Seminar 12 - Traumatic Head Injury Flashcards
List the clinical features of wound infection
Signs and symptoms of infection – pain, localized swelling, redness or heat
Purulent discharge
Unexplained persistent pyrexia
Malodor from the wound
Spreading – crepitus, malaise, loss of appetite
How does the body normally deal with cells which have had their DNA damaged by UV
DNA damage is sensed by checkpoint kinases e.g. ATM and ATR
These send out signals that upregulate the expression and stability of p53
This arrests cells in the G1 phase of cell cycle and promotes either high-fidelity DNA repair or the elimination of cells that are damaged beyond repair
In DIC where are the procoagulants released from
They can be released from a variety of locations such as the placenta in obstetric complications and damaged tissues in severe trauma and burns.
Which microbiology style tests may be performed on wound infection
Organisms isolated from the aseptically obtained wound culture
Gram stain for infective organisms; staining for fungal elements
Test for antigens from the organism through ELISA
Detection of antibody response to organism in host sera
PCR to detect small amounts of microbial DNA
List the ABCDE warning signs of melanoma
Asymmetry
Border – Ragged, notched, uneven, blurred
Color – Shades of black, brown and tan (variegated)
Diameter – Usually larger than 6mm (increasing diameter)
Evolving – Has been changing; texture of mole may become hard or lumpy
List potential causes of high grade sarcoma
Genetic conditions
Radiation – emergence of radiation-induced genetic mutations that encourage neoplastic transformation
Chronic lymphedema
Environmental carcinogens – Infection-induced soft-tissue tumour is Kaposi sarcoma resulting from human herpesvirus type 8 in patients with HIV
Infection
Trauma
What is a subarachnoid haemorrhage
Extravasation of blood into the subarachnoid space (SAS).
List the microscopic features of subacute (evolving) focal ischaemic infarcts
At 48-72hrs phagocytic cells are evident. In the following 2-3weeks they will become the predominant cell
The macrophages can persist in these lesions for months to years and they become stuffed with blood or products of myelin breakdown
As early as one week after the insult reactive astrocytes and newly formed vessels can be seen at the infarcts periphery
Astrocytes at the edge of the lesion will progressively enlarge, divide and develop a network of cytoplasmic extensions as liquefaction and phagocytosis continues
List the immediate compensatory mechanisms for rising ICP
Decrease in CSF volume by moving it out of foramen magnum
Decrease in blood volume by squeezing sinuses
Non-infectious vasculitis can also cause focal ischaemic CVA - true or false
True
Polyarteritis Nodosa and other non infectious vasculitis can cause single or multiple infracts in the brain
List some examples of high grade sarcoma
Clear cell sarcoma Dermatofibrosarcoma protuberans Ewing sarcoma Extraskeletal myxoid chondrosarcoma Liposarcoma
Describe a systemic wound infection
Systemic infection from a wound affects the body as a whole, with microorganisms spreading throughout the body via the vascular or lymphatic systems.
Systemic inflammatory response, sepsis and organ dysfunction are signs of systemic infection
What consequences of SAH tend to occur in the first few days post-bleed
Increased risk of additional ischaemic injury from vasospasm affecting vessels bathed in extravasated blood
Which mutations are often seen in melanoma
Mutations that disrupt cell cycle control genes e.g. CDKN2A
Mutations that activate pro-growth signaling pathways e.g. RAS and PI3K/AKT signaling
Mutations that activate telomerase e.g. TERT
Why do people in ICU experience weakness and stiffness
Muscles weaken due to long periods of inactivity.
This happens quicker when they are on a ventilator.
Why are ICU patient’s at high risk of complications
They will already be severely unwell with most having an issue with one or more organs.
This already makes them vulnerable to complications such as infection and AKI.
List the pathological features of secondary haemorrhagic infarcts
The evolution and features of these infarcts are the same as ischemic infarcts
Blood extravasation and resorption will also be seen within them
Extensive intracerebral haematomas may be seen alongside the haemorrhagic infracts if the patient is on anticoagulants
How do the ventricles appear in communicating and non-communicating hydrocephalus
Communicating - all 4 ventricles enlarged
Non-communicating - 4th ventricle normal whilst others enlarged
4th normal as CSF can’t flow into is as well due to obstruction
What are the two main triggers of DIC
Release of procoagulants into the bloodstream and the injury of endothelial cells.
Which cancers are most associated with DIC
Acute promyelocytic leukemia
Adenocarcinomas of the lung, pancreas, colon and stomach
If a person is unable to complete a GCS test - e.g. eye opening w/ facial injuries, verbal if intubated- how do you record it
Should be recorded as NT (not testable)
Infarcts in focal ischaemic CVA can be divided into which groups
Non haemorrhagic and secondary haemorrhagic infarcts
The deficits that are caused by a focal ischemic CVA can improve over time - true or false
True
Due to resolution of local oedema and reversal of injury to the penumbra
List common symptoms of cellulitis
Involved site(s): red, hot, swollen, tender
Borders are not elevated or sharply demarcated
Regional lymphadenopathy
Malaise, chills, fever, toxicity