Homeostasis, Inflammation and Cellular Response - Cheat Sheet
Your last-minute revision companion for mastering homeostasis mechanisms, stress adaptation, cellular injury, inflammatory response, fluid shifts, and shock management. This cheat sheet condenses all testable content into rapid-fire reference points critical for the PRC NLE.
Homeostasis and Stress Adaptation
Common values
Value
37°C (98.6°F)
Symbol
Temp
Quantity
Normal body temperature set point
Value
7.35–7.45
Symbol
pH
Quantity
Normal blood pH
Value
70–100 mg/dL
Symbol
Glucose
Quantity
Normal serum glucose (fasting)
Important facts
- GAS Stage 1 — Alarm: 'Fight-or-flight' response; sympathetic nervous system and HPA axis activate.
- GAS Stage 1 hormones: Epinephrine and norepinephrine (catecholamines) increase HR, BP, RR, blood glucose; shunt blood to vital organs.
- GAS Stage 2 — Resistance (Adaptation): Body attempts to adapt and return to homeostasis; if stressor resolved, recovery occurs.
- GAS Stage 3 — Exhaustion: If stressor is prolonged/overwhelming, adaptive reserves deplete → physiologic decline, disease, or death.
- Cortisol (stress hormone): Raises blood glucose (hyperglycemia), suppresses inflammation and immunity, promotes protein/fat catabolism.
- Aldosterone (stress hormone): Promotes sodium and water retention → increased blood volume and blood pressure.
- ADH (Antidiuretic Hormone): Conserves water; elevated in stress → fluid retention, lower serum osmolarity.
- Local Adaptation Syndrome (LAS): Localized stress response of a body part or tissue (e.g., inflammatory response at wound).
- Postoperative patients commonly show: hyperglycemia (cortisol), fluid retention (aldosterone/ADH), lowered immunity (cortisol suppression).
- Stress hormones prepare for 'fight-or-flight': ↑HR, ↑BP, ↑RR, ↑blood glucose, ↓digestion, ↓immunity — all shift resources to survival.
Key definitions
Homeostasis
Example
Rising body temperature triggers sweating and vasodilation to return temperature to set point (~37°C).
Body's tendency to maintain a stable internal environment (temperature, pH, fluid volume, electrolytes, glucose) within narrow physiologic limits through negative feedback loops.
Negative Feedback Loop
Example
High blood glucose → insulin release → glucose uptake → blood glucose decreases.
A change from set point triggers a response that REVERSES that change, restoring equilibrium.
Positive Feedback Loop
Example
Labor contractions → oxytocin release → stronger contractions (ends with delivery).
A change triggers a response that AMPLIFIES that change (rare; usually self-limiting).
Stress
Example
Post-operative patient experiences surgical trauma (physiologic) + fear of pain (psychological).
Any real or perceived threat to homeostasis; triggered by physiologic (trauma, infection, surgery) or psychological (fear, anxiety) stressors.
General Adaptation Syndrome (GAS)
Example
Surgical patient: acute stress response (alarm) → adaptation and healing (resistance) → complications if prolonged (exhaustion).
Body's nonspecific three-stage response to any stressor: alarm → resistance → exhaustion.
Diagrams to know
- Three stages of General Adaptation Syndrome with hormone and physiologic changes at each stage
- Negative feedback loop (set point → change → response → reversal to set point)
- HPA axis activation pathway: Stressor → Hypothalamus → Anterior Pituitary → Adrenal Cortex → Cortisol release
Cellular Injury and Adaptation
Important facts
- Cellular adaptations are REVERSIBLE responses to stress or altered environment; cell injury occurs when stress exceeds adaptive capacity.
- ATROPHY (↓size) vs HYPERPLASIA (↑number) vs HYPERTROPHY (↑size) — all are adaptive responses to changed demand.
- METAPLASIA is a change in CELL TYPE (one epithelium to another), not size or number; Barrett's esophagus is classic (squamous → columnar).
- DYSPLASIA is the ONLY POTENTIALLY PREMALIGNANT adaptation; other adaptations are benign.
- Most common cause of cellular injury: HYPOXIA (inadequate oxygen delivery); followed by ischemia, toxins, infection, immune injury, malnutrition.
- Necrosis is uncontrolled and inflammatory; apoptosis is orderly and clean — the body's 'self-destruct button'.
- Apoptosis is essential for normal development, tissue turnover, and removal of damaged/infected cells without collateral damage.
- Necrotic tissue appears pale, coagulated, or liquefied depending on type; apoptotic bodies are membrane-bound and phagocytosed cleanly.
Key definitions
Atrophy
Example
Immobilized leg muscles shrink; hand muscles atrophy in spinal cord injury.
Reversible decrease in cell size due to disuse, denervation, or reduced blood supply.
Hypertrophy
Example
Cardiac muscle enlarges in hypertension; bicep muscles enlarge with weightlifting.
Reversible increase in cell size due to increased workload or hormonal stimulation.
Hyperplasia
Example
Breast tissue proliferation in pregnancy; bone marrow hyperplasia in chronic hypoxia.
Reversible increase in the NUMBER of cells due to increased demand.
Metaplasia
Example
Respiratory epithelium (ciliated columnar) → stratified squamous in smokers' airways.
Reversible change from one mature cell type to another in response to chronic irritation.
Dysplasia
Example
Cervical dysplasia detected on Pap smear; can progress to cervical cancer if untreated.
Disordered, abnormal cell growth; loss of size/shape uniformity; often premalignant; may be reversible early on.
Necrosis
Example
Myocardial necrosis in MI; tissue necrosis in severe burns.
Uncontrolled cell death from injury; cells rupture and release contents, triggering inflammation.
Apoptosis
Example
Removal of webbing between fingers in fetal development; death of activated T-cells after immune response.
Programmed, orderly cell death; cell shrinks and fragments without rupturing; minimal inflammation.
Diagrams to know
- Spectrum of cellular adaptations: Atrophy → Normal → Hypertrophy/Hyperplasia/Metaplasia → Dysplasia → Cellular Injury (Necrosis/Apoptosis)
- Cell injury continuum: Reversible injury (swelling, organelle dysfunction) → Irreversible injury (necrosis)
The Inflammatory Response
Common values
Value
4,500–11,000 cells/μL
Symbol
WBC
Quantity
Normal WBC count
Value
>11,000 cells/μL (leukocytosis)
Symbol
Leukocytosis
Quantity
Elevated WBC in infection/inflammation
Value
0–20 mm/hr
Symbol
ESR
Quantity
Normal ESR (adult female)
Value
<3 mg/L
Symbol
CRP
Quantity
Normal C-reactive protein
Important facts
- INFLAMMATION is NOT the same as INFECTION; infection is inflammation caused specifically by microorganisms.
- Five cardinal signs: Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Functio laesa (loss of function) — ALL LOCAL SIGNS.
- Systemic signs of inflammation: FEVER (prostaglandin action on hypothalamus), LEUKOCYTOSIS (elevated WBC), MALAISE, ↑C-reactive protein, ↑ESR.
- Key inflammatory mediators: Histamine (vasodilation, permeability), Bradykinin (pain, vasodilation), Prostaglandins (fever, pain, vasodilation), Leukotrienes (permeability, chemotaxis).
- Vasodilation → redness and heat; increased capillary permeability → fluid shift into tissues → swelling (edema).
- Neutrophils are FIRST responders (arrive in minutes to hours); macrophages follow (hours to days) and clean up debris.
- A 'LEFT SHIFT' on WBC differential means increased immature neutrophil bands (stab cells); indicates acute, severe infection.
- C-reactive protein (CRP) is an acute-phase reactant; elevated in inflammation/infection; used to assess inflammation severity.
- ESR (Erythrocyte Sedimentation Rate): RBCs settle faster when inflammation present (elevated fibrinogen); nonspecific but useful screening.
- Chronic inflammation can lead to fibrosis (excess collagen), tissue damage, and disease (rheumatoid arthritis, Crohn's disease).
Key definitions
Inflammation
Example
Redness, warmth, swelling, pain, and loss of function at a wound site or around a splinter.
Body's protective, NONSPECIFIC response to tissue injury or invasion; aims to neutralize/destroy harmful agents, limit spread, prepare tissue for healing.
Five Cardinal Signs of Inflammation (Local)
Example
Sprained ankle: red, warm, swollen, painful, unable to bear weight.
Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain), Functio laesa (loss of function).
Histamine
Example
Allergic reaction: histamine release → itching, redness, swelling (hives).
Key inflammatory mediator released by mast cells and basophils; causes vasodilation and increased capillary permeability.
Bradykinin
Example
Burn injury: bradykinin release → severe pain and increased vascular permeability.
Inflammatory mediator that causes pain and vasodilation; product of the kinin cascade.
Prostaglandins
Example
NSAIDs block prostaglandin synthesis → reduced pain, fever, and inflammation.
Inflammatory mediators that promote vasodilation, increased permeability, pain, and fever; derived from arachidonic acid.
Leukotrienes
Example
Asthma: leukotriene release → bronchoconstriction and airway inflammation.
Inflammatory mediators (derived from arachidonic acid) that increase vascular permeability and promote leukocyte chemotaxis.
Chemotaxis
Example
Neutrophils migrate toward a bacterial infection site following cytokine gradients.
Directed movement of white blood cells toward a site of inflammation in response to chemical signals.
Phagocytosis
Example
White blood cell engulfs and destroys a bacterium; macrophage clears dead neutrophils.
Process by which neutrophils and macrophages engulf and destroy pathogens, dead cells, and debris.
Diagrams to know
- Vascular and cellular events in inflammation: Injury → Mediator release → Vasodilation + ↑Permeability → Fluid exudation + Leukocyte migration → Phagocytosis
- Timeline of inflammatory cell arrival: Neutrophils (0–24 hrs) → Macrophages (24 hrs+)
- Sources and actions of key inflammatory mediators (histamine, bradykinin, prostaglandins, leukotrienes)
Wound Healing
Common values
Value
0–3 days
Symbol
Phase 1
Quantity
Duration of inflammatory phase
Value
3–21 days
Symbol
Phase 2
Quantity
Duration of proliferative phase
Value
21 days–2 years
Symbol
Phase 3
Quantity
Duration of maturation phase
Important facts
- INFLAMMATORY PHASE (0–3 days): Hemostasis, inflammation, débridement of dead tissue; neutrophils and macrophages dominate.
- PROLIFERATIVE PHASE (3–21 days): Fibroblasts produce collagen, angiogenesis, granulation tissue formation, epithelialization; needs protein, vitamin C, zinc.
- MATURATION/REMODELING PHASE (21 days–2 years): Collagen is reorganized and cross-linked; scar tissue matures; wound strength increases gradually.
- Primary intention heals fastest with least scar; secondary intention is slower with more scarring; tertiary is combination.
- IMPAIRED HEALING risk factors: Poor perfusion (diabetes, vascular disease), corticosteroid use, malnutrition (protein, vitamin C, zinc deficiency), infection, age >65, obesity.
- Vitamin C is essential for collagen synthesis; deficiency (scurvy) leads to poor wound healing.
- Protein is needed for collagen formation; zinc promotes epithelialization and immune function; iron needed for collagen cross-linking.
- A moist wound environment speeds healing; excessive dryness or excessive moisture both impair healing.
- Macrophages remove dead tissue AND promote fibroblast recruitment; essential to healing process.
- Infection greatly delays healing by prolonging inflammation and consuming nutrients; cleanliness and asepsis are critical.
Key definitions
Primary Intention (Primary Closure)
Example
Surgical incision closed immediately with sutures; heals with minimal scarring.
Healing of a clean, approximated wound with minimal scar tissue; edges are brought together (sutures, staples).
Secondary Intention
Example
Pressure ulcer or large laceration left open; heals slowly, from inside out, with more scarring.
Healing of an open wound from the base up by granulation tissue; more scar tissue forms.
Tertiary Intention (Delayed Closure)
Example
Contaminated wound left open for 3–5 days to allow cleaning and granulation, then sutured.
Initial open healing (secondary), followed by delayed closure (primary) when wound is clean.
Granulation Tissue
Example
Pink/red tissue visible in a healing pressure ulcer as it fills in from the base.
New tissue formed during healing; rich in fibroblasts, collagen, and new blood vessels; appears red and bumpy.
Diagrams to know
- Three phases of wound healing timeline: Inflammatory (0–3 days) → Proliferative (3–21 days) → Maturation (21 days–2 years)
- Cellular and molecular events at each phase of healing
- Comparison of primary vs. secondary vs. tertiary intention healing timelines and scarring
Fluid Shifts in Illness
Formulas
Hydrostatic Pressure (HP) > Oncotic Pressure (OP) → Fluid MOVES OUT into tissues
Meaning
HP = pushing force of fluid against vessel walls; OP = pulling force of plasma proteins (albumin). When HP > OP, net fluid shift is outward → edema.
Watch out
Do NOT confuse direction: HIGH HP pushes fluid OUT; LOW OP allows fluid to stay OUT. Both cause edema but through different mechanisms.
When to use
Explain edema in heart failure (↑HP), liver disease/malnutrition (↓OP), burns, sepsis.
Hydrostatic Pressure (HP) < Oncotic Pressure (OP) → Fluid is PULLED into vessels
Meaning
When OP exceeds HP, the pulling force of plasma proteins draws fluid back into circulation.
Watch out
During reabsorption phase (e.g., post-burn diuretic phase), excess fluid re-entering circulation can cause FLUID OVERLOAD and pulmonary edema if not monitored.
When to use
Diuretic phase (fluid reabsorption): as intravascular volume is restored, oncotic pressure pulls fluid back from tissues.
Common values
Value
3.5–5.5 g/dL
Symbol
Albumin
Quantity
Normal serum albumin
Value
>2.5 g/dL (minimum)
Symbol
Critical
Quantity
Albumin needed for oncotic pressure
Value
30–50 mL/hr
Symbol
UOP
Quantity
Target urine output during reabsorption
Important facts
- Third-spacing is the SILENT THREAT: total body water may be normal or HIGH, but INTRAVASCULAR volume is DEPLETED → hypovolemia signs despite visible edema.
- Classic presentation of third-spacing: Hypotension, tachycardia, low urine output (signs of hypovolemia) BUT edema, ascites, or visibly swollen tissues.
- Causes of third-spacing: Severe burns, sepsis, major surgery, bowel obstruction, peritonitis, cirrhosis, hypoalbuminemia (malnutrition, liver disease, nephrotic syndrome).
- Albumin is the MAIN plasma protein maintaining oncotic pressure; low albumin is a major cause of edema (seen in malnutrition, liver disease, nephrotic syndrome).
- Nursing management: Monitor I&O carefully; daily weights; serum albumin; hemodynamic status (BP, HR, CVP if available); anticipate REABSORPTION PHASE.
- Reabsorption phase (e.g., post-burn diuretic phase): As inflammation resolves, capillary integrity improves, and fluid re-enters circulation → risk of FLUID OVERLOAD.
- During reabsorption phase: Watch for pulmonary edema, congestive heart failure, hypertension; may need diuretics; monitor urine output (should be 30–50 mL/hr).
- Starling equation balances hydrostatic and oncotic pressures; shifts in either can cause pathologic edema.
- Generalized edema often involves both mechanisms: ↑HP (venous congestion) AND ↓OP (protein loss or synthesis failure).
Key definitions
Third-Spacing
Example
Severe burn patient: fluid shifts into interstitial space and bowel lumen; intravascular volume depletes despite visible edema and ascites.
Abnormal shift of fluid from intravascular space into 'third' space (interstitium, peritoneal cavity, pleural space, bowel lumen) where it is NOT readily accessible.
Hydrostatic Pressure
Example
In heart failure, elevated venous pressure → elevated capillary hydrostatic pressure → fluid forced into tissues.
The 'pushing' force exerted by fluid against vessel walls; higher in capillary arteriolar end.
Oncotic (Colloid Osmotic) Pressure
Example
Low serum albumin (liver disease, malnutrition) → decreased oncotic pressure → fluid remains in tissues despite normal hydrostatic pressure.
The 'pulling' force created primarily by plasma proteins (especially albumin); draws fluid into vessels.
Diagrams to know
- Capillary fluid dynamics: Arterial end (↑HP drives fluid out) vs. Venous end (↑OP pulls fluid in)
- Third-spacing pathophysiology: Normal distribution → intravascular depletion + interstitial/cavity accumulation
- Timeline of third-spacing and reabsorption phases in burns
Introduction to Shock
Common values
Value
>90 mmHg
Symbol
SBP
Quantity
Normal systolic BP
Value
<90 mmHg systolic
Symbol
Shock BP
Quantity
Hypotension in shock
Value
≥30 mL/hr (≥0.5 mL/kg/hr)
Symbol
UOP
Quantity
Target urine output in shock
Value
0.5–1.5 mmol/L
Symbol
Lactate
Quantity
Normal serum lactate
Value
>2 mmol/L
Symbol
Lactic acidosis
Quantity
Elevated lactate in shock
Important facts
- HYPOVOLEMIC SHOCK is the MOST COMMON type (hemorrhage, dehydration, burns, third-spacing).
- In shock, cells lack oxygen and switch to ANAEROBIC METABOLISM → lactate production → LACTIC ACIDOSIS → cell death and organ failure.
- Shock has FOUR stages: Initial → Compensatory → Progressive → Refractory (irreversible).
- INITIAL STAGE: Cellular changes begin (anaerobic metabolism, lactic acid formation); often NO obvious clinical signs; critical window to detect.
- COMPENSATORY STAGE: Sympathetic and endocrine activation (catecholamines, RAAS, ADH). HR↑, RR↑, cool clammy skin, oliguria, restlessness. BP is OFTEN STILL NORMAL — this is the KEY WINDOW TO INTERVENE.
- RESTLESSNESS and ANXIETY are OFTEN THE EARLIEST SIGNS of inadequate cerebral perfusion in shock; do NOT dismiss them as 'just anxiety.'
- PROGRESSIVE STAGE: Compensation fails. Hypotension develops, worsening acidosis, altered mental status (confusion, lethargy), reduced urine output, organ hypoperfusion.
- REFRACTORY (IRREVERSIBLE) STAGE: Profound organ failure; multiple organ dysfunction syndrome (MODS); recovery is NO LONGER POSSIBLE; death is imminent.
- Classic shock signs (most types): Hypotension, tachycardia, tachypnea, cool clammy skin, oliguria, altered consciousness.
- EXCEPTION — NEUROGENIC SHOCK: Bradycardia (NOT tachycardia) + warm, dry skin (NOT cool clammy); due to loss of sympathetic tone.
Key definitions
Shock
Example
Septic patient: massive vasodilation → blood pooling → decreased perfusion to vital organs → organs fail → death.
A life-threatening state of INADEQUATE TISSUE PERFUSION and CELLULAR OXYGENATION; cells switch to anaerobic metabolism → lactic acidosis → cell death.
Tissue Perfusion
Example
Low cardiac output (heart failure) or low oxygen (severe anemia) both reduce tissue perfusion.
Delivery of oxygenated blood to tissues; perfusion = cardiac output × vascular resistance × oxygen content.
Hypovolemic Shock
Example
Trauma patient with severe bleeding; fluid shifts out of vessels in peritonitis.
Shock due to loss of circulating blood volume; most common type. Causes: hemorrhage, dehydration, third-spacing, burns.
Cardiogenic Shock
Example
Acute myocardial infarction with loss of >40% of left ventricular function → cardiogenic shock.
Shock due to failure of the heart to pump effectively. Causes: MI, acute heart failure, severe dysrhythmias, cardiac tamponade.
Distributive (Vasogenic) Shock
Example
Septic shock: bacterial toxins cause severe vasodilation and capillary leak.
Shock due to MASSIVE VASODILATION causing maldistribution and pooling of blood volume; total volume may be normal but perfusion is inadequate.
Septic Shock
Example
Gram-negative sepsis releases endotoxin (LPS) → cytokine storm → vasodilation → shock.
A subtype of distributive shock caused by systemic infection; characterized by vasodilation, increased capillary permeability, and profound inflammation.
Anaphylactic Shock
Example
Penicillin allergy → mast cell degranulation → histamine/tryptase release → vasodilation, edema, airway constriction.
A subtype of distributive shock; severe, IgE-mediated allergic reaction with rapid vasodilation and bronchoconstriction.
Neurogenic Shock
Example
Spinal cord transection at C5 → loss of sympathetic vasoconstriction → hypotension with BRADYCARDIA (NOT tachycardia).
A subtype of distributive shock caused by spinal cord injury above T6; loss of sympathetic tone causes vasodilation.
Obstructive Shock
Example
Tension pneumothorax compresses the heart → decreased cardiac output → shock.
Shock due to physical obstruction to blood flow. Causes: cardiac tamponade, tension pneumothorax, pulmonary embolism, aortic dissection.
Diagrams to know
- Four stages of shock: Initial → Compensatory → Progressive → Refractory, with signs at each stage.
- Pathophysiology of each shock type: hypovolemic (volume loss), cardiogenic (pump failure), distributive (vasodilation), obstructive (mechanical obstruction).
- Cellular cascade in shock: Tissue hypoperfusion → anaerobic metabolism → lactate production → acidosis → organelle dysfunction → cell death.
- Compensatory mechanisms in early shock: SNS activation (↑HR, ↑contractility), RAAS activation (↑aldosterone → Na/H2O retention), ADH release (↑water retention).
Reactions or equations
Cardiac Output (CO) = Heart Rate (HR) × Stroke Volume (SV)
Note
Sympathetic activation in compensatory shock increases HR to maintain CO; if HR cannot compensate (e.g., neurogenic shock with bradycardia), shock worsens.
Conditions
In shock: CO may be ↓ from low HR (heart failure, bradycardia) or low SV (hypovolemia, cardiogenic).
Mean Arterial Pressure (MAP) = Cardiac Output (CO) × Systemic Vascular Resistance (SVR)
Note
In septic/anaphylactic shock, vasodilation drops SVR; in hypovolemic shock, both CO and SVR are compromised.
Conditions
In distributive shock: CO may be normal/high but SVR is massively decreased → hypotension despite normal/high volume.
Priority Nursing Management in Shock
Common values
Value
30 mL/kg over 3 hours (or 1–2 L over 10–20 min in acute hemorrhage)
Symbol
IVF
Quantity
Crystalloid bolus for shock resuscitation
Value
>90 mmHg
Symbol
Target SBP
Quantity
Target systolic BP in compensatory shock
Value
>94% (on supplemental O2)
Symbol
SpO2
Quantity
Target SpO2 in shock
Value
<1 hour of recognition
Symbol
Golden hour
Quantity
Time to initiate antibiotics in sepsis
Important facts
- ABCs in SHOCK: Airway & Breathing (high-flow oxygen is PRIORITY for oxygenation) → Circulation (large-bore IVs, fluids, blood products).
- OXYGEN is the #1 priority in shock: Tissue hypoxia is the core problem; high-flow O2 (target SpO2 ≥94%) is initial life-saving intervention.
- Large-bore IV access (18-20 gauge) is ESSENTIAL for rapid fluid/blood administration; avoid small-bore lines.
- Fluid resuscitation: ISOTONIC CRYSTALLOIDS (0.9% NaCl, lactated Ringer's) for most shock types; 30 mL/kg bolus in first 3 hours (Surviving Sepsis Campaign).
- BLOOD PRODUCTS for hemorrhagic shock: Target permissive hypotension (SBP 90 mmHg) until surgical control; massive transfusion protocol if needed.
- POSITION: Supine with legs elevated 30°–45° (modified Trendelenburg) to promote venous return UNLESS respiratory distress or head injury contraindicated.
- MONITOR CONTINUOUSLY: Vital signs (HR, BP, RR), urine output (target ≥30 mL/hr), SpO2, level of consciousness, CVP/PAWP if available.
- VASOPRESSORS (norepinephrine, epinephrine): Use ONLY AFTER adequate fluid resuscitation; correct hypotension and improve perfusion.
- EPINEPHRINE (IM 0.3–0.5 mg) is first-line for anaphylactic shock; repeat at 5–15 min intervals if no response.
- ANTIBIOTICS for septic shock: Start within 1 hour of recognition; broad-spectrum empirically until culture/sensitivity results.
- CARDIOGENIC SHOCK requires CAUTIOUS fluid administration to avoid pulmonary edema; inotropes (dobutamine) and mechanical support (IABP, LVAD) may be needed.
- NEUROGENIC SHOCK: Bradycardia + hypotension; may need ATROPINE for bradycardia and FLUIDS/VASOPRESSORS for BP support.
- Treat the UNDERLYING CAUSE: Control bleeding in hemorrhage, antibiotics/source control in sepsis, epinephrine in anaphylaxis, emergent revascularization in MI.
Key definitions
Primary Survey (ABCs in Shock)
Example
Trauma patient: check airway (intubate if needed) → high-flow O2 (SpO2 >94%) → two large-bore IVs → crystalloid bolus → supine position with legs up.
Airway/Breathing → Circulation: ensure patent airway, provide high-flow O2, establish IV access, administer fluids/blood, position supine with legs elevated.
Diagrams to know
- Shock management algorithm: Recognition → ABCs (airway/O2/IVs) → Fluid resuscitation → Vasopressors if needed → Treat underlying cause
- Fluid responsiveness assessment: Does the patient's BP/urine output improve with fluid bolus? If no, consider cardiogenic shock or need for vasopressors.
Must remember
- HOMEOSTASIS = stable internal environment maintained by NEGATIVE FEEDBACK loops; stress triggers GENERAL ADAPTATION SYNDROME with three stages: Alarm (fight-or-flight) → Resistance (adaptation) → Exhaustion (failure).
- The BIG THREE stress hormones: CORTISOL (raises glucose, suppresses immunity), ALDOSTERONE & ADH (retain sodium and water) — explain postop hyperglycemia, fluid retention, and lowered immunity.
- CELLULAR ADAPTATIONS are reversible: Atrophy (↓size), Hypertrophy (↑size), Hyperplasia (↑number), Metaplasia (change cell type) — ONLY dysplasia is premalignant.
- Five CARDINAL SIGNS of INFLAMMATION (LOCAL): RUBOR (redness), CALOR (heat), TUMOR (swelling), DOLOR (pain), FUNCTIO LAESA (loss of function) — MUST memorize for NLE.
- KEY INFLAMMATORY MEDIATORS: Histamine (vasodilation, permeability), Bradykinin (pain), Prostaglandins (fever, pain, vasodilation), Leukotrienes (permeability, chemotaxis) — each has distinct action.
- THIRD-SPACING is the SILENT TRAP: Intravascular volume is DEPLETED (hypotension, tachycardia, oliguria) despite visible edema and ascites — HIGH ONCOTIC PRESSURE pulls fluid into tissues; LOW HYDROSTATIC PRESSURE keeps it there.
- SHOCK = inadequate tissue perfusion → anaerobic metabolism → lactic acidosis → cell death; HYPOVOLEMIC is most common; NEUROGENIC is the EXCEPTION (bradycardia, warm skin, not tachycardia/cool).
- FOUR stages of SHOCK: Initial (cellular changes, ↔BP) → Compensatory (↑HR/RR, cool skin, oliguria, BP often normal — GOLDEN WINDOW) → Progressive (hypotension, altered mental status) → Refractory (irreversible, death).
- RESTLESSNESS and ANXIETY are EARLIEST signs of shock — cerebral hypoperfusion; do NOT dismiss as 'just anxiety' — suspect shock immediately and act.
- SHOCK MANAGEMENT ABCs: Airway & high-flow O2 (priority for oxygenation) → Large-bore IVs + crystalloid fluids → Supine with legs elevated → Monitor I&O, vitals, urine ≥30 mL/hr → Treat underlying cause (antibiotics for sepsis, epinephrine for anaphylaxis, surgery for hemorrhage).
Last minute tips
- In NLE scenario questions about shock, always check for restlessness and anxiety FIRST — these are the earliest signs of inadequate cerebral perfusion in the compensatory stage when BP is still normal. This is your critical action trigger.
- For third-spacing questions, remember: Patient has HYPOTENSION + OLIGURIA (hypovolemia signs) BUT ALSO edema/ascites visible. This paradox is the hallmark. Mechanism: low albumin OR high capillary hydrostatic pressure keeps fluid OUT of vessels.
- Neurogenic shock is the EXCEPTION — it has BRADYCARDIA (sympathetic loss) and WARM DRY skin, NOT the tachycardia and cool clammy skin of other shock types. Know this inside-out; it appears on almost every exam.
- For cardiogenic shock, the rule is CAUTIOUS fluids to avoid pulmonary edema — this is opposite to hypovolemic/septic shock where you give aggressive fluids. The question will test if you know the difference.
- Wound healing phases memory: Inflammatory phase needs blood clotting and immune cells; Proliferative phase (3–21 days) NEEDS protein, vitamin C, and zinc — this is when the patient should be well-nourished; Maturation is the long remodeling phase (weeks to years). Nutritional deficiency impairs healing most in the proliferative phase.
Comparison tables
Cellular Adaptations vs. Injury
| Process | Cell Size Change | Cell Number Change | Cell Type Change | Reversibility | Cause | Example |
|---|---|---|---|---|---|---|
| Atrophy | Decrease | No | No | Reversible | Disuse, denervation, reduced blood supply | Immobilized leg muscles |
| Hypertrophy | Increase | No | No | Reversible | Increased workload, hormone stimulation | Cardiac muscle in hypertension |
| Hyperplasia | No (overall ↑) | Increase | No | Reversible | Increased demand | Breast tissue in pregnancy |
| Metaplasia | Variable | Variable | YES — Change | Reversible (early) | Chronic irritation | Squamous cells in smokers' airways |
| Dysplasia | Variable (disordered) | Increase (disordered) | No | Possibly reversible (early); may progress | Chronic irritation, carcinogens | Cervical dysplasia |
| Necrosis (Cell Death) | Cell ruptures | Loss | N/A | Irreversible | Severe injury (ischemia, trauma) | MI, severe burns |
| Apoptosis (Programmed Death) | Cell shrinks & fragments | Loss (orderly) | N/A | Irreversible | Genetic program (normal/pathologic) | Embryonic webbing removal |
Four Types of Shock — Quick Comparison
| Shock Type | Primary Problem | Cause | Key Features | Fluid/Drug Response | Exception to Note |
|---|---|---|---|---|---|
| Hypovolemic | Low intravascular volume | Hemorrhage, dehydration, burns, third-spacing | Tachycardia, cool clammy skin, oliguria, hypotension | Responds to crystalloid + blood; permissive HTN in trauma | Most common type |
| Cardiogenic | Heart pump failure | MI, acute HF, dysrhythmias, tamponade | Pulmonary edema, jugular venous distension, weak pulses | Cautious fluids; inotropes + mechanical support | AVOID fluid overload; risk of pulmonary edema |
| Distributive (Septic) | Massive vasodilation + maldistribution | Infection (gram-neg > gram-pos), toxins | Warm flushed skin (early), tachycardia, wide pulse pressure | Aggressive fluids + vasopressors + antibiotics | Early septic shock may have WARM skin, not cool |
| Distributive (Anaphylactic) | Massive vasodilation + airway edema | Severe IgE allergic reaction (drugs, food, insect sting) | Urticaria, stridor, wheezing, hypotension, angioedema | IM epinephrine (0.3–0.5 mg) FIRST; then IVF + antihistamines | Airway management is CRITICAL; epinephrine is life-saving |
| Distributive (Neurogenic) | Loss of sympathetic tone | Spinal cord injury (T6 and above) | BRADYCARDIA + hypotension + WARM DRY skin | Fluids + vasopressors; atropine if severe bradycardia | BRADYCARDIA (not tachycardia); warm skin (not cool clammy) |
| Obstructive | Physical block to blood flow | Tamponade, tension pneumothorax, PE, aortic dissection | JVD, muffled heart sounds, unequal breath sounds | Treat the obstruction (pericardiocentesis, chest tube, thrombolytics) | Fluid may worsen tamponade; definitive treatment is mechanical |
Stages of Shock — Key Differences
| Stage | Cellular Event | BP Status | Key Signs & Symptoms | Reversibility | Nursing Priority |
|---|---|---|---|---|---|
| Initial | Anaerobic metabolism begins; lactate ↑ | Often NORMAL | Often NO obvious signs; cellular changes only | Reversible if recognized early | HIGH INDEX of SUSPICION; look for restlessness, anxiety |
| Compensatory | SNS activation, RAAS, ADH; CO remains adequate | Often MAINTAINED (≥90 mmHg) | HR↑, RR↑, cool/clammy skin, oliguria, restlessness, anxiety, normal mentation | Reversible with intervention | AGGRESSIVE RESUSCITATION — this is the golden window |
| Progressive | Compensation fails; severe acidosis, organelle damage | HYPOTENSION develops | Hypotension, altered mentation (confusion, lethargy), severe oliguria, mottled skin, weak pulses | May be reversible with aggressive intervention; risk of MODS | Continue resuscitation + treat underlying cause; consider vasopressors |
| Refractory (Irreversible) | Profound cell death; multiple organ failure | Severe hypotension, unresponsive to fluids/drugs | Unresponsiveness, anuria, no perfusion signs, profound acidosis, DIC | IRREVERSIBLE; death imminent | Supportive care; consider withdrawal of support; focus on comfort |
Inflammatory Mediators — Sources and Actions
| Mediator | Source | Primary Actions | Clinical Trigger | Blocked By |
|---|---|---|---|---|
| Histamine | Mast cells, basophils | Vasodilation, ↑capillary permeability, itching | Immediate allergic reaction, mast cell degranulation | Antihistamines (H1, H2 blockers) |
| Bradykinin | Kinin cascade (plasma proteins) | Pain, vasodilation, ↑permeability | Tissue injury, burn, angioedema | ACE inhibitors (indirectly); no direct blocker |
| Prostaglandins | Arachidonic acid metabolism (many cell types) | Vasodilation, ↑permeability, pain, FEVER | Tissue injury, inflammation | NSAIDs, corticosteroids (inhibit arachidonic acid release) |
| Leukotrienes | Arachidonic acid metabolism (WBCs, mast cells) | ↑capillary permeability, chemotaxis, bronchoconstriction | Allergic reaction, asthma | Leukotriene inhibitors (montelukast); aspirin, NSAIDs |
| Cytokines (TNF-α, IL-1, IL-6) | Activated macrophages, T cells | Fever, systemic inflammation, endothelial activation, sepsis cascade | Infection, severe injury, sepsis | Monoclonal antibodies (research); supportive care in sepsis |
Wound Healing Phases — Cellular and Molecular Events
| Phase | Timeline | Primary Cells | Main Events | Nutritional Needs | Impairment Factors |
|---|---|---|---|---|---|
| Inflammatory (Hemostasis) | 0–3 days | Platelets, neutrophils, macrophages | Blood clotting, hemostasis, débridement of dead tissue, inflammatory mediator release | Basic (energy) | Infection, excessive dryness, hypovolemia |
| Proliferative (Granulation) | 3–21 days | Fibroblasts, endothelial cells, myofibroblasts | Collagen synthesis, angiogenesis, granulation tissue formation, epithelialization | Protein, vitamin C, zinc, iron | Malnutrition, corticosteroids, poor perfusion (diabetes), infection |
| Maturation (Remodeling) | 21 days–2 years | Fibroblasts (reorganizing collagen) | Collagen cross-linking, scar maturation, wound strength increase | Protein, vitamin C (ongoing) | Chronic inflammation, repeated injury, excessive tension on wound |
Diagrams
Homeostasis, Inflammation & Cellular Response — Master Concept Map
Comprehensive mind map showing the interconnection between homeostasis maintenance, stress adaptation (GAS), cellular responses (adaptation vs. injury), inflammation, fluid dynamics, and shock classification. Use this to see the 'big picture' and how all concepts relate.
Shock Recognition & Management Algorithm
Step-by-step flowchart for recognizing and managing shock. Emphasizes the critical 'golden window' of the compensatory stage (when BP is often still normal), the ABCs of management, and shock-specific interventions. Use this to practice rapid clinical decision-making.
Four Stages of Shock Progression
State diagram illustrating the progressive nature of shock from initial cellular injury through compensatory and progressive stages to irreversible refractory shock. The key takeaway: the compensatory stage is when BP is often STILL NORMAL, making early recognition of signs like restlessness critical for intervention.
Wound Healing Timeline & Nutritional Needs
Timeline showing the progression of wound healing phases with the critical nutrition window highlighted during the proliferative phase (days 3–21). This visual emphasizes when protein, vitamin C, and zinc are most essential for preventing impaired healing.
Cellular Adaptation vs. Injury Decision Tree
Decision tree for distinguishing between reversible cellular adaptations (atrophy, hypertrophy, hyperplasia, metaplasia) and irreversible cellular injury (necrosis vs. apoptosis). This helps students quickly recognize what type of cellular response is occurring based on the clinical scenario.