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Patho > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Health

A

A state of complete physical, mental, and social wellbeing, and not merely the a sense of disease and infirmity

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2
Q

Determinants of health

A
  • Biology and behavior
  • physical and social environment
  • gov policies and interventions
  • access to quality health care
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3
Q

Disease

A

Any deviation from or interruption of the normal structure or function of a part, organ, or system of the body that is manifested by a characteristic set of symptoms or signs

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4
Q

Organic disease

A

Structural changes

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5
Q

Examples of organic diseases

A

Inflammation, infection, bone break

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6
Q

Functional disease

A

No morphologic abnormalities

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7
Q

Asymptomatic

A

Disease present (abnormal physical finding) but NOT associated with symptoms or discomfort

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8
Q

Symptomatic

A

Disease present WITH associated symptoms

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9
Q

Disease continuum

A

One end: severe, life-threatening, disabling illness
Other end: complete mental and physical well-being

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10
Q

Pathology and physiology

A

Deals with the study of the structure and function of cells, tissues and organs within the body

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11
Q

Pathophysiology

A

The pathology and physiology of disease, focuses on the mechanisms underlying disease

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12
Q

What does pathophysiology do

A

Basis for preventive and therapeutic health measures and nursing practice

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13
Q

Etiologic factors

A

Causes of disease

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14
Q

Examples of etiologic factors

A

Biologic agents
Physical forces
Chemical agents
Nutritional excesses or deficits

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15
Q

Important concepts about etiology

A
  • a single disease agent can affect more than a single organ
  • a number of different disease agents can affect the same organ
  • most diseases are multifactorial
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16
Q

Etiology

A

Describes what sets the disease process in motion

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17
Q

Risk factors

A

Predisposing conditions for a particular disease

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18
Q

Congenital risk factors

A

Present at birth

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19
Q

Acquired risk factors

A

Caused by events that occur after birth

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20
Q

Categories of risk factors

A
  • genetic
  • disease associated
  • treatment associated
  • environmental
  • lifestyle/behavioral
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21
Q

Pathogenesis

A

Sequence of cellular and tissue events that take place from the time of initial contact with an agent until the ultimate expression of disease
- how the disease process evolves “how things come to be wrong”

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22
Q

Morphology

A

The fundamental structure of cells or tissues
- cells -> tissues -> organs -> organ systems

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23
Q

Histology

A

Relation to morphology
- deals with the study of the cells and extracellular matrix of body tissues

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24
Q

Lesions

A

Relation to morphology
- Represents a pathologic or traumatic discontinuity of body organ or tissue

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25
Q

Signs

A

Objective (can be measured) manifestation of an illness or disorder
- can be seen, heard, measured or felt by clinician

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26
Q

Symptoms

A

Subjective (cannot be measured) evidence of an illness or disorder
- changes in the body or its function that is perceived by the patient as indicating the presence of disease

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27
Q

Syndrome

A

A compilation of signs and symptoms characteristic of a specific disease state

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28
Q

Complications

A

Possible adverse extensions of a disease or outcomes from treatment

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29
Q

Sequelae

A

Lesions or impairments that follow or are caused by a disease

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30
Q

Diagnosis

A

Designation as to the nature or cause of a health problem
- involves weighing competing possibilities and selecting most likely one accounting for the clinical presentation

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31
Q

What diagnosis is based on

A

Health history and physical examination

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32
Q

Deductive reasoning

A

From general to specific
- concerned with the rules for determining when an argument is valid

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33
Q

Inductive reasoning

A

From specific to general
- concerned with the soundness of inferences for which the evidence is not conclusive

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34
Q

Probability theory

A

Inductive reasoning
- what is the probability that the conclusion is true given the evidence in question

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35
Q

Major categories of diagnostic tests

A
  • clinical laboratory tests
  • tests of electrical activity
  • radioisotope studies
  • endoscopy
  • ultrasound
  • x ray
  • magnetic resonance imaging (MRI)
  • positron emission tomography (PET scan)
    -cytologic and histologic exams
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36
Q

Validity

A

(Accuracy)
- refers to the extent to which a measurement tool measures what it is intended to measure

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37
Q

Reliability

A

(Consistency)
- refers to the extent to which an observation, if repeated, gives the same result

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38
Q

Reference range

A

Determined for each test by each laboratory
- usually defined by testing healthy volunteers and plotting the frequency distribution

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39
Q

How reference ranges are conformed

A

Gaussian bell shaped curse
- hopefully fall in 95 percentile
- ranges are reported as 2 standard deviations away from the mean

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40
Q

Acute disorder

A

Usually self limiting and relatively severe

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41
Q

Chronic disorder

A

Implies long term process
- continuous symptoms/severity of disease over time

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42
Q

Exacerbation

A

Seen in chronic disorders
- varying degrees of aggravation of symptoms/severity of disease

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43
Q

Subacute disease

A

Intermediate between acute and chronic
- not as severe as acute and not as prolonged as chronic

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44
Q

Preclinical stage

A

Disease is not clinically evident but is destined to progress to overt clinical disease

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45
Q

Subclinical disease

A

Not clinically apparent and not destined to become clinically apparent

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46
Q

Clinical disease

A

Characterized by signs and symptoms

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47
Q

Carrier status

A

Refers to an individual who harbors an organism but is without clinical manifestation
- does not have the disease but can still infect others

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48
Q

Classifications of disease

A
  • congenital and hereditary
  • inflammatory
  • degenerative
  • metabolic
  • neoplastic
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49
Q

Congenital and hereditary disease

A

Genetic abnormality, intrauterine injury or integration of genetic and environmental factors

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50
Q

Inflammatory disease

A

Non-specific reaction to an injurious agent

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51
Q

Degenerative disease

A

Deterioration of various parts of the body

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52
Q

Metabolic disease

A

Disturbances of cellular energy processes

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53
Q

Neoplastic disease

A

Benign or malignant
Characterized by abnormal cell growth

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54
Q

Stress response

A

State of affairs arising when a person relates to situations in certain ways
- successfully adapt
- maladaptive resulting in disease

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55
Q

How are people disturbed by situations

A

Not by the situation itself but by the way they appraise and react to situations

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56
Q

How stress effects health

A

Stressful demands that exceed a persons coping abilities result in reactions such as disturbances of cognition, emotion and behavior that can adversely affect health and well being

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57
Q

Homeostasis

A

Purposeful maintenance of a stable internal environment maintained by coordinated physiologic processes that oppose change

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58
Q

How the physiologic control system works

A

Opposes change by operating on negative feedback mechanisms

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59
Q

Components of physiologic control system

A
  • sensor that detects change
  • integrator/comparator that sums and compares incoming data
  • effector system that returns the sensed function to within the set point range
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60
Q

Cannon’s general features of homeostasis

A
  • constancy requires mechanisms that act to maintain it
    -steady state conditions require that any tendency towards change automatically be met with facts that resist
  • the regulating system that determines the homeostatic state consists of a number cooperating mechanisms acting simultaneously or successively
  • does not occur by chance, result of organized self governance
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61
Q

Control systems

A

A collection of interconnected components that function to keep physical or chemical parameter of the body relatively constant

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62
Q

Jobs of control systems

A

Regulate cellular function
Control life processes
Integrate functions of different organ systems

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63
Q

Negative feedback mechanisms

A
  • maintains stability in system
    When function or value decreases below the set point of the system interjects and causes it to increase and vis Vera with an irregular increase
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64
Q

Positive feedback mechanism

A
  • interjects instability in the system
    Produces a cycle in which the initiating stimulus produces more of the same
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65
Q

Stress

A

State manifested bu a specific syndrome of the body developed in response to stimuli

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66
Q

Stimuli

A

Stressors
- endogenous: internal
- exogenous: external

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67
Q

General Adaption Syndrome (GAS)

A
  • G: the effect is a general systemic reaction
  • A: the response is in reaction to a stressor
  • S: the physical manifestations are coordinated and dependent on each other
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68
Q

Alarm (stage of GAS)

A
  • CNS aroused and defenses mobilized
  • epinephrine and norepinephrine released, increases heart rate, force on contraction, O2 intake and mental activity
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69
Q

Resistance or adaption (stage of GAS)

A
  • Sympathetic NS response
    -“adrenaline rush”
  • body responds to stressor & attempts to return to homeostasis
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70
Q

Exhaustion (stage of GAS)

A
  • continuous stress causes progressive breakdown of compensatory mechanisms
  • body can no longer produce hormones and organ damage begins (onset of disease)
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71
Q

Properties of the stressor

A

Type:
Eustress (good stress)
Distress (disease infection)
Intensity/severity:
Mild
Moderate
Severe
Duration:
Acute
Chronic

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72
Q

Conditions of the person being stressed

A

Physical, psychological, emotional and social state

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73
Q

Conditions of person being stresses effects

A

Susceptibility
Adaptive capacity and response

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74
Q

Eustress

A

Mild, brief, controllable
- perceived as positive stimuli to emotional and intellectual growth and development

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75
Q

Distress

A

Severe, protracted, uncontrollable situations of psychological and physical health
- disruptive of health

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76
Q

Conditioning factors

A

Refers to influence of the adaptive capacity of the person
Internal: genetic predisposition, age, sex
External: exposure to envi agents, life experiences dietary, social support

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77
Q

How stress response is mediated

A

Neuroendocrine-immune interactions
Combined efforts of the nervous and endocrine systems
- they integrate signals received along neurosensory pathways and from circulating mediators in the bloodstream

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78
Q

Stress effect on immune system

A
  • response is meant to protect person from acute threats to homeostasis
  • neural response and hormones are usually not around long enough to damage tissues
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79
Q

If a stress response is hyperactive…

A

Also occurs if stress response becomes habituated
psychological and behavioral changes can become a threat to homeostasis

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80
Q

If a stress response is hypoactive…

A

Person may be more susceptible to diseases associated with overactivity of the immune system

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81
Q

Hypothalamic-Pituitary-Adrenal cortex (HPA)

A

Neuroendicrine response
- mediated by glucocorticoids secreted by the adrenal cortex
- cortisol

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82
Q

Sympathetic nervous system (SNS)

A

Neuroendicrine response
- mediated by catecholamines secreted by the adrenal medulla
- epinephrine and norepinephrine

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83
Q

Major glucocorticoid in body

A

Cortisol

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84
Q

Functions of cortisol in stress response

A
  • stimulates the breakdown of muscular protein in AA
  • help lipids break down fatty acids and glycerol
  • promotes hepatic gluconeogenesis (synthesis of glucose) from AA, glycerol and fatty acids
  • inhibits tissues from utilizing glucose, making more available to the brain
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85
Q

Permissive action of cortisol

A
  • allows small amounts of glucose to be used for lipolysis and bronchodilation needed for the stress response
  • decreases hormone production, reproductive function, bone formation and RBC and WBC formation (inhibits immune response)
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86
Q

Adrenal catecholamines

A

Epinephrine and norepinephrine
- almost all norepinephrine is converted to epinephrine
- exert their effects in target organs as they travel through alpha and beta receptors

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87
Q

Alpha receptors

A
  • found in arteries in smooth muscle
  • when stimulated by epinephrine and norepinephrine, cause arteries to constrict to help return blood to heart
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88
Q

Beta 1 receptors

A
  • located in heart
  • when stimulated, cause the heart to beat faster and contract more forcefully to increase cardiac output
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89
Q

Beta 2 receptors

A
  • located in the lungs
  • when stimulated cause the bronchioles to dilate
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90
Q

Epinephrine and norepinephrine during stress response

A

Keep blood glucose levels high, thereby inhibiting metabolic activities like digestion

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91
Q

Epinephrine increases

A
  • Preparation for fight or flight response
  • mobilizes energy stores and increases blood glucose and fatty acids
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92
Q

Cortisol increases

A
  • mobilizes energy stores by increasing blood glucose, amino acids and fatty acids
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93
Q

Glucagon increases

A

Hormone that releases glucose from the liver
- increases blood glucose and fatty acids

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94
Q

Insulin decreases

A

Allows glucose to stay in the blood

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95
Q

Systems that keep circulating volume and blood pressure high (stress)

A

Renin-angiotensin-aldosterone system (RAA)
Anti-diuretic hormone system (ADH or Vasopressin)

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96
Q

Renin-angiotensin-aldosterone system (RAA) stress response

A
  • conservation of salt and water
  • increase in plasma volume
  • increase in arteriolar vasoconstriction to maintain/elevate blood pressure
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97
Q

Anti-diuretic hormone system (ADH) stress response

A
  • increase in plasma volume (control water)
  • increase in arteriolar vasoconstriction to maintain/elevate blood pressure
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98
Q

HPA Axis stress response

A

Secretion of cortisol to mobilize energy stores
- raise blood glucose, AA and fatty acids (use as energy)

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99
Q

Sympathetic nervous system stress response

A

Epinephrine (facilitated by cortisol)
- raise blood glucose and fatty acids
- vasoconstrict as it flows through alpha receptors that cause the initiation of the RAA system due to less flow to the kidneys

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100
Q

stress effects which hormones

A

Growth, thyroid, reproductive

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101
Q

Body system adaption to stress Growth

A

Acute stress: increased levels of thyroid hormones to generate energy and respond to threat
Chronic stress: decreased levels of growth and thyroid hormones (conserve energy)

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102
Q

Body system adaption Immunity

A

Exact mechanisms unclear BUT share common pathways
Hormones and neuroopeptides can alter immune function
Immune system can modulate Neuroendicrine function

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103
Q

Body system adaption Reproduction

A

Inhibition of reproductive hormones cause amenorrhea (a sense of menstruation) and infertility

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104
Q

Cerebral cortex and stress

A

Involved with vigilance, cognition and focused attention

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105
Q

Limbic system and stress

A

Involved with emotional response (fear, excitement, rage, anger)

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106
Q

Thalamus and stress

A

Relay center - important in receiving, sorting and distribution sensory input

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107
Q

Hypothalamus and stress

A

Coordinates response of the endocrine system and autonomic nervous system

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108
Q

Pituitary gland and stress

A

Releases hormones that govern vital processes

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109
Q

Reticular activating system (RAS) and stress

A

Modulates mental alertness

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110
Q

Definition of stress

A

A state manifested by symptoms that arise from the coordinated activation of the neuroendocrine and immune systems

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111
Q

Purpose of hormones and neurotransmitters released during stress

A

Catecholamines (epinephrine) and cortisol
- alert the individual to a threat or challenge to homeostasis
- enhance cardiovascular and metabolic activity of other systems in order to manage the stressor
- focus the energy of the body by suppressing the activity of other systems that are not immediately needed

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112
Q

What systems are suppressed during stress response

A

Immune ,digestive and reproductive

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113
Q

What is the stress response designed to be

A

Acute and self limited
SUPPOSED TO BE

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114
Q

When pathophysiologic changes occur (stress response)

A
  • a component of the system fails
  • the neural & hormonal connections among the components of the system are dysfunctional
  • the original stimulus for the activation of the system is prolonged or of such magnitude that it overwhelms the ability of the system to respond appropriately
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115
Q

Physiologic stress

A

Chemical or physical disturbance in the cells or tissue fluid produced by a change, either in the external environment or within the body itself, that requires a response to counteract the disturbance

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116
Q

Components of physiologic stress

A
  • exogenous or endogenous stressors initiating the disturbance
  • chemical or physical disturbance produced by the stressor
  • the body counteracting response to the disturbance
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117
Q

Adaption

A

The ability to respond to challenges of physical or psychological homeostasis and to return to a balanced state
- affected by individual differences

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118
Q

Appraisal of the event

A

Cognitive perception of the meaning or significance of the threat

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119
Q

Coping mechanisms

A

Emotional and behavioral responses used to manage threats to physiologic or psychological homeostasis

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120
Q

Factors affecting ability to adapt

A
  • previous learning
  • physiologic and anatomic reserves
  • time
  • genetic endowment
  • age
  • health status
  • nutrition
  • sleep wake cycle
  • hardiness
  • psychosocial factors
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121
Q

Effects of acute stress ANS

A

(fight or flight) pounding headache, moist skin, stiff neck, arousal, alertness, vigilance, cognition, attention

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122
Q

Effects of acute stress (life saving ability)

A

diversion of blood to essential body function increases alertness and cognitive functional

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123
Q

Effects of acute stress (detrimental)

A

Overwhelm response mechanisms can be life threatening

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124
Q

Effects of chronic stress

A
  • neural and hormonal connections among the components becomes dysfunctional
  • system may become over or under active
  • NIOSH: stress in a health hazard of the work place
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125
Q

Effects of chronic stress are linked to

A

Cardiovascular, gastrointestinal, immune and neurological diseases
Depression, alcoholism, drug abuse, eating disorders, accidents and suicide

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126
Q

Causes of PTSD

A

Combat, major catastrophic events, airplane crashes, terrorist bombings and rape or child abuse

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127
Q

PTSD is characterized by

A

Intrusion: occurrence of flashbacks in which past traumatic event is relived
Avoidance: emotional numbing and disruption of important personal relationships - often associated w/ depression
Hyperarousal: increases irritability and exaggerated startle reflex

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128
Q

Treatment of PTSD

A

Debriefing, crisis intervention, medications for anxiety and depression

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129
Q

Methods for studying physiologic manifestations of the stress responses

A
  • electrocardiographic recording of heart rate
  • blood pressure measurement
    -electrodermal measurement of skin resistance associated with sweating
    Biochemical analyses of hormone levels
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130
Q

Treatment of stress disorders

A

Relaxation
Imagery
Music therapy
Massage therapy
Biofeedback

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131
Q

Physical and chemical barriers to infections

A
  • skin
  • mucous membranes and secretions
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132
Q

Inflammatory response

A

Non specific
- fever and inflammation
- occur after tissue injury or infection
- immediate and general protection against invasion by a wide range of pathogens
- involves phagocytic WBCs, anti microbial substances, natural killer cells

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133
Q

Immune response

A

Specific
- identifies self from non-self
- recognizes & eliminates altered host cells
- develops more slowly & involves specific cells to combat a particular pathogen

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134
Q

1st line of defense mechanical factors

A
  • skin
  • mucous membrane
  • mucus
  • hairs
  • cilia
  • lacrimal apparatus
  • saliva
  • urine
  • defecation & vomiting
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135
Q

1st line of defense chemical factors

A
  • acid pH of skin
  • unsaturated fatty acids
  • lysozyme
  • gastric juice
  • vaginal secretions
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136
Q

2nd line of defense internal defenses

A
  • antimicrobial proteins: interferons and complement system
  • natural killer cells
  • Phagocytes
  • inflammation
  • fever
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137
Q

Natural killer cells

A

Help induce apoptosis of viral/tumor cells

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138
Q

Complement system

A

Proteins kill organisms that don’t belong

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139
Q

Phagocytes

A

Engulf and destroy bacteria, foreign particles and dead cells

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140
Q

Lymph nodes

A
  • distribute along lymphatic vessels
  • filter lymph fluid & remove bacteria and toxins from circulation through phagocytic activity
  • proliferation of immune cells
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141
Q

Thymus

A
  • located in mediastinum
  • produces T- lymphocytes
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142
Q

Spleen

A
  • largest lymph organ
  • reservoir for blood
  • macrophages clear cellular debris and process hemoglobin
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143
Q

Tonsils

A
  • Produce lymphocytes
  • guard against airborne and ingested pathogens
  • last organ to catch pathos before digestion
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144
Q

Red bone marrow

A

Houses stem cells that develop into lymphocytes

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145
Q

Primary lymphatic organ

A

Provide environment for stem cells to divide and mature
Red bone marrow: RBC WBC platelets mature
Thymus gland: T cells mature

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146
Q

Secondary lymphatic organs and tissues

A

Sites where most immune responses occur
Lymph nodes: macrophages
Spleen: macrophages
Lymphatic nodules: collect and filter debris

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147
Q

Lymphatic flow

A

Drains toxins, waste and infectious things to large blood vessels
- lymph fluids does NOT have RBC but is similar to blood (low protein count)

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148
Q

Microbial factors

A

Virulence: how serious it is
Dose: how much exposure
Portal of entry: eyes, ears, nose, cut, urethra, anus, surgery
Organ preference

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149
Q

Host resistance

A

Ability of the body to ward off disease

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150
Q

Host susceptibility

A

Vulnerability or lack of resistance to disease

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151
Q

Host factors

A

Age, immunity, genetics, nutrition, underlying or pre-existing diseases, health habits, stress, psychological factors

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152
Q

Environment and disease

A

Humidity, poor sanitation, crowded living, pollution, dust

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153
Q

Biologic agents

A

Allergens
Infectious organisms
- viruses, bacteria, mycoplasma, rickettsiae, fungi, parasites
Vaccines can combat

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154
Q

Chemical agents

A

Toxins
Dust

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155
Q

Physical gents

A

Kinetic energy
- ex: bullet wounds, blunt trauma, vehicular injuries
Radiation
Thermal
Social and psychologic stressors

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156
Q

Infection

A

Tissue destroying microorganisms enter and multiply in the body
Categorization by severity
- Minor: colds, ear infections
- life-threatening: sepsis

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157
Q

Sepsis

A

Infection, contamination

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158
Q

Bacteremia

A

Presence of bacteria in the blood

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159
Q

Viremia

A

Presence of virus particles in the blood

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160
Q

Septicemia

A

Systemic infection in which pathogens are present in the blood having spread from an infection in any part of the body

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161
Q

Viruses

A

Microscopic genetic parasites
- consist of a protein coat that surrounds a nucleic acid core which may contain RNA or DNA
- have no metabolic capability, most require a host cell to replicate (obligate intracellular parasites)
- some can reproduce outside of a living cell
- capable of remaining dormant for long periods of time

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162
Q

Bacteria

A
  • single celled microorganisms
  • no true nucleus
  • reproduce by cell division
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163
Q

Cell damaging proteins of bacteria

A

Endotoxins: released when the bacterial cell wall decomposes
Exotoxins: released during cell growth

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164
Q

Classifications of bacteria

A

Shape: coccus (spherical), spirillum (helical), bacillus (elongated)
Growth requirements
Motility
O2 requirements: aerobic vs anaerobic
Gram stain: positive purple, negative does not retain stain

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165
Q

Mycoplasmas

A
  • 1/3 the size of bacteria
  • capable of reproducing independently
  • do NOT have a rigid cell wall
  • some cause pneumonia
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166
Q

Rickettsiae

A
  • depends upon host cell division
  • have a rigid cell division
  • human infection caused by bite of an infected arthropod
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167
Q

Fungi

A
  • non-photosynthetic microorganisms that reproduce asexually (cell division)
  • relatively large
  • contain a true nucleus
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168
Q

Classifications of Fungi

A

Yeasts: round, single-celled facultative anaerobes (can live w/ or w/out O2)
Molds: filament-like , multinucleated, aerobic microorganisms

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169
Q

Mycotic infections or mycoses

A

Infections caused by fungi that release mycotoxins
- most are mild, unless they become systemic or the patient’s immune system is compromised, opportunistic infection

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170
Q

Parasites

A
  • depend on a host for food and protective environment
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171
Q

Protozoa

A

Parasite
- minute unicellular animals
-transmission by arthropod vector or contaminated food/water

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172
Q

Examples of Protozoa infections

A

Malaria, amebic dysentery

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173
Q

Helmiths

A

Worm like parasites
- transmitted by ingestion of fertilized eggs or larva penetration of the skin
- most common in developing countries

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174
Q

Arthropods

A

Parasite
- have jointed exoskeletons and paired jointed legs
- can serve as vectors for other diseases

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175
Q

Examples of arthropods

A

Ticks, mosquitoes, biting flies

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176
Q

Ectoparasites

A

Organisms that live on the outside of the body
- transmitted through contact with infected clotting, bedding or grooming articles

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177
Q

Examples of ectoparasites

A

Mites, lice and chiggers

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178
Q

Normal body flora

A

Harmless microorganisms that reside in or on the body
- found on skin and in the nose, mouth, pharynx, distal intestine, colon, distal urethra and vagina
- many useful functions

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179
Q

Normal body flora on skin

A

About 100,000 per square centimeter

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180
Q

Useful function of intestinall flora

A

Synthesize vitamin K

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181
Q

Host factors are influenced by

A

Genotype/phenotype
Nutritional status
Immune system
Social behavior

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182
Q

Environment and infection

A

Influences the probability and circumstances of contact between the host and the agent
Includes:
Sanitation and living conditions
Pollution
Social, political and economic factors

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183
Q

Pathogen

A

Disease causing agent

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184
Q

Reservoir

A

Habitat in which an infectious agent normally lives and grows

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185
Q

Examples of reservoirs

A

Human: symptomatic or asymptomatic
Animal: zoonoses
Environmental: plants, soil and water

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186
Q

Portal of exit

A

Path by which an agent leaves the source host

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187
Q

Transmission

A

How pathogens are passed

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188
Q

Modes of transmission

A

Direct: direct contact, droplet spread
Indirect: airborne, vehicleborne, vectorborne

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189
Q

Portal of entry

A

A gent enters susceptible host
Respiratory
Oral
Skin
Intravenous
Gastrointestinal

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190
Q

New host

A

Final link is a susceptible host

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191
Q

Granulocytes

A

Type of immune cell (WBC) w/ granules (small particles) w/ enzymes realized during infection, allergic reactions and asthma

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192
Q

Types of granulocytes

A

Neutrophils
Bands (immature neutrophils)
Basophils
Eosinophils

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193
Q

Agranulocytes

A

Types of WBC that lacks granules

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194
Q

Types of agranulocytes

A

Lymphocytes
Monocytes

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195
Q

Cellular elements of peripheral smear

A

Granulocytes
Agranulocytes
RBC
Platelets

196
Q

White blood cells

A

Protect body against harmful bacteria and infection

197
Q

Neutrophils

A

WBC type of Granulocyte
Phagocytosis “pyogenic” infections

198
Q

Basophils

A

WBC type of Granulocyte
Involved in allergies and inflammatory response

199
Q

Eosinophils

A

WBC type of Granulocyte
Release heparin and histamine
- involved in delayed allergic reaction
- has role in parasitic infections

200
Q

Monocytes

A

WBC type of agranulocyte
Phagocytosis
Severe infections

201
Q

Lymphocytes

A

WBC type of agranulocyte
Viral infections

202
Q

B-cells

A

W/ lymphocytes
Mature into plasma cells and release antibodies

203
Q

T-cells

A

W/ lymphocytes
Regulate cell mediated immunity

204
Q

Macrophages

A
  • Lack surface receptors for specific antigens
  • Have receptors for Fc region (tail region of antibody) and for the compliment
  • ingest and process antigen and deposit it on its own surface
205
Q

MHC

A

Group of membrane bound proteins that code for antigens

206
Q

MHC class 1

A

Communicate w/ macrophages to alert T cells to destroy foreign antigen (help identify foreign vs host)
Each person has unique

207
Q

MHC class 2

A

Send chemicals to T cells to organize the killing of macrophages that have engulfed foreign invades

208
Q

Secreting cytokines

A

Job of macrophages
Tumor necrosis factor (TNF) and interleukin-1 which produce fever

209
Q

Dendritic cells

A

Mononuclear phagocytes that are another type of antigen presenting cell
- different function than dendritic cells in the nervous system
- communicate w/ innate and adaptive immune systems with central role in fighting infection and maintaining organ integrity

210
Q

Main function of dendritic cells not NS

A

Activation of naive T cells not previously subjected to an antigen

211
Q

Reticuloendothelial system

A

Destroy abnormal cells or at end of life cells

212
Q

Lung macrophages

A

Alveolar macrophages

213
Q

Liver macrophages

A

Kupffer’s cells

214
Q

Tissue macrophages

A

Lymph nodes and spleen

215
Q

Intestine macrophages

A

Peyer’s patches

216
Q

CNS macrophages

A

Microglial cells

217
Q

Skin macrophages

A

Langerhans’ cells

218
Q

Connective tissue macrophages

A

Histiocytes

219
Q

Absolute WBC count

A

Actual number
More important

220
Q

Relative WBC count

A

Percentage

221
Q

Finding absolute value WBC

A

Relative value (%) x total WBC

222
Q

Increased values of WBC terms

A

Leukocytosis
Neutrophilia
Lymphocytosis
Monocytosis
Eosinophilia
Basophilia

223
Q

Decreased values WBC terms

A

Leukopenia
Neutropenia
Lymphopenia
Monocytopenia
Eosinophilia
Basopenia

224
Q

Increased WBC count means

A

Infections, inflammation, tissue necrosis, leukemia neoplasia (cancer)
Also trauma and stress

225
Q

Decreased WBC count means

A

Chemotherapy, radiation therapy, marrow infiltrative diseases, overwhelming infections, dietary deficiencies, autoimmune diseases

226
Q

Age and WBC count

A

Newborns and infants have higher WBC values
Elderly may not develop increased WBC even with severe infection

227
Q

Critical WBC values

A

< 2500 cells/mm3
> 30,000 cells/mmm3

228
Q

Erythrocyte sedimentation rate (ESR)

A

Serologic indicator of inflammation and infection
- rate that RBCs settle out of anti-coagulated blood in 1 hour

229
Q

How ESR works

A

Inflammatory and necrotic processes cause an alteration in blood proteins, RBCs rend to clump together in a column like manner and thus are heavier and settle out faster when in vertical tube
-NOT diagnostic just provides info

230
Q

ESR and acute infections

A

Usually does not elevate for 6 to 24 hours and peaks after several days

231
Q

C-Reactive Protein (CRP)

A

Serologic indicator of inflammation and infection
- an abnormal protein synthesized by the liver and present in blood during ant process that involves tissue necrosis, trauma, inflammation or infection
- classic and most dramatic acute phase reactant
NONSPECIFIC

232
Q

Readings of CRP

A

Levels increase up to 1000 x normal and decrease rapidly when inflammatory process regresses
Good indication of healing and response to Tx

233
Q

Culture

A

Saliva, blood, urine and CSF (cerebral spinal fluid) and other specimen
- sample placed in culture media to allow organism to grow and be identified

234
Q

Sensitivity with cultures

A

Antimicrobial effectiveness determined by placing various antibiotic disks on the culture medium

235
Q

Important to remember about in vitro tests

A

They do NOT reflect plasma concentrations or attainable concentrations at the site of infection and do NOT take into account local factors (like pH) that may affect the activity of the drug

236
Q

Serial dilution

A

Way of performing Calc to determine how many separate colonies are present
- from this a Calc of viable cells in the original suspension can be made

237
Q

Urinalysis markers of infection

A

Appearance and color
Odor
PH
Leukocyte esterase
Nitrates

238
Q

Appearance and color urinalysis

A

Could may be caused by pus (necrotic WBC, RBC or bacteria)
Pseudomonas may make it green

239
Q

Odor urinalysis

A

Foul because of UTI

240
Q

PH urinalysis

A

Bacteria may cause increase
Urea-splitting bacteria case urine to be alkaline (increase)

241
Q

Leukocyte esterase urinalysis

A

Screening test to detect leukocytes
90% accurate

242
Q

Nitrites urinalysis

A

Screening test for identification of UTIs
Bacteria produce an enzyme called reductase which can reduce nitrates to nitrites
50% accuracy
False + if contaminated with vaginal sec reactions

243
Q

Stool culture

A

Normal stool contains indigenous bacteria and fungo
Presence of urine may inhibit bacterial growth causing false neg
- unrelenting fever and abdominal pain
- if immunocompromised normal flora in stool can become pathogenic

244
Q

Pathogenic bacteria found in stool

A

Salmonella, shingella, campylobacter, yersinia

245
Q

Acute inflammatory response

A

Rapid and nonspecific
Protective response to cellular injury from any cause
Can only occur in vascularized tissue

246
Q

Acute inflammatory response results in

A

Accumulation of fluids and cells at the site
“-itis” : inflammation

247
Q

Inflammation

A

Reaction of vascularized tissue to local injury
It is active, aggressive and nonspecific
NOT synonymous with infection; colonization alone does NOT produce inflammation
Tissue response is the same regardless of the cause

248
Q

Causes of inflammation

A

Infection by microorganisms
Heat and cold
Radiation
Trauma
Chemicals
Ischemic damage

249
Q

Hypoxia

A

Lack of sufficient O2 in cells

250
Q

Hypoxemia

A

Lack of O2 in blood

251
Q

Ischemia

A

Reduced blood supply
Gradual porgessive or sudden acute

252
Q

Arteriosclerosis

A

Gradual narrowing of the arteries
Causes ischemia

253
Q

Thrombosis

A

Complete blockage of an artery by a blood clot
Causes ischemia

254
Q

Embolus

A

A blood clot that has traveled from a distant site
Causes ischemia

255
Q

Anoxia

A

Total lack of O2

256
Q

Infarction

A

Cell death

257
Q

Acute vascular response

A
  • immediate arteriolar vasoconstriction -> vasodilation -> swelling (edema) and erythema (redness) -> hyperemia
  • increased capillary permeability -> allows fluid to escape into tissue -> swelling -> fluid dilutes toxins
  • pain and impaired function d/t tissue swelling and release of chemical mediators
258
Q

Acute cellular response WBC

A

Move towards damaged cells
Phagocytosis of dead cells and organisms

259
Q

Acute cellular response platelets

A

Move towards damaged cells and control any excess bleeding in area

260
Q

Acute cellular response mast cells

A

Release heparin to maintain blood flow to area

261
Q

Acute phase response cellular response

A

Granulocytes
Mononuclear phagocytes
Margination and emigration of leukocytes
Chemotaxis
Phagocytosis

262
Q

Acute cellular response neutrophil

A

Primary phagocyte
- arrive early
- polymorphonuclear (PMNs or polys) or segmented (segs)

263
Q

Acute cellular response eosinophils

A

Allergic reactions and parasitic infection s
Release chemical mediators causing inflammation

264
Q

Acute cellular response basophils

A

Mast cells in tissues
Inflammation and allergic reaction
Contain histamine -> mediator of inflammation

265
Q

Acute cellular response Leukocytosis

A

Increase WBCs

266
Q

Mononuclear phagocytes

A

Largest WBC (3-8%)
3-4x longer lifespan
Mature into macrophages

267
Q

Acute cellular response mononuclear phagocytes

A

W/in 48 hours monocytes and macrophages are predominant cell type
Can phagocytize larger material than neutrophils
Migrate to local lymph nodes and play role in specific immunity
Role in chronic inflammation -> wall off material that cannot be digested

268
Q

Margination of leukocytes

A
  • release of chemical mediators and cytokines affect endothelial cells of capillaries
  • causes expression of adhesion molecules
  • leukocytes marginate (pavementing)
269
Q

Adhesion molecules

A

Cause WBC to stick to area of vessels

270
Q

Pavementing

A

Moving to the side closer to the invader

271
Q

Chemical mediators

A

Histamine, leukotrienes and kinins

272
Q

Emigration of leukocytes

A

Follows Margination
Diapedesis (moving) through capillary walls in order to attack

273
Q

Acute response chemotaxis

A
  • Leukocytes wander through tissue guides by:
    Secreted cytokines (chemokines, IL-8)
    Bacterial and cellular debris
    Complement fragments (C3a C5a)
  • migration in response to chemical signal -> increases probability of sufficiently localized cellular response
274
Q

Acute response phagocytosis

A

Neutrophils and macrophages engulf and degrade bacteria and cellular debris

275
Q

4 steps of phagocytosis

A

Chemotaxis: chemical attraction of WBC to area
Adherence plus opsonization: coats the antigen with antibody (Fc) or complement (C3a)
Engulfment
Intracellular killing: via enzymes, defensins, toxic products

276
Q

Phagocytosis engulfment

A

Pseudopods surround and enclose particle in phagocytic vesicle (phagosome)
Merge with lysosome
Antibacterial molecules and enzymes digest

277
Q

Acute phase response

A
  • changes in concentrations of plasma proteins
  • increase in erythrocyte sedimentation rate
  • fever
  • increase in number of leukocytes
  • skeletal muscle catabolism (break down)
  • negative nitrogen balance
278
Q

Histamine

A

Main chemical mediator of inflammation
- released by basophils, platelets, and mast cells
- responsible for both parts of vascular response to inflammation

279
Q

Vasodilation causes (inflammation)

A

Increased blood flow + increased capillary permeability

280
Q

Histamine also stimulates

A

Bronchoconstriction (H1 receptors)
Gastric acid secretion (H2 receptors)

281
Q

Plasma proteases

A

Inflammatory mediator
Contributes to vascular phase of inflammation through fibrinopeptides formed during final step of clotting process

282
Q

Bradykinins (inflammatory mediator plasma protease)

A

increases capillary permeability and causes pain

283
Q

Kinins (inflammatory mediator plasma proteases)

A

activated complement proteins and clotting factors

284
Q

Prostaglandins

A

Inflammatory mediator
- produces from arachodonic acid found in the cell membranes via cyclooxygenase metabolic pathway
- PGE and PGE2 important in inflammation
- increase blood flow and capillary permeability
Cause fever
Stimulate pain receptors

285
Q

What blocks proglandins

A

NSAIDs
Ibuprofen, alive, etc

286
Q

Leukotrienes

A

Inflammatory mediator
- increase vascular permeability
- affects adhesion of WBC to capillary
- acts as chemo-attractants

287
Q

SRSA

A

Slow reacting substance of anaphylaxis
Key role in bronchoconstriction in asthma

288
Q

Platelet activation factor

A

Inflammatory mediator
- generated from a complex lipid in cell membranes
- affect a variety of cell types
- induces PLT aggregation
- activates neutrophils
- potent eosinophil chemo-attractant

289
Q

Cytokines

A

Inflammatory mediator
- peptide produced by variety of immune and inflammatory cells
- function as local hormones that affect host response to injury or infect
- multiple effects -> serve as a communication link between immune and inflammatory system

290
Q

Producers of cytokines

A

Macrophages, monocytes, neutrophils, lymphocytes
Noninflammatory cells: fibroblasts and endothelial cells

291
Q

Inflammatory cytokines

A

IL-1, IL-6, TNF, interferon-y
- promote fever and malaise + stimulate T-cell activity
- released from macrophages and monocytes ( IL-1 and TNF) or activated T-cells (IL-6, TNF and interferon)
- activate B-cells: plasma cells and secrete antibodies

292
Q

IL-2

A

Cytokine
Decreased by activated T-helper
This with TNF: stimulate cytotoxic T-cells which attack and kill cancer cells or cells infected with a virus
Alerts macrophages to increase phagocytosis

293
Q

Hematopoietic colony stimulating factors

A

Increase WBC during infection

294
Q

IL-10

A

Noninflammatory cytokine
Decrease activation of B-cells

295
Q

Inflammatory exudates

A

Fluid, plasma protein, cell contents

296
Q

Serous

A

Watery, low protein (plasma)
Ex: blister that pops

297
Q

Fibrinous

A

Fibrinogen -> thick sticky mesh work, like a clot
Ex: strep throat, bacterial pneumonia

298
Q

Membranous

A

Develop on mucous membrane surface -> necrotic cells enmeshed in fibrino-purulent (pus) exudate
Ex: colon inflammation

299
Q

Purulent or suppurative

A

Contains pus

300
Q

Pus

A

WBCs - neutrophils and macrophages, proteins, tissue debris)

301
Q

Hemorrhagic

A

Leakage of RBCs (blood)

302
Q

Acute inflammation

A

With intact immune system - usually self limited and rapidly controlled by host defenses

303
Q

Chronic inflammation

A

Self-perpetuating and last for weeks or months
- involves proliferation of fibroblasts instead of exudates which increases the risk of scarring

304
Q

Irritants found in chronic inflammation

A

Typically low grade, persistent (talc, silica, asbestos) or moderate to low virulence (tubercle bacillus, treponema pallium, actinomyces) that are unable to penetrate deeply or spread rapidly

305
Q

Types of chronic inflammation

A

Non-specific
Granulomatous

306
Q

Abscess

A

A localizes area of inflammation containing a purulent exudate

307
Q

Typical set up of an abscess

A

typically have a central necrotic core containing purulent exudates surrounded by a layer of neutrophils

308
Q

Fibroblasts and abscesses

A

May eventually enter area and wall off to make it inaccessible to antibiotics
- often requires surgical incision and drainage

309
Q

Ulceration

A

A site of inflammation on an epithelial surface (skin and GI tract), have become necrotic and eroded

310
Q

What is ulceration usually associated with

A

Subendothelial inflammation

311
Q

What can cause ulceration

A

Injury to epithelial surface to because of vascular compromise

312
Q

Chronic lesions and ulceration

A

The area surrounding the ulceration develops fibroblast in proliferation with scarring and accumulation of chronic inflammatory cells

313
Q

Chronic inflammatory cells

A

Macrophages and lymphocytes

314
Q

Granuloma formation

A

Happens when the acute inflammatory response is unsuccessful at ridding the body of foreign particles which causes chronic inflammation

315
Q

When does granuloma formation occur

A

When giant cells (fused macrophages) engulf large foreign particles

316
Q

How granuloma formation works

A

A 1-2 mmm lesion - mass of macrophages surrounded by lymphocytes
Outside: encases by a collagen network and may eventually calcify -> lesion becomes encapsulated and isolated
Inside: debris decays and forms a liquid that may diffuse out leaving behind only a tick walled casing

317
Q

What is granuloma formation associated with

A

Foreign bodies such as splinters, sutures, silica, asbestos and microorganisms that cause Tb and syphilis

318
Q

Acute phase response: systemic manifestations

A
  • changes in concentrations of plasma proteins: liver increases synthesis of acute phase proteins such as fibrinogen and C-reactive proteins
  • increased ESR
  • fever
  • lethargy (effects of interleukins and TNF)
319
Q

Systemic manifestations in bacterial infections

A

^ number of leukocytes
^ number and immaturity of circulating neutrophils by stimulating production in the bone marrow

320
Q

“Shift to the left”

A

Increase in the number of bands (immature neutrophils)

321
Q

Systemic manifestations in parasitic infections and allergic reactions

A

Eosinophilia

322
Q

Systemic manifestations in viral infections

A

Neutropenia and lymphocytosis

323
Q

Systemic manifestations in overwhelming infections in the presence of other debilitating diseases

A

Leukopenia

324
Q

Systemic manifestations in skeletal muscle catabolism & neg nitrogen balance

A

Amino acids are used for immune response and tissue repair

325
Q

Lymphadenopathy

A

Characterized by a localized or generalized enlargement of the lymph nodes or lymph vessels

326
Q

Lymphadenitis

A

Inflammatory condition of the lymph nodes
- may be enlarged hard, smooth or irregular
- may be red, feel hot or tender to the touch

327
Q

Location of node in lymphadenitis

A

Indicative of the site of origin of disease
- affected nodes are proximally located along the lymphatic drainage pathway

328
Q

Pain of nodes

A

Painful: associated with inflammatory process
Non-painful: more characteristic of neoplasms

329
Q

Opportunistic infection

A

Infections that occur as a result of altered or weakened host immune system

330
Q

Autoimmune disorders

A

Hyperactive immune system
- inflammatory response related to injury to one’s own body tissues

331
Q

Pyrexia

A

Fever - elevation in body temp
- cardinal manifestation of disease
- raised by toxins released during inflammatory process
- do NOT minimize or ignore

332
Q

Fever following major surgery or MI

A

Low grade temp is normal for 1st 48-72 hours

333
Q

Where is body’s thermostat

A

Hypothalamus

334
Q

Pyrogens

A

Fever producers

335
Q

Exogenous pyrogens

A

Gram +/- bacteria
Endotoxins
Viruses
Fungi
Yeast
Protozoa

336
Q

Endogenous pyrogens

A

PMNs
Macrophages
T4 cells release fever producers in response to injury (IL1,IL6, TNF)
Malignancies, Ag-Ab reactions and graft rejections

337
Q

Fever production

A

Endogenous pyrogens stimulate release of PgE from hypothalamus
Stimulates release of NE from adrenal medulla
Lowers Ca around hypothalamic cells
Increases firing rate

338
Q

Prodromal stage of fever

A

General malaise, fleeting aches and pains

339
Q

Stage 1 of fever

A

Cold and shaking chill state
- 10-40 min with rapid, steady rise in Temp ->
- cellular metabolism ->
- vasoconstriction and cessation of sweating

340
Q

Stage 2 of fever

A

Flush stage
- Thermostats rest cutaneous vasodilation ->
- Skin warm and flush ->
- Dehydration

341
Q

Stage 3 of fever

A

Defervescence
- initiation of sweating

342
Q

Intermittent fever

A

Returns to normal at least every 24 hours

343
Q

Remittent fever

A

Varies a few degrees in either direction

344
Q

Sustained or continuous fever

A

Increased temperature with minimal variation

345
Q

Recurrent or relapsing fever

A

One or more episode of fever each lasting several days with one or more days of normal temp b/w episodes

346
Q

Fever of Unknown Origin

A

T> 101 present for > 3 weeks
Causes: malignancies, infections, cirrhosis

347
Q

Treatment for fever

A
  • Modifications of external environment: tepid baths & cooling blanket
  • treatment of underlying causes
  • fluid replacement and simple carbohydrates
  • antipyretics: acetaminophen, NSAIDs, ASA (aprinin)
348
Q

fever in children

A
  • Common: 2/3 of all children < 3 yrs
  • low vs high risk: based on prob of progression to bacteremia and meningitis
  • S/S toxicity: lethargy, poor feeding, hypoventilation and poor O2, cyanosis
349
Q

Fever in elderly

A
  • normal body temp and circadian pattern often altered in elderly
  • lower basal temp
  • 20-30% with serious infection present with absent or blunted febrile response
350
Q

only liquid tissue

A

Blood
Has some solid components
RBC WBC platelets

351
Q

Composition of blood

A

-Plasma (55%)
About 50% water
About 5% plasma substances
-Formed Elements (45%)
Less than 1% WBC and platelets
Almost 45% RBC

352
Q

Plasma proteins in blood

A

Albumin, globulins, fibrinogen, electrolytes, dissolved gases, waste products of metabolism, nutrients, vitamins, cholesterol

353
Q

All cells start as

A

Pluripotent stem cells

354
Q

Control of progenitor cell differentiation

A
  • hematopoietic growth factors (stimulate cells to proliferate and differentiate)
  • each progenitor cell responds to only a certain growth factor
  • some growth factors act non-specifically on several
355
Q

Where are many growth factors released from

A

Immune and inflammatory cells

356
Q

Colony stimulating factors

A

Growth factors for specific lines of cells
- GCSF: granulocyte colony stimulating factor erythropoietin

357
Q

RBCs

A
  • no nucleus, mitochondria or ribosomes
  • cannot reproduce
  • contain hemoglobin that carry O2 to cells
358
Q

Shape of RBCs

A

Biconcave disks
High surface area allows for rapid diffusion
Small and flexible -> squeeze through capillary beds

359
Q

Growth of RBCs

A
  • unipotential stems cells are in bone marrow
  • response to growth factors and become erythoblasts (6 days in bone marrow)
  • turn into reticulocytes (1 day in bone marrow one day in blood)
  • become erythrocytes (RBC)
360
Q

Lifespan of erythrocyte

A

120 days

361
Q

Required for synthesis of erythrocyte

A

Iron, folic acid, vitamin B12

362
Q

Erythoblast

A

Progenitor for Erythrocyte

363
Q

Reticulocyte

A

Immature RBC

364
Q

Erythrocyte

A

RBC

365
Q

Myeloblast

A

Progenitor for granulocyte

366
Q

Monoblast

A

Progenitor for monocyte which becomes macrophages

367
Q

Prolymphoblast

A

Progenitor for lymphoid stem cells which become B-lymphocytes and T-lymphocytes

368
Q

Breakdown of RBCs

A

RBC disintegrate and release Hgb into circulation

369
Q

Liver and spleen and breakdown of RBCs

A

Phagocytize old RBCs
- globulin: converted into AA (build into proteins) to be reused in body
- iron: stored in liver and spleen until reused
- rest of molecules: converted to bilirubin and excreted in stool a bile or in urine

370
Q

Transferrin

A

Carries iron to bone marrow where Hgb synthesized

371
Q

Hemoglobin

A

Consists of heme and protein globulin
- about 300 molecules per RBC

372
Q

Hemoglobin binding sites

A

4 sites for O2 per Hgb

373
Q

Abnormal Hgb molecules

A

> 100 types that carry O2 poorly and can make patients anemic

374
Q

Hematocrit

A

% of blood taken up by RBCs
Range depends on sex and age

375
Q

Rules of 3

A

RBC x 3 = HGB
Hgb x 3 + Hct

376
Q

Mean Corpuscular Volume

A

MCV = Hct / RBC
Relates to cell size
Normal: 87 - 103 micrometer^3

377
Q

Microcytic

A

Cells too small in size

378
Q

Normocytic

A

Cells of normal size

379
Q

Macrocytic

A

Cells too large in size

380
Q

Mean Corpuscular Hemoglobin Concentration

A

MCHC = Hgb / Hct
Norm: 32- 36 g/dL

381
Q

Hypochromic

A

Cells with too little Hgb

382
Q

Normochromic

A

Cells with normal amount of Hgb

383
Q

Hyperchromic

A

Cells with too dense Hgb

384
Q

Mean Corpuscular Hemoglobin

A

MCH = Hgb / RBC
Normal: 27 - 32 pg
Reflects both size of RBC and concentration of Hgb in RBC

385
Q

Low value of MCH

A

Cause hypochromia or microcytosis or both
Not particularly helpful because it doesn’t differentiate

386
Q

Red cell distribution width

A

Standard deviation of the MCV
Measure of the degree of uniformity of RBC size

387
Q

Thalassemia

A

Uniform sized cells (normal level RDW)

388
Q

Iron deficiency anemia and clinical descriptors

A

Decreased cell size
Increased RDW

389
Q

Problem with MDW

A

Sensitivity is high but specificity is low
So if it is normal you can rule out iron deficiency anemia but if its high it can be many types of anemia

390
Q

Reticulocyte count

A

The number of RBCs containing RNA (convert to DNA within 24 hrs)
Good indicator of bone marrow function

391
Q

Most reliable measure of RBC production

A

Reticulocyte count (# of reticulocytes vs %)
Automated methods more accurate than manual

392
Q

Absolute Reticulocyte count

A

% reticulocytes x RBC count

393
Q

Spherocytes

A

RBC shape
Small and round
Decrease O2 carrying ability

394
Q

Ellipyocytes

A

RBC shape
Elliptical or oval
Decrease O2 carrying ability

395
Q

Sickle

A

RBC shape
Crescent shaped
Decrease O2 carrying ability

396
Q

Target cells

A

RBC shape
Thin cells with less Hgb

397
Q

Anisocytosis

A

Abnormal size of RBC
Caused by severe anemia

398
Q

Poikilocytosis

A

Abnormal shape of RBC
Caused by severe anemia

399
Q

Spherocytosis

A

Spherical RBCs without pale center
Caused by heredity

400
Q

Stomatocytosis

A

RBC with slit-like areas of enteral pallor
Caused by congenital hemolytic anemia

401
Q

Target cells on peripheral smear

A

RBCs with dark center + periphery and clear ring in between
Caused by thalassemia and hemoglobinopathies

402
Q

Basophilic stippling

A

Punctuate stippling when Wright-stained
Caused by lead posioning

403
Q

Anemia

A

Decreased RBCs or Hgb or Hct

404
Q

Causes of Anemia

A

Disorder in RBC production
Evelvated loss of RBCs
- chronic bleeding (loosing a little everyday for months)
- sudden hemorrhage (trauma)
- excess lysis/cell destruction (destroying more than making)

405
Q

Anemia symptom expression depends on

A

Duration and severity
Age and health status of host

406
Q

Symptoms of anemia manifestation

A

Relates to reduction in delivery of O2 to cells (hypoxemia)

407
Q

Symptoms of anemia

A
  • Listlessness, FATIGUE, irritability, WEAKNESS, PALLOR
  • ^ RR DYSPNEA AND SOB, - ^ HR, palpitations, angina (chest pain)
  • heart failure & ischemia id pre-existing CV disease: pictorial, intermittent claudication, dizziness or giddiness
408
Q

Classifications of anemia

A

Rate of development: acute or chronic
Morphology (shape)
Hemoglobin content
Type of defect or etiology

409
Q

Production defect

A

Lack of necessary building blocks to make RBCs

410
Q

Destruction defect

A

Bone marrow destruction or hemolysis

411
Q

Genetic defects in Hemoglobin

A

Sickle cell anemia

412
Q

Microcytic hypochromic anemia causes

A

Iron deficiency
Thalassemia
Chronic systemic diseases

413
Q

Microcytic normochromic anemia causes

A

Chronic systemic disease

414
Q

Normocytic normochromic anemia causes

A

Anemia of chronic disease
Acute blood loss
Hemolytic anemia
Renal failure
Liver disease
Hypothyroidism
Sickle cell anemia
Hypersplenism

415
Q

Normocytic hypochromic anemia causes

A

Lead poisoning (plumbism)
Chronic systemic diseases

416
Q

Normocytic hyperchromic anemia causes

A

Hereditary spherocytosis

417
Q

Marcocytic normochromic anemia causes

A

Folic acid deficiency
Vitamin B 12 deficiency
Alcoholism
Chromic liver disease
Hypothyroidism
Aplastic anemia
Myelodysplastic syndromes
Drug induced (chemo)

418
Q

Macrocytic hypochromic anemia causes

A

Some Macrocytic anemias with superimposed iron deficiency

419
Q

Disorders of Red Cell production anemias causes

A

Inadequate/inaccessible iron
Lack of folic acid
Lack of vitamin B12
Lack of globulin
Bone marrow disease (leukemia)
Deficiency of erythropoietin (as in renal failure)

420
Q

Causes of aplastic anemia

A

Idiopathic
Radiation
Chemo

421
Q

Aplastic anemia

A

Disease where the body stops producing enough new blood cells

422
Q

Lab results of aplastic anemia

A

Normocytic
Normochromic
Decreased Reticulocyte count

423
Q

S/S of aplastic anemia

A

Hypoxemia
Decrease in bone marrow function (myelosuppression)
Infection
Bleeding

424
Q

Tx for aplastic anemia

A

Stop drugs
Transfusions
Bone marrow transplant

425
Q

Causes of iron deficiency

A

Decreased intake or absorption
Chronic blood loss

426
Q

S/S of iron deficiency

A

Hypoxemia

427
Q

Lab results of iron deficiency

A

Microcytic
Hypochromic
Increase total iron binding capacity
Decreased ferritin

428
Q

Tx of iron deficiency

A

Iron- dietary, supplements, parenteral iron (IV)

429
Q

Iron deficiency anemia

A

Microcytic (decreased MCV)
Hypochromic (decreased MCHC)
Decreased production of Hgb due to decreased availability of iron

430
Q

Most common cause of anemia (all ages)

A

Iron deficiency

431
Q

Menorrhagia

A

Heavy menstrual bleeding, often with clots for 7-10 days
One of the most common causes of iron deficiency anemia

432
Q

Occult GI loss

A

Up to 50-75 mL of blood per day
Even a well-balanced diet and increased Fe uptake by transferrin cannot offset losses
One of the most common causes of iron deficiency anemia

433
Q

Normal serum iron results

A

Male: 75-275
Females: 65-165
Newborn: 100-250
Child: 50-129

434
Q

Where iron in the body is stored

A

70% in Hgb of RBCs
30% in form of ferritin and hemosiderin

435
Q

Serum iron tests

A

Test usually measures iron bound to transferrin
Provides indirect measure of rate of dilevery to tissues
Of little diagnostic value by itself

436
Q

Serum iron tests affected by

A

Hemolysis, time of day, transfusion, menstruation, supplementation

437
Q

Iron-phosphorous-protein complex

A

Contains about 23% iron
Formed in intestinal mucosa by union of ferric iron with the protein apoferritin

438
Q

Serum ferritin test

A

Amount of ferritin is directly related to total body iron stores
Good marker for iron deficiency anemia

439
Q

Contradictions of serum ferritin test

A

Increased tissue damage causes false elevation
Administration of iron supplements ^ levels 2-3 for oral and within 24 hrs for parenteral
Not affected by blood transfusion

440
Q

Transferrin concentration test

A

Transferrin is globulin in the blood that binds and transports iron 1/3 bound with iron 2/3 reserve
Can be measured directly or estimated from the total iron binding capacity (TIBC)

441
Q

Total iron binding capacity (TIBC)

A

Maximum iron-binding capacity of transferrin and other iron binding globulins
- some labs do not perform - more of an indication of liver function and nutrition

442
Q

Transferrin and iron stores

A

Inversely relates b/c stores are there and don’t need to move as much

443
Q

Things that affect transferrin

A

Inflammation, loss of protein, nutritional status, liver disease

444
Q

Transferrin saturation test

A

The % of transferrin and other mobile iron-binding proteins that are saturated with iron
The ration of serum iron to iron binding capacity
Transferrin sat (%) = [(serum iron level)/(TIBC)]

445
Q

Normal transferrin saturation

A

20-50%
Iron deficiency associated with low sat (<15%)

446
Q

Dietary iron

A

10-20 mg Fe in average diet
Only 1-2 mg of Fe absorbed from intestines

447
Q

Menstruating females and dietary iron

A

Lose 30 mg with each period

448
Q

Pregnancy and children birth and dietary iron

A

Loss of 650 mg to fetus and intrapartal bleeding

449
Q

Storage of dietary iron

A

500-1500 mg stored as ferritin and hemosiderin in reticuloendothelial cells of macrophage system (liver, spleen and bone marrow) and muscle as myoglobin

450
Q

Manifestations of iron deficiency anemia

A

Same as those for all anemias
- brittle, spoon shaped nails
Glossitis
Web in upper esophagus
Pica

451
Q

Glossitis

A

Smooth, red sore tongue

452
Q

Pica

A

Habitual eating of non-nutritive substances (clay, laundry starch, ice, paint)

453
Q

Tx of iron deficiency anemia

A

Correct underlying causes
Ferrous sulfate given with meals
- give liquid form w/ straw bc stains teeth
- IM must use Z-track tech in deep tissue
Reticulocytosis in 4-5 days
Therapy
Transfusion

454
Q

Megaloblastic anemia

A

Impaired synthesis of DNA in RBC precursors in bone marrow
Macrocytic, ^ MCV and fewer in number

455
Q

Causes of megaloblastic anemias

A

Most often due to Vitamin B12 or folic acid deficiency

456
Q

Vitamin B12

A

Must be supplied in food: meat, eggs, milk, cheese
Absorbed in terminal ileum
Absorbed only when in complex with intrinsic factor
Largely stored in liver

457
Q

Intrinsic factor

A

A mucoprotein secreted by parietal cells of gastric mucosa
Help absorb Vitamin B12 by binding with ingested cobalamine (VB12) and then adhering to receptor site in the distal ileum where it is absorbed into the blood and transported to the lover for storage or bone marrow for erythropoiesis

458
Q

How vitamin B12 cause anemia

A

Dietary inadequacy
Intrinsic factor problem (does not produce for years)
Decreased Absorption from defect in ileum
Consumption by parasites or unusual bacteria

459
Q

Serum vitamin B12 and folate test

A

Vitamin B12: 100-700 pg/ml
Folic acid: 2-20 neg/ml

460
Q

Interfering factors of serum vitamin B12 and folate test

A

VB12: ^ in pregnancy, oral contraception, high does Vitamin A or C, smoking
Folic acid: folic acid antagonists, hemolysis, transfusion

461
Q

Pernicious anemia causes

A

Inadequate production of IF (intrinsic factor)
Interference with bonding of IF-cobalamine (type 1 blocking antibody)
Interference with bonding of IF and cobalamine complex at the ideal receptor sites (type 2 binding antibody)
Test with intrinsic factor antibody test

462
Q

Causes of vitamin B12 deficiency

A

Decreased intake, intrinsic factor or ETOH use

463
Q

Vitamin B12 lab results

A

Macrocytic
Normochromic
Decreased B12

464
Q

S/S of VB12 deficiency

A

Hypoxemia
Neurological symptoms
Premature grey hairs
Vitiligo
Low BP
Lemon-yellow skin
Fever
Splenomegaly
Yellow-blue color blind

465
Q

Neurologic VB12 deficiency S/S

A

Early:
Inability to preform fine motor skills
Loss of vibratory sense and 2 point discrimination
Progressive:
Paresthesias (hallmark of VB12 def) numbness and tingling
Weakness
Uncoordination
Ataxia
Personality changes
Late:
Urinary/fecal incontinence
Spastic paralysis
Confusion
Psychosis

466
Q

Tx of VB12 deficiency

A

^ VB12 in diet
Parenteral VB12

467
Q

Other causes of VB12 deficiency

A

Pernicious Anemia
Total gastrectomy (removes source of intrinsic factor)
Vegetarian diet
Chronic alcoholism
Spruce and celiac disease
Resection of ileum

468
Q

Causes of folic acid deficiency

A

Decreased intake
Increase ETOH use
Increased demand
Drugs

469
Q

Lab results folic acid deficiency

A

Macrocytic
Normochromic
Decreased serum folate

470
Q

S/S folic acid deficiency

A

Hypoxemia

471
Q

Tx of folic acid deficiency

A

^ intake
Supplements

472
Q

Causes of acute anemia d/t blood loss

A

Trauma
Surgery

473
Q

Lab results of acute anemia d/t blood loss

A

Normocytic
Normochromic
^ Reticulocyte count

474
Q

S/S of acute anemia d/t blood loss

A

Volume depletion
Decreased BP
^ HR
Shock

475
Q

Tx of acute anemia d/t blood loss

A

Hemostasis
Oxygen
Transfusion

476
Q

Causes of chronic anemia d/t blood loss

A

GI bleed (ulcer)
Menstruation

477
Q

Lab results of chronic anemia d/t blood loss

A

Microcytic
Hypochromic
^ Reticulocyte count

478
Q

S/S of chronic anemia d/t blood loss

A

Hypoxemia

479
Q

Tx of chronic anemia d/t blood loss

A

Treat cause
Iron therapy

480
Q

Anemia of chronic disease (anemia of inflammation)

A

Very common
Seen with malignancy, chronic infection or inflammation

481
Q

Anemia of chronic disease lab results

A

Typically Normocytic and normochromic
Or slightly hypochromic

482
Q

Results of anemia of chronic disease

A

RBC survival softened but no compensatory ^ in production
R/T hyperactive immune system resulting in ^ destruction w/out ^ production

483
Q

Polycythemia

A

Defined as an abnormally high total red cell mass
Hct> 50% taken up by RBC
Often accompanies rise in WBC and PLT

484
Q

Relative polycythemia

A

Hct rises with loss of plasma volume

485
Q

Absolute polycythemia

A

Primary = polycythemia Vera - common in men between 40-60, proliferative disorder
Secondary = arises from an ^ in erythropoietin, usually as compensation rom chromic hypoxia

486
Q

Complication of polycythemia

A

^ blood volume and viscosity
Viscosity can interfere with cardiac blood flow
Hypertension
Venousstasis
Thromboembolism

487
Q

Treatments for polycythemia

A

Primary: focus is to reduce blood viscosity, often with periodic phlebotomy, drug therapy or bone marrow transplant
Secondary to hypoxia: correct that proble with O2

Patho (6 decks)

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