Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Patho Test 1 > TEST 3: Shock > Flashcards

TEST 3: Shock Flashcards

1
Q

Basic principles of shock
(Lecture, p. 1557)

A

-Inadequate tissue perfusion—> decreased oxygen and nutrient delivery —> impaired cellular metabolism

-Can have increased oxygen demand and nutrients (hyper metabolic state)
-Can have decreased removal of cellular waste

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cellular changes in shock
(Lecture, p.1558)
BLUEPRINT

A

Main problem of shock at the cellular level:
-We switch from aerobic to anaerobic metabolism (d/t overconsumption of oxygen)

When anaerobic metabolism starts:
-Increased lactate, metabolic acidosis, increase in the oxy-hgb dissociation

-Next, protein metabolism increases, causing increased muscle wasting( decreased real and cardiac muscle strength) decrease immunoglobulin (will decrease your immune response) and increased cellular edema (inflammatory response that activates the clotting cascade)

-Lastly, decreased ATP, which increase intracellular Na/ water, decreased circulating volume, and can also trigger the clotting cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Metabolic changes in shock
(Lecture)
1559

A
  1. Increased glucose (from catecholamine, cortisol, and growth hormone release; BUT insulin resistance) which causes:
    Increased protein breakdown, increased pyruvate, increased lactate (also increases insulin resistance)
  2. Inability to use glucose/increased insulin resistance causes:
    Increased gluconeogensis and glycogenolysis (which deplete energy store and increase cell failure), also increase Lipolysis (so you increase the amount of free fatty acids and triglycerides).

INTERESTING: except in the liver, kidneys and muscles, the body’s cells have extremely limited stores of glycogen. The total body stores can fuel the metabolism for only about 10 hours. Though depletion of fat and glycogen stores is not considered organ failure, but contributes considerably to Cellular failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

General shock management
(Lecture)

A

-Consider patient history, risk factors, clinical situation

-Tx: address under lying cause, improve tissue perfusion, improve oxygen delivery, support metabolic demands and manage hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Stages of shock
(Lecture)

A
  1. Compensated:
    Where the body is still able to compensate for relative or absolute fluid loss (patient is able to maintain adequate BP and cerebral perfusion)
    —-vasoconstriction, increased HR & contractility maintain CO, activation of RAAS
  2. Decompensated:
    Late phase of shock where body’s compensatory mechanisms are unable to maintain adequate perfusion to the brain and vital organs
    —-vascular collapse, decreased CO (all the predictable symptoms)
  3. Irreversible:
    Rapid deterioration of the cardiovascular system and the compensatory mechanisms have failed—> MODS–> DEATH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cardiogenic Shock etiology & characteristics
(Lecture, p. 1567)

A

Results from the inability of the heart to pump adequate blood to the tissues and organs

3 primary etiologies:
-Decreased contractility (pump failure): from MI, sepsis, contusion, dysrythmia, papillary muscle rupture
-Impaired diastolic filling: arrhythmias
-Obstruction: PE, tamponade, valve disorders, tumors, wall defects

-Caused by extensive myocardial damage and aggravated by inflammatory response

Defining characteristics: hypotension and hypoperfusion despite adequate LV filling pressure & intravascular volume

-Also results in metabolic acidosis and is often fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cardiogenic shock compensatory mechanisms
(Lecture, p. 1567)

A

2 main mechanisms

  1. Decreased CO = Activates RAAS and stimulates ADH (which increases volume) —> preload, SV, HR increase—> causes systemic and pulmonary edema (causing dyspnea)
  2. Decreased CO = activates catecholamine compensatory release—>
    Causing increased SVR, preload, SV, HR—>which increases myocardial oxygen requirements (worsening the failure/ shock)—> leading to decreased CO/ EF
    —> worsened tissue perfusion, low BP
    —> ischemia, impaired cell metabolism, worsening myocardial dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cardiogenic shock manifestations/ treatment
(Lecture, p. 1567)

A

-Caused by inadequate perfusion to the heart and lungs

Manifestations:
-CP, dyspnea, faintness, impending doom
-Tachycardia, tachypnea, hypotension, JVD, low CO
-Signs of poor perfusion: mottling, cyanosis, low UO
-Extra heart sounds, pulm edema, hypoxemia
-Elevated end organ lab values (LFT/ BUN/ Creat)

-Treatment: support the pump, remove the obstruction/ PCI to open coronary arteries, IABP, impella, ECMO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hypovolemic Shock
(Lecture, p. 1568)

A

-Caused by reduced intravascular volume (preload) from loss of whole blood (hemorrhage), plasma (burns), or interstitial fluids (diaphpresis, DM, emesis, diuretics) in large amounts, which reduces CO.

-Symptoms occur with 15% of intravascular volume loss

Etiologies:
-Whole blood: hemorrhage
-Plasma: burns
-Interstitial fluids: diaphoresis, DM, DI, emesis, diarrhea, diuretics

Defining characteristics: compensatory mechanisms up to a certain point and then they fall off a cliff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hypovolemic shock compensatory mechanisms
(Lecture, p. 1569)

A

Decreased volume causes decreased CO= interstitial fluid shift into intravascular spaces, aldosterone and ADH to increase fluid reabsorption, and splenic discharge (disgorges stored rbc’s and plasma)

Decreased volume caused decreased CO= catecholamine release—> increase SVR /HR/ contractility (which increases CO)

Note, if loss continues, compensatory mechanisms fail and tissue perfusion is further decreased

Prompt control of hemorrhage is main goal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hypovolemic shock manifestations/ treatment
(Lecture, p. 1568)

A

-High SVR: pallor and cool extremities
-Thirst
-Oliguria
-Low Preload (RA/ CVP) and tachycardia

Treatment:
Fluid/ blood replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Neurogenic shock (aka vasogenic)
(Lecture, p. 1566)

A

-Widespread, massive vasodilation that results from an imbalance between the parasympathetic and sympathetic nervous system stimulation of vascular smooth muscle

-Etiologies (anything that stimulates parasympathetic activity and inhibits sympathetic activity) :
-Trauma: spinal cord or medulla
-Conditions that deprive medulla of oxygen or glucose
-Depressive drugs, anesthetic agents, severe emotional distress, pain

Defining characteristics: hypotension with bounding peripheral pulses and flash cap refill/ bradycardia

GEM hallmark sign of neurogenic shock is very low SVR (hypotension) as well as bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Neurogenic shock compensatory mechanisms
(Lecture)

A

-Really no body compensatory mechanisms IN the body WE have to do something (Ie vasopressin)

Imbalance between sympathetic and parasympathetic stimulation= massive vasodilation—> causing decreased vascular tone—> causing decreased SVR—> leading to inadequate CO and decreased tissue perfusion—> leads to impaired cellular metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Anaphylactic Shock
(Lecture, p. 1565)

A

-Is the outcome of a widespread inflammatory and vasodilatory reaction to an allergic antigen (usually a protein)

-Etiologies: exposure to allergic antigen

-Anaphylactoid type— cold, exercise, and medication contaminants (not IgE mediated, non immunologic)

Defining characteristics: similar to neurogenic shock with vasodilation, peripheral pooling, and tissue edema/
Bronchoconstriction

Mediators:
Histamine, kinins, prostaglandins, complement, leukotrienes, serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Anaphylactic shock compensatory mechanisms
(Lecture)

A

-The second type of shock that doesn’t have internal compensatory mechanisms WE must intervene to treat

Antigen exposure—> trigger inflammatory response—> mild to severe response (usually more extreme)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Anaphylactic Shock manifestations/ treatment
(Lecture, p.1566)

A

Manifestations:
-CV: hypotension, diaphoresis, pallor
-Resp: SOB, cough, rhinorrhea, throat tightening, wheezing,
-GI: N/V/D, abdominal pain
-Cutaneous: erythema, pruritis, urticaria, angioedema
OMINOUS: anxiety, confusion, impaired mentation (sign of worsening shock)

Treatment:
-Epi to stop mast cell degranulation, fluid resuscitation, antihistamines, steroids

17
Q

Septic shock
(Lecture, p. 1560)

A

-Is the endpoint of a physiologic state of hypoperfusion with profound underlying circulatory, cellular, and metabolic abnormalities (subset of sepsis)

-Etiology: Infection
-Gram negative and positive bacteria, virus, or fungus related
-can be anywhere: PNA, bloodstream, intravascular catheter, intraabdominal, urosepsis, surgical wound.

18
Q

Overview of shock categories
(P.1560)

A

Distributive > septic + anaphylactic + neurogenic

Cardiogenic

Hypovolemic

Obstructive

Note— initial management for all is to discover, diagnose and correct/ remove underlying cause

19
Q

The sepsis spectrum
(Lecture)

A

SIRS —>sepsis —>septic shock—> MODS

20
Q

Obstructive shock
(P.1569)

A

-Associated with a mechanical obstruction to and/ or from the heart (generally within the great vessels of the heart) that causes inadequate cardiac output

-Commonly combined with cardiogenic shock

-Usually due to PE, tension pneumo, or cardiac tamponade

-Potentially life threatening due to hemodynamic instability

21
Q

SIRS
(Lecture)

A

-Reaction to anything that stimulates the inflammatory response (can be both infectious and non infectious)

Cause: infection, trauma, pancreatitis, burns etc.

CARS (compensatory Anti-inflammatory response syndrome)

-SIRS Criteria:

Temp >38 or <36
HR > 90
RR > 20 or PaC02 <32
WBC > 12,000 or <4000, or > 10% bands

22
Q

Sepsis
(Lecture)

A

-Life threatening organ dysfunction caused by a deregulated host response to infection

Defining characteristics— systolic hypotension <90 and organ dysfunction

23
Q

SOFA Score
(Lecture)

A

Sequential organ failure assessment score :
-P/ F ratio (with or without mechanical ventilation)
-Platelet count (heme function)
-Glasgow coma score (neuro, anything less than patients normal is positive)
-Bilirubin (liver function)
-MAP (cardio function)
-Creatinine (kidney function)

*Considered positive if score increases two points= organ dysfunction due to hypoperfusion (aka positive sofa score)

-Quick SOFA score (qSOFA)
Used on patients not in the icu
-RR> 22
-GCS < 15
SBP < 100

If 2/3 are true, considered positive for sepsis organ dysfunction (best measure outside of icu ie clinic)

24
Q

How bacteremia works
(Lecture)

A

Bacteremia—> gram negative bacteria release endotoxins or gram positive bacteria release exotoxins, which both cause—> release of pro inflammatory cytokines, which causes activation of—> complement system, coagulation system, kinin system, neutrophil, endothelial, and monocyte-macrophage cell activity, which then —> anti inflammatory cytokine release —> endothelial cell dysfunction, ultimately resulting in—> capillary leak, micro vascular thrombus, cell adhesion, tissue hypoxia, apoptosis, impaired vascular tone, free radical damage

–Inadequate to diagnose sepsis especially without organ dysfunction (1563)

25
Q

Sepsis manifestations
(Lecture)

A

General:
-Hypo/hyperthermia, tachycardia, tachypnea, AMS, edema, hyperglycemia, cyanosis, mottling

Inflammatory:
-Leukocytosis or leukopenia, bandemia, elevated CRP, elevated procal

Hemodynamic:
-SBP< 90/Map <70, or an SBP decrease >40
-SvO2>70
-Cardiac index > 3.5L/min

Organ dysfunction:
-PF ratio <300, oliguria, creatinine increase, coagulopathy, ileus, thrombocytopenia, hyperbilirubinemia

Tissue dysfunction: lactic acidosis, decreased cap refill

1562-1563

26
Q

Septic shock
(Lecture)

A

-Subset of sepsis with profound circulatory, cellular, metabolic abnormalities (greater risk of mortality)

*Defining characteristics— vasopressors to maintain MAP > 65, low SVR and vasodilation, lactic > 2, without hypovolemia

1563

27
Q

MODS

Definition

Causes

Risk Factors

Prognosis

A

Progressive dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to a severe illness or injury.

Causes:
Sepsis/septic shock MOST COMMON CAUSE
severe trauma, major surgery, burns, circulatory shock, acute pancreatitis, ARF, ARDS, Blood transfusion, Heat stroke, Liver failure, mesenteric ischemia, propofol infusion syndrome, DIC, and tissue necrosis.

Risk:
Elderly, significant tissue injury, pre-existing conditions

Prognosis:
2 systems fail 54% mortality
5 systems fail 100% mortality

1570

28
Q

Primary MODS

A

Organ injury directly associated with a specific insult, generally ischemia, or decreased perfusion from shock or trauma, burn, soft tissue necrosis, or invasive infection.

Localized tissues/organs
GENERALIZED HYPOPERFUSION IN PRIMARY MODS USUALLY CANNOT BE DETECTED CLINICALLY

The insult does create a stress response initiating hormones, especially catecholamines. This response is “PRIMED” not active.

1570

29
Q

Secondary MODS

A

Progressive organ dysfunction from excessive inflammatory reaction after a latent period following an initial injury, in organs distant from the original injury.

Thought to be triggered by the second (often mild) insult not the primary injury, but produces an immense and disproportionate response secondary to being “primed” resulting in self perpetuating inflammation

1570

30
Q

Pathophysiology of secondary MODS

A
  • macrophages trigger inflammatory cytokines->endothelial damage-> neutrophils -> more tissue damage-> more inflammation-> nitric oxide (vasodilation)-> microvascular thrombi-> DIC!!

-Stress response-> catecholamines->hypermetabolism-> high O2 consumption-> catabolic state-> LOW SVR

-Neutrophils activated-> inflammation-> ROS -> damage endothelium.

Complement, kallikrein-kinin, coagulation and fibrinolytic cascades are ALL activated.
-Hyperinflammatory, hypercoagulable state that contributes to vasodilation, vasopermeability, cardiovascular instability, endothelial dysfunction, and clotting abnormalities!! OOF

-Bacterial translocation (gut hypothesis), maldistribution of blood, hypermetabolism, myocardial depression, supply-dependent oxygen consumption (demand exceeds supply), if O2 restored reperfusion injury.

1171-1175

31
Q

High and Low metabolism pathways

A

High: increased metabolic rate attempt to compensate for lack of energy but leads to accelerated depletion of energy stores and exacerbates cellular damage.

Low: cells slow their metabolism due to lack of substrates & O2, functionality is reduced, energy deficiency and repair/growth/maintenance are impaired

RESULT: dysfunctional ion pumps cause increase in Na & water -> cellular swelling possibly lysis
-toxic metabolites accumulate, acidosis, enzymes alter protein functions, increasing cellular injury and death.

organizer

32
Q

SIRS vs Sepsis

A

SIRS:
can be infectious or non-infectious in nature
Systemic inflammatory signs with no confirming infection

Sepsis:
always a dysfunctional response to infection
infection root cause of organ dysfunction

33
Q

Sepsis vs Septic Shock

A

Sepsis:
organ dysfunction from infection response

Septic Shock:
progression of sepsis with sustained hypotension despite fluid resuscitation, evidence of tissue hypoperfusion (elevated lactic)

34
Q

Septic Shock vs MODS

A

Septic Shock:
Acute circulatory failure requiring immediate intervention

MODS:
Longer term progression of organ failure, often following septic shock, where multiple organ systems are now impaired due to prolonged hypoperfusion and inflammation

35
Q

MODS timeline

A

Initial: 0-24hrs
Fever, tachycardia, dyspnea, AMS, hypermetabolic state

Intermediate: 24-72hrs
ARDS

Progressive: 7-10 days
Persistent hypermetabolic & hyperdynamic state, bacteremia, multisystem organ failure (liver, kidney, GI)

Late: 14-21 days
Worsening Organ failure, potentially evolving to death

Chronic: 21+ days
Lingering symptoms, gradual improvement or DEATH

Advanced Patho Test 1 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions