Pathology (intro) Flashcards
What are the 2 types of autopsy?
Hospital and medico-legal
What are the aims of a hospital autopsy?
To determine, clarify or confirm medical diagnoses that remains unknown or unclear prior to death.
Accounts for <10% UK autopsies.
What are the aims of a medico-legal autopsy?
To determine cause & manner of death & identify decedent.
Accounts for >90% UK autopsies.
What are the 2 subtypes of medico-legal autopsies?
Coronial & forensic.
When is a coronial autopsy used?
When death is not due to unlawful action e.g. natural, drowning, accidents, peri/post op.
When is a forensic autopsy used?
When death is suspected to be due to unlawful actions e.g. homicide, death in custody, neglect, any from coronial list which may be due to involvement of a 3rd party.
Which 4 questions should be asked in an autopsy?
Who, when, where, how?
Which 3 types of deaths are referred to the coroner? Give examples of each.
Presumed natural - cause unknown, not seen by doc in last 14 days.
Presumed iatrogenic - peri/post op, anaesthetic, illegal abortion, complications of therapy.
Presumed unnatural - accidents, fires, industrial.
Who refers deaths for autopsies?
Doctors do not have a statutory duty but do have a common law duty.
Registrar of BDM has a statutory duty.
Relatives and police can also.
Which types autopsies does a histopathologist perform?
Hospital and coronial.
Forensic pathologist performs forensic.
What are the 5 stages of an autopsy?
History/scene, external exam, evisceration, internal exam, reconstruction.
Describe the aim and features of an external exam.
To identify the deceased.
Formal identifiers, gender, age, body habitus, jewellery, tattoos, clothing.
Describe the features of an evisceration.
Y shaped incision from behind ears to clavicle then down midline.
Open body cavities, examine organs in situ, remove all thoracic & abdominal organs, remove brain.
Described the features of an internal exam.
Heart & great vessels - narrowing of coronary arteries = IHD. Lungs, trachea, bronchi - pneumonia, emphysema, tumours. Liver, gall bladder, pancreas. Upper GI tract. Spleen, thymus if present, lymph nodes. GU tract & renal. Endocrine organs. CNS.
Define acute inflammation.
The initial and often transient local physiological response to tissue injury.
State 6 causes of acute inflammation.
Microbial infections - bacteria, viruses.
Bacterial toxins - exotoxins.
Hypersensitivity reactions - parasites, TB.
Physical agents - trauma, burns, ionising radiation.
Chemicals - corrosives.
Tissue necrosis - e.g. resulting from ischaemia.
State the 5 macroscopic features of acute inflammation and why they occur.
- Rubor (redness/erthyema) - capillary dilation.
- Calor (heat) - hyperaemia & vasodilation, also chem mediators=systemic fever.
- Tumor (swelling) - oedema, new connective tissue formation.
- Dolor (pain) - oedema=tissue distortion, pus under pressure, chem mediators e.g. bradykinin, psotoglandins, serotonin.
- Loss of fxn - movement consciously & reflexively inhib by pain, severe swelling may physically immobilise tissues.
State 3 main processes involved in the acute inflammatory response.
- Increase in vessel calibre & consequently flow
- Increased vascular permeability & formation of fluid exudate
- Formation of cellular exudate
Define oedema.
The abnormal accumilation of fluid in the interstitium. Often presents as swelling.
Describe how vessel calibre changes in acute inflammation & the effects of this.
Precapillary sphincters (formed from smooth muscle of arteriolar wall) relax, capillary dilatation & hyperemia.
Describe the mechanism of increased vascular permeability/ formation of the fluid exudate in acute inflammation.
Capillary hydrostatic pressure is increased, also results in escape of plasma proteins into extravasc space thus increased colloid osmotic pressure there, thus increased vascular permeability = net flow of protein-rich fluid (exudate) out of vessels.
Also endothelial cells have pores between them which are opened up when contractile proteins are stim by chem mediators.
State the causes of immediate transient, immediate sustained & delayed prolonged increased vascular permeability.
Immediate transient - chem mediators (histamine, bradykinin, NO, C5a, PAF)
Immediate sustained - severe direct vascular injury e.g. trauma.
Delayed prolonged - endothelial cell injury e.g. x rays, bacterial toxins.
