0% found this document useful (0 votes)
23 views5 pages

Homeostasis and Metabolic Response to Injury

Uploaded by

LUCKY GAMING
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
23 views5 pages

Homeostasis and Metabolic Response to Injury

Uploaded by

LUCKY GAMING
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

1.

Basic concepts of homeostasis, metabolic changes in injury and their


mediators

Introduction:
Homeostasis is the ability of the body to maintain a stable internal environment despite external stress.
Injury and surgery disrupt this balance, leading to metabolic and endocrine changes aimed at survival.

Phases of response:
- Ebb phase (0–48 hrs): ↓ metabolism, ↓ O2 use, hypothermia.
- Flow phase (>48 hrs): hypermetabolism, ↑ O2 consumption, catabolism.

Mediators:
- Catecholamines, cortisol, glucagon → hyperglycemia, lipolysis.
- Cytokines (IL-1, TNF-α) → inflammation, fever.
- ADH, aldosterone → water & sodium retention.

Clinical relevance:
- ↑ calorie & protein needs.
- Risk of infection, poor healing.
- Management: resuscitation, nutrition, glycemic control.
2. Factors affecting metabolic response to injury

Introduction:
The magnitude of metabolic response to injury varies depending on several host and external factors.

Factors:
- Age: Children & elderly have exaggerated response.
- Nutritional status: Malnutrition worsens catabolism.
- Severity/type of injury: Burns > trauma > elective surgery.
- Comorbidities: Diabetes, renal, hepatic disease alter response.
- Medications: Steroids blunt response, β-blockers reduce catecholamine surge.
- Anesthesia/analgesia: Adequate pain control reduces stress.

Clinical significance:
- Tailor fluid & nutrition to patient’s profile.
- Anticipate complications in high-risk patients.
3. Basic concepts of perioperative care

Introduction:
Perioperative care covers pre-, intra-, and post-operative management to ensure safe surgical
outcomes.

Preoperative care:
- History, exam, investigations.
- ASA risk assessment.
- Optimization of comorbidities.
- Informed consent.

Intraoperative care:
- Monitoring: ECG, BP, O2 sat.
- Fluid balance.
- Asepsis & anesthesia safety.

Postoperative care:
- Pain control (NSAIDs, opioids, epidural).
- Fluids/electrolytes balance.
- Prevention of complications: DVT, pneumonia, wound infection.

Summary: Good perioperative care reduces morbidity and improves recovery.


4. Pathophysiology of shock, types, principles of resuscitation

Introduction:
Shock = state of inadequate tissue perfusion → anaerobic metabolism → lactic acidosis.

Types:
- Hypovolemic (hemorrhage, dehydration).
- Cardiogenic (MI, arrhythmias).
- Distributive (septic, anaphylactic, neurogenic).
- Obstructive (PE, tamponade).

Pathophysiology:
- ↓ perfusion → cellular hypoxia.
- Anaerobic glycolysis → lactate accumulation.
- Cellular failure → MODS.

Resuscitation principles (ABC):


- Airway: ensure patency.
- Breathing: oxygen, ventilation.
- Circulation: IV fluids (crystalloids), blood transfusion.
- Monitor urine output, lactate.
- Use vasopressors if fluid refractory.
5. Clinical features and treatment of shock

Clinical features:
- General: hypotension, tachycardia, tachypnea.
- Skin: cold, clammy (except septic – warm).
- CNS: confusion, restlessness.
- Renal: oliguria.
- Lab: metabolic acidosis, ↑ lactate.

Treatment:
- Rapid recognition & ABC management.
- Oxygen supplementation.
- IV fluids: crystalloids first-line.
- Blood transfusion if hemorrhagic.
- Vasopressors: norepinephrine in septic shock.
- Treat underlying cause (e.g., antibiotics in sepsis, surgery for bleeding).

Summary: Shock is life-threatening but reversible if treated early with fluids, oxygen, and
cause-specific therapy.

You might also like