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patho > class 4 stress response > Flashcards

class 4 stress response Flashcards

1
Q

GENERAL
ADAPTATION
SYNDROME (GAS)

A

Alarm stage (DOESNT LAST LONG)
* Mobilization of defenses
* Hypothalamus
* Sympathetic nervous system
* Adrenal glands (CORTISOL)
-fight or flight, adrenaline release

Resistance stage
-the body tries to overcome stressors
* Elevation of hormone levels
* Body systems operate at peak performance levels.
-if this level fails, exhaustion begins

Final stage
* Resolution or death

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2
Q

SIGNIFICANT EFFECTS
OF
STRESS RESPONSE

A

 Elevated blood pressure and increased heart rate
 Bronchodilation and increased ventilation
 Increased blood glucose levels
 Arousal of the central nervous system
 Decreased inflammatory and
immune responses

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3
Q

when CNS is activated, it then stimulates what

A

hypothalamus which controls everything

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4
Q

STRESS AND DISEASE: SPECIFIC PROBLEMS

A

 Headache
- May develop during or after stress response

 Stomatitis (ulcers in the mouth) and necrotizing periodontal disease

 Prolonged vasoconstriction
- Can impair function or necrosis in gastrointestinal tract or kidneys

 Precipitating factor
- Chronic infections
- Physical and/or emotional distress

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5
Q

POTENTIAL EFFECTS OF PROLONGED
OR SEVERE STRESS

A

 Renal failure
- Prolonged severe vasoconstriction
- Ischemia(loss of o2 to tissue) causes cell damage.

 Stress ulcers
- Vasoconstriction and glucocorticoids
- Decrease in mucosal regeneration and mucus production

 Infection
- Depression of the inflammatory and immune responses

 Slowed healing
-Following trauma or surgery
-Increased secretion of glucocorticoid—reduction in protein synthesis and tissue regeneration
-Increased catecholamine levels—vasoconstriction, reduced nutrients and oxygen to the tissue

 Post-traumatic stress disorder
- Serious consequence of major disaster or personal threat
- Usually occurs within 3 months of event
-May cause symptoms years later
- High risk of developing dependence on drugs and/or alcohol

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6
Q

neurotransmitter stress response (serotonin)

A

During stress, the body may increase serotonin synthesis to help stabilize mood. However, chronic stress can impair serotonin receptor function, leading to:

Downregulation: Fewer receptors are available.
Desensitization: Receptors become less responsive.

As a result, even with more serotonin, the brain struggles to use it effectively, which can contribute to mood disorders like anxiety and depression, as well as cognitive and physical health issues. Managing stress through techniques like mindfulness and exercise can help support serotonin balance.

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7
Q

Immune Stress Response

A

Interaction:
Stress activates the nervous and immune systems during the alarm phase of General Adaptation Syndrome (GAS).

Negative Effects:
Chronic stress impairs the immune system’s ability to produce protective factors (e.g., cytokines, antibodies).

Conclusion:
This leads to a reduced immune response, increasing susceptibility to infections and health issues.

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8
Q

Biogenic amine hypothesis for depression and mania

A

Depression: deficiency of catecholamine, especially norepinephrine

Mania: excess amines

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9
Q

Permissive hypothesis for depression and mania

A

Affective disorders are due to decreased concentrations of serotonin

 Depression results from decreases in both serotonin and catecholamine
levels

 Mania results from increased catecholamine but decreased serotonin levels

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10
Q

Dysregulation hypothesis

A

Depression and other affective disorders result from a failure in the regulation
of catecholamine activity

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11
Q

DEPRESSION – ASSESSMENT &
SCREENING

A

Generally underdiagnosed

 Screening methods
 “Two quick question” screening
 Clinical interview to determine if the patient meets the Diagnostic & Statistical Manual of
Mental Disorders (DSM-5)
 Patient Health Questionnaire (PHQ-9)
 Hamilton Rating Scale for Depression

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12
Q

Medical conditions associated with depression

A

COPD, migraines, epilepsy, etc)

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13
Q

treatment of depression

A

 Lifestyle-self care

 Self-management

 Psychotherapy
 Cognitive behavioural therapy
 Interpersonal therapy

 Pharmacological management

 Electroconvulsive therapy (ECT)

 Repetitive transcranial magnetic stimulation

 Vagus Nerve stimulation

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14
Q

Antidepressants – four primary classes

A

 Tricyclic antidepressants (TCAs)

 Selective serotonin reuptake inhibitors (SSRIs)

 Selective norepinephrine reuptake inhibitors (SNRIs)
 Atypical antidepressants

 Monoamine oxidase inhibitors (MAOIs)

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15
Q

why are SSRIs and SNRIs usually used first

A

Cause fewer adverse effects than tricyclics and MAOIs

Have very few drug–drug or drug–food interactions

Takes about 2 to 4 weeks before improvement of symptoms can be seen

little or no effect on cardiovascular system

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16
Q

most common SSRI

A

citalopram (Celexa)
Escitalopram (cipralex)

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17
Q

common SNRI

A

venlafaxine (Effexor) also used for menopause

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18
Q

Mechanism of action (SSRIs)

A

 Selectively inhibit serotonin reuptake

 Have little or no effect on norepinephrine or dopamine reuptake

 Result in increased serotonin concentrations at nerve endings

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19
Q

Mechanism of action (SNRIs)

A

Selectively inhibit serotonin and norepinephrine

Result increase in these NT levels

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20
Q

ANTIDEPRESSANTS:
ADVERSE EFFECTS on CNS

A

, dizziness, anxiety, insomnia,
fatigue

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21
Q

ANTIDEPRESSANTS:
ADVERSE EFFECTS on GI

A

Nausea, diarrhea,
constipation, dry mouth

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22
Q

ANTIDEPRESSANTS:
ADVERSE EFFECTS

A

sexual dysfunction and weight gain, Suicidal ideation, serotonin
syndrome

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23
Q

SEROTONIN SYNDROME

A

-Caused by excess serotonin in the brain

 SSRI + TCAs or MAO inhibitors can cause serotonin syndrome (SES)

 Hyperpyrexia, hypertension, sweating, tremors, ataxia (discoordination)

 Mental status changes: confusion, anxiety, & restlessness

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24
Q

SSRI discontinuation syndrome

A

 Occurs when SSRI/SNRI treatment stopped suddenly

 Symptoms include

 Dizziness, confusion,

 Lethargy

 Paresthesia (Tingly arms/feet)

 Vivid dreams

 Nausea

 Electric shock sensations

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25
Q

SSRIS/SNRIS NURSING CONSIDERATIONS

A

Maximum therapeutic effects may take up to 5 weeks

 Assess for drug history, especially other anti-depressant medications

 Increased risk of suicide as drug approaches therapeutic concentration

 Assess for baselines of weight, liver function

 Provide education to patient regarding adherence and SSRI discontinuation syndrome

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26
Q

TRICYCLIC ANTIDEPRESSANTS mechanism of action

A
  • considered second line

-Reuptake Inhibition: TCAs primarily work by inhibiting the reuptake of neurotransmitters, particularly serotonin and norepinephrine, increasing their levels in the brain, causing accumulaton at the nerve endings.

-Additional Effects: They also affect other neurotransmitter systems, including histamine and acetylcholine, contributing to both therapeutic effects and side effects.

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27
Q

TRICYCLIC ANTIDEPRESSANTS:
DRUG EFFECTS (blockades)

A

 Blockade of norepinephrine reuptake
 *Antidepressant (desired), tremors, tachycardia, others

 Blockade of serotonin reuptake
 *Antidepressant (desired), nausea, headache, anxiety, sexual dysfunction

Corrects the imbalance between norepinephrine &
Serotonin at the nerve endings in the CNS

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28
Q

TRICYCLIC
ANTIDEPRESSANTS Anticholinergic effects (results from blocking acetylcholine)

A

Blurred vision, dry mouth, GI mobility issues

 Sedation (blockade of histamine receptors)

 Impotence/sexual dysfunction (effects on serotonin)

 Orthostatic hypotension (blockade of alpha-1 adrenergic receptors) (DROPPING BP WHEN YOU STAND UP)

 Weight gain

Increases falls in elderly because of effects.

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29
Q

TCAS Interactions

A

 CNS depressants – enhance sedation

 Sympathomimetics

 Anticholinergics

 MAO inhibitors

 Oral Contraceptives

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30
Q

TCAS contradictions

A

 Dysrhythmias, recent MI

 Narrow-angle glaucoma (NAG)

 Benign prostatic hyperplasia (BPH)

31
Q

TRICYCLIC
ANTIDEPRESSANTS:
OVERDOSE

A

 Overdose is lethal—70 to 80% die before reaching the hospital

 CNS and cardiovascular systems are
mainly affected (cardiotoxicity)

 Death results from seizures or dysrhythmias

32
Q

MONOAMINE OXIDASE INHIBITORS MAOIS mechanism of action and what are they used for

A

MAOIs inhibit the MAO enzyme system in the CNS, By inhibiting MAO, more NE, DA or 5HT is available for release by the neuron
More NE, DA or 5HT released into synapse to stimulate receptors

 Amines (dopamine, serotonin, norepinephrine) are not broken down, resulting in higher levels in the brain

 This results in the alleviation of symptoms of depression

 Used for atypical depression, some mood disorders & Parkinson`s disease

33
Q

Common Adverse Effects of MAOI

A

 Orthostatic hypotension
 Headache
 Insomnia
 Diarrhea

34
Q

MAOIS INTERACTIONS

A

 Insulin and oral hypoglycemic
 Enhances hypoglycemia

 Antihypertensive agents
 Profound hypotension

 SSRIs
 Serotonin syndrome

 Foods containing tyramine
 MAO inhibitors prevent breakdown of dietary tyramine
 Tyramine promotes release of NE which causes acute hypertension, palpitations, occipital headache, flushing, sweating,
nausea

35
Q

HYPERTENSIVE CRISIS AND TYRAMINE

A

 Ingestion of foods or drinks with the amino acid tyramine leads to hypertensive crisis, which may lead to cerebral
hemorrhage, stroke, coma, or death

 Avoid foods that contain tyramine!

36
Q

MAOIS: OVERDOSE

A

 Symptoms appear 12 hours after ingestion

 Symptoms include tachycardia, circulatory collapse, seizures,
coma

 Treatment is aimed at protecting the brain and the heart and
eliminating toxin
 Gastric lavage (washing out stomach)
 Urine acidification (makes it acidic)
 Hemodialysis

37
Q

MAOIS NURSING CONSIDERATIONS

A

 May take 4 – 8 weeks for therapeutic effects

 Increased risk for suicide as drug approaches therapeutic levels

 Assess for contraindications including liver and renal function, cardiovascular disease

 Provide education regarding diet and avoiding foods that contain tyramine, interactions, and adherence

 Provide education re: caffeine avoidance

 Wear medical alert bracelet

38
Q

bipolar disorder cause and characteristics

A

-Exact cause is unknown; excess excitatory NT ( glutamate & NE); decreased inhibitory NT (GABA)

 Patients alternate between depression and extreme mania

 Suicide risk is high; significantly impacts social and occupational functioning

39
Q

Symptoms of mania (excessive CNS stimulation)

A

 Agitation, intense excitement, elevated mood, talkativeness (pressured speech)

 Impulsive behavior, short attention span

 No thoughts to consequences of actions

40
Q

medication used for bipolar

A

 Mood stabilizers
- Lithium carbonate
- Valproic acid

 Atypical Antipsychotics

41
Q

PROTOTYPE DRUG LITHIUM mechanism of action and therapeutic class

A

 Therapeutic classification
- Mood stabilizer, used for bipolar disorder

 Mechanism of Action
- inhibiting glutamate (excitatory NT) action
- Protecting neurons that are damaged when GABA levels are low
- Decreased release of NE
- Increases 5HT production and release
- Narrow therapeutic index/range

42
Q

Adverse Effects – Initial effects of lithium

A
  • Muscle weakness
  • Lethargy
  • Nausea, vomiting
  • Polyuria, nocturia
  • Headache, dizziness
  • Tremors
  • Confusion
43
Q

Adverse Effects – long-term effects of lithium

A
  • Kidney impairment
  • Proteinuria, albuminuria
  • glycosuria
  • Cardiovascular
  • Dysrhythmias
  • Circulatory collapse
  • Leukocytosis
  • Hypothyroidism, goiter
  • Lithium decreases production of
    thyroid hormones
44
Q

ELECTROCONVULSIVE THERAPY

A

Electroconvulsive therapy (ECT) is a medical treatment for severe mental health conditions, primarily major depressive disorder, that involves the application of electrical currents to the brain to induce a brief seizure.

45
Q

ECT used with mania

A

-In the presence of extreme and sustained agitation.
- In the presence of “manic delirium.”

46
Q

ECT used with schizophrenia

A

 Positive symptoms with abrupt or recent onset.
 Catatonia. (unresponsivness)
 History of good response to ECT.

47
Q

Vagus nerve stimulation (VNS)

A

surgical implantation VNS into left chest wall; the device is connected to a thin, flexible wire that is wrapped around vague nerve (left side of neck); believe that stimulation of nerve increases the level of
neurotransmitters

48
Q

Light or phototherapy

A

artificial lighting that is 5-20 times brighter that usual indoor lighting; used to simulate sunlight

49
Q

Generalized Anxiety Disorder (GAD)

A

 Excessive anxiety that lasts more than 6 months

 Symptoms include restlessness, fatigue, difficulty focusing, sense of dread, sleep
disturbances

 ANS effects are common as part of stress response

50
Q

Panic Disorder

A

 Intense apprehension, immediate feelings of fear, terror, impending doom,
increased sympathetic effects

51
Q

Social Anxiety Disorder or Social Phobia

A

 Unreasonable fear of being judge, ridiculed or embarrassed by others

 Type of phobia

52
Q

Obsessive Compulsive disorder (OCD)

A

 recurrent, intrusive thoughts or repetitive behaviors

 Obsessions (thoughts) & compulsions (behavior)

53
Q

Situational Anxiety

A

anxiety that arises in response to a specific situation or event.

54
Q

Non-pharmacologic Treatment of Anxiety
Disorders

A

 Counseling
 Cognitive-Behavioral therapy
 Support groups
 Complementary and Alternative medicines

55
Q

Brain Areas Associated with Anxiety Disorders

A

Limbic System and Reticular Formation

56
Q

limbic system

A

– associated with emotion, learning
and memory

 Connects to hypothalamus to mediate
responses related to anxiety, fear, anger

 Hypothalamus influences sympathetic response

57
Q

Reticular Formation

A

 Stimulation of reticular formation increases arousal and alertness

 Inhibition of reticular formation promotes
drowsiness and sleep

 In anxiety, messages from hypothalamus and limbic area carried by way of reticular activating system (RAS) to the cortex – this is thought to be basis of fear and anxiety

58
Q

low levels of what neurotransmitter is associated with anxiety and depression

A

serotonin

59
Q

Norepinephrine

A

effects on the systems associated with physical sensations of anxiety
(cardiovascular, respiratory, GI systems via stimulation of sympathetic nervous system

60
Q

GABA

A

most abundant inhibitory neurotransmitter

Inhibitory neurotransmitter in the thalamic, hypothalamic and limbic system

61
Q

Corticotropin-releasing hormone (CRH)

A

neuropeptide & hormone found in many areas of the brain; it is the initial hormone released from the hypothalamus that activates one of the major stress response systems (hypothalamic-pituitary-adrenal (HPA) axis

62
Q

Physiological symptoms are related to
the activation of the SNS; the flight or
fight response is activated (sympathetic)

A

Tachycardia
 Shortness of breath (SOB)
 Pounding in the ears
 Hypertension
 Excessive sweating (diaphoresis)
 Dry mouth

63
Q

Physiology symptoms caused by the
PSNS (parasympathetic)

A

 Abdominal cramping
 Diarrhea
 Fatigue
 Urinary urgency
 Numbness and tingling of the
extremities
 Additional symptoms include
restlessness, difficulty focusing, sense
of dread, sleep disturbances

64
Q

when are Benzodiazepines used

A

as adjunctive therapy for short term use

65
Q

Drugs Classes Used to Treat Anxiety and Sleep Disorders

A

 CNS depressants

 Antidepressants

66
Q

examples of CNS depressants

A

 CNS depressants

 Benzodiazepines

 Barbiturates (rarely prescribed – responsible for content of this drug under seizures)

 Nonbenzodiazepine Anxiolytics

67
Q

indication for use of benzo

A

 GAD: Adjunctive therapy early in treatment (acute anxiety or agitation); beneficial while
waiting for SSRIs to become effective, times of acute crisis

 Also classified as a sedative/hypnotic – insomnia

 Seizure disorders, alcohol withdrawal, pre-medication prior to procedures/surgery

68
Q

mechanism of action of benzo

A

 Depresses activity in the CNS by binds to GABA A receptors causing inhibition of post-synaptic neurons in thalamus, hypothalamus, limbic system

 Stimulate (potentiates) GABA receptors in the brain – GABA is inhibitory – hence it cause CNS relaxation/sedation

69
Q

Barbiturates for anxiety & Insomnia

A

 Simply put – they are RARELY if ever used for anxiety/insomnia!

 Power CNS depressant

 Significant side effects

 Withdrawal symptoms extremely severe & can be fatal

 Overdose is a medical emergency
 Hypotension, respiratory depression, & shock
 Activated charcoal, gastric lavage, etc

 Psychological and physical dependence is high

70
Q

Insomnia:
Prototype Drug Zopiclone MOA and onset

A

Exerts specific agonist action at central GABA receptors

very rapid, must be taken right before bed

71
Q

Insomnia:
Prototype Drug Zopiclone therapeutic effects

A

 Sedative – hypnotic
 Short term (ideally) & chronic treatment of insomnia

72
Q

Zopiclone adverse effects

A

 Generally mild
 Bitter taste in the mouth & dry mouth - common
 Nausea & dyspepsia (heartburn)
 Day-time drowsiness (requires education)
 Anterograde amnesia

73
Q

What are amines

A

 Amines (dopamine, serotonin, norepinephrine)

patho (6 decks)

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