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EXAM Prep Flashcards

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1
Q

Types of Traumatic Neurological Emergency Presentations:

A

Traumatic Brain Injury TBI: Concussions, Contusions, Skull Fractures, Traumatic Subdural/ Subarachnoid Haemorrhage

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2
Q

Symptoms of Traumatic Neurological Presentations

A

Headache

Confusion

Loss of Consciousness

Seizures

Focal Neurological deficits

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3
Q

Types of Non-Traumatic Neurological Presentations:

A

Stroke (Ischaemic or Haemorrhagic)

Seizures (Generalised or Focal)

Meningitis / Encephalitis

Brain Tumours

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4
Q

Pathophysiology of Ischaemic Stroke

A

Occlusion of a cerebral artery, leading to decreased blood flow and ischemia

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5
Q

Assessment of Ischaemic Stroke

A

Fast acronym (Face, Arms, Speech, Time)

CT scan to differentiate from Haemorrhagic Stroke

Neurological observations

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6
Q

Management of Ischaemic Stroke

A

Reperfusion

Thrombolytics (e.g. tPA) if within time window

Antiplatelet therapy and rehabilitation

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7
Q

Pathophysiology of Haemorrhagic Stroke

A

Rupture of a blood vessel in the brain, leading to increased intracranial pressure

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8
Q

Assessment of Haemorrhagic Stroke

A

Fast acronym (Face, Arms, Speech, Time)

CT scan to differentiate from ischaemic stroke

Neurological observations and Vital signs

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9
Q

Management of Haemorrhagic Stroke

A

Control of blood pressure (aim for less than 140mm Hg)

Surgical Intervention (e.g. Clipping or coiling of aneurysms)

Regular monitoring for complications

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10
Q

Thunderclap Headache is more likely to be symptom of what stroke

A

Haemorrhagic

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11
Q

What is autoregulation

A

The brain’s ability to maintain constant blood flow despite changes in perfusion pressure.

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12
Q

What is Cerebral Perfusion

A

CPP = Mean Arterial Pressure (MAP) - Intracranial Pressure (ICP). Normal CPP is crucial for adequate brain function. CPP should be maintained above 70-80mmHg

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13
Q

Nursing Care of The Patient Presenting with a Neurological Emergency

A

Management of Airway / breathing: Ensure airway is clear, administer oxygen as needed, intubation may be required.

Continuous monitoring of neurological status, vital signs

Administering medications

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14
Q

Interventions to Decrease ICP

A

Hyperventilate: Aim for 30 -35 CO2

Head up elevated 30 degrees

Use tape rather than tube ties if patient is intubated

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15
Q

Diabetes as a Co-morbidity to Neurological Presentations

A

Factor of atherosclerosis, significant impact on cardiovascular system, can compete with stroke management and recovery

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16
Q

Diabetes Management as a Co-morbidity to Neurological Emergencies

A

Maintain tight glycaemic control to reduce complications and improve outcomes

Monitor blood glucose levels regularly

Work with a diabetes educator or specialist when needed for comprehensive care.

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17
Q

Cushing’s Triad

A

Bradycardia

Widened pulse pressure

Irregular respirations

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18
Q

Pathophysiology of Haematology and Oncology Presentations

A

Nadir = Period after chemotherapy when blood counts are at their lowest (usually 7-14 days after chemotherapy)

Neutrophils are involved in the acute inflammatory response to infection and the removal of bacteria by phagocytosis.

Low levels of WBC make it harder for the body to fight infection making patients more susceptible to infection

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19
Q

Nursing and Medical Assessment, Interventions and Management for Febrile Neutropenia

A

Comprehensive patient assessments (history, physical exams, lab tests)

Aim to identify source (blood cultures, chest x-ray, specimens and swabs)

Administer broad spectrum intravenous antibiotics (IVABs) within 30 minutes of presentation (take blood cultures prior if able)

Collaborate with multidisciplinary teams (e.g. ICU, or med Onc) for holistic management

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20
Q

Complications of Chemotherapeutics

A

Febrile Neutropenia

Thrombocytopenia (bleeding risk)

Anaemia (hypoxia)

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21
Q

Common Side Effects of Chemotherapeutics

A

Nausea

Vomiting

Fatigue

Alopecia

Myelosuppression

Increased Infection Risk

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22
Q

Management Strategies for Complications and Side effects of Chemotherapeutics

A

Use of antiemetics

Growth factors

Pain management

Supportive care

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23
Q

Assessment of Dental Conditions

A

Monitor for oral mucositis, infections and dental cavities especially in immunocompromised patients

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24
Q

Assessment of ENT conditions

A

Assess for hoarseness, stridor, dysphagia and hearing loss

Also ask patient to open mouth properly. Look for swelling and how fast patient opened their mouth

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25
Interventions for Dental and ENT Conditions
Drainage of the abscess Referral to specialist teams Management of pain Treatment of Infection
26
Pathophysiology of Depression and Anxiety
Depletion of serotonin or dopamine, symptoms = low mood (depression), Anxiety = overwhelming feelings of worry, nervousness and fear, neurochemical dysregulation
27
Assessment of Depression and Anxiety
Use standardised tools Clinical interviews Be respectful Establish a rapport Speak calmly and in short sentences, Assess suicide risk or harm to others
28
Management of Depression and Anxiety
Consider psychotherapy Pharmacotherapy (SSRIs and SNRIs) Referral to mental health team, Encourage other supports Support healthy coping mechanisms.
29
Pathophysiology of Hyperthermia and Heat Related Illness
Hyperthermia occurs when the body produces or absorbs more heat than it can dissipate Mechanisms include: - Impaired thermoregulation - Excessive heat production
30
Assessment of Heat Exhaustion
A-E primary survey Skin temperature and moisture Mental status evaluation Symptoms: Heavy sweating, weakness, dizziness, nausea, headache Core temp <40 degrees Celsius
31
Assessment of Heat Stroke
Primary survey Skin temperature and moisture mental status evaluation Symptoms: Altered mental status, cessation of sweating, rapid heart rate, hypotension, seizures, and hot and dry skin Core temp >40
32
Management of Hyperthermia and Heat Related Illness
Supportive care and management of complications Intubation + muscle relaxants to prevent shivering Administer cool IV fluids Remove clothing Continuous assessment of vital signs and neurological status.
33
Assessment of Orthopaedic / Musculoskeletal Trauma
Initial Survey: A-E History: Mechanism of injury, pain level and functional ability Neurovascular observations Physical Exam: Inspect for deformities, swelling, bruising and range of motion
34
5 Ps of the Neurovascular Assessment
Pallor Pulselessness Pain Paraesthesia Paralysis
35
Management Strategies for Orthopaedic / Musculoskeletal Trauma
Immobilisation: Use splints, casts, traction to stabilise fractures Pain Management: Administer analgesics as needed Surgical Intervention: May be necessary for severe fractures or dislocations Procedural sedation: For painful relocation and casts.
36
Nursing Care for Orthopaedic / Musculoskeletal Trauma
Pain relief Regular neurovascular assessments Elevating effected limb Assistance with ADLs
37
Complications for Orthopaedic / Musculoskeletal Trauma
Compartment syndrome DVT Non-union of fractures
38
Confounding Factors in Trauma Management
Age, pre-existing conditions and comorbidities Medications and anticoagulants (can mask signs of shock, increased risk of injury) Older age, paediatric patients, obesity.
39
Pathophysiology of Blunt Abdominal Trauma
Caused by non-penetrating forces (e.g. Motor vehicle accidents, falls). It may lead to organ laceration, contusion, or haemorrhage without disrupting the skin
40
Assessment of Blunt Abdominal Trauma
Mechanism of injury, associated symptoms (e.g. Pain, nausea), look for signs of internal bleeding (hypotension, tachycardia), tenderness, distension or rigidity, ultrasound (FAST), CT scan for abdominal injuries
41
Management of Blunt Abdominal Trauma
Stabilisation (IV fluids, blood products as needed), surgery may be required for significant haemorrhage or organ injury, monitoring for complications such as compartment syndrome or delayed haemorrhage.
42
Pathophysiology of Penetrating Abdominal Trauma
Involves an object piercing the abdomen (e.g. Stab wounds, gunshot wounds). The injury may directly damage organs or cause bleeding
43
Assessment of Penetrating Abdominal Trauma
History (type of weapon, depth of injury), Examine for entry and exit wounds, signs of peritonitis (rebound tenderness, guarding), CT scan or diagnostic peritoneal lavage may be used.
44
Management of Penetrating Abdominal Trauma
Immediate surgical intervention often needed for repair and to control bleeding, prophylaxis for infections and ongoing monitoring for sepsis
45
Assessment for Abdominal Trauma
Continuous monitoring of vital signs and signs of shock Thorough abdominal assessment (inspection, palpation, percussion, auscultation) Monitoring for changes in mental status indication potential hypovolemia or sepsis
46
Interventions for Abdominal Trauma
Administer IV fluids and blood products as ordered Pain management Prepare for possible surgical interventions Educate the patient and family about the condition and treatment plan
47
Complications of Abdominal Trauma
Infection (peritonitis, abscess formation) Organ failure (Kidney, liver) Chronic pain or gastrointestinal dysfunction
48
Management of Abdominal Emergencies in the Elderly
Comorbidities: Elderly patients often have multiple health issues that complicate diagnosis and treatment (e.g. Diabetes, cardiovascular disease) Atypical Presentations: Symptoms may be less pronounced (e.g. Altered mental status instead of pain) Medication Effects: Increased sensitivity to medications and potential for adverse drug interactions Surgical Risks: Higher operative risks and longer recovery times
49
ATOD Assessment
Determine the type and amount of alcohol, tobacco and other drugs used Evaluate for withdrawal symptoms or overdose signs
50
ATOD Interventions
For alcohol withdrawal, consider medications like benzodiazepines and monitoring in a safe environment. Provide counselling and support for cessation Refer to addiction services if needed
51
Nursing and Medical Care for Patients With ATOD Dependence
Monitor for complications of ATOD use (e.g. Liver disease from alcohol, respiratory issues from tobacco) Provide education on the risks of continued use and benefits of cessation Implement harm reduction strategies as appropriate. ETOH or other withdrawal scores
52
Pathophysiology of DKA
Occurs due to absolute insulin deficiency. Lack of insulin leads to increased lipolysis, producing free fatty acids that are converted to ketones, causing metabolic acidosis. More commonly found in T1DM.
53
Pathophysiology of Hyperglycaemic Hyperosmolar State (HHS):
Characterised by severe hyperglycaemia, significant dehydration, and high serum osmolality without significant ketoacidosis. Insulin levels are of sufficient to prevent ketogenesis but inadequate to control blood sugar levels. More commonly found in T2DM.
54
Fluid and Electrolytes in DKA
DKA typically involves dehydration, electrolyte imbalances (especially potassium) and acidosis due to ketone accumulation.
55
Presentation of DKA
Rapid onset (hours to days), polyuria, polydipsia, weight loss, abdominal pain, vomiting, fruity breath (due to acetone), altered mental status
56
Presentation of HHS
Presentation: Gradual onset (days to weeks), polyuria, polydipsia, confusion, lethargy, severe dehydration, hypotension, and elevated serum osmolality.
57
Medical Management of Diabetes
Insulin Therapy: Initiated in both DKA and HHS to lower blood glucose Fluid Resuscitation: Isotonic saline in DKA; may start with normal saline in HHS, transitioning to 0.45% if hypernatremia is present. Electrolyte Management: Monitoring and replacement of potassium, magnesium and phosphate as needed. Laboratory Values: Blood glucose, electrolytes, ketones and regular venous blood gases.
58
Nursing Management of Diabetes
Monitoring: Vital signs, neurological status, fluid intake/output. Education: Importance of adherence to medication, dietary management, recognising symptoms of hypo/hyperglycaemia and when to seek help Support: Emotional and psychological support, especially for patients experiencing severe illness.
59
Microvascular Complications with Diabetes
Retinopathy: Damage to retinal blood vessels, leading to vision loss Nephropathy: Kidney damage due to chronic hyperglycaemia, leading to end-stage renal disease Neuropathy: Nerve damage causing pain, tingling or loss of sensation.
60
Macrovascular Complications with Diabetes
Increased risk of cardiovascular diseases (CVD) due to atherosclerosis, leading to heart attack and stroke.
61
Pathophysiological Changes With Diabetes
Persistent hyperglycaemia leads to glycation of proteins, resulting in vascular and nerve damage Inflammation and oxidative stress contribute to complications, exacerbated by metabolic syndrome.
62
Fluid and Electrolytes in HHS
HHS involves profound dehydration and hypernatremia, with potential electrolyte imbalances but typically less severe than in DKA.
63
Core temp > 41 degrees increasingly leads to what?
Protein denaturing Loss of energy producing processes Loss of cell membrane function
64
Management of HHS
Fluid replacement (more aggressive than in DKA), insulin therapy (often less intensive) and careful monitoring of electrolytes.
65
Management of DKA
Immediate insulin therapy, fluid replacement (with isotonic fluids) electrolyte monitoring (especially potassium) and treatment of acidosis.
66
Cushing's Triad: Widening pulse pressure
As ICP becomes higher than MAP, CPP decreases. CNS is activated in response causing vasoconstriction to increase MAP to maintain CPP resulting in widening pulse pressures.
67
Cushing's Triad: Bradycardia
The baroreceptors at the aortic arch and carotid sinuses sense the increased BP and stimulate the vagus nerve in response slowing down the heart rate.
68
Cushing's Triad: Irregular breathing
Increased ICP compresses the brainstem particularly the medulla and pons which regulate breathing leading to abnormal breathing patterns and Cheyne-stokes
69
Monro Kellie Doctrine
Within a fixed volume an increase in one component will show reciprocal decrease in the other remaining 1 or 2 Increased ICP results in decreased CSF and blood flow
70
Special court in abdo traumas
Kids: Blood loss differs, soft bones / less abdo protection Elderly: comorbidities, poly pharmacy, less physiological reserve Obstetrics: Placental abruption, Uterine rupture, feto-maternal haemorrhage
71
GCS and head injury characterisation
GCS 14-15 - mild head injury GCS 9-13 - Moderate head injury GCS 3-8 - Severe Head Injury

Emerg Nursing (1 decks)

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