Pathophysiology Unit 2 | Chapter 6 (Porth 5th Edition) Flashcards

1
Q

Homeostasis

A

The maintenance of a stable internal environment despite external changes, crucial for normal physiological functioning.

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2
Q

Constancy of the Internal Environment

A

A principle of homeostasis where the body regulates variables like temperature, pH, and electrolyte balance within narrow limits.

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3
Q

Control Systems

A

Biological mechanisms (e.g., nervous and endocrine systems) that monitor and adjust physiological processes to maintain homeostasis.

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4
Q

Negative Feedback

A

A regulatory mechanism where a system’s output reduces or inhibits the process, maintaining stability (e.g., insulin lowering blood glucose).

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5
Q

Positive Feedback

A

A mechanism that amplifies a response (e.g., oxytocin during childbirth), often leading to an endpoint.

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6
Q

Stress

A

A state of threatened or perceived disruption to homeostasis, triggering physiological and psychological responses.

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7
Q

Stress Response

A

The body’s adaptive reaction to stressors, involving neuroendocrine and immune system activation.

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8
Q

General Adaptation Syndrome (GAS)

A

Hans Selye’s three-stage model (alarm, resistance, exhaustion) describing the body’s response to prolonged stress.

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9
Q

Alarm Stage

A

Initial phase of GAS, characterized by fight-or-flight activation via the SAM axis and HPA axis.

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10
Q

Resistance Stage

A

Second phase of GAS, where the body attempts to adapt and restore homeostasis using sustained cortisol release.

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11
Q

Exhaustion Stage

A

Final phase of GAS, resulting in resource depletion, immune suppression, and vulnerability to disease.

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12
Q

Neuroendocrine Responses

A

Stress-induced activation of the HPA axis (cortisol) and SAM axis (adrenaline/noradrenaline).

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13
Q

HPA Axis

A

Hypothalamic-Pituitary-Adrenal axis: CRH → ACTH → cortisol release, regulating metabolism and immune function during stress.

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14
Q

SAM Axis

A

Sympathetic-Adrenal-Medullary axis: Activates the sympathetic nervous system, releasing adrenaline and noradrenaline for immediate stress response.

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15
Q

Cortisol

A

Glucocorticoid hormone released during stress; suppresses inflammation, increases blood glucose, and modulates immune function.

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16
Q

Catecholamines

A

Adrenaline and noradrenaline; enhance alertness, heart rate, and energy mobilization during acute stress.

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17
Q

Immune Responses to Stress

A

Stress alters immune function via cortisol (suppression) and cytokines (pro-inflammatory signals).

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18
Q

Psychoneuroimmunology

A

Study of interactions between psychological processes, the nervous system, and immune function during stress.

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19
Q

Cytokines

A

Signaling proteins (e.g., IL-6, TNF-α) released during stress; can promote inflammation or immune suppression.

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20
Q

Allostasis

A

The process of achieving stability through physiological or behavioral change in response to stressors.

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21
Q

Allostatic Load

A

The cumulative physiological wear and tear from chronic stress, leading to health risks (e.g., hypertension, diabetes).

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22
Q

Coping Mechanisms

A

Strategies (problem-focused or emotion-focused) to manage stress, such as planning, social support, or avoidance.

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23
Q

Adaptation

A

Successful adjustment to stress, restoring homeostasis without long-term physiological or psychological harm.

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24
Q

Maladaptation

A

Ineffective coping leading to chronic stress, dysfunction, or disorders (e.g., anxiety, cardiovascular disease).

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25
Q

Resilience

A

The ability to recover from stress, influenced by genetics, upbringing, and social support.

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26
Q

Acute Stress Effects

A

Short-term responses: increased heart rate, heightened senses, and energy mobilization via SAM axis activation.

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27
Q

Chronic Stress Effects

A

Long-term consequences: hypertension, immunosuppression, gastrointestinal issues, and mental health disorders.

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28
Q

Posttraumatic Stress Disorder (PTSD)

A

A disorder following trauma, characterized by flashbacks, hypervigilance, and emotional numbness.

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29
Q

Hyperarousal

A

PTSD symptom involving exaggerated startle response, irritability, and difficulty sleeping.

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30
Q

Fight-or-Flight Response

A

Immediate physiological reaction to threat, mediated by the SAM axis to prepare for action.

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31
Q

Immune Suppression

A

Reduced immune function due to chronic cortisol exposure, increasing infection and cancer risk.

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32
Q

Psychosomatic Disorders

A

Physical illnesses (e.g., ulcers, asthma) exacerbated or caused by psychological stress.

33
Q

Cognitive Behavioral Therapy (CBT)

A

A treatment for stress disorders, focusing on changing maladaptive thought patterns and behaviors.

34
Q

Mindfulness-Based Stress Reduction (MBSR)

A

Therapeutic approach using meditation and awareness to manage stress and improve adaptation.

35
Q

SSRIs

A

Selective serotonin reuptake inhibitors; antidepressants used to treat chronic stress and PTSD by modulating serotonin levels.

36
Q

Beta-Blockers

A

Medications (e.g., propranolol) that reduce SAM axis effects, alleviating physical symptoms of acute stress.

37
Q

Social Support

A

A protective factor against stress, improving coping and reducing allostatic load through emotional and practical assistance.

38
Q

Feedback Inhibition

A

Mechanism where end-products (e.g., cortisol) inhibit earlier steps in a pathway (e.g., CRH/ACTH release).

39
Q

Pro-inflammatory Cytokines

A

Immune molecules (e.g., IL-1, IL-6) that promote inflammation, often elevated during chronic stress.

40
Q

Psychogenic Stress

A

Stress originating from psychological sources (e.g., anxiety, trauma) rather than physical threats.

41
Q

Eustress

A

Positive stress that enhances motivation and performance (e.g., preparing for a competition).

42
Q

Distress

A

Negative stress causing dysfunction, often overwhelming an individual’s coping abilities.

43
Q

Hypothalamus

A

Brain region initiating the HPA axis by releasing CRH in response to stress.

44
Q

Adrenal Cortex

A

Produces cortisol in response to ACTH stimulation during the HPA axis activation.

45
Q

Adrenal Medulla

A

Releases adrenaline and noradrenaline as part of the SAM axis during acute stress.

46
Q

Telomeres

A

Protective DNA caps that shorten with chronic stress, linked to accelerated aging and disease.

47
Q

Exposure Therapy

A

Treatment for PTSD involving gradual, controlled exposure to trauma-related stimuli to reduce fear.

48
Q

Biofeedback

A

Technique teaching control over physiological stress responses (e.g., heart rate) through real-time monitoring.

49
Q

Emotion-Focused Coping

A

Managing stress by regulating emotional reactions (e.g., meditation, seeking support).

50
Q

Problem-Focused Coping

A

Addressing stressors directly through planning, problem-solving, or altering the situation.

51
Q

Oxidative Stress

A

Cellular damage from reactive oxygen species (ROS), exacerbated by chronic stress and inflammation.

52
Q

Glucocorticoid Receptors

A

Proteins that bind cortisol, mediating its effects on metabolism, immune function, and gene expression.

53
Q

Epigenetics

A

Changes in gene expression (without altering DNA) due to stress, influencing vulnerability to disorders.

54
Q

Vasopressin

A

Hormone released with CRH during stress, enhancing water retention and blood pressure.

55
Q

ACTH

A

Adrenocorticotropic hormone; stimulates cortisol release from the adrenal cortex.

56
Q

CRH

A

Corticotropin-releasing hormone; triggers ACTH release from the pituitary gland.

57
Q

Noradrenaline

A

Neurotransmitter in the SAM axis, increasing alertness and redirecting blood flow during stress.

58
Q

Sympathetic Nervous System

A

Activates fight-or-flight responses, increasing heart rate, dilating pupils, and inhibiting digestion.

59
Q

Parasympathetic Nervous System

A

Promotes rest-and-digest functions, counterbalancing the sympathetic response post-stress.

60
Q

Psychophysiological Disorders

A

Conditions like migraines or hypertension where stress contributes to physical symptoms.

61
Q

Burnout

A

A state of emotional exhaustion and reduced performance due to chronic workplace stress.

62
Q

Acute Stress Disorder

A

Short-term anxiety and dissociation following trauma, potentially progressing to PTSD if unresolved.

63
Q

Hypocortisolism

A

Abnormally low cortisol levels, linked to chronic fatigue and fibromyalgia in some stress-related disorders.

64
Q

Psychosocial Stressors

A

Environmental factors (e.g., poverty, discrimination) that induce stress and affect health outcomes.

65
Q

Neuroplasticity

A

The brain’s ability to reorganize itself, influenced by stress and adaptive coping mechanisms.

66
Q

Stress Inoculation

A

Training individuals to handle stress through gradual exposure and skill-building, enhancing resilience.

67
Q

Limbic System

A

Brain region (including amygdala and hippocampus) involved in emotional processing and stress response regulation.

68
Q

Amygdala

A

Detects threats and activates the HPA and SAM axes in response to perceived danger.

69
Q

Hippocampus

A

Regulates memory formation and cortisol feedback; atrophy occurs with chronic stress.

70
Q

Type A Behavior Pattern

A

Personality trait (competitiveness, urgency) linked to higher stress and cardiovascular risk.

71
Q

Type B Behavior Pattern

A

Personality trait (relaxed, patient) associated with lower stress reactivity.

72
Q

Telomerase

A

Enzyme that lengthens telomeres; reduced activity under chronic stress accelerates cellular aging.

73
Q

Stress-Related Cardiomyopathy

A

Heart dysfunction (e.g., Takotsubo syndrome) triggered by extreme emotional stress.

74
Q

Gastrointestinal Stress Effects

A

Symptoms like irritable bowel syndrome (IBS) or ulcers due to altered gut motility and microbiota.

75
Q

Psychogenic Fever

A

Elevated body temperature caused by psychological stress without infection.

76
Q

Adrenergic Receptors

A

Bind adrenaline/noradrenaline, mediating effects like increased heart rate and vasoconstriction.

77
Q

Hypocretin/Orexin

A

Neurotransmitters regulating arousal and wakefulness, disrupted in stress-related sleep disorders.

78
Q

Stress Granules

A

Cellular structures formed during stress to prioritize survival by halting non-essential protein synthesis.