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Health & Illness 2 Kathleens Final > Midterm > Flashcards

Midterm Flashcards

1
Q

What is intoxication?

A

Behavioural and physical symptoms from substance use.

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2
Q

What is craving?

A

Desire to use substance. A symptom associated with substance use disorder.

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3
Q

What is tolerance?

A

Increasing need in the amount of substance to achieve its reward.

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4
Q

What is withdrawal?

A

Syndrome of symptoms that occur with sudden cessation of drug use.

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5
Q

What is habituation?

A

Very short term, neurons receive a repetitive stimulus and chemically inhibit their own receptors to restrict stimulus short term.
You learn to ignore the stimulus or modify your behaviour short term. It is meant to allow primal suffering like hunger pains or sleep in loud places

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6
Q

What is adaptation?

A

Eventually through habituation neurons will permanently restrict enough receptors to permit functioning in presence of stimulus.
Stimulus has to increase to be effective.

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7
Q

CAGE questionnaire

A

Alcohol consumption
C- cut down on drinking
A- have people annoyed you by criticizing drinking
G- have you ever felt guilty about your drinking
E- have you ever had a drink in the am to calm your nerves or cure hangover ( eye opener )

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8
Q

Biological reward

A

Dopamine release, drugs increase dopamine in the pleasure area of the brain giving the brain extra dopamine which produces a positive reward for drug use.

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9
Q

Social effect

A

Peer pressure, self medication, grief, anxiety, social isolation, etc.

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10
Q

Substance induced disorders

A

Temporary and reversible. Cause by intoxication and immediate effects of cessation (withdrawals)
Effects the can causing physiological, psychological and behavioural effects

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11
Q

Substance use disorders

A

Form continued, frequent use of substance.

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12
Q

Behavioural disorders

A

That produce a reward response, gambling addiction, food addiction, sex addiction.

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13
Q

Potential signs of substance use

A

Fatigue, headache, sexual dysfunction, appearing older than age ,unexplained skin changes and life issues

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14
Q

Self stigma

A

Internalized negative messages, low self esteem shame

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15
Q

Societal stigma

A

Negative labels and judgement, discrimination

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16
Q

Structural stigma

A

Policies that increase stigma healthcare stigma, healthcare challenges, workplace challenges

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17
Q

Harm reduction

A

Reduces harms associated with substance use across the continuum of use
Ex. Safe injection sites, mobile sites, clean needles, sharps, safe injection kits

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18
Q

Prescription dependence vs addiction

A

Dependence: ordinary biological consequence of taking certain meds for weeks to years, not abusing your body is just use to it

Addiction: continued drug use in the face of negative consequences, involves cravings, lack of control and overuse despite it being harmful

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19
Q

Health care warning signs of misuse / addiction

A

Nightshift, extreme fatigue, unreliability, charting errors

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20
Q

What’s an opioid?

A

CNS depressant, medically is used as a analgesic
Derived from the opium poppy.

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21
Q

Phases of opioid addiction.

A

Phase 1- euphoria. Rush occurs almost immediately. May see facial flushing and deepening of voice.
Phase 2- sense of extreme well being. Endorphin reaction occurring.
Phase 3- lethargy to unconsciousness
Phase 4- once opioid is metabolized, user seeks additional drugs to avoid painful withdrawal.

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22
Q

What is opioid intoxication?

A

Constricted pupils, euphoria, slurred speech, psychomotor retardation, drowsiness, decreased RR, bp.

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23
Q

Long term use of opiods

A

Liver damage - jaundice, fatigue, ascities, abdominal discomfort
Damaged veins
Reduced appetite causes malnutrition
Risk for death from RESPIRATORY ARREST, hypoventilation, apnea
Social consequences,poor self management

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24
Q

Can opioids induce constipation?

A

Yes, can cause peristalsis. Ensure bowel health, using laxative and stool softeners
High risk for bowel obstructions and fissures

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25
Q

Sign of a overdose

A

Slow breathing, hard to wake, discolouration, pupils small, choking, dizzy

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26
Q

What do you use if someone overdoses?

A

Narcan , call 911
This induces withdrawal immediately, will wake up agitated

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27
Q

Withdrawal: stress reaction

A

Mediated by ANS due to stress from stopping addictive behaviour, ranges from mild to extreme

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28
Q

Withdrawal: rebound symptoms

A

Adaptive changes in the brain that counter effects of addiction continue despite cessation
Opposite of drug choice

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29
Q

Opioid withdrawal happens when?

A

4-6 6 hours after last use, peaks at 2-3 days, resolves 5-7 days

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30
Q

Diagnostics

A

Observation and patient account, generally subjective data. Use of dsm.
Blood and urine test can detect drug and alcohol metabolites as well as hepatitis and liver disease

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31
Q

Nursing assessment

A

Health history, ensure therapeutic communication through building trust and support. Use motivational interviewing

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32
Q

What is motivational interviewing?

A

Nurse listens more than speaks, provide empathy, positive reinforcement and encouragement, do not argue, discrepancies should be pointed out in a respectful manner

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33
Q

Recovery

A

Early: 1 month- 1 year
Sustained: 1-5 years
Stable: 5+ years

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34
Q

Methadone

A

Synthetic full opioid agonist and long lasting

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35
Q

Buprenorphine

A

Treats opiate withdrawal and craving
Long acting partial opioid agonist
Produces less euphoria

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36
Q

Suboxone

A

Bupremorphine + naloxone

Treats opiate withdrawal and craving, must take sublingual if the naloxone is activated for example crushing or injecting it will cause immediate withdrawal

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37
Q

Sublocade

A

Long acting buprenorphine, once monthly injection
Continuous release to sustain medication levels for 28 days

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38
Q

What are carries?

A

Multiple-day doses at a time from a pharmacy, then you carry nome
This requires trust and frequent Drug tests

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39
Q

Self awareness

A

Introspection, exploration of thoughts, emotions and values

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40
Q

Self esteem

A

Individual likes Or values themselves

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41
Q

Self concept

A

Body image, role performance, personal identity

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42
Q

Anorexia nervosa

A

Refusal to maintain minimally normal weight for height
Self worth is defined by shape of body and weight
Intense fear of gaining weight
Preoccupation with food and peculiar handling of food
Behavioural restriction of caloric intake
May binge and purge but primarily restricted behavior
Can start at 7 high correlation with OCD, anxiety

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43
Q

Signs and symptoms of anorexia nervosa

A

Starvation, lytes imbalance, dehydration, caloric restriction, excessive exercise, low calcium, estrogen deficiency.
Lanugo, cola extremities, constipation, abnormal ECG, yellow skin, impeded bone density, peripheral edema.

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44
Q

Assessment

A

Comprehensive physical assessment
Eating habits, perception of health and body

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45
Q

Hospitalization criteria

A

Weight loss greater than 85% temp under 36 hr under 40 systolic bp under 90 severe dehydration glucose under 2.2 electrolytes imbalance hepatic renal or cv compromise and suicidality and failure to adhere treatment plan

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46
Q

Treatment

A

SSRIs and Prozac reduce OCD behaviour after reaching maintenance weight
Antipsychotics may help with delusions or overactivity
Atypical antipsychotics can improve mood and decrease OCD symptoms

• Goal is to reach 90% ideal body weight (when most females can menstruate)
• Milieu Therapy

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47
Q

Refeeding syndrome

A

Critical risk, Increasing nutrition following period of starvation can cause refeeding syndrome. It can be fatal if not appropriately recognized and treated due to electrolyte and metabolic disturbances
This is caused by a shift of fluid and electrolytes

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48
Q

Deficiency and signs

A

Thiamine: wernicke korsakoff syndrome (confusion, weak eye muscles, ataxia, psychosis, amnesia, confabulations)
Phosphate: muscle weakness, parenthesis, cardiac arrhythmias
Magnesium: organ systems
Potassium: weakness, hyperventilation, ECG changes including T wave flattening and u waveformation

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49
Q

Risk factors for developing reseeding

A

Electrolytes, weight loss, intake, BMI,fat, muscles loss,disease

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50
Q

Prevention and treatment

A

Before refeeding: identify risks, baseline bloodwork, medical assessment and correct electrolyte imbalance begin on oral supplement
After initiation:start low and go slow- build up to full feeding over 3-7 days. Monitor vitals, ECG,bloodwork and serology and treat/replace imbalances prn

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51
Q

Bulimia nervosa

A

Repeated episodes of binge eating followed by compensatory behavior may use vomiting, excessive exercise,misuse of laxatives, diuretics, significant disturbance in perception of body shape and weight -tend tonover around a ideal body weight, there’s a high correlation with anxiety and depression-typically seen in ages over 12.

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52
Q

Bulimia nervosa complications

A

Bradycardia, hypotension, cardiac arrhythmia, electrolyte imbalance, elevated bicarb, dehydration, esophageal tears, diminished chewing, loss of dental arch, Russells sign (knuckle callus), abdominal pain and gastric dilation, parotid glandenlargement

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53
Q

Treatment for bulimia nervosa

A

Antidepressants
Prozac shown to lessen relapse
Correcting electrolyte imbalance

CBT is highly effective Interpersonal therapy
Generally more ready to establish
therapeutic relationship as they understand behaviours are problematic

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54
Q

Outcomes for bulimia nervosa

A

Vitals, impulse control, weight maintenance, hope

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55
Q

Binge eating disorder

A

Repeated episodes of binge eating after which there is significant emotional distress, episode induce guilt, depression, embarrassment and self disgust. Strong correlation with anxiety and depression

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56
Q

Treatment for binge eating

A

Antidepressants (may regain weight once stopped)
Stimulants
Prozac shown to lessen relapse
Dialectical behaviour therapy effective in reducing binging (talk therapy to manage thoughts, emotions, relationships)

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57
Q

Bariatric surgery

A

Preop: Understand post-op dietary requirements, supports, and management strategies
Screened for psychiatric comorbidities
Minimum 12 month recovery from eating disorder, suicide attempt, psychiatric hospitalization, etc.
Receive counselling and education lifestyle changes
Post op: Close follow up from interprofessional team monthly for 6 months, then every 2 months for the remainder of the first year post surgery

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58
Q

Feeding disorders

A

Inability or difficulty eating or drinking sufficient quantities to maintain nutrition.
May be affected by prematurity, failure to thrive, autism, and various cognitive disorders
Typically onset is in childhood, may continue into adulthood or resolve.

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59
Q

Examples of feeding disorders

A

Avoidant and restrictive
Pica- persistent eating of none food such as dirt, rocks, chalk
Rumination- undigested food is returned to the mouth and then rechewed reswallowed or spit out

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60
Q

Lifespan consideration of early age

A

Preterm babies have higher risk of
collapsing alveoli
Less alveolar surface area for gas exchange
Narrow branching of peripheral airway is easily obstructed

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61
Q

Lifespan consideration of older age

A

Reduced max inspiratory and expiratory force
Weaker cough Alveoli lose elasticity
Diminished strength of respiratory muscles

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62
Q

Tripod positioning

A

Optimizes the mechanics of respirations by taking advantage of the accessory muscles of the neck and upper chest to get more air to the lungs

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63
Q

What is asthma ?

A

Chronic airway trapping and inflammation leading to narrowed bronchioles
Linked to environmental triggers
Episodes can be reversible
May lead to scaring, fibrosis and thickening of basement membranes
Can be seasonal and year round

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64
Q

Triggers of asthma

A

Infection
Allergens
Exercise
Irritants

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65
Q

Asthma symptoms

A

Frequent coughing
SOB
chest pain
Difficulty breathing
Use inhaler
Night cough
Wheezing
Common cold

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66
Q

Diagnostics of asthma

A

Spirometry is the preferred diagnostic test for asthma.
Bronchodilators must be held 6-12 hours prior to testing.
Testing is done both before and after the use of bronchodilator to determine if obstruction is reversible and degree of response

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67
Q

Spirometry measures what?

A

Forced vital capacity (FVC) - the largest amount of air that you can blow out after you take your biggest breath in.
Forced expiratory volume (FEV1)- the amount of air you can blow out of your lungs in the first second

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68
Q

Very mild

A

Well controlled with reliever needed only occasionally

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69
Q

Mild

A

Well controlled with single low dose controller, reliever needed twice a week or less

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70
Q

Moderate

A

Well controlled with low to moderate dose dual controller with occasional reliever needed twice a week or less.

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71
Q

Severe

A

Controlled with high dose dual controller and additional medications with reliever needed twice a week or less or unable to achieve control

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72
Q

A patient with asthma should receive what first ?

A

Bronchodilator and then steroid

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73
Q

Client teaching

A

Avoid contact with triggers (minimize them if unavoidable)
Proper use of medications
Keep rescue inhaler on person at all times Regularly check peak flow meter to ensure remaining
in green zone
Primary prevention of respiratory illnesses
Do not avoid exercise!

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74
Q

Assessment findings of asthma

A

Lung sounds: commonly hear wheezing, may also hear crackles, rhonci, or stridor
Assess breathing effort, respiration rate (tachypnea), thorax symmetry, expansion of chest,
Oxygen status. Take a spO2 reading and assess for indicators of hypoxia such as skin, lip, and nail colour. Assess cognition.
Heart rate increased from work of breathing, and body’s attempt to compensate impaired gas exchange
Temp: may be increased as exacerbations often brought on from infections such as pneumonia
Pediatric: flared nares, chest wall retracts on inspiration, grunts, cyanosis when sucking, breaks in feeding

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75
Q

Asthma attacks

A

acute exacerbation
1. Early compensation- hyperventilation and fatigue. Fatigue helps the body compensate through rest which reduces oxygen demand.
HR and RR increase to optimize oxygen delivery to the cells
2. Late compensation- hypoventilation as they tire and respirations slow. Results in respiratory acidosis.

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76
Q

Status asthmatics

A

Most extreme acute asthma attack; patient fails to respond to standard treatment
Results in hypoxia, hypercapnia, and acute respiratory failure
Most commonly brought on by viral illnesses, food allergy, poor treatment adherence, discontinuation of mediation, or increased allergen exposure
Increased airway resistance with air trapping and hyperinflation of the lungs
Produces extreme anxiety and fear, worsening hyperventilation
Patient fatigue leads to co2 retention, respiratory acidosis, and can end with respiratory arrest, cardiac arrest, cor pulmonale, pneumothorax, etc.
Sternocleidomastoic, intercostal, and superclavicular muscle retractions
Pulses paradoxus (10mmHg drop in SBP from end-expiratory to end-inspiratory blood pressure)
Cannot finish a sentence (1-2 words), RR >30

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77
Q

Risk for status asthmaticus

A

History of past near-fatal asthma attack requiring intubation
Poor perception of dyspnea and hypercapnia
Recurrent hospitalizations or deterioration
despite chronic oral steroid use
History or coronary artery disease

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78
Q

What is COPD?

A

Chronic obstruction of airflow
Progressive disease
Usually insidious onset
Starts confined to lungs but as it progresses
causes skeletal muscle dysfunction, altered nutrition, HF, etc.

Can be classified as emphysema or chronic
bronchitis, but more often a combination of the two.

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79
Q

Cardinal symptoms

A

dyspnea, shortness of breath, difficulty breathing, limited activity

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80
Q

Emphysema

A

Pink puffer
Alveolar (diffusion) problem
Increase co2 retention
Minimal cyanosis
Pursed lip breathing
Dyspnea and increase RR
hyperresonance on chest percussion
Orthopneic
Barrel chest
Exertional dyspnea
Prolonged expiratory time
Short jerky sentences
Use of accessory muscles to breathe
Thin appearance

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81
Q

Think pink for emphysema

A

Pink sink and pursed lips
Increased chest circumference
No chronic cough
Keep tripoding

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82
Q

Chronic bronchitis

A

Blue bloater
Dusky and cyanotic
Recurrent cough and increase sputum production
Hypoxia
Hypercapnia (increase pcO2)
Respiratory acidosis
Increase hgb
Increase RR
Exertional dyspnea
High incidence in heavy cigarette smokers
Digital clubbing
Cardiac enlargement
Use of accessory muscles
Leads to right sided heart failure

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83
Q

Think blue for chronic bronchitis

A

Blue
Longer term cough
Unusual lung sounds
Edema

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84
Q

Diagnosis of COPD

A

Spirometry (FEV/FVC ratio less than 70%)
Workup may include
● CXR
● Medical history
● Physical examination
● Walking test (desat)
● EKG (heart failure)
● ABGs

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85
Q

Nursing interventions for COPD

A

• Lung sounds (wheezing, crackling)
• Work of breathing and use of accessory
muscles
• Need for suctioning
• Sputum production (?culture needed; high
risk for pneumonia)
• O2 sats. We want it between 88-93%
• Oxygen supplementation as ordered
• Pursed lip breathing/huff coughing
• May use nebulizer treatments, inhalers

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86
Q

Client education for COPD

A

QUIT SMOKING (most effective intervention)
Drug therapy (how to appropriately use medications)
Pursed lip breathing
Huff coughing
Oxygen therapy (we typically want low-
flow, humidified oxygen for home use)
Encourage flu and pneumonia vaccinations

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87
Q

Pursed lip breathing

A

Prolongs exhalation and prevents bronchiolar collapse and air trapping. Improves oxygenation, slows RR, and decreases dyspnea
-Relax neck and shoulders
-Inhale through nose for 2 seconds
-Pucker lips like a whistle or blowing out a candle
-Exhale slowly and gently through lips for 6 seconds

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88
Q

Huff coughing

A

Facilitates removal of secretions, reduces fatigue, and conserves energy
1. Patient assumes a sitting position with neck slightly flexed, shoulders relaxed, knees flexed, and forearms supported by a pillow and, if possible, with feet on the floor.
2. Patient then drops their head and bends forward while using slow, pursed-lip breathing to exhale.
3. Sitting up again, patient uses diaphragmatic breathing to inhale slowly and deeply.
4. Patient repeats steps 2 and 3 another three or four times to facilitate mobilization of secretions.
5. Before initiating a cough, patient should take a deep abdominal breath, bend slightly forward, and then cough three or four times on exhalation (huff coughing). Patient may need to support or splint the thorax or abdomen to achieve a cough of maximum effectiveness.

89
Q

Nutrition for COPD

A

Rest prior to eating approx. 30m Use bronchodilators prior to meal Small frequent meals
High calorie/protein
Avoid gassy food (pressure on diaphragm)
Increase fluids if not contraindicated to thin mucus
Avoid exercise 1 hour pre and post meal

Dry mouth and weight loss are frequent in COPD

90
Q

What is BIPAP?

A

BIPAP pushes air into your lungs then reduces pressure on exhalation. Since hypoxemia is the drive to breathe in severe COPD, this allows a return to normal breathing. This will reduce CO2 retention, assist in correction of acid-base imbalance, and allow respiratory muscles to rest as it forcibly induces gas exchange.

91
Q

What is stress?

A

A feeling of pressure or emotional strain to which the body has a physiological response. It is a Series of reactions to demands with the full reaction determined by duration severity resources and coping mechanisms

92
Q

Ranges of stress

A

Neutral : day to day manageable stress
Challenge manageable : moderate to greater stress that needs existing and potentially new resources and coping actions
Severe: not manageable, stress exceeds coping capacity

93
Q

Stress may be what?

A

Acute: most typical and short in duration
Episodic acute: self inflicted from taking on unrealistic assignments
Chronic: perceptual or sustained demand, threat or pressure that is harmful to health

94
Q

Selyes adaptation syndrome

A

●Alarm Stage is the physiological response to stress (you are trembling prior to your midterm and feel anxious)
●Resistance Stage is when the body attempts to repair after the initial shock/stress. If your body never sends the signal that the stress is finished, you continue with high stress hormones and long term effects are seen. (the exam is over but you still can’t focus on your other courses)
●Exhaustion: prolonged stress leads to exhaustion physically, emotionally, mentally in which you may experience burnout or mental heath crisis (it’s been weeks since your exam but you’re anxious and depressed. You can’t sleep. You don’t know how you can finish the semester).

95
Q

Impact of chronic Stress

A

Weight gain: cortisol helps with controlling fat/protein/carb burning.
High glucose: cortisol releases stored glucose and is a contributing factor to T2DM

96
Q

Who’s at risk for stress

A

Demographic: middle age, women
Socioeconomic: low income
Children have fewer coping skills
Adolescents: focus on body image and new independence
Older adults: fewer social supports

97
Q

Cognitive Appraisal

A

Appraising a stressor and assessing, categorizing, and evaluating it; framing the stressor in respect to their own well-being

98
Q

Positive coping strategies may be:

A

Problem-Focused
Generate solutions to reduce or eliminate stressors

Emotion-Focused
Regulate emotional response that occurs in the given situation. Focus on emotional control through self-regulation and behaviour

Meaning-Focused
Drawing on values, beliefs, and goals to modify personal interpretations and responses to the situation

99
Q

Common positive coping strategies

A

●Education, Social support, Exercise, Therapeutic lifestyle change, Music therapy, Relaxation strategies, Alternative therapies
●Oxytocin stimulated by touch, warm temperature, vibration, electroacupuncture, olfactory clues, social interaction

100
Q

Maladaptive coping strategies

A

Do not address the underlying issue and may negatively affect you further.

Commonly seen maladaptive coping strategies include alcohol/substance abuse, smoking, excessive eating, denial, and avoidance.

101
Q

Physiological

A

Caused by stress incurred due to injury or illness such as stroke, MI, Cancer, or Traumatic Injury

102
Q

Psychological

A

Most commonly seen in stressors encountered on a regular basis such as occupational pressure, academic pressure, financial pressure, or major life events such as experiencing the loss of child through SIDS

103
Q

SIDS

A

Sudden Infant Death Syndrome (SIDS) is the sudden death of a seemingly healthy infant that remains unexplained after all other possible causes have been ruled out through autopsy, death scene investigation, and review of medical history.

104
Q

SIDS facts

A

SIDS occurs between birth and 12 months of age. Most common between month 2-3

95% of cases before 6 months of age.

Death occurs during sleep

SIDS is associated with suboptimal physiologic regulation and a combination of several intrinsic and extrinsic factors. The most preventable risk factor is sleeping in a prone position.

105
Q

Triple risk of SIDS

A

1.Underlying Vulnerability (may have brainstem abnormalities that decrease arousal signals, possible gene polymorphisms)

2.Trigger event (prone sleeping, cardiac dysfunction, infection)

3.Vulnerable developmental stage (2-4 months marked by changes in cardiac, ventilatory, and sleep-wake patterns)
●Brainstem abnormalities/immaturity may be due to prematurity, low birth weight, or in multiples (twins, triplets, etc)

106
Q

Intrinsic factors

A

●Things you cannot change
●Low APGAR
●Genetics/Receptor not well studied at the moment; research is emerging
●5-HT 1A receptors are in the medulla (responsible for breathing)

107
Q

Extrinsic factors

A

●Things you have control over/interventions we can have in place to reduce risk
●We want to sleep in the same ROOM but not the same bed.
●Overheating can lead to hyperthermia which may contribute to difficulty breathing
•Temperature, safe bedding, No smoke

108
Q

safety/SIDS risk reduction

A

Alone (baby shouldn’t sleep with pillows, blankets, stuffies, bumper pads)
Back (sleep SUPINE)
Crib (NO bed-sharing) and Cigarettes (no smoke)

109
Q

Protective factors against SIDS

A

Pacifier use
Use of a fan
Breastfeeding
Vaccination

110
Q

Clinical manifestation

A

SIDS is silent. there may be frothy, blood-tinged secretions from their mouth and nares.

Internal findings may include respiratory tract inflammation, pulmonary edema, and intrathoracic petechiae

Diagnosis is confirmed through autopsy which rules out other potential causes of death

111
Q

On arrival to scene of a baby who’s passed of SIDS

A

•Environment prior to resuscitation efforts
•Temperature of the room
•Temperature of the infant
•Ventilation/heating in home
•Location of infant
•Condition of bed/crib
•Infant’s clothing
•Presence or absence of bedding and soft objects in bed
•Presence or absence of marks on infant’s body
•Caregiver reactions

112
Q

Assessment for nurse (SIDS)

A

First on the scene is usually police or EHS. Be mindful to give no indication of wrongdoing, abuse, or neglect first minutes are crucial
Sleep environment should remain untouched
Once in ER, usually no resuscitation efforts
Ask factual questions, allow the investigator to have parents fully recount the experience; we are not asking them to relive the trauma multiple times
Physician usually initiates discussion of the autopsy with the nurse present for support
Allow them to say goodbye to their infant and assist them in getting to their car or arranging transportation
Follow up care in home
Phone family physician and infant’s family physician to inform them of the tragedy
Educate mother on ceasing lactation if she is breastfeeding

113
Q

Traumatic Injury

A

Traumatic injury not only causes a physiological stress response, but psychological stress when inadequate attention is paid to all concerns during their health crisis.

114
Q

Do say

A

“It’s understandable that you feel this way”

“It wasn’t your fault; you did the best you could”

“I am so sorry that this happened”

“Things will get better. You will feel better, although things may never be the same again”

“These are normal reactions to an abnormal situation”

115
Q

Don’t say

A

“It could have been worse”

“you can always get another pet/car/house/have another child/get married again, etc.”

“It’s best if you just stay busy”

“I know just how you feel”

“you need to get on with your life. If I were you, I would…”

116
Q

Change in Health Status

A

Situational crisis may result from extraordinary, unanticipated situations such as a drastic, unexpected change in health status.

117
Q

Phase I of crisis

A

•Confronted by the problem. Respond with feelings of increased anxiety. Problem-solving.

118
Q

Phase 2

A

•Confronted by the problem. Respond with feelings of increased anxiety. Problem-solving.

119
Q

Phase 3

A

•Trial and error fails, escalate to panic level. Some form of resolution may be reached with new coping mechanisms

120
Q

Phase 4

A

•Crisis unresolved, coping skills ineffective, may transition to mental health emergency

121
Q

Physical disability

A

A wide and evolving range of permanent, temporary, or intermittent impairments, both physical and mental, which can result in functional limitations as the person interacts with their environment, others and potentially with socially constructed barriers

122
Q

Common barriers faced by those with physical disabilities

A

Physical, lack of assistive technology, perception and attitude, transportation, social, programs and policy

123
Q

Those with physical disabilities may experience

A

Grief, HRH, selfesteem issues, mood disorders

124
Q

Acid base balance

A

Process of regulating the pH, bicarb concentration and partial pressure of carbon dioxide of body fluids
Blood ph needs to be regulated for optimal organ and cellular function

125
Q

What is acidotic?

A

Ph<7.35

126
Q

What is alkalotic?

A

Ph >7.45

127
Q

Acid production

A

Generation of acid through cellular metabolism

128
Q

Acid buffering

A

Process to control changes in pHl

129
Q

Acid secretion

A

Removal of acid from the body

130
Q

Optimal acid base balance

A

• Acid excretion keeps pace with acid production
• Buffers are not overwhelmed
• The blood pH is maintained in the normal
range of 7.35 to 7.45

131
Q

Acidosis caused by

A

Retention of too much acid Loss of too much base
• Respiratory acidosis
➢ CO2 retention= ↑PaCO2
• Metabolic acidosis
➢ HCO3 loss or H+ retention = ↓HCO3

132
Q

Respiratory acidosis

A

pH <7.35 PCO2 >45
• Too much Carbonic Acid production
• Cause hypoventilation leading to increase PCO2
Respiratory Compensation
• Hyperventilation to decrease PCO2 Renal Compensation
• Increase HCO3
• H+ is secreted and NH3 produced

Hypoventilation -headache -Decrease LOC

133
Q

Respiratory acidosis clinical findings

A

Causes of Hypoventilation and Increase CO2
• COPD
• Pulmonary Edema
• Neuromuscular disease
• OHS
• Opioid overdose

134
Q

Metabolic acidosis

A

pH<7.35 HCO3<22
• Too much metabolic acid production
• More metabolic acid than kidneys can excrete
• Loss of HCO3 base Renal Compensation
• Increase H+ secretion Respiratory Compensation • Hyperventilation ↓ PCO2

Excessive metabolic acid production • DKA
• Lactic acidosis (tissue hypoxia) Decrease H+ Excretion
• Oliguria
Loss of Bicarbonate

135
Q

Metabolic acidosis clinical findings

A

Decrease LOC
• Hyperventilation(lungs compensating)
• Abdominal Pain
• Nausea and vomiting

136
Q

Alkalosis

A

Caused by:
➢ Retention of too much base loss of too much acid
• Respiratory acidosis ➢ PCO2 loss
• Metabolic acidosis
➢ HCO3 excess or H+ loss

137
Q

Respiratory alkalosis

A

pH >7.45 PCO2<35
• Too little carbonic acid production
• Cause hyperventilation Respiratory Compensation • Hypoventilation
Renal Compensation
• Decrease HCO3
• Decrease secretion of H+ , less NH3 production

Hyperventilation and Decrease PCO2
• Hypoxia
• Acute Pain
• Anxiety
• Asthma attack

138
Q

Respiratory alkalosis clinical findings

A

• Decreased LOC • Diaphoresis
• Hyperventilation

139
Q

Metabolic alkalosis

A

pH>7.45 HCO3>26 mmol/L
• Too little metabolic acid
• Too much HCO3 or acid excretion > acid production
Renal Compensation
• Decrease secretion of H+ Respiratory Compensation • Hypoventilation

Severe vomiting
hypovolemia
Hypokalemia
Diuretic therapy

140
Q

Metabolic alkalosis

A

Decreased LOC
• Hypoventilation (lungs compensating)
• Volume depletion
• hypokalemia

141
Q

Respiratory support

A

Bronchodilators
• High flow oxygen→ WOB and Oxygenation
• Noninvasive ventilation → WOB, CO2 clearance, oxygenation
• Invasive ventilation →Mechanical ventilation, Control RR, VT, PEEP, FIO2

142
Q

Compensation?

A

If ph is not normal it is fully compensated

143
Q

Methods of heat loss

A

Convection: transfer of heat from the body to moving liquid or air
Evaporation: sweat is vaporized at the skin at the surface
Conduction: the transfer of heat from the body to a cooler surface by direct contact
Radiation: transfer of heat via electromagnetic waves

144
Q

Hypothalamus

A

The thermostat of the body

145
Q

Hypothermia

A

Accidental: environment exposure, complication from a serious systemic disorder
Therapeutic: induced reduction in heat to preserve tissue and reduce edema and preventing ischemia

146
Q

Hypothermia treatment

A

Passive warming:dry, warm clothing,warm drinks, exercise
Active warming: warm blankets, heating pads, warm baths, heated environments
Core rewarding: warm IVF, gastric lavage, peritoneal lavage, inhaled warm O2

147
Q

Age considerations for hyperthermia

A

Infants: unable to take measures to control temp, completely dependent on caregivers
Older adults: decreased sweating, reduced perception of temp.

148
Q

Hyperthermia treatment

A

Cool bath, cold fluid lavage,cooling blankets, antipyretics and cool IVF

149
Q

Assessment for impaired thermoregulation

A

History: age, health history, fam history, social history, recent injury / illness, environmental exposure

150
Q

Basic symptoms of hyper

A

Fever, hot chills, shivering, dizziness,

151
Q

Basic symptoms hypo

A

Feeling cold, shivering, muscle cramps

152
Q

Symptoms for both

A

General malaise, loss of appetite and lethargy

153
Q

Physical assessment

A

Rectal temp is Most accurate and reliable
Hyperthermia: skin flushed, warm, not to touch, dry skin and mucous membranes, decreased output, dehydration. Confusion, delirium, coma
Hypothermia: cool skin, slow capillary refill, pale/cyonotic. Impaired cognition-poor coordination below 34- muscle rigidity and shivering stops below 30 c

154
Q

Malignant hyperthermia

A

A rare metabolic disease characterized by hyperthermia and rigidity of skeletal muscles

155
Q

What is malignant hyperthermia triggered by?

A

Anesthetic drugs during general anesthesia (most risk in OR and recovery)

156
Q

What happens in the body with malignant hyperthermia?

A

General anesthetic and a paralytic are given to the patient (most often halothane and succinylcholine prior to surgery)
These medications activate the Ryanodine receptors, however, because of a mutation these receptors are unable to close
This causes an influx of calcium into the muscle and leads to prolonged contraction of muscles (rigidity)
Because of the prolonged contraction, muscles have a high oxygen demand which in turn increases CO2 production

157
Q

What med is given in case of malignant hyperthermia?

A

Dantrolene
When giving IV, monitor ECG, vitals, lytes, and urine output continuously

158
Q

Anyone known to MH should what?

A

Wear medical alert identifier

159
Q

Brain injury

A

Biggest risk of death occurs at 3 separate times
Immediately at the time of brain injury
Two hours post injury
Three weeks post injury

160
Q

What does comminuted mean?

A

Many fractured pieces, shattering

161
Q

What does compound mean?

A

Broken bone pierces skin

162
Q

Skull fracture

A

Linear or depressed
Simple, comminuted, compound
Open or closed

163
Q

Diffuse injury

A

Concussion diffuse axonal injury

164
Q

Focal injury

A

Lacerations, confusions, hematomas, cranial nerve injury

165
Q

Skull fracture

A

Monitor for CSF leaks (halo sign), battle’s sign, or bilateral periorbital ecchymosis.Assess all rhinorrhea or otorrhea for CSF. Do NOT insert NG tube

166
Q

Signs of skull fractures

A

Battle sign = basilar fracture
Positive halo sign = CSF

167
Q

Diffuse axonal injury

A

This kind of injury is caused by the tearing of axon (thin fibres that connects neurons for communication) due to the impact.

12-24 hours to fully develop, so may worsen with time after initial injury

90% of people with DAI remain in a vegetative state.

168
Q

What is a contusion

A

Bruising of the brain tissue
Areas of hemorrhage, infarction, necrosis, edema
Commonly seen at fracture sites and coup- contrecoup or injuries.
Prognosis dependent on amount of bleeding around contusion

169
Q

Laceration

A

Tearing of the brain tissue, depressed and open fractures or penetrating injuries
Poor prognosis
Intracerebral hemorrhage

170
Q

Emergency management of head injuries

A

Initial:
Ensure airway
Stabilize cervical spine
Administer 02
Establish IV access for NS or Ringer’s
Control external bleeding with pressure dressing
Assess for rhinorrhea, otorrhea, scalp wounds
Remove clothing

171
Q

Emergency Management of Head Injuries

A

Ongoing:
Administer fluids with caution
Anticipate need for intubation
Assume cervical spine injury
Maintain temperature control
Monitor vitals, GCS, cardiac rhythm, pupil size and reactivity
Keep head elevated ~30 degrees
Administer appropriate medications
Immediately notify of Cushing’s triad (bradycardia, irreg resp, increased systolic BP.)

172
Q

Potential assessment findings

A

Bruising, battle sign, raccoon eyes
Depressed skull
Lacerations to head
Cheyne-Stokes respirations
Hyperventilation
Decreased 02
Asymmetry of face
Incontinence
Confusion
CSF leak
Decreased LOC
Speech problems
Involuntary movement
Seizure
Unequal or dilated pupils

173
Q

Diagnostics

A

CT #I option
MRI best to detect lesions
Transcranial Doppler
Cervical spine xray
GCS tool

174
Q

Epidural hematoma

A

Bleed between dura and inner surface of the skull
Neuro emergency

175
Q

Subdural hematoma

A

Bleeding between dura and arachnoid layer of meningeal covering
Usually venous in origin
Occurs 2-14 days of injury, may enlarge
Acute, subacute, chronic

176
Q

Intraparenchymal hematoma

A

Bleeding in brain tissue

177
Q

Subarachnoid hematoma

A

Traumatic forces damage vascular structures in subarachnoid space

178
Q

Intracranial pressure

A

Intracranial pressure is determined by the pressure exerted from total volume of CSF, brain tissue, and blood

An increase in any one of these factors without a decrease in the others results in increased ICP

Normal ICP is 5-15mmHg
If there a sustained pressure >20mmHg it must be treated

Monitor for Cushing’s Triad

179
Q

Cushings triad

A

Cushing’s Triad: high systolic BP, low HR, irregular respirations
May see an external ventricular drain (EVD) closed system that allows the drainage of CSF
Treat with drugs like mannitol (hyperosmotic agents reduce edema)

180
Q

TBI and thermoregulation

A

Fever without the presence of infection is a contributor to secondary brain damage after a brain injury.

Hyperthermia can contribute to worsening cerebral hypoxia

Fever increases metabolic demands, increases agitation, shivering, pain, and likelihood of seizure.

Ensure patients are kept at a stable temperature. Do not overcorrect. If patients become too cold, shivering will be induced and metabolic workload will increase

181
Q

ICP

A

High metabolism from increased ICP = fever
Injury and edema to the brain cause an influx of blood to the area; contributes to fever. Increased blood flow contributes to increased ICP.
Brain injury can cause sensitivity to temp changes (hypothalamus injured)
Increased temp = increased metabolism/02 demand. This with potentially augmented blood flow (remember that high temp causes vasodilation) can lead to cerebral ischemia.

182
Q

Treatment of TBI and complications

A

Stabilize vitals and perfusion status

183
Q

Craniotomy

A

To elevate depressed bone and remove fragments

184
Q

Craniectomy

A

Removal, if large bones are destroyed

185
Q

Cranioplasty

A

Improve appearance

186
Q

CSF drain

A

Drain via ventriculostomy . Intermittent drainage using 3-way stopcock with close monitoring of cerebral perfusion pressure

187
Q

Burr hole

A

Alleviate pressure from cerebral edema

188
Q

Timely diagnostic

A

Prevent secondary injury due to increased pressure/cerebral edema

189
Q

Thyroid

A

The thyroid is a small, butterfly-shaped gland located at the base of the neck, just below the Adam’s apple. The thyroid gland makes two main hormones: thyroxine (T-4) and triiodothyronine (T-3). These hormones affect every cell in the body. They support the rate at which the body uses fats and carbohydrates.

190
Q

TRH

A

Thyrotropin releasing hormone
Released by the hypothalamus

191
Q

TSH

A

Thyroid stimulating hormone
Released by the anterior pituitary

192
Q

Thyroid hormones

A

Triiodothyronine (t3) and thyroxine (t4)
Released by the thyroid
Cannot be made without iodione

193
Q

Hormones

A

Hypothalamus detects low blood levels of thyroid hormones and releases Thyrotropin Releasing Hormone (TRH)
TRH stimulates the anterior pituitary gland to release Thyroid Stimulating Hormone (TSH)
TSH stimulates the thyroid to release T3, T4, and/or Calcitonin

194
Q

Hyperthyroidism

A

Also known as thyrotoxicosis

hyperactivity of the thyroid gland with sustained increase in thyroid hormones

195
Q

Types of hyperthyroidism

A

Graves
Toxic nodular goiter
Hyper functioning thyroid adenoma
Jod-base Dow syndrome
Neonatal hyperthyroidism

196
Q

Graves’ disease

A

Usually women aged 20-40
Genetic risk (autoimmune)
Abnormal antibodies (including thyroid stimulating immunoglobulin; TSI) mimic TSH and create false signals to TSH receptors to release more T3 and T4 which results in excess hormone.

197
Q

Toxic nodular goiter

A

Aka plumbers disease. Some areas, of thyroid more responsive to TSH than others causing uneven growth. Mutation occurs in TSH receptor during division becoming toxic

198
Q

Hyperfunctioning of thyroid adenoma

A

Follicular cells grow uncontrollably forming a benign tumor

199
Q

Jod-basedow syndrome

A

Lodine-induced thyrotoxicsis following a hefty dose of iodine

200
Q

Neonatal hyperthyroidism

A

Birthing parent has graves disease and hormones cross the placenta and affect the infant

201
Q

Hyperthyroid diagnostics

A

RAIU→radioactive iodine uptake
CIDs → color flow Doppler sonography: increase blood flow due to thyroid hyperactivity
Ultrasounds→ visual benign, malignant nodules
Serology →decrease TSH, increase T3 and T4

202
Q

Symptoms of hyperthyroidism → think fast

A

Enlarged thyroid, Hair loss, tremors, tachypnea, insomnia, anxiety, diarrhea, ophthalmopathy, weight loss/increased appetite, infertility, heat, intolerance, diaphoresis, tachycardia, hyperactivity

203
Q

Graves ophthalmopathy

A

20-50% experience exophthalmos (protrusion of the eyeball from the orbit)

This happens due to impaired venous drainage from the orbits due to inflammatory response of the autoimmune disease resulting in edema. The increased pressure pushes the eyeball forward.

Risk of dry, irritated eyes as lids may not be able to fully close. Can result in corneal ulcers, vision loss, ocular muscle weakness leading to diplopia

204
Q

Treatment options

A

Thyroid ectomy : preop requiring lab testing, thyroid imaging and laryngal exam. Risk of hormonal leakage during removal and risk of thyroid storm. Beware hypocalcemia.
Pharmacologic therapy: anti-thyroid medication, beta blockers for symptom management.
Radioactive iodine therapy: destroys thyroid overtime, but is unsafe for pregnant women

205
Q

Thyroid storm

A

Life-threatening condition, hyper thyroid symptoms are greatly exaggerated, occurs with cessation of treatment, infection, or post surgery.

Heat intolerance develops into high fever, tachycardia advances to cardiac dysrhythmias, hyperactivity/anxiety advance to confusion, seizure, coma.

Treat with beta blockers, thyroid hormone reduction (thioamides, radioactive iodine preparations)

206
Q

Hypothyroidism

A

Hypo-activity of thyroid gland with sustained decrease in thyroid hormones

207
Q

Primary hypothyroidism

A

The thyroid gland is the problem. There aren’t enough thyroid hormones being utilized or produced for a variety of reasons.

208
Q

HaShimoto’s thyroiditis

A

Most common cause of hypothyroidism, is a autoimmune disease

responds to damage by increasing size and number of follicular cells causing the thyroid to enlarge

Antibodies continue to cause damage to the point where thyroid function is destroyed.

209
Q

Iodine deficiency

A

Iodine is required to convert t3 and T4

210
Q

Congenital hypothyroidism

A

Random or inherited genetic mutation
Doesn’t develop normally or as expected

211
Q

Iatrogenic

A

Develops in response to hyperthyroid treatment such as a thyroidectory

212
Q

Medication induced

A

Excessive consumption of anti-thyroid medications
Side effect of medication such as lithium

213
Q

Secondary hypothyroidism

A

The body isn’t producing TSH and therefore inhibiting the stimulation needed for thyroid hormone release.

214
Q

Pituitary

A

Tumors to the anterior pituitary gland can suppress the release of TSH

215
Q

Hypothalamus disorder

A

Brain injuries that result in damage of hypothalamus may inhibit the release of TRH or the hypothalamus ability to detect hormone levels appropriately

216
Q

Symptoms of hypothyroidism- think slow

A

Goiter, weight gain,fatigue, cold intolerance, constipation, muscle weakness, headache, poor concentration and memory, bradycardia, anemia, myxedema, lethargy, infertility and menstrual irregularities

217
Q

Treatment of hypothyroidism

A

Synthroid

Take medication an hour before other medications on an empty stomach

If taking GI medications, must space them at least 4 hours apart as they decrease absorption

Increases myocardial oxygen demands; risk for angina/dysrhythmias

218
Q

Patient education with hypothyroidism

A

It is important that those on thyroid hormone replacement therapy understand the signs and symptoms of HYPERthyroidism (dose can be too high)
Never abruptly stop taking therapy
Be aware thyroid therapy may take time to take effect
Be aware thyroid preparations potentiate effects of anticoagulants and decrease effect of digitalis compounds; may need closer monitoring

219
Q

Myxedema coma

A

Life threatening

occur with in times of great stress (infection, surgery) or with cessation of treatment or failure to begin treatment. Higher risk with use of sedatives.

Cold intolerance develops into hypothermia, drowsiness evolves into coma, etc.

Treat aggressively. Vital functions must be supported. IV thyroid hormone replacement and glucocorticoid therapy.

Health & Illness 2 Kathleens Final (2 decks)

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