Seminar 12 - Traumatic Head Injury Flashcards

1
Q

List the clinical features of wound infection

A

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

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2
Q

How does the body normally deal with cells which have had their DNA damaged by UV

A

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

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3
Q

In DIC where are the procoagulants released from

A

They can be released from a variety of locations such as the placenta in obstetric complications and damaged tissues in severe trauma and burns.

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4
Q

Which microbiology style tests may be performed on wound infection

A

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

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5
Q

List the ABCDE warning signs of melanoma

A

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

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6
Q

List potential causes of high grade sarcoma

A

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

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7
Q

What is a subarachnoid haemorrhage

A

Extravasation of blood into the subarachnoid space (SAS).

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8
Q

List the microscopic features of subacute (evolving) focal ischaemic infarcts

A

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

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9
Q

List the immediate compensatory mechanisms for rising ICP

A

Decrease in CSF volume by moving it out of foramen magnum

Decrease in blood volume by squeezing sinuses

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10
Q

Non-infectious vasculitis can also cause focal ischaemic CVA - true or false

A

True

Polyarteritis Nodosa and other non infectious vasculitis can cause single or multiple infracts in the brain

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11
Q

List some examples of high grade sarcoma

A
Clear cell sarcoma 
Dermatofibrosarcoma protuberans
Ewing sarcoma
Extraskeletal myxoid chondrosarcoma
Liposarcoma
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12
Q

Describe a systemic wound infection

A

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

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13
Q

What consequences of SAH tend to occur in the first few days post-bleed

A

Increased risk of additional ischaemic injury from vasospasm affecting vessels bathed in extravasated blood

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14
Q

Which mutations are often seen in melanoma

A

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

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15
Q

Why do people in ICU experience weakness and stiffness

A

Muscles weaken due to long periods of inactivity.

This happens quicker when they are on a ventilator.

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16
Q

Why are ICU patient’s at high risk of complications

A

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.

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17
Q

List the pathological features of secondary haemorrhagic infarcts

A

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

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18
Q

How do the ventricles appear in communicating and non-communicating hydrocephalus

A

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

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19
Q

What are the two main triggers of DIC

A

Release of procoagulants into the bloodstream and the injury of endothelial cells.

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20
Q

Which cancers are most associated with DIC

A

Acute promyelocytic leukemia

Adenocarcinomas of the lung, pancreas, colon and stomach

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21
Q

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

A

Should be recorded as NT (not testable)

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22
Q

Infarcts in focal ischaemic CVA can be divided into which groups

A

Non haemorrhagic and secondary haemorrhagic infarcts

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23
Q

The deficits that are caused by a focal ischemic CVA can improve over time - true or false

A

True

Due to resolution of local oedema and reversal of injury to the penumbra

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24
Q

List common symptoms of cellulitis

A

Involved site(s): red, hot, swollen, tender
Borders are not elevated or sharply demarcated
Regional lymphadenopathy
Malaise, chills, fever, toxicity

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25
Q

Which vessels are most commonly the cause of subarachnoid haemorrhage

A

Usually arise in arterial bifurcation in circle of Willis

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26
Q

What is defined as a high speed RTA

A

Anything over 30 mph classified as ‘high speed’.

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27
Q

List medical management options for raised ICP

A

Use diuretics (mannitol, hypertonic saline, furosemide, urea)
Barbiturate coma
Anti-epileptics

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28
Q

What causes the contralateral hemiparesis in extradural haematoma

A

Compression of cerebral peduncle

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29
Q

What causes the ipsilateral pupillary dilatation in extradural haematoma

A

The expanding haematoma causes herniation of uncus of temporal lobe which compresses the pupillary fibres of CN III

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30
Q

Which patients are at higher risk of bleeding in reactive gastritis

A

Those with respiratory failure or coagulopathy

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31
Q

List some infections that can cause ARDS

A
Sepsis 
Diffuse pulmonary infection
Viral, mycoplasmic and pneumocystis pneumona 
Miliary TB
Gastric aspiration
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32
Q

When do watershed infarcts typically occur

A

Usually occur if the global ischemia is due to severe hypotensive episodes
Most commonly seen in patients who have been resuscitated after cardiac arrest.

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33
Q

List acute complications of an ICU stay

A
ICU delirium 
DVT and PE
GI ulcers and bleeds 
Kidney failure 
Liver damage 
Pressure ulcers
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34
Q

What interventions may be performed after a focal ischaemic CVA to reduce the risk of further events

A

If due to carotid atheromatous plaques then carotid endarterectomy will be done
If there is narrowing or occlusion of vessels then angioplasty and stenting can be performed
All patients, unless contra indicated, will be placed on either a DOAC or warfarin from 2 weeks following the event

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35
Q

List the potential mechanisms of death in DIC

A

Thrombotic complications such as ischaemia and multi-organ dysfunction

Life-threatening haemorrhage due to the consumption of clotting factors

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36
Q

What is bazex syndrome

A

Condition which leads to follicular atrophoderma, multiple basal cell carcinomas, local anhidrosis

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37
Q

How does a subdural haemorrhage present

A

Slowly evolving neurologic symptoms, often with a delay from the time of injury

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38
Q

Why can haemoperitoneum go unnoticed

A

It is bleeding into a free, internal space

May not produce symptoms until they go into hypovolemic shock

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39
Q

What causes kidney failure in ICU

A

Often caused by shock, infection or medication

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40
Q

What is the main cause of haemorrhage in the epidural space (extradural)

A

Trauma

Usually associated with temporal skull fracture in adults - disrupts the middle meningeal artery

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41
Q

What is the most common injury type seen in RTAs

A
Blunt force injuries 
Bruises (external) - e.g. seat belt 
Contusions (internal)
Lacerations - includes flaying
Abrasions - includes road rash
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42
Q

What is the most common cause of wound infection following appendix/biliary surgery

A

Gram-negative bacilli and anaerobes

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43
Q

List some of the late phase (healing) complications of SAH

A

Meningeal fibrosis and scarring - sometimes causes obstruction of CSF flow as well as interruption of the normal pathways of CSF resorption

Survivors also at risk of hydrocephalus

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44
Q

How do burns cause DIC

A

Major trigger is the release of procoagulants such as TF

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45
Q

List causes of increased central venous pressure that can lead to raised ICP

A

Venous sinus thrombosis
Heart failure
Obstruction of jugular veins

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46
Q

List possible symptoms seen in an anterior cerebral artery stroke

A
Disinhibition and speech perseveration
Primitive reflexes
Altered mental status
Impaired judgement
Contralateral weakness - greater in  arms, 
Contralateral cortical sensory deficits
Gait apraxia
Urinary incontinence
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47
Q

What is the most common cause of wound infection following gastroduodenal surgery

A

Gram-negative bacilli and streptococci

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48
Q

How does a ruptured saccular aneurysms present clinically

A

Sudden, excruciating headache (“worst headache ever”) - due to blood at high arterial pressure entering SAS

Rapid loss of consciousness
Neck stiffness + photophobia – meningeal irritation
Headache with N+V – raised ICP or meningeal irritation.
Confusion, seizures.
CN III palsy – posterior communicating artery aneurysm.

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49
Q

Describe the effect of endothelial injury in the pathogenesis of DIC

A

The injury exposes the subendothelial matrix which can activate the platelets and coagulation pathway.
This causes thrombi to form due to fibrin deposition.

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50
Q

List risk factors for basal cell skin cancer

A
Radiation exposure 
Gene mutations – TP53 gene mutations in BCC
Arsenic exposure through ingestion – Treat asthma and psoriasis 
Immunosuppression 
Xeroderma pigmentosum 
Nevoid basal cell carcinoma syndrome 
Bazex syndrome 
Previous nonmelanoma skin cancer
Skin type – albinism 
Rombo syndrome 
Alcohol consumption 
Hydrochlorothiazide use – potent photosensitizer
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51
Q

Which genes have been linked to an increases risk of focal ischaemic CVA

A

Mutations in F2, F5, NOS3, ALOX5AP and PRKCH

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52
Q

Risk of additional ischaemic injury due to extravasated blood is of greatest significance in SAH in which locations

A

Basal SAH

Vasospasm can involve the major vessels of the Circle of Willis.

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53
Q

What is the most frequent cause of spontaneous SAH

A

Rupture of a saccular (berry) aneurysm

They are found in ~2% of population

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54
Q

List the most common causes of DIC

A
Malignancy 
Sepsis 
 Major trauma 
Obstetric events 
Hypoxia, acidosis and shock can all cause endothelial injury and contribute to DIC.
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55
Q

List the microscopic features of cellulitis

A

Clusters of neutrophils
Invading adipose tissue extensively -> Fat necrosis
Seen in deeper tissue

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56
Q

List some of the potential complications of haemorrhagic CVA

A

A large proportion of survivors will be left with some form of neurological deficit which will depend on the site and size of the haemorrhage and therefore the location and extent of damaged tissue

It is possible however to have a gradual improvement of the deficits that are left over weeks to months following the event as the haematoma is gradually removed

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57
Q

What skin and hair changes may be experienced by ICU patient’s

A

Lots of ICU survivors experience dry skin and hair loss.

Usually improves with time

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58
Q

What is rombo syndrome

A

Autosomal dominant condition distinguished by basal cell carcinoma and atrophoderma vermiculatum, trichoepitheliomas, hypotrichosis milia, and peripheral vasodilation with cyanosis

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59
Q

List the morphological features of global cerebral ischaemia

A

The brain will become oedematous and swollen and so the gyri will widen and the sulci will narrow
The will be poor demarcation between the white and gray matter on the cut surface.
Over time the microscopic features of irreversible ischemic injury will evolve and they mimic the changes in infarcts

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60
Q

Which types of basal cell carcinoma will get radiation therapy

A

Advanced and extended lesion that are not suitable for surgery
Can be due to allergy to anesthetics, current anticoagulant therapy

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61
Q

List potential differentials for normal pressure hydrocephalus

A
Other forms of dementia
Cervical myelopathy
All urinary problems
Parkinson’s disease
Depression
Etc.
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62
Q

List the macroscopic features of basal cell carcinoma

A

Present as pearly papules containing prominent dilated sub-epidermal blood vessels (telangiectasias)
Advanced lesions may ulcerate and cause extensive local invasion of bone or facial sinuses

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63
Q

List risk factors for presence of berry aneurysms

A

Increased incidence in 1st degree relatives.

Increased incidence with certain Mendelian disorders - AD PCKD, Ehlers-Danlos type IV, NF1, Marfan’s, fibromuscular dysplasia of extracranial arteries, and coarctation of aorta.

Other predisposing factors: cigarette smoking and HTN.

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64
Q

Which medical therapies are used for the treatment of high-grade sarcoma

A

Ifosfamide and doxorubicin-based chemotherapy

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65
Q

List causes of haemorrhagic CVA

A
Hypertension 
Cerebral amyloid angiopathy (CAA)
Trauma
Aneurysm rupture,
Anticoagulation
Vasculitis
Thrombolysis
Coagulopathy
Arteriovenous malformations
Venous and cavernous angiomas
Intracranial neoplasms 
Cocaine use
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66
Q

Why do symptoms develop rapidly in an extradural haemorrhage

A

Rapidly evolving since blood under high arterial pressure is extravasating from the vessel into the potential space between the periosteum and the dura

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67
Q

List risk factors for developing HAP

A

The biggest risk factor is mechanical ventilation - very common in ICU.

Also severe underlying disease, immunosuppression, prolonged antibiotics and invasive instrumentation like catheters.
All may be seen in ICU

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68
Q

What is an extradural haemorrhage

A

The accumulation of blood in the (potential) space between the periosteal dura and the bone

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69
Q

How do you distinguish between focal and global ischaemic brain injury

A

The distinction between them is not due to pathological differences but rather the amount of brain that is involved.

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70
Q

What are the 2 most serious subtypes of brain herniation

A

Uncal herniation- displacement of the medial part of the temporal lobe (uncus) below the tentorium cerebelli

Tonsillar herniation- the cerebellar tonsils are forced downwards through the foramen magnum, causing compression on the brainstem (fatal if left untreated)

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71
Q

What happens when the intracranial compensatory mechanisms become exhausted

A

This is when no further drainage of blood or CSF is possible.
At this point, the equilibrium becomes disrupted and the patient enters adecompensated statewhere intracranial pressure will begin to rise

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72
Q

What is the most serious form of skin cancer

A

Malignant melanoma

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73
Q

What is the most common cause of wound infection following orthopedic surgery

A

S aureus and coagulase-negative staphylococci

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74
Q

Describe the pathological features of the vessels in haemorrhagic CVA

A

Any vessel affected by cerebral amyloid angiopathy will be rigid and therefore will not collapse during processing and sectioning
The hyaline material that is deposited in CAA is not made from collagen like it is in normal hyaline arteriosclerosis but rather b amyloid

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75
Q

Describe the features of a class 4 - dirty/infected surgical wound

A

Purulent inflammation present
Preoperative perforation of viscera
Penetrating traumatic wounds >4 hours

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76
Q

List the main complications of raised ICP

A

Seizures
Stroke
Neurological damage
Death

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77
Q

List the macroscopic features of wound infection

A

Purulent discharge from surgical site or wound or drain placed in the wound
Discoloration of tissues both within and at the wound margins
Friable, bleeding granulation tissue
Lymphangitis - red line spreading from wound

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78
Q

What is non-communicating hydrocephalus

A

Occurs when the flow of CSF is blocked along one or more of the narrow
passages connecting the ventricles.

Aqueductal stenosis results from a narrowing of the aqueduct of Sylvius,
(between the third and fourth ventricles)

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79
Q

Describe the natural progression of squamous cell skin carcinoma

A

If untreated they will destroy nearby healthy tissue

Then spread to the lymph nodes or other organs which can be fatal

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80
Q

What is the most common cause of wound infection following head and neck surgery

A

S aureus, streptococci, anaerobes and streptococci present in an oropharyngeal approach

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81
Q

What effect can DIC have on the kidney

A

The kidneys may have small thrombi in the glomerulus which can lead to reactive swelling, microinfarcts or even bilateral renal cortex necrosis.

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82
Q

Steroids improve the outcome in diffuse axonal injury - true or false

A

False

The make it worse

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83
Q

The kidney failure seen in ICU patients is always temporary - true or false

A

False
It can be short-term/temporary in some cases
BUT
In others it can become a lifelong disease (may need dialysis).

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84
Q

Describe the inflammatory phase of wound infection

A

Begins with coagulation cascade to limit bleeding
Platelet reaction & reversible opening of endothelial cell junctions to allow passage of neutrophils and monocytes
Inflammatory exudate fills the wound in hours

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85
Q

What is brain herniation

A

A shifting of the brain parenchyma itself in response to high ICP

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86
Q

The rate of CSF drainage by a shunt can be altered - true or false

A

True
VP shunts have pressure valve (palpate behind auricle) that can be set
with a specially designed magnet/kit.
Can be set to drain more or less CSF by changing rate based on patient needs

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87
Q

Describe a local wound infection

A

Local infection is contained in one location, system or structure.
Occurs when bacteria or other microbes move deeper into the wound tissue and proliferate at a rate that invokes a response in the host

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88
Q

List the potential GCS scores for verbal response

A
5 – Orientated response
4 – Confused conversation 
3 – Inappropriate words 
2 – Incomprehensible sounds 
1 – No response
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89
Q

Why might ICU patients end up with longer term breathing issues after their stay

A

If the patient was on a ventilator their chest muscles will become weaker.
May require chest exercises or physio to improve breathing.

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90
Q

Describe the pathogenesis of haemorrhagic CVA caused by CAA

A

Ab peptides are deposited in the walls of medium and small cortical, meningeal and cerebellar vessels

Once the vessels walls have amyloid deposited within them it weakens them which makes them more vulnerable to rupture = haemorrhage

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91
Q

How does normal pressure hydrocephalus present

A

Hakim’s triad: abnormal gait, urinary incontinence, dementia

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92
Q

Why do babies get massive heads with hydrocephalus

A

Because their fontanelles haven’t fused so the skull can expand to cope with pressure
Not seen in adults’

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93
Q

Repeat bleeding is common in SAH - true or false

A

True

prognosis worsens with each bleed

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94
Q

How common are CVAs

A

They are incredibly common
Someone in the UK has a CVA every 3.5minutues
15million people suffer a CVA annually worldwide
¼ of individuals in the UK who suffer a CVA will die within a year and >1/2 that survive will be left with a permanent disability

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95
Q

Which countries have the highest rates of melanoma

A

Australia and New Zealand
10-20% arise in the head and neck region
Incidence is increasing worldwide though

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96
Q

It is common for children to present with a skull # and extradural haemorrhage - true or false

A

False
Children have a deformable skull which means that temporary displacement of skull bones can lacerate underlying vessels without fracture.
In adults, a fracture is likely to be seen.

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97
Q

What are the most common causative organisms of HAP

A

Most common organisms are gram +ve cocci (s.aureus) and gram -ve rods (enterobacteriaceae and pseudomonas)

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98
Q

Which processes initiate ARDS

A

ALI/ARDS is initiated by the injury of pneumocytes and pulmonary endothelium
It begins a cycle of inflammation and lung damage

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99
Q

Squamous cell skin carcinoma is more common in which sex

A

2-3 times more common in men than women due to higher cumulative lifetime UV exposure

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100
Q

What can cause reactive gastritis

A

The main cases are severe trauma, burns, intracranial disease, major surgery, severe illness and other forms of physiological stress

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101
Q

List surgical management options for raised ICP

A

Surgical decompression
Remove mass lesions
CSF diversion

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102
Q

What are lobar haemorrhages

A

Haemorrhages that effect the lobes of the cerebral hemispheres
Type of haemorrhagic CVA

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103
Q

What determines the prognosis of ARDS

A

Prognosis varies with age of the patient, cause and the number of organs involved.

Cause - pneumonia 86% and trauma 38% mortality

3 organs or more is invariably fatal

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104
Q

What is communicating hydrocephalus

A

This is when the flow of CSF is blocked after it exits the ventricles.
Called communicating because the CSF can still flow between the
ventricles, which remain open

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105
Q

What causes a fat emboli

A

They occur in those that have suffered large fracture

Can also get bone marrow emboli

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106
Q

What are the 3 subtypes of reactive gastritis ulcers

A

Stress ulcers
Curling ulcers
Cushing ulcers

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107
Q

Describe the process of endothelial activation in ARDS

A

Occurs early on

Pneumocyte injury is sensed by the alveolar macrophages which then start to secrete mediators like TNF which act on the nearby endothelium
Another mechanism is via circulating inflammatory mediators which activate it directly - occurs in sepsis or systemic illness

Some cells will get damaged by the mediators in the process, but others start to express adhesion molecules, procoagulant proteins and chemokines.

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108
Q

A GCS score of 8 or below requires which interventions

A

GCS ≤8 indicates intubation

ICP monitoring where GCS ≤8 w/ abnormal CT head

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109
Q

What can cause ARDS

A

Can be caused by direct lung injury or occur secondary to severe systemic illness

Several genes have been linked to ARDS - mostly linked to coagulation or inflammation

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110
Q

What effect does an extradural haemorrhage have on the surrounding structures

A

As it enlarges, it strips the dura from the bone but is restrained at the sutures
Gives the convex/lemon shaped appearance

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111
Q

Describe the maturation phase of wound infection

A

Dominant features – wound contraction, scar formation, remodeling

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112
Q

Which type of CVA is more common - ischaemic or haemorrhagic

A

Ischaemic - they account for 82-92% of CVA’s

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113
Q

What is the most common cause of ganglionic intracerebral haemorrhage

A

Hypertension

Associated with deep brain (ganglionic) parenchymal haemorrhages.

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114
Q

Where do most berry aneurysms present

A

90% of saccular aneurysms are near major arterial branch points in the anterior circulation
Multiple aneurysms exist in 20-30% of cases

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115
Q

What increase the risk of developing ICU delirium

A

Increased risk from infection, kidney, heart or lung failure and certain drugs.
Specific patients will also be at a higher risk: elderly and those with existing memory/cognitive issues.

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116
Q

List possible symptoms seen in a vertebrobasilar artery stroke

A
Vertigo
Nystagmus
Diplopia
Visual field defects
Dysphagia
Dysarthria
Facial hypaesthesia
Syncope
Ataxia
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117
Q

What can cause an increased production of CSF

A

Choroid plexus papilloma

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118
Q

ICU survivors are two to five times more likely to die compared with age and sex-matched population controls - true or false

A

True

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119
Q

Haemorrhagic CVAs are most common in which age group

A

They most often occur in mid to late adult life ( peak incidence approx 60yrs)

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120
Q

Describe the features of a class 1 - clean surgical wound

A
Uninfected operative wound
No acute inflammation
Closed primarily
Respiratory, gastrointestinal, biliary, and urinary tracts not entered
No break in aseptic technique
Closed drainage used if necessary
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121
Q

What are the two main microscopic patterns of basal cell carcinoma

A

Multifocal superficial type – Multifocal growths originating from the epidermis and sometimes extending

Nodular lesions growing downward deeply into the dermis as cords and islands of variably basophilic cells w/ hyperchromatic nuclei, embedded in a mucinous matrix and often surrounded by fibroblasts and lymphocytes

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122
Q

List the macroscopic features of cellulitis

A

Swelling, erythema, warmth
Petechiae or hemorrhage
Necrotic
Involves deeper dermis and subcutaneous fat

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123
Q

Describe how the release of TNF can trigger DIC

A

It causes the endothelial cells to express tissue factor and decrease thrombomodulin expression which tips the balance towards coagulation
It also promotes the adhesion of leukocytes (via adhesion molecule expression) which damage the cells.

These processes can cause widespread deposition of fibrin within the microvasculature (forms clots)

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124
Q

Describe the humoral theory of cerebral blood flow autoregulation

A

Theory is that it is the action of metabolic by-products that controls flow

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125
Q

It is common to see microbleeds in the brains of those with CAA - true or false

A

True

They have weakened vessels that are prone to rupture

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126
Q

ARDS can occur as a result of cardiopulmonary bypass - true or false

A

True

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127
Q

List the most common symptoms of DIC

A

Microangiopathic anaemia
Dyspnoea, cyanosis and respiratory failure
Oliguria and acute renal failure
Bleeding and bruising – can occur anywhere
Convulsions and coma
Circulatory collapse and shock

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128
Q

What determines the survival of an ischaemic portion of the brain

A

It will depend on the duration of the ischemia, the magnitude and rapidity of the reduction of blood flow an the presence of collateral circulation

These factors also determine the clinical presentation of cerebrovascular disease as they determine the site and size of the damaged area

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129
Q

What is the biggest predictor of prognosis in reactive gastritis

A

How quickly/easily the underlying condition can be treated

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130
Q

Describe the treatment of ARDS

A

No specific treatments for ALI/ARDS

Overview - admit to ICU, give supportive therapy and treat the underlying cause.
Supportive resp - CPAP or most need careful ventilation
Supportive circulation - monitoring and careful fluid management
Most need nutritional support

Ventilation usually needed at high pressure due to stiffening of the lungs.

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131
Q

Which type of CVA do bone marrow emboli typically cause

A

Focal ischemic CVA

Appears as widespread haemorrhagic lesions in the white matter

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132
Q

Describe the typical appearance of a basal cell carcinoma

A
Waxy papules with central depression
Pearly appearance
Erosion or ulceration, often central
Bleeding, especially when traumatized
Crusting
Rolled (raised) border
Translucency
Telangiectases over the surface
Slow growing (0.5 cm in 1-2 y)
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133
Q

What is DIC

A

It is an acute, subacute or chronic thrombohaemorrhagic disorder that is characterised by the excessive activation of the coagulation pathway and the formation of thrombi in the microvasculature

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134
Q

What is the main mechanism of death in reactive gastritis

A

Fatal GI bleeds or the consequences of GI perforation.

One study reported a mortality rate of 46% in critically ill patients with GI bleeding, compared with 21% inpatients without bleeding.

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135
Q

Describe the pathogenesis of reactive gastritis

A

Biggest underlying cause is thought to be local ischaemia.
This can be caused by systemic hypotension or reduced blood flow caused by stress-induced vasoconstriction of the vessels supplying the GI tract.
Redistribution of blood flow occurs in conditions like sepsis
In some cases, there is increased release of the vasoconstrictor endothelin-1 which also contributes

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136
Q

List some of the complications associated with drains and catheters

A

Central venous catheters can result in bloodstream infections

Urinary catheters have a high risk of causing UTI

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137
Q

List the microscopic features of ARDS

A

Diffuse alveolar damage, interstitial and intra-alveolar damage, inflammation and fibrin deposition are all seen.
Inflammation characterised by scattered neutrophils and macrophages

Presence of the waxy hyaline membranes in the alveoli - consisting of fibrin-rich oedema and necrotic epithelial cells

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138
Q

Describe the role of metabolic autoregulation in the autoregulation of cerebral blood flow

A

Arterioles dilate in response to chemicals, e.g. lactic acid and CO2

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139
Q

What is pulmonary oedema

A

The presence of excess interstitial fluid within the alveoli

It can result from haemodynamic disturbances (cardiogenic) or increased capillary permeability due to microvascular injury (non-cardiogenic).

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140
Q

How is the GCS score used

A

Generally used to categorise traumatic brain injury into mild (13-15), moderate (9-12) and severe (3-8)
Part of the APACHE II scoring system, which is used to predict ICU mortality

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141
Q

How common are wound infections

A

A survey sponsored by WHO demonstrated a prevalence of nosocomial infections in the range of 3-21%, with wound infections accounting for 5-34% of the total

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142
Q

It is possible to determine whether a CVA is ischemic or haemorrhagic from the clinical presentation alone -true or false

A

False

Not possible

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143
Q

List potential complications of aneurysm clipping

A
Stroke
Seizure
Vasospasm
Bleeding
The clip being placed incorrectly so that it does not stop the bleeding or blocks another artery
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144
Q

List some of the complications associated with tracheostomies

A

Patients will be unable to speak to begin with which can be distressing.

Will leave a scar.

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145
Q

What are ganglionic haemorrhages

A

Haemorrhages effecting the basal ganglia and thalamus

Type of haemorrhagic CVA

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146
Q

What is the most common region of the brain to get a focal ischemic CVA due to an emboli

A

The territory supplied by the middle cerebral artery

It is as common for each hemisphere in this territory to be effected

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147
Q

How does sepsis cause DIC

A

Endotoxins released in sepsis can inhibit endothelial expression of thrombomodulin directly or indirectly by stimulating immune cells to make TNF
Can also activate factor XII
These trigger coagulation

Antigen-antibody complexes are also sometimes produced in response to infection and can activate the classic compliment pathway and secondarily activate platelets = coagulation

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148
Q

List the consequences of PPI treatment

A

PPI low incidence of adverse effects or drug interactions.

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149
Q

Describe the pathogenesis of a haemorrhagic CVA

A

Brain tissue is damaged due to a raise in ICP
Blood from the ruptured vessels compresses the surrounding tissue causing it to become infarcted.
The presence of the blood in the parenchymal tissue and the associated oedema will raise the ICP pressure which will damage the brain tissue

The brain also becomes infracted due to a loss of blood supply
The blood that is leaking from the ruptured vessels was intended for somewhere so the site it was intended for will become ischemic

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150
Q

What is the normal ICP in a newborn

A

1.5-6 mmHg (often < 0)

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151
Q

What are the main causes of subarachnoid haemorrhage

A

Trauma - typically associated with underlying parenchymal injury.
e.g. RTA

Vascular abnormality (AV malformation or aneurysm)

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152
Q

The onset of DIC is always sudden - true or false

A

False
It can be sudden - e.g. in sepsis
However in other cases it can be more insidious and chronic - e.g. in malignancy or dead foetus

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153
Q

Describe the myogenic theory of cerebral blood flow autoregulation

A

Theory is that it is a direct reaction of smooth muscle to the stretch

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154
Q

How are surgical wounds classified

A

Class 1 - clean
Class 2 - clean-contaminated
Class 3 - contaminated
Class 4 - dirty infected

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155
Q

Obstruction to CSF flow leads to what

A

Hydrocephalus

This causes increase ICP

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156
Q

Head injury is a common cause of death and disability in RTAs - true or false

A

True

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157
Q

Some cells in the CNS will be more sensitive to ischemia than others - true or false

A

True
Neurones are the most sensitive
Astrocytes and glial cells are also particularly sensitive

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158
Q

List symptoms of severe cellulitis infections

A
Systemic – violaceous color and bullae 
Lymphangitic spread, crepitus, hemodynamic instability 
Cutaneous hemorrhage 
Skin sloughing 
Skin anesthesia 
Rapid progression 
Gas in the tissue
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159
Q

Uraemia can cause ARDS - true or false

A

True

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160
Q

Describe how PTCH mutations lead to basal cell carcinoma

A

PTCH protein is a receptor for sonic hedgehog (SHH), a component of the Hedgehog signaling pathway

Typically have a germline loss-of-function mutation in one PTCH allele
The second normal allele is inactivated in tumours by an acquired mutation, usually caused by exposure to mutagens (particularly UV light)

In this ‘off’ state PTCH exists in a complex with another transmembrane protein called SMO
Binding of SHH to PTCH releases SMO
This activates the transcription factor GLI1 which turns on the expression of genes that support tumor cell growth and survival

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161
Q

List the pathological features of lacunar infarcts

A

They are lake shaped, hence the name, <15mm wide and can be single or multiple
Microscopically they show gliosis surrounding areas of tissue loss
The vessels that are effected can also have a widening of their perivascular spaces which is termed etat crible

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162
Q

What is the purpose of craniotomy in haemorrhagic CVA

A

To remove the collected blood and damaged brain tissue to relive the pressure on the surviving brain
Done if bleeds are large

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163
Q

Which features of haemorrhagic CVA suggest a poor prognosis

A

A low GCS suggests a high mortality and poor prognosis

A large blood volume at presentation also suggests a poorer prognosis
Very large bleeds or bleeds that extend into the ventricular system can be devastating

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164
Q

Which age group is most prone to facial cellulitis

A

adults > 50 yo

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165
Q

List complications of shunts for hydrocephalus

A

Mechanical failure
Infections
Obstructions

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166
Q

Which type of CVA do fat emboli typically cause

A

Focal ischemic CVA

They tend to cause shower embolisation

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167
Q

How can hydrocephalus be classified

A

As communicating vs non-communicating

As congenital vs acquired

Or by aetiology

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168
Q

List local complications of wound infection

A

Delayed and non-healing of wound

Abscess formation

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169
Q

How do CVAs caused by fat emboli typically present

A

Present with generalised cerebral dysfunction, a lack of localising signs and disturbances of higher cortical function

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170
Q

Describe the neurogenic theory of cerebral blood flow autoregulation

A

Theory is that it is the action of perivascular nerves that controls flow

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171
Q

List potential causes of pulmonary oedema due to undetermined origin

A

High altitude

Neurogenic - CNS trauma

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172
Q

List the microscopic features of melanoma

A

Cells are usually larger than normal melanocytes
They have enlarged nuclei with irregular contours and chromatin clumped at periphery of nuclear membranes
Prominent red nucleoli (eosinophilic)

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173
Q

ICP is determinant of cerebral perfusion pressure - true or false

A

True

CPP = MAP – ICP

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174
Q

List the macroscopic features of melanoma

A

Striking variations in color, appearing in shades of black, brown, red, dark blue and gray
Zones of white or flesh-colored hypopigmentation appear on occasion due to focal regression
Irregular and notched border
Radial growth – horizontal spread of melanoma within the epidermis and superficial dermis
Vertical growth phase – is often heralded by the appearance of a nodule

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175
Q

What is the GCS scored out of

A

15
eyes out of 4
verbal response out of 5
motor response out of 6

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176
Q

Which parts of the brain may be involved in a intra-parenchymal brain haemorrhage

A

Selective involvement of the crests of gyri, where the brain is in contact with the inner surface of the skull (frontal & temporal tips, orbitofrontal surface)

Petechial haemorrhages in an area of previously ischaemic brain, usually following the cortical ribbon.

“Lobar” haemorrhage involving subcortical white matter and often with extension into the SAS.

Centred in the deep white matter, thalamus, basal ganglia, or brainstem; may extend into the ventricular system.

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177
Q

List common ICU interventions/devices that often lead to complications

A
Ventilators 
Tracheostomy 
IV lines and pumps 
Feeding tubes 
Drains and catheter 
Drugs
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178
Q

What is ICP

A

Theintracranial pressure
It is the pressure within the cranium of the skull
It is measured in millimeters of mercury mmHG

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179
Q

What determines the extent of a focal ischaemic CVA

A

The duration of the ischemia and the extent of collateral blood supply
This also determines the size, location and shape

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180
Q

List the macroscopic features of reactive gastritis

A

Lesions range from shallow erosions to ulcers that penetrate the gastric mucosa.

The ulcers are typically rounded, under 1cm in diameter and usually have a black/brown base due to staining by the acid digesting blood products.

These lesions are found anywhere in the stomach and usually occur in multiples.

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181
Q

What are the 3 main injury categories in RTA

A

Acceleration/ deceleration (may occur even w/out an impact)
1 impact w/ vehicle
2 impact w/ road or stationary object

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182
Q

How do you treat wound infection

A

Antibiotic prophylaxis
Each surgical specialty, body region and operation type needs to have its strategy to treat due to different microbial spectrum
Early surgical debridement - however, re-opening of surgical site can cause significant morbidity
Sepsis Treatment – antibiotics

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183
Q

Where do most basal cell carcinomas occur

A

Occurs mostly on face, head and neck, and hands

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184
Q

Which organisms commonly cause wound infection

A

Patient’s own endogenous flora

e.g. staphylococci (S.aureus strain is most common), MRSA, streptococci, enterococci

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185
Q

List the macroscopic features of non-haemorrhagic infarcts

A

There will not be much change in their appearance in the first 6 hrs of irreversible injury

The tissue will be soft, swollen and pale and the gray-white matter junction will become indistinct by 48hrs

Between 2-10 days - The brain will become friable and gelatinous
As oedema resolves in the viable adjacent tissue the ill defined border between infracted and normal tissue will become defined

The tissue will then liquefy which will eventually leave a cavity that is filled with fluid which c will keep expanding until all dead tissue has been cleared. This occurs from day 10 and lasts for 3 weeks

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186
Q

List the clinical features of high-grade sarcoma

A

Gradually enlarging painless mass
Can become quite large, esp. in thigh and retroperitoneum
Pain or symptoms associated with compression by the mass – paresthesias or edema in an extremity
Constitutional symptoms rarely – fever and/or weight loss

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187
Q

Which systemic factors can increase the risk of wound infection

A
Age
Malnutrition
Hypovolemia
Poor tissue perfusion
Obesity
Diabetes
Steroids and other immunosuppressants
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188
Q

What would happen if a brain tumour continued togrow without intervention

A

The intracranial pressure will rise to such a degree that the final cranial component, the brain parenchyma, will shift in position and become displaced, this is termedherniation

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189
Q

Which operative characteristics can increase the risk of wound infection

A
Poor surgical technique
Lengthy operation
Intraoperative contamination
Prolonged preoperative stay in the hospital 
Hypothermia
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190
Q

List some acceleration/deceleration injuries than may be seen in RTA

A

Diffuse axonal injury - caused by shearing forces on brain

Aortic dissection - shearing forces generated by arch of aorta continuing forward whilst descending aorta anchored to thoracic spine

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191
Q

How does hydrocephalus affect the surrounding brain tissue

A

The excess fluid increases the size of the ventricles and puts pressure on the brain.
This can damage brain tissues and cause a range of impairments in brain function.

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192
Q

Describe the structure of the pia mater

A

Adherent to the brain parenchyma and spinal cord.

Thin and highly vascularised - helps nourish the underlying neural structures

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193
Q

Describe the typical appearance of a squamous cell carcinoma of the skin

A

Preceded by actinic keratoses

A shallow ulcer with heaped-up edges, covered by a plaque

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194
Q

Which organisms are the most common of cellulitis from bite wounds

A
Capnocytophaga canimorsus (dog)
Eikenella corrodens (human)
Pasteurella multocida (dog or cat)
Streptobacillus moniliformis (rat)
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195
Q

What causes berry aneurysms

A

Aetiology is unknown but absence of SM and intimal elastic lamina in affected vessel suggests that they are developmental abnormalities.

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196
Q

When might you see burns in a RTA

A

May see if vehicle catches fire but unlikely in RTCs otherwise

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197
Q

List the complications of TPA treatment used in focal ischaemic CVAs

A
Haemorrhagic CVA
Hypotension
Fluid accumulation on the brain
Pericarditis
Cardiac tamponade
Arrhythmia
Heart failure
Fluid accumulation in the lungs
Seizures
Swelling of the vocal cords
Internal bleeding
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198
Q

List potential causes of haemodynamic pulmonary oedema

A
Left-sided heart failure 
Volume overload
Pulmonary vein  
Hyperalbuminemia 
Kidney (nephrotic or protein-losing enteropathies) and liver disease
Infections - e.g. bacterial pneumonia 
Lung trauma  
Liquid aspiration
Inhales gases -
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199
Q

Which masses can lead to an increase in ICP

A
Tumour
Infarct
Contusions
Haematoma
Abscess

They distort surrounding brain by increasing pressure

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200
Q

Hypersensitivity reactions to what substances can cause ARDS

A

Drugs

Organic solvents

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201
Q

How common is reactive gastritis in ICU patients

A

Most patients admitted to ICU will have some histological evidence of gastric mucosal damage.
In 1-4% of these patients, the bleeding is so severe that transfusions are required.

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202
Q

What exacerbates the cyanosis and hypoxaemia in ARDS

A

They are exacerbated by the V/Q mismatch - occurs because some areas affected and some not

203
Q

What causes a stress ulcer in reactive gastritis

A

Most common in sepsis, shock or severe trauma

204
Q

What are the two main types of CVA

A

Ischaemic and haemorrhagic

205
Q

What is the main cause of subdural haemorrhage

A

Trauma

May follow minor trauma - particularly in elderly

206
Q

What is the most common site of metastases in high-grade sarcoma

A

Lung

207
Q

DVT/PE prophylaxis is recommended for all ICU patients - true or false

A

true

208
Q

What is the only definitive treatment for DIC

A

Treat the underlying cause

209
Q

List some chemical injuries that can cause ARDS

A

Heroin or methadone overdose
Acetylsalicylic acid - aspirin
Barbiturate overdose
Paraquat

210
Q

Describe the mechanism through which the CNS tissue is damaged in a CVA

A

As the blood flow becomes reduced the neurones will cease functioning
Once the cells become ischaemic they will have a reduction of ATP as they can no longer complete oxidative phosphorylation due to a lack of O2.
This reduction of ATP leads to cell and organelle swelling which causes cell death through necrosis
The ischemia will also cause an inappropriate release of glutamate which will further damage neurones by causing an influx of Ca ions into them (excitotoxicity)
It also though that some of the cells in a CVA die through apoptosis

211
Q

What is the Monroe-Kellie doctrine

A

It describes the relationship between the contents of the cranium and intracranial pressure

The increased volume of any of the contents leads to a decrease volume of one or both of the others

212
Q

What is wound contamination

A

Wound contamination is the presence of non-proliferating microbes within a wound at a level that does not evoke a host response

213
Q

Describe the pathogenesis of high grade sarcoma

A

Start with genetic mutations - e.g. loss of function of tumour suppressor gene like p53

Soft-tissue tumours grow centripetally
They will reach anatomic limits and then breach compartmental boundaries
This allows them expand more quickly due to a lack of fascial boundaries

Peripheral portion of the tumor compresses surrounding soft tissue which leads to formation a well-defined compression zone of fibrous tissue & inflammatory cells
The reactive zone surrounding it together form a pseudocapsule that encloses the tumor

Will eventually progress to metastatic disease

214
Q

Describe the role of CO2 in the autoregulation of cerebral blood flow

A

CO2 is a potent dilator!

Increased CO2/increased BP → vasodilation

Decreased CO2/decreased BP → vasoconstriction

215
Q

Which type of intracranial haemorrhage appears in a crescent moon shape on CT/MRI

A

Subdural

216
Q

Which cells in the brain are most sensitive to ischaemia

A

Neurones are the most sensitive
Astrocytes and glial cells are also particularly sensitive

The most sensitive neurones to ischemia, and therefore the neurones that are damaged first in these events, are; the pyramidal neurones in the hippocampus, cerebellar purkinje cells and pyramidal neurones in the cerebral cortex ( especially the ones in layers 3 and 5).

217
Q

What is the most common cause of lobar intracerebral haemorrhage

A

Cerebral amyloid angiopathy

218
Q

What are the main types of vascular disease that cause focal ischemic CVAs

A

Emboli from distant sites
Thrombosis within cerebral vessels
Other vasculidites

219
Q

How common is DVT in ICU patients

A

Prevalence of about 30%.

220
Q

List common injury patterns

A
Blunt force - bruises, lacerations, abrasions 
Sharp force - incisions and stabs 
Gunshot 
Burns - heat, electrical chemical
Head injuries
221
Q

What is Terson syndrome

A

Vitreous haemorrhage associated with SAH

222
Q

Describe the path of CSF flow

A

Secreted from the choroid plexus in the lateral ventricles
It flows through the ventricle system to the subarachnoid space (Magendie and Luschka)
This then enters the venous system through the arachnoid granulations

223
Q

List risk factors for developing cellulitis

A

High risk: Elderly, diabetes
Post-surgery
Varicella infection - cellulitis can complicate varicella
MRSA
Bite wounds, lacerations and puncture wounds

224
Q

What is normal pressure hydrocephalus

A

A chronic idiopathic condition (accumulation of CSF) commonly seen in the elderly

225
Q

Which countries have the highest rates of basal cell carcinoma

A

Affect countries near equator

Highest rates occur in South Africa and Australia, areas that receive high amounts of UV radiation

226
Q

How can genetics impact the development of squamous cell skin cancer

A

Sporadic tumours will have acquired defects (also seen in their precursors)
e.g. loss of p53 function

These defects also have a relationship with the damage caused by sun exposure

227
Q

When is radiation used in the treatment of high grade sarcoma

A

If the patient refuses or cannot tolerate surgery

228
Q

Which gene is associated with Nevoid basal cell carcinoma syndrome (NBCCS)

A

PTCH – a tumour suppressor gene
Typically have a germline loss-of-function mutation in one PTCH allele
The second normal allele is inactivated in tumours by an acquired mutation, usually caused by exposure to mutagens (particularly UV light)
This leads to the cancer

229
Q

What innervates the dura mater

A

Innervation from CN V

Pain in meningitis is from stretching of dura detected by CV V

230
Q

What are the main causes of the cardiac mural thrombi

A
MI
AF
Valvular disease - mitral stenosis, prosthetic valves, endocarditis
Severe heart failure
Dilated cardiomyopathy
231
Q

Which parts of the body may strike the interior of the car in an RTA

A

Head = Windscreen/ window/ front pillar
May cause injury such as skull fracture, cerebral haemorrhage or contusions etc.

Chest +/- abdomen =- Dashboard/ door
May cause injury such as rib fractures, pulmonary contusions, splenic and hepatic lacerations etc.

Lower body = Car body or chassis
May cause injury such as leg/femur fractures etc.

232
Q

Why is the incidence of wound infection likely underestimated

A

Most wound infections occur when the patient is discharged, and these infections may be treated in the community without hospital notification

233
Q

How do you manage reactive gastritis

A

Main management is treating the underlying condition.
PPI or H2 receptor antagonist can be given prophylactically to lessen the impact of gastric ulceration in high-risk patients.

234
Q

Describe the pathogenesis of lacunar infarcts

A

Due to the Hx the effected vessels develop arteriosclerosis (which is also called small vessel disease because it effects vessels between 40-900um in diameter)

The disease can then progress to cause thrombosis and complete vessel occlusion which will ultimately lead to cavitary infarcts known as lacunar infracts

235
Q

Describe the pathological features of ganglionic intracerebral haemorrhage caused by HTN

A

Vessel wall abnormalities including accelerated atherosclerosis in larger arteries, hyaline arteriosclerosis in smaller arteries, and (if severe) proliferative changes + frank necrosis of arterioles.

The arterioles with hyaline change are thickened and more vulnerable to rupture

236
Q

When is chemotherapy used in the treatment of high grade sarcoma

A

Can be used as medical treatment

Also used to reduce the risk of metastatic disease following multimodality treatments without amputation

237
Q

Which age groups are more likely to get cellulitis

A

A higher incidence of cellulitis in individuals older than 45 years
More common in geriatric patients

Certain age groups are at higher risk in some unique scenarios (e.g. children)

238
Q

Describe the structure of the arachnoid mater

A

Directly under dura, contains connective tissue and is avascular.
CSF contained in space under arachnoid mater, the subarachnoid space.

Arachnoid granulations are small projections of arachnoid membrane into dura venous sinuses that allow CSF to re-enter venous circulation

239
Q

List the morphological features of diffuse axonal injury

A

Widespread, often asymmetric, axonal swellings that appear within hours of injury and can persist for much longer.
Swelling best seen using silver impregnation techniques or with immune-peroxidase stains for axon transport proteins, e.g., amyloid precursor protein and alpha-synuclein

May also see focal haemorrhagic lesions
Later, increased number of microglia seen in damaged areas of cerebral cortex, and subsequently there is degeneration of the involved fibre tracts.

240
Q

What is an ischaemic CVA

A

Impairment of blood supply and oxygenation of the CNS tissue which results in ischemia and hypoxia of the brain tissue.
They can either be global or focal

241
Q

What causes mesenteric bruising in RTA

A

Can occur when seatbelts are worn due to position of lap belts
Causes compression of closed bowel loops and mesenteries between impacting surface and spine

242
Q

What is the incidence of ARDS in ICU units

A

A 2016 study found it to be 10.6%

243
Q

How does UVB radiation cause melanoma

A

Cause multiple genetic changes which leads to malignant transformation of melanocytes

244
Q

Describe the microscopic appearance of a saccular (berry) aneurysm

A

The arterial wall adjacent to aneurysm neck shows some intimal thickening + attenuation of the media.

Smooth muscle and intimal elastic lamina do not extend into the neck and are absent from the aneurysm sac itself – made up of thickened hyalinised intima and an adventitia covering.

245
Q

Haemorrhagic CVA has a higher mortality than ischemic CVA - true or false

A

True

Although they are less common

246
Q

How can systemic acidosis lead to reactive gastritis

A

It alters the intracellular pH of the gastric mucosal cells and disrupts the pH gradient that usually promotes the wash-out of acid

247
Q

List the microscopic features of healed focal ischaemic infarcts

A

The astrocytic response will recede after several months which will leave a dense network of glial fibres admixed with new capillaries and perivascular connective tissue

A gliotic layer of tissue separates the cavity from the meninges and subarachnoid space

248
Q

List causes of brain swelling that can lead to raised ICP

A
Ischaemia/anoxia
Acute liver failure
Encephalopathy,
Idiopathic intracranial hypertension
Hypercarbia

These all decrease CPP, but cause minimal tissue shift

249
Q

Which causes, other than atheromatous plaques,

should be considered in young patients with thrombosis causing focal ischemic CVA

A
Antiphospholipid syndrome
Protein C and S deficiency
Pregnancy
Sickle cell disease
Cocaine and amphetamines
250
Q

Where do most squamous cell skin carcinomas occur

A

70% occur on head and neck

251
Q

What are the most common patterns of intracerebral haemorrhages

A

Ganglionic
May originate in putamen (50-60%), thalamus, pons, cerebellar hemispheres (rare), and other brain regions

Lobar
Occurs in small- and medium- calibre leptomeningeal, cortical and cerebellar vessels.

252
Q

List the clinical signs seen if a haemorrhagic CVA occurs in the cerebellum

A
Facial weakness
Ipsilateral ataxia
Gaze paresis
Sensory loss
Skew deviation
Miosis 
Deceased conscious level
253
Q

List potential complications of craniotomy

A
Seizure
Stroke
Brain swelling
CSF leak
Nerve damage
Loss of some mental function
254
Q

What is the main complication of DVT in ICU

A

Can lead to a PE

255
Q

What is a haemorrhagic CVA

A

These are when the tissue infarction is due to rupture of a parenchymal vessel meaning areas of tissue are no longer supplied with blood
It also results in bleeding into the brain parenchyma

256
Q

Trauma to the pterion commonly cause which type of intra-cranial haemorrhage

A

Extradural

257
Q

List potential complications of mannitol treatment

A
Arrhythmia
Hypotension
Pulmonary congestion
Acidosis
Skin necrosis
Convulsion
Anaphylaxis
258
Q

How can you diagnose raised ICP

A

Medical history and physical exam including a neurological exam to test senses, balance and mental status
LP - measures the pressure of CSF
CT head - GOLD standard
MRI - shows more detail

259
Q

Why might a stay in ICU lead to liver damage

A

May become damaged as a side effect of medications used to treat other important conditions.
Also at risk due to shock, infection etc.

260
Q

Describe a Cushing ulcer in reactive gastritis

A

Can be gastric, duodenal or oesophageal and typically arise in those with intra-cranial disease
Has an increased risk of perforation

261
Q

What is the most common cause of lobar haemorrhages

A

The main cause of these is cerebral amyloid angiopathy (CAA)

262
Q

List the microscopic features of acute focal ischaemic infarcts (first 48hrs)

A

Eosinophilic neuronal necrosis (“dead red neurones”) will be seen in the neurones in the effected area. ( 6-12hrs)

Vasogenic and cytotoxic oedema will both be present (6-12hrs)

The normal tinctorial characteristics of gray and white matter structures will be lost (6-12hrs)

Myelinated fibres will disintegrate and glial cells, predominantly astrocytes, and endothelial cells will swell (6-12hrs)

There will be progressive neutrophilic emigration which will eventually drop of (which is never as prominent as it s following an MI) ( up to 48hrs)

263
Q

What is reactive gastritis

A

This is a type of gastritis that occurs in the context of severe trauma, burns, intracranial disease, major surgery, severe illness and other forms of physiological stress

264
Q

In the absence of pathology,normal homeostatic mechanismsmaintain a normal intracranial pressure - true or false

A

True

They respond to small fluctuations in intracranial volume

265
Q

Where in the saccular aneurysm does rupture usually occur

A

Rupture usually occurs at apex of sac

Blood goes into the SAS, the brain substance, or both.

266
Q

Describe the structure of the dura mater

A

Lies directly beneath skull or vertebral column.
It is the thickest and toughest (fibrous) layer.

In skull there are 2 layers - periosteal (outmost) and meningeal (innermost)
The dural venous sinuses are enclosed between the layers
The layers also form the dural septae when they separate - falx cerebri and tentorium cerebelli etc.

In spine: meningeal part only.

267
Q

What is the most common site of melanoma

A

10-20% arise in the head and neck region

268
Q

What is the most common cause of ganglionic haemorrhages

A

The major cause is hypertension

269
Q

List the clinical signs seen if a haemorrhagic CVA occurs in the caudate nucleus

A

Confusion
Contralateral hemiparesis
Conjugate gaze paresis

270
Q

How does ICU delirium present

A

May present with hallucinations, confusion, may not recognise surroundings or people, difficulty remembering or understanding information

As per normal delirium you get hyperactive and hypoactive forms
Usually temporary and last days/weeks, some use meds to treat but not well supported

271
Q

When would extensive intracerebral haematomas be seen alongside secondary haemorrhagic infracts

A

If the patient is on anticoagulants

272
Q

List the clinical signs seen if a haemorrhagic CVA occurs in the thalamus

A
Contralateral sensory loss and hemiparesis
Homonymous hemianopia
Gaze paresis
Miosis
Confusion 
Aphasia
273
Q

What is the most common cause of wound infection following urology procedures

A

Gram-negative bacilli

274
Q

Describe the transformation of a non haemorrhagic to secondary haemorrhagic infarct

A

It is called secondary haemorrhagic transformation

You only get this transformation of the initial causative event lasted long enough to damage the small blood vessels in the effected area as it is there damage that allows the haemorrhage into the infarct when reperfusion occurs

The haemorrhages in these infarcts are usually petichiael but can be multiple or confluent

275
Q

List some of the complications associated with IV lines and pumps

A

Associated with bruising and sometimes even scars.

Infection risk.

276
Q

What effect can DIC have on the lungs

A

Many fibrin thrombi can be seen in the alveolar capillaries.
May be associated with pulmonary oedema and fibrin exudation which forms the hyaline membranes.

277
Q

Describe the macroscopic appearance of a saccular (berry) aneurysm

A

thin-walled outpouching usually on an arterial branch point along the circle of Willis, or a major vessel just beyond
Few mm to 2-3cm in diameter
Bright red, shiny surface and a thin, translucent wall.
Atheromatous plaques, calcification or thrombi may be found in the wall or lumen of the aneurysm.
Sometimes there is evidence of prior haemorrhage - brownish discolouration of adjacent brain and meninges
Neck of aneurysm may be wide or narrow.

278
Q

Describe the clinical features of global cerebral ischaemia

A

The clinical outcome in these cases will vary depending on the insult’s severity and length
If it is only a mild case then the patient may only have a transient post-ischemic confusional state followed by a complete recovery
Unfortunately it is also possible for the patient to be left with irreversible CNS damage

279
Q

What is the definition of cerebrovascular accident

A

This is when there is tissue infarction in the brain as a consequence of altered blood flow

280
Q

How do you calculate cerebral blood flow

A

Cerebral perfusion pressure divided by cerebral vasc resistance

281
Q

How does ARDS progress

A

Symptoms appear rapidly and then the patient will progress to respiratory failure.

282
Q

List the three main causes of CSF flow problems

A

Obstruction - obstructive hydrocephalus

Increased production

Decreased absorption - communicating hydrocephalus

283
Q

Describe the features of a class 2 - clean-contaminated surgical wound

A

Elective entry into respiratory, biliary, gastrointestinal, urinary tracts and with minimal spillage
No evidence of infection or major break in aseptic technique
Example: appendectomy

284
Q

What effect do the clots have in DIC

A

They can cause ischaemia of affected or vulnerable organs by occluding the vessels
It also leads to a microangiopathic anaemia as the red cells fragment as they try to squeeze through the occluded vessels

285
Q

How do you differentiate reactive gastritis from chronic gastritis

A

In reactive gastritis the scarring and blood vessel thickening that is typically seen with chronic gastric ulcers is absent.

286
Q

Describe the pathological features of invasive squamous cell carcinoma

A

Nodular, variable keratin production (appreciated grossly as hyperkeratotic scale), may ulcerate
Shows variable degrees of differentiation

287
Q

What are the 3 main types of intracranial haemorrhage

A

Subarachnoid, intracerebral, extradural

288
Q

What proportion of ICU patients will develop AKI

A

50%

289
Q

How common are long-term mental health effects after ICU stay

A

In one study of survivors of acute lung injury, 36% were found to have depression, about 40% anxiety, and 62% PTSD
Unsurprising as it is a very traumatic experience for both patient and family

290
Q

Which part of the brain is most affected in diffuse axonal injury

A

Affect central areas: brainstem (95%; immediate death), corpus callosum, parasagittal areas, interventricular septum, hippocampal formation

Brain has different areas of mass and densities, when pressure or shearing forces are applied these areas will move/strain with different force. Occurs where density difference is greatest (grey/white interface).

291
Q

How do you differentiate reactive gastritis from normal peptic ulcers

A

Reactive gastritis ulcers can be found anywhere in the stomach and usually occur in multiples

Normal peptic ulcers are usually solitary and found in the antrum

292
Q

Which types of haemorrhagic CVA are usually due to underlying cerebrovascular disease

A

Haemorrhages in the brain parenchyma and the subarachnoid space

293
Q

How do you treat hydrocephalus

A

Usually surgical treatment to restore and maintain normal cerebrospinal fluid levels in the brain - shunts etc.

294
Q

What is the main management of focal ischaemic CVA

A

The gold standard is IV TPA within 4.5hrs of symptoms starting
If the cause is a particularly large clot them embolectomy may be performed to remove it

295
Q

Hydrocephalus is most common in which age groups

A

Occurs more frequently among infants and adults 60 and over

296
Q

List the delayed compensatory mechanisms for rising ICP

A

Decrease in extracellular fluid

297
Q

What is the definition of stroke

A

This is the clinical term for a CVA and it is defined as the acute onset of neurological symptoms that last >24hrs and can be explained by a vascular mechanism

298
Q

Which types of haemorrhagic CVA are usually due to trauma

A

Epidural and subdural haemorrhages

299
Q

Which regions of the brain are most sensitive to ischaemia

A

The border/watershed regions where to ends of an arterial supplies territory meet.
The border between the anterior and middle cerebra hemispheres is the most at risk of these areas in the cerebral hemispheres in these events
These areas will be damaged first in global ischaemia

300
Q

What is the normal ICP for an adult

A

7–15mmHg

301
Q

Hypertension related intraparenchymal haemorrhages typically originate in which part of the brain

A

The putamen, thalmus, cerebellar hemispheres, pons or other regions of the brain

302
Q

What is xanthochromia

A

Yellow CSF
Seen in SAH
CSF would initially be blood-tinged from SAH but the delay allows the blood to be broken down into haem then bilirubin = yellow

303
Q

Mucus from some adenocarcinomas can act as a procoagulant - true or false

A

True

In some cases it can activate factor X and aid coagulation

304
Q

High-grade sarcomas tend to invade locally - true or false

A

True

They will have ill-defined margins as a result

305
Q

Which signs are more common in patients with haemorrhagic CVAs than patients with ischemic CVAs

A

Headache, altered mental status, seizures, marked Hx and nausea and vomiting

With the exception of the Hx this is due to the fact that these signs are caused by raised ICP which is more of a feature in haemorrhagic CVA

306
Q

List some of the complications of high grade sarcoma

A
Skin ulceration
Thrombocytopenia
Hemorrhage
Fracture 
(depending on histopathologic category and anatomic site)
307
Q

What determines the risk of saccular aneurysm rupture

A

Most frequent in 5th decade (slightly F>M)

Risk of rupture depends on size and location of aneurysm :(<7mm is low risk and posterior circulation is higher risk)

FH and co-morbidity (e.g. PCKD or HTN)

1/3 cases are associated with acute increases in intracranial pressure e.g., straining with stool

308
Q

How does haemorrhage in the epidural space present (extradural)

A

Often have a brief LOC followed by short lucid period (regain consciousness and awareness)

Patient will then deteriorate and exhibit symptoms e.g., headache, vomiting, contralateral hemiparesis & ipsilateral pupillary dilatation
Rapidly evolving neurologic symptoms that require intervention.

309
Q

Describe the process of neutrophil adhesion and in ARDS

A

Neutrophils will adhere to the molecules expressed by the endothelium and migrate into the interstitium and alveoli

They degranulate and release many inflammatory mediators such as proteases, cytokines, ROS, neutrophil epithelial traps - directly injure lung

This starts the lung inflammation associated with ARDS

310
Q

Where do most melanomas occur

A

Occurs mostly on the trunk in white males and lower legs and back in white females

311
Q

List risk factors for DVT in ICU

A

Associated with increased duration of ventilation and longer ICU stay.
Longer they are in ICU the longer they are immobile = higher DVT risk

Some patients are more at risk: cancer, infections, trauma or genetics.

312
Q

Cerebrovascular disease is the most prevalent cause of mortality and morbidity from neurologic disease in the US - true or false

A

True

It is also the fifth leading cause of death in the US

313
Q

What is the definition of Transient Ischemic Attack

A

This is when the clinical signs of a CVA last < 24Hrs

314
Q

What is the most common cause of wound infection following obs/gynae surgery

A

Gram-negative bacilli, enterococci, anaerobes, group B streptococci

315
Q

If the protective functions of p53 are lost, how does the body deal with DNA damaged by UV

A

Loss of protective functions of p53
DNA damage induced by UV light is repaired by error-prone mechanisms
This leads to rapid accumulation of mutations & carcinogenesis
This creates mutations that are passed down to daughter cells = cancer

316
Q

ARDS is associated with which lifestyle factors

A

More common and worse in chronic alcoholics and smokers

317
Q

What are some of the risk factors for long-term cognition issues after ICU stay

A

delirium, hypotension, hypoxemia, prolonged sedation, and hypoglycemia

318
Q

How do you treat cellulitis

A

Oral or IV penicillin (drug of choice for initial treatment) unless patient has known penicillin allergy
Antifungal medications if necessary
Warm soaks to the site to help relieve pain and decrease edema by increasing vasodilation
Pain medication is needed
Elevation of infected extremity

Can be treated as outpatient with oral therapy but some do require admission and IV antibiotics

319
Q

Where in the cerebral vessels are emboli most likely to lodge

A

At sites where vessels branch or sites where there is already luminal narrowing

320
Q

List systemic complications of wound infection

A

Cellulitis
Osteomyelitis
Septicemia – Death (distant hematogenous spread of bacteria and sepsis)

321
Q

Which type of intracranial haemorrhage appears in a bi-convex, ‘lemon-shaped’
area on CT/MRI

A

Extradural

May also see mass effect & brain herniation

322
Q

How do you treat squamous cell skin carcinoma

A

Electrodessication and Curettage – treat localized, superficial lesion
Surgical excision
Radiation therapy
Systemic treatment – chemotherapy, immunotherapy

323
Q

How can cellulitis progress to a more serious illness

A

Uncontrolled contiguous spread (lymphatic or circulatory systems)

324
Q

What effect can DIC have on the CNS

A

The thrombi can cause microinfarcts which result in carrying neurological symptoms

325
Q

How can intracerebral haemorrhage cause secondary infarction

A

The collection of blood compresses the adjacent parenchyma

The compression causes secondary infarction

326
Q

Why does the brain have high O2 requirements

A

The brain needs a constant supply of energy and it gets this energy through aerobic metabolism

327
Q

What are the goals of therapy in raised ICP

A

Maintain CPP

Prevent ischaemia and brain compression

328
Q

List causes of intra-parenchymal brain haemorrhage

A

Trauma -contusions
Ischaemia -haemorrhagic conversion of an ischaemic infarct
Cerebral amyloid angiopathy (CAA)
Hypertension

Tumours -primary or metastatic
Associated with high-grade gliomas or certain metastases (melanoma, choriocarcinoma, RCC).

329
Q

What is the most common cause of squamous cell skin carcinoma

A

DNA damage induced by exposure to UV light

Tumour incidence is proportional to the degree of lifetime sun exposure

330
Q

What is the main determinant of prognosis in DIC

A

The underlying condition

The prognosis varies greatly between patients

331
Q

How long does it take neurological symptoms of a focal ischaemic CVA to appear

A

The neurological deficits usually develop over minutes but can progress and develop over several hours

332
Q

Pancreatitis can cause ARDS - true or false

A

True

333
Q

List some of the complications associated with medications on ICU

A

All come with their own side effects
One example would be certain antibiotics causing a C.diff infection

Also have to consider drug interactions

334
Q

Describe the pathological features of in-situ squamous cell carcinoma

A

They appear as sharply defined, red, scaling plaques

Cells with atypical nuclei involve all levels of epidermis

335
Q

What are the clinical features of reactive gastritis

A

The most common sign is actually the GI bleeding

This may present as haematemesis, melena and/or coffee ground vomit.

336
Q

How common is ICU delirium

A

Also 60-80% ventilator patients will develop delirium.

337
Q

Describe the pathogenesis of cellulitis

A

Usually follows a breach in the skin e.g. fissure, cut, laceration, insect bite or puncture wound
In some cases: no obvious portal of entry; may be due to microscopic changes in the skin or invasive qualities of certain bacteria

Organisms on skin & its appendages gain entrance to the dermis and multiply leading to cellulitis
Contamination -> Colonization -> Infection

338
Q

How can inflammation lead to focal ischaemic CVA

A

If there is an inflammatory process in a blood vessel it can cause luminal narrowing and occlusion and therefore cerebral infarcts
e.g. infective vasculitis

339
Q

What is nevoid basal cell carcinoma syndrome

A

Autosomal dominant disorder which can result in the early formation of multiple odontogenic keratocysts, palmoplantar pitting, intracranial calcification, and rib anomalies
Can lead to multiple basal cell skin carcinomas

340
Q

Why might ICU patients end up with incontinence after their stay

A

After using a catheter, the pelvic muscles can become weak, and patients may struggle to control their bladder
Continence should return to normal with time.

341
Q

Most basal cell carcinomas have mutations affecting which signalling pathway

A

Hedgehog signaling - mutations cause uncontrolled signalling
This pathway controls polarity and CNS development during embryogenesis and regulates follicle formation and hair growth

342
Q

What is the most common mechanism of death in ARDS and what is its mortality

A

Most common mechanism of death is from sepsis, multi-organ failure or severe lung injury.

A 2016 study found mortality to be between 35-46%

343
Q

What is diffuse axonal injury

A

Shearing/tearing of brain axons at microscopic level
Caused by mechanical forces - mainly rotational acceleration which causes unrestricted head movement.
One of the most common and important pathologic features of traumatic brain injury (TBI)

344
Q

How does hypertension lead to haemorrhagic CVA

A

Hx causes accelerated atheroscelrosis in larger arteries, hyaline arterioscelrosis in smaller arteries and if sever can cause proliferative changes or frank necrosis in arterioles
The arteriolar walls that have been altered by hyaline changes are thickened but are more vulnerable to rupture = haemorrhage

345
Q

Describe the morphological appearance of intracerebral haemorrhage

A

Characterised by a central core of clotted blood that compresses the adjacent parenchyma
The compression causes secondary infarction
Anoxic neuronal and glial
changes + oedema
Oedema eventually resolve, haemosiderin- and lipid-laden macrophages appear + proliferation of reactive astrocytes is seen (periphery of lesion).
Cellular events then resemble those that occur after cerebral infarction

346
Q

Describe the clinical effects of intracerebral haemorrhage

A

These bleeds can be clinically devastating if a large part of brain is involved or there is extension into ventricular system

Can be clinically silent if affecting smaller regions or evolves like an infarct

347
Q

List the 3 meningeal layers

A

Dura mater
Arachnoid mater
Pia mater

348
Q

How do you manage a haemorrhagic CVA

A

Any patient that is anticoagulated will get transfusion of blood products to reverse the effects of the anticoagulation
Osmotic diuretics (Mannitol) - to reduce the ICP
Antihypertensive medication
If the bleed is large then a craniotomy can be performed
AVM and aneurysms can occasionally be repaired surgically
Bleeding aneurysms can be managed with clipping or endovascular embolisation

349
Q

How common are long-term cognition issues after ICU stay

A

40-80% of ICU patients will develop some form of cognitive issue such as forgetfulness or not being able to think clearly

350
Q

Describe the clinical outcomes of severe global cerebral ischemia

A

Patients will have widespread neuronal death irrespective of the regional vulnerabilities
If the patient does survive this event they will likely remain in a persistent vegetative state or may meet the criteria for brain death.
If the individual remains ventilated in a persistent vegetative state they will end up with respirator brain due to the brain gradually undergoing widespread liquefaction

351
Q

What is the most common cause of an infective vasculitis leading to focal ischemic CVA

A

Opportunistic infection like aspergillosis in someone immunosuppressed by syphilis
TB can also cause an infective vasculitis leading to a focal Ischemic CVA

352
Q

How do obstetric events cause DIC

A

Procoagulants can enter the circulation from the amniotic fluid, placenta or dead retained foetus

353
Q

What is a a watershed area of the brain

A

These regions are the regions where to ends of an arterial supplies territory meet

354
Q

List the clinical features of haemorrhagic CVA

A

Acute onset neurological signs (stroke) -exact signs depend on the region of the brain affected
It is possible for a haemorrhagic CVA to be clinically silent if a small enough region is affected
Patients are also often hypertensive as Hx is the most common underlying cause of these bleeds
Headache, altered mental status, seizures, marked Hx and nausea and vomiting

355
Q

What is the normal ICP in a young child

A

3-7 mmHg

356
Q

List the clinical signs seen in an lobar haemorrhagic CVA

A

Contralateral hemiparesis or sensory loss
Homonymous hemianopia
Contralateral conjugate
Gaze paresis
Abulia - absence of willpower or an inability to act decisively
Apraxia - inability to perform learned (familiar) movements on command
Neglect

357
Q

What is the most common type of non-melanoma skin cancer

A

Basal cell carcinoma - accounts for 80% of cases

Squamous cell makes up the other 20%

358
Q

Why are tracheostomies performed on ICU patients

A

Often used if someone is in ICU for a long time as ventilation tubes can cause damage and are uncomfortable.

359
Q

What causes secondary haemorrhagic infarcts in focal ischaemic CVA

A

They occur because of reperfusion injury that follows either therapeutic or spontaneous restoration of blood flow

360
Q

How does geography affect the incidence of squamous cell skin carcinoma

A

Live close to equator tend to present SCC at a younger age

Highest incidence: Australia

361
Q

What is the other name for non-communicating hydrocephalus

A

Obstructive hydrocephalus

362
Q

What is the ideal placement for a venous line and why

A

Subclavian vein is ideal placement as lower infection rate

363
Q

Describe the proliferation phase of wound infection

A

Begins as cells that migrate to the site of injury start to proliferate - cellularity of wound increases
Angiogenesis, epithelial cell & fibroblast proliferation
Marginal basal cells migrate across the wound -> epithelialized
Number of inflammatory cells decreases with the increase in stromal cells

364
Q

Describe the incidence of high grade sarcoma

A

Annual incidence of soft-tissue sarcomas ranges from 15 to 35 per 1 million population
The incidence increases steadily with age;
Slightly higher in men than in women

365
Q

How do the lungs recovery from ARDS

A

Recovery can take some time as epithelial necrosis and inflammation prevent the surviving cells from helping to resorb the oedema.

If the inflammatory stimuli decreases, macrophages can start to remove the debris from the alveoli, and they release growth factors which stimulate fibroblasts and collagen deposition.
This leads to fibrosis of the alveolar walls

Type II cells proliferate to repair the alveolar lining - they also replace type I cells, so lining is altered.
Uninjured capillary epithelial cells will also proliferate to repair the endothelium.

366
Q

List the potential GCS scores for eyes

A

4 – Eyes opening spontaneously
3 – Eyes opening to sound
2 – Eyes opening to pain
1 – No response

367
Q

How does DIC eventually increase bleeding risk

A

This widespread formation of clots causes consumption of the clotting factors and platelets which will eventually lead to an increases bleeding risk

This also occurs due to a release of plasminogen which cleaves fibrin and digests clotting factors V and VIII, reducing their availability further
The fibrin degradation products also inhibit platelet aggregation, fibrin polymerisation and thrombin = decreased clotting

368
Q

List possible symptoms seen in a posterior cerebral artery stroke

A
Contralateral homonymous hemianopsia
Cortical blindness
Visual agnosia
Altered mental status
Impaired memory
369
Q

What causes ICP

A

An increase in volume of any one of the intracranial components - brain, CSF, blood

370
Q

The majority of extradural haematomas follow a skull fracture - true or false

A

True

85%

371
Q

How does pulmonary oedema occur in ARDS

A

Endothelial activation and injury makes the capillaries leaky which leads to interstitial and alveolar oedema

372
Q

The type II alveolar cells become damaged in ARDS - true or false

A

True

This reduces surfactant and impacts gas exchange

373
Q

How do lacunar infarcts present

A

The presentation will depend on their location.

They can be clinically silent or they can cause severe neurological impairment

374
Q

Which blood products may be used in DIC and why

A

Blood products such as FFP, platelets and cryoprecipitate can be used to replace the missing components

375
Q

What is wound colonisation

A

Colonisation refers to the presence of microbial organisms within the wound that undergo limited proliferation without evoking a host reaction

376
Q

List the microscopic features of high grade sarcomas

A
Spindle cell pattern
Large pleomorphic neoplastic cells
Hyperchromatic 
Abnormal mitotic figure 
Positive for vimentin by immunohistochemical staining
377
Q

What can cause obstruction to CSF flow

A

Masses

Chiari Syndrome

378
Q

Which genes are associated with lobar intracerebral haemorrhage

A

Apolipoprotein E (ApoE) – e2 or e4 allele increases risk of bleeding

AD forms are assoc. with with APP gene mutations

379
Q

What is the purpose of the dural septae

A

They restrict displacement of the brain, like a seatbelt

380
Q

Describe the role of pressure autoregulation in the autoregulation of cerebral blood flow

A

Arterioles dilate or constrict in response to changes in BP or ICP

381
Q

List some of the complications of treatment for high grade sarcoma

A

Surgery - infection or wound dehiscence
Infection (from immunosuppression)
Postirradiation sarcoma ( usually >10 years after radiation therapy)

382
Q

How does a subarachnoid haemorrhage present

A

Thunderclap’ headache, often rapid neurologic deterioration

Secondary injury may emerge and is associated with vasospasm

383
Q

Describe the appearance of the infarct caused by ischaemia of the border between the anterior and middle cerebral arteries

A

Tends to form a cortical wedge shaped infarct a few cm from the interhemispheric fissure
Infarct usually shows secondary haemorrhagic transformation
Commonly bilateral.

384
Q

List the most common clinical signs of a focal ischaemic CVA

A

The main clinical symptoms are focal neurological deficits that depend on the site of the brain that is effected

May have hemiparesis, monoparesis, quadriparesis, hemisensory deficits, monocular/binocular visual loss, visual field deficits, diplopia, dysarthria, facial droop, ataxia, vertigo, aphasia, sudden drop in conscious level
These signs can be independent but patients tent to have multiple of them

385
Q

DIC has a huge range of clinical presentations which vary with cause - true or false

A

True

386
Q

Discuss the mortality rate for high-grade sarcoma

A

High-grade soft tissue sarcomas over 10 cm in diameter have an approximate 50% mortality rate
Those over 15 cm in diameter have an approximate 75% mortality rate

387
Q

Give an overview of the pathogenesis of ARDS

A
Pneumocyte damage
Endothelial activation 
Neutrophil adhesion and degranulation 
Capillary leakage leading to oedema 
Recovery via resolution of inflammation, fibrosis and proliferation of surviving cells
388
Q

What is the typical mechanism of death in focal ischaemic CVA

A

If enough brain tissue is destroyed then these events can be fatal themselves

The oedema that they cause could also raise the ICP leading to brainstem herniation

389
Q

What is the most common causative organism for infections in ICU

A

Bacteria

390
Q

What causes pressure ulcers

A

Caused by prolonged immobilisation - as seen in ICU.

The pressure causes the skin to be deprived of blood flow, which can result in skin breakdown.

391
Q

Cerebral blood flow can remain constant over which BP range

A

50-150 mmHg

Below or over this blood flow becomes disrupted
Below = artery collapse, impaired dilatation and ischaemia
Above - force causes dilatation, you get increased flow and oedema

392
Q

List some of the complications associated with feeding tubes

A

Risks associated with misplacement

393
Q

What is hydrocephalus

A

It is the buildup of fluid in the cavities (ventricles) deep within the brain

394
Q

How does diffuse axonal injury present

A

Reduced consciousness and coma

Can lead to vegetative state

395
Q

List the consequences of H2 receptor antagonist treatment

A

H2 antagonists have the potential for the development of tolerance, and can have adverse effects (e.g., confusion or agitation)

396
Q

Cerebral amyloid angiopathy commonly causes which pattern of haemorrhage

A

Lobar pattern of intra-cerebral/intra-parenchymal haemorrhage involving the subcortical white mater, often with extension into the SAS

397
Q

How do you diagnose ARDS

A
Requires 4 features to be present:
Acute onset 
Bilateral infiltrates on CXR 
Pulmonary capillary wedge pressure <19mmHg or a lack of clinical congestive heart failure (measured via pulmonary artery catheter 
Refractory hypoxaemia
398
Q

What is another name for reactive gastritis

A

Stress-Related Mucosal Disease

399
Q

Why is the incidence of squamous cell skin carcinoma rising

A

Due to aging population, improved detection, increased use of tanning beds, environmental factors e.g. depletion of the ozone layer

400
Q

Which factors increase the risk of developing reactive gastritis

A

Increasing number of days of mechanical ventilation

Increasing length of ICU stay.

401
Q

What is the most common location for an extradural haematoma

A

Temporoparietal region
Usually due to disruption of middle meningeal artery (anterior branch is vulnerable since it runs under pterion)

Less commonly in the frontal, occipital or posterior fossa regions

402
Q

What can cause decreased absorption of CSF

A

SAH
Meningitis
Malignant meningeal disease

403
Q

How can you prevent additional ischaemic injury from vasospasm in SAH

A

High-fluid intake (.>3500ml/day) and CCBs to prevent vasospasm
CCBs dilate the vessels

404
Q

What causes a focal ischaemic CVA

A

These occur because a localised area of the brain has a reduction or cessation of blood flow due to either partial or complete arterial obstruction

405
Q

Why is HAP often life-threatening in the ICU

A

It is superimposed on the already severe illness.

406
Q

What effect can thrombotic occlusion of the cerebral arteries have

A

The thrombi may cause antegrade extension or fragmentation and distal embolisation

Cause focal CVA

407
Q

List the potential outcomes for someone with ARDS

A

Those that survive will often recover their pulmonary function, but some are left with interstitial fibrosis and chronic pulmonary disease

408
Q

Can wound infection be fatal

A

Yes

77% of deaths of surgical patients were related to surgical wound infection

409
Q

List the microscopic features of basal cell carcinoma

A

Tumor cells resemble those in the normal basal cell layer of epidermis
Arise from epidermis or follicular epithelium
Appear as either a multifocal superficial or nodular pattern
Palisading
Basaloid cells within dermis
In sections, stroma retracts away from the carcinoma -> create clefts or separation artifacts that assist in differentiating basal cell carcinomas

410
Q

What is the most common site for cellulitis

A

The leg

411
Q

What determines the prognosis of a haemorrhagic CVA

A

The severity of the CVA and the location and size of the bleed
Very large bleeds or bleeds that extend into the ventricular system can be devastating

412
Q

Why do the lungs become stiff in ARDS

A

Type II alveolar cells are damaged which leads to a lack of surfactant

413
Q

Where are thrombi commonly found in DIC

A

In the brain, heart, lungs, kidneys, adrenals and liver.

414
Q

List possible symptoms seen in a middle cerebral artery stroke

A

Contralateral hemiparesis and hypaesthesia
Ipsilateral hemianopsia
Gaze preference towards side of lesion
Agnosia
Receptive or expressive aphasia -if lesion in dominant hemisphere
Neglect and inattention

415
Q

What temporary sensation changes may be experienced by ICU patient’s

A

Certain medications can alter hearing or leave a strange taste.
IV feeding can alter taste when patients start eating again - may taste stronger or different
Eyes can be dry and sore from long periods of sedation, or they can be swollen and puffy due to fluid administration.

416
Q

How do you manage a subarachnoid haemorrhage

A

Urgent non-contrast CT for head trauma
If normal do LP = may show xanthochromia
CT angio – identify location of abnormality & provide route for endovascular coiling.
Craniotomy + microsurgical clipping of aneurysm
Secure the aneurysm <48hrs for reduced rupture risk and lower disability rates.

417
Q

List the clinical signs seen if a haemorrhagic CVA occurs in the brainstem

A
Facial weakness
Quadriparesis
Gaze paresis
Occular bobbing
Decreased conscious level 
Autonomic instability
418
Q

Which type of anaemia is seen in DIC

A

Microangiopathic anaemia

Caused by red cells fragmenting as they try to squeeze through the occluded vessels

419
Q

Which types of basal cell carcinoma will get topical therapy

A

Nonrecurring and superficial

Typically low-risk patients with superficial BCC who cannot undergo surgery or radiation

420
Q

DIC is an acquired conditions - true or false

A

True
It occurs as a result of another illness/event
Does not occur on its own

421
Q

What is xeroderma pigmentosum

A

An autosomal recessive disease which results in the inability to repair UV-induced DNA damage
Can lead to squamous and basal cell skin cancer

422
Q

How can causes of increased ICP be classified

A
By their mechanism
Can be: 
Mass 
Brain swelling 
An increase in central venous pressure
423
Q

Where does melanoma typically metastasise to

A

May occur locally - within or around the primary site

In the regional lymph node basins

Or distally:
Remote skin (away from the melanoma scar)
Remote lymph node(s)
Viscera
Skeletal
CNS sites
424
Q

Which sharp force injuries are often seen in RTAs

A

Incisions – May see (‘dicing’ or otherwise) due to shattered glass/ ejection through window/ windscreen

Stab wounds/ puncture wounds – May be the result of impact w/ loose objects e.g. pens (much rarer)

425
Q

What forms the hyaline membranes seen in ARDS

A

The protein rich oedema fluid and dead type II cells become organised into the hyaline membranes

426
Q

What is the most common cause of thrombotic occlusion of the cerebral arteries

A

Acute changes in atherosclerotic plaques

The carotid bifurcation, origin of the middle cerebral artery and both ends of the basilar artery are the most common sites effected

427
Q

List risk factors for squamous cell skin cancer

A

UV exposure - fair skin and albinism make you vulnerable
Immunosuppression -Iatrogenic and noniatrogenic e.g. in organ transplant recipients or HIV patients respectively
carcinogens
HPV infection
Hydrochlorothiazide use
Dermatoses e.g. Xeroderma pigmentosum, Dystrophic epidermolysis bullosa, Epidermodysplasia verruciformis, Erosive lichen planus

428
Q

Describe the morphological appearance of old intracerebral haemorrhages

A

Areas of parenchymal cavitary destruction with a rim of brownish discolouration.

429
Q

List the potential limitations of GCS scoring

A

Assessment impaired by intoxication
Poor reproducibility between clinicians, especially motor responses
Often reported as a total score rather than constituent parts – same score may predict vastly different outcomes depending on point distribution
May miss unilateral pathology

430
Q

What are the 3 components within the skull

A

Brain -80%

Blood - 10%
Cerebrospinal fluid -10%
100-150ml of each

431
Q

Describe the mortality of focal ischaemic CVA

A

The Framingham and Rochester stroke studies suggested that the 30 day mortality was 19% and that the 1yr survival rate was 77%
The prognosis will however depend upon the individual patients, their premorbid condition and age, post stroke complication and the severity of the event

432
Q

Describe the natural progression of basal cell skin carcinoma

A

They enlarge slowly
Rarely metastasise
Do need treated as they can be locally destructive
They can become large, cause disfigurement, spread to other parts of body and cause death

433
Q

What is intracerebral haemorrhage

A

Rupture of small intraparenchymal vessel leading to primary haemorrhage within brain

434
Q

Describe the natural history of SAH

A

25-50% die with the first rupture
Those that survive often improve and recover consciousness in mins
Repeat bleeding is common and unpredictable; prognosis worsens with each bleed

435
Q

What is the most common cause of wound infection following vascular surgery

A

S aureus, Staphylococcusepidermidis, gram-negative bacilli

436
Q

What is the most common antibiotic used to treat wound infection

A

Cefazolin 1-2g

Used for all except colorectal surgery wounds (they use Cefotetan or cefoxitin plus oral neomycin and oral erythromycin)

437
Q

List the mechanisms involved in the autoregulation of cerebral blood flow

A

Pressure autoregulation
Metabolic autoregulation

CO2 levels

438
Q

List some inhaled irritants that can cause ARDS

A

Oxygen toxicity
Smoke
Irritant gases or chemical

439
Q

List the 3 main phases of wound infection

A

Inflammatory phase
Proliferative phase
Maturation phsae

440
Q

What is the main cause of lacunar infarcts

A

Hypertension that effects the deep penetrating arteries that supply the basal ganglia, hemispheric white matter and brainstem

441
Q

List some of the serious illnesses that can result from cellulitis

A

Lymphangitis , abscess formation and gangrenous cellulitis or necrotizing fasciitis

Spreads along deep fascia – high mortality if spread to trunk (cannot move) -> cyanotic or septic shock

GABHS and S. aureus produce toxins that may mediate a more severe systemic infection -> septic shock -> death

442
Q

Which cancers are associated with intra-parenchymal brain haemorrhage

A

High-grade gliomas or certain metastases - melanoma, choriocarcinoma, RCC

443
Q

What causes Kaposi sarcoma

A

Seen in patients with HIV/AIDS

Caused by infection with the human herpesvirus type 8

444
Q

List early signs and symptoms of a raised ICP

A
Decreased level of consciousness
Headache
Pupillary dysfunction +/- papilloedema
Changes in vision
Nausea and vomiting
445
Q

List non-medical/surgical management options for raised ICP

A

Maintain head in midline to facilitate blood flow
Loosen tube ties, collars etc.
Put head of the bed at 30-45 degrees elevation
Avoid gagging, coughing etc.
Decrease environmental stimuli
Treat hyperthermia
Maintain fluid balance and normal electrolytes
Maintain normocarbia

446
Q

Describe the role of inflammatory mediators in diffuse axonal injury

A

Pro- and anti-inflammatory mediators; cytokines and interleukins appear to have a role
IL-6 levels are higher in non-survivors

447
Q

Which patients are most at risk of haemorrhagic CVA due to CAA

A

CAA is most common in the elderly so they are at most risk

Polymorphisms in ApoE resulting in the presence of E2 or E4 increase the risk of haemorrhagic CVA in patients with CAA

448
Q

List some hematological conditions that can cause ARDS

A

Transfusion-associated lung injury

DIC

449
Q

All infarcts in focal ischaemic CVA will start out as non haemorrhagic infarcts/ischemic infarcts - true or false

A

True

This is because the brain has an end arterial supply and a lack of collaterals

450
Q

List the potential GCS scores for movement response

A
6 – Obeys commands 
5 – Localises to pain 
4 – Normal flexion/ withdrawal from pain 
3 – Abnormal flexion to pain 
2 – Abnormal extension to pain
1 – No response
451
Q

List the clinical signs seen if a haemorrhagic CVA occurs in the putamen

A

Contralateral sensory loss and hemiparesis
Contralateral conjugate gaze paresis
Aphasia
Neglect
Apraxia - inability to perform learned (familiar) movements on command
Homonymous hemianopia

452
Q

List potential causes of focal ischemic CVA

A

Embolism
Fat or bone marrow emboli
Thrombotic occlusion of the cerebral arteries
Inflammatory conditions

453
Q

List risk factors for melanoma

A

Exposure to sunlight, particularly UV-B radiation
Light-colored skin
Presence of freckling and benign nevi
Genetics – familial atypical multiple mole and melanoma (FAMMM) syndrome

454
Q

How do you treat basal cell carcinoma

A

Removal of the tumour with the best possible cosmetic result
If fat is reached -surgical excision
Topical Treatment - e.g. topical 5-fluorouracil 5%
Radiation
Photodynamic therapy
Systemic Retinoids
Hedgehog Pathway Inhibitors e.g. Vismodegib, Sonidegib
Checkpoint Inhibitor

455
Q

Why might ICU patients end up with voice changes after their stay

A

Being on a ventilator can cause someone’s voice to change due to a sore throat and extremely dry mouth

456
Q

Is reactive gastritis reversible

A

Yes
If the underlying cause is treated the mucosa will heal via complete re-epithelialisation within days to weeks.
In a healthy patient the lesions do not recur.

457
Q

Which areas of the brain are typically affected by lacunar infarcts

A

In descending order of frequency ;

Putamen, globus pallidus, thalmus, internal capsule, deep white matter, caudate nucleus and pons

458
Q

Describe the role of excitotoxicity in diffuse axonal injury

A

Excitatory amino acids (glutamate) activate NMDA receptors

Ca2+ mediated activation of proteases and lipases

459
Q

List some of the long term complications of ICU

A
Weakness and stiffness 
Fatigue 
Loss of appetite and weight loss 
Sleep problems 
Depression, anxiety and PTSD 
Issues with mental ability/cognition
Skin and hair changes 
Temporary sensation changes 
Breathing issues 
Voice changes 
Incontinence
460
Q

Why do people in ICU experience weight loss

A

Associated with a loss of appetite

The weight loss can be due to muscle loss

461
Q

List potential causes of pulmonary oedema due to alveolar wall injury

A
Infections - e.g. bacterial pneumonia 
Lung trauma  
Liquid aspiration - gastric content or near drowning
Inhales gases - high O2, smoke 
Radiation
Systemic inflammatory response syndrome - sepsis, burns etc.
Blood-transfusion related 
Drugs and chemicals - chemo agents etc.
462
Q

What is the most common cause of haemorrhagic CVA

A

Hypertension

It is responsible for >50% of clinically significant haemorrhages

463
Q

Which organisms are the most common of cellulitis in the elderly/diabetics (general cases)

A

GAS

S aureus

464
Q

What is more common malignant or benign soft tissue tumours

A

Benign soft-tissue tumors occur at least 10 times more frequently than malignant ones

465
Q

How does immunosuppression lead to squamous cell skin carcinoma

A

It reduces host surveillance and increasing the susceptibility of keratinocytes to infection and transformation by viruses, particularly HPV subtype 5 and 8

E.g. chronic immunosuppression as a result of chemotherapy/organ transplantation

466
Q

Which surgical therapies are used for the treatment of high-grade sarcoma

A

Complete local excision for benign soft-tissue tumors

Extremity sarcoma may get larger surgery such as: 
Intracapsular excision and amputation
Marginal excision and amputation
Wide excisions and amputation
Radical excision and amputation
467
Q

What is ARDS

A

a clinical syndrome of progressive respiratory insufficiency caused by diffuse alveolar damage in the setting of sepsis, severe trauma or diffuse pulmonary infection

468
Q

At which ICP is intervention required

A

A value above 20mmHg usually signifies the point at which intervention may be required to avoid significant or life-threatening consequences.

469
Q

How do you treat melanoma

A

Biopsy – evaluate the thickness of lesion
Excisional biopsy – for small lesions or large lesions in cosmetically favorable locations
Punch biopsy
Excision
Mohs micrographic surgery
Adjuvant systemic therapy for:
(1) those with stage IIB or III with high risk of recurrence
(2) distant metastases

470
Q

What causes a Curling ulcer in reactive gastritis

A

These occur in the proximal duodenum following severe burns or trauma

471
Q

How can intracranial disease lead to reactive gastritis

A

The GI lesions are thought to occur as a result of direct stimulation of the vagal nuclei which triggers gastric acid hypersecretion

472
Q

Which wound characteristics can increase the risk of wound infection

A

Nonviable tissue in wound
Haematoma
Foreign material
Pre-existent sepsis

473
Q

List some of the complications of a focal ischaemic CVA

A

1/2 of patients will be left with some from of disability/ neurological deficit - will depend in the severity and location of the infarct
There is however usually some improvement in the patients condition in the first few months following the stroke

474
Q

What causes endothelial injury in DIC

A

Can occur due to inflammation, antigen-antibody complexes, extreme temperatures and microorganisms.
Leukocytes damage cells by releasing ROS and proteases

475
Q

What causes global cerebral ischaemia

A

This occurs when there is a generalised reduction of cerebral perfusion (i.e. due to shock, severe hypotension or cardiac arrest) or if the blood is not able to carry as much O2 ( i.e. CO poisoning)

476
Q

What is the most common cause of wound infection following colorectal surgery

A

Gram-negative bacilli and anaerobes

477
Q

How do you diagnose DIC

A

Based on clinical observation and blood tests.

Blood tests include: 
Fibrinogen levels
Platelets
PT and PTT 
D-dimers
478
Q

If the occlusion that is causing a focal ischemic CVA is in a large artery what is the most likely cause

A

An emboli

479
Q

List some physical injuries that can cause ARDS

A
Mechanical trauma - including head injury
Pulmonary contusions
Near-drowning
Fractures with fat embolism
Burns 
Ionising radiation
480
Q

Describe the features of a class 3 - contaminated surgical wound

A

Nonpurulent inflammation present
Gross spillage from gastrointestinal tract
Penetrating traumatic wounds < 4 hours
Major break in aseptic technique

481
Q

List the microscopic features of ARDS in the organisation phase

A

In this stage, type II pneumocytes proliferate and granulation tissue forms in the alveoli (walls and spaces)

In most cases this resolves but in some fibrotic thickening occurs which is scarring.

482
Q

Any disruption of O2 supply to the brain will cause damage to the brain - true or false

A

True
This is because it can no longer meet its energy requirements
Can be due to reduced perfusion or hypoxemia

483
Q

Describe a spreading wound infection

A

Spreading infection describes the invasion of the surrounding tissue by infective organisms that have spread from a wound

484
Q

Which organisms are the most common of cellulitis in hospital acquired cases

A

<24 hours postoperatively: GABHS or Clostridium perfringens

Acinetobacter baumannii – emerging multidrug-resistant pathogen

485
Q

List late signs and symptoms of a raised ICP

A
Coma
Fixed, dilated pupils
Hemiplegia
Cushing’s triad - bradycardia, increase BP and altered respiration pattern
Hyperthermia
Increased urinary output
486
Q

Describe the pathological features of haemorrhagic CVA

A

A central core of clotted blood that will compress the adjacent parenchyma is found within acute primary parenchymal haemorrhages .
The compression that this clotted blood causes will lead to secondary infarction of the effected tissue and so anoxic neuronal injury, glial changes and oedema will be seen
Over time the oedema will resolve and there will be an appearance of heamosiderin and lipid laden macrophages. Additionally there will be proliferation of reactive astrocytes at the lesions edges
The cellular events follow the same time course as cerebral infarction (Focal Ischemic CVA infarctions)
Once the haemorrhage is old there will be areas of parenchymal cavitary destruction that have a rim of brownish discolouration

487
Q

What is the normal ICP in an older child

A

10-15 mmHg

488
Q

Basal cell carcinoma rarely metastasise - true or false

A

True

489
Q

Why does in increase any one of the intracranial components cause an increase in pressure

A

Because the cranium is fixed - cannot accommodate change

490
Q

Describe the pathological features of lobar intracerebral haemorrhage caused by CAA

A

Amyloidogenic peptides are deposited in vessel walls - makes them rigid
The deposits also weakens vessel wall and can cause haemorrhage

Looks similar to hyaline arteriosclerosis on H&E stain except the material in CCA consists of beta-amyloid rather than collagen and is in a different location

491
Q

What is the most common mechanism of death from haemorrhagic CVA

A

The build up of blood in the tissue and associated cerebral oedema raising the ICP and causing herniation of the brainstem

492
Q

How can you prevent pressure ulcers

A

Routine position changes done to reduce risk

493
Q

List potential complications of endovascular embolisation of an aneurysm

A

Thromboembolic events or perforation of the aneurysm

494
Q

Which type of cellulitis is seen in children under 3

A

Buccal cellulitis caused by H influenzae type B

Perianal cellulitis with GABHS

495
Q

Which molecule is being considered as a new biomarker for traumatic brain injury

A

Plasma levels of von Willebrand factor
May also be able to indicate severity

VWF is a glycoprotein released in endothelium in response to local trauma - indicator of traumatic microvascular injury.
It can act as a biomarker of cerebrovascular pathology
Increased expression of the factor is associated with vascular and neurodegenerative dementia

496
Q

When is surgical resection and adjuvant therapy used in the treatment of high grade sarcoma

A

For recurrent and metastatic disease

497
Q

What is photodynamic therapy

A

Process of using specific wavelengths of light to photoexcite porphyrins
Used in the treatment of BCC

498
Q

List the macroscopic features of ARDS

A

Lungs are heavy, firm, red and boggy in the acute phases.

Lesions are not evenly distributed so some areas are stiff and poorly ventilated whilst others remain normal.

499
Q

How long can it take to recover from an ICU stay

A

These issues can persist for several months and may require ongoing treatment.
E.g., physical recovery can take up to 18 months and will require slowly building up strength.

500
Q

List some of the complications associated with ventilators

A

They are the biggest risk factor for hospital-acquired lung infection.
Thought to be because its easier for bacteria to get in as bypassing the defenses of nose and mouth

Can cause barotrauma (injury to body due to changes in barometric (air) or water pressure) or even GI bleeds.

Some patients may experience weaning errors

501
Q

List common sources of emboli that occlude the cerebral vessels

A

Cardiac mural thrombi are most common

Thromboemboli from atherosclerotic plaques, most commonly in the carotids, are the second most common

Rarer sources of the emboli include; paradoxical emboli, fat, tumour and air emboli or thromboembolic emboli from cardiac surgery

502
Q

What are the 3 most common sites of hospital acquired infection

A

Lungs
Blood
Urine

503
Q

List the symptoms of ARDS

A

Severe dyspnoea and tachypnoea
Tachycardia

Progresses to:
Respiratory failure
Hypoxaemia - often refractory in response to O2
Cyanosis
Peripheral vasodilation
Bilateral fine inspiratory crackles
Respiratory acidosis - lungs not functioning
Lungs become stiff due to a lack of surfactant

504
Q

List the microscopic features of reactive gastritis

A

Acute stress ulcers are well demarcated, and the adjacent mucosa is typically normal.

Serositis may be present.