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Surgery, Opthalmology, Otolaryngology, and Rhinology > Surgery > Flashcards

Surgery Flashcards

1
Q

what is shock?

A
  • Failure to meet the metabolic needs of the cell or tissue.
  • DECREASED TISSUE PERFUSION

-can be a direct consequence of etiologies such as:
HYPOVOLEMIC/HEMORRHAGIC
CARDIOGENIC
NEUROGENIC
SEPTIC (due to released of molecules or cellular products that result in cellular or endothelial activation)

-initial injury is reversible but if the injury is prolonegd enough, it becomes irreversible

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2
Q

What is the general approach to the management of patients in shock?

A
  • assuring secure airway with appropriate ventilation
  • control of hemorrhage
  • restoration of vascular volume and tissue perfusion
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3
Q

What is the mainstay of treatment of hemorrhagic or hypovolemic shock?

A

Volume resuscitation with blood products

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4
Q

What processes should be prevented or monitored in hemorrhagic shock?

A

hypothermia
acidemia
coagulopathy

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5
Q

What is the mainstay of treatment of hemorrhagic or septic shock?

A
  • fluid resuscitation
  • appropriate antibiotic therapy
  • control of source of infection

(drainage of infected fluid collection,
removal of infected foreign body,
debridement of devitalized tissue)

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6
Q

What are the classifications of shock?

A 
hypovolemic
cardiogenic
septic (vasogenic)
neurogenic
traumatic
obstructive
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7
Q

What is the final common pathway for profound and prolonged shock?

A

vasodilatory shock

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8
Q

What is septic shock or vasodilatory shock?

A

the results of dysfunction of the endothelium and vasculature secondary to circulating inflammatory mediators and cells or as a response to prolonged and severe hypoperfusion

  • failure of the vascular smooth muscles to constrict appropriately
  • there is peripheral dilation with resultant hypotension
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9
Q

What is the most frequent form of vasodilatory shock?

A

septic shock

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10
Q

What type of shock is a by product of the body’s response to disruption of the host-microbe equilibrium resulting in invasive or severe localized infection?

A

septic shock

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11
Q

What are the 2 classification of sepsis according to the magnitude of systemic inflammatory reaction?

A

sepsis
severe sepsis
septic shock

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12
Q

How does sepsis, severe sepsis, and septic shock differ from each other?

A

sepsis has evidence of infection and systemic signs of inflammation like fever, leukocytosis, and tachycardia.

severe sepsis is sepsis with hypoperfusion with signs of organ dysfunction (not yet hypotensive)

septic shock has more significant evidence of tissue hypoperfusion and systemic hypotension

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13
Q

In sepsis, prompt search of infection is necessary. What are the possible locations of infection?

A
  • wounds (inspect all wounds)
  • intravenous catheters
  • blood cultures
  • adjunctive imaging studies to find the location of infection or abscess that is not visible externally
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14
Q

Why is long term, empiric, broad spectrum antibiotic use should be minimize?

A
  • to reduce the development of resistant organism
  • to avoid complications like fungal overgrowth and antibiotic-associated colitis from overgrowth of clostridium difficile
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15
Q

What is the role of corticosteroid?

A

They are class of drugs that lowers the inflammation of the body. They also reduce the immune system activity.

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16
Q

What the essential management for septic shock?

A
  1. Adequate airway and ventilation (intubate if necessary)
  2. Fluid resuscitation with balanced salt solutions
  3. Empiric antibiotics that target the most likely pathogen. Switch to narrow spectrum if culture result is out.
  4. Percutaneous drainage or operative management for those with fluid collections, infected foreign body (artificial valve), and devitalized tissue. Antibiotic therapy may not be effective if these are present.
  5. Vasopressor (norepi- preferrred, then epi, then arginine vasopressin)
  6. Intensive insulin therapy (maintenance of blood glucose at 80-110 mg/dL) for those with persistent hypergylcemia and insulin resistance
  7. Use of lower tidal volume if with ARDs
  8. Others like antiendotoxin antibodies, anticytokines antibodies, cytokine receptor antagonist, immune enhances, NO synthase inhibitor, O2 radical scavengers)
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17
Q

What is the most common cause of cardiogenic shock?

A

acute and extensive MI

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18
Q

What is cardiogenic shock?

A

CIRCULATORY PUMP FAILURE leading to diminished forward flow with subsequent hypoxia, in the setting of adequate vascular volume

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19
Q

What is the hymodynamic criteria for cardiogenic shock?

A 
sustained hypotension (SBP<90mmhg for 30 mins)
reduced cardiac index (<2.2 L/min/m2)
elevated PAWP (>15mmHg)
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20
Q

What are possible causes of cardiogenic shock?

A 
Acute MI (most common)
Free wall rupture
Cardiac tamponade
Acute mitral regurgitation
Ventricular septal defect
Arrhythmia
End-stage cardiomyopathy
Myocarditis
Severe myocardial contusion
Left ventricular flow obstruction
Obstruction to ledt ventricular filling
Metabolic
drug reactions
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21
Q

What are the signs of cardiogenic shock?

A 
hypotension
cool and mottled skin
depressed mental status
tachycardia
diminished pulses

dysrhythmia, precordial heave, distal heart tones

In evalutation of possible cardiogenic shock, other causes of hypotension must be excluded (hemorrhagic, sepsis, pulmonary embolism, and aortic dissection)

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22
Q

What diagnostic tools are used for confirmation of a cardiac source of shock?

A

ECG, echocardiography

Others like CXR, ABG, Electrolytes, CBC, and cardiac enzymes may also help.

23
Q

What are the effects of dobutamine?

A

It has an effect on both B1 and B2 adrenergic receptors.
B1- increases cardiac output by increasing cardiac rate and contractility
B2- vasodilate vascular peripheral vascular beds, lower peripheral resistance, and lower systemic blood pressure

24
Q

What inotropic supports.drugs are used in profound cardiac dysfunction?

A 
Dobutamine
Dopamine (similar effects with dobutamine but in lower doses, thus preferrable)
25
Q

What are the effects of epinephrine?

A

stimulates both alpha and beta receptors

It increases cardiac contractility and heart rate through its actions on beta1 receptor but also vasoconstrict peripheral vessel through its action on alpha1

26
Q

How would you check for the status of peripheral vasculature blood flow?

A

capillary refill time
peripheral pulses
urine output

27
Q

What is an obstructive shock?

A

From mechanical obstruction of venous return

28
Q

What are the causes of obstructive shock?

A 
Pericardial tamponade
Pulmonary embolus
Tension pneumothorax
IVC obstruction
-DVT
-gravid uterus on IVC
-neoplasm
Increases intrathoracic pressure
-excess PEEP
-neoplasm
29
Q

What are the classic findings for tension pneumothorax?

management?

A
  • respiratory distress
  • HYPOTENSION
  • diminished breath sounds over one hemithorax
  • hyperresonance
  • JUGULAR VENOUS DISTENSION
  • SHIFT OF MEDIASTINAL STRUCTURES to the unaffected side

Pleural decompression by needle decompression at 2nd ICS midclavicular line (gush of air will be heard)

30
Q

What do you call the inflammatory mediators released in response to tissue injury during a soft or bony injury?

A

damage-associated molecular patterns

-these are somewhat similar in pathogen-associated molecular patterns

31
Q

What is a third spacing?

A

translocation of intravascular volume into the peritoneum, bowel, burned tissues, or crush injury sites. This is the phenomenon of fluid distribution after a major trauma involving blood loss.

this serves as the basis for the treatment of hemorrhagic shock with RBCs and lactated Ringer’s solution or isotonic saline.

32
Q

What are the core principles in the management of critically injured pariten?

A

control of airway with proper ventilation

control of active hemorrhage

appropriate volume resuscitation with blood products with limited volume of crystalloid

recognized hypoperfusion

excessive resuscitation may exacerbate the bleeding

33
Q

What are the three phases of shock?

A

compensated
decompensated
irreversible phase

34
Q

What is the goal of neuroendocrine response (sympathetic and RAAS etc) to hemorrhage?

A

maintain perfusion to heart and the brain through

  1. PERIPHERAL VASOCONSTRICTION (SNS)
  2. INHIBITION OF FLUID EXCRETION (RAAS)
35
Q

What are the AFFERENT SENSORS/RECEPTORS that send signal to the brain during an event of hemorrhage?

A

Baroreceptors (in atrium, aortic arch, carotid bodies)

Chemoreceptors (aorta, carotid bodies)

36
Q

What is the normal action of normal inactivated baroreceptors?

A

normally it inhibits the ANS action

If sudden drop of pressure is detected by the baroreceptors, it also stops to inhibit the ANS, thus ANS actions are promoted. These include peripheral vasoconstriction.

37
Q

What are the body’s cardiovascular responses to hemorrhage?

A
  1. increased cardiac rate
  2. venous and arterial vasoconstriction
  3. shunting of blood away from less essential organ like G
    I
  4. autoregulation of brain and heart makes it unaffected by ANS activation (this is to maintain adequate perfusion of blood to heart and brain)
  5. induces catecholamine release
  6. increase circulating glucose availability to peripheral tissue (HYPERGLYCEMIA and INSULIN RESISTANCE)
38
Q

What are the body’s hormonal responses to hemorrhage?

A
  1. Activation of H-P-A axis (releasing cortisol and epinephrine)
  2. RAAS system is activated (prevent sodium excretion, thus, water excretion)
  3. Releasing of ADH or vasopressin by the pituitary
39
Q

What cytokine is the earliest cytokine that respond to an injurious stimuli? This is produced by monocytes, macrophages and T-cells.

A

TNF alpha

its half-life is 90 minutues, compared to IL-1 which only has minutes

40
Q

What is the function of TNF alpha once released in the bloodstream?

A

TNF alpha can:

  1. produce peripharal vasodilation
  2. activate other cytokines
  3. induce procoagulant activity
  4. stimulate a wide array of cellular metabolic changes
41
Q

What is the half-life and function of IL-1 in shock?

A

Half-life is only 6 minutes.

Its function is to produce a FEBRILE RESPONSE by activating prostaglandins in the posterior hypothalamus. and causes anorexia by activating the satiety center

also augments secretion of ACTH, glucocorticoids and endorphins

stimulate release of IL2, 4, 6. 8. GM-CSF. and interferon gamma

42
Q

What is the function of IL2 in shock?

A

activates other lymphocyte and natural killer cells

43
Q

What cytokine is elevated in response to hemorrhagic shock, major operative procedures or trauma? this cytokine plays a role in the development of alveolar damage and ARDS.

A

IL6

44
Q

What are the signs of possible intra-abdominal hemorrhage?

A

abdominal distension
abdominal tenderness
visible abdominal wounds

Do diagnostic ultrasound or diagnostic peritoneal lavage

45
Q

What diagnostic tests should be ordered if patient came in from sustained high energy blunt trauma?

A

CT scan to assess for head, chest, or abdominal bleeding

46
Q

What are the classic findings for cardiac tamponade?

A

Becks triad (hypotension, muffled heart sounds, increased JVP)

dyspnea
orthopnea
peripheral edema
chest pain
tachycardia
47
Q

What the emergency management for cardiac tamponade?

A

pericardial decompression by pericardiocentesis

needle pericardiocentesis may not be helpful in evacuating clotted blood

48
Q

What is a neurogenic shock?

A

refers to diminished tissue perfusion as a result of LOSS OF VASOMOTOR TONE to peripheral beds due to spinal cord injury.

This results to increased vascular capacitance, decreased venous return, and decreased cardiac output

49
Q

What are the classical findings for neurogenic shock?

A 
BRADYCARDIA
HYPOTENSION
cardiac dysrhythmias
reduce cardiac output
decreased vascular resistance
50
Q

What management can be done to neurogenic shock?

A

secure airway and ventilation
fluid resuscitation

ADMINISTRATION OF VASOCONSTRICTOR

51
Q

What are the two important goals in the treatment of shock?

A

adequate organ perfusion

tissue oxygenation

52
Q

how would you know if resuscitation is complete in treating shock?

A

O2 debt is repaid

tissue acidosis is corrected (means no anaerobic metabolism occurring)

aerobic metabolism restored

53
Q

How would you quantify O2 debt?

A

Lactate levels

Base deficits

Surgery, Opthalmology, Otolaryngology, and Rhinology (4 decks)

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