WK 6

• Psychology is the scientific study of behaviour. Attempts to understand people and individual differences in behaviour.
• Psychological determinants: learning (modelling/reinforcement), personality (characteristics/traits), affect (emotions/mood) and cognitions (beliefs/thoughts/attitudes)
• Psychology can promote + maintain health. Prevent + treat illness. Identify psychological basis of illness. Improve healthcare systems.
• Health & Illness Landscape

  • Industrialised communities:

  • Shift from infectious diseases to chronic and ‘lifestyle’ conditions

  • Focus on improving quality of life and standards of living

  • Defining new health concerns - mental health, positive wellbeing, health promotion.

  
  

  • Developing communities:

  • Absence of basic care standards: clean water, hygiene, malnutrition

  • Low basic health literacy
• Disease: physiological dysfunction, illness: the experience of being sick, sickness: a particular status, position or role in society that is justified by either the presence of disease or to the experience of illness
• Health: physiological absence of dysfunction
• Being Healthy: experience of wellbeing
• Health Role: a particular status, position or role in society that cannot make reference to, or assume the responsibilities (or excuses) of , either the presence of disease or to the experience of illness
• Medical Model:

  Emphasises the physiological basis and presentation of illness and disease states.

  • Overreliance on this model may lead to: • Failure to consider the whole person • Seeing all people as the same • Ignoring the healthy / well person
• Biopsychosocial (BPS) Model:

  Approach that recognises the biological and genetic basis of many illnesses and the role of psychological, social, cultural, environmental and economic factors. • Examines the interplay
• Choosing between models consider: acute vs chronic, treatment vs prevention + health promotion, intervention vs recovery, groups with unique needs (children/indigenous)
• BPS model uses biology, interaction, holism and mutuality
• Biology: gender, illness, disability, immune function, genetic vulnerability, neurochemistry stress reactivity, med effects. SOcial context: social supports, family background, cultural traditions, social/economic status, education. Psychology: learning/memory, attitudes/beliefs, personality, behaviours, emotions, coping skills, past trauma
• Principal functions of CVS: oxygen delivery (important for structural + functional integrity of tissues + organs), nutrient delivery, hormone delivery, removal of metabolites.
• Oedema = Accumulation of extracellular interstitial fluid. Clinical and gross morphological recognition: Soft tissue swelling + Fluid accumulation in body ‘serous’ cavities.

  Interstitial fluid accumulation in tissues visible microscopically, without injury to cell constituents
• Oedema mechanisms: Increased net hydrostatic capillary pressure. Decreased counteractive plasma protein osmotic pressure. Increased vascular permeability (especially if no pressure issues). Obstruction of lymphatic drainage
• Hyperaemia (active process, increased blood flow) and Congestion (passive process, blood outflow obstruction, decreased inflow)
• Haemorrhage = blood loss after vessel wall rupture. From vessels of any size at any site. Usually following trauma/injury. Can be 'spontaneous' from small vessels in persons with defective haemostasis. Blood loss = external (beyond skin surface), into body cavity, or into tissue
• External Haemorrhage: Capillaries (small, oozing). Venous (slow flow, dark red). Arterial (pulsatile flow, bright red). Arterial more likely to be fatal than venous haemorrhage - but can be severe (severed jugular veins)
• Internal Haemorrhage: any size, any site. Potential external evidence: blood in vomit/faeces - can be altered (melaena) or unrecognised (faecal occult blood). May be concealed into body cavity. From closed trauma or disease eg ectopic pregnancy
• Tissue Haemorrhage: Any size, any site. Smallest = microscopic extravasation. Small = skin/mucosa (1-2mm petechiae, >3mm ecchymoses). Medium-large = haematoma (bruise). Massive = ruptured abdominal aortic aneurysm into retroperitoneal tissue
• Haemostasis: is a series of events designed to keep blood as fluid in circulation and minimise blood loss from sites of vessel injury/rupture
• Haemostasis: Bleeding from vascular injury minimised by: Constriction of injured vessel walls by nervous reflexes and chemical mediators, clotting (platelet aggregation + conversion of soluble plasma protein fibrinogen into fibrin following coagulation cascade)
• Thrombosis: thrombus formed within intact vessel, instead of at site of rupture. Obstructs blood flow + harmful. Pathogenesis: Virchow's triad: endothelial injury (hypercholesterolemia, inflammation) + change in blood flow (stasis [AF, bed rest], Turbulence [atherosclerotic vessel narrowing]) and hypercoagulability (inherited: factor V Leiden, or acquired: disseminated cancer)
• Endothelial Injury for thrombosis: In arteries - substantial pathological lesion in tunica intima eg complicated atheromatous plaque. In veins - inflammation or invasion by cancer, minor endothelial damage
• Change in blood flow for thrombosis: turbulence over lesions/plaques in arteries. stasis in veins. both in heart.
• Change in blood coagulability for thrombosis: primary (inherited) eg thrombophilia (factor V leiden mutation, protein C deficiency. May not become evident until adult life. Secondary (acquired, more common). after surgery, trauma childbirth, immobilisation, prolonged bed rest. additional: infection with disseminated intravascular coagulation, cancer (paraneoplastic syndromes, autoimmune, heparin complications)
• What is the macroscopic appearance of a thrombus?

  Solid or semi-solid material in vessel lumen
• How is a thrombus attached to the vessel wall?

  With varying firmness
• What color is a thrombus typically described as?

  Red-brown
• What is the texture of a thrombus?

  Friable
• In which direction does a thrombus extend?

  In the direction of blood flow
• What is the initial microscopic event in thrombus formation?

  Platelet aggregation
• What follows platelet aggregation in thrombus formation?

  Fibrin deposition with clotting cascade activation
• In fast blood flow, which component is dominant in thrombus formation?

  Platelets
• In slow blood flow, which component becomes prominent in thrombus formation?


  Fibrin
• What are "lines of Zahn"?

  Alternating layers of red blood cells and platelets held together with fibrin
• Where do lines of Zahn form?

  In flowing blood vessels
• How do lines of Zahn develop over time?

  They form over time in flowing blood
• How can lines of Zahn help pathologists?

  They help establish thrombus versus post mortem blood clotting