test 1 Flashcards

(77 cards)

1
Q

pathophysiology of raised ICP

A
  • the cranium is a closed box and there is no space for its contents to expand
    -when intracranial pressure increases
  • the pressure compresses the blood vessels in the brain which reduces blood flow
    -this causes hypoxia of blood tissue and hypoxic brain tissue becomes oedematous and further decreases blood flow, which further increases intracranial pressure
    -as a result of brain oedema, the drainage of CSF decreases which can also increase the ICP.
    -there is an increased level of carbon dioxide in the brain which can lead to tissue necrosis
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2
Q

what are the causes of ICP

A
  • cerebral oedema
  • space occupying lesions such as tumours, haematomas
  • Increased in arterial blood flow, for example in respiratory failure
  • A decrease in venous drainage, for example jugular obstruction, the head-down position or straining
  • An obstruction to the flow of Cerebrospinal fluid (CSF), for example congenital abnormalities e.g. hydrocephalus or following trauma e.g. scull fractures
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3
Q

what are the clinical manifestations

A
  • Restlessness, headache, confusion
  • Loss of consciousness, convulsions, projectile
    vomiting
  • Decorticate/decerebrate posture or spasms
  • Reduced response to sensory stimuli
  • Cushing’s triad of symptoms: raised systolic blood
    pressure (widened pulse pressure), slow bounding pulse and papilledema
  • Focal neurological signs, such as abnormal pupil
    reactions
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4
Q

Explain cushings triad as a main symptom of ICP

A

increased systolic bp
decreased pulse and respiration

hypertension, bradycardia, apnea (irregular respirations)

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5
Q

what is meningtitis

A

Infection and Inflammation of the lining around the brain and spinal cord Caused by bacteria, viruses, fungi or parasites.

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6
Q

what is the difference between septic and aseptic meningitis

A

septic
Meningitis is caused by bacteria
Characterized by pus formation
Contagious and fatal
Epidemic form (outbreak)

aseptic
Infection with other infectious agents
Meningitis caused by viruses
Not life threatening
Common type and contagious

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7
Q

pathophysiology of meningitis

A

In meningitis, the meninges become swollen and inflamed

Inflammatory exudate increases intracranial pressure

Infection causes an increases in CSF production

The inflammatory reaction causes irritation of the cerebral tissues

The meninges become inflamed and irritated

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8
Q

relate the pathophysiology to the clinical manifestations

A

Fever- Meninges become swollen and inflamed.

Neck stiffness and headache -Because of the inflamed and irritated meninges

Convulsions, -The inflammatory reaction causes irritation of cerebral tissues.

Hydrocephalus-Inflammatory scar tissue may block the CSF drainage channels.

Epilepsy -Because of scar tissue in the meninges

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9
Q

what are the clinical manifestations

A

fever, headache and neck stiffness, epilepsy, hydrocephalus, convulsions, positive kernigs and brudzinski;s sign, photophobia, skin lesions and rashes, classic triad

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10
Q

definition of epilepsy and what is primary and secondary

A

A convulsion or fit is often a symptom of underlying disease. Most convulsions are idiopathic.

primary- idiopathic
secondary- cause is known and epilepsy is a symptom of another underlying condition

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11
Q

causes of epilepsy

A

-Trauma such as birth injuries
-Congenital defects of the central nervous system
-Inborn errors of metabolism
-Infectious diseases e.g. meningitis and/or encephalitis
-Hyperpyrexia (Children): febrile convulsions
-Brain tumours
-Vascular lesions
-Acidosis, hypoxia and or electrolyte disturbances
-Drug or alcohol intoxication

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12
Q

pathophysiology of epilepsy

A

In a normal brain they are billions of neurons which can be either excitatory or inhibitory. Excitatory neurons stimulate others to fire action potentials and transmit electrical impulses while inhibitory neurons suppress this process to prevent excessive firing therefore a balance between inhibition and exhibition of neurons is essential for normal brain functioning

In Epilepsy there is an up regulation of excitatory neurons and down regulation of inhibitory neurons causing lots of neurons to fire synchronously at the same time

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13
Q

petit mal epilepsy (absence seizures)

A

This is characterised by a sudden and momentary blankness of expression or a facial or a limb twitch. The patient does not usually fall and incontinence is unusual. Blank stare, lip smacking or eye blinking.

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14
Q

grand mal epilepsy

A

This is characterised by a generalised convulsion that follow a definite pattern.There is usually an aura followed by the tonic stage, the Clonic stage and finally the convulsive stage. The patient usually loses consciousness and passes from the unconscious state into a deep sleep. There may be incontinence of urine and faeces during the seizure. The patient may also injure themselves during the seizure by biting their tongue or hitting objects when falling

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15
Q

partial seizures

A

Partial seizures do not involve the whole of the brain they occur within a limited part of the brain.
Simple partial seizures such as jacksonian seizures do not entail any alteration in consciousness however a complex partial seizure are accompanied by a loss of consciousness.

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16
Q

tonic seizures

A

Are associated with stiffening of muscles or increased muscle tone and may cause the person to fall often backwards

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17
Q

atonic seizures

A

Are characterised by sudden loss of muscle tone which may cause the person to collapse or drop down

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18
Q

clonic seizures

A

Are associated with rhythmic jerking muscle movement most commonly affecting neck, face, arms and legs

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19
Q

myoclonic seizures

A

Sudden brief jerks or twitches of muscles. Patient’s typically react as if they are hit by a jolt of electricity.

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20
Q

tonic clonic seizures

A

These are a combination of muscles stiffening and jerking. It also involves a sudden loss of consciousness and loss of bladder control

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21
Q

what are the drug therapies used in epilepsy

A

phenobarbital- all forms of epilepsy except petit mal or myoclonic seizures

phenytoin- all forms of epilepsy except petit mal or myoclonic seizures

primidone- used orally to control generalised tonic clonic (grand mal) and focal seizures

Valproic acid – All forms of epilepsy. Drug of first choice in the treatment of tonic-clonic seizures as part of the syndrome of generalized epilepsy.

Carbamazepine – used as a first-line agent for the management of generalized and focal seizures – not effective in the treatment of absence seizures (petit mal) or atonic seizures.

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22
Q

what is status epilepticus

A

most serious complication. it usually consists of recurrent seizures with no interval of normal consciousness in between. this can lead to brain damage and hypoxia

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23
Q

Factors that precipitate status epilepticus include:

A

interruption of anticonvulsant medication,
fever,
concurrent infection or
other illness.

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24
Q

systemic lupus erythematosis

A

(SLE) is a chronic autoimmune disease where the body attacks its own tissues causing inflammation and damage

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25
risk factors for CVD
-pre existing disease such as HPT which puts strain on the heart -age, the older you are, the more likely to develop atherosclerosis -gender (females are less prone to atherosclerosis than males except after menopause when there is no oestogen) -smoking (nicotine causes damage to arterial endothelium which increases clotting and making platelets more sticky which increases coagulability of the blood.
26
what are the causes of impaired cerebral circulation
Transient ischaemic attacks Cerebral thrombosis Cerebral embolism
27
Transient ischaemic attacks
Temporary dysfunction due to ischemia. Blood flow to the brain decreases or stops for period of time. The onset attack is rapid and last less than 24 hours. most TIA's last 30 mins
28
Cerebral thrombosis
This type of stroke is usually due to atherosclerotic occlusion. The onset is gradual occurring over hours or even days
29
atherosclerotic occlusion
plague forms on the lining of the arteries, the plague grows and the lining of the artery gets damaged and the plaque ruptures which leads to a big clot forming and limits and blocks the blood flow.
30
Cerebral embolism
Cerebral embolism is caused by blood atheromatous material that is broken off from the arterial wall or pieces of calcified heart valves in patients with rheumatic heart disease. The onset is abrupt and are not typically preceded by transient ischaemic attacks.
31
intracerebral haemorrhage
haemorrhage inside the brain. Most catastrophic. The onset is abrupt. this haemorrhage occurs within the brain and involves small blood vessels. caused by trauma and spontaneous rupture. There is an increased risk for pts with diabetes and hpt.
32
epidural or extradural haemorrhage
Blood comes from a bleeding artery and collects between the dura mater and the skull, rapidly increasing pressure on the brain. This happens as a result of trauma to the head or skull fractures. the pt appears to recover completely but may have raised ICP days later.
33
subarachnoid haemorrhage
blood fills in the space between the arachnoid and pia mater. due to sponatenous rupture or head injury. the patient will feel a thunderclap headache which will feel like a kick to the head
34
subdural haemorrhage
due to trauma in the head especially within the elderly. Causes clotting abnormalities and rupture of small vessels in between the arachnoid and dura mater
35
pathophysiology of atherosclerosis
- atherosclerosis (plaque build up in the arteries) - plaque is a sticky substance made up of cholesterol, fat and calcium and other substances in the blood - plaque over time begins to grow and harden therefore blocking and limiting blood flow in the arteries -therefore the arteries become narrower and limits the flow of oxygen rich blood - large plaques may become necrotic.
36
Hemiparesis
Hemiparesis Manifestation: Weakness of the face, arm, and leg on the same side (due to a lesion in the opposite hemisphere). Nursing implications: Place objects within patient’s reach on the nonaffected side. Instruct the patient to exercise and increase the strength on the unaffected side.
37
Hemiplegia
Hemiplegia Manifestation: Paralysis of the face, arm and leg on the same side (due to a lesion in the opposite hemisphere) Nursing implications: Encourage the patient to provide range-of motion exercise to the affected side. Reposition the patient every 2 hours. Maintain body alignment in functional position. Exercise unaffected limb to increase mobility, strength, and use. Support patient during the initial ambulation phase.
38
ataxia
Ataxia Manifestation: Staggering, unsteady gait Unable to keep feet together; needs a broad base to stand. Nursing implications: Provide supportive device for ambulation (walker, cane). Instruct the patient not to walk without assistance or supportive device.
39
Dsyarthia
Dysarthria Manifestation: Difficulty in forming words Nursing implications: Provide the patient with alternative methods of communicating. Allow the patient sufficient time to respond to verbal communication. Support the patient and family to alleviate frustration related to difficulty in communicating.
40
dsyphagia
Manifestation: Difficulty in swallowing Nursing implications: Test the patient’s pharyngeal reflexes before offering food or fluids. Assist the patient with meals. Place food on the unaffected side of the mouth. Allow time to eat.
41
Homonymous hemianopsia
Homonymous hemianopsia (loss of half of the visual field) Manifestation: Unaware of persons or objects on side of visual loss. Neglect of one side of the body. Difficulty judging distances. Nursing implications: Place objects within intact field of vision. Approach the patient from side of intact field of vision. Instruct/remind the patient to turn head in the direction of visual loss to compensate for loss of visual field. Encourage the use of eyeglasses if available. When educating the patient, do so within patient’s intact visual field.
42
paraesthesia
Paresthesia (occurs on the side opposite the lesion) Manifestation: Sensation of numbness, tingling, or a ‘pins and needles’ sensation. Difficulty with proprioception. Nursing implications: Instruct patient that sensation may be altered. Provide range of motion to affected areas and apply corrective devices as needed. If numbness is present, protect the affected areas from injury and burns.
43
loss of peripheral vision
Manifestation: Difficulty seeing at night. Unaware of objects or the borders of objects. Nursing implications: Place objects in center of patient’s intact visual field. Encourage the use of a cane or other object to identify objects in the periphery of the visual field. Driving ability will need to be evaluated.
44
Diplopia
Manifestation: Double vision. Nursing implications: Explain to the patient the location of an object when placing it near the patient. Consistently place patient care items in the same location.
45
Expressive aphasia
Expressive aphasia Manifestation: Unable to form words that are understandable; may be able to speak in single-word responses Nursing implications: Encourage patient to repeat sounds of the alphabet. Explore the patient’s ability to write as an alternative means of communication.
46
Receptive aphasia
Receptive aphasia Manifestation: Unable to comprehend the spoken word; can speak but may not make sense. Nursing implications: Speak clearly and in an unhurried manner to assist the patient in forming the sounds. Explore the patient’s ability to read as an alternative means of communication.
47
Global (Mixed) Aphasia
Global (mixed) aphasia Manifestation: Combination of both receptive and expressive aphasia. Nursing implications: Speak clearly and in simple sentences, use gestures or pictures when able. Establish alternative means of communication.
48
Cognitive deficits
Cognitive Deficits Manifestation: Short and long-term memory loss. Decreased attention span. Impaired ability to concentrate. Poor abstract reasoning. Altered judgement. Nursing implications: Reorient patient to time, place, and situation frequently. Use verbal and audititory cues to orient patient. Provide familiar objects (family photo’s, favorite objects). Use noncomplicated language. Match visual tasks with a verbal cue; holding toothbrush, simulate brushing of teeth while saying, ‘I would like to brush your teeth now’. Minimize distracting noises and views when providing education to the patient. Repeat and reinforce instructions frequently.
49
Emotional deficits
Emotional Deficits Manifestation: Loss of self-control. Emotional lability. Decreased tolerance to stressful situations. Depression. Withdrawal. Fear, hostility, and anger. Feelings of isolation. Nursing implications: Support patient during uncontrollable outbursts. Discuss with the patient and family that the outbursts are due to the disease process. Encourage patient to participate in group activity. Provide stimulation for the patient. Control stressful situations, if possible. Provide a safe environment. Encourage patient to express feelings and frustrations related to disease process.
50
what is Multiple sclerosis
Multiple sclerosis (MS) is a progressive disorder of the central nervous system, characterized by demyelination and plague formation in the brain and the spinal cord.
51
Clinical manifestations of MS
* Fatigue * Weakness * Difficulty with coordination * Loss of balance * Numbness * Pain can contribute to social isolation. * Diplopia * Depression
52
Myasthenia gravis def
Myasthenia gravis is a disease of the neuromuscular junction, characterised by generalised and progressive muscular weakness
53
pathophysiology of Myasthenia gravis
In Myasthenia Gravis, antibodies are formed that attack and block acetylcholine receptors on the postsynaptic membrane of the neuromuscular junction, impairing normal neurotransmission and causing muscle weakness.
54
causes of Myasthenia gravis
Not well known. Stress is thought to play a role in both triggering and exacerbating the disease.
54
clinical manifestations of myasthenia gravis
* Muscle weakness and fatigue * Visual problems (diplopia, ptosis, and weakness of the extra-ocular muscles) * Slurred speech, difficulty in swallowing * Sleepy, mask-like expression * Slurred speech * Difficulty in swallowing
55
management of myasthenia gravis
* Anticholinesterase agents such as pyridostigmine * Steroids * Immunosuppressive agents * Thymectomy- surgery to remove thymus * Plasmapheresis – procedure in which the plasma containing the autoantibodies is separated from the red blood cells. The plasma is discarded and and the erythrocytes are returned to the patient, together with the fluid to maintain hydration.
56
myasthenic crisis
Myasthenic Crisis – most serious complication of myasthenia gravis (exacerbation of symptoms) Respiratory distress and varying degrees of dysphagia, dysarthria (difficulty speaking), eyelid ptosis, diplopia and prominent muscle weakness are symptoms of myasthenic crisis. The patient is placed in an INTENSIVE CARE UNIT FOR CONSTANT MONITORING because of associated intense and sudden fluctuations in clinical condition. Ongoing assessment for respiratory failure is essential (respiratory rate, depth, breath sounds) Blood is drawn for arterial blood gas analysis. Endotracheal intubation and mechanical ventilation may be needed. Physiotherapy, including postural drainage to mobilise secretions and suctioning to remove secretions. Tube feedings if the patient cannot swallow
57
def guillian barre syndrome
Guillain-Barre syndrome, also known as polyradiculitis or acute autoimmune inflammatory demyelinating polyneuropathy, is a clinical syndrome involving both the peripheral and cranial nerves. It is characterised by paraesthesia, muscle weakness and paralysis.
58
causes guillian barre syndrome
* The autoimmune reaction is believed to be initiated by a viral infection * The disease is often preceded by a flu-like illness, followed by the onset of the symptoms of Guillain-Barre. * This is an occasional illness during the seroconversion stage of HIV/Aids
59
clinical manifestations of guillian barre syndrome
Progressive muscle weakness and diminished reflexes of the lower extremities Hyporeflexia and weakness may progress to tetraplegia Demyelination of the nerves that innervate the diaphragm and intercostal muscles results in neuromuscular respiratory failure Paraesthesia of the extremities, sensory distortions and decreased or absent tendon reflexes. Cranial nerve demyelination can result in a variety of clinical manifestations. Cranial nerve (9,10,3,12) involvement occurs, causing difficulty in swallowing, chewing, and talking. Optic nerve demyelination may result in blindness
60
trigeminal neuralgia def
A condition characterised by episodes of excruciating pain along the distribution of the fifth cranial (trigeminal) nerve, which includes: * The lips * Gums, * Cheek, * Chin and occasionally the eye A variety of stimuli can trigger an episode, such as light touch or contact with hot or cold objects. The condition usually occurs in elderly individuals and the causes are unknown
61
trigeminal neuralgia pharmacological therapy
Anticonvulsant agents, such as Carbamazepine (Tegretol), relieve pain in most patients with trigeminal neuralgia by reducing the transmission of impulses at certain nerve terminals. Serum levels must be monitored to avoid toxicity.
62
bells palsy def
The condition is characterised by paralysis of the facial muscles, with ptosis, drooping at the corner of the mouth and salivation due to inflammation or compression of the facial nerve by tumours. Bell’s Palsy is caused by unilateral inflammation of the seventh cranial nerve, which results in weakness or paralysis of the facial muscles on the affected side.
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bells palsy clinical manifestations
* Speech is usually difficult due to paralysis of the facial muscles, which may also cause the lower eyelids to droop, resulting in the cornea drying out. * The face is distorted from paralysis of the facial muscles, decreased lacrimation (tearing) occurs * The patient experiences painful sensations in the face, behind the ear, and in the eye. * The patient may also experience speech difficulties and may be unable to eat on the affected side because of weakness or paralysis of the facial muscles.
64
nursing management for bells palsy
Eyes should be protected, especially during sleep and a splint can be used to prevent excessive drooping of the lower part of the face. Excessive salivation and drooling may be embarrassing for the patient: this should be wiped away or suctioned Moisturising eye drops during the day and eye ointment at bedtime may help prevent injury. Sunglasses may be worn during the day to decrease evaporation from the eye. The nurse can suggest massaging the face several times daily, using a gentle upward motion, to maintain muscle tone. Facial exercises, such as wrinkling the forehead, blowing out the cheeks, and whistling, may be performed with the aid of a mirror to prevent muscle atrophy. Exposure of the face to cold and drafts is avoided.
65
definition of fracture
A fracture is a break in the continuity of a bone caused by applied force during trauma, disease (pathological fracture) or prolonged pressure on the bone (stress fracture).
66
pathophysiology of a fracture
In a fracture, there is a break in continuity of a bone, results in the periosteum being stripped off from the bone and blood vessels supplying. The edges of the bone may damage surrounding soft tissue and blood vessels, resulting in bleeding into the bone and tissues, including joint cavities if joints are involved. A haematoma may form, increase the swelling in the area.
67
principles of traction
-Traction is continuous and must be taken that the weights are not disturbed. -The patient must maintain a good body alignment in the centre of the bed the whole time and therefore pressure care must be provided. -The weights that constitute the pull must hang freely and not rest on the bed or the floor. -Ensure that the patient does not slip down in the bed as this will move the weights towards the floor. -There must be no knots on the ropes to allow for free running in the grooves of the pulleys. Devices for traction must be fitted with foot support to prevent plantar flexion or foot drop.
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complete fracture
There is a clean break of the bone; the broken parts are often displaced; this type of fracture can be closed/simple or open
68
closed or simple fracture
The bone is broken into two parts (complete fracture) with no break in the skin
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open fracture
The bone is completely broken and there is a wound that opens to the exterior (open compound fracture); or there is a wound that opens to the exterior through which a bone is protruding (open complex fracture); the wound may be clean or contaminated
70
comminuted fracture
There are many fragments at the point of the break as a result of crush injury
71
compression fracture
The vertebral column has been compressed as a result of a fall from a height in an upright position and has absorbed the shock of the fall
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depressed fracture
This applies to the skull where a blunt blow causes a dent that presses on the brain substance
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impacted fracture
A bone fragment slips over the other fragment
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incomplete or greenstick fracture
This applies in children where the one side breaks while the other side is bent
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pathologic fracture
These are related to disease and can occur without any trauma, eg in osteoporosis, bone metastasis