total blindness without visible change in the eye, typically due to disease of the optic nerve , spinal cord, or brain)
-slurred speech
-hemiparesis
-altered consciousness
-hypertension
-cardiovascular collapse

384
Q

strabismus repair concerns

A

forced duction testing
OR
oculogastric reflex
MH

385
Q

intraocular surgery concerns

A

proper control of IOP
akinesia
drug interactions and associated systemic diseases

386
Q

retinal detachment surgery

A

OCR
proper control if IOP
nitrous oxide interaction with air
sulfur hexafluoride or perfluorocarbons

387
Q

complications of needle based ophthalmic anesthesia

A

-extraocular muscle injury leading to postop strabismus, diplopia
-intra-arterial injection producing immediate convulsions
-central retinal artery occlusion
-inadvertent brain stem anesthesia–>contralateral amaurosis, mydriasis, muscle paresis, neurocardiopulmonary compromise, death

388
Q

Cranial nerve II

A

optic
provides visual information from retina
sensory

389
Q

cranial nerve III

A

oculomotor
-innervation of the extraocular muscles
innervation of the pupil and ciliary muscles
motor

390
Q

CN IV

A

trochlear
innervation of the superior oblique muscles
motor

391
Q

CN VI

A

abducens
innervation of the lateral rectus muscles
motor

392
Q

CN VII

A

facial
innervation of the muscles of facial expression
motor/sensory

393
Q

Cranial nerve 10

A

vagus
parasympathetic innervation associated with oculocardiac reflex

394
Q

What is the most common form of arthritis?

A

osetoarthritis

395
Q

What is osteoarthritis?

A

chronic degenerative joint disease that causes the breakdown of cartilage and bone in the joints
-develop slowly and worsen gradually
-pain, stiffness, swelling

396
Q

Are women or men more likely to develop osteoarthritis?

A

women especially over age 50Risk factors

397
Q

Risk factors for osteoarthritis

A

-obesity
-hx of injury
-overuse from repetitive movements of joints
-family hx of OA
-malformed joints

398
Q

What is rheumatoid arthritis?

A

long-term autoimmune disease that causes joint inflammation and pain
-immune system attacks its own tissues
-pain welling stiffness loss of function

399
Q

Which arthritis is symmetrical?

A

rheumatoid
osteo=asymmetrical

400
Q

RA can affect:

A

-heart
-lungs
-blood
-nerves
-eyes
skin

401
Q

What is RA triggered by?

A

-autoimmune disorder triggered by an antigen in genetically predisposed persons, chronic inflammatory disease involving diffuse joints and organ systems
-activated endothelial cells attract adhesion molecules that stimulate T cells and B lymphocytes
-release of cytokines (tumor necrosis factor, interleukins) accelerate the inflammatory process
-B lymphocytes produce antibodies (rheumatoid factor_ that further increase cytokine production
-eventually cartilage and articular surfaces are destroyed

402
Q

_____% of RA patients have measurable levels of rheumatoid factor

A

75

403
Q

Which joints are involved in RA first?

A

metacarpophalangeal and interphalangeal joints of hands

404
Q

What is the most frequently involved joint of the leg in RA?

A

knee

405
Q

upper cervical spine is affected in RA in _____% of patients

A

85

406
Q

In RA, atlantoaxial and subaxial instability can lead to ______________.

A

compresssion of the spinal cord

407
Q

Affected Larynx in RA results in ______________.

A

limitation vocal cord movement and laryngeal mucosal edema–>airway obstruction

408
Q

What is the common case of mortality in RA?

A

cardiovascular disease
-high incidence of subclinical cardiac dysfunction

409
Q

_________ is present in 20-50% of RA patients.

A

Pericarditis
can produce restrictive pericarditis and cardiac tamponade

410
Q

Heart problems with RA

A

-CAD
-myocarditis
-aortitis (aortic root dilation, aortic valve insufficiency)
-diastolic dysfunction
-dysrhythmias
-pumonary HTN

411
Q

pulmonary changes in RA

A

-interstitial lung disease
-reduced oxygen diffusing capacity
-obstructive and restrictive lung disease
-pulmonary nodule
-pulmonary effusions

412
Q

true/false: mild anemia is present in almost every RA patient

A

-decreased erythropoiesis (process of RBC production) are SE of drug therapy

413
Q

Nerve complications of RA

A

-peripheral nerve compression from joint destruction and non compressive neuropathies secondary to vasculities of blood vessels supplying affected nerves
-cervical myelopathy secondary to cervical spine compression

414
Q

rheumatoid vasculitis can affect:

A

-cerebral blood vessels resulting in headache, hemiparesis, aphasia and confusion

415
Q

4 groups of antirheumatic drugs

A
  1. NSAIDS-reduce pain and inflammation
  2. corticosteroids-side effects limit use
  3. DMARDs-target T and B cells. Methotrexate very effective and initial choice
  4. Biological DMARDS-target inflammatory mediators such as TNF and interleukins
416
Q

intubation techniquie for RA

A

one that minimizes cervical movement is recommended
-awake intubation, video laryngoscopy, or flexible fiberscope-assisted tracheal intubatoin

417
Q

incidence of atlanto axial (first joint between skull and C-spine) subluxation may exceed _____%, flexion of neck can compress spinal cord.

A

40

418
Q

What does cricoarytenoid arythritis produce?

A

edema of the larynx and may decrease the size of the glottis inlet–>smaller tube size

419
Q

Should anti-tnf biologic we withheld before surgery?

A

yes

420
Q

What is anykylosing spondylitis?

A

type of arthritis causing inflammation of the joints and ligaments of the spine
severe cases-causes vertebrae to fuse leading to rigid inflexible spine
-inflammation causes stiffness

421
Q

What does ankylosing spondylitis affect

A

peripheral joints: knees , ankles , hips
some develop eye disease uveitis, skin 9psoriasis, or gut (IBD)

422
Q

Does ankylosing spondylitis have acure?

A

no, but excercise, pT/OT to improve mobility and posture,, medications to manage pain

423
Q

General anesthesia for ortho

A

-rendered senseless to pain
-unconscious and unaware
-good physiologic control
-positioning

424
Q

Regional anesthesia for ortho

A

-good relaxation
-may result in less blood loss
-lower rate of DVT
-can be continued for post-op analgesia
-intraop sedation can be titrated to effect
-length of procedure
-can isolate effect to surgical area
-can be combined with GA
-less N/V
-accelerated hospital discharge

425
Q

hypotensive technique for ortho procedures

A

-deliberate hypotension in order to decrease overall blood loss 40–50%
-reduced need for transfusion
-used with neuraxial
-MAP 50-65, SBP 80-90

426
Q

potential risks for hypotensive technique

A

cerebral perfusion and stroke
heart attack

427
Q

How do the organs manage during hypotensive technique?

A

brain, heart, liver and kidneys have the ability to autoregulate flow by intrinsic elasticity of vascular smooth muscles-baroreceptors and chemoreceptors

428
Q

Are epidural veins valveless?

A

yes!

429
Q

spinal surgery posterior approach prone position

A

-pressure on abdomen causes inferior vena cava compression, increased bleeding from valveless epidural veins, reducing CO and increasing risk of lower limb thrombosis
-adequate foam padding under chest and anterior superior iliac spines
-arms not abducted more than 90 degrees and positioned with slight internal rotation to reduce risk fo brachial plexus stretching
-ulnar nerve at risk with elbow flexed
-eyes taped, goggles

430
Q

anterior approach to thoracocolumbar spine is ______position.

A

lateral

431
Q

adult spine surgery transfusion ranges from _____ to ____%

A

50-80%

432
Q

Most blood loss during spinal instrumentation and fusion during spine surgery occurs with _________

A

decortication and proportional to the # of vertebral level involved

433
Q

decreased blood losss and transfusion requireents during spinal sx

A

-preoperative autologous donation
-proper positioning
-use of intraop blood salvage
-administration of TXA

434
Q

TXA is an analogue of ________.

A

lysine

435
Q

MOA TXA

A

acts by competitively blocking the lysine binding site of plasminogen which leads to inhibition of fibrinolysis
-antifibrinolytic
-can reduce blood loss by 30-40%

436
Q

contraindications to TXA

A

-history of blood clots in the lungs (PE) or vein (DVT)
-coagulopathy (DIC)
-severe renal insufficiency or chronic kidney disease
-hx of acute subarachnoid hemorrhage
-coronary or vascular stents placed within 6 months to 1 year

437
Q

intraoperative monitoring for spinal surgery considered mandatory if cord is at risk of injury when:

A

-corrective forces applied to spine
-osteotomies are made
-spinal canal is surgically invaded

438
Q

3 methods of IOM

A

-wake-op test
-sSEP
MEP

439
Q

anesthesia requirements for wake up test

A

-reliable but quickly antagonied
-wakening should be smooth
-no pain during test
-no recall (recall occurs in 0-20%)

440
Q

What do SEEPs assess

A

dorsal column pathways of proprioception and vibation supplied by posterior spinal arteries
altered by neural injury, volatile anesthetics, hypercarbia, hypoxia, hypotension and hypothermia

441
Q

Latency

A

time it takes for an electrical impulse to travel from stimulation site to recording site, measured in milliseconds (MS)

442
Q

amplitude

A

size of the response measured in microvolts (uV)

443
Q

if muscles controlled by C5 nerve roots (Deltoid, biceps, brachialis and brachioradialis) are flaccid, partial ______ should be expected.

A

diaphragmatic

444
Q

spinal shock occurs immediately after injury and lasts up to ______ weeks.

A

3

445
Q

lesions above the cardiac accelerator fibers are at _______________ cause bradycardia

A

T1-T4

446
Q

Complete cord transection above _____ -85% go on to exhibit autonomic hyperreflexia

A

T5

447
Q

what is autonomic hyperreflexia?

A

-severe paroxysmal HTN with bradycardia from the baroreceptor reflex, dysrhthmias, and cutaneous vasoconstriction below and vasodilation above the level of injury
-induced by distension of bladder or rectum or any noxious stimulus including surgery
-remove stimulus, deepen anesthesia, direct-acting vasodilator
-seizures, intracranial hemorrhage or MI

448
Q

respiratory failure and mechanical ventilation with cervical lesions at _______.

A

C3-C5

449
Q

Lesions b/w ______-significant alterations in respiratory function due to loss of abdominal and intercostal support

A

C5-C7
-vital capacity reduction of 60%
-atelectasis and risk of infection d/t inability to cough and clear secretion

450
Q

succinylcholine for first _____hours after injury

A

48 hours
-after that proliferation of ach receptors in muscle can cause hypersensitivity to depolarizing
-mar
- muscle relaxants-marked hyperkalemia
-maximal hyperkalemia risk from sux b/w 4 weeks and 5 months after spinal injury
-may rise to 14 mEq/L-V-fib, cardiac arrest
-non-depolarizing agents okay

451
Q

goal of MILS (manual inline stabilization)

A

to apply sufficient opposite forces to head and neck to limit the movement during airway intervention
-recommended by current ATLS guidelines

452
Q

surgery for scoliosis is considered when?

A

cobb angle , a measure of curvature exceeds 50 degrees in thoracic or 40 degrees in lumbar spine

453
Q

goal in scoliosis surgery

A

goal is to halt progression of condition, partially correct deformity, prevent further respiratory and cardiac deterioration
-pulmonary function acutely deteriorates for 7-10 days after surgery

454
Q

cobb angle 10 degrees

A

minimum angulation

455
Q

cobb angle 20-40 degrees

A

back brace and PT

456
Q

cobb angle >50 degrees thoracic and 40 degrees lumbar

A

corrective surgery

457
Q

measurement of cobb angle

A

-draw lines paralell to upper border of superior vertebral body and lower border of lowest vertebral vertebrae of the structural curve then erecting perpendicular from these lines to cross each other
-angle between these perpendicular is the angle of the curvature

458
Q

venous air embolism s/s

A

-unexplained hypotension
-increased ET nitrogen concentration
-fall in ETCO2

459
Q

tx of VAE

A

flood surgical site with saline
-control sites of air entry
-reposition with surgical site below the right atrium
-aspirate air from multiorific CVC
-cessation of inhaled nitrous oxide

460
Q

study shos that lower rate of perioperative nerve injury in patients who received ______ block

A

interscalene

461
Q

radial nerve palsy in up to _____% of humeral shaft fractures

A

17

462
Q

What injury is associated with proximal humerus fractures

A

axillary nerve and brachial plexus injury

463
Q

Hemodynamic changes in beach chair

A

B/P at head wil lbe lower than arm
-every 20cm of height difference-15mmHg difference in arterial pressure
-reports of strokes but autoregulation is sufficient-no associated increase in neurologic outcome
=report of stroke but autoregulation is sufficient -no associated increase in neurologic outcome

464
Q

four nerves of brachial plexus

A

-radial
-musculocutaneous
-ulnar
-median

465
Q

advantages of peripheral nerve blocks

A

-earlier discharge
-decreased risk of hospital admission following rotator cuff repair
-lower 30 day mortality
-decreased incidence of thromboembolic events
-lower transfusion requirements and less blood loss
-dereased length of stay, cost and hospital complications
-superior pain control

466
Q

How long can brachial plexus catheters be left in

A

4-7 days postop

467
Q

anterior approach to hip and pelvic surgery

A

-gaining favor for tissue sparing
-smaller incision
-potential for less pain
-faster recovery
-improved mobility

468
Q

posterior surgical approach to hip and pelvic surgery

A

-most performed
-lateral decubitus position, arms neutral and abducted/flexed less than 90 degrees
-axillary roll to prevent compression of brachial plexus and axillary artery
-GA-airway accessed prior to positioning
-RA -sitting or lateral

469
Q

why is knee surgery more painful recovery

A

high incidence b/c TKA involves cutting and cementing of 2 long bones (femur and tibia)

470
Q

intraocular proceudre imporatnt viarable

A

-globe akinesia
-patient movement
-control of IOPin

471
Q

extraocular procedure imporatnt variables

A

-significance of IOP fades , elicitation of oculocardiaca reflex becomes concern

472
Q

_______extraocular muscles move eye within their orbit to various positions

A

6

473
Q

4 layers of eyelid

A
  1. conjunctiva
    -2. cartilagenous tarsal plate
  2. muscle layer-orbicularis and levator palpebrae
  3. skin
474
Q

blood supply to eye/ orbit by emans of

A

branches of internal and external carotid arteries

475
Q

venous drainage of eye through

A

central retinal vein then all veins empty into cavernous sinus

476
Q

trochlear nerve supplies what

A

superior oblique muscle

477
Q

abducens nerve supplies what

A

lateral rectus muscle

478
Q

trigeminal nerve

A

most complex ocular and adnexall innervation

479
Q

3 layers of eye

A
  1. sclera
  2. uveal tract (iris, ciliary body and choroid)
  3. retina
480
Q

What transmits optic nerve and ophthalmic artery as well as sympathetic nerve from carotid plexus?

A

optic foramen

481
Q

2/3 of aqueous humor is formed where

A

posterior chamber by ciliary body in an active secretory process involving both the carbonic anhydrase and cytochrome oxidase systems

482
Q

remaining 1/3 of aqueous humor formed by

A

passive filtration of aqueous humor from vessles on anteriors surface of iris

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