1.3 Immunity, Inflammation, Infection Flashcards
transfer of antibodies from a mother to her infant and breast feeding.
natural acquired passive immunity
when a person is naturally exposed to antigens, becomes ill, and recovers. The body creates it’s own antibodies.
naturally acquired active immunity
Vaccinations, your body makes the antibodies after vaccinations.
artificially acquired active immunity
first type of antibody to respond to acute infection “first you got to get it from your mother!”
IgM
As we get over the infection and our bodies remember; they are much smaller.
IgG
Found in secretions and on mucous membranes, also in breastmilk!
IgA
Describe the manifestations of acute inflammation, including diagnostic testing
Rubor (redness) Tumor (swelling) Calor (heat) Dolar (pain) Functio laesa (loss of function) Malaise
____ is an autmatic response to cell injury that neutralizes harmful agents and removes dead tissue
inflammation
relatively short duration; non specific early response to injury. aimed primarily at removing the injurious agent and limiting tissue damage
acute inflammation
longer duration lasting for days to years.
chronic inflammation
2 types of inflammatory mediators
plasma derived (liver) Cell-derived (WBCs, Platelets, Endothelial cells)
3 concepts for plasma proteins
coagulation factors (clot formation)
Complement system (complement cascade)
Kinins (bradykinin, kallidin)
increases vascular permeability that causes contractions of smooth muscle and dilation of blood vessels
bradykinin
a part of the immune system that enhances or complements the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promotes inflammation, and attack the pathogenic cell membrane
complement system
regulated acid production in GI tract
Histamine
dilates arterioles by stimulating release of nitric oxide
histamine
increases permeability of capillaries to allow WBCs and proteins so they can enter tissues
Histamines
trigger smooth muscle contractions in the bronchioles
leukotrines
increase permeability of venules
leukotrines
formed by the oxygenation of arachidonic acid by cyclooxygenases 1 and 2 (COX-1 & COX-2)
prostaglandins
induce vasodilation
prostaglandins
inhibit platelet aggregation
prostaglandins
induce fever by activating thermoregulatory center in hypothalamus
prostaglandins
can cause bronchoconstriction
prostaglandins
what is the opposite of prostaglandins?
Thromboxane A2
induces vasoconstriction
thromboxane A2
facilitates platelet aggregation
Thromboxane A2
is a potent eosinophil chemoattractant that moves eosinophils to the site of injury
platelet activating factor (PAF)
a very important mediator that induces fever, hypotension, tachycardia, release of neutrophils
cytokines
_____ storm can be lethal
cytokines
3 local response vascular changes that may occur with inflammation:
immediate transient response
immediate sustained response
delayed hemodynamic response
this local response occurs with minor injury
immediate transient response
this local response occurs with more serious injury and continues for several days and damages the vessels in the area
immediate sustained repsonse
this local response increased in capillary permeability that occurs 4 - 24 hours after injury
delayed hemodynamic response
in what stage do prostaglandins and leukotrienes affect blood vessels?
vascular stage
in what stage are arterioles and venules dilated causing cells to adhere to and migrate through endothelium?
vascular stage
redness and warmth and dilation are a result of which stage?
vascular stage
in what stage are capillaries more permeable and allows work to damaged tissue? this allow allows exudate to escape from the tissues. swelling and pain is a result.
vascular state
watery fluid that is low in protein content and results of plasma entering inflammed site
serous exudate
occurs when there is severe tissue injury that causes damage to blood vessels or a significant leakage of RBCs from the capillaries
sanguineous exudate
we see liquidy exudate as well as blood in the clear fluid
serasanguineous exudate
fibrinous exudate
contains fibrinogen that makes a sticky meshwork in the fibers of a blood clot
necrotic cells get into the membrane of the tissues
membranous exudate
exudate that contains pus. pus is also known as degraded WBCs and tissue debris.
Prulent (suppurative)
White blood cells that are involved in inflammation
ganulocytes & monocytes
examples of granulocytes
neutrophils
eosinophils
basophils
mast cells
monocytes are converted to ____ so that they can devour pathogens or damaged cells
monocytes
____ enter the injured area, express adhesive proteins, and attach to the blood vessel lining
leukocytes
what inflammatory mediators do leukocytes release at the injury area?
histamine serotonin PAF Cytokines Nitric oxide
which leukocytes participate in the acute inflammatory response?
eosinophils
monocytes
neutrophils
what plays a role in the acute phase of the immune response?
granulocytes and monocytes
in what stage do inflammatory mediators cause WBC production causing WBC count to rise?
cellular stage
two types of leukocytes participate in the acute inflammatory response:
granulocytes (neutrophils, eosinophils, and basophils)
Monocytes (the largest of the WBCs)
in what stage does fever, lethargy, and skeletal muscle breakdown occur?
systemic acute-phase response
in what stage does the liver make fibrinogen and C-reactive protein (CRP)? this facilitates in clotting, binding to pathogens, and moderate inflammatory responses
systemic acute-phase response
_____ is where macrophages accumlate in the damaged area and keep releasing inflammatory mediators?
chronic inflammation
this type of inflammation is where fibroblasts proliferate and scar tissue forms
nonspecific chronic inflammation
this type of inflammation is where macrophages mass together around foreign bodies and connective tissue surrounds and isolates the mass
granulomatous inflammation
What 3 drugs are anti-inflammatory agents?
Salicylates
NSAIDs
Acetaminophen (paracetamol)
this drug blocks the inflammatory response, has fever blocking properties, and analgesic properties
salicylates
this drug inhibits the synthesis of prostaglandins
salicylate
this drug is prohibited to children under 19 who have had a viral infection
salicylates
this drug can cause Reye syndrome: liver failure, brain damage
Salicylate
this drug to drug interaction needs to be noted because it interferes with absorption
salicylate
symptoms of salicylism
dizziness tinnitus difficulty hearing nausea vomiting diarrhea confusion
what is tinnitus?
ringing in the ears
symptoms of acute salicylate toxicity
hyperpnea, tachypnea, hemorrhage, excitement, confusion, pulmonary edema, seizures, tetany, metabolic acidosis, fever, coma
what is the prototype of salicylate?
aspirin
non-selective NSAIDs inhibit what?
COX-1 and COX-2
this drug inhibits synthesis of prostaglandins
NSAID
GI bleeding is a contradiction of what drug?
NSAID
this drug-to-drug interaction of decreased diuretic effect, decreased beta-blockers, and lithium toxicity of which drug?
NSAID
what is the prototype of NSAIDs
Ibuprofen
this drug selectively inhibits COX-2
COX-2 inhibitors
what is the prototype for COX-2 inhibitors?
Celecoxib
what drug-to-drug interaction must be noted with COX-2 inhibitors?
sulfonamides (SULFA ALLGERGY!)
this drug causes severe renal or hepatic dysfunction, late pregnancy
Celecoxib
this drug can lead to stevens-johnson syndrome which is a skin rash that can be lethal
Celecoxib
as a pyretic, this drug acts directly on thermoregulatory cells of hypothalamus. it causes vasodilation and diaphoresis both which lower body temp
acetaminophen
what is the prototype of acetaminophenl?
paracetamol aka tylenol
this drug is associated with significant risk of liver damage especially in overdose
acetaminophen
this drug is often used in combination with opioid analgesics
acetaminophen
this steroid hormone is produced in the adrenal cortex
corticosteroids
this drug is a contrast with non-steroidal anti-inflammatory drugs (NSAIDS)
corticosteroids
this drug is a short term treatment of many inflammatory disorders
glucocorticoids
this drug gives the body a chance to heal from the effects of inflammation
glucocoroticoids
what is a serious adverse reaction of glucocorticoids?
Hyperglycemia. this effects the glucose levels so be careful with diabetic patients.
this drug can cause adrenal insufficiency which is the suppression of the adrenals. prolong use can cause adrenal glands to atrophy.
glucocorticoids
what is the prototype of glucocorticoids?
prednisone
tissues that contain the functioning cells of an organ or body part
parenchymal
what is the support tissue of parenchymal tissue?
stromal tissues
what are 3 types of body cells
Labile
Stable
Permanent cells
continue to divide and replicate throughout life, replacing cells that are continually being destroyex
labile
this type of body cell stops dividing when growth ceases
stable
this body cell cannot undergo mitotic division
permanent cells
this body cell cannot undergo mitotic division
permanent cells
how can wounds heal?
Primary healing and secondary healing
this is when tissue create small, clean wounds and have no tissue loss
primary healing
this is when tissue has great loss that needs to be replaced and tissue contamination. Example: burn
secondary healing
what are the 3 stages of wound healing?
inflammatory phase
proliferative phase
maturational or remodeling phase
in this phase of wound healing, blood clot and phagocytes occur to stop the bleeding and destroy pathogens
inflammatory phase
what will promote wound healing?
increased blood flow and oxygen delivery
what is the main objective of the inflammatory response?
increased blood flow and oxygen delivery
this is the body’s physiologic response to injury
inflammation
this is the body’s physiologic response that provides defense and protection against foreign substances that lead to disease?
immunity
this is the invasion of multiplication of microorganisms in body tissues
infection
Granulocytes are _____
phagocytes
____ are by far the most prevalent of the granulocytes
neutrophils
_____ are granulocytes that are involved in the allergic reactions and can attack parasites such as worms
eosinophils
____ are granulocytes that are also involved in allergic reactions and are able to release histamine, which helps trigger inflammation, and heparin, which prevents blood from clotting
Basophils
this monocyte is a the bridge from innate to adaptive systems
dendritic cells
excessive or inappropriate activation of the immune response to harmless non-self antigens
hypersensitivity
this occurs when the body is damaged by the immune system, rather than by the antigen (often called allergen)
hypersensitivity
what are the 4 types of hypersensitivity reactions?
Type 1: IgE-mediated
Type 2: antibody-mediated
Type 3: complement-mediated
Type 4: cell-mediated
this type of hypersensitivity is commonly called “allergic reactions”
Type 1 hypersensitivity
this type of hypersensitivity causes systemic or anaphylactic reactions
Type 1 hypersensitivity
These are examples of what type of hypersensitivity: rhinitis, food allergies, bronchial asthma, hives, and atopic dermatitis
Type 1 hypersensitivity
systemic response to the inflammatory mediators released in type 1 hypersensitivity
anaphylaxus
histamine, acetylcholine, kinin, leukotrienes, and prostaglandins all cause what?
vasodilation
what will happen if arterioles vasodilate throughout the body?
BP drops. No blood flow in the body.
acetylcholine, kinin, leukotrienes, and prostaglandins all cause what?
bronchoconstriction
what will happen when bronchioles constrict?
Decrease the ability to inhale and exhale. No oxygen flow in the body.
_____ has a very strong genetic predisposition. These people have frequent hypersensitivity to multiple allergens.
atopy or atopic reactions
this type of hypersensitivity is cytotoxic. meaning the certain immune cell is doing the damage.
Type 2 hypersensitivity
in this type of hypersensitivity, IgG or IgM attack antigens on cell surfaces.
Type 2 hypersensitivity
this type of hypersensitivity reaction is evident in blood transfusion and Rh disease
Type 2 hypersensitivity
in this type of hypersensitivity reaction, antibodies bind to receptors and cause dysfunction. i.e Graves disease; myasthenia
Type 2 hypersensitivity
in this type of hypersensitivity, an inflammatory response leads to tissue damage.
type 2 hypersensitivity
this type of hypersensitivity reaction occurs when free-floating antigen + antibody = circulating immune complex
type 3 hypersensitivity
this type of hypersensitivity causes: autoimmune vascultiis glomerulonephritis serum sickness arthus reaction
type 3 hypersensitivity
in this type of hypersensitivity reaction, immune complexes deposit on walls of blood vessels and activate complement. usually complement is a good thing but in this case, over reaction is causing damage to the blood vessels. example: Vasculitis
Type 3 hypersensitivity
in this type of hypersensitivity reaction, it is cell-mediated and sensitized T cells are attacking antigen
Type 4 hypersensitivity
in this type of hypersensitivity reaction, is cell mediated and DELAYED compared to the others.
Type 4 hypersensitivity
in this type of hypersensitivity reaction, it destroys all cells with a virus even if it’s not damaging a cell.
type 4 hypersensitivity
in this type of hypersensitivity reaction, we see a delayed-type hypersensitive in TB test, allergic dermatitis test, and hypersensitivity pneumonitis.
Type 4 hypersensitivity
what type of hypersensitivity reaction would be involved in latex allergy?
Type 1 or Type 4.
Type 1 causes anaphylaxis
Type 4 causes allergic dermatitis, skin reaction.
this is when the immune system attacks self-antigens
autoimmune disorder
Normally, self-reactive immune cells are killed in the lymphoid organs or suppressed by regulatory T cells. In ____, this self tolerance breaks down. Instead the immune system will destroy its own body tissues.
Autoimmunity
When testing for autoimmune diseases, _____ will appear in the blood.
antitissue antibodies. i.e antithyroid antibodies
A chronic inflammatory diseases characterized by formation of autoantibodies and immune complexes (type 3 hypersensitivity)
Systemic Lupus Erythematosus
In what autoimmune disorder do we see an increased production of autoantibodies, particularly antinuclear antibodies which attack the nucleic acid that make the DNA in the cells. Ultimately damages DNA.
Lupus
T/F: patients who suffer from autoimmune disease have hypoactive immune systems
false, in autoimmune diseases, the immune system is HYPERactive. It is attacking self-antigens and destroys its own body tissues.
This is when there is an inadequate immune response due to impaired function of insufficient production of immune factors.
Immunodeficiency
in ______ genetic mutation that causes decreased production (poorly functioning) components of the immune response (B cells, T cells, immunoglobins, complements, etc)
Primary (heritable) Immunodeficiency
in ______ this is caused by another disease.
Aids, cancers (bone marrow and blood cells), medications (immunosupression), and environmental toxins
Secondary (acquired) immunodeficiency
A person who has an immunodeficiency of any kinds is said to be ______. They are vulnerable to opportunistic infections.
Immunocompromised
This is referred to when bacteria are not causing harm and may be beneficial
Colonization
This is referred to when bacteria are harmful and causing disease
infection
Microorganisms that are normally living in or on the body. Some are useful, many have no effect. These are opportunistic pathogens that are capable of causing disease if health and immunity are weakened.
Microflora
This is a type of infectious agent that is small modified infectious host proteins. They are abnormally shaped versions of our own proteins. The cause normal proteins to shape like them.
Prion
This is a type of infectious agent has a protein coat surrounding a nucleic acid core. It has no metabolic enzymes of their own. They insert their genome into host cell’s DNA. They use cell’s metabolic machinery to make new versions of itself.
viruses
This is a type of infectious agent are cells without membrane-bound organelles (prokaryotes). They can live independently and use infected organism for food and shelter.
Bacteria
This is a type of infectious agent can produce toxins.
Bacteria
This is a type of infectious agent most require a cooler temperature than human core body temperature. So most infections are on the surface of the body.
Fungi
This is a type of infectious agent includes protozoa, malaria, dysentery, roundworms, tapeworms, ticks, mosquitoes, mites, lice, fleas.
Parasites
____ means bacterial toxins in the blood
sepsis or septicemia
What are the common adverse effects of antibiotics?
GI upset & Superinfection.
What are the 2 most common superinfections?
Clostridium difficile & Candidiasis (yeast)
These antibiotics are grouped together in the class called Beta Lactam antibiotics.
Penicillin (including carbapenems) and cephalosporins
Inflammatory bowel diseases occurs where?
primarily in the colon, small intestine, and the rectum
2 examples we discuss for IBD
Crohn disease
Ulcerative colitis
IBD with granulomatous lesions
Crohn disease
IBD that is primarily submucosal
Crohn disease
IBD that skips lesions
Crohns disease
IBD that occurs primarily in ileum, secondarily colon
Crohn disease
IBD with rare rectal bleeding
Crohn disease
IBD where fistulas, strictures, perianal accesses are common
Crohn disease
IBD where development of cancer is uncommon
Crohn disease
IBD where ulcerative, exudative lesions
Ulcerative colitis
IBD that is primarily mucosal
Ulcerative colitis
IBD with continuous lesions
Ulcerative colitis
IBD primarily in rectum and left colon
Ulcerative colitis
IBD where rectal bleeding is common
Ulcerative colitis
IBD where fistulas, strictures, perianal abscesses are rare
Ulcerative colitis
IBD where development of cancer is relatively common
Ulcerative colitis
IBD with “cobblestone” appearance
Crohn disease
Stage of Crohn disease: People with mild to moderate Crohn disease are able to eat food normally without dehydration, fevers, stomach pain, blockages in their intestine, or losing more than 10% of body weight
Mild to moderate stage
Stage of Crohn disease: If patient does not respond to treatment if they have high fevers, significant weight loss, stomach pain, or tenderness, occasional nausea or vomiting, or significant anemia
Moderate to severe stage
Stage of Crohn disease: have symptoms despite taking steroids, or have high fevers, persistent vomiting, blockages in their intestine, or an abcess
Severe stage
treatment of crohn disease
corticosteroids
antibiotics
cells in adaptive immunity
B & T cells
