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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

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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

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3
Q

2 mechanisms to clear pathogens

A

the process of phagocytosis
◦ the production of antibodies

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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

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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

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6
Q

fibrosis

A

scarring damage

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7
Q

what do chemical mediator do

A

create a response

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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

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9
Q

damaged tissue and cells release what

A

chemcial mediators into blood and ISF

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10
Q

6 chemical mediators

A

histamine, leukotrienes, bradykinin,
complement, cytokines, and prostaglandins

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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)

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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)

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13
Q

Complement system

A
  • enhances phagocytosis process to get rid of damaged and unwanted cells
  • complement proteins are primarily serine proteins
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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
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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)

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16
Q

Chemical Mediators derived from
Arachidonic Acid

A

 Prostagladins
 Leukotrienes
 Thromboxane

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17
Q

where does arachidonic acid pathway take place

A

inside cell

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18
Q

Both part of arachidonic pathway

A
  • Lipoxygenase pathway
  • Cyclooxygenase pathway
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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

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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

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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

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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

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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
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24
Q

what produces a fever

A

pyrogens

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25
Q

Systemic Manifestations:
Acute Phase Response (blood)

A

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

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26
Q

Leukocytosis

A

Increased numbers of white blood cells,
especially neutrophils (neutrophils usually indicate bacterial infection)

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27
Q

Differential count

A

Proportion of each type of white blood cell
altered, depending on the cause

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28
Q

Plasma proteins (inflammation diagnostics)

A

Increased fibrinogen and prothrombin

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29
Q

C-reactive protein (inflammation diagnostics)

A

A protein not normally in the blood, but appears with acute inflammation and necrosis within 24–48 hours

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30
Q

Increased erythrocyte sedimentation rate (inflammation diagnostics)

A

Elevated plasma proteins increase the rate at which red blood cells settle in a sample, indicates inflammation

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31
Q

Cell enzymes (inflammation diagnostics)

A

Released from necrotic cells and enter tissue fluids and blood: may indicate the site of inflammation

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32
Q

SIRS (Systemic Inflammatory
Response Syndrome)

A

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)

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33
Q

Treatment of Inflammation

A

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

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34
Q

PRICE

A

protect, rest, ice, compress, elevate

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35
Q

Chronic Inflammation

A

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.

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36
Q

Types of wound healing: Resolution

A

◦ Minimal tissue damage; tissue returns to normal
◦ Mild sunburn

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37
Q

Types of wound healing: Regeneration

A

◦ Occurs in cells capable of mitosis; damaged tissue is replaced by identical tissue
-cardiac cells are not capable of mitosis

38
Q

Types of wound healing: Replacement

A

◦ 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
Q

4 stages of healing

A

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
Q

Healing by Primary intention

A

Incision or open wound is immediately
closed (sutures/staples/glue)
Risk of infection is minimal
-closed wound

41
Q

Healing by Secondary intention

A

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
Q

Healing by Tertiary Intention

A
  • 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
Q

ruptured stomach ulcer will also release what

A

air, which will feel hard and tender

43
Q

As long as what ions are produced, the stomach will remain neutral

A

As long as HCO3 is produced, Hydrogen ions from HCl there will be no mucosal injury

44
Q

What is a peptic ulcer and what does it effect.

A

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
Q

2 types of peptic ulcers

A

Duodenal
◦ more often in 30-50 yr age group
most common type of peptic ulcer
Gastric (stomach)
◦ more common after age 60

46
Q

what are most peptic ulcers caused by

A

H. Pylori infections

47
Q

2nd most common cause of peptic ulcer

A

the use of aspirin and NSAIDs (inhibits bicarb),

48
Q

manifestations of peptic ulcer

A

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
Q

Complications of ulcer

A

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
Q

perforation of ulcer

A

-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
Q

Gastric Outlet Obstruction of ulcer

A

◦ 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
Q

Diagnosis of ulcer

A

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
Q

treatment of ulcer

A

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
Q

stress ulcer

A

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
Q

Zollinger-Ellison Syndrome

A

Gastrinoma (Gastrin-secreting tumor)
◦ Ulceration becomes inevitable

56
Q

Chrons disease

A

ulceration in the small intestine
(although can occur anywhere in GI tract from mouth to anus)

57
Q

ulcerative colitis

A

ulceration in the large intestine
(Colon) and rectum is almost always involved

58
Q

characteristics of ulcerative colitis

A

 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
Q

Manifestations
(Ulcerative Colitis)

A

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
Q

results of ulcerative colitis

A

Dehydration
Weight loss
Anemia
Fever
Due to: Fluid loss, bleeding, and inflammation

61
Q

Complications
(Severe Ulcerative Colitis)

A

Toxic Megacolon
◦ Dilation of the colon with signs of toxicity
Anal fissures, hemorrhoids, perirectal abscess
Cancer of the colon
Systemic Complications

62
Q

Drug classes used to manage inflammation

A
  • NSAIDs
  • Non-specific COX antagonists (ie ASA)
  • COX-2 specific antagonists (ie celecoxib)
  • Systemic Glucocorticoids
  • prednisone
  • Antihistamines
  • Acetaminophen for pyrexia
63
Q

Nonsteroidal
AntiInflammatory
Drugs
(NSAIDs)

A
  • 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
Q

What is the function of arachidonic acid?

A
  • 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
Q

what is the only benefit to blocking COX 1

A

MI, stroke is the only benefit

66
Q

where is cox 2 usually found

A

at site of infection

67
Q

three classes of NSAIDS

A

Salicylates (ASA)- Aspirin
Ibuprofen and like drugs- Advil, mortin
COX 2 antagonists- celibrix

68
Q

indications of NSAIDs

A
  • Analgesic (reduce pain)
  • Anti-inflammatory
  • Antipyretic (reduce fever)
  • Anticoagulant
    (salicylates)
69
Q

Analgesic: what is it and how does it work

A

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
Q

Antipyretic: what is it and how does it work

A

to reduce fever
* Inhibit prostaglandin E2 within the area of the brain that controls temperature

71
Q

Salicylates: what is it and how does it work

A
  • Have antiplatelet activity (decreases ability to clot)
  • Inhibit platelet aggregation
72
Q

NSAID: Acetylsalicylic Acid (ASA) and mechanism of action

A
  • 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
Q

NSAID: Ibuprofen (Motrin, Advil)and mechanism of action

A
  • 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
Q

NSAIDS Adverse effects

A
  • 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
Q

COX-2 Inhibitors (ie celecoxib [Celebrex])

A
  • 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
Q

Systemic Glucocorticoids

A
  • 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
Q

Systemic Glucocorticoids method of action

A
  • 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
Q

what are synthetic glucocorticoids used for

A
  • Autoimmune diseases (RA, SLE, etc)
  • Asthma, COPD
  • Inflammatory bowel disease
  • Selected neoplasias (cancer)
  • Selected viral and bacterial infections including shingles
79
Q

Antipyretic Drugs
(Acetaminophen,
Tylenol) mechanism of action

A
  • 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
Q

Antipyretic Drugs (Acetaminophen,
Tylenol) therapeutic effects and uses

A

Mild to moderate pain
* Osteoarthritis of the hip or knee
* Dysmenorrhea
* Dental procedures
* Headache and myalgia
* Fever

81
Q

serious effects of antipyretic drugs

A
  • Hepatotoxicity, acute liver failure
  • Renal failure
  • Pancytopenia
  • OVERDOSE can cause severe hepatotoxicity (liver in a toxic state), liver failure & death
82
Q

Nursing Considerations for Patients Receiving Antipyretic Therapy

A
  • 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
Q

Pharmacotherapy
of PUD (peptic ulcer disease) and GERD (gastroesophageal reflux) classification of drugs and rugs used

A

-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
Q

H2-Receptor Antagonists therapeutic uses

A
  • 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
Q

H2-Receptor Antagonists mechanism of action

A
  • 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
Q

H2-Receptor Antagonists adverse effects and drug interactions

A
  • 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
Q

Pharmacotherapy with Proton Pump Inhibitors (PPIs), what do they do and therapeutic uses

A
  • 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
Q

PPIs mechanism of action

A
  • 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
Q

Pharmacotherapy
of H. pylori
Infection

A
  • 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

patho (6 decks)

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