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Pathophysiology > Anti inflammatory drugs 2 > Flashcards

Anti inflammatory drugs 2 Flashcards

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1
Q

Ischemia is called what?

A

↓ arterial blood flow

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2
Q

Short-term compensations for ishemia is what?

A

Short-term compensations → anaerobic metabolism

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3
Q

One long-term compensation for ishemia is what?

A

One long-term compensation → angiogenesis “collateral circulation”

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4
Q

Treatment is aimed at what for ishemia?

A

Treatment is aimed at improving/restoring blood flow and increasing oxygen levels in the bloo

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5
Q

Types of Necrosis

A

coagulative
Liquefactive
Caseous
Gangrene

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6
Q

Describe Coagulative necrosis

A

ischemia, free radical, still looks like a cell for a while, may have viable cells around it

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7
Q

Describe Liquefactive necrosis

A

bacterial (WBC enzymes dissolve tissue

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8
Q

Describe Caseous necrosis

A

coagulated tissue no longer recognizable, cheese like appearance

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9
Q

Describe Gangrene and the two types?

A

gangrene – build-up of decomposing dead tissue, usually refers to appendage/limb with ischemic necrosis
•dry chronic/slow
•wet acute/quick/possible bacteria

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10
Q

What are the two types of cell injury?

A

lethal and sublethal

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11
Q

Cell Adaptation to Sublethal Injury are

A 
Adaptive changes:
•Atrophy (↓ number or size)•
Hypertrophy (↑ size)•
Hyperplasia (↑ number)•
Metaplasia (new type)
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12
Q

maladaptive changes:

A

maladaptive changes:
•Dysplasia (abnormal change)is an abnormal differentiation of dividing cells that results in changes in their size, shape, and
appearance
•Anaplasia (↑ immature)

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13
Q

Describe “collateral circulation?

A

“collateral circulation” – develop additional small arterial vessels from other local arteries that re-route blood around a blocked artery

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14
Q

Excessive apoptosis can lead to?

A

Excessive apoptosis can lead to atrophy

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15
Q

Define Debridement?

A

medical removal of dead, damaged, or infected tissue to improve healing in the remaining healthy tissue

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16
Q

What are the three ways of Debridement?

A 
Surgical Removal (scraping/curettage, cutting away)
•Enzymatic Creams & Dressings (break down dead tissue)
•Mechanical Irrigation (with syringe of NS
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17
Q

Define autolysis?

A

The body will use natural enzymes to break down dead tissue andphagocytes to remove it

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18
Q

What are the three Non-Specific (Innate) Immune Response

A

Skin and mucous memebrane
mononuclear phagocytes
inflammatory response

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19
Q

What are the four ways of inflammatory response?

A

Vascular response
Cellular response
Chemical mediators
exudate formation

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20
Q

In Skin and Mucous membranes what antimicrobial peptides kills bacteria, fungi and viruses

A

Antimicrobial peptides “defensins” can kill many bacteria, fungi and viruses

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21
Q

What are the three functions of Phagocytes

A

Removal of old or damaged cells
Recognition, destruction and removal of invading agents such as microorganisms
Participation in the inflammatory and immune response

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22
Q

Free, mobile phagocytes are called?

A

Monocytes in blood

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23
Q

When monocytes enter the tissue they are called what and what is the difference between both life spans?

A

Monocytes circulate in the blood/lymph/spleen and enter into tissue to become macrophage
Monocytes ~ 1-day half-life, macrophage ~ live for months

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24
Q

Fixed (resident) phagocytes are called and where are they located?

A

Specialized tissue macrophages in the liver, spleen, bone marrow, lungs, lymph nodes, nervous system (specific name

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25
Q

Tissue macrophages are _______ phagocytes and are “on-site” ready to work
•Constant surveillance, involved in ______ & ______

A

Tissue macrophages are “bigger & better” phagocytes and are “on-site” ready to work•Constant surveillance, involved in inflammation & immunity

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26
Q

Is inflammation always caused by infection and explain the difference?

A

– inflammation may be caused by injury other than infection; infections almost always involve inflammati

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27
Q

What are the four major steps involved in inflammation?

A

Restore hemostasis (stops bleeding using platelets and coagulation)
Neutralize and destroy invading and harmful agents
Limit the spread of harmful agents to other tissue
Prepare any damaged tissue for repair by clean

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28
Q

intensity of inflammatory response depends on?

A

intensity of response depends on extent and severity of injury and the health of the individual’s inflammatory response system

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29
Q

Prolonged inflammation may do what and what is evident?

A

Prolonged inflammation may impair healing and result in an accumulation of macrophages, fibroblasts, and collagen called a granuloma – fibrosis and scarring are evident

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30
Q

In inflammation what are the two Vascular Response

A

Vasoconstriction (local, short) to control bleeding Vasodilation & Increased Permeability (resources to sit

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31
Q

Platelets form _______ and coagulation forms _______ to control bleeding
•Platelets and other local cells release what and what is it used for?

A

latelets form plug and coagulation forms fibrin to control bleeding
•Platelets and other local cells release proinflammatory mediators such as histamine – causes local capillary vasodilation & increased permeability (bring fluid and resources such as proteins and white cells to site of injury

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32
Q

Vasodilation results in _____ – increased blood flow to the area (redness, erythema)

A

Vasodilation results in hyperemia – increased blood flow to the area (redness, erythema)

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33
Q

increased permeability in the capillary allows plasma proteins (albumin) to move into the interstitial space causing what and what is the MOA?

A

increased permeability in the capillary allows plasma proteins (albumin) to move into the interstitial space accompanied by fluid movement, edema and swelling

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34
Q

What keeps the bacteria from spreading and what releases the growth factors that begins the healing process.

A

Fibrin from the clot traps bacteria and keeps it local

•Platelets release growth factors that begin the healing process.

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35
Q

Describe chemotaxis?

A

chemotaxis – use of released chemicals to call WBC to the area

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36
Q

Describe Margination and diapedesis

A

Margination and diapedesis – method of WBC leaving capillary and entering interstitial area –

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37
Q

Neutrophils response time what and what is the lifespan?

A

Neutrophils – phagocytes, most abundant, early response (6-12h), short life (24-48h), destroy invading bacteria, foreign material and remove injured cell de

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38
Q

What is stimulated to produce/increase neutrophils and what stimulates it. When neutrophils is increased what does it do to the WBC count.

A

The bone marrow is stimulated by released chemical mediators to create/release more neutrophils → causes an increase in the WBC count, particularly the neutrop

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39
Q

If demand is high to fight bacterial infection what happens to neutrophils?
What is immature neutrophil called and mature neutrophil called?
Describe what we mean by a “shift to the left”?

A

If demand is high, immature neutrophils will be released causing a rise in plasma “band neutrophils” (immature neutrophils) (mature neutrophils are “segmented neutrophils”. An ↑ in band and ↓ in segmented neutrophils is called a “shift to the left” and is commonly seen in severe or prolonged bacterial infections where neutrophils are used at a rapid rate or for a long duration(run low on mature neutrophil

40
Q

When do monocytes arrive?

what is the major role of the monocytes?

A

Monocytes – phagocytes, arrive in 3-7 days, enter tissue and become macrophages, major role in cleaning debris so healing can begin, longer life span – may continue work for weeks

41
Q

Describe the eosinophils and what is it effective against?

A

Eosinophils – large, less abundant, effective against larger parasites and release chemicals that can destroy them.

42
Q

What do the Basophils release? and what scenarios are the active in?
Do they have more selective roles?

A

Basophils – more selective role, release pro-inflammatory histamine and heparin, active in allergy and asthma

43
Q

Mast Cells – reside in where?
triggered by ?
massive release of _______ to trigger inflammation, active in ______

A

Mast Cells – reside in skin and mucous membranes near the body surface, triggered by contact and foreign invaders, massive release of histamine to trigger inflammation, active in allerg

44
Q

Monocytes & Macrophages secrete what?

A

– cytokines & bradykinins,

45
Q

What are the functions of bradykinin

A

vasodilation
Smooth muscle contraction
Stimulation of pain sensor

46
Q

cytokines functions?

A

Messengers – tell other cells toparticipate, increase activit

47
Q

Endothelium cells are involved.

A

Endothelium cells – diapedesis, prostaglandins

48
Q

The characteristics of the exudate often changes with?

A

The characteristics of the exudate often changes with the cause of inflammation

49
Q

What are the four types of inflammatory exudate?

A

Serous – watery clear to light pink – low cell and protein content, seen early in inflammation (blister, pleural effusion)
Catarrhal (uncommonly used term) – accelerated mucous production (runny nose)
Purulent (pus) – WBC, microorganisms, liquified dead cells and other debris – purulent drainage(creamy, thick, may be green or yellow)
Hemorrhagic – necrosis of vessel wall with uncontrolled bleeding (hematoma)
Fibrinous – excess fibrin leading to excessive fibrinous connective tissue – may cause tissues to adhere to each other (adhesio

50
Q

watery or serous exudate occurs with?

A

watery or serous exudate occurs with allergy, burns, or viral infection

51
Q

A purulent or pus exudate is typical of a

A

bacterial infection.

52
Q

Systemic Clinical Manifestations due to release in bloodstream of PG, cytokines,complement activation

A

-Fever (PG effect on hypothalamus) Stages of the Febrile Response
-ANS may increase muscle tone/shivering (increases temperature)and decrease sweating/peripheral blood flow (reduce heat
Paradoxically may feel the “chills” as the body tries to reach hypothalamus new higher set-point
4.Malaise, nausea and anorexia5.
Increased pulse and respiratory rate (rise in metabolic rate with fever

53
Q

What are the types of inflammation?

A

Acute inflammation
subacute inflammation
chronic inflammation

54
Q

Acute inflammation – healing occurs in how many weeks? – Is there any residual damage left.
What is the protein that is associated with the acute phase and when measured it can serve as a marker for what?

A

Acute inflammation – healing occurs in 2-3 weeks – usually no residual damage. C-reactive protein (CRP) is an acute phase protein that can be measured in the blood as a “marker” of inflammation.

55
Q

Subacute inflammation and Acute inflammation acute what is the difference

A

Subacute inflammation – as acute but lasts longer – few mont

56
Q

How long is chronic inflammation?

What is the side effect on local healthy tissue?

A

Chronic inflammation – weeks or months or even years, chemical process continues or is repeated, and local healthy tissue is injured, may have fibrous scaring or tissue loss e.g. rheumatoid arthriti

57
Q

What is the final phase of the inflammatory response? n

A

The healing process

58
Q

What is Regeneration?

A

Regeneration – replacement of lost cells and tissues with cells of the same type.

59
Q

Describe the labile cells and what are they?

Describe the permanent cells and what are they?

A

Labile cells divide constantly and regenerate quickly – skin, lymphoid organs, bone marrow, mucous membranes of GI/GU/Reproductive tracts.

Permanent cells such as neurons of the CNS and cardiac muscle do not regene

60
Q

How do most tissues heal?

A

Repair – most tissues heal with connective tissue re

61
Q

What are three ways of repair

A

Primary intention
secondary intention
Tertiary intention

62
Q

Primary Intention is for what kind of injuries?

A

Primary Intention – two well approximated margins (matched edges) such as a surgical wound or paper cut –

63
Q

Primary intention has three phases and what are they?

A
  • Initial (Inflammatory) Phase
  • Granulation (Proliferative/Reconstructive) Phase
  • Maturation Phase and Scar Contraction
64
Q
  • How long does the inflammatory phase last?
  • What releases growth factors?
  • What is the function of fibrin in this phase
A

3-5 days, edges are aligned/sutured/stapled – clotting, inflammation, clean up of debris, platelet release growth factor, clot begins to dissolve, fibrin forms framework for future capillary growth and migration of epithelial cell

65
Q

Granulation tissue

A

proliferating fibroblasts (immature connective tissue cells that migrate to healing site and secrete collagen to organize and strengthen the healing site - fibrous or scar tissue
)proliferating capillaries sprouts (angioblasts)
WBCs and a loose fluid matri

66
Q

Describe the granulation tissue?

A

Granulation tissue is pink, highly vascular and very delicate (friable), at risk for injury/dehiscence and resistant to infection.

67
Q

-During inflammation what do macrophages release and what does it stimulate?

A

Changes in blood composition: During inflammation, macrophages release colony stimulating factors (CSF) that stimulate the formation of granulocytes and monocytes in the bone marrow.

68
Q

Changes in blood composition: During inflammation leads to what?

A

results in an increase in circulating WBCs (seen on CBC), known as leucocytosis, especially circulating neutrophils

69
Q

During inflammation what happens to transferrin production and what does it limit?

A

transferrin production is decreased, which could limit the availability of iron to replicating bacteria.

70
Q

What is released from the macrophages and lymphocytes and what does it stimulate________

A

IL-6 released from macrophages and lymphocytes increase protein synthesis in the liver including complement proteins and C-reactive protein, which activate monocyte

71
Q

What happens to the ESR during inflammation and it is due to what?

A

erythrocyte sedimentation rate (ESR) increases during inflammation due to the addition of plasma proteins

72
Q

Describe the secondary intention repair?

What happens to the inflammation and exudate in this kind?

A

secondary Intention – wounds with a wide or irregular margin that cannot be approximated – venous ulcers, pressure ulcers, trauma Large defect, gaping or erosion – much more inflammation and exudate present.

73
Q

Describe the tertiary intention?

A

Tertiary Intention – delayed primary intention – contaminated wound deliberately left open (dog bite) and is later surgically closed – results in a much larger scare

74
Q

Skeletal muscle metabolism:
The metabolic rate increases in the presence of what?
The increased catabolism that follows results in what?
Conically, this can cause profound ?

A

skeletal muscle metabolism: The metabolic rate is increased in the presence of pyrogens. The increased catabolism that follows results in accelerated protein break-down
Chronically, this can cause profound muscle wasting called cachexia.

75
Q

An acute inflammatory response involves

A

An acute inflammatory response involves
rapid onset,
localization of tissue damage
rapid resolution of tissue damage

76
Q

NSAIDS, ASA effective for treating afrible patients but what is the contradiction in children and teens?

A

NSAIDS, ASA effective but associated with Reye’s Syndrome in children and teens, generally avoided

77
Q

acetaminophen generally safe , effective, drug of choice, many different formulations (age related – associated with poisonings under ____

A

acetaminophen generally safe , effective, drug of choice, many different formulations (age related – associated with poisonings under 6 yoa

78
Q

Prolonged fever children →

•Prolonged fever adults →

A

Prolonged fever children → risk febrile seizure
•Prolonged fever adults → tissue breakdown, high energy requirement, reduced mentation, delirium, coma, especially older adults, rarely fata

79
Q

Assessing the Febrile Patient for Acetaminophen Administration what do we look out for

A 
Discomfort/pain, malaise, headache, body ache•
Confirm Febrile (temperature, route)
•Monitor for Dehydration (fluid intake, turgor)
•Hepatic function (labs, N/V, chills, abd pain)
•Renal function (labs, fluids and electrolytes, u/o)
80
Q

What are the major signs of adverse event when acetaminophen is administered?

A

Signs of adverse events – liver toxicity #1 (hepatic necrosis) with over-use, especially combined with alcohol, limit 4g/d, hidden in many combination OTC medications, no anti-inflammatory action,
- inhibits metabolism of the anticoagulant warfarin (Coumadin) increasing risk of bleeding

81
Q

Anti-Inflammatory Drugs

A

Most decrease the natural inflammatory response
•Most are non-specific to injury or allergy
•Few are specific to a disorder (e.g. gout)
•Recall: inflammatory response can be local or systemic.

82
Q

NSAIDS are used for what kind of inflammation?

A

mild to moderate inflammation

83
Q

Describe some of the functions of NSAIDS?

A

Analgesic, antipyretic, anti-inflammatory

•High safety margin, OTC

84
Q

COX II inhibition leads to ↓

COX I inhibition leads to

A
  • COX II inhibition: ↓inflammation, pain, fever

* COX I inhibition: GI Irritation, reduced renal perfusion, reduced platelet aggregation (ASA, 7-10d lifespan of pl

85
Q

COX I & COX II drugs are?

COX II only are?

A

COX I & COX II: ASA, ibuprofen, naproxen

•COX II only: Celecoxib (Celebrex

86
Q

NSAIDS:At higher doses, GI symptoms often intolerable, they can be reduced by?

A

GI symptoms reduced when taken with food or milk

87
Q

Abuse of NSAIDS can lead to what?

A

Abuse can lead to renal failure (acute tubular necrosis)

88
Q

What can happen to adults with ASA toxicity?

A

Adults, caution: tinnitus and hearing loss with ASA toxicity

89
Q

When is the optimal effect of NSAIDS?

A

Optimal effects in 1-3 weeks

90
Q

What are the contraindications for NSAIDS?

A
  • Avoid alcohol, liver impairment, renal impairment
  • Avoid with oral anticoagulants – increases action
  • ASA not for children – Reye’s Syndrome (liver/brain swell
91
Q

What effect does ASA have on ibuprofen?
What effect does NSAIDS have on diuretics?
Is acetaminophen an anti-inflammatory drug?
What is the risk when take with some herbal treatments?
Avoid if history of what with NSAID use

A

ASA reduces effect of ibuprofen•
May reduce effect of some diuretics (renal perfusion)
•Increased risk of bleeding with some herbal treatments
•Avoid if history of nasal polyps, angioedema, bronchospasm with NSAID use•
No overdose antidote
•NOTE: Acetaminophen is NOT an anti-inflammatory

92
Q

To cause an anti-inflammatory reaction prednisone (Glucocorticoids ) has to be used at what kind of dose and when we have low cortisol addison’s disease which of dose do we use?

A

Potent anti-inflammatory at higher-than-physiologic doses, including acute and severe inflammation (also used in low-cortisol conditions such as Addison’s disease, at normal physiologic levels/doses

93
Q

prednisone (Glucocorticoids ) is used for long term or short term use? and for how many days?

A

Short-term use (4-10d) r/t serious adverse effect

94
Q

What the half life of the prednisone?

Glucocorticoids is naturally produced by?

A

Half-life 3.5h, adrenal suppression lasts 30-36h – titrate off dose
Naturally produced by adrenal gland

95
Q

Glucocorticoids suppress the release of what?

Inhibit synthesis of __________ by COX II pathway

What does it do to the immune systeM

A

Suppress histamine release
–Inhibit synthesis of prostaglandins by COX II pathway
–Suppress some phagocytes, lymphocytes: immuno suppress

Pathophysiology (6 decks)

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