Week 2 (ch. 4-7) Flashcards
Etiology of pain
Infection Ischemia Tissue necrosis Stretching inflammation Chemicals Burns
Somatic pain
Conducted by sensory nerves
- skin, bone, muscle
Visceral pain
Sympathetic nerve fibers
- organs
Nociceptors
Pain receptors
What kind of nerve endings do nociceptors have
Sensory nerve endings
What are nociceptors stimulated by?
Thermal, chemical, or mechanical/physical stimuli
Where are nociceptors located?
Present in most tissues
Pain threshold
Level of stimulation needed to activate pain receptors
Describe the pathway in which nociceptors allow you to feel pain
Nociceptors, spinal chord, pain
Dermatome
Spinal nerve impulse from certain area of the skin
— used to test areas of sensory loss or pain
What does dermatome help us figure out?
Helps us determine the site of spinal cord injury
Pain response involved what?
Involves responses such as stress response, emotional response, physical response
Gate control theory
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
Gate control theory: what causes closed gates to occur
Closed gates occur do to other sensory stimuli that diminish the pain sensation
Ex. Ice
Describe the analgesia system
Release of opiate-like chemicals (endorphins, serotonin)
- block pain impulse
- secreted by inter neurons in the CNS
Signs / symptoms of pain
Elevated BP
Tachycardia (increased heart beat)
Restless / lack of movement
Guarding
Referred pain
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)
Phantom pain
Perceived pain in lost limb
- doesn’t respond to typical pain therapy
- resolves in weeks to months
- not fully understood
Perception of pain
Depends on many factors different from person to person
Acute pain
Sudden, sharp Localized or generalized Thermal and physical Tissue damage - skin and mucosa membranes Short term
What fibers are responsible for acute pain?
A delta fibers
Chronic pain
Dull, aching, burning Generalized Thermal, physical, chemical Muscle, tendons, myocardium, digestive, skin Long term, debilitating
What fibers are responsible for chronic pain
C fibers
Central pain
Due to damage of brain or spinal cord
- localized or large area
- persistent
Ex. Tumor on spinal cord
Neuropathic pain
Due to damage or disease of peripheral nerves
- tingling, burning, or shooting
Ex. Trigeminal neuralgia
Ischemic pain
Due to sudden loss of blood flow to tissue or organ
- aching, burning, prickling
Cancer-related pain
Advance of tumor growth
- increased pressure on nerve endings, stretching of tissues, obstruction of vessels, ducts or intestines
- acute or chronic
Pain management: medications
Analgesics
Tylenol
NSAIDS
Narcotics
Pain management: non-pharmacological approach
Stress reduction, relaxation therapy, distraction, acupuncture, hypnosis
Pain management: anesthesia locations
Local, spinal (regional), general
What are the lines of defense?
First line - mechanical barrier (nonspecific) Second line - phagocytosis and inflammation (nonspecific) Third line (specific)
First line of defense - mechanical barrier (nonspecific)
Skin, tears, saliva
Second line of defense - phagocytosis and inflammation (nonspecific)
Neutrophils and macrophages destroy foreign matter, bacteria, cell debris
How do we interpret a complete blood count (CBC) test
We look at the second line of defense (neutrophils and macrophages). If these counts are high, there is an immune response
Third line of defense (non-specific)
Production of antibodies or sensitized lymphocytes after exposure to specific substances
What would be an example of 3rd line of defense
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
In what line of defense does inflammation occur?
Second life of defense
What is the purpose of inflammation?
Localize and remove injurious agent
What are the causes of inflammation?
Tissue injury (foreign body, sprain, ischemia, etc.) allergy, infection, burn
How is inflammation not the same as infection
Infection is a cause of inflammation, just as a burn
What does inflammation display as?
Redness, swelling, warmth, pain, possible loss of function to the area
What does -itis stand for
Inflammation
Steps of inflammation
- Release of bradykinins from injured cells
- Activation of pain receptors by bradykinins
- Mast cells and basophils release histamine
- Capillary dilation (bradykinin and histamine)
- Increased blood flow and capillary permeability
- Bacteria may enter the tissue
- Neutrophils and monocytes come to the injury
- Neutrophils phagocytize the bacteria
- Macrophages leave bloodstream for phagocytosis of microbes
Cytokines (acute inflammation)
Communicators in the tissue fluid send messages to lymphocytes macrophages, immune system and hypothalamus (induced fever)
Describe the process of acute inflammation
- Damage occurs —> Mast cells and platelets release Chemical mediators into the interstitial fluid and blood —> Affects vessels and nerves in affected area
- Cytokines: Communicators in tissue fluid send a messages to lymphocytes, macrophages, immune system, and hypothalamus (fever)
- Anti-inflammatory and anti-histamines (most of them) reduce the effects of these chemical mediators
What does the release of chemical mediators do?
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
Chemical mediators attract what?
Leukocytes (neutrophils monocytes macrophages) into the interstitial space
— these destroy and remove by phagocytosis
Chemical mediators: what happens once phagocytic cells die?
Lysosomal enzymes get released, which damage nearby sells thus prolonging inflammation
Chemical mediators: what happens due to excessive fluid and proteins collected in the interstitial space?
The swelling results in increased pressure on the capillary, resulting in decreased blood flow. This decreases the removal of waste
Why is it important to inactivate chemical mediators?
To prevent unnecessary prolonging of inflammation
Local effects of inflammation
Redness (erythema), heat, swelling (edema), pain
Loss of function
Exudate
Systemic effects of inflammation
Fever, malaise, fatigue, headaches, anorexia
— Fever is mild and less inflammation caused by infection, then the fever will be more severe
Why can a high-grade fever be beneficial
It can impair growth and reproduction of organisms
Serous exudate
Watery, consist primarily of fluid, some proteins, and white blood cells
Fibrinous exudate
Thick, sticky, high cell and fiber content
Purple to exudate
Thick, yellow-green, contains more leukocytes, cell debris, and microorganisms
Ex. Assess
Abscess
A localized pocket of purulent exudate in solid tissue
Hemorrhagic exudate
Present when blood vessels are damaged
What is the course of a fever?
- Release of pyrogens in circulation
- Reset hypothalamus control —> high
- Body response that increases body temp. (Voluntary and involuntary)
- The rest of this has to be in book I can’t see it on PowerPoint (learning activity)
Leukocytes is
Increase WBC in blood
What are the diagnostics used for inflammation?
- Leukocytosis
- Elevated serum C-reactive protein (CRP)
- Elevated erythrocytes sedimentation rate (ESR)
What happens in leukocytosis
- Often see increase in immature neutrophils referred to as “shift to the left”
- Differential count (proportion of each type of WBC)
— helps distinguish between bacterial or viral agent/infection
Potential complications of acute inflammation: infection
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
Complications of acute inflammation: muscle spasm
My be initiated by inflammation
Protective response to pain
What causes chronic inflammation
If the cause to acute inflammation was not eradicated, or chronic irritation (smoking)
Describe characteristic of chronic inflammation
— Less swelling and exudate than seeing in acute inflammation
—More lymphocytes, macrophages, fibroblasts
—More tissue destruction and scar tissue
— formation of granuloma
Granuloma
Mass of cells with necrotic center covered with connective tissue
Treatment of inflammation: medications
Acetylsalicylic acid (asprin)
Acetaminophen (Tylenol)
NSAID (ibuprofen)
Steroids
Acetylsalicylic acid (asprin)
Analgesic effect and antipyretic affect
Acetaminophen (Tylenol)
Analgesic effect and antipyretic affect, but does not affect inflammatory response
NSAID (Ibuprofen)
Anti inflammatory and analgesic and antipyretic effect
Steroids (to treat inflammation)
End in -one
Treat of inflammation: no medication
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)
Healing: resolution
Damaged cells recover
Healing: regeneration
Damaged cells replaced (occurs in liver)
Healing: replacement
CT replaces the damaged cells (scar)
Healing process in injurry
Blood clot forms (seals area) - inflammation surrounds area-phagocytosis occurs - granulation tissues grows
What factors promote healing?
Youth Good nutrition Good circulation Clean area No infection or further trauma to area
What factors delay healing
Age Poor nutrition Poor circulation Anemia Certain chronic disease Infection Prolonged use of glucocorticoids
Scar complication: loss of function
Due to loss of normal cells, don’t have typical function
Scar complications: contractors and obstructions
No elastic and shrinks over time
Scar complication: hypertrophic
Overgrowth, keloid
Scar complication: ulceration
Blood supply impaired around scar tissue resulting in tissue damage
How many cells do bacteria have?
1 - unicellular
How does bacteria replicate?
Binary fission
What factors influence growth/duplication of bacteria?
Lack of nutrients / o2
Increase metabolic waste
Changes in pH
Changes in temp
Bacteria: bacilli
Rod shape organisms
Bacteria: spirochete
Include spiral forms and vibrio app.
Bacteria: cocci
Spherical forms
- diplocicci
- streptococci
- staphylococci
Bacteria: structure
Rigid cell wall - protects the bacteria, gives shape
— gram positive and negative vary in thickness
Bacteria cell membrane
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
Bacteria capsule
Not all bacteria have it, offers additional protection
- GP - it is located outside the cell wall
- GN - its located outside outer membrane
Bacteria flagella and fimbriae
Aide in movement or attachment
Pili
Form of fimbriae that transfer genetic material
Bacteria cytoplasm
Contains chromosome, ribosome, RNA and plasmids
What are plasmids
Usually contain genetic information converting drug resistance
Bacteria structure secrete what?
Toxins and enzymes
Bacteria: exotoxins
Gram positive
- secreted, often interferes with nerve conduction
Bacteria: endotoxins
Gram negative
- present in cell wall
- released after death of bacterium
- cause fever, weakness, and effect circulation leading to septic shock
Bacteria: enzymes
Damage tissue and promote the spread of infection
Bacteria: endospores
Latent form of bacteria
- survive long periods of time
- resistant to heat and other adverse conditions (disinfectants)
Viruses
Small, obligate intracellular parasites - require a living host
Virus: protein coat
Come in many shape and sizes, can change quickly (mutate)
Virus: nucleic acid
DNA or RNA
- method of classification
- RNA —> some viruses contain reverse transcriptase enzyme to convert RNA to DNA…occurs when it enters host cell
Virus: infection process?
- Attach to host cell
- Genetic material enters cell
- Viral RNA/DNA take control of the host cell
- New viruses are assembled
- New viruses released by lysis of host cell or by budding from host cell
- New viruses then infect nearby cell and repeat process
Virus: latent
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
Why can viruses cause difficulty in us developing immunity
The mutate (change slightly in reproduction)
Where can viruses hide on us
In our cells
Why do viruses reply so much on our cells to survive?
Lack own metabolic process or structure
What happens if viruses alter host chromosomes
Lead to development of malignant cells / cancer
Chlamydia
Common STI may result in infertility and PID
Birth with Chlamydia infants may have eye infections / pneumonia
Rickettsiae
Gram-negative, transmitted by insect vectors (tick/lice), attack vessel walls causing rash and small hemorrhages
- ex. Rocky Mountain fever
Mycoplasmas
Lack cell wall, makes antimicrobials not affective in treatment
- common cause of pneumonia
Fungi are ____
Eukaryotic
Protozoa are ______
Eukaryotic
Explain structure of Protozoa
Unicellular
Lack cell wall
Many live independently, others are obligate parasites
Pathogens are usually _____
Parasites
What are some examples of Protozoa diseases
Trichomoniasis
Malaria
Amebic dysentery
Helminths
Vary in size
Three stages of life (ovum, larva, adult)
Enter body through skin or ingestion
Example of helminths
Pinworm, tapeworm
Prions
Not fully understood; protein-like agent
Transmitted by ingestion of infected tissues
Example of prions
Creutzfeldt-Jakob disease — progress rapidly and fatal
Algae
Fresh and marine waters
Main component of plankton, typically not of concern to humans
What are the places in the body that do not have resident flora (sterile)
Lungs, brain, blood, bladder, kidney
Opportunistic infection
If our normal flora gets to a part of the body where it isn’t suppose to be, it can cause disease
Infection occurs when a microbe/parasite ______
Has the opportunity to reproduce on/in the bodies tissues
Endemic
Specific infections occur within a population
Epidemic
Infection occurs outside normal area / region or occur in higher than expected rates
Reservoir
Source of infection
— person with known infection, person with asymptomatic, animal, contaminated water, soil, food or equipment
Carrier
Transmits the organism but never acquires the infection
Mode of transmission: direct contact
Direct touching
— intercourse, kissing
Mode of transmission: indirect contact
Carried on an intermediary
— food or fomite (bed linen, instruments)
Mode of transmission: droplet
Oral or respiratory (sneezing)
Mode of transmission: aerosol
Respiratory tract that remain suspended in air
Mode of transmission: vector
Insect or animal carry (malaria)
Nosocomial infections
Infections that happen in healthcare facilities
- 10-15% of pt. Acquire
Reason for nosocomial infections
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
What are the most frequent nosocomial infections?
Pneumonia, post surgical, c. Diff, MRSA
Host Resistance: interferons-proteins
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
What factors decrease the hosts resistance?
Age, immunodeficiency, malnutrition, chronic disease, genetic susceptibility, stress, inflammation/trauma that effects integrity of the skin, impaired inflammatory response (long term glucocorticoid use)
Virulence
Degree of pathogenicity (disease causing) of a microbe
How is virulence commonly expressed
Case fatality rate
- percentage of fatalities that occur within the number of those who delevoped disease from microbe
Newly emerging disease
- different strains of common infections such as influenza
- spread beyond normal endemic areas
Superbugs
Multi drug resistant forms of existing diseases
- TB
- s. Aureus
Infection control requires 2 approaches which are:
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)
Incubation period
The time between entry of organism to appearance of signs and symptoms. This varies considerably with different organisms
Prodromal period
Early symptoms stage, non-specific symptoms
—Fatigue, loss of appetite, headache
— evident varies with dif. Organism
Acute period
Infectious disease develops fully
- s/s at peak
- Length of period Depends on violence of pathogen and host resistance
Recovery phase
S/s subside, body processes return to normal
What is the physiology of infection
Incubation period, prodromal period, acute period, recovery phase
Local infection
Confined to certain area
Focal infection
Spread from local to other tissues
Systemic infections
Spread to several sites and tissue fluids, typically circulatory
Mixed infections
Multiple agents present at same time
Primary infections
First time exposed
Secondary infections
Occur after primary typically by opportunistic
Ex. Thrush after antibiotic use
Sub clinical infections
Do not cause s/s; may persis long periods
Signs and symptoms of local infections
Pain/tender, swelling, redness, warmth, swollen lymph nodes, exudate
Lymphadenopathy
Swollen lymph nodes
What kind of exudate does bacteria vs virus have
Bacteria = pus / purulent Virus = serous (clear)
S/s of systemic infection
Fever, fatigue, weakness, headache, nausea
severe infections include confusion, seizures, loss of consciousness
How do you diagnose infection
Culture and staining techniques
- drug sensitivity tests
- can take 48 hours or great
Diagnosis of infection: immunological testing of body fluids
Antigen ID
Antibody tiger
Diagnosis of infections: blood test
Variations in numbers of leukocytes
- differential count
- C-reactive protein
- erythrocyte sedimentation rate (ESR) - elevated
Leukocytosis
Bacterial infection
Leukopenia
Viral infection
Differential count
Changes in distribution of leukocytes
Treatment of infection
Bodies defense usually does the job
Antimicrobial usage
Why is antimicrobial usage limited
To reduce development of drug resistance
- need to be taken appropriately
- taken Prophylactically in high-risk patients prior to invasive procedures
Antibiotic
Drugs derived from organisms
Can also be made synthetically
Antimicrobial
Anti…bacterial, viral, fungal
Bacteriostatic
Drugs that inhibit the reproduction of bacterial
Bactericides
Drugs that kill bacteria
Broad spectrum
Effect against both gram+ and gram- organisms
Narrow spectrum
Effective against EITHER gram+ or gram- (one or the other)
First generation drug
Original drug class
Second generation drug
Later version, which may be more effective, more tolerable, or more easily administered
What are the 5 way in which antibiotics can work
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
Antiviral modes of action
Drugs may act by…
A. Blocking entry into host cell
B. Inhibiting gene expression
C. Inhibiting assembly of the virus
Antifungal mode of action
A. Can interfere with mitosis in fingers
B. Can increase fungal membrane permeability
C. Most antifungal agents administered topically to skin or mucous membrane
Why might antifungal meds be toxic to human or animal cells
Because fungal are eukaryotic cells and antifungal agents are therefore often toxic to animal or human cells
— treatment requires strict medical supervision
Antiprotozoal mode of action
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
Defense mechanisms: specific
System response to specific substance, cell, toxin or Protein sign as foreign
Recognizes foreign and potential threat and removes it
Bodies defense mechanism: nonspecific
Inflammation, phagocytosis
What are the lymphoid structures
Lymph nodes, spleen, tonsils, lymphatic circulation, intestinal lymphoid tissue
Basic structures that all the immune system to function
What are the immune cells
Lymphocytes, macrophages
— ID and removal of bad stuff
What are the tissues involved in immune cell development
Bone marrow and thymus
— maturation of immune cells
Where do immune cells originate
Bone marrow
What does thymus do
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
Antigens
Foreign substances or human cell surface molecules, unique to each individual
Self antigens
Present on plasma membrane, immune system ignore self-cells
Macrophages
Large phagcytic cells that interpret and engulf foreign substances
Where are macrophages
Liver, lungs and lymph nodes
What is the primary cells in immune system and what do they do
Lymphocytes
— WBC produced in bone marrow
T lymphocytes (t-cells)
Cell-mediated immunity (recognize antigen - target cell - and destroy it, then reproduce to continue to battle the antigen)
Where are t lymphocytes made and where do they go?
From stem cells in bone marrow
Differentiate into thymus
Memory T cells
Remain for years ready to attack if invader returns
B lymphocytes (b cells)
Produce antibodies / immunoglobulins
Humoral immunity
Where do B lymphocytes reside
Mature in bone marrow then move to spleen and lymphoid tissue
Antibodies / immunoglobulins
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
IgG
Most common in blood
IgM
First to increase in immune response
IgA
In secretions
- tears, mucous membranes, colostrum
IgE
Allergic reactions
- causes release of histamine and other chemicals
- release in inflammation
IgD
Attached to B cells
Activates B cells
Complement system
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
Chemical medications are involved in what / functions
Involved in inflammation and immune reaction
Signaling, causing cellular damage
Immune system diagnostic tests: titer (titre)
Measures levels of serum immunoglobulins
Immune system diagnostic tests: indirect Coombs’ test
Detects Rh blood compatibility
Immune system diagnostic tests: MHC typing
Tissues matching before transplantation procedures
Natural immunity
Species specific
Innate immunity
Gene specific, seen by ethnicity
Primary immune response
Exposure to antigen, takes 1-2 weeks, tested by serum antibodies in tigers
Secondary immune response
Repeat exposure of same antigens, faster and higher antibody levels
Active immunity
Own body (T and B cells)
Active natural immunity
Acquired after exposure to antigen
Body makes antibodies for that antigen
Active artificial immunity
Antigen purposefully introduced to body then antibodies are made
Can be dead or weakened antigen
Ex. Vaccines
Passive immunity
Transferred from one to another
Passive natural immunity
IgG mom to fetus from placenta
Breast milk
Passive artificial immunity
Injection of antibodies from one person or animal to a different person
Ex. Snake antivenom, rabies antiserum
Vaccines
Create herd immunity - decrease spreading of infection
Emerging
Newly identified infectious disease
Re-emerging
Disease previously controlled now developing cases again
What are the two types of rejection
Host vs graft disease
Graft vs host disease
Host vs graft disease
Recipients immune system attack the transplanted tissue, seen with kidney transplant
Graft vs host disease
Graft/tissue T cells attack the host/recipient cells, scene with bone marrow transplants
Hyperacute rejection
Immediately after transplant
Acute rejection
Occurs after several weeks of transplant
Chronic/late rejection
Months or years after transplant, see gradual degradation
Tissue and organ transplant treatment (immunosuppressant): common drugs
Cyclosporine, azathioprine, prednisone
— concern for high risk or recipient developing functions due to decreased immune function
— includes opportunistic infections and cancer cells
Type I hypersensitivity: allergic
Common - caused by allergen
- hay fever, food allergies
Can involve mucosa of nasal or digestive tract
Causative agent of type 1 hypersensitivity
Exposed to allergen, develop IgE, mast cells
Complications of type 1 hypersensitivity
Anaphylaxis
Treatment of type 1 hypersensitivity
Medications (epinephrine, steroids, antihistamines)
O2
Stabilize BP
Systemic response of type 1 hypersensitivity
Airway obstruction, decreased BP from release of histamine, hypoxia
Type II hypersensitivity: cytotoxic
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
Type III hypersensitivity: immune complex hypersensitivity
Antigen combines with antibody
— forms immune complexes, deposited in tissue
— activation of complement system
Process causes inflammation and tissue destruction
Ex. Glomerulonephritis, rheumatoid arthritis
Type IV hypersensitivity: cell-mediated or delayed hypersensitivity
Delayed response by sensitized T lymphocytes
- release of lymphokines
- inflammatory response
- destruction of antigen
Ex. Tuberculin test, contact dermatitis, allergic skin rash
Primary immunodeficiency
Development failure in the system
Secondary immunodeficiency
Acquires loss of immune response from specific cause
- Infection, splenectomy, liver disease, immunosuppressive drugs
Effect of immundeficiency
Predisposes individual to develop opportunistic infections from normal flora, vulnerable to microbes
Immunodeficiency treatments
Prophylactic antimicrobial’s, replacement therapy for antibodies
What does HIV destroy
Helper T cells - CD4 lymphocytes
