Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > Week 2 (ch. 4-7) > Flashcards

Week 2 (ch. 4-7) Flashcards

1
Q

Etiology of pain

A 
Infection
Ischemia 
Tissue necrosis
Stretching inflammation
Chemicals
Burns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Somatic pain

A

Conducted by sensory nerves

- skin, bone, muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Visceral pain

A

Sympathetic nerve fibers

- organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Nociceptors

A

Pain receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What kind of nerve endings do nociceptors have

A

Sensory nerve endings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are nociceptors stimulated by?

A

Thermal, chemical, or mechanical/physical stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where are nociceptors located?

A

Present in most tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pain threshold

A

Level of stimulation needed to activate pain receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the pathway in which nociceptors allow you to feel pain

A

Nociceptors, spinal chord, pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Dermatome

A

Spinal nerve impulse from certain area of the skin

— used to test areas of sensory loss or pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does dermatome help us figure out?

A

Helps us determine the site of spinal cord injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pain response involved what?

A

Involves responses such as stress response, emotional response, physical response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gate control theory

A

Built into pathways
- modify entry of pain to spinal chord and brain
- can be open or closed
—> open allows pain to continue on path
—> closed reduces or modifies the path of pain impulses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Gate control theory: what causes closed gates to occur

A

Closed gates occur do to other sensory stimuli that diminish the pain sensation
Ex. Ice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the analgesia system

A

Release of opiate-like chemicals (endorphins, serotonin)

  • block pain impulse
  • secreted by inter neurons in the CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Signs / symptoms of pain

A

Elevated BP
Tachycardia (increased heart beat)
Restless / lack of movement
Guarding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Referred pain

A

Pain felt in an area away from the source of the pain due to sensory fibers from different sources connecting at a single level of the spinal cord
- ex. Left neck / arm pain source is ischemia in the heart (heart attack)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Phantom pain

A

Perceived pain in lost limb

  • doesn’t respond to typical pain therapy
  • resolves in weeks to months
  • not fully understood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Perception of pain

A

Depends on many factors different from person to person

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Acute pain

A 
Sudden, sharp
Localized or generalized
Thermal and physical
Tissue damage - skin and mucosa membranes
Short term
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What fibers are responsible for acute pain?

A

A delta fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Chronic pain

A 
Dull, aching, burning 
Generalized
Thermal, physical, chemical
Muscle, tendons, myocardium, digestive, skin 
Long term, debilitating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What fibers are responsible for chronic pain

A

C fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Central pain

A

Due to damage of brain or spinal cord
- localized or large area
- persistent
Ex. Tumor on spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Neuropathic pain

A

Due to damage or disease of peripheral nerves
- tingling, burning, or shooting
Ex. Trigeminal neuralgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Ischemic pain

A

Due to sudden loss of blood flow to tissue or organ

- aching, burning, prickling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Cancer-related pain

A

Advance of tumor growth

  • increased pressure on nerve endings, stretching of tissues, obstruction of vessels, ducts or intestines
  • acute or chronic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Pain management: medications

A

Analgesics
Tylenol
NSAIDS
Narcotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Pain management: non-pharmacological approach

A

Stress reduction, relaxation therapy, distraction, acupuncture, hypnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Pain management: anesthesia locations

A

Local, spinal (regional), general

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the lines of defense?

A 
First line - mechanical barrier (nonspecific) 
Second line - phagocytosis and inflammation (nonspecific)
Third line (specific)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

First line of defense - mechanical barrier (nonspecific)

A

Skin, tears, saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Second line of defense - phagocytosis and inflammation (nonspecific)

A

Neutrophils and macrophages destroy foreign matter, bacteria, cell debris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How do we interpret a complete blood count (CBC) test

A

We look at the second line of defense (neutrophils and macrophages). If these counts are high, there is an immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Third line of defense (non-specific)

A

Production of antibodies or sensitized lymphocytes after exposure to specific substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What would be an example of 3rd line of defense

A

An example of this would be having the chickenpox as a child and then saying you can’t get them again. It is due to the antibodies produced during the first exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

In what line of defense does inflammation occur?

A

Second life of defense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the purpose of inflammation?

A

Localize and remove injurious agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the causes of inflammation?

A

Tissue injury (foreign body, sprain, ischemia, etc.) allergy, infection, burn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How is inflammation not the same as infection

A

Infection is a cause of inflammation, just as a burn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What does inflammation display as?

A

Redness, swelling, warmth, pain, possible loss of function to the area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What does -itis stand for

A

Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Steps of inflammation

A
  1. Release of bradykinins from injured cells
  2. Activation of pain receptors by bradykinins
  3. Mast cells and basophils release histamine
  4. Capillary dilation (bradykinin and histamine)
  5. Increased blood flow and capillary permeability
  6. Bacteria may enter the tissue
  7. Neutrophils and monocytes come to the injury
  8. Neutrophils phagocytize the bacteria
  9. Macrophages leave bloodstream for phagocytosis of microbes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Cytokines (acute inflammation)

A

Communicators in the tissue fluid send messages to lymphocytes macrophages, immune system and hypothalamus (induced fever)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe the process of acute inflammation

A
  1. Damage occurs —> Mast cells and platelets release Chemical mediators into the interstitial fluid and blood —> Affects vessels and nerves in affected area
  2. Cytokines: Communicators in tissue fluid send a messages to lymphocytes, macrophages, immune system, and hypothalamus (fever)
  3. Anti-inflammatory and anti-histamines (most of them) reduce the effects of these chemical mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What does the release of chemical mediators do?

A

A. Vasodilation (increase in diameter of arterioles) —> hyperemia (increase blood flow to an area)

B. Increased capillary permeability = plasma proteins and fluid move to interstitial space

C. Globulins serve as antibodies

D. Fibrinogen makes fibrin mesh around the affected area to localize the agent

E. Blood clotting also makes fibrin mesh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Chemical mediators attract what?

A

Leukocytes (neutrophils monocytes macrophages) into the interstitial space
— these destroy and remove by phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Chemical mediators: what happens once phagocytic cells die?

A

Lysosomal enzymes get released, which damage nearby sells thus prolonging inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Chemical mediators: what happens due to excessive fluid and proteins collected in the interstitial space?

A

The swelling results in increased pressure on the capillary, resulting in decreased blood flow. This decreases the removal of waste

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Why is it important to inactivate chemical mediators?

A

To prevent unnecessary prolonging of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Local effects of inflammation

A

Redness (erythema), heat, swelling (edema), pain
Loss of function
Exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Systemic effects of inflammation

A

Fever, malaise, fatigue, headaches, anorexia

— Fever is mild and less inflammation caused by infection, then the fever will be more severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Why can a high-grade fever be beneficial

A

It can impair growth and reproduction of organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Serous exudate

A

Watery, consist primarily of fluid, some proteins, and white blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Fibrinous exudate

A

Thick, sticky, high cell and fiber content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Purple to exudate

A

Thick, yellow-green, contains more leukocytes, cell debris, and microorganisms
Ex. Assess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Abscess

A

A localized pocket of purulent exudate in solid tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Hemorrhagic exudate

A

Present when blood vessels are damaged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the course of a fever?

A
  1. Release of pyrogens in circulation
  2. Reset hypothalamus control —> high
  3. Body response that increases body temp. (Voluntary and involuntary)
  4. The rest of this has to be in book I can’t see it on PowerPoint (learning activity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Leukocytes is

A

Increase WBC in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the diagnostics used for inflammation?

A
  1. Leukocytosis
  2. Elevated serum C-reactive protein (CRP)
  3. Elevated erythrocytes sedimentation rate (ESR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What happens in leukocytosis

A
  1. Often see increase in immature neutrophils referred to as “shift to the left”
  2. Differential count (proportion of each type of WBC)
    — helps distinguish between bacterial or viral agent/infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Potential complications of acute inflammation: infection

A

A. Micro organisms can more easily penetrate edematous tissues
B. Some microbes resist phagocytosis
C. The inflammatory exudate also provides an excellent medium for micro organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Complications of acute inflammation: muscle spasm

A

My be initiated by inflammation

Protective response to pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What causes chronic inflammation

A

If the cause to acute inflammation was not eradicated, or chronic irritation (smoking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Describe characteristic of chronic inflammation

A

— Less swelling and exudate than seeing in acute inflammation
—More lymphocytes, macrophages, fibroblasts
—More tissue destruction and scar tissue
— formation of granuloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Granuloma

A

Mass of cells with necrotic center covered with connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Treatment of inflammation: medications

A

Acetylsalicylic acid (asprin)
Acetaminophen (Tylenol)
NSAID (ibuprofen)
Steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Acetylsalicylic acid (asprin)

A

Analgesic effect and antipyretic affect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Acetaminophen (Tylenol)

A

Analgesic effect and antipyretic affect, but does not affect inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

NSAID (Ibuprofen)

A

Anti inflammatory and analgesic and antipyretic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Steroids (to treat inflammation)

A

End in -one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Treat of inflammation: no medication

A

RICE (rest, ice, compression, elevation)

Cold (in acute to vasoconstrict) - reduce edema and pain

Heat - recovery/chronic,To improve circulation allowing for removal of waist and extra fluid (promotes healing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Healing: resolution

A

Damaged cells recover

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Healing: regeneration

A

Damaged cells replaced (occurs in liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Healing: replacement

A

CT replaces the damaged cells (scar)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Healing process in injurry

A

Blood clot forms (seals area) - inflammation surrounds area-phagocytosis occurs - granulation tissues grows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What factors promote healing?

A 
Youth
Good nutrition
Good circulation
Clean area
No infection or further trauma to area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What factors delay healing

A 
Age
Poor nutrition
Poor circulation
Anemia 
Certain chronic disease
Infection
Prolonged use of glucocorticoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Scar complication: loss of function

A

Due to loss of normal cells, don’t have typical function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Scar complications: contractors and obstructions

A

No elastic and shrinks over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Scar complication: hypertrophic

A

Overgrowth, keloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Scar complication: ulceration

A

Blood supply impaired around scar tissue resulting in tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How many cells do bacteria have?

A

1 - unicellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How does bacteria replicate?

A

Binary fission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What factors influence growth/duplication of bacteria?

A

Lack of nutrients / o2
Increase metabolic waste
Changes in pH
Changes in temp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Bacteria: bacilli

A

Rod shape organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Bacteria: spirochete

A

Include spiral forms and vibrio app.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Bacteria: cocci

A

Spherical forms

  • diplocicci
  • streptococci
  • staphylococci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Bacteria: structure

A

Rigid cell wall - protects the bacteria, gives shape

— gram positive and negative vary in thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Bacteria cell membrane

A

Controls movement of material in and out of cell

  • GP = cell membrane located inside cell wall
  • GN = cell membrane location on both sides of cell wall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Bacteria capsule

A

Not all bacteria have it, offers additional protection

  • GP - it is located outside the cell wall
  • GN - its located outside outer membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Bacteria flagella and fimbriae

A

Aide in movement or attachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Pili

A

Form of fimbriae that transfer genetic material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Bacteria cytoplasm

A

Contains chromosome, ribosome, RNA and plasmids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are plasmids

A

Usually contain genetic information converting drug resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Bacteria structure secrete what?

A

Toxins and enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Bacteria: exotoxins

A

Gram positive

- secreted, often interferes with nerve conduction

99
Q

Bacteria: endotoxins

A

Gram negative

  • present in cell wall
  • released after death of bacterium
  • cause fever, weakness, and effect circulation leading to septic shock
100
Q

Bacteria: enzymes

A

Damage tissue and promote the spread of infection

101
Q

Bacteria: endospores

A

Latent form of bacteria

  • survive long periods of time
  • resistant to heat and other adverse conditions (disinfectants)
102
Q

Viruses

A

Small, obligate intracellular parasites - require a living host

103
Q

Virus: protein coat

A

Come in many shape and sizes, can change quickly (mutate)

104
Q

Virus: nucleic acid

A

DNA or RNA

  • method of classification
  • RNA —> some viruses contain reverse transcriptase enzyme to convert RNA to DNA…occurs when it enters host cell
105
Q

Virus: infection process?

A
  1. Attach to host cell
  2. Genetic material enters cell
  3. Viral RNA/DNA take control of the host cell
  4. New viruses are assembled
  5. New viruses released by lysis of host cell or by budding from host cell
  6. New viruses then infect nearby cell and repeat process
106
Q

Virus: latent

A

Virus enters cell
Replicate either slowly or not from some time later
May enter coat/capsid into cell membrane of host cell
—> this alows the cell to recognize viral invader and attach by immune system

107
Q

Why can viruses cause difficulty in us developing immunity

A

The mutate (change slightly in reproduction)

108
Q

Where can viruses hide on us

A

In our cells

109
Q

Why do viruses reply so much on our cells to survive?

A

Lack own metabolic process or structure

110
Q

What happens if viruses alter host chromosomes

A

Lead to development of malignant cells / cancer

111
Q

Chlamydia

A

Common STI may result in infertility and PID

Birth with Chlamydia infants may have eye infections / pneumonia

112
Q

Rickettsiae

A

Gram-negative, transmitted by insect vectors (tick/lice), attack vessel walls causing rash and small hemorrhages
- ex. Rocky Mountain fever

113
Q

Mycoplasmas

A

Lack cell wall, makes antimicrobials not affective in treatment
- common cause of pneumonia

114
Q

Fungi are ____

A

Eukaryotic

115
Q

Protozoa are ______

A

Eukaryotic

116
Q

Explain structure of Protozoa

A

Unicellular
Lack cell wall
Many live independently, others are obligate parasites

117
Q

Pathogens are usually _____

A

Parasites

118
Q

What are some examples of Protozoa diseases

A

Trichomoniasis
Malaria
Amebic dysentery

119
Q

Helminths

A

Vary in size
Three stages of life (ovum, larva, adult)
Enter body through skin or ingestion

120
Q

Example of helminths

A

Pinworm, tapeworm

121
Q

Prions

A

Not fully understood; protein-like agent

Transmitted by ingestion of infected tissues

122
Q

Example of prions

A

Creutzfeldt-Jakob disease — progress rapidly and fatal

123
Q

Algae

A

Fresh and marine waters

Main component of plankton, typically not of concern to humans

124
Q

What are the places in the body that do not have resident flora (sterile)

A

Lungs, brain, blood, bladder, kidney

125
Q

Opportunistic infection

A

If our normal flora gets to a part of the body where it isn’t suppose to be, it can cause disease

126
Q

Infection occurs when a microbe/parasite ______

A

Has the opportunity to reproduce on/in the bodies tissues

127
Q

Endemic

A

Specific infections occur within a population

128
Q

Epidemic

A

Infection occurs outside normal area / region or occur in higher than expected rates

129
Q

Reservoir

A

Source of infection

— person with known infection, person with asymptomatic, animal, contaminated water, soil, food or equipment

130
Q

Carrier

A

Transmits the organism but never acquires the infection

131
Q

Mode of transmission: direct contact

A

Direct touching

— intercourse, kissing

132
Q

Mode of transmission: indirect contact

A

Carried on an intermediary

— food or fomite (bed linen, instruments)

133
Q

Mode of transmission: droplet

A

Oral or respiratory (sneezing)

134
Q

Mode of transmission: aerosol

A

Respiratory tract that remain suspended in air

135
Q

Mode of transmission: vector

A

Insect or animal carry (malaria)

136
Q

Nosocomial infections

A

Infections that happen in healthcare facilities

- 10-15% of pt. Acquire

137
Q

Reason for nosocomial infections

A

Many contagious disease present, overcrowding, contaminated instruments, immunocompromised/ weak pt., transmission from staff, food trays, many microbes in building including many that are drug resistant

138
Q

What are the most frequent nosocomial infections?

A

Pneumonia, post surgical, c. Diff, MRSA

139
Q

Host Resistance: interferons-proteins

A

Produced by host cells in response to virus invasion of cell

Influenced by activity of nearby cells - increase those host cells resistance to that virus causing a disruption in the viral replication

Stimulate the immune response

140
Q

What factors decrease the hosts resistance?

A

Age, immunodeficiency, malnutrition, chronic disease, genetic susceptibility, stress, inflammation/trauma that effects integrity of the skin, impaired inflammatory response (long term glucocorticoid use)

141
Q

Virulence

A

Degree of pathogenicity (disease causing) of a microbe

142
Q

How is virulence commonly expressed

A

Case fatality rate

- percentage of fatalities that occur within the number of those who delevoped disease from microbe

143
Q

Newly emerging disease

A
  • different strains of common infections such as influenza

- spread beyond normal endemic areas

144
Q

Superbugs

A

Multi drug resistant forms of existing diseases

  • TB
  • s. Aureus
145
Q

Infection control requires 2 approaches which are:

A

Standard precautions used in all settings with all clients when body fluids may be exchanged. Gloves, hand washing

Specific precautions in clients diagnosed with a particular infection. These are used in addition to standard precautions (droplet)

146
Q

Incubation period

A

The time between entry of organism to appearance of signs and symptoms. This varies considerably with different organisms

147
Q

Prodromal period

A

Early symptoms stage, non-specific symptoms
—Fatigue, loss of appetite, headache
— evident varies with dif. Organism

148
Q

Acute period

A

Infectious disease develops fully

  • s/s at peak
  • Length of period Depends on violence of pathogen and host resistance
149
Q

Recovery phase

A

S/s subside, body processes return to normal

150
Q

What is the physiology of infection

A

Incubation period, prodromal period, acute period, recovery phase

151
Q

Local infection

A

Confined to certain area

152
Q

Focal infection

A

Spread from local to other tissues

153
Q

Systemic infections

A

Spread to several sites and tissue fluids, typically circulatory

154
Q

Mixed infections

A

Multiple agents present at same time

155
Q

Primary infections

A

First time exposed

156
Q

Secondary infections

A

Occur after primary typically by opportunistic

Ex. Thrush after antibiotic use

157
Q

Sub clinical infections

A

Do not cause s/s; may persis long periods

158
Q

Signs and symptoms of local infections

A

Pain/tender, swelling, redness, warmth, swollen lymph nodes, exudate

159
Q

Lymphadenopathy

A

Swollen lymph nodes

160
Q

What kind of exudate does bacteria vs virus have

A 
Bacteria = pus / purulent 
Virus = serous (clear)
161
Q

S/s of systemic infection

A

Fever, fatigue, weakness, headache, nausea

severe infections include confusion, seizures, loss of consciousness

162
Q

How do you diagnose infection

A

Culture and staining techniques

  • drug sensitivity tests
  • can take 48 hours or great
163
Q

Diagnosis of infection: immunological testing of body fluids

A

Antigen ID

Antibody tiger

164
Q

Diagnosis of infections: blood test

A

Variations in numbers of leukocytes

  • differential count
  • C-reactive protein
  • erythrocyte sedimentation rate (ESR) - elevated
165
Q

Leukocytosis

A

Bacterial infection

166
Q

Leukopenia

A

Viral infection

167
Q

Differential count

A

Changes in distribution of leukocytes

168
Q

Treatment of infection

A

Bodies defense usually does the job

Antimicrobial usage

169
Q

Why is antimicrobial usage limited

A

To reduce development of drug resistance

  • need to be taken appropriately
  • taken Prophylactically in high-risk patients prior to invasive procedures
170
Q

Antibiotic

A

Drugs derived from organisms

Can also be made synthetically

171
Q

Antimicrobial

A

Anti…bacterial, viral, fungal

172
Q

Bacteriostatic

A

Drugs that inhibit the reproduction of bacterial

173
Q

Bactericides

A

Drugs that kill bacteria

174
Q

Broad spectrum

A

Effect against both gram+ and gram- organisms

175
Q

Narrow spectrum

A

Effective against EITHER gram+ or gram- (one or the other)

176
Q

First generation drug

A

Original drug class

177
Q

Second generation drug

A

Later version, which may be more effective, more tolerable, or more easily administered

178
Q

What are the 5 way in which antibiotics can work

A

Interfere with bacterial cell wall synthesis
Increase permeability of bacterial cell membrane
Interfere with protein synthesis
Interfere with synthesis of essential metabolites
Inhibit synthesis of nucleic acids

179
Q

Antiviral modes of action

A

Drugs may act by…
A. Blocking entry into host cell
B. Inhibiting gene expression
C. Inhibiting assembly of the virus

180
Q

Antifungal mode of action

A

A. Can interfere with mitosis in fingers
B. Can increase fungal membrane permeability
C. Most antifungal agents administered topically to skin or mucous membrane

181
Q

Why might antifungal meds be toxic to human or animal cells

A

Because fungal are eukaryotic cells and antifungal agents are therefore often toxic to animal or human cells
— treatment requires strict medical supervision

182
Q

Antiprotozoal mode of action

A

Similar characteristics to antifungal agents (could damage human cells because Protozoa are eukaryotic)

Many Pathogenic protozoa have several stages in their life cycle. Require treatment with different agents at different stages of the cycles

183
Q

Defense mechanisms: specific

A

System response to specific substance, cell, toxin or Protein sign as foreign
Recognizes foreign and potential threat and removes it

184
Q

Bodies defense mechanism: nonspecific

A

Inflammation, phagocytosis

185
Q

What are the lymphoid structures

A

Lymph nodes, spleen, tonsils, lymphatic circulation, intestinal lymphoid tissue

Basic structures that all the immune system to function

186
Q

What are the immune cells

A

Lymphocytes, macrophages

— ID and removal of bad stuff

187
Q

What are the tissues involved in immune cell development

A

Bone marrow and thymus

— maturation of immune cells

188
Q

Where do immune cells originate

A

Bone marrow

189
Q

What does thymus do

A

Famous programs immune system to ignore self-antigens during fetal development
—If this doesn’t occur it can cause an auto immune disorder where the body doesn’t recognize self

190
Q

Antigens

A

Foreign substances or human cell surface molecules, unique to each individual

191
Q

Self antigens

A

Present on plasma membrane, immune system ignore self-cells

192
Q

Macrophages

A

Large phagcytic cells that interpret and engulf foreign substances

193
Q

Where are macrophages

A

Liver, lungs and lymph nodes

194
Q

What is the primary cells in immune system and what do they do

A

Lymphocytes

— WBC produced in bone marrow

195
Q

T lymphocytes (t-cells)

A

Cell-mediated immunity (recognize antigen - target cell - and destroy it, then reproduce to continue to battle the antigen)

196
Q

Where are t lymphocytes made and where do they go?

A

From stem cells in bone marrow

Differentiate into thymus

197
Q

Memory T cells

A

Remain for years ready to attack if invader returns

198
Q

B lymphocytes (b cells)

A

Produce antibodies / immunoglobulins

Humoral immunity

199
Q

Where do B lymphocytes reside

A

Mature in bone marrow then move to spleen and lymphoid tissue

200
Q

Antibodies / immunoglobulins

A 
Specific proteins 
Present in body fluids
Bind to specific matching antigen and destroy it 
Key in immunity to specific diseases
Can be administered to treat disease
201
Q

IgG

A

Most common in blood

202
Q

IgM

A

First to increase in immune response

203
Q

IgA

A

In secretions

- tears, mucous membranes, colostrum

204
Q

IgE

A

Allergic reactions

  • causes release of histamine and other chemicals
  • release in inflammation
205
Q

IgD

A

Attached to B cells

Activates B cells

206
Q

Complement system

A

Activated during immune reactions with IgG or IgM
Group of inactive proteins circulating in blood
C1-C9
Causes cell damage and further inflammation when activated

207
Q

Chemical medications are involved in what / functions

A

Involved in inflammation and immune reaction

Signaling, causing cellular damage

208
Q

Immune system diagnostic tests: titer (titre)

A

Measures levels of serum immunoglobulins

209
Q

Immune system diagnostic tests: indirect Coombs’ test

A

Detects Rh blood compatibility

210
Q

Immune system diagnostic tests: MHC typing

A

Tissues matching before transplantation procedures

211
Q

Natural immunity

A

Species specific

212
Q

Innate immunity

A

Gene specific, seen by ethnicity

213
Q

Primary immune response

A

Exposure to antigen, takes 1-2 weeks, tested by serum antibodies in tigers

214
Q

Secondary immune response

A

Repeat exposure of same antigens, faster and higher antibody levels

215
Q

Active immunity

A

Own body (T and B cells)

216
Q

Active natural immunity

A

Acquired after exposure to antigen

Body makes antibodies for that antigen

217
Q

Active artificial immunity

A

Antigen purposefully introduced to body then antibodies are made
Can be dead or weakened antigen
Ex. Vaccines

218
Q

Passive immunity

A

Transferred from one to another

219
Q

Passive natural immunity

A

IgG mom to fetus from placenta

Breast milk

220
Q

Passive artificial immunity

A

Injection of antibodies from one person or animal to a different person
Ex. Snake antivenom, rabies antiserum

221
Q

Vaccines

A

Create herd immunity - decrease spreading of infection

222
Q

Emerging

A

Newly identified infectious disease

223
Q

Re-emerging

A

Disease previously controlled now developing cases again

224
Q

What are the two types of rejection

A

Host vs graft disease

Graft vs host disease

225
Q

Host vs graft disease

A

Recipients immune system attack the transplanted tissue, seen with kidney transplant

226
Q

Graft vs host disease

A

Graft/tissue T cells attack the host/recipient cells, scene with bone marrow transplants

227
Q

Hyperacute rejection

A

Immediately after transplant

228
Q

Acute rejection

A

Occurs after several weeks of transplant

229
Q

Chronic/late rejection

A

Months or years after transplant, see gradual degradation

230
Q

Tissue and organ transplant treatment (immunosuppressant): common drugs

A

Cyclosporine, azathioprine, prednisone
— concern for high risk or recipient developing functions due to decreased immune function
— includes opportunistic infections and cancer cells

231
Q

Type I hypersensitivity: allergic

A

Common - caused by allergen
- hay fever, food allergies
Can involve mucosa of nasal or digestive tract

232
Q

Causative agent of type 1 hypersensitivity

A

Exposed to allergen, develop IgE, mast cells

233
Q

Complications of type 1 hypersensitivity

A

Anaphylaxis

234
Q

Treatment of type 1 hypersensitivity

A

Medications (epinephrine, steroids, antihistamines)
O2
Stabilize BP

235
Q

Systemic response of type 1 hypersensitivity

A

Airway obstruction, decreased BP from release of histamine, hypoxia

236
Q

Type II hypersensitivity: cytotoxic

A

Antigen is present on cell membrane
— Maybe normal body component or exogenous

Circulating IgG react with antigen
— Distraction by phagocytosis or cytolytic enzymes

Example: response to incompatible blood transfusion

237
Q

Type III hypersensitivity: immune complex hypersensitivity

A

Antigen combines with antibody
— forms immune complexes, deposited in tissue
— activation of complement system

Process causes inflammation and tissue destruction

Ex. Glomerulonephritis, rheumatoid arthritis

238
Q

Type IV hypersensitivity: cell-mediated or delayed hypersensitivity

A

Delayed response by sensitized T lymphocytes

  • release of lymphokines
  • inflammatory response
  • destruction of antigen

Ex. Tuberculin test, contact dermatitis, allergic skin rash

239
Q

Primary immunodeficiency

A

Development failure in the system

240
Q

Secondary immunodeficiency

A

Acquires loss of immune response from specific cause

- Infection, splenectomy, liver disease, immunosuppressive drugs

241
Q

Effect of immundeficiency

A

Predisposes individual to develop opportunistic infections from normal flora, vulnerable to microbes

242
Q

Immunodeficiency treatments

A

Prophylactic antimicrobial’s, replacement therapy for antibodies

243
Q

What does HIV destroy

A

Helper T cells - CD4 lymphocytes

Pathophysiology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions