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SCORE+DECKER UAMS > DECKER > Flashcards

DECKER Flashcards

1
Q

what is the initial injury that triggers the immune response in a transplant?

A

ischemia-reperfusion injury

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2
Q

Describe the mechanism of ischemia-reperfusion injury

A
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3
Q

Is ischemia-reperfusion injury worse in deceased or living donor transplants? Why?

A

deceased, brain death is associated with upregulation and activation of the complement cascade as well as generalized ischemia 2/2 activation of the sympathetic system in its attempt to increase cerebral perfusion pressure

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4
Q

What are some ways that the donor graft can be damaged during harvesting?

A
  • warm ischemia time (after vessel clamping)
  • cold ischemia time (after refrigeration)
  • manipulation of the graft
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5
Q

Why are HLA proteins central in the discussion of alloantigens when speaking of transplant rejection?

A

they are highly polymorphic, widely expressed, and capable of eliciting a uniquely large polyclonal T cell response

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6
Q

Describe class 1 HLAs

A
  • expressed by most of the nucleated cells
  • can only be recognized by CD8 coreceptors
  • present intracellular peptides (including viruses/bacteria)
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7
Q

Describe class II HLAs

A
  • present extracellular antigens to T cells
  • are present on APCs
  • recognized only by CD4 coreceptors
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8
Q

What other alloantigens in the immune system (other than HLA) can cause rejection despite identical HLA complex genes?

A

minor histocompatibility antigens

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9
Q

Know this schematic: APC and T cell interaction and the anti-rejection med targets

A
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10
Q

What are the different categories of methods of presentation of APVs to recipient T cells?

A

direct, indirect, semi-direct

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11
Q

What major cell line makes up adaptive immunity? How do they contribute to rejection?

A

T cells

  • defined broadly by surface markers CD4 or CD8
  • T helper 1s (CD4) produce IL-2, which proliferates CD8 Ts
  • T helper 2s produce other ILs, active B cells and eos
  • CD8 Ts can directly induce allograft cell death
  • T(reg) cells can suppress other T activation
  • Memory Ts produce cytokines faster
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12
Q

What major cells are present in innate immunity? What are their functions?

A
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13
Q

What is the leading cause of death in patients under the age of 45?

A

trauma

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14
Q

What is the number one cause of death in the first hour of trauma?

A

hemorrhage

  • nearly 40% of trauma deaths are 2/2 hemorrhage
  • In the Prospective, Observational, Multicenter, Major Trauma Transfusion (PROMMTT) study the median time to hemorrhagic death was only 2.6 hours.
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15
Q

What should the pre-hospital fluid resuscitation be like for penetrating trauma patients?

A

Patients with penetrating injuries, who received very little fluid resuscitation until they reached the operating room (OR) had a higher rate of survival than patients who were resuscitated in the prehospital phase and in the trauma bay.6 Additionally, they had fewer complications and shorter lengths of stay.

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16
Q

What is the pre-hospital recommendation on tourniquet use?

A

all law enforcement, fire, and emergency medical services, and concerned citizens be supplied with and trained on how to apply tourniquets

low rate of complications, but attention must be paid to tourniquet time

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17
Q

How do you assess airway in trauma patients?

A
  • ask their name
  • assume spine instability until exam done
  • can do chin lift/jaw thrust while maintaining inline stability
  • maintain stability while intubating
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18
Q

Describe the use of medication in RSI?

A
  • no bag-mask (inc risk of aspiration)
  • administer rapid induction agent, then NMB, then ETT
  • best meds are fastest w/ short duration w/o HDS fx
  • ex: etomidate 2-3 mg, succ 100 mg vs roc 70 mg, ETT
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19
Q

How do you manage a difficult airway in the trauma bay?

A
  • be prepared and well stocked
  • anticipate in head, neck, face trauma
  • stock: suction x2, oropharyngeal airway, nasal cannula, laryngoscopes, multiple ETT sizes 5-8, LMA, bougie, tape, cricothyroidotomy kit
  • prep for surgical airway if difficulty intubating and oxygenating
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20
Q

How do you perform a cricothyroidotomy?

A
  • as long as you can mask, you can re-attempt ETT
  • longitudinal incision at cricothyroid membrane
  • incise membrane transversely
  • spread membrane
  • small ETT (5 or 6) should be placed through the incision
  • ensure location in trach w/ ET CO2, ensure not mainstem w/ BL breath sounds
  • secure the tube in place w/ tape and note the level of insertion at teeth
  • look for your tube in CXR
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21
Q

How do you assess breathing in a trauma patient?

A
  • look: symmetrical chest rise, gross trauma
  • listen: bilateral breath sounds
  • feel: crepitus
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22
Q

Diagnose tension pneumothorax?

A
  • clinical
  • absent breath sounds on one lung
  • tracheal deviation
  • hypotension
  • no need for XR to confirm before management
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23
Q

How do you manage tension PTX?

A
  • needle decompression vs tube thoracostomy depending on skill and staff
  • needle: 2nd intercostal space at mid-clavicular line, convert to tube thoracostomy for definitive mgmt
  • tube: 4-5th intercostal space at mid-axillary line, place posteriorly and superiorly
  • do not place chest tubes through existing wound
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24
Q

How do you assess circulation in the trauma patient?

A
  • check pulses in all extremities
  • measure blood pressure
  • obtain access
  • manage hemorrhage
25
Q

How do you control active superficial or extremity hemorrhage in a trauma patient?

A
  • compression is the first-line - direct pressure
  • pack large wounds w/ gauze and hemostatic agents
  • tourniquets can be used for extremities
26
Q

What is ideal vascular access in the trauma patient?

A
  • large bore (18 gauge at least) short catheters
  • avoid access in injured extremities
  • place central lines opposite proximal vein injuries
  • if there is an intraabdominal vascular injury, keep in mind that femoral or lower extremity access sites may not deliver meds/fluids
  • IO can be used - noncollapsible vessel; proximal humerus or tibia, sternum; faster and easier than central lines
27
Q

How do you assess disability in a trauma patient?

A
  • pupil reactivity
  • gross motor/sensation x4
  • rectal tone
  • GCS (when 8, intubate)
  • spinal precautions until this check is normal
28
Q

Describe the early management in a suspected TBI in the trauma bay?

A
  • suspect TBI in head trauma w/ dec GCS
  • noncon head CT to eval
  • dec ICP: elevate HoB, not tight C collar, hypertonic saline
  • avoid routine hyperventilation and hypothermia
  • hyperventilation can be used in an impending hernia
29
Q

What does “exposure” mean in the trauma ABCDE mnemonic?

A
  • full removal of garments
  • log-roll w/ in-line stabilization to assess back and spine
  • bilateral axilla, perineum need to be visualized
  • cover with warm blankets after exposure to prevent hypothermia
30
Q

What is the lethal triad in trauma injury?

A

acidosis, coagulopathy, hypothermia

31
Q

In the severely injured trauma patient, what pathophysiological derangement should be minded?

A

trauma induced coagulopathy

32
Q

What is the preferred resuscitative fluid for patients who require large volume in the trauma bay?

A

blood

  • if losing blood from the chest, trauma chest tubes can be used to autotransfuse blood
33
Q

How does traditional coagulopathic lab work compare w/ ROTEM/TEG in guiding resuscitation for trauma patients?

A

In 2015, a randomized control trial, using a TEG-based algorithm versus conventional coagulation assays (international normalized ratio (INR), partial thromboplastin time (PTT), fibrinogen, and D-Dimer) in trauma patients, showed the goal-directed resuscitation to have a mortality benefit. Twenty (36.4%) patients, who received blood product transfusions based on conventional coagulation assays, died in comparison with 11 (19.6%) who were managed with TEG (p=0.049).

34
Q

How does 4F-PCC compare to FFP in normalizing elevated INR in trauma patients?

A

In a randomized control trial, comparing FFP with 4F-PCC in patients with international normalized ratios (INRs)greater than 2 who required urgent surgical intervention, a significant difference in time to INR reversal and achievement of hemostasis was documented.

35
Q

What is idarucizumab?

A

monoclonal antibody approved to reverse the direct thrombin inhibitor, dabigatran

36
Q

What are some commonly encountered antithrombotics and methods for reversal?

A
37
Q

What does “damage control resuscitation” mean?

A
  • balanced blood product resuscitation early
  • permissive hypotension
  • warm the patient, correct acidosis
  • The Pragmatic, Randomized Optimal Platelet and Plasma Ratios (PROPPR) study, trauma patients in need of massive transfusion (MT) demonstrated that patients who received a 1:1:1 ratio had an improved survival at 3 hours and a reduction in death due to exsanguination in the first 24 hours compared with patients who received a 1:1:2 ratio.
38
Q

How do you know which trauma patients need massive transfusion?

A

The Assessment of Blood Consumption or ABC score

2 or greater will likely need MTP

39
Q

What is the role of TXA in the trauma patient?

A

to treat hyperfibrinolysis (a known component of coagulopathy)

  • severe trauma patients requiring MTP (ABC score 2)
  • give only within 3 hrs of injury
  • 1g on arrival, then 1g over 8 hours
40
Q

Define supraventricular tachycardia.

A

Occurring at or above the SA node w/ rate >100

41
Q

What is SVT classification based on? What are the different kinds?

A

origin

  • sinus tachycardia
  • junctional tachycardia
  • atrial tachycardia
  • atrial fibrillation w/ RVR
  • atrial flutter
  • multiatrial tachycardia
42
Q

What is the evaluation of a patient w/ suspected SVT?

A
  • focused H&P
  • vitals
  • EKG - narrow QRS w/ rate 180-220
  • labs - anemia, lytes, hyperthyroidism
  • +/- echo and CXR
43
Q

How do you identify sinus tachycardia?

A
  • EKG - regular QRS complex w/ normal P waves at an increased rate
44
Q

What are the characteristics of atrial fibrillation?

A

disorganized atrial electrical activity: EKG - absent P waves, irregular QRS

45
Q

Atrial fibrillation is often self-limiting. If it lasts >48 hrs, there is an increased risk of what?

A

TIAs, stroke

46
Q

How do you determine the risk/benefit of anticoagulation use in a patient with atrial fibrillation?

A

CHADS2

  • CHF
  • HTN
  • Age >75
  • DM
  • Stroke/TIA (2)
47
Q

How do you manage a patient with unstable atrial fibrillation?

A
  • synchronized cardioversion
  • amiodarone: 300 mg/1 hr, 10-50 mg/hr x24 hr
  • continues >48 hrs: CHADS2 for anticoag
48
Q

How do you manage new atrial fibrillation w/ RVR in a stable patient?

A
49
Q

What medication do you use in a stable patient with a history of heart failure (EF<40) and new atrial fibrillation w/ RVR?

A

amiodarone

50
Q

What medication do you use in a stable patient with a history of COPD and new atrial fibrillation w/ RVR?

A

diltiazem

51
Q

How do you recognize atrial flutter?

A

EKG shows organized atrial electrical conduction at a highly increased rate (250-350). “Buzz saw” appearance on strip.

52
Q

How do you manage new atrial flutter in a stable patient?

A

Short-term management of atrial flutter consists of agents such as flecainide, propafenone, and amiodarone.

Long-term should be followed by cardiology for possible ablation.

53
Q

What is an atrioventricular reciprocating tachycardia?

A

accessory pathway of electrical conduction that allows propagation of the signal back up through the ventricle and to the atria, causing tachycardia

54
Q

What arrhythmia is atrioventricular reciprocating tachycardia associated with?

A

WPW

55
Q

What are EKG characteristics of AVRT

A

pre-excitation of the ventricular response shown by “delta waves”

56
Q

How do you treat AVRT?

A

Vagal maneuver is the first line of treatment in stable patients. IV adenosine can help break the circuit. All patients with AVRT should be started on β-blockers, and a cardiology referral is warranted for possible ablation.

57
Q

Atrioventricular nodal reentry tachycardia (AVNRT) is the most common form of paroxysmal supraventricular tachycardia (PSVT) and accounts for 60 to 70% of PSVT cases. What does EKG look like?

A

regular, narrow-complex w/ rate in 120s to 250s; inverted P waves in II, III, aVF (this can be hidden d/t simultaneous depolarization of atria and ventricles)

58
Q

How do you treat AVNRT?

A

β-blockers or nondihydropyridine calcium-channel blockers. Digoxin is often not preferred, as it has shown to have lower efficacy and a higher side-effect rate. Type Ic and type III antiarrhythmics can be used. As with atrial flutter, all patients with AVNRT should be considered for catheter ablation, as it has a cure rate of 95%.

SCORE+DECKER UAMS (29 decks)

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