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Pathophysiology > W.4: Shock syndrome > Flashcards

W.4: Shock syndrome Flashcards

1
Q

Definition of shock

A

A physiological state characterized by a significant, systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery and insufficient removal of cellular metabolic products, resulting in tissue injury.

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2
Q

Perfusion: Oxygen, nutrient delivery and CO2 elimination requires 4 things..

A
  1. A properly beating heart
  2. Adequate transport medium, blood and Hb
  3. An intact functioning vessel system
  4. A functioning respiratory system
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3
Q

Short term perfusion problems will lead to?

A
  • Syncope
  • Orthostatic collapse
  • Carotis hyperesthesia
  • Electric shock
  • Spinal cord injury
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4
Q

Long term perfusion issues leads to?

A

Shock syndrome

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5
Q

Vessel tone is controlled by

A

The sympathetic and parasympathetic nervous system

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6
Q

Function of pre-capillary sphincters

A

They control blood flow through the capillaries in response to oxygen demand of the tissue

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7
Q

Compensated shock

A

Body is able to compensate and maintain tissue perfusion

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8
Q

Progressive shock

A

Body begins to loose its ability to compensate - inadequate perfusion begins

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9
Q

Irreversible shock

A

Cell and tissue damage result in multisystem organ failure leading to death

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10
Q

Shock stage I (potentially reversible)

A

Low cardiac output or vasodilation (-> compensated hypotension)

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11
Q

Shock stage II (potentially reversible)

A

Decreased perfusion, major end-organ dysfunction (-> decompensated hypotension) -> microcirculatory failure, endothelial damage

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12
Q

Shock stage III (irreversible)

A

Cellular membrane injury (-> Cellular death)

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13
Q

Cell death, steps

A
  1. Hypoxia -> anerobic met. -> lactic acid accumulation -> Na/K-pump fails
  2. Ion shift: Na into cell -> brings water with it
  3. Cell swelling
  4. Mitochondrial swelling -> no prod. of ATP
  5. Lysosomes released, cell membrane breaks
  6. Cell destruction -> tissue death
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14
Q

Some clinical markers of shock (5)

A
  • Brachial sys. BP: <110mmHg
  • Sinus tachycardia: >90bpm
  • Shock index: RRsys/pulse <= 1 (norm=2)
  • Resp. rate: <7 or >29 breaths/min
  • Urine ouput: <0.5ml/kg/hr
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15
Q

What is hypovolemic shock?

A

Classic shock, which is the most common. It is the standard used to compare other forms of shock in differential diagnosis. (Hemorrhagic->blood loss, dehydration->fluid loss)

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16
Q

What is obstructive shock?

A
  • Pulmonary embolism/blocked pulmonary circulation
  • Tension pneumothorax/increased intrathoracic pressure
  • Cardiac tamponade/pressure on myocardium. Decreased preload.
17
Q

What is cardiogenic shock?

A

Heart (pump) failure (40% of myocardium damaged by AMI)

18
Q

Types of distributive shock (3)

A
  • Neurogenic
  • Anaphylactic
  • Septic
19
Q

Neurogenic shock

A

Spinal cord injury, drug overdose or poisoning which affects nervous systems ability to maintain vascular tone leading to vasodilation.

20
Q

Anaphylactic shock

A

Vasodilation and fluid shifting from capillary to cell. Leads to micro clotting and smooth muscle contraction (bronchospasm)

21
Q

Septic shock

A

Vasodilation and fluid shifting due to overwhelming infection.

22
Q

Causes of hypovolemic shock

A
  • Hemorrhage: eg. trauma, surgery, hemothorax, hematoma..
  • Fluid loss from GI: Diarrhea, vomiting
  • Fluid loss from urinary tract: Diabetes, salt-wasting disorders, adrenocortical insufficiency, diuretics
  • Fluid loss from the skin: Excessive burn, skin inflammation
  • Internal sequestration of fluid: Loss of volume into the interstitial space or body cavities
23
Q

E/NE stimulate alpha receptors to cause..

A

Vasoconstriction

24
Q

E/NE stimulate beta receptors to cause..

A

Bronchodilation and cardiac stimulation

25
Q

Causes of cardiogenic shock

A
  • Impaired pump function
  • Myocardial infarction
  • Asthma
  • Severe acidosis
  • Barbiturate intoxication
  • Toxins of septic shock
  • Valvular stenosis, septal rupture
  • Pericardial tamponade
  • Pneumothorax
  • Embolism
26
Q

Characteristics of distributive shock

A
  • Normovolemia
  • Normotension
  • Decreased TPR (generalized vasodilation)
  • Increased CO
  • Redness, fever
  • Increased HR
27
Q

What happens when we have long lasting hypoperfusion of tissues?

A
  • Accumulation of metabolites
  • Decreased peripheral resistance: cerebral ischemia, cardiac ischemia
  • Positive feedback mechanisms
28
Q

Mediators in shock

A
  1. Amins (histamine, serotonine)
  2. Lipids (eicosanoids, PAF)
  3. Proteolytic cascade (kinin-kallikrein, complement system, clotting factors, plasminogen)
  4. Cytokines (interleukins, TNF, GCSF, GFs, IFs)
  5. Free radicals (O2-, NO, lipid and protein peroxides)
29
Q

Reaction of muscle tissue in shock

A

Glucose uptake increases, glucose ox. dec. -> pyruvate and lactate release inc., inc. protein degradation -> keton acids

30
Q

Pathological changes of kidney in shock

A

Part of MOF (multiple organ failure) because of:

  • Vasoconstriction
  • Decrease of concentrating ability
  • Decrease of the urin quantity
  • Degradation of tubular epithel, anuria (failure of the kidney to produce ruin), uraemia (increased urea in the blood)
  • Dialysis
31
Q

Pathological changes of lungs in shock

A

Part of MOF (mortality 70%), overactivation of immune responses, liquid sequestration in alveola, adult respiratory distress syndrome (ARDS)

32
Q

Role of adipose tissue in shock

A

Shock is fatal in obese people, centralization of circulation -> stop flow in adipose tissue -> anaerob metabolism, cell death, reperfusion injury, danger of ARDS

33
Q

Changes of lipid metabolism in shock

A

Increased lactic acid, pyruvate, alanin, ketonic acid, fatty acid synthesis

34
Q

Anaphylactic shock is caused by

A
  • Person exposed to antigen that triggers IgE activated mast cells
  • Decreased sympathetic innervation of vasculature caused by drugs (eg. Penicillin) or foods (eggs, nuts, seafood)

Pathophysiology (14 decks)

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