NLE Foundations of Medical-Surgical Nursing — Homeostasis, Inflammation and Cellular ResponseRevision Notes

Exam Tips

• Know the three GAS stages by name and their clinical signs: Alarm (fight-or-flight, catecholamines, HPA activation), Resistance (adaptation, attempt to return to homeostasis), Exhaustion (reserves depleted, organ failure, death possible).
• For any question about a postoperative patient with high blood glucose, fluid retention, or low WBC function — think cortisol, aldosterone, ADH as the underlying mechanism.
• The hypothalamic-pituitary-adrenal (HPA) axis is the key endocrine pathway of the stress response — expect it to appear in anatomy/physiology-integrated NLE items.
• LAS vs GAS: LAS is LOCAL (e.g., redness at a wound site). GAS is SYSTEMIC (e.g., the whole-body response to major trauma).

Key Points

• Homeostasis is the body's continuous effort to keep the internal environment stable — temperature, pH (7.35–7.45), fluid volume, electrolytes, and blood glucose — within narrow physiologic limits.
• Negative feedback loops are the primary mechanism: a change from the set point triggers a corrective response that reverses the change. Example: rising blood glucose triggers insulin release, lowering glucose back to normal.
• Positive feedback loops amplify a response rather than reverse it. These are less common and are seen in uterine contractions during labor and platelet aggregation during clotting.
• A stressor is anything that threatens homeostasis — physiologic (trauma, infection, surgery, hemorrhage) or psychological (fear, grief, anxiety).
• Hans Selye's General Adaptation Syndrome (GAS) describes the body's nonspecific, three-stage response to any stressor.
• The Local Adaptation Syndrome (LAS) is a localized response to a local stressor — such as inflammation at a wound site.
• Key stress hormones and their effects: Cortisol — raises blood glucose, suppresses inflammation and immunity, promotes protein and fat catabolism. Aldosterone — promotes renal sodium and water retention, raising blood volume and pressure. ADH (antidiuretic hormone) — conserves water at the renal collecting duct.
• Clinical implication: Postoperative and critically ill patients commonly show stress-induced hyperglycemia, fluid retention (oliguria), and temporary immunosuppression — all driven by cortisol, aldosterone, and ADH.

Definitions

Section Title

Homeostasis and the Stress Response

Common Mistakes

• Confusing negative feedback (which restores balance) with positive feedback (which amplifies change). Remember: NEGATIVE = corrects the deviation; POSITIVE = amplifies it.
• Thinking all three GAS stages always occur sequentially in every patient. Many resolve in the resistance stage; exhaustion only occurs with prolonged or overwhelming stress.
• Forgetting that cortisol SUPPRESSES immunity — students often incorrectly associate a stress response with enhanced immunity.
• Overlooking psychological stressors. Fear, grief, and anxiety activate the same HPA axis as physical injury.

Exam Tips

• HYPOXIA is always the most common cause of cellular injury — make this your default answer if the cause is not specified.
• Know the progression: Normal Cell → Adaptation (atrophy, hypertrophy, hyperplasia, metaplasia) → Dysplasia (pre-malignant) → Neoplasia (malignant).
• For NLE scenarios involving smoking: think metaplasia of respiratory epithelium and understand why these patients lose the mucociliary clearance mechanism.
• Apoptosis questions often appear in the context of cancer nursing — malignant cells have DEFECTIVE apoptosis, so they survive when they should die.

Key Points

• Cells respond to stress by adapting their size, number, or type before progressing to injury and death.
• Atrophy: decrease in cell SIZE — seen in disused muscle (e.g., a limb in a cast) or denervated tissue.
• Hypertrophy: increase in cell SIZE — seen in cardiac muscle hypertrophy in hypertension, or uterine muscle in pregnancy.
• Hyperplasia: increase in cell NUMBER — seen in breast tissue during pregnancy, or compensatory liver regeneration.
• Metaplasia: REVERSIBLE change from one mature cell type to another — seen in respiratory epithelium of smokers (columnar ciliated → squamous). This is the cell's way of surviving an adverse environment.
• Dysplasia: DISORDERED, abnormal cell growth with variation in size and shape — often a PRE-MALIGNANT change. Not the same as metaplasia.
• When injury exceeds adaptive capacity, cell death occurs by necrosis or apoptosis.
• Necrosis: UNCONTROLLED, pathologic cell death caused by injury (infarction, toxins, infection). Provokes an inflammatory response. Types include coagulative (most common, e.g., MI), liquefactive (brain, abscess), caseous (TB), gangrenous, and fat necrosis.
• Apoptosis: PROGRAMMED, orderly cell death — genetically controlled, does NOT provoke inflammation. Normal in embryonic development, immune cell regulation, and aging.
• The MOST COMMON cause of cellular injury is HYPOXIA (insufficient oxygen delivery). Other causes: ischemia, physical agents (heat, radiation), chemical agents (drugs, toxins), infectious organisms, immune reactions, and nutritional deficiencies.

Definitions

Section Title

Cellular Injury and Adaptation

Common Mistakes

• Confusing hypertrophy (bigger cells) with hyperplasia (more cells). Tip: HyperTROPHY = TROPHY-sized cells (bigger); HyperPLASIA = more PLACES for cells (more cells).
• Thinking metaplasia is always abnormal — it is actually a PROTECTIVE ADAPTATION. However, it becomes problematic because the new cell type may lack the function of the original (e.g., loss of cilia in smokers impairs mucus clearance).
• Confusing dysplasia with metaplasia. Metaplasia = organized but different cell type (REVERSIBLE). Dysplasia = DISORDERED, abnormal, potentially pre-malignant.
• Saying necrosis and apoptosis are the same. Key differentiator: Necrosis = causes INFLAMMATION; Apoptosis = does NOT cause inflammation.

Exam Tips

• Memorize the 5 cardinal signs using the Latin terms: Rubor, Calor, Tumor, Dolor, Functio Laesa. NLE commonly uses the Latin terms.
• NSAID mechanism: blocks prostaglandin synthesis → reduces fever, pain, and inflammation. This is why NSAIDs are used for dysmenorrhea, headache, and post-inflammatory pain.
• The order of WBC response in inflammation: NEUTROPHILS first (phagocytose acutely), then MACROPHAGES (clean up and activate adaptive immunity).
• CRP and ESR are both nonspecific inflammation markers — elevation supports but does not confirm infection. Used to MONITOR treatment response.
• Systemic signs of inflammation (fever, leukocytosis, malaise, elevated CRP/ESR) are always secondary to the LOCAL cardinal signs in the inflammatory cascade.

Key Points

• Inflammation is the body's NONSPECIFIC, protective response to tissue injury or invasion — it is not exclusive to infection.
• Infection is a SPECIFIC cause of inflammation (caused by microorganisms). Inflammation can also be caused by chemical injury, ischemia, trauma, or immune reactions.
• Purpose of inflammation: neutralize and destroy harmful agents, limit their spread, remove debris, and prepare the tissue for healing.
• Chemical mediators released at the site of injury include: HISTAMINE (from mast cells and platelets — primary mediator of early vasodilation and increased permeability), BRADYKININ (causes pain, vasodilation, increased permeability), PROSTAGLANDINS (cause pain, fever, vasodilation — target of NSAIDs and aspirin), and LEUKOTRIENES (prolong and intensify the response, important in asthma).
• Vascular response: vasodilation (increases blood flow → redness and heat) + increased capillary permeability (plasma proteins and fluid leak into tissue → edema).
• Cellular response: WBCs — primarily NEUTROPHILS (arrive first, 6–12 hours; phagocytose bacteria and debris) then MACROPHAGES (arrive later, clean up remaining debris and stimulate further immune response) — migrate to the site by CHEMOTAXIS.
• PHAGOCYTOSIS is the process by which neutrophils and macrophages engulf and destroy pathogens, dead cells, and debris.
• The five CARDINAL SIGNS of LOCAL inflammation: Rubor (redness), Calor (heat), Tumor (swelling/edema), Dolor (pain), Functio Laesa (loss of function).
• SYSTEMIC manifestations: Fever/pyrexia (prostaglandins reset the hypothalamic thermostat), Leukocytosis (elevated WBC count, normal 5,000–10,000/mm³; elevated suggests inflammation/infection), Shift to the left (increased BANDS — immature neutrophils — in the CBC differential, indicating acute demand for WBCs), Malaise, elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).
• ACUTE inflammation is short-lived (days to weeks), predominantly neutrophilic, and usually resolves. CHRONIC inflammation is prolonged (weeks to years), predominantly mononuclear (lymphocytes, macrophages), and is associated with ongoing tissue damage (e.g., rheumatoid arthritis, TB).

Definitions

Section Title

The Inflammatory Response

Common Mistakes

• Confusing inflammation with infection. INFLAMMATION is the body's response (can be caused by many things). INFECTION is one CAUSE of inflammation (specifically from microorganisms).
• Forgetting the FIFTH cardinal sign — Functio Laesa (loss of function). Students often only recall four.
• Mixing up which WBC arrives FIRST at an inflammatory site: NEUTROPHILS arrive first (6–12 hours). Macrophages come later to clean up.
• Not knowing what 'shift to the left' means — it does NOT mean the CBC values shifted; it means there are more IMMATURE neutrophils (bands) in the blood.
• Thinking fever is always dangerous and must be immediately treated. Mild fever is BENEFICIAL — it slows microbial growth and enhances immune function. Intervention is priority when fever is very high (>39°C–40°C) or causes discomfort.

Exam Tips

• Memorize the 3 phases: Inflammatory (Days 1–4, hemostasis and phagocytosis), Proliferative (Days 4–21, collagen and granulation), Maturation (Day 21 onward, scar remodeling).
• Nutritional mnemonic for wound healing: PROTEIN + VIT C + ZINC = healing TRIO. Any patient with poor wound healing — assess nutritional status first.
• For evisceration: MOIST STERILE SALINE GAUZE → supine position → knees flexed → call surgeon. Do NOT attempt to push organs back.
• Keloid formation is more prevalent among Filipino, Asian, and African patients — a clinically relevant and culturally sensitive NLE point.

Key Points

• Wound healing occurs by three types of intention based on wound characteristics: PRIMARY intention (clean, well-approximated wound edges, e.g., surgical incision closed with sutures — minimal scarring, fastest healing), SECONDARY intention (wound left open to heal from the base up by granulation tissue — more scarring, longer healing, e.g., infected wound or pressure ulcer), TERTIARY intention / DELAYED PRIMARY closure (wound initially left open, then closed later after edema or infection resolves).
• Phases of wound healing: (1) INFLAMMATORY PHASE (Days 1–4): hemostasis and inflammation, phagocytosis of debris, wound appears red and swollen — this is NORMAL, not a sign of infection. (2) PROLIFERATIVE PHASE (Days 4–21): fibroblasts synthesize collagen, granulation tissue forms, wound contracts, epithelialization occurs. Requires: protein, vitamin C, and zinc. (3) MATURATION/REMODELING PHASE (Day 21 onward, up to 2 years): collagen remodeled, scar tissue matures and strengthens (gains up to 80% of original tissue strength).
• Factors IMPAIRING wound healing: poor tissue perfusion (peripheral arterial disease, vasoconstriction), diabetes mellitus (impaired leukocyte function, microangiopathy), corticosteroid use (suppresses inflammation needed for healing), malnutrition (especially protein and vitamin C deficiency), infection, obesity, old age, radiation therapy, and anemia.
• Complications of wound healing: Dehiscence (wound edges separate — risk 5–12 days post-op), Evisceration (abdominal organs protrude through the wound — surgical emergency), Keloid formation (excessive scar tissue extending beyond wound margins — more common in darker-skinned individuals), Hypertrophic scar (excessive scar within wound margins), Fistula (abnormal tract between two epithelium-lined surfaces), and Contracture (scar tissue restricts movement).
• Nursing responsibilities: maintain moist wound environment, ensure adequate nutrition (high-protein diet, vitamin C supplements), prevent infection with aseptic technique, monitor for signs of wound infection (purulent drainage, increasing redness/warmth beyond expected, fever, increasing pain), and educate patients on proper wound care and nutrition.

Definitions

Section Title

Wound Healing

Common Mistakes

• Thinking the inflammatory phase of wound healing means the wound is infected — early redness and swelling are NORMAL and EXPECTED in the first 3–4 days.
• Forgetting the key nutritional requirements for the proliferative phase: PROTEIN (for collagen synthesis), VITAMIN C (for collagen cross-linking), and ZINC (for cell proliferation and immune function). Expect a diet-related wound healing question in the NLE.
• Confusing dehiscence (wound edges separate — skin and tissue only) with evisceration (organs come out). Evisceration is the more critical emergency.
• Not remembering that corticosteroids IMPAIR wound healing by suppressing the inflammation needed for healing — a key drug-related complication.

Formulas

Exam Tips

• The NLE may present a burn or septic patient with edema AND low blood pressure, low urine output, and tachycardia — recognize this as THIRD-SPACING causing hypovolemia, not fluid overload.
• Urine output is a key indicator of intravascular volume and renal perfusion. Target: AT LEAST 30 mL/hr in adults (0.5 mL/kg/hr). Values below this require urgent reporting.
• Remember the PUSH vs. PULL rule: Hydrostatic pressure PUSHES fluid out (elevated in CHF). Oncotic pressure PULLS fluid in (reduced in hypoalbuminemia).
• Daily weight is the GOLD STANDARD for monitoring fluid status. A sudden weight gain of 1 kg overnight = approximately 1 liter of fluid retention.

Key Points

• The body has three fluid compartments: INTRACELLULAR fluid (ICF — 40% body weight), EXTRACELLULAR fluid (ECF — 20% body weight, divided into intravascular plasma and interstitial fluid), and the concept of a 'THIRD SPACE' — an area where fluid accumulates but is not functionally available.
• THIRD-SPACING is the abnormal shift of fluid from the intravascular space (blood vessels) into a space where it cannot be readily used — the interstitium (edema), peritoneal cavity (ascites), pleural cavity (pleural effusion), pericardial sac, or bowel lumen.
• Causes of third-spacing: BURNS (the most classic example), SEPSIS, MAJOR SURGERY, BOWEL OBSTRUCTION, PANCREATITIS, LIVER FAILURE / HYPOALBUMINEMIA.
• The DANGER of third-spacing: Total body water may be NORMAL or EVEN HIGH, but the INTRAVASCULAR VOLUME IS DEPLETED. The patient shows signs of HYPOVOLEMIA (hypotension, tachycardia, decreased urine output, decreased CVP) despite VISIBLE EDEMA. This is why you may see a burned patient who is severely swollen but going into shock.
• HYDROSTATIC PRESSURE is the PUSHING force of fluid against vessel walls. When elevated (e.g., in congestive heart failure, venous obstruction), it forces fluid OUT of vessels into tissues, causing edema.
• ONCOTIC PRESSURE (Colloid Osmotic Pressure) is the PULLING force created primarily by plasma ALBUMIN. When albumin is low (e.g., liver disease, malnutrition, nephrotic syndrome), the pulling force is reduced and fluid STAYS in the tissues, causing edema.
• After the acute injury phase (e.g., after a burn), the REABSORPTION PHASE occurs (typically 48–72 hours post-burn) when third-space fluid re-enters the circulation, causing INCREASED blood volume and risk of FLUID OVERLOAD — nursing must monitor for signs of pulmonary edema and heart failure during this phase.
• Nursing monitoring for third-spacing: Strict intake and output (I&O), DAILY WEIGHTS (most accurate assessment of fluid status — 1 kg = approximately 1 liter of fluid), serum albumin levels, assessment for edema, and hemodynamic monitoring (blood pressure, heart rate, CVP, urine output — target minimum 30 mL/hr).

Definitions

Section Title

Fluid Shifts in Illness — Third-Spacing

Common Mistakes

• Assuming an edematous patient is fluid-OVERLOADED. Third-spacing patients can be severely edematous but INTRAVASCULARLY DEPLETED — treatment is volume replacement, not diuretics (which would worsen the hypovolemia).
• Forgetting the REABSORPTION PHASE after burns — failing to anticipate fluid overload when third-space fluid re-enters circulation at 48–72 hours.
• Not performing daily weights — students focus on I&O records but forget that daily weight is the MOST ACCURATE way to assess fluid changes.
• Confusing hydrostatic and oncotic pressure. Mnemonic: HYDROSTATIC = PUSH (pushes fluid OUT); ONCOTIC = PULL (pulls fluid IN using albumin as the magnet).

Formulas

Exam Tips

• The NLE commonly tests: earliest signs of shock (restlessness, anxiety, tachycardia), the compensatory stage (BP still normal), and neurogenic shock (bradycardia + warm skin).
• Priority interventions always follow ABCs: Airway → Breathing (O2) → Circulation (IV access, fluids). This is your answer framework for any shock scenario.
• Urine output ≥30 mL/hr is the TARGET — values below this in a shock patient require immediate reporting and intervention.
• For anaphylactic shock: EPINEPHRINE 1:1,000 IM (lateral thigh) is the FIRST and PRIORITY drug — not antihistamines, not steroids first.
• Lactic acidosis = marker of anaerobic metabolism = marker of shock severity. Elevated serum lactate confirms inadequate tissue oxygenation.
• In the Philippine hospital setting, under RA 9173, nurses have the authority and responsibility to initiate emergency interventions and collaborate with the interdisciplinary team. Document all assessments, interventions, and patient responses.

Key Points

• SHOCK is a life-threatening physiologic state of INADEQUATE TISSUE PERFUSION AND CELLULAR OXYGENATION, regardless of the cause.
• When cells are deprived of oxygen, they switch from AEROBIC to ANAEROBIC METABOLISM. This produces LACTIC ACID, leading to METABOLIC ACIDOSIS, cellular dysfunction, organ failure, and death.
• FOUR TYPES of shock based on etiology: (1) HYPOVOLEMIC — loss of circulating volume (hemorrhage, severe dehydration, burns, third-spacing) — MOST COMMON TYPE. (2) CARDIOGENIC — pump failure (MI, severe heart failure, dysrhythmias). (3) DISTRIBUTIVE — massive inappropriate vasodilation causing blood maldistribution, subdivided into SEPTIC (infection), ANAPHYLACTIC (severe allergic reaction), and NEUROGENIC (spinal cord injury — loss of sympathetic tone). (4) OBSTRUCTIVE — physical obstruction to blood flow (cardiac tamponade, tension pneumothorax, massive pulmonary embolism).
• FOUR STAGES of shock: (1) INITIAL: anaerobic metabolism begins, lactic acid builds up — few or NO clinical signs visible. (2) COMPENSATORY: sympathetic nervous system, RAAS, and ADH activate to restore pressure — HR increases, vessels constrict, BP often STILL NORMAL. RESTLESSNESS AND ANXIETY are the EARLIEST CLINICAL SIGNS. (3) PROGRESSIVE: compensatory mechanisms FAIL — hypotension, worsening acidosis, mental status changes, oliguria, organ hypoperfusion. (4) REFRACTORY (IRREVERSIBLE): profound multi-organ failure — recovery is no longer possible even with intervention.
• GENERAL CLINICAL MANIFESTATIONS of shock: Hypotension (SBP <90 mmHg), Tachycardia (HR >100 bpm), Tachypnea, Cool and clammy skin (vasoconstriction — EXCEPT in early DISTRIBUTIVE shock where skin is WARM and FLUSHED due to vasodilation), Oliguria (<30 mL/hr), Altered LOC (confusion, restlessness, agitation).
• SPECIAL FEATURES: NEUROGENIC shock presents with BRADYCARDIA and WARM, DRY skin (NOT tachycardia and cool skin) due to loss of sympathetic tone. CARDIOGENIC shock requires CAUTIOUS fluid administration to avoid worsening pulmonary edema — DO NOT aggressively give IV fluids. ANAPHYLACTIC shock — epinephrine (1:1,000 IM) is the priority drug.
• PRIORITY NURSING MANAGEMENT (ABCs): (A) Airway — ensure patent airway. (B) Breathing — administer HIGH-FLOW OXYGEN via non-rebreather mask. (C) Circulation — establish LARGE-BORE IV ACCESS (2 large-bore peripheral IVs), administer ISOTONIC CRYSTALLOIDS (0.9% NaCl or Lactated Ringer's) for hypovolemic and most distributive shock. For hemorrhagic shock — blood products (packed RBCs). POSITION: SUPINE with LEGS ELEVATED (modified Trendelenburg) UNLESS contraindicated (respiratory distress, head injury, suspected spine injury). MONITOR continuously: vital signs, urine output (target ≥30 mL/hr), LOC, O2 saturation.
• VASOPRESSORS (e.g., norepinephrine, dopamine) are added once adequate volume is restored, to maintain MAP ≥65 mmHg. TREAT THE CAUSE: Epinephrine for anaphylaxis, antibiotics for sepsis, reperfusion therapy (PCI/thrombolytics) for cardiogenic shock from MI.
• MODS (Multiple Organ Dysfunction Syndrome) is the end-stage complication of unresolved shock — progressive failure of two or more organs (kidneys, lungs, liver, heart, brain). High mortality.

Definitions

Section Title

Introduction to Shock

Common Mistakes

• Assuming a NORMAL blood pressure rules out shock — in the COMPENSATORY STAGE, BP is often still normal. Look for TACHYCARDIA, RESTLESSNESS, and DECREASED URINE OUTPUT as early warning signs.
• Giving large amounts of IV fluids to a CARDIOGENIC shock patient — this is dangerous and will worsen pulmonary edema. Cardiogenic shock = cautious, limited fluids.
• Forgetting that NEUROGENIC shock causes BRADYCARDIA and WARM skin — not the typical cool, clammy, tachycardic presentation. Spinal cord injury context is the clue.
• Not recognizing restlessness and anxiety as the EARLIEST signs of shock — dismissing these as 'patient anxiety' rather than signs of cerebral hypoperfusion.
• Confusing the Trendelenburg position and modified Trendelenburg. MODIFIED TRENDELENBURG (legs elevated, body supine) is used in hypovolemic shock to increase venous return. Standard Trendelenburg (head down) is no longer recommended.