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WorksheetsModule 6 Shock -
Total questions: 20
Worksheet time: 7mins
Shock is a clinical syndrome caused by:
Excessive nutrient delivery to the cells
Adequate tissue perfusion
Inadequate tissue perfusion
Increased blood viscosity
The three key components required to prevent shock are:
Strong bones, adequate electrolytes, oxygen reserves
Effective lungs, adequate hemoglobin, strong muscles
Effective pump (heart), adequate vasculature, sufficient blood volume
High blood sugar, normal potassium, effective clotting
Common physiologic responses in all shock types include:
Hypertension, hypometabolism, fluid overload
Tissue hypoperfusion, hypermetabolism, inflammatory activation
Vasodilation, bradycardia, hyperkalemia
Hyperglycemia, hypercalcemia, dehydration
In shock, the shift from aerobic to anaerobic metabolism leads to:
Increased ATP production
Enhanced oxygen utilization
Lactic acid accumulation → metabolic acidosis
Hyperoxygenation of tissues
In the compensatory stage of shock, catecholamine release results in:
Decreased heart rate and vasodilation
Increased heart rate, increased contractility, vasoconstriction
Fluid excretion and decreased contractility
Decreased blood flow to the heart, brain, and lungs
Clinical manifestations in the compensatory stage of shock include:
Severe hypotension and coma
Tachycardia, tachypnea, cool pale skin, decreased urine output, anxiety
Cyanosis, anuria, multi-organ dysfunction
Hyperactive bowel sounds, warm dry skin
In the progressive stage of shock, the failure of compensatory mechanisms leads to:
Improved tissue perfusion
Worsening tissue hypoperfusion
Increased oxygen delivery
Enhanced metabolic activity
Clinical manifestations in progressive shock include:
Strong bounding pulses, warm skin, normal urine output
Severe hypotension, tachycardia, weak or absent pulses, cool clammy skin
Euphoria, hyperactivity, increased GI motility
Increased blood pressure, bradycardia, dry skin
The irreversible stage of shock is defined as:
Reversible with aggressive fluid therapy
Mild organ dysfunction with possible recovery
Organ damage so severe that treatment is ineffective → survival not possible
Compensated tissue perfusion despite hypotension
A first-line fluid in the management of shock is:
0.9% Normal Saline or Lactated Ringer’s (isotonic crystalloids)
Albumin (colloid solution)
3% Hypertonic saline
Plasma expanders only
A major risk of excessive crystalloid resuscitation is:
Metabolic alkalosis
Systemic and pulmonary edema, abdominal compartment syndrome
Hypernatremia
Hypoglycemia
The most common cause of cardiogenic shock is:
Acute myocardial infarction (extensive LV damage)
Severe dehydration
Spinal cord injury
Anaphylaxis
In hypovolemic shock, early clinical manifestations include:
Restlessness, anxiety, thirst, tachycardia, tachypnea, cool clammy skin
Anuria, coma, cyanosis
Severe hypotension and multi-organ dysfunction
Hypertension, bradycardia, flushed warm skin
Diagnostics in hypovolemic shock typically reveal:
Elevated CVP and PCWP
Decreased CVP and PCWP
Elevated troponin
Increased creatinine clearance
In neurogenic shock, the unique clinical manifestation is:
Severe tachycardia with hypotension
Hypotension with bradycardia and warm dry skin
Hypotension with tachypnea and cool clammy skin
Hypertension with bounding pulses
Anaphylactic shock is characterized by:
Slow onset, mild allergic reaction, preserved airway
Severe, life-threatening allergic reaction with rapid airway compromise and hypotension
Gradual blood loss and dehydration
Mild tachycardia with adequate perfusion
The first-line treatment for anaphylactic shock is:
Epinephrine IM (0.3-0.5 mg)
Oxygen alone
Corticosteroids as the main therapy
Antihistamines as the primary treatment
Early clinical manifestations of septic shock (“warm phase”) include:
Fever, warm flushed skin, bounding pulse, tachycardia, tachypnea
Cool clammy skin, weak pulses, hypotension
Anuria, cyanosis, coma
Bradycardia and hypothermia
A key laboratory finding in shock indicating tissue hypoperfusion is:
Elevated bilirubin
High sodium levels
Increased lactate
Normal ABG
Multi-Organ Dysfunction Syndrome (MODS) is defined as:
Single organ dysfunction following trauma
Progressive, potentially fatal dysfunction of two or more organ systems
