Critical

Question 1

ARDS

Answer 1

Acute Respiratory Distress syndrome

Acute inflammatory lung injury
- Life threatening clinical syndrome occurring
- Secondary to an inciting event - such as shock, sepsis, trauma or transfusion

Inflammatory response
- With pro inflammatory IL 1, 6 and TNF alpha

Alveolar damage occurs, with damage to both endothelium and epithelium of the lung
- Leading to increased permeability - both via direct damage and the inflammatory cascade
- With loss of surfactant
- And accumulation of protein rich fluid

This affects gas exchange and lung compliance
- Causing alveolar collapse
- Impaired oxygenation and resp failure

Which can exacerbate pulmonary HTN and shock

And can be exacerbated by ventilation

Diffuse infiltrates throghout lungs

Diagnosis - Berlin criteria
- Inciting event last 7 days
- Bilateral effusions not explained by overload
- Absence of other lung injury as cause (HF, pneumonia)
- Resp compromise - impaired PaO2 to FIO2 ration

Tx
- resp support in ICU
- Can need prone
- Steroids

Question 2

Wound Healing

Answer 2

• Haemostasis - blood and lymphatic fluid move in, with clotting cascade, vasoconstriction and platelet plug formation, before vasolidation to bring more factors
  • Inflammatory phase - thrombocytes, WBC. PDGF and platelet factor, TGF B and complement, VEGF. Fibroblasts are recruited.
• Proliferative phase - days 5-7 - fibroblasts lay down collagen, matrix and angiogenesis occurs. Re-epithelialization.
• Remodelling - from 3rd week, alterations in collagen breakdown and reforming as wound matures, scar contracture.

Question 3

Wound healing factors affecting

Answer 3

Factors affecting wound healing
- Intrinsic - infection, diabetes, nutrition, vitamins, pain, genetics, ischaemia
- Extrinsic - mechanical, foreign bodies, necrotic tissue, temp, infection, chemical stressors, drugs
- Aberrations - Keloid, granulation, fibroblast

Question 4

Types of wound

Answer 4

Types of Wound
- Clean - skin major source
- Clean contaminated - risk - 5-10%
- Contaminated - emergency operations
- Dirty

Question 5

Dressings

Answer 5

Dressings
- Films - Gas and water permeable, micro impermeable - for clean supf wounds
- Foams - allevyn - maintains moist environment, absorbent (not good for dry wounds)
- Alginates - kaltostat, alginic acid from seaweed - hydrophilic absorbs exudate to give moist environment, haemostatic
- Hydrogels - mostly water, for rehydrating dry wounds, autolytic enviroment
- Hydrocolloids - duoderm - polymers - soft gel, can be occlusive barrier.

Question 6

VAC

Answer 6

Negative Pressure Wound therapy
* VAC dressing
* Therapeutic helps to promote acute or chornic healing of wounds
* Subatmospheric pressure to wound environment
* Change every 3-4 days

* Mechanism - drwas out lfuid from the wound, increases blood flow, cleanage and drainage 
* Contraindications infection malig, necrosis fistulas

Question 7

Primary Haemostasis

Answer 7

Haemostasis

Divided into primary and secondary haemostasis
* Primary haemostasis is a platelet plug formation
* Secondary haemostasis is the clotting cascade

Primary haemostasis
* Platelet adhesions
* Platelet aggregation
* Fibrinogen
* vWF

* Problems
	○ Low platelet count
	○ Platelet dysfunction 

	○ Causes mucocutaneous bleeding, petechiae and ecchymosis

Question 8

Secondary haemostasis clotting cascade

Answer 8

Secondary Haemostasis
* Coag cascade includes intrinsic and extrinsic pathways, leading to common pathway
* Both involve the sequential activation of a series of clotting factors

* Extrinsic activation
	○ Tissue injury causes exposure of tissue factor
	○ This goes with VIIa
* Intrinsic activation
	○ Exposure of factor XII in blood to a negatively charged surface 
		§ XII, IX, XI, VIII
* Common pathway
	○ Factor X activated 
	○ Go to V 
	○ Go to Prothrombin II to thrombin IIa 
	○ Go to Fibrinogen I to Fibrin Ia 

Fibrin reinforces and enmeshes with the platelet plug

Calcium is needed for several steps

Question 9

Clot breakdown / anti thrombotic

Answer 9

Clot Breakdown

TPA breaks plasminogen down into plasmin
* Inhibited by tranexamic acid

Plasmin breaks
* Fibrin broken down into FDPs including D dimers

Antithrombotic pathways

Prot C and Prot S
* Thrombin binds to thrombomodulin on endothelial cells
* Activates Prot C and Prot S
* Turn off Va

Tissue factor pathway inhibitor
* Turns off Xa

Antithrombin
* Protease inhibitor
* Turns off clotting
* Xa, IIa