class 2 Flashcards
1
Q
what is lymphatic system
A
Provides the body the ability to resist injury and
infection
Consists of cells, vessels, and tissues that survey
your body
Your lymph nodes are the main lymphoid organ of
the body
◦ Filled with macrophages and lymphocytes
2
Q
WBC
A
White blood cells play an important role in the
Inflammatory process:
◦ Granulocytes: Neutrophils, eosinophils, basophils and
monocytes and macrophages
◦ Their primary role is Phagocytosis
3
Q
2 mechanisms to clear pathogens
A
the process of phagocytosis
◦ the production of antibodies
4
Q
Defense Mechanisms (3)
A
1st line – Nonspecific defense
◦ Skin, mucous membranes, tears (Physical Barrier), Flora in the gut
2nd line – Nonspecific defense
◦ Phagocytes (neutrophils, macrophages), natural killer cells (release toxins) and interferons (Cellular Barrier)
◦ Complement system, fever, inflammation (Process barrier)
3rd line – Specific defense; immune response (antibodies)
◦ Production of unique antibodies or sensitized lymphocytes
following exposure to specific substances
5
Q
what is inflammation
A
Body’s nonspecific response to tissue injury, it wants to contain the injury
It is a normal response
It is a necessary response
Involves processes that attempt to minimize injury
to the body; protective mechanism
6
Q
fibrosis
A
scarring damage
7
Q
what do chemical mediator do
A
create a response
8
Q
3 Stages of Acute Inflammation
A
Vascular Stage
◦ Vasodilation and increase in vascular permeability
◦ (Bradykinin activates pain receptors & pain sensation stimulates mast cells & basophils to release histamine)
Cellular Stage
◦ Delivery of leukocytes (neutrophils) to the site of injury
Leukocyte Activation and Phagocytosis
◦ Phagocytosis- the cell killing
9
Q
damaged tissue and cells release what
A
chemcial mediators into blood and ISF
10
Q
6 chemical mediators
A
histamine, leukotrienes, bradykinin,
complement, cytokines, and prostaglandins
11
Q
Chemical Mediators: plasma derived mediators
A
(1) Plasma-derived mediators
◦ Acute-Phase proteins- bring about fever and inflammation
◦ Complement Cascade/System
◦ Clotting/fibrinolytic System
◦ Kinin System (bradykinin)
12
Q
Chemical Mediators: cell-derived mediators
A
(2) Cell-derived mediators
◦ Neutrophils & macrophages (lysosomal enzymes),platelets (serotonin), mast cells (histamine)
◦ Leukocytes (Prostaglandins,Leukotrienes, Platelet Activating Factor)
◦ Leukocytes, macrophages (Nitric oxide, Oxygen derived free radicals)
◦ Macrophages, lymphocytes, endothelial cells (Cytokines)
13
Q
Complement system
A
- enhances phagocytosis process to get rid of damaged and unwanted cells
- complement proteins are primarily serine proteins
14
Q
Histamine & Inflammation
A
- Chemical Mediator
involved in acute
inflammation
Produced by Basophils
and Mast cells
Causes vasodilation of
blood vessels
Increases permeability of
capillaries
15
Q
Cytokines & Inflammation
A
Cytokines are an inflammatory mediator
There are cytokines involved in acute
inflammation and other cytokines involved in chronic inflammation
Interleukins, interferons, tumor necrosis factors- (TNF) are examples of cytokines (inflammatory mediator)
16
Q
Chemical Mediators derived from
Arachidonic Acid
A
Prostagladins
Leukotrienes
Thromboxane
17
Q
where does arachidonic acid pathway take place
A
inside cell
18
Q
Both part of arachidonic pathway
A
- Lipoxygenase pathway
- Cyclooxygenase pathway
19
Q
Lipoxygenase pathway
A
1) lipoxygenase pathway
2) Leukotriene receptor antagonist
3)Leukotrines
4) Induces smooth muscle contractions, constricts pulmonary airways, Increases microvascular permeability
20
Q
Cyclooxygenase pathway
A
1) Consists of Cox 1 and Cox 2
2) Aspirin, NSAIDs
Can either create Prostaglandins or Thromboxane
Prostaglandin- Induces vasodilation and bronchoconstriction, and inhibits inflammatory process.
Thromboxane- Vasoconstriction, bronchodilation, promotes platelet function
21
Q
COX 1
A
The good effects: COX-1 protects
the gut reduces gastric acid
secretion and increases mucous),
supports renal function, promotes
platelet aggregation
-helps release chemical mediators
Inhibition of COX-1 results in the
following harmful effects:
◦ GASTRIC EROSION AND
ULCERATION
◦ BLEEDING TENDENCIES
◦ RENAL IMPAIRMENT
22
Q
COX 2
A
The bad effects, COX-2 found at
the sit of injury and mediates
inflammation and sensitizes pain
receptors to painful stimuli)
Inhibition of COX-2 results largely
in beneficial effects:
◦ SUPPRESSION OF INFLAMMATION
◦ ALLEVIATION OF PAIN
◦ REDUCTION OF FEVER
◦ PROTECTION AGAINST
COLORECTAL CANCE
23
Q
Fever
A
- prevents mircoorganisms from growing
Non-specific body defense
Accelerates the body defenses and repair
processes
◦ Fever can be beneficial if it impairs the growth and
reproduction of pathogens.
If excessive it can harm the body
24
Q
what produces a fever
A
pyrogens
25
Systemic Manifestations:
Acute Phase Response (blood)
Leukocytosis (Increased WBC in the blood)
◦ WBC’s increases to15.0-20.0 X 109 cells/L (Normal 4.0-10.0 X 109 cells/L)
Lymphadenitis (swollen lymph nodes)
Elevated C-reactive protein (CRP) (When elevated indicates inflammation)
Elevated ESR (erythrocyte sedimentation rate) (indicates inflammation)
Increased plasma proteins and cell enzymes in the serum
◦ Isoenzymes are specific cell enzymes
◦ For Example: If the liver is inflamed you will see a rise in the liver enzymes in the blood – AST and ALT
26
Leukocytosis
Increased numbers of white blood cells,
especially neutrophils (neutrophils usually indicate bacterial infection)
27
Differential count
Proportion of each type of white blood cell
altered, depending on the cause
28
Plasma proteins (inflammation diagnostics)
Increased fibrinogen and prothrombin
29
C-reactive protein (inflammation diagnostics)
A protein not normally in the blood, but appears with acute inflammation and necrosis within 24–48 hours
30
Increased erythrocyte sedimentation rate (inflammation diagnostics)
Elevated plasma proteins increase the rate at which red blood cells settle in a sample, indicates inflammation
31
Cell enzymes (inflammation diagnostics)
Released from necrotic cells and enter tissue fluids and blood: may indicate the site of inflammation
32
SIRS (Systemic Inflammatory
Response Syndrome)
Fever (Over 38oC)
Increased HR (Over 90 beats/min)
Increase RR (first clinical indicator); hypoperfusion could cause lactic acid; infection of the lungs
WBCs (Macrophages-cytokines-increased white cells neutrophils followed by monocytes); Leukocytosis (above 12,000)
33
Treatment of Inflammation
ASA –reduces pain and fever & inflammation
Acetaminophen – reduces fever and pain; not inflammation
NSAIDs – reduce inflammation, pain, and fever
Corticosteroids – reduce inflammation; short term use due to side effects
34
PRICE
protect, rest, ice, compress, elevate
35
Chronic Inflammation
More tissue destruction occurs
Less swelling & exudate
The presence of more lymphocytes, macrophages, and fibroblasts
More scar tissue
Examples:
◦ Rheumatoid arthritis is characterized by chronic
inflammation
◦ Other examples: Glomerulonephritis, Pericarditis, Neuritis
◦ Chron’s disease is an inflammatory bowel disease.
36
Types of wound healing: Resolution
◦ Minimal tissue damage; tissue returns to normal
◦ Mild sunburn
37
Types of wound healing: Regeneration
◦ Occurs in cells capable of mitosis; damaged tissue is replaced by identical tissue
-cardiac cells are not capable of mitosis
38
Types of wound healing: Replacement
◦ By connective tissue (scar or fibrous tissue)
◦ Extensive tissue damage or cells are incapable of mitosis
◦ Chronic inflammation or infections result in more fibrous
tissue
39
4 stages of healing
1) Homeostasis- formation of the blood clot
2) Inflammatory process- Phagocytic WBC migrate to wound, Neutrophils ingest and remove bacteria
3) Proliferative- Fibroblasts synthesize and secrete collagen, angiogenisis (formation of new blood vessesl). Want to see it very vascular.
4) Remodeling- Formation of scar
40
Healing by Primary intention
Incision or open wound is immediately
closed (sutures/staples/glue)
Risk of infection is minimal
-closed wound
41
Healing by Secondary intention
Occurs when the wound edges cannot be
approximated
A granulation tissue matrix (a form of collagen that is very vascular, delicate) must be built to fill the wound defect
Prolonged phase of inflammation because there is more time required for phagocytosis of necrotic tissue
Sometimes healing is hastened by use of a skin graft
42
Healing by Tertiary Intention
- wound is left open
If a wound is contaminated, this technique
may be used to decrease the chance of
infection
◦ The wound is initially cleansed and observed for several days
◦ Once the wound appears clean, it is surgically closed
43
ruptured stomach ulcer will also release what
air, which will feel hard and tender
43
As long as what ions are produced, the stomach will remain neutral
As long as HCO3 is produced, Hydrogen ions from HCl there will be no mucosal injury
44
What is a peptic ulcer and what does it effect.
Can affect one or all layers of the stomach or duodenum
Begins with breakdown of the mucosal layer
Usually associated with acute inflammation
Healed ulcers prone to ulceration
Affects both men and women
45
2 types of peptic ulcers
Duodenal
◦ more often in 30-50 yr age group
most common type of peptic ulcer
Gastric (stomach)
◦ more common after age 60
46
what are most peptic ulcers caused by
H. Pylori infections
47
2nd most common cause of peptic ulcer
the use of aspirin and NSAIDs (inhibits bicarb),
48
manifestations of peptic ulcer
Pain
◦ Burning, gnawing, nagging or aching pain near the midline in the epigastrium (epigastric area)
◦ Chronic and intermittent
Tend occur at intervals of weeks or months
During an exacerbation, pain is daily
◦ Frequently occurs when the stomach is empty
Usually 2-3 hours after meals and at night
◦ Relieved by Antacids or ingestion of food
49
Complications of ulcer
Hemorrhage (ulcer has eroded a blood vessel)
◦ Hematemesis (bright red or coffee ground
appearance caused by blood mixing with acid)
Important!! Circulatory shock may develop, depending on the
amount of blood lost
May require immediate correction of blood loss & emergency
surgery
◦ Melena (black tarry stools)
50
perforation of ulcer
-A complication of an ulcer is caused when the ulcer erodes through the walls of the stomach and duodenal wall.
-Peritonitis, Excruciating pain, not relieved by food or antacids, tender rigid abdomen
51
Gastric Outlet Obstruction of ulcer
◦ A complication caused by Interference with the passage of gastric contents; Result of repeated episodes of injury, inflammation & scaring
◦ Feeling of fullness/heaviness after meals, reflux, anorexia after eating, N&V, weight loss, abd. Pain, vomit undigested food
52
Diagnosis of ulcer
History (√ aspirin and NSAID use)
Test for H. Pylori
◦ Blood test/stool test- IgM antibodies to H. Pylori
◦ Urea breath test (indicates H pylori infection)
◦ Biopsy
Lab findings
◦ Hypochromic anemia
◦ Occult blood in the stools
Barium Swallow (x-ray studies)
Endoscopy
53
treatment of ulcer
Antibiotics (2 or more)
Mucosal protective agents
◦ Binds to ulcer tissue & serves as a barrier to acid, pepsin, & bile; do not give with antacids
Antacids
◦ Used to decrease or neutralize the acid in the stomach
H2-receptor antagonist
◦ Block acid secretion by parietal cells
Proton pump Inhibitors
◦ Inhibit acid production
Reduce exacerbating factors (ie) avoid aspirin, NSAIDs, caffeine
54
stress ulcer
Develop in relation to major physiologic stress
Patients with large surface area burns, trauma, sepsis, acute respiratory distress syndrome, severe liver failure, and major surgical procedures
First indicator is usually a hemorrhage due to rapid onset
55
Zollinger-Ellison Syndrome
Gastrinoma (Gastrin-secreting tumor)
◦ Ulceration becomes inevitable
56
Chrons disease
ulceration in the small intestine
(although can occur anywhere in GI tract from mouth to anus)
57
ulcerative colitis
ulceration in the large intestine
(Colon) and rectum is almost always involved
58
characteristics of ulcerative colitis
Ulcerative lesions in the mucosal layer
◦ Extends from the rectum into colon in a continuous pattern
Inflammatory process
◦ Damages the mucosal barrier
◦ Mucosa is hyperemic, and edematous
Severe inflammation
◦ Mucosa hemorrhages, inflammatory lesions may ulcerate, abscesses may form
Chronic inflammation
◦ The mucosal layer often develops pseudopolyps (severe episodes of inflammation)
The bowel wall thickens due to repeated inflammatory episodes (can lead to closure of the lumen)
59
Manifestations
(Ulcerative Colitis)
Diarrhea (urgent)
Rectal Bleeding
◦ Stools contain blood and mucous
Cramping abdominal pain
Anorexia, weakness, fatigue
Varied severity
Mild- less than 4 stools daily, no toxicity
Moderate- more than 4 stools, min toxicity
Severe more than 6 stools per day & toxicity
(fever, tachycardia, anemia, elevated ESR)
60
results of ulcerative colitis
Dehydration
Weight loss
Anemia
Fever
Due to: Fluid loss, bleeding, and inflammation
61
Complications
(Severe Ulcerative Colitis)
Toxic Megacolon
◦ Dilation of the colon with signs of toxicity
Anal fissures, hemorrhoids, perirectal abscess
Cancer of the colon
Systemic Complications
62
Drug classes used to manage inflammation
* NSAIDs
* Non-specific COX antagonists (ie ASA)
* COX-2 specific antagonists (ie celecoxib)
* Systemic Glucocorticoids
* prednisone
* Antihistamines
* Acetaminophen for pyrexia
63
Nonsteroidal
AntiInflammatory
Drugs
(NSAIDs)
* NSAIDs antagonize (block) cyclooxygenase
(COX), an enzyme necessary for
production of prostaglandins
* Prostaglandins are pro-inflammatory and
cause vasodilation
* Inflammation associated with action of
COX-2 thus it is ideal to block COX-2
rather than COX-1 and COX-2
* Inhibition of COX-1 associated with
undesirable effects of NSAIDs (side effects)
64
What is the function of arachidonic acid?
* Arachidonic acid is important because the human body uses it as a
starting material in the synthesis of two kinds of essential substances,
the prostaglandins and the leukotrienes.
* However, when a triggering event (i.e., injury) occurs arachidonic acid
production is stimulated in excess the release of excess prostaglandins and
leukotrienes result in the inflammatory response
* Inflammation, edema, headache, and pain
65
what is the only benefit to blocking COX 1
MI, stroke is the only benefit
66
where is cox 2 usually found
at site of infection
67
three classes of NSAIDS
Salicylates (ASA)- Aspirin
Ibuprofen and like drugs- Advil, mortin
COX 2 antagonists- celibrix
68
indications of NSAIDs
* Analgesic (reduce pain)
* Anti-inflammatory
* Antipyretic (reduce fever)
* Anticoagulant
(salicylates)
69
Analgesic: what is it and how does it work
for treatment of headaches, mild to moderate pain, and inflammation
* Block the chemical activity of either or both cyclooxygenase (COX) enzymes
(prostaglandin [PG] pathway) and lipoxygenases (leukotriene [LT] pathway)
* Result: limits the undesirable inflammatory effect of PGs
70
Antipyretic: what is it and how does it work
to reduce fever
* Inhibit prostaglandin E2 within the area of the brain that controls temperature
71
Salicylates: what is it and how does it work
* Have antiplatelet activity (decreases ability to clot)
* Inhibit platelet aggregation
72
NSAID: Acetylsalicylic Acid (ASA) and mechanism of action
* Irreversibly inhibits cyclo‐oxygenase enzyme, so blocks synthesis of
prostaglandins and thromboxane A2.
* Therefore, reduces platelet aggregation (COX-1 activity)
* Cardiovascular risk reduction
* Salicylates (ASA) are contraindicated in children (under 18 ) with flulike
symptoms, as its use is strongly associated with Reye’s syndrome (neurological condition)
73
NSAID: Ibuprofen (Motrin, Advil)and mechanism of action
* Therapeutic effects and uses
* Relief of fever and mild to moderate pain associated with chronic
symptomatic rheumatoid arthritis (RA) and osteoarthritis
* Myalgia, headache, dental pain, and dysmenorrhea
* Fever (antipyretic properties)
Mechanism of action:
* Block action of COX-1 and COX-2, reducing prostaglandin production
74
NSAIDS Adverse effects
* Bleeding (platelets don't stick cause of inhibition of COX 1 and 2)
* Anorexia, nausea, vomiting,
constipation or diarrhea, heartburn, GI
irritation
* Dizziness, drowsiness, headache
* Polyuria, azotemia, cystitis, increased
BUN and creatinine, hematuria
More serious effects:
* Hypotension, congestive heart failure
* Peripheral edema
* Aplastic anemia, leukopenia
* GI ulceration
* Occult blood loss
* Hepatotoxicty
* Nephrotoxicity
* Decreased hemoglobin and hematocrit (if theres blood loss)
75
COX-2 Inhibitors (ie celecoxib [Celebrex])
* Block COX-2 but not COX-1
* Indicated for mild to moderate pain and inflammation associated with
RA and osteoarthritis, dysmenorrhea
* Less GI bleeding and ulcer formation than with ibuprofen or aspirin (because it isnt blcoking COX 1)
76
Systemic Glucocorticoids
* Glucocorticoids are powerful anti-inflammatory agents with many
indications (arthritis, asthma, neoplasia)
* Duration of use is limited as therapeutic doses of glucocorticoids are
associated with many adverse effects
* GI irritation, hyperglycemia, Cushing’s syndrome, electrolyte
imbalances
* Different dosing regimens are used to reduce the appearance of adverse
effects
77
Systemic Glucocorticoids method of action
* Suppress immune responses and inflammation (inhibits arachidonic pathway, suppresses filtratioin of phagocytes)
* Inhibit the synthesis of chemical mediators (prostaglandins, leukotrienes,
histamine) to reduce swelling, warmth, redness and pain.
* Suppress infiltration of phagocytes, so damage from lysosomal enzymes is
averted
* Have greater anti-inflammatory effects than NSAIDS
78
what are synthetic glucocorticoids used for
* Autoimmune diseases (RA, SLE, etc)
* Asthma, COPD
* Inflammatory bowel disease
* Selected neoplasias (cancer)
* Selected viral and bacterial infections including shingles
79
Antipyretic Drugs
(Acetaminophen,
Tylenol) mechanism of action
* Inhibits COX activity in CNS but
not in rest of body
* Antipyretic action may be due
to action at hypothalamus
* Does not suppress platelet
aggregation
* Does not decrease renal blood
flow of cause renal impairment
80
Antipyretic Drugs (Acetaminophen,
Tylenol) therapeutic effects and uses
Mild to moderate pain
* Osteoarthritis of the hip or knee
* Dysmenorrhea
* Dental procedures
* Headache and myalgia
* Fever
81
serious effects of antipyretic drugs
* Hepatotoxicity, acute liver failure
* Renal failure
* Pancytopenia
* OVERDOSE can cause severe hepatotoxicity (liver in a toxic state), liver failure & death
82
Nursing Considerations for Patients Receiving Antipyretic Therapy
* Assessment
* Obtain a complete health history including allergies and drug history, recent surgeries, fever, and trauma
* Obtain vital signs
* Planning
* Patient to experience a reduction of fever
* Provide education regarding drug action, precautions, and possible adverse effects
* Interventions
* Monitor hepatic and renal function
* Use caution with alcoholic patients
* Use with caution with patients with diabetes mellitus (acetaminophen can promote hypoglycemia)
83
Pharmacotherapy
of PUD (peptic ulcer disease) and GERD (gastroesophageal reflux) classification of drugs and rugs used
-The classification of these drugs are H2 antagonists
* Drugs that reduce acid secretion
* H2-receptor antagonists
Proton pump inhibitors (PPIs)
* Anticholinergics
* Prostaglandins
* Drugs that neutralize acid
* Antacids
* Antibiotics
* Amoxicillin, clarithromycin,
tetracycline, metronidazole
84
H2-Receptor Antagonists therapeutic uses
* Available OTC and by prescription
* Therapeutic effects and uses
* Duodenal ulcers, gastric ulcers
* Hypersecretory conditions (ie ZES)
* Heartburn, GERD
* Used off-label to counter medications that promote development of peptic ulcers
85
H2-Receptor Antagonists mechanism of action
* Block histamine at the H2 receptors of acid-producing parietal cells (stomach)
* Reduces production of hydrogen ions, resulting in decreased production of HCl acid
* Suppresses acid secretion in the stomach
86
H2-Receptor Antagonists adverse effects and drug interactions
* Serious adverse effects
* Blood dyscrasias, especially neutropenia and thrombocytopenia
* Confusion may occur rarely, usually in elderly or with IV dosing
* High doses may result in gynecomastia, impotence, or loss of libido in
men
* Drug interactions
* All H2 antagonists may inhibit the absorption of drugs that require an acidic GI environment for absorption (because its decreasing acid in the stomach)
* Smoking has been shown to decrease the effectiveness of H 2 blockers
87
Pharmacotherapy with Proton Pump Inhibitors (PPIs), what do they do and therapeutic uses
* PPIs H+/K+ pump on parietal cells, reducing acid secretion in the
therapy of PUD and GERD
* Acid secretion is significantly reduced compared H2 receptor
antagonist & have a longer duration of action
* Therapeutic effects and uses
* By prescription, approved for short-term, 4- to 8-week
therapy of active peptic ulcers
* OTC, indicated for relief of heartburn
88
PPIs mechanism of action
* Reduces acid secretion in stomach by irreversibly binding to
the H+/K+ pump
* Proton pump inhibitors irreversibly bind to the hydrogen–potassium–ATPase enzyme
* This bond prevents the movement of hydrogen ions from the
the parietal cell into the stomach
* Result: hypo or achlorhydria—reduction or absence of HCL in
gastric secretions
89
Pharmacotherapy
of H. pylori
Infection
* Antibiotics usually given with drug that
reduces acid secretion (PPI or H2
blocker)
* Two or more antibiotics (given with PPI) usually given at
same time to prevent development of
resistance to antibiotics
* Beta-lactamase, macrolides and
tetracyclines are used together
