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BNKN602 > Patho & Interventions > Flashcards

Patho & Interventions Flashcards

1
Q

Asthma: definition

A

A respiratory condition whereby the airway may tighten, partially close, swell and make more mucus when faced with certain triggers. this causes difficulty breathing.

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2
Q

Asthma: aetiology

A

is thought to be caused by a combination of genetic and environmental factors. this included
- exercise- induced asthma, can worsen when air is cold or dry
- occupational asthma, triggered by workplace irritants such as chemicals, fumes, gases or dust
- allergy-induced asthma, triggered by airborne substances such as pollen, smoke, tobacco, pet fur.

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3
Q

Asthma: pathophysiology

A

an inflammatory response is triggered by allergens= mucous secretion that occludes small airways and bronchial hyperreactivity
airway inflammation = swelling or oedema of the membranes that line the bronchi and bronchioles
mast cells, when activated, release chemical called mediators which cause inflammatory response, leading to an increased blood flow and movement of white blood cells to the area and bronchoconstriction.
alveoli in areas distal to airway obstruction become hyper-inflated
air trapping within the alveoli causes increased pressure that decreases alveolar perfusion causing a ventilation/ perfusion (V/Q) mismatch. this will initially cause hypoxaemia and eventually cause hypercapnia leading to asthma symptoms.

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4
Q

Asthma: interventions/ assessments

A

bronchodilators through nebuliser or spacer
administer 02 as prescribed
sit patient upright
reassurance
education
mobilise/ rest as tolerated
monitor sputum.
posterior chest
peak flow

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5
Q

COPD: definition

A

A group of lung diseases that block airflow and make it difficult to breathe.
Emphysema
Chronic Bronchitis
Asthma

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6
Q

COPD: signs and symptoms

A

SOBE
increased RR
decreased SP02
increased HR
fever
chills
Wheeze
Crackles on inspiration
Cough
dullness on percussion
chronic cough
fatigue
sputum production
increased frequency of chest infections
tripod positioning
clammy skin/ diaphoresis
dizziness

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7
Q

COPD: assessment/ interventions

A

encourage fluids to moisten secretions
position upright to maximise air entry
educate breathing techniques. pursed lip breathing, exhalation of c02
bronchodilators
ABS

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8
Q

COPD: pathophysiology

A

tobacco smoke/ air pollution causes
inflammation of the airway epithelium, which leads to
infiltration of inflammatory cells and release of cytokines, which can cause
systemic effects (muscle weakening and loss)
this can lead to continuous bronchial irritation and inflammation
- chronic bronchitis (bronchial oedema, hypersecretion of mucus, bacteria; colonisation of airways

or
breakdown in lung elastic tissue
- Emphysema (destruction of alveolar septa and loss of elastic recoil of bronchial walls)

both of which can result in
- airway obstruction, air trapping, loss of surface area for gas exchange, frequent exacerbations (infection, bronchospasm), Evident by Dyspnea, cough, hypoxemia, hypercapnia or pulmonia.

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9
Q

COPD: Emphysema:

A

affects the air sacs, which are balloon like spaced in the lungs. over time the air sacs are slowly destroyed, which reduced air exchange in the lungs.

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10
Q

Pneumonia: signs and symptoms

A

SOBE
increased RR
decreased SP02
increased HR
fever
chills
Wheeze
Crackles on inspiration
Cough
dullness on percussion

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11
Q

Pneumonia:

A

acute infection of the lung parenchyma

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12
Q

Pneumonia: Assessments/ interventions

A

administer ABs
encourage fluid intake, IV fluids
encourage coughing technique
position upright
cooling cares
educate good hand hygiene.

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13
Q

Pneumonia: pathophysiology

A
  1. bacteria invades spaced between cells and alveoli
  2. inflammatory response + alveolar macrophages try to control infection
  3. fluid and mucus buildup in lungs
  4. impaired gas exchange and circulation
  5. ventilation exceeds pulmonary perfusion (V/Q) mismatch.
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14
Q

influenza: definition

A

influenza is an acute inflammation of nasopharynx, trachea and bronchioles with congestion, oedema and the possibility of necrosis of respiratory structures.

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15
Q

influenza: signs and symptoms

A

fever
cough
sore throat
runny/ stuffy nose
body aches
headaches
chills
upset stomach

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16
Q

influenza: pathophysiology

A
  1. virus enters the respiratory tract attaching to epithelial cells
  2. enters host cell and uses host DNA to replicate the disease
  3. new viral spores are released from host cell
  4. destruction/ desquamation of trachea and bronchi means on basal layer of epithelium remains
  5. damage to epithelial cell wall causes oedema and possibly haemorrhage of submucosa leading to cell death
  6. necrotic cells may undergo phagocytosis by macrophages, recruiting neutrophils
  7. results in alveolar wall oedema causing ineffective gas exchange.
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17
Q

influenza: aetiology

A

there are age groups more susceptible to influenza including
- elderly
- young children and pregnant women
- adults and children with chronic disorders of pulmonary and or circulatory systems
- those living in nursing homes or long term care.

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18
Q

influenza: assessments and interventions

A

administer bronchodilators
encourage fluids
cooling cares
educate hand hygiene
prevention (immunisation)

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19
Q

pulmonary embolism: definition

A

is a blockage in one of the pulmonary arteries in the lungs

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20
Q

pulmonary embolism: signs and symptom

A

SOV
chest pain
cough
increased HR or palpitations
decreased SP02

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21
Q

pulmonary embolism: Aetiology

A

a pulmonary embolism is caused by blood clots that travel from the legs, or rarey other parts of the body. (DVT deep vein thrombosis)
risk factors include
- conditions and disorders that blood clotting as a result of venous stasis
- decreased mobility
- hypercoagulability
- pregnancy and injury to endothelial cells that line vessel
- no matter the source, a blood clot becomes an embolus when all or part of it breaks away from the site of formation into the bloodstream

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22
Q

pulmonary embolism: assessments/ interventions

A

administer anticoagulants
encourage regular mobilisation and position changes
reassure and educate about PE treatment options
administer 02 as required.

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23
Q

ischaemic heart disease: definition

A

increases myocardial oxygen demand and decreased myocardial oxygen delivery results in ineffective myocardial oxygen perfusion

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24
Q

ischaemic heart disease: signs and symptoms

A

can range from no symptoms, to chest pain, to a heart attack.

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25
Q

ischaemic heart disease: pathophysiology

A
  1. atherosclerosis leads to heart damage and necrosis of the myocardium
  2. heart damage leads to cardiac arrest/ arrhythmias.
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26
Q

ischaemic heart disease: aetiology

A

coronary artery disease (CAD) is the most common type of heart disease and happens with the arteries that supply blood to the heart muscle (coronary artery) become hardened and narrowed.
- A gradual blockage can result in angina.
- A sudden or severe blockage can result in heart attack or cardiac arrest.

Risk factors
- HTN
- smoking
- diabetes
- high fat and cholesterol diet

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27
Q

ischaemic heart disease: assessments and interventions

A

lifestyle changes, medications, angioplasty and surgery.
physical exercise, smoking cessation, weight loss, low fat diet
GTN spray
medications
- statin (decreased liver’s production of harmful cholesterol)
- blood thinners (helps prevent blood clots from forming, dissolves old ones)
- beta blockers (slows heart rate and decreases blood pressure)
- calcium channel blockers (relaxes blood vessels)
- heart medications (helps reduce chest pain or pressure caused by blockage in arteries of heart)

coronary stent
- tube placed in the arteries of the heart to keep them open
coronary angioplasty
- unblocking an artery by inflating a balloon inside it. A stent may also be inserted to hold artery open
coronary artery bypass surgery.

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28
Q

Atherosclerosis: definition

A

the build up of fats, cholesterol and other substances in and on the artery walls.

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29
Q

Atherosclerosis: signs and symptoms

A

Atherosclerosis often has no symptoms until a plaque ruptures or the build up is severe enough to block blood flow.
- chest pain.
- SOB
- Fatigue
- tightening of the chest

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30
Q

Atherosclerosis: pathophysiology

A
  1. an irritant is present, e.g. lipids, high blood pressure, toxins, diabetes.
  2. damage occurs to the endothelium by the irritant- a crack of fissure is formed.
  3. LDL cholesterol deposits accumulate in the artery wall known as fatty streaks
  4. LDL oxidases and sends signals to the immune system and monocytes (WBC) arrive
  5. monocytes convert to macrophages and consume the cholesterol
  6. macrophages fill up on cholesterol and die = foam cells
  7. formation of foam cells = release of cytokines
  8. smooth muscle cells migrate into expanding fatty plaque forming a lipid cap
  9. smooth muscle cells also deposit calcium into the fatty plaque, hardening it and causing bulging into the artery lumen
  10. blood flow is decreased(resistance increased)and compliance is reduced (less flexibility)
  11. ongoing inflammation= plaque rupture, thermogenic material inside cap is exposed= arriving platelets from a thrombus
  12. a thrombus is formed and occludes the artery causing ischemia or infarction
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31
Q

Atherosclerosis: aetiology

A

high blood pressure
high cholesterol
high triglycerides
smoking and or sources or tobacco
insulin resistance, obesity or diabetes
inflammation from diseases such as arthritis, lupus or infections or inflammation of unknown cause.

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32
Q

Heart failure: definition

A

is the heart’s inability to consistently pump enough blood to organs and tissues.

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33
Q

Heart failure: pathophysiology

A
  1. MI or cardiac dysfunction / structural abnormality impairs ability of the left ventricle to fill with or eject blood
  2. poor ventricular function/ myocardial damage leads to decreased stroke volume and cardiac output
  3. leads to a neurohormonal response
  4. either sympathetic system activated to increase cardiac workload or RAAS cc c pathways activated
  5. results in vasoconstriction and sodium + fluid retention
  6. further stress on the ventricular wall and remodeling leads to heart failure.
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34
Q

Heart failure: aetiology

A

commonly caused by IHD (decreased contraction, ventricular filling or both). more common among the elderly.
can be caused by AF, HTN, diabetes smoking, drinking excessively , HIV and some cytotoxic drugs.

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35
Q

Heart failure: assessment and intervention

A

ensure daily weights
start FBC and fluid restrictions
educate on healthy eating and exercise
furosemide?

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36
Q

Chronic renal failure/ kidney injury: definition

A

progressive irreversible loss of kidney function and decreased GFR for at least three months.
can lead to AKI, interventions aim to prevent AKI

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37
Q

Chronic renal failure/ kidney injury: signs and symptoms

A

Nausea
Vomiting
Loss of appetite
Fatigue and weakness
Sleep problems
Urinating more or less
Decreased mental sharpness
Muscle cramps
Swelling of feet and ankles
Dry, itchy skin
High blood pressure (hypertension) that’s difficult to control
Shortness of breath, if fluid builds up in the lungs
Chest pain, if fluid builds up around the lining of the heart

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38
Q

Chronic renal failure/ kidney injury: pathophysiology

A

.

39
Q

Chronic renal failure/ kidney injury: aetiology

A

At the early stages people have no symptoms:
Diabetes
Hypertension
Smoking
Obesity
Ethnicity
Gender men>women
Age - kidney function decreases with age
Specific conditions – glomerulonephritis

40
Q

Chronic renal failure/ kidney injury: assessments and interventions

A

Nursing interventions:
Maintain adequate nutrition
Fluid restriction
Promote activity & rest as tolerated
Provide skin care
Provide education on condition & complications
Provide culturally appropriate care
Psychological/emotional l support
Support for smoking cessation

41
Q

Acute kidney failure/ kidney injury: definition

A

Acute kidney injury (AKI)occurs when the kidneys are unable to remove the body’s metabolic waste or perform their seven regulatory functions – in particular, for cardiac week - maintenance of BP and electrolyte regulation

42
Q

Acute kidney failure/ kidney injury: signs and symptoms

A

passing less urine (pee) than usual
very concentrated urine, or urine looking yellow/brown/red in colour
loss of appetite
nausea or vomiting
fatigue and short of breath
feeling confused, anxious and restless, or sleepy
swelling of legs or other body parts
pain in abdomen or lower back.

43
Q

Acute kidney failure/ kidney injury: pathophysiology

A

.

44
Q

Acute kidney failure/ kidney injury: assessment and intervention

A

Assessments:
Fluid balance chart (FBC)
Daily weigh (1kg of weight = 1L retained fluid)
Skin integrity
Vital signs → EWS
Capillary refill time (CRT)
Palpate and/or scan the bladder
Bloods – GFR, electrolytes, CBC
Ability to manage ADLs

45
Q

DVT: signs and symptoms

A

throbbing pain in 1 leg (rarely both legs), usually in the calf or thigh, when walking or standing up
swelling in 1 leg (rarely both legs)
warm skin around the painful area
red or darkened skin around the painful area – this may be harder to see on brown or black skin
swollen veins that are hard or sore when you touch them

46
Q

DVT: definition

A

DVT (deep vein thrombosis) is a blood clot in a vein, usually in the leg.

47
Q

DVT: pathophysiology

A

Deep venous thrombosis usually begins in venous valve cusps. Thrombi consist of thrombin, fibrin, and red blood cells with relatively few platelets (red thrombi); without treatment, thrombi may propagate proximally or travel to the lungs.

  1. Decreased or mechanically altered blood flow
  2. Trauma to blood vessels stimulates the clotting cascade
  3. Platelets aggregate at the site, especially where venous statis is present
  4. Platelets and Fibrin form the initial clot
  5. Decreased blood flow leads to decreased oxygenation and increase in hematocrit (increase in RBC in the blood volume)
  6. RBC are trapped in the fibrin meshwork
  7. Clot may completely occlude blood vessel or embolus may travel to other parts of the body (lungs or brain).
48
Q

DVT: Virchow’s triad

A

Virchow’s Triad distills the multitude of risk factors for DVT into three basic elements favouring thrombus formation: venous stasis, vascular injury and hyper coagulability.
Clinical, biochemical, and radiological tests are used to increase the sensitivity and specificity for diagnosing DVT.

49
Q

Paralytic ileus: definition

A

The condition where the motor activity of the bowel is impaired, usually without the presence of a physical obstruction.

50
Q

Paralytic ileus: signs and symptoms

A

Abdominal bloating, abdominal distension, Gas, Constipation, Nausea and vomiting, dehydration.

51
Q

Paralytic ileus: pathophysiology

A

Paralytic ileus occurs when the muscle contractions that move food through your intestines (peristalsis) are temporarily paralyzed.

  1. SNS activated intra operatively and bowel motility inhibited
  2. Increase in cytokines and inflammatory mediators decrease bowel motility
  3. Peristalsis slows then stops
  4. This leads to decreased movement of faecal matter through the bowel
52
Q

Traumatic brain injury: signs and symptoms

A

Loss of consciousness from several minutes to hours
Persistant headache or headache that worsens
Repeated vomiting or nausea
Convulsions or seizures
Dilation of one or both pupils
Clear fluids draining from nose and ears
Inability to awaken from sleep

53
Q

Traumatic brain injury: pathophysiology

A

Traumatic brain injury occurs when a traumatic event causes that brain to move rapidly within the skull, leading to damage.
Damage of neuronal tissues associated with TBI fall into two categories:
Primary injury, which is directly caused by mechanical forces during initial insult; and secondary injury, which refers to further tissue and cellular damages following primary insult.

54
Q

Traumatic brain injury: definition

A

Brain dysfunction caused by an outside force, usually a violent blow to the head.

55
Q

ischemic/ hemorrhagic stroke: signs and symptoms

A

Motor deficits – most obvious – include: mobility, respiratory function, swallowing and speech, gag reflex, self care abilities
Hemiplegia (paralysis) / hemiparesis (weakness)
Ataxia = altered coordination of movement & posture (cannot coordinate movement – lost sense of where body part is located, staggering/abnormal walking movements)
Dysphagia = altered swallow

Communication –
Speech = aphasia (inability to use or comprehend words), expressive & receptive dysphasia – depending on area affected these will differ eg – damage to Wernickes area – may have fluent aphasia – faulty understanding of written or spoken words, might produce a string of words with no meaning (word salad), or damage to Brocca area – non fluent – inability to properly form words (know what they want to say but cannot speak the words)

Intellectual Function – Both memory and judgement may be impaired, L side damage more likely to result in memory problems, R side tends to mean pt is impulsive

Spatial perceptual - more common with R side – patients may deny their illness or their body parts. Neglect of one side of body (may be made worse by homonymous hemianopia) , spatial orientation – can’t judge distances, agnosia – cant recognise an object by sight, touch or hearing, and apraxia – inability to carry out learned sequential movements on command

Affect - may have trouble controlling emotions, responses may be exaggerated or unpredictable, depression an issue, frustration, lability

Focus in on terminology
Hemianopia / diplopia
Memory – short & long term affected, low attention & concentration, altered judgement & abstract thought
Emotional lability

Elimination – symptoms more often temporary than permanent but need to consider functional incontinence (resulting from cognitive, functional or environmental factors)

56
Q

ischemic stroke: pathophysiology

A

Ischaemic cascade:
- disrupted blood flow
- Anaerobic respiration
- Lactic acid
- Insufficient ATP

Ion imbalance:
- Increase in intracellular calcium
- Increase Glutamate
- Vasoconstriction

Enlarged area of infarction into penumbra:
- Cell membrane and proteins break down
- Formation of free radicals
- Proteins production decreased
- Cell injury and death

57
Q

hemorrhagic stroke: pathophysiology

A

Ruptured vessel:
- Explosive eruption of blood from vessel into surrounding brain tissue and structure
- Haematoma develops
- Exposure of brain to blood, an increase in intracranial pressure caused by sudden entry of blood into the tissue, and secondary ischaemia result from reduced blood flow/perfusion.

ion imbalance:
- Mismatch between blood flow and metabolic demand
- Breakdown of sodium/potassium pump maintaining cellular function
- Anaerobic respiration to produce ATP
- Increased production of lactic acid

Cell death:
Altered pH
Cell membrane and proteins break down
- Formation of free radicals
- Cell injury and death

58
Q

ischemic/ hemorrhagic stroke: aetiology

A

Modifiable contributing factors:
- High cholesterol
- diabetes
- Obesity
- Inactivity
- Smoking and ETOH
- Hypertension

Non-modifiable contributing factors:

Age
More common in over 55-year-olds

Gender
Women have a higher incidence of stroke than men

Ethnicity
NZ Maori have a greater incidence than non-Maori
Greater incidence in South Asian and African/Caribbean population

Genetics
Small vessel disease in approx. 7% of stroke in young adults

59
Q

ischemic/ hemorrhagic stroke: assessments and interventions

A

Nursing interventions:
Maintain head of bed 30◦
to facilitate jugular venous drainage and help reduce intracranial pressure

Maintain systolic blood pressure within prescribed parameters (often < 180mmHg)
to reduce the potential for further bleeding or ischaemic changes

Continuous neurological observations
to help identify deterioration to initiate timely intervention and treatment

Ensure correct positioning of paralysed limbs
to prevent contractures and maximise function for rehabilitation

Ensure patient is kept NBM until swallow is assessed by Speech and Language Therapist
to prevent aspiration of oral fluid and food

Administer prescribed aspirin orally or enterally
to impede clotting and prevent further ischaemia

Turn the patient regularly
to maintain skin integrity and prevent pressure injury if the patient cannot move themselves

60
Q

Spinal cord injury: definition

A

A spinal cord injury (SCI) is damage to the tight bundle of cells and nerves that sends and receives signals from the brain to and from the rest of the body.

61
Q

Spinal cord injury: signs and symptoms

A

HTN (>20mmHg pt baseline) - Bradycardia
Headaches
Blurred vision
Facial Flushing
Diaphoresis above level of injury
Anxiety and restlessness.

62
Q

Spinal cord injury: pathophysiology

A
  1. Noxious stimulus (distended bladder, constipation etc.)
  2. Signals transmitted to spinal cord to initiate SN activation (> HR, > BP - vasoconstriction, > RR)
  3. HTN stimulates baroreceptors in carotid bodies. Brain initiates PN activity to reduce BP by slowing HR (bradycardia)
  4. Signals to reverse SN activity sent from brain via spinal cord to vasodilate blood vessels, slow HR. This occurs ABOVE SCI level
  5. Signals cant pass BELOW level of injury. if noxious stimulus continues, ascending signals continue to initiate SN activity.
  6. Results in increasing HTN (associated headache, blurred vision) bradycardia, vasodilation ABOVE SCI level and vasoconstriction BELOW.
63
Q

Spinal cord injury: Types of spinal cord injury

A

Transient concussion (reversible)

Contusion - Bursed

Laceration- Cut to cord

Compression - Squashed cord

Transection (irreversible) - cut straight through spinal cord

64
Q

Spinal cord injury: assessments and interventions

A

Interventions:
Put the person into sitting position 90◦ to help lower the BP
Loosen clothing
Assess for the probable cause and remove
Continue to assess vital signs (Q2-3min BP)
Administer GTN as prescribed if SBP > 150mmHg (short acting anti-hypertensive medications only)

65
Q

Compartment syndrome: Definition

A

A painful and dangerous condition caused by pressure build-up from internal bleeding or swelling of tissues.
The pressure decreases blood flow, depriving muscles and nerves of required nourishment.

Occurs in long bone fractures.

66
Q

Compartment syndrome: signs and symptoms

A

Bulging or visible swelling of the muscle.
Feeling like the muscle is fuller, swollen or somehow larger than normal.
Numbness.
Muscle pain that is stronger than you’d expect from the injury.
Severe pain when you stretch the muscle.
Tightness in the muscle.
Tingling or burning sensation in or under your skin, called paresthesias.

67
Q

Compartment syndrome: pathophysiology

A

Fluid enters a fixed volume compartment (eg from bleeding)
Increase in tissue and venous pressure
This pressure exceeds capillary perfusion pressure
Capillaries collapse
Muscle and nerve ischemia occurs
OR…
External compression (eg plaster cast)
Decrease in size of compartment
Increase in intracompartment pressure and decrease in arteriolar pressure
Leads to muscle and nerve ischemia

68
Q

Compartment syndrome: aetiology

A

Acute compartment syndrome can also occur after injuries without bone fractures, including:

Crush injuries
Burns
Overly tight bandaging
Prolonged compression of a limb during a period of unconsciousness
Surgery to blood vessels of an arm or leg
A blood clot in a blood vessel in an arm or leg
Extremely vigorous exercise, especially eccentric movements (extension under pressure)

69
Q

Compartment syndrome: The 5 P’s of neurovascular assessment relating to compartment syndrome

A

Pain, Pallor (pale appearance), pulselessness, paresthesia (burning or prickling sensation), poikilothermia (temperature control).

70
Q

Autonomic dysreflexia: definition

A

Autonomic dysreflexia isan abnormal, overreaction of the involuntary (autonomic) nervous system to stimulation. The most common cause of Autonomic dysreflexia is spinal cord injuries.

71
Q

Autonomic dysreflexia: signs and symptoms

A

Hypertension
Bradycardia
Sweating
Flushing
Pupillary constriction
Nasal congestion
Pale cool skin
Piloerection (goose bumps)

72
Q

Autonomic dysreflexia: aetiology

A

ingrown toenail, constipation intense pain, kinked catheter, distended bladder, urinary tract infection, pressure injury

73
Q

Autonomic dysreflexia: pathophysiology

A
  1. Strong discomfort/pain stimulus sending signal into spinal cord via intact peripheral nerves below T6 lesion
  2. CNS senses this input as it travels up the spinal cord evoking a massive Peripheral sympathetic response through spinal reflexes and sends the Sympathetic Nervous System signals and vessels vasoconstrict below the level of the T6 injury
  3. Vessels continue to constrict as they are trying to send signals to the brain -
    peripheral artery hypertension occurs
  4. Brain detects hypertensive crisis through baroreceptors in carotid and aortic arch but CAN’T get the signal to relax vessels and decrease blood pressure into the lower extremities because the spinal cord is severed
  5. Brain attempts two maneuverers to halt hypertensive crisis

May…
6. Attempts to Shut down sympathetic surge by sending descending inhibitory impulses
Impulses unable to travel to most sympathetic outflow areas due to spinal cord injury at T6 or above
OR….
6. Attempts to decrease peripheral BP by slowing Heart Rate through an intact vagus (parasympathetic) nerve
Compensatory bradycardia is inadequate, and hypertension continues

  1. Sympathetic nerves prevail below level of spinal injury and parasympathetic nerves prevail above level of injury causing vasodilation above the level of injury (T6) and Vasoconstriction below T6 injury causes increase BP and the vagus nerve causes bradycardia.
  2. Reflex hypertension eases with removal of noxious stimulus
74
Q

Myocardial infarction:

A

A myocardial infarction (commonly called a heart attack) is an extremely dangerous condition that happens because of a lack of blood flow to your heart muscle. The lack of blood flow can occur because of many different factors but is usually related to a blockage in one or more of your heart’s arteries. Without blood flow, the affected heart muscle will begin to die. If blood flow isn’t restored quickly, a heart attack can cause permanent heart damage and death.

75
Q

myocardial infarction: signs and symptoms

A

Chest pain (angina). This can be mild and feel like discomfort or heaviness, or it can be severe and feel like crushing pain. It may start in your chest and spread (or radiate) to other areas like your left arm (or both arms), shoulder, neck, jaw, back or down toward your waist.
Shortness of breath or trouble breathing.
Fatigue.
Trouble sleeping (insomnia).
Nausea or stomach discomfort. Heart attacks can often be mistaken for indigestion or heartburn.
Heart palpitations.
Anxiety or a feeling of “impending doom.”
Sweating.
Feeling lightheaded, dizzy or passing out.

76
Q

myocardial infarction: pathophysiology.

A

myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function. Prolonged myocardial ischemia activates a “wavefront” of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyocytes in the infarcted heart.

77
Q

myocardial infarction: aetiology

A

Coronary artery spasm.
Rare medical conditions: An example of this would be any disease that causes unusual narrowing of blood vessels.
Trauma: This includes tears or ruptures in the coronary arteries.
Obstruction that came from somewhere else in your body: A blood clot or air bubble (embolism) that gets trapped in a coronary artery.
Electrolyte imbalance.
Eating disorders: Over time, these can damage your heart and ultimately result in a heart attack.
Takotsubo or stress cardiomyopathy.
Anomalous coronary arteries (a congenital heart defect you’re born with where the coronary arteries are in different positions than normal in your body. Compression of these causes a heart attack).

78
Q

myocardial infarction: assessments and interventions

A

Interventions:
Supplemental oxygen
Medications
Education

79
Q

Angina: definition

A

a type of chest pain caused by reduced blood flow to the heart

80
Q

Angina: signs and symptoms

A

Discomfort, heaviness or tightness of the chest which may spread to the back, shoulders, neck or jaw. Other people describe it as a dull ache
Discomfort in the arm, neck or jaw with no chest discomfort
The discomfort can range from mild or dull to severe.

81
Q

Angina: aetiology

A

Angina is usually caused by coronary artery disease (also called atherosclerosis), which is the build-up of plaque in the walls of your arteries

82
Q

Angina: pathophysiology

A

Almost invariably, angina is associated with significant obstruction of at least one major coronary artery.
Oxygen demands not met. Normally, the myocardium extracts a large amount of oxygen from the coronary circulation to meet its continuous demands.
Increased demand. When there is an increase in demand, flow through the coronary arteries needs to be increased.
Ischemia. When there is blockage in a coronary artery, flow cannot be increased, and ischemia results which may lead to necrosis or myocardial infarction.
Schematic Diagram for Angina Pectoris via Scribd.

83
Q

Atelectasis: definition

A

Partial or complete collapse of a lobe or the entire lung, common post op complication.

84
Q

Atelectasis: signs and symptoms

A

Atelectasis often causes no symptoms on its own, though some underlying conditions that lead to atelectasis (like COPD) can cause symptoms.

However symptoms that may be experienced are:
Trouble breathing/shortness of breath (dyspnea).
Coughing.
Chest pain.
Rapid breathing (tachypnea).
Skin and lips turning blue.
Increased HR
Decreased O2
Decreased chest expansion on one or both sides

85
Q

Atelectasis: pathophysiology

A

Reduced ventilation or blockage

Obstruction of air to and from alveoli

Trapped air absorbed into bloodstream, blockage stops further air entering alveoli

Area of lung becomes airless

Lung collapse

Respiratory distress

86
Q

Atelectasis aetiology :

A

.

87
Q

Atelectasis: assessments and interventions

A

Intervention:
Deep breathing exercises
- DBE aim to allow as much oxygen in as possible to increase lung expansion and remove any sputum that may be present. DBE can re-expand the lung tissue such as alveoli that are unable to be inflated correctly during atelectasis.

Nursing actions to prevent atelectasis:
1. Spirometer is used to help the lungs to strengthen by encourage deep, full breaths. The pt aims to breathe in slowly and hold their breath for as long as comfortable. this device should be used at least 10 times every hour to promote recovery.
2. Administer bronchodilators
3. Have pt sitting upright to increase lung expansion and gas exchange
4. Education on breathing techniques and importance of coughing to excrete mucous.

88
Q

Meningitis: definition

A
89
Q

Meningitis: Pathophysiology

A

There are two types of meningitis, Bacterial and viral.
Bacterial- the entry of bacteria into the cerebrospinal fluid (CSF) and bacterial growth in this compartment leading to inflammation within the CSF and the adjacent brain tissue.
Viral - Once the virus has replicated and caused dysfunction within the immune system, it is able to cross the BBB (Blood-brain barrier) where it enters the cerebrospinal fluid

90
Q

Meningitis: risk factors

A

Not having completed childhood vaccinations, Children under the age of 5 years and adults over 50 years, living in overcrowded houses and co morbidities.

91
Q

Meningitis: Signs and symptoms

A

Infants and children- Fever, crying, unsettled, irritable, vomiting, sleeping, harder to wake, reluctant to walk, rash
Teens and adults- Fever, Headache, vomiting, sleeping, confusion, delirious, Unconscious, joint pain, aching muscles, stiff neck, photophobia, rash.

92
Q

Stoma: definition

A

An opening on the abdomen. connected to either the digestive system or urinary system to allow waste to divert out of the body.

93
Q

Stoma: colostomy, ileostomy, and urostomy

A

Colostomy: Opening from the large intestine through the abdomen. can be temporary or permanent. can be located in ascending, transverse, descending, or sigmoid.

Ileostomy: opening in the abdomen wall located on the right lower abdomen, at the end of the ileum.

Urostomy: opening in the abdominal wall. re- directs urines away from the bladder thats diseased or injured.

94
Q

Stoma: pt education

A

Pouches needs to be changed every 3-7 days but the pouch needs to be emptied regularly every day to decrease the risk of infections. it can take the stoma a few days to work correctly therefore, slowly introduce foods.

BNKN602 (21 decks)

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