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Advanced Patho Exam 4 > Exam 4: MODS > Flashcards

Exam 4: MODS Flashcards

1
Q

define shock

A

The circulatory system fails to adequately perfuse cells (tissues and organs) with arterial blood → impaired cellular metabolism → cell dysfunction.

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2
Q

what is aerobic catabolism perfused with?

A

normally perfused with arterial blood

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3
Q

what is glucose molecule broken down by?

A

glycolysis

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4
Q

what happens to pyruvic acid in the presence of o2? (aerobic catabolism)

A

pyruvic acid in the presence of O2 enters the mitochondria and undergoes oxidative phosphorylation → results in the production of large amount of ATP

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5
Q

what is ATP

A

energy unit of all cells, is used to drive energy dependent functions=very important for cell survival

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6
Q

what happens to pyruvic acid in anaerobic catabolism?

A

b/c theres not oxygen→ the pyruvic acid cannot enter the mitochondria so instead it coverts to lactic acid

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7
Q

what is one of our critical measures for shock?

A

lactic acid
- serum measurement of lactic acid is called lactate→ when lactate levels increase, the assumption is the cell do not have enough O2 and is producing lactic acid as byproduct

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8
Q

what is the byproduct of aerobic catabolism?

A
  • CO2 (which we exhale) and water
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9
Q

what does a strong pulse indicate?

A

good strength of cardiac contraction

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10
Q

assessing perfusion: clinical level (5)

A
  • Vital signs (heart rate and blood pressure)
  • SaO2
  • skin color and temperature
  • strength of pulse
  • organ function (well perfused organs function normally). if organ not well perfused, then expect some of the markers for organ function to be abnormal→cardiac (troponin), kidneys (BUN/creatinine), pancreas (amylase/lipase), liver (transaminase)
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11
Q

Assessing perfusion: cellular level (3)

A

a. Saturation of tissue hemoglobin with oxygen (StO2) using modified oximeter with near infrared spectroscopy. Continuous monitoring and trending. “Normal” value 45-95% depending on anatomic location.
b. Serum lactate levels: Lactate byproduct of anaerobic metabolism
c. Capillary refill: Simple bedside measure using < 3 seconds as cut off for normal

B&C should be paired

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12
Q

what is the difference, advantages, disadvantages of tissue oxygen oximeter compared to pulse ox

A

the difference is the light penetration is deeper than a pulse ox→ thought to go into the deeper tissue
advantages: provides continuous recording of how tissues are perfused
disadvantages: the absolute normal is so wide from 45-95%. that its the trend thats more important than the absolute #→wide because it depends on where the pulse ox is placed.

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13
Q

what does the presence of lactate indicate?

A

the presence of lactate, especially in the excess of 2 mml/L, suggest an anaerobic metabolism process→key indicator for shock

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14
Q

Assessing perfusion: Variables that affect perfusion: Tissue oxygen extraction

A
  1. Tissue oxygen extraction ratio (O2 ER) =
    =tissue O_2 consumption (V ̇O_2 ):tissue O_2 delivery (D ̇O_2)
    = 250 mLs/min:1000 mLs/min = .25 or 25%
  2. Perfusion decreases if the tissues require (i.e., consume) more O2 then can be delivered
    a. Conditions that increase VO2: Fever, tachycardia, hypertension, muscle effort, etc.
    b. Conditions that decrease DO2: Anemia, hypoxemia, decreased cardiac output, etc.
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15
Q

assessing perfusion: Pathophysiology of shock regardless of etiology

A
  1. Decreased tissue perfusion starts the process → impairs O2 & glucose delivery and use.
  2. Impaired O2 delivery and use → anaerobic metabolism:
    a. ↓ATP & ultimately ↓circulatory volume
    b. ↑protein catabolism → ↓ protein (albumin) → ↓circulatory volume + edema
    c. ↑lactate → metabolic (lactic) acidosis → ↓O2 affinity for hemoglobin worsening hypoxemia
  3. Impaired glucose delivery and use
    a. ↑glucose but not available/properly utilized by cells for glycolysis →↑pyruvate → ↑lactate
    b. catecholamines, cortisol, and growth hormone (stress response)
    i. ↑lipolysis → free fatty acids
    ii. ↑gluconeogenesis → proteolysis →↓albumin
    iii. ↑glycogenolysis → depleted energy stores
  4. Result of the above (1-3): clotting, inflammation, lysosomal destruction of tissue, and cellular failure → perpetuates ↓tissue perfusion.
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16
Q

describe oxyhemoglobin dissociation curve shifts in metabolic acidosis

A

in metabolic acidosis oxyhemoglobin dissociation curve shifts to the RIGHT
- shifting to the right is good for tissues because O2 is released from hgb more readily, but shifting to right also impairs the ability of hgb to pick up O2 at the lungs→so contributes to our anaerobic metabolism

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17
Q

define gluconeogenesis

A

break down of non-glucose stores for energy= primarily the form of protein

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18
Q

define glycogenolysis

A

release of glycogen stores in the liver= fewer stores for energy

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19
Q

what is the consequences of impaired O2 delivery and use and impaired glucose delivery and use?

A

the consequence is decrease tissue O2 delivery and increase tissue O2 demand

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20
Q

shock continuum (stages)

A

Initial (subtle findings) ↔ Compensatory ↔ Progressive→Refractory

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21
Q

shock stage: initial (subtle findings)

A

Pathophysiologic event → decreased perfusion.
Switch to anaerobic metabolism.
VS often normal, anxious.

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22
Q

shock stage: compensatory (4)

A

SNS (NE and Epi) & RAA & ADH boost volume and pressure.
VS: ↑ HR/↓ BP.
Skin cool and clammy.
Urine output low.

*aldosterone and ADH: boost volume
*NE and Epi: boost BP
*angiotensin: causes vasoconstriction

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23
Q

shock stages: progressive

A

Compensatory mechanisms failing.
Anaerobic metabolism →systemic cell & tissue ischemia.
Organ systems fail.
VS & clinical findings worsen.

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24
Q

shock stages: refractory

A

Multiple organ dysfunction → death.

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25
Q

Shock classified by etiology: hypovolemic

A

Hypovolemic: Inadequate tissue perfusion due to reduced intravascular volume (preload).

Etiology: Hemorrhage, burns, medical conditions: diabetes mellitus and insipidus, insensible losses: sweating, vomiting, diarrhea.

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26
Q

clinical manifestations: hypovolemic shock (4)

A

Predictable based on pathophysiology:
- Hypotension
- tachycardia
- cool clammy skin
- decreased preload.
- Subtle based on degree of volume loss.

a. Compensatory mechanisms maintain ~ normal BP through stage II.
b. Early warning signs: Pulse pressure (SBP – DBP), respiratory rate, and urine output
c. Narrow pressure changes: Systolic preserved while diastolic initially rises. Late stages S/D drop together.

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27
Q

Shock classified by etiology: obstructive

A

Inadequate tissue perfusion d/t obstruction of blood flow through the cardiovascular system.

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28
Q

what are the three types of obstructive shock?

A
  • pulmonary embolism
  • cardiac tamponade
  • tension pneumothorax
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29
Q

describe pathophysiology obstructive shock: pulmonary embolism

A

Thrombus blocks circulation →
heart doesn’t fill →
↓ cardiac output → ↓ tissue perfusion.

PE: clot in the pulm artery that carries venous blood→ theres an obstruction of blood flow from PA through pulm capillaries, PV and left side of heart

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30
Q

obstructive shock: PE-history

A

-deep vein thrombosis
- clotting disorder

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31
Q

obstructive shock: PE-S/S

A
  • jugular vein distention→KEY characteristic!
  • hypotension
  • tachycardic
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32
Q

obstructive shock pathophysiology: cardiac tamponade

A

Blood in the pericardial sac compresses the heart →
heart doesn’t fill → ↓ cardiac output → ↓ tissue perfusion.

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33
Q

obstructive shock: cardiac tamponade- history

A

chest trauma → penetrating with knife, rib fracture that penetrate the sac

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34
Q

obstructive shock: cardiac tamponade- S/S (4)

A
  • Muffled heart sounds → KEY finding
  • Hypotensive
  • tachycardic
  • jugular venous distension.
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35
Q

obstructive shock pathophysiology: Tension pneumothorax

A

Air enters pleural space with each breath and cannot escape → lung and mediastinal structures compressed & shift → ↓ cardiac output → ↓ tissue perfusion.

**mediastinal structures shift away from the collapsed lung

36
Q

obstructive shock: Tension pneumothorax- History

A

Chest trauma → sucking chest wound.

37
Q

obstructive shock: Tension pneumothorax- S/S (4)

A
  • Absent breath sounds one side.→ KEY indicator
  • Hypotensive
  • tachycardic
  • Jugular venous distension
38
Q

Shock classified by etiology: cardiogenic

A

Inadequate tissue perfusion due to depressed myocardial contractility.→ problem with the heart ability to pump

  1. Etiology: Usual culprits: acute myocardial infarction and/or exacerbation of heart failure.
39
Q

cardiogenic shock: risk factors

A

Conditions that accelerate atherosclerotic disease (uncontrolled HTN, dyslipidemia, smoking) → coronary artery disease → myocardial infarction → heart failure

40
Q

cardiogenic shock: clinical manifestations

A

Subjective findings depend on etiology. Physical findings categorized as those due to inadequate tissue perfusion and those due to pulmonary congestion.

  • AMS
  • pulmonary congestion/edema: tachypnea, dyspnea, hypoxemia, crackles → alveoli filled of fluid
  • weak thready pulses
  • hypotension and tachycardia
  • S3 heart sound
  • cool skin, cyanosis, mottling,
  • kidneys : decrease UO, increase BUN/Cr
41
Q

what is the abnormal heart sound of cardiogenic shock?

A
  • S3 heart sounds
  • “this abnormal heart sound occurs early in diastole, a filling time for the heart. the ventricles should be mostly empty and blood form the atrium should dump into there but if heart and ventricle are failing and not pumping out enough blood, then at the beginning of diastole, when its suppose to fill easily, the blood thats entering the left ventricle at the beginning of diastole makes a little rumbling sound→ indicating the heart is full of fluid”
42
Q

Shock classified by etiology: distributive

A

Emphasis: Sepsis → septic shock ↔ multiple organ dysfunction syndrome (MODS).

  1. Etiology: Infection
43
Q

define sepsis

A

Life-threatening organ dysfunction caused by a dysregulated host response to infection. ( person has an infection and their immune and inflammatory response to the infection is typically exaggerated, the exaggerated immune and inflammatory response causes organ dysfunction) Organisms include bacteria (gram + staph and strep; and – e coli, klebsiella, pseudomonas), viruses, fungi, and protozoa.

Common culprits: Lower respiratory, lower GI tract infections and genital urinary tract .

44
Q

define septic shock

A

Progression of sepsis to shock state:
i. decreased tissue perfusion: vasopressors (norepinephrine) to maintain MAP > 65 mmHg → BP is dropping because of vasodilation.
ii. impaired cellular metabolism with serum lactate levels > 2 mmol/L

45
Q

what is MODS

A

Often (but not always) a complication of sepsis. Dysfunction of two or more organ systems resulting from an uncontrolled host inflammatory response→ same thing as dysregulated host response to an infection, same process but now have specific organ damage

46
Q

Sepsis: risk factors

A
  • Extremes of age (<1/> 65)
  • immunosuppression
  • chronic illnesses
  • hospitalizations.
47
Q

pathophysiology of distributive shock

A

Sepsis → Septic shock → MODS

48
Q

define PAMP

A
  • pathogen associated molecular particles
  • these are pathogens recognized by macrophages
49
Q

what PAMPs does gram (+) bacteria have on its surface?

A

lipoteichoic acid

50
Q

what PAMPs does gram (-) bacteria have on its surface?

A

lipopolysaccharides

51
Q

what PAMPs does gram (+) and gram (-) both share on its surface?

A

peptidoglycan

52
Q

what does dysregulated host response mean?

A

it means pro-inflammatory response is much greater than anti-inflammatory

53
Q

what does the combination of pro-inflammatory cytokines and anti-inflammatory cytokines cause?

A

endothelial cell dysfunction/disrupts the endothelium

54
Q

pathophysiology of AMS in sepsis

A

cytokines cause endothelial cell dysfunction in the vascular circulation in the brain→ those effects are referred to as sepsis associated encephalopathy→ pathophysiology based change in mental status

55
Q

what does endothelial dysfunction contribute to?

A
  • capillary leak→ allows fluid and large molecules to enter the interstitial space and separates the capillary from the blood vessel from the tissue its suppose to supply nutrients to
56
Q

what is vasodilation mediated by in distributive shock?

A
  • vasodilation is mediated by histamine and nitric oxide
  • vasodilation is the definition of distributive shock→ the blood vessels are dilated, pressure very low, this decreases perfusion.
57
Q

what happens to nitric oxide in sepsis?

A

it goes up in patient with sepsis and it contributes to vasodilation

58
Q

what are the proinflammatory cytokines that are released during sepsis? (3)

A
  • Tumor necrosis factor alpha (TNF-a)
  • interleukins (IL-1, IL-6)
  • interferons (IFN-a, INF-b, INF-y)
59
Q

what is chemotaxis of leukocytes?

A

just means that leukocytes come towards that activated tissue macrophage

60
Q

what are toll like receptors (TLR) stimulated by?

A

microbial PAMPs→ can be stimulated by lipopolysaccharides, lipoteichoic acid, peptidoglycans

61
Q

what happens when tissue macrophages are activated by PAMPs

A

it results in an inflammatory response and its both pro-inflammation and anti-inflammation
*pro-inflammatory response is greater than anti-inflammatory response

62
Q

what are the acute phase proteins?

A

-C-reactive proteins and fibrinogen
*when we have cytokines, these proteins levels increase → thats our measurement we have inflammatory process going on

63
Q

what is the clotting system activated by?

A

clotting system is activated by tumor necrosis, interleukin 1 and interleukin 6→ probably d/t vessel wall damage

64
Q

why is permeability a problem in septic shock?

A
  • fluid leaked from blood vessel into the interstitial space
  • large molecules, like albumin, move into the interstitial space and now we get fluid and large molecules filling the interstitial space→ this separates the blood vessels from the tissue that it supplies blood to b/c theres more fluid, albumin, and molecules in the interstitial space→ contributes to decreased tissue perfusion
65
Q

activated clotting system also activates the kinin system → what can bradykinin cause?

A

causes downstream effects like histamine-like effects, vasodilation, leakiness (fluid and large molecules entering the interstitial space separating the capillary from the tissue it supplies nutrients to), and vasodilation characteristics of sepsis and distributive shock

66
Q

what does neutrophil do when it reaches the interstitial space?

A
  • it helps eliminate the bacteria (benefical)
  • the neutrophil releases free radicals or reactive oxygen species→ these substances are damaging to the surrounding tissues (not beneficial)
67
Q

what is every blood vessel in your circulatory system lined with?

A

it is lined with endothelium
→ the combination of pro-inflammatory and anti-inflammatory blood vessels disrupts the endothelium

68
Q

define Multiple organ dysfunction syndrome

A

Progressive dysfunction of two or more organ systems resulting from an uncontrolled host inflammatory response to a severe illness or injury.

69
Q

etiology of MODS

A

Sepsis and septic shock (commonly) or any severe pathophysiologic process that triggers a systemic inflammatory response by the host.

70
Q

risk factors: MODS

A
  • Extremes of age, especially older adults
  • significant tissue injury
  • co-morbid conditions

**same as patients with sepsis)

71
Q

what is the definition of primary MODS

A

one organ thats been hypo-perfused or ischemic that is inflamed.→ that inflammation primes the inflammatory system

72
Q

pathophysiology of MODS

A

impaired perfusion or ischemia to an organ thats caused by either pathogen or damage→ causes activations of macrophages locally with stress response (that organ is damaged)→ this sets up the inflammatory system to react to a second insult→ now widespread endothelial dysfunction which leads to uncontrolled systemic inflammatory/stress response

73
Q

what are the triggers of disseminated intravascular coagulation? (3)

A
  • trauma
  • sepsis
  • injury to endothelium
74
Q

what is needed for vascular smooth muscles to contract?

A

-myosin
- actin
- calcium

75
Q

process nitric oxide favors vasodilation

A

1) increased NO levels→ decrease phosphorylation myosin
2) NO changes the amount of calcium inside a cell→ see a decease in cytoplasmic calcium

76
Q

why does encephalopathy occur during organ dysfunction?

A

encephalopathy occurs b/c pathophysiologic events are going on systemically→ it occurs early and throughout the patients experience with sepsis

mechanisms for causes:
- there is damage to neurons itself
- BBB is altered→ its a blood vessel with endothelium that is altered by the effects of cytokines and plasma proteins→ so these blood vessels dilate, theyre suppose to be tight junctions, which is wha keeps substances from the bloodstream from entering the interstitial space, are destroyed→ now there’s fluid, albumin and inflammatory mediators entering the interstitial space and directly damaging the neurons

77
Q

Time frame for organ dysfunction: 24 hours (5)

A
  • Low-grade fever
  • tachycardia
  • tachypnea
  • dyspnea
  • a general hyperdynamic and hypermetabolic state
78
Q

Time frame for organ dysfunction: 24-72 hours

A

Adult/acute respiratory distress syndrome: Arterial hypoxemia (PaO2/FiO2 < 300 mmHg).

79
Q

what are the long term effects of endothelial and intra-alveolar events?

A

both type 1 and type 2 pneumocytes are damaged

80
Q

type 1 pneumocyte function

A

where gas exchange occurs

81
Q

type 2 pneumocytes function

A

produce surfactant→ allows your alveoli to open and close normally

*in the absence of surfactant, the alveoli tend to collapse all the way down and do not want to open=atelectasis

82
Q

Time frame for organ dysfunction:7-10 days (3)

A
  • Endotoxemia (GI bacteria enters blood stream): Positive blood cultures.
  • Acute kidney injury: Acute oliguria (urine output <0.5 mL/kg/h); Creatinine increase >0.5 mg/dL
  • Hepatic failure: Hyperbilirubinemia (plasma total bilirubin >4 mg/dL or 70 mmol/L)
83
Q

Time frame for organ dysfunction: >10 days (2)

A
  • Hematologic disorders: Disseminated intravascular coagulation (clotting) and fibrinolysis (elevated INR > 1.5 or PTT > 60 s; thrombocytopenia (platelet count <100,000/m3); elevated D-dimers.
  • Cardiac failure (impaired perfusion): Transition from warm (vasodilation) to cold (vasoconstriction) shock.
84
Q

Time frame for organ dysfunction: 14-21 days

A

death

85
Q

what are the interventions of the first hour bundle?

A
  1. measure lactate level→ remeasure lactate if initial lactate elevated (>2 mmol/L)
  2. obtain blood cultures before administering abx
  3. administer broad spectrum abx
  4. begin rapid administration of 30 mL/kg crystalloid (LR or 0.9) for hypotenson or lactate >4 mmol/L
  5. apply vasopressors if hypotensive during or after fluid resuscitation to maintain MAP >65 mmHg

Advanced Patho Exam 4 (4 decks)

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