Test 3 revision Flashcards

1
Q

What is a traumatic brain injury?

A

Traumatic brain injury (TBI) is an aquired injury that occurs when there is disruption in the normal function of the brain due to a bump, blow or jolt to the head or a penetrating head injury.

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2
Q

What are the two categories of a traumatic brain injury?

A

blunt/closed TBI: skull & dura mater remain intact and brain is NOT exposed to external environment

penetrating/open TBI: penetration or damage of skull & dura mater occurs and the brain is exposed to the external environment

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3
Q

What is a primary traumatic brain injury?

A

Primary injury:
tissue damage that occurs at the moment of trauma. This includes damage to tissue via penetration or compression and shearing forces associated with blunt trauma.

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4
Q

What is a secondary traumatic brain injury and what can it include?

A

Secondary injury:
Occurs in the hours to days after the primary injury and involves the inflammation, oedema and bleeding that occurs in response to the primary injury.

Secondary injury can include metabolic & electrolyte imbalances, neurotransmitter excitotoxicity, mitochondrial dysfunction, apoptosis and/or ischemia.

Secondary injury is going to have an impact on intracranial pressure (ICP) and can be even more detrimental than the primary injury in some cases.

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5
Q

How can you determine the severity of a TBI?

A

Brain imaging is used to distinguish between focal/ diffuse injuries
AND
to identify any intracranial hemorrhage/hematoma.

The Glasgow Coma Scale is often used to assess the neurological impact of a TBI and provides a rough guide to the severity of the TBI:

Mild TBI: score 13-15
Moderate TBI: score 9-12
Severe TBI: score 3-8

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6
Q

What is the management of a TBI?

A

A major component of TBI treatment is the monitoring and management of intracranial pressure (ICP) and cerebral perfusion pressure (CPP).

As well as monitoring and mainatining
- ventilation
- blood pressure
- electrolyte levels
- blood glucose levels
- temperature regulation.

Seizures are commonly associated with TBI, and thus seizure prophylaxis is important.

Affected/damaged tissue may need to be removed.

Penetrating injuries carry a risk of infection, so antibiotics are commonly used.

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7
Q

Whats a focal brain injury?

A

Focal brain injury refers to areas of localised damage

Either blunt (closed) or penetrating (open) TBI can result in focal injury.

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8
Q

What can a primary focal brain injury result in? Can result in either of both

A

Contusion: Injury to brain tissue (bruise from damage to the cells and blood vessels of a focal area. Pia mater is still intact in a contusion. Brain contusions result from coup and countercoup injuries.)

Intracranial hematoma: Accumulation of blood (clotted) within the cranium

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9
Q

What is the difference between a coop and contrecoup contusion

A

coup injury (1): injury occurring at the initial point of forceful impact. This includes compression damage occurring directly below the site(s) of impact (a & c) as well as any associated shearing injury (b).

contrecoup injury (2): injury occurring in areas of the brain opposite from the site of initial impact due to rebound effect (a) and associated shearing injury (b).

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10
Q

What are the different kinds of intracranial hemorrhage/hematoma? (4)

A

1) Epidural (extradural) hematoma
2) Subdural hematoma
3) Subarachnoid hemorrhage
4) Intracerebral hemorrhage

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11
Q

What are the layers of the brain? (Outermost to inner most)

A

Scalp, skull, dura mater, arachnoid mater, subarachnoid space, pia mater, and brain

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12
Q

Whats a epidural (extradural) hematoma

A

blood accumulation between the skull and outer layer of the dura mater. Blood loss may be arterial (most common) or venous

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13
Q

Whats a Subdural hematoma

A

blood accumulation between the dura mater and arachnoid mater. May be acute or chronic. Blood loss is typically venous and as pressure increases from the clot, blood vessels are compressed, reducing further bleeding.

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14
Q

What is a Subarachnoid hemorrhage

A

Bleeding within the subarachnoid space (between the arachnoid and pia mater). Blood mixes with the cerebrospinal fluid (CSF).

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15
Q

What is a Intracerebral hemorrhage?

A

Bleeding into the brain.

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16
Q

What is a diffuse brain injury? And what does it range from?

A

Widespread brain damage. Damage to neurons throughout the brain. Characterized by general disturbances in neuronal function

Diffuse brain injury ranges from concussion (mild form of TBI) to severe diffuse axonal injury (DAI) with coma.

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17
Q

What is a diffuse axonal injury (DAI)?

A

Is associated with the majority of neurons firing action potentials simultaneously following concussion.

This leads to release of glutamate resulting in excitotoxicity, which alters normal neuronal ion transport. Abnormal ion transport can disrupt mitochondrial function and ATP prodution, therefore reducing the neurons ability to generate and propagate action potentials.

DAI occurs due to shearing forces generated within the brain at impact. It can be visualized by multiple, small lesions within the white matter tracts of the brain. The majority of individuals with severe DAI will not wake up from their coma.

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18
Q

What are the percentages of intracranial volume?

A

10% cerebral blood volume

10% cerebrospinal fluid (CSF)

80% brain tissue

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19
Q

What is the normal intracranial pressure?

A

5-15mmHg.

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20
Q

How does the brain accommodate for changes in intracranial pressure?

A

Small increases in the volume of one component can typically be compensated for by small decreases in another component, but only up to a certain point.

If compensation is not adequate, intracranial pressure (ICP) continues to rise, leading to life-threatening conditions.

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21
Q

What are reasons ICP may rise?

A
  • brain tumours
  • cerebral oedema (increased intra- or extracellular fluid in brain tissue) from infection
  • intracranial hemorrhage/hematoma
  • hydrocephalus (accumulation of CSF)
  • cerebral vasodilation (e.g. in response to hypercapnia, hypoxia)
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22
Q

What are symptoms of a high ICP?

A

◦ Decreased Glasgow Coma score – difficulty staying awake
◦ Central neurogenic hyperventilation
◦ Widening pulse pressure
◦ Bradycardia (but bounding)
◦ Firstly the pupils will constrict, and be sluggish. Then once the pressure continues to rise: Ipsilateral dilation and fixation (the pupil on the side of the bleed/herniation) is large
and unresponsive. The other pupil is still constricted. As pressure increases, the brain herniates through the foramen magnum, down into the neck. Bilateral dilated and fixed pupils.

  • Reduced consciousness and impairment of sensory and motor functions (e.g. reduced response to pain, weakness) leading to coma
  • Decreased ventilation leading to alterations in breathing patterns. Ultimately reducing respiration
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23
Q

What happens when ICP is too high?

A

When the pressure in the brain raises enough that it is equal to the blood pressure in the cranial arteries, then there is no pressure gradient to push blood out of the arteries into the brain.

Hypoxia and hypercapnia occur. This then causes acidosis in the brain

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24
Q

What’s the difference between a concussion and an axonal diffusion injury?

A

Technically, the difference between a concussion and a diffuse axonal
injury is that a person is diagnosed with a concussion if they are unconscious for 6 hours or less

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25
Q

What are special needs of the brain?

A

The brain does not store large amounts of glycogen or ATP.

The brain cannot do anaerobic respiration. The brain must have a constant supply of blood to bringm oxygen and glucose or it will start to die very quickly.

15-20% of the blood from the left ventricle goes directly to the brain.

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26
Q

What is the nursing Assessment for TBI

A

Glasgow Coma Score

Mild TBI: 13-15
Moderate TBI: 9-12
Severe TBI: 3-8

Reflexes
◦ Pupils: PERRLA

Equalization
◦ Equality of strength in left versus right arms and legs
◦ Drift: Can the arms stay up for a count of 10, legs for a count of 5?
◦ Ataxia: Finger to nose rapidly

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27
Q

What are nursing interventions for ICP?

A

◦ Head of the bed at least 30 degrees

◦ Corticosteroids to decrease oedema

◦ Administer mannitol (osmotic diuretic) or possibly hypertonic saline (3%)

◦ Cooling to lower brain and body metabolic requirements

◦ Induce hyperventilation to reduce CO2 level and induce vasoconstriction

◦ Keep blood pressure high enough for perfusion

◦ Seizure prophylaxis

◦ Monitor ICP and prepare for surgery or medically induced coma

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28
Q

What is the function of the skin?

A

Protection
Sensation
Metabolic
Temperature regulation
Absorption
Excretion
Blood reservoir

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29
Q

What is Cellulitis?

A

Cellulitis is a bacterial infection of the dermis and subcutaneous tissue that can easily, and rapidly spread.

It more commonly occurs in older adults, though a particular type- periorbital cellulitis- occurs in children.

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30
Q

What bacteria is the most common with a Cellulitis infection?

A

Most commonly “streptococcus pyogenes”
or
“staphylococcus aureus (staph infection)

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31
Q

How is cellulitis typically acquired and where is it usually located?

A

Occurs when the skin barrier is broken and bacteria have access to the lower dermis and fatty tissue layers.

Can be via cut, insect bite, burn, scrape, puncture wound, or patches of dry skin.

Most commonly found on the legs

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32
Q

What are risk factors for cellulitis?

A

People with..
- Diabetes
- Venous diseases
- Lymphoedema
- Leg ulcers
- Oedema
- IV drug use
- Over weight
- Have a weakened immune system
- Other skin diseases (eczema or athletes foot)
- Already have a swollen arm or leg
- Have had cellulitis before

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33
Q

What are symptoms of cellulitis?

A

Red, swollen, painful, blisters, warmth. Sometimes there are blisters filled with yellow fluid.

May develop fever if infection becomes symptomatic.

Can cause sepsis if enters the blood stream, low blood pressure, high fever.

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34
Q

What is the treatment for cellulitis?

A

Treatment: Antibiotics (oral or IV), elevate legs, wound care and antibiotic creams, possibly compression stocking to reduce fluid

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35
Q

How to prevent cellulitis?

A

Bandage, keep skin wounds clean, antibiotic cream, heal exciting breaks in the skin.

Diabetes or poor circulation: Examine feet every day, moisturize, avoid injury

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36
Q

What are pressure Injuries?

A

“localized damage to skin and/or underlying tissue as a result of pressure or pressure in combination with shear”

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37
Q

What causes pressure in pressure injuries?

A

Bones – skin, subcutaneous tissue, and muscle caught between bone and a hard surface are under great pressure

Mechanical devices – oxygen tubing, canes, bed rails, catheters, nasogastric tubes

Pressure occludes blood vessels, which causes ischemia

Muscle may actually be affected first as it is less resistant than skin

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38
Q

What causes shearing?

A

Skin and subcutaneous tissue may stay in place due to friction against a surface

When moved, or when sliding down in a chair, muscle and bone may move

This shears the skin and subcutaneous tissue from the muscle

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39
Q

How many stages of pressure injuries are there?

A

6

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40
Q

What are the stage pressure injuries are there?

A

Stage 1, stage 2, stage 3, stage 4, unstageable and deep tissue injury

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41
Q

What is pressure injury stage 1?

A

Skin remains intact with localized area of erythema or discolouration that is non-blanchable (Does NOT change color/lighten when pressure (e.g. finger-press) is applied)

(Just red no skin breakage)

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42
Q

What is pressure injury stage 2?

A

Partial-thickness skin loss. Dermis intact but exposed. No granulation tissue, slough, or necrosis

Partial thickness injury that exposes the dermis; may appear blister-like.

(Skin that appears when a blister pops)

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43
Q

What is pressure injury stage 3?

A
  • Full thickness loss of skin that exposes the hypodermis (Adipose tissue, granulation tissue visible).
  • Ulcer typically has rolled edges.
  • Eschar and slough may be visible at the edges but do not cover the wound
  • No exposure of muscle, fascia, bone, tendon, ligament, or cartilage
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44
Q

What is pressure injury stage 4?

A

Full thickness loss of skin that exposes further underlying tissues such as fascia, tendon/muscle, ligament, bone, etc.

Slough or eschar may be present but do not cover the wound

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45
Q

What is an unstageable pressure injury?

A

Full thickness loss of skin (stage 3 or 4) but slough, eschar and/or necrosis cover the wound so damage is unable to be confirmed

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46
Q

What is a deep tissue pressure injury?

A

Injury in tissues deep to the skin which appears as a persistent, non-blanchable, deep red, maroon or purple discolouration or blood-filled blister (skin may or may not be intact).

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47
Q

How can you prevent pressure injuries?

A

Repositioning, using supportive surfaces that distribute or relieve pressure (e.g. certain types of mattresses), reducing exposure to sustained moisture (e.g. due to incontinence), reducing shear and friction forces, etc.

Further management may include wound dressing/treatment, debridement, infection prevention/management, pain management and nutritional/hydration management.

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48
Q

What’s gastroenteritis?

A

Gastroenteritis is inflammation of the lining of the stomach and the intestines.

It is usually caused by an infectious agent but can also be a reaction to medication or poisons.

The pathophysiology of gastroenteritis is different for different kinds of infections.

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49
Q

Why is gastroenteritis critical in children?

A

Children have a greater percentage of water which increases their risk of dehydration.

In addition children have immature kidneys (so cannot reabsorb water as well) and they have a great surface area to weight so can lose water easier

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50
Q

What are examples of viral gastroenteritis?

A

Rotavirus
Norovirus

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51
Q

How is viral gastroenteritis transmitted?

A

Transmitted faecal-orally

Occurs when microorganisms from an infected stool of one person enter the mouth of another.

Germs are transferred from hand to mouth because the hands have touched contaminated items and have not been well washed afterwards.

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52
Q

How does viral gastroenteritis affect the body?

A

Viruses invade and take over the cells that line the stomach and the gut

These are the cells that first absorb nutrients and water from the stomach and intestines

Additionally, the viruses release toxins that cause the death of surrounding cells.

Ultimately, the intestines cannot absorb nutrients and water well,
and even lose some of the fluid that they do have in their tissue

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53
Q

What are symptoms of viral gastroenteritis?

A

Symptoms start with vomiting followed by watery diarrhoea

Low fever is present, but high fever is typically not from a gastroenteritis virus.

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54
Q

What are some examples of bacterial gastroenteritis?

A

Clostridium difficile (Cdiff)
Campylobacter
Shigella
Salmonella

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55
Q

How does bacterial gastroenteritis spread?

A

The spread of gastroenteric bacteria is usually through undercooked food (especially chicken or eggs) or unpasteurized milk.

C. diff used to be thought of as a nosocomial infection (one obtained through the hospital) but it is now prevalent in the community

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56
Q

What is the two mechanisms of bacterial gastroenteritis?

A

Release of a toxin –
in some cases, the bacteria itself doesn’t even have to get into the body, but if the toxin made by the bacteria is taken in and is not killed by sufficient heat in cooking. The toxin causes the cells that line the gut to stop taking in water and nutrients and instead to
dump fluid and electrolytes into the gut, causing diarrhoea.

Invasion by the bacteria itself –
Bacteria get into the mucosa. The immune system responds by causing inflammation, which can cause ulceration of the tissue of the intestines and bleeding.

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57
Q

What are the symptoms of bacterial gastroenteritis?

A

Cramping and vomiting followed by diarrhoea

Bacterial gastroenteritis is more likely (not always) to present with a high fever and bloody or mucous-filled diarrhoea.

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58
Q

What are complications of GASTROENTERITIS IN CHILDREN?

A

Diarrhoea requires three or more loose stools in a day. Unless stools are loose and unless there are at least three
stools in a day, diarrhoea is not generally diagnosed or treated.

Dehydration/Hypovolemia (liquid portion of the blood (plasma) is too low):
- Sunken fontanels in a baby; dry mucosal membranes, sunken eyes, decreased tears.
- Weight loss – especially for a baby
- Rapid thready pulse; decreased blood pressure; dizziness

Hyponatremia
- Less sodium = less nervous activity
- Apathy, weakness
- Depressed reflexes, twitches

Hypokalaemia
- Less potassium = less muscle
- Muscle weakness that can lead to paralysis
- Pulse may be bradycardic from lack of potassium or can be tachycardic from dehydration

Metabolic acidosis
- Rapid breathing to blow out the acid
- As acidosis gets worse, especially with low potassium, may greatly increase bradycardia

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59
Q

How to care for children with severe GASTROENTERITIS?

A

Monitor diarrhoea, dehydration and electrolyte & acid-base imbalances.

Treatment
* Handwashing with soap, not just gel

At home:
* Oral rehydration therapy (ORT)
* Usually prepackaged.
* Rough guide: A litre of water, 6
teaspoons of sugar, and ½
teaspoon of salt.
* If child will not drink, may need
ondansetron to reduce nausea and to
give ORT with a syringe.

In hospital:
* NG fluids, possibly with electrolytes
* Possibly medication for diarrhoea;
however, if diarrhoea is from an
infectious cause, medication may not
be given so that the body can wash
the pathogen out of the body.
* Feeding as soon as child will take in
food.

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60
Q

What’s rheumatic fever?

A

Rheumatic fever causes inflammation, of the heart, blood vessels and joints.

Can be caused by inadequately treated strep throat or scarlet fever.

Rheumatic fever is caused by Group A (Beta-haemolytic) streptococcus bacteria. There are over 100 strains of group A strep bacteria, but the one that causes rheumatic fever is often Strep pyogenes.

61
Q

How does rheumatic fever occur?

A

Our skin and respiratory tract are colonised with Group A strep bacteria, but they can cause cellulitis, gastroenteritis, and strep throat when uncontrolled. Group A strep is generally spread by droplets or direct contact.

Rheumatic fever occurs after an infection of the throat with group A strep, called strep pharyngitis or strep throat.

Cellulitis can also be caused by group A strep, but rheumatic fever is more closely linked to strep throat than to cellulitis.

62
Q

What is the pathophysiology of rheumatic?

A

When a child has strep throat, the immune system makes antibodies to the Strep bacteria. One of the major antigens on the group A Strep that the immune system attacks is called the “M protein”.

Unfortunately, the group A strep’s M-protein looks very much like proteins found on the heart muscle, heart valves, synovial lining of the joints, the nerves, and skin/subcutaneous tissues.

In acute rheumatic fever, the child’s immune system then starts attacking these other sites in the body. When the immune system attacks these sites, especially the heart, it forms Aschoff bodies (are nodules found in the hearts).

T-cells and phagocytic cells travel through the blood to come to the cells with proteins that look like the strep M-protein. At these areas, the phagocytic immune cells attack the body cells and the proteins around them.

Eventually, like in other areas with inflammation, they wall themselves off and create a nodule of collagen (scar tissue). This breakdown of the joints, heart, skin, and even nervous tissue causes the symptoms associated with acute rheumatic fever.

63
Q

What are symptoms of rheumatic fever?

A

Occurs 2 to 4 weeks after strep throat

Not everyone with acute rheumatic fever gets the same symptoms but will develop some of the following:

  • High fever
  • The Jones Criteria: Joint pain (migrating polyarthritis). The arthritis generally starts in the lower legs and “migrates” upward over time.
  • Carditis – chest pain and shortness of breath. Acute rheumatic fever typically affects the valves and the endocardium (inner lining).This causes the valves not to be able to close properly so that some blood flows the wrong way when the heart pumps (Mitral regurgitation, aortic regurgitation).
  • Skin nodules – from the collections of collagen under the skin.
  • Erythema marginata – a red, non-itchy rash.
  • Sydenham’s chorea – involuntary tics from the face or arms.
64
Q

How to assess for rheumatic fever?

A
  • Patient history that includes recent respiratory infection
  • Draw labs to assess for inflammation and for antibodies to Strep antigens
  • Auscultate for left sided heart murmur
  • Assess for heart failure, especially left sided symptoms
  • ECG for heart rhythm
  • Assess for joint pain and inflammation that is moving upward
  • Assess skin for new nodules (Especially hands)
  • Assess for new rashes, especially if non-itchy
  • Assess for tics or neurological changes
65
Q

How to treat rheumatic fever?

A
  • Obtain throat culture of any school age child with sore and red throat
  • Provide antibiotics: penicillin (long term)
  • Provide anti-inflammatory medications: aspirin
  • Prednisone is given if there is pericarditis – inflammation of the sac around the heart
  • Provide medications for heart failure; Diuretics; ACE or ARB; Beta blocker; Possibly calcium channel blockers if atrial fib is present; Low sodium diet
  • Ensure adequate oxygenation
  • Emotional support for decreased function with chorea
  • Long term care; Prophylactic antibiotics; Heart valve replacement
66
Q

What is strep throat?

A

A bacterial infection that causes red throat/ tonsils, fever, painful swallowing, body aches, and swollen lymph nodes.

67
Q

What are complications of strep throat?

A

Heart Disease
- Initially, rheumatic fever causes mitral and aortic regurgitation.
- Blood flows backwards when the heart pumps. You can hear this by a murmur in a stethoscope?

Heart disease symptoms:
Dyspnoea, tripod positioning, possible jugular venous distention

Over time, the valves can harden and narrow, causing stenosis

The back up of blood from the valves stretches the heart. Also, the heart muscle is damaged from the immune system.
These two changes lead to
* Atrial fibrillation
* Left sided heart failure

Acute Glomerulonephritis
Occurs 1to 3 weeks after Strep throat or Group A Strep skin infection

Antibodies bind to antigens on the
group A Strep bacteria. These antibody-antigen complexes float through the blood. They flow to the glomerulus of the kidneys, but are too big to filter into
the urine. The body tries to clear out the antigen-antibody complexes with
inflammation. The inflammation destroys the lining of the glomeruli and leaves it with a sort-of scar tissue. Scar tissue doesn’t filter well, so the
kidneys end up not filtering, and the
body goes into Acute Renal Failure
Intrarenal – the glomeruli are inside the
kidney

68
Q

What is osteoarthritis?

A

Osteoarthritis is an inflammatory condition associated with degeneration of joint tissues.

There is degradation of the articular cartilage in joints, ultimately leading to damage to the bone surfaces and synovial membrane. The joint becomes painful and mobility is decreased due to stiffening of the joint.

Hip joint wearing down = hip replacement

69
Q

What are risk factors to osteoarthritis?

A

Age
Inflammation
Joint injury
Mechanical stress and obesity
Neurological disorders
Genetics
Medications

70
Q

What is a fracture?

A

A bone fractures (breaks) when force is applied to the bone which exceeds the bones tensile or compressive strength.

Bone fractures may occur as a result of trauma or pathological processes which have weakened the bone, and any bone in the body can be affected.

Fractures tend to be more common in young males and the elderly (65+ years).

71
Q

What is a complete fracture?

A

Bone broken all the way through (bone separated into at least 2 pieces)

72
Q

What is an incomplete fracture?

A

Break does not go all the way through the bone (bone remains in one piece)

73
Q

What is an open (compound) fracture?

A

Bone penetrates the skin (skin is also broken)

74
Q

What is a closed (simple) fracture?

A

Skin remains intact, bone does not penetrate

75
Q

What is a comminuted fracture?

A

Bone is broken into more than two pieces

76
Q

What is a occult fracture?

A

Break is not obvious or easily discernible

77
Q

What is an avulsion fracture?

A

Fragment of bone at ligament/tendon attachment point breaks off

78
Q

What is a linear fracture?

A

Break is parallel to the long axis of the bone

79
Q

What is a transverse fracture?

A

Break is horizontal through the bone

80
Q

What is an oblique fracture?

A

Break is at an oblique angle to the long axis of the bone

81
Q

What is a spiral fracture?

A

Break curves around the cortical (compact) bone

82
Q

What is a displaced fracture?

A

Broken bone ends are mis-aligned

83
Q

What is a Impacted fracture?

A

Broken bone ends are pushed into each other

84
Q

Signs and symptoms of a bone fracture

A
  • tenderness and/or pain
  • unnatural alignment/deformity
  • swelling
  • muscle spasm
  • impaired sensation
  • decreased mobility/limb function
85
Q

What are complications of fractures?

A
  • Fat embolism (most commonly associated with long bones) (particles of fat get into your bloodstream and block blood flow) Long bones can have fat in them. When you break a bone, fat can move across the blood vessels and become a ebolise.
  • Hypovolemic shock: Because bones are rich in blood, If the break is severe enough and bleeding cannot be contained, could be a risk to HS from hemorrhage.
  • Bone necrosis if blood supply compromised
  • Infection (More likely if open fracture)
  • Delayed union of bone pieces (mal- union & non-union). Delayed healing process.
86
Q

What is the process of fracture healing?

A

1) Hematoma
- Blood accumulation around break

2) Soft callus
- Fibrous CT and fibrocartilage replace hematoma + new blood vessel formation

3) Hard callus
- Bone tissue replaces soft callus tissue

4) Remodeling
- Bone remodeling to sculpt bone original shape (or as close as possible)

87
Q

What are treatment options for fractures?

A

1) Immobilisation (e.g. via splint, plaster cast)

2) Reduction: realignment of displaced fractures

3) Traction: use of weight/steady pulling force to stretch muscles and surrounding tissue to allow realignment of bone fragments

4) External fixation: pins & screws driven into bone fragments and attached to external plate to hold bones in place

5) Open reduction & internal fixation: surgical procedure exposing fracture site to allow re-alignment and then pins, screws, plates and/or rods to maintain alignment

88
Q

What is Parkinson’s disease

A

Parkinson’s disease is a movement disorder of the nervous system.

Loss of dopaminergic neurons within the substantia nigra of the brain.

These are neurons that secrete dopamine into parts of the basal ganglia (Key part that controls your body’s voluntary movements) and therefore play a role in somatic motor control (skeletal muscle movements).

89
Q

What are symptoms of Parkinson’s disease?

A

Tremor (resting)
Rigidity or muscle stiffness
Bradykinesia (Slowed movement) or akinesia (No movement (e.g. lack of initiating movement)

The above signs can be associated with decreased facial movements/expression, postural & gait alterations and speech or swallowing alterations.

Additional signs & symptoms develop due to the wider impact of dopamine loss in the brain and may include autonomic effects (e.g. drooling, constipation, urinary retention) and cognitive effects (e.g. depression, dementia).

90
Q

What are risk factors to Parkinson’s disease?

A

No known cause

It typically occurs after the age of 40 and is more common in males.

Probably a specific genetic or environmental component.

91
Q

What are treatments to parkinson’s disease?

A

No treatment to stop the disease are get neourns back.

Levodopa (L-dopa): a dopamine precursor that is converted to dopamine by the remaining neurons in the substantia nigra (thus effectiveness reduces over time)

Dopamine agonists: trigger dopamine receptors to stimulate the necessary neuronal signals

Anticholinergics: dopamine-acetylcholine balance in the basal ganglia is important for proper signaling, as dopamine levels decrease, an imbalance develops, thus anticholinergics attempt to restore the balance

Deep brain stimulation: electrical stimulation of certain brain regions to alleviate the symptoms associated with improper signaling

Supportive care, e.g. physiotherapy, occupational therapy

92
Q

What does the term tonic mean in regards to seizures?

A

State of increased muscle tone & rigidity

93
Q

What does the term clonic mean in regards to seizures?

A

State of alternating muscle contraction & relaxation

94
Q

What is status epilepticus?

A

A serious complication of epilepsy when seizure activity of tonic-clonic seizures (mostly) is sustained for longer than 5 minutes or there are recurrent seizures without recovery of consciousness in between.

Status epilepticus is a medical emergency because seizure activity increases oxygen demand and ventilation is temporarily suspended during the seizure.

Therefore is the seizure activity is sustained, the brain will quickly be deprived of oxygen.

Cerebral hypoxia - neuronal death - respiratory failure. LIFE THREATENING

95
Q

What is schizophrenia

A

A disorder that affects a person’s ability to think, feel and behave clearly.

Psychosis “a severe form of mental disorder in which thinking is disconnected from external reality”
Includes:
- Sensory hallucinations
- Delusions
- Disorganized speech

96
Q

What does positive schizophrenia symptoms cause?

A

Adding stuff thats not there

Excess of normal experiences
- Sensory hallucinations, delusions, disorganized speech and behaviour

97
Q

What is the pathology of positive symptoms?

A

MESOLIMBIC pathway in the brain – “reward pathway”. Pathway involved in addiction.

Normally dopamine runs through this system and we get happy. Too much dopamine in this pathway is when schizophrenic symptoms arise.

Dopamine is the chemical that attaches to receptors to trigger the feelings of reward.

Reward causes an increase in dopamine in the mesolimbic system, but so does acute stress. It is thought that the purpose of this is to increase a feeling of reward to help get through a stressful situation.

Chronic stress, however, will often decrease the amount of dopamine in the mesolimbic pathway.

Additionally people with schizophrenia have more receptors so dopamine have more to bind to.

98
Q

Tell me about D2-receptors and its involvement with schizophrenia?

A

There are 5 kinds of dopamine receptors throughout the body. The D2-receptors are the main ones associated with schizophrenia.

In patients with schizophrenia, there is noted to be an increase in D2-receptors in the mesolimbic pathway.

Excessive activation of the D2 receptors in the mesolimbic pathway have been repeatedly related to the positive symptoms of schizophrenia.

99
Q

What is the pathology of negative symptoms?

A

Things we are taking away

Reduction in normal function

Apathy, lack of motivation, inability to initiate action, emotional blunting, poor concentration, decreased speech, decreased pleasure

100
Q

What is the pathology of negative symptoms?

A

Negative symptoms occur from TOO LITTLE dopamine through the MESOCORTICAL pathway.

Starts at the same place as the reward pathway, but instead it runs to the front of the brain

  • Important in maintaining attention, working memory, and planning.
  • This pathway uses both dopamine and serotonin.
  • It is thought that by decreasing dopamine in this pathway that it comparatively increases serotonin, which leads to the negative symptoms.
101
Q

WHAT IS BIPOLAR DISORDER?

A

Bipolar disorder is considered a mood disorder.

Bipolar is noted to have both periods of mania and then later periods of depression

102
Q

What are symptoms of bipolar?

A

Bipolar symptoms are not due to a single neurotransmitter; however, there are changes in the balance of
neurotransmitters in the brain during manic and depressive episodes.

Manic Symptoms
- Excessive excitement, agitation and energy (usually euphoria)
- Risk taking behaviour (gambling, business investments)
- Racing thoughts
- Grandiosity with feelings of well-being and self confidence
- Rapid, pressured speech (often tangential or with flight of ideas)
- Highly distractible
- Rapid heart rate, elevated blood pressure
- Impulsivity; increased risk of suicide

Bipolar Depression Symptoms
- Anhedonia
- Slowed movement/behaviour
- Low mood or sadness
- Fatigue
- Guilt/worthlessness
- Difficulty concentrating

103
Q

Whats the pathophysiology of bipolar symptoms?

A

In manic episodes, there is an increase in glutamate, noradrenaline, and dopamine.

Glutamate causes an increase in excitability of the neurons, so more neurons are firing more frequently. It is extremely important in neuroplasticity and making new neural connections and learning. Glutamate levels are higher when awake – and manic episodes are often preceded by difficulty sleeping. However, too much glutamate over a long period leads to the death of neurons.

Noradrenaline
Normally released from the adrenal glands during acute stress. It is also a neurotransmitter for the sympathetic
nervous system.

Dopamine – may contribute to psychosis often (not always) found in acute mania

During the depressive phase of bipolar, there is a decrease of noradrenaline

104
Q

What do 1st generation Anti-Psychotics (Neuroleptics) do?

A

Block dopamine receptors so that the neurotransmitter dopamine cannot excite the next neuron in the pathway to signal

105
Q

What are some 1st Generation Antipsychotics (Typical antipsychotics)

A

Haloperidol (Haldol)
Zuclopenthixol (Accuphase)

(There are 5 different dopamine receptors. Antipsychotics are antagonists to the D2 receptor
– Blocking the D2 receptor reduces the positive symptoms of schizophrenia)

106
Q

What are some side effects of 1st Generation/Typical Antipsychotics (Neuroleptics)?

A

Sedation

Extrapyramidal Side Effects:
Movement dysfunction such as
- Dystonia (continuous spasms and muscle contractions)
- Akathisia (may manifest as motor restlessness), etc)
- Rigidity (Cogwheel)

Dopamine is one of the neurotransmitters that helps the basal ganglia maintain this fluidity.

107
Q

What medication is given to to stop extrapyramidal side effects?

A

Benztropine (Cogentin)

108
Q

What do second Generation (Atypical) Anti-Psychotics do?

A

Block D2 receptors but also block Serotonin (5HT) receptors

Blocking both receptors allows for a better balance between dopamine and serotonin

Because 2nd Gen anti-psychotics do a better job balancing the dopamine and serotonin in this pathway, they do better at managing negative symptoms.

109
Q

What are examples of 2nd Generation (Atypical) Anti-psychotics

A
  • Olanzapine
  • Risperidone
  • Quetiapine
  • Clozapine
110
Q

What are the side Effects of 2nd generation antipsychotics?

A

Two important things to remember for 2nd Gen Antipsychotics

Doesn’t have (as much)
- Extrapyramidal Side Effects; Tardive Dyskinesia; Sometimes sedation

But has a is more associated with
- Rapid weight gain (especially olanzapine)
- Hypotension (they also block some receptors in the Sympathetic Nervous System)

Risperidone: Hyperprolactinemia
Quetiapine: Sedation

111
Q

What are clozapine side effects

A

Clozapine is the most effective antipsychotic. However, it cannot be tried until the client has failed
2 other anti-psychotics. T

his is because of the severity of the side effects:
– Agranulocytosis (requires repeated blood tests)
– Anticholinergic side effects – to the point of intestinal obstruction and hypersalivation
– More extreme hypotension and sedation than the other 2nd generation

112
Q

What are issues with lithium?

A

Narrow therapeutic range
■ There is a very small range between when lithium becomes effective and when it becomes toxic
■ Requires repeated blood tests to make sure client is in effective range

The effects of sodium regulation
■ Because lithium is replacing sodium through the channels in the cell, changing the amount of
sodium in the body can dramatically affect the lithium level.
■ Lithium is increased by anything that causes hyponatremia. What gets rid of sodium?
– Vomiting, sweating, exercise, low sodium diets, high fever

Medications that interfere with lithium
■ SSRIs and other anti-depressants – can cause serotonin syndrome
■ NSAIDS and other medications that affect the kidney, because the kidney excretes excess lithium

Renal tubular damage may occur with prolonged therapy so monitoring of renal function is essential in patients on lithium therapy

112
Q

What is the purpose of lithium

A

lithium is a mood Stabiliser to treat bipolar disorder.

Lithium is an element in the same row of the periodic table as sodium and potassium meaning it can flow through the same channels as sodium, but it doesn’t move out of cells as easily
as sodium.

Since the action potential to create and pass on signals from neurons is all based on the polarization of the cell due to moving sodium ions across it, lithium reduces the excitability of the
neurons so that they can chill

This causes a balance in the levels of neurotransmitters in the brain.

Amazingly, lithium does not change the neurotransmission of people not affected by bipolar, so it stops excessive excitability without hindering appropriate excitability

113
Q

What is the gradual up-titration of lithium?

A

1 to 3 weeks for a response from lithium.

Goal range for acute phase: 0.8 1.2mmol/L

Goal maintenance range: 0.6-0.8mmol/L

Mild toxicity symptoms start at 1.5mmol/L

114
Q

What are symptoms of lithium toxicity?

A

Early symptoms of lithium toxicity:
Confusion, vomiting, tremor, slurred speech, increased sleep

Late symptoms of lithium toxicity:
Blurred vision, visual colour changes, ataxia, dysrhythmia, trembling, convulsions, increased urine

115
Q

Whats treatment for lithium toxicity?

A

Gastric lavage; diuresis; hemodialysis

116
Q

What are adverse effects of lithium?

A

Nausea, anorexia, vomiting, diarrhoea
Thirst and polyuria
Tremor, weakness
Hypothyroidism (due to interference with iodination)
Mental confusion
Teratogenesis
Oedema and weight gain
Nephrogenic diabetes insipidus

117
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

118
Q

What is the pathway of pain?

A

Pain starts with stimulating primary
nociceptors (first order neurons) (Sensory). Run from the perheery into the dorsal horn spinal cord/brain stem.
-
Neurotransmitter crosses over the synapse and causes action potential in second order neuron. SOD ends and transmit signals to thalamus, within the ascending spinothalamic tract of the spinal cord and brainstem.
-
Tertiary sensory neurons then transmit signals from the thalamus to other brain regions, including the:
primary somatosensory cortex
limbic system
prefrontal cortex

119
Q

Whats peripheral neuropathic pain?

A

The pain sensory nerves going to the brain or the spinal cord are damaged.

Brain doesn’t realise that the pain is coming from the nerve

It localises the pain as coming from the place where the receptor is located. Presents as burning, numbness or electric shock

120
Q

Whats an example of peripheral neuropathic pain?

A

Diabetic neuropathy
Neuralgias
Complex regional pain syndromes

121
Q

Explain diabetic neuropathy.

A

Unmyelinated axons are directly affected by hyperglycemia and ischemia by diabetes.

The longer the axons the greater the risk for neurophy

122
Q

When does pain perception occur?

A

The perception of pain occurs once nociceptive signals reach specific areas of the brain via tertiary sensory neurons.

123
Q

What is morphine?

A

Opioid analgesic

Gold standard for potency, therapeutic effect, and side effects

Obtained by opium poppies

Morphine is not highly protein-bound (35%) and is relatively hydrophilic so crosses only slowly into the CNS

124
Q

What are opioid antagonists

A

Opioid antagonists are medications that block the activation of opioid receptors in your central or peripheral nervous systems. In other words, these medications block the effects of opioids. They’re key to treating opioid overdose, opioid use disorder and other conditions.

respiratory depression

125
Q

What are examples of opioid antagonists?

A

Naloxone and Naltrexone

126
Q

What is an opioid?

A

A chemical that works by binding to opioid receptors. Receptors found in the CNS, PNS and the gi tract.

Used to treat acute and chronic pain.

Can alleviate severe delbitaibg pain

127
Q

What is endometriosis

A

Tissue similar to the ones that grow in your uterus grow in other parts of your body.

Ectopic endometrium called lesions respond to hormones, grow with blood supply, and break down/ shed- irritation & of the surrounding tissue - inflammation- scarring adhesion -

It is not known what causes endometriosis; there are a few theories (e.g. retrograde menstruation, embryological tissue origin) and growing evidence that an improper immune response may be involved.

128
Q

What is treatment for endometriosis

A

Hormonal therapy- Contreceptive pill

Surgery to remove scaring/ lesions, hysterectomy, oophorectomy

129
Q

What is breast cancer?

A

Primary breast cancer is usually described as non-invasive or invasive and classified according to where the abnormal cell proliferation begins.

Breast cancer is the most common cancer in females, but it can also occur in males (although is very rare).

130
Q

What is non-invasive breast cancer?

A

Ductal carcinoma in-situ originates within the epithelial cells lining the ducts of the breast and the growing mass remains within the duct. This type carries the risk of becoming invasive ductal carcinoma.

Lobular carcinoma in-situ is not really a breast cancer, as it is not invasive or potentially invasive. It is localized cell growth within the lobules.

131
Q

What is invasive breast cancer?

A

Invasive ductal carcinoma is the most common type of breast cancer. It develops from cells lining the ducts of the breast that then spread to the surrounding tissue. There are a number of rarer, sub-types of invasive ductal cancer.

Invasive lobular carcinoma is the second most common type of breast cancer. It originates with epithelial cells in the lobules that then spread to surrounding tissues.

132
Q

What are the risk factors for breast cancer

A

early age of menarche and late age of menopause

nulliparity or late 1st pregnancy

genetics (e.g. BRAC genes) and family history

environmental factors (e.g. poor diet, smoking, lack of physical activity, increased weight after menopause, alcohol use)

133
Q

What is a testicular torsion?

A

This is a twisting of the spermatic cord which disrupts blood supply to the testis. This can occur spontaneously, or as a result of physical exertion or trauma, most commonly in younger aged males around the time of puberty. Vascular engorgement and ischemia occur, which can eventually lead to testicular necrosis and loss of function.

134
Q

What are symptoms to testicular torsion?

A

There is typically a rapid onset of scrotal swelling and pain. Other signs & symptoms may include nausea/vomiting, fever, loss of the cremaster reflex and a horizontally positioned testis.

Emergency management is required as irreversible changes can occur within 4-6 hours. It is treated with detorsion (manual untwisting), possibly followed by surgery.

135
Q

What is Benign prostatic hyperplasia (BPH)?

A

Benign prostatic hyperplasia (BPH) is a non-cancerous enlargement of the prostate gland.

Common in men over 50. Often considered a normal part of aging.

136
Q

What are symptoms of Benign prostatic hyperplasia

A

Weak inconsistent stream of urine
Have to strain when urinating
Pain during urination
Trouble initiating urination

137
Q

What is treatment to benign prostatic hyperplasia

A
  • relieving obstruction & allowing urine to flow normally.
    Finasteride shrinks prostate gland by inhibiting conversion of testosterone
138
Q

What is a spinal cord injury?

A

Spinal cord injury involves damage to the spinal cord that results in some alteration to normal function. The impact of the injury can range from temporary disruption of function to permanent loss of function. Spinal cord injury may be a result of trauma or disease processes that cause damage. Most commonly, spinal cord injury occurs due to trauma of the vertebral column associated with:

motor vehicle accidents
falls
violence
sporting injuries, e.g. diving

139
Q

What is a complete spinal injury

A

Total loss of sensory and motor functions below the lesion/level of injury.

140
Q

What is a incomplete spinal injury

A

Some level of function remains below the lesion/level of injury.

141
Q

What is cord concussion?

A

Temporary disruption of cord function.

142
Q

What is cord contusion?

A

Bruising of neural tissue with temporary loss of cord function.

143
Q

What is Cord laceration

A

Tearing of neural tissues with loss of cord function. Return of function may be possible with very minor damage, otherwise likely to be permanent loss.

144
Q

What is Cord transection

A

Severing of spinal cord causing permanent loss of function.

145
Q

What is primary spinal cord injury?

A

Spinal cord injury involves the initial damage to the spinal cord (primary injury)

The primary injury produces mechanical disruption to the vertebral column (e.g. vertebral fracture or dislocation), causing cord contusion, compression, laceration or transection. This focal damage of the spinal cord injures neurons and oligodendrocytes and disrupts vasculature and the blood-spinal cord barrier.

146
Q

What is secondary spinal cord injury?

A

Secondary injury involves the cascade of events that result from the primary injury. These include microscopic hemorrhaging within the spinal cord and/or surrounding meninges and the infiltration of inflammatory chemicals and cells into the spinal cord. These subsequently cause swelling of the spinal cord which leads to functional impairment and vascular impairment. These factors then lead to further damage to the spinal cord (i.e. cellular dysfunction & death) via increased pressure and cord compression and ischemic injury.

147
Q

What is spinal shock?

A

Immediately following the primary injury, spinal shock occurs. Spinal shock involves the loss of spinal cord activity at and below the level of injury, including:

loss of all reflexes (somatic & autonomic)
paralysis of skeletal muscles
decreased or no sensation

pinal shock also results in an inability to activate thermoregulatory mechanisms (e.g. vasoactivity, sweating) and thus the individual’s body temperature is determined by the external temperature. Spinal shock can last a few days to a few months and can make it difficult to determine the actual extent of injury and functional loss.