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NSC2500 - Pharm & Physiology > Pain and Infection > Flashcards

Pain and Infection Flashcards

1
Q

What are the parts of the body the that are generally considered micro-organism free?

A
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2
Q

What is considered normal microbiota on the human body? (URT, Stomach, Large Intestine, Vagina, Skin, LTR, Mouth)

A

Upper Respiratory Tract: Stapphylococcus pneumonia
Stomach: Yeasts such as Candida app.
Large Intestine: Escherichia coli
Vagina: Candida albicans
Skin: Staphylococcus epidermidis
LTR: No normal microbiota
Mouth: Step spp.

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3
Q

Define opportunistic pathogens

A

Microorganisms that do not normally cause disease but may do so if moved to a new site (wound or burn) or in the immunocompromised.

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4
Q

What are health-care infections compared to non-health care infections

A

Health care: occurs at least 48 hours after admission or specific time after discharge.
Causative agents: Bacteria (MOST), then fungal then viruses.
Site of infection usually include: urinary tract, surgical wounds, LRT, skin , blood

Non-health care: Can be from endogenous infection or other causative agents.

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5
Q

Define Bacteria (prokaryote)

A

Very simple cells that are unicellular with no nuclear membrane, mitochondria, Golgi bodies or endoplasmic reticulum, reproduces by binary fission

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6
Q

Define Archera

A

Lack nuclei, have unique membrane, able to live in extreme environments.

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7
Q

Define Eukaryote

A

Complex cells with membrane bound nucleus

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8
Q

Define virus

A

Not a cell but a particle, genetic material DNA or RNA (NOT BOTH), obligate intracellular parasite.

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9
Q

What parts of a healthy person are usually Microbe-free?

A

Middle and inner ear, sinuses, muscles, glands, organs, circulatory system, brain and spinal cord, ovaries and testes, blood, saliva, urine in kidneys and in bladder, cerebrospinal fluid.

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10
Q

What parts of the body are colonised harmlessly by a mix of microbes?

A

Skin and mucous membrane.

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11
Q

What is the difference between prokaryotic and eukaryotic cells?

A

Prokaryotic: Unicellular, very simple structure, genetic material not enclosed, no internal organelles.

Eukaryotic: Unicellular (protozoa, yeasts) or multicellular (fundi, algae)
genetic material enclose.

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12
Q

What are the pathogenic microbes?

A

Bacteria, fungi, protists/protozoa,

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13
Q

What are the shapes of the bacterial cells (Morphology)

A

Coccus (Spherical), Bacillus (Rod Shaped), Spirillum (Spiral Forms)

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14
Q

how does bacteria move?

A

Flagella

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15
Q

What are the growth requirements for microorganism to survive?

A

Oxygen, Moisture, Temperature, pH, Nutrients.

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16
Q

To cause a disease a microbe must do what?

A

Gain entry to host, attach to host tissue, multiply.

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17
Q

What are the two types of bacterial toxins?

A

Endotoxins, Exotoxins

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18
Q

What is coagulase?

A

Forming plasma clot

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19
Q

What is streptokinase?

A

Dissolves clots

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20
Q

What is Scaled Skin Syndrome or SSS?

A

Staphylococcal Scaled Skin Syndrome (SSSS) caused by strains of S. aureus that produce epidermolytic exotoxins, exofoliatins break down the desmosomes and skin layers come apart.
Outer layers of skin shed exposing red inner layer
septicaemia may result

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21
Q

What is Staphylococcus aureus ?

A

is predominantly associated with skin infections (boils and impetigo) can also cause pneumonia, sinusitis, meningitis, osteomyelitis, endocarditis etc.

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22
Q

What is MRSA?

A

Methicillin Resistant Staphylococcus aureus (MRSA) is a major issue in hospitals especially in bone infections (osteomyelitis) and surgical sites.
Surgeries can provide entry points
Treatment: Vancomycin is the drug of choice for MRSA.

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23
Q

What is cellulitis?

A

acute bacterial infection usually superficial but can spread to subcutaneous tissues and blood (via the lymphatic system)
Infected tissues become hot, painful and swollen.
Over, chills and lymph node enlargement can occur

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24
Q

What causes cellulitis?

A

Streptococcus Progenies or Staphylococcus sp.

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25
Q

Explain the urogenital tract in bio biology include how infections enter the body and defences.

A

Predominantly sexually transmitted diseases/infections
Enter the skin or mucosa of penis, external genitalia, vagina, cervix, urethra.
Defences include normal microbiota, pH, sphincter’s as mechanical barriers and mucus.

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26
Q

What are the entries for the respiratory tract? and examples

A

Upper and lower both have moist epithelia, Upper has mucus, cilia and normal microbiota, lower has alveolar macrophages and mucus in the bronchioles.
Examples: Streptococcal sore throat, meningitis, diphtheria, whooping cough, influenza, measles, mumps, rubella, common cold, fungi causing pneumonia.

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27
Q

What are RTIs? Explain.

A

Respiratory Tract infections.
Many microbial pathogens tend to be associated with specific sites on the host. Their incidence may also be influenced by Patient age, underlying illness, length of stay if in hospital, history of smoking, immunocompromised.

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28
Q

What are the two types RTIs?

A

Upper respiratory tract, lower respiratory tract.

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29
Q

Explain middle ear infections

A

Acute otitis media (AOM)
Streptococcus pneumonia, respiratory syncytial virus (RSV)
predominantly in small children esp 6-18 month olds.

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30
Q

What is acute otitis media?

A

Earache, fever, vomiting, lethargy.
Diagnosis will require an examination of ear.
Antibiotic treatment only reduces pain within 24 hours in about 5% of patients
most cases resolve spontaneously
complications can result in tearing of the tympanic membrane

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31
Q

What is bacteria pharyngitis ?

A

AKA Strep throat
Streptococcus pyogenes, gram positive pathogen able to cause many disease
Common in children 5 - 15 years
Rapid onset with no cough or mucus associated with cold
Treatment is necessary - can lead to rheumatic fever or rheumatic heart disease.

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32
Q

What are the symptoms of epiglottis?

A

Drooling, Difficulty swallowing, Difficulty in breathing, Noisy inhalation (Stridor), Child can’t breathe unless sitting up, poor ventilation leads to increased blood C02 leading to lethargy and confusion, Rapid inflammation can lead to airway obstruction, inability to breathe, death

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33
Q

What can an infection of epiglottis mean?

A

May lead to swelling and blockage of windpipe, medical emergency with rapid onset of complete obstruction in 3-6 hours for sever cases.

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34
Q

What is the treatment for Epiglottis? Both preventative and therapeutic

A

Preventative: Vaccination (Haemophilus influenzae, Streptococcus pneumoniae)

Therapeutic: Endotracheal tube, tracheostomy, antibiotics

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35
Q

What are some bacterial infections in the LRT?

A

Whooping Cough, Lung Abscesses, Tuberculosis, Pneumonia.

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36
Q

What is Whooping Cough?

A

Pertussis, Infective agent Bordetella pertussis, droplet transmission, if unvaccinated can result in sever complications.

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37
Q

Explain Sepsis

A

is the body’s response to bacterial infection.
Risk factors include trauma, burns, weakened immune systems, chronic illness, wound infections, invasive medical procedures.

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38
Q

What are exogenous sources of infection in a health care facility?

A

Other patients with infections, staff with infections, normal microbiota of other patients, Beds, sheets and sinks, hospital strains colonising other patients and staff, medical equipments, disinfectants, medications.

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39
Q

What are the endogenous sources of infection in a health care facility?

A

Patients own normal microbiota, hospital organism colonising patients, primary infection.

40
Q

What are the different modes of transmission and examples?

A

Contact (Direct, Faecal/ora;, Droplet, indirect contact), Air (Droplet or dust particles etc), Vehicle (Contaminated food, water, drugs, blood or body fluids), Vector (Mosquitoes, flies, rats or other vermin).

41
Q

What is a susceptible host?

A

Individuals degree of resistance to a pathogen, susceptible to the violence and number of miccorganisms producing infection.

42
Q

How to break the chain of transmission?

A

Infection control

43
Q

What is a live vaccine?

A

Reversion, organism may mutate back to virulent form and cause and full blown disease in people that have an immunocompromised immune system

44
Q

What is a inert vaccine?

A

Fewer side effects, lower immunogenicity

45
Q

What is an antimicrobial?

A

Chemotherapy (Introduction of specific chemical compound/drug to the body to elicit a desired response preferably without causing harm)
Antibiotic/antimicrobial - Compound that in small amounts exhibits microbiostatic or microbicidal properties.
Microbiostatic - Inhibits reproduction
Mircobiocidal - Kills microbes.

46
Q

What is antimicrobial therapy?

A

Kill or inhibit growth of microorganism or produced toxin (Antibacterial, fungal, viral, protozoal, toxin)

47
Q

What is selective toxicity?

A

Kill or inhibit disease causing microorganism, with little or no damage to host cell.

48
Q

What causes a disruption cell wall synthesis?

A

B-lactams, Natural penicillin, semi-synthetic penicillin, cephalosporins, Carbapenems, Monobactams , glycopeptides.

49
Q

What disrupts the protein synthesis ?

A

Aminoglycosides, tetracyclines, Macrolides, Oxazolidinones, streptogramins and lincosamides, chloramphenicol, fusidic acid.

50
Q

What causes disruption to nucleic acid synthesis?

A

Sulfonamides, Quinolones, Rifamycins, Nitroimidazoles.

51
Q

What inhibits the cell membrane function?

A

Polymyxins

52
Q

What are anti fungal drugs? With description

A

Azoles - Inhibit synthesis of sterols by inhibiting enzymes (have greater affinity for fungal enzymes than human enzymes)
Polyenes - Combine with a major sterol component inc ell membrane -> leakage of cell contents -> cell death.

53
Q

What is antimicrobial resistance?

A

Determines the choice of drug dictated by several factors. Site of infection, infecting organism, route of admission, antimicrobial sensitivity.

54
Q

Define Pain threshold

A

Minimum intensity when perceive stimulus as painful eg pressure or pain

55
Q

Define Pain Tolerance

A

Maximum level that can be tolerated

56
Q

Explain the gate control theory of pain

A

Top panel: No input, the inhibitory neuron’s prevents signals being sent to the brain
Middle Panel: More large fibre stimulation so both inhibitory and protection neuron’s prevents signals going to the brain
Bottom Panel: More small fibre stimulation so interneuron is inactivated and so a PAIN signal is sent to the brain

57
Q

Explain the classification of somatic and visceral pain states

A

Somatic: Localised; injury/disease of skin, musculoskeletal/joints, tissue stimulation to lead to binding of receptors.
Visceral: No clear loci, internal organ dysfunction (eq myocardial ischaemia, renal calculi, functional disease)

58
Q

Explain the classification of neuropathic, nociceptive and mixed pain, pain states

A

Neuropathic: Somatosensory system affected (post-herpetic neuralgia)
Nociceptive: Injury of skin, muscle, tendons, ligaments, bones, joints
Mixed: eg Cancer - tumour and/or treatment sequelae (eg surgery, chemotherapy, radiation)

59
Q

What are the mechanisms of pain and define each

A

Activation- of peripheral nociceptors stimuli (Mechanical, Thermal, Chemical, Polymodal) Transduction and transmission
(A delta Fibres, C fibres) and modulation (Attenuation of signal by intrinsic inhibitory pathways in the peripheral and central nervous systems before perceived as unpleasant)

60
Q

What causes of range of pain experienced?

A

Hyperalgesia (Increased pain from normally painful stimuli)
Allodynia (Pain experienced from normally non-painful stimuli)
Implicated (Neurotrophines, Postagladnins, bradykins, cytokines)

61
Q

What are nociceptors?

A

Sensory receptors, free nerve endings located in the skin, muscle, joints, bone, viscera. Categorised by responses to mechanical, thermal, chemical stimuli.

62
Q

What are thermal receptor potential (TRP) channels?

A

Ion channels with several members involved in nociception etc

63
Q

Chemical Mediators of Pain?

A

Cytokines, Substance P, BradyKinin, Prostaglandins, Capsaicin, 5-Hydoxytryptamine, Glutamate, Gamma-aminobutyric acid.

64
Q

What is analgesia?

A

The reduction or control of pain

65
Q

What are the opioid receptors?

A

Are in reality the endogenous receptors for the endogenous opioid peptides.
Are all G coupled receptors, widely distributed in central nervous system.
Drugs may act as agonists at all receptors, or agonists at some and antagonists at other receptors.

66
Q

What do opioids and GPCRs inhibit?

A

Adenylate cyclase.

67
Q

What are the useful side effects of opioid drugs?

A

Depress cough reflex. GIT motility reduction.

68
Q

What are the opioid drug classes? And examples

A

Full agonists (Morphine, Herion, Codeine, Pethidine)
Partial/Mixed Agonists (Combination of agonist and antagonist on different receptors eg pentazocine, buprenorphine),
Antagonists (Little/no effect on its own blocks opiod receptors eg naloxone, naltrexone

69
Q

What is inflammation?

A

The sum of the host’s defences against an infectious or noxious stimuli (Primary defence Mechanisms)
Two phases (Acute/Innate- seconds to hours , Adaptive - slow days to weeks).
Sometimes these responses can also damage ‘self’ tissue.

70
Q

What are the characteristic of inflammation? An explain each

A

Heat/redness - Localised vasodilation due to increase in inflammatory mediators acting on local circulation
Localised oedema (swelling) - Leakage of plasma fluid, proteins and immune cell to site due to inflammatory mediators cause contraction of endothelial cells -> opening of tight junctions
Pain- Firing of sensory nerve fibre due to mechanical damage to nerves or action of inflammatory mediators.
Loss of function - Guarding of movement (temporary); Extensive tissue damage as seen in chronic inflammatory conditions.

71
Q

what are inflammatory mediators?

A

Intracellular chemical messenger released by inflammatory cells (mainly WBC and platelets) to orchestrate and regulate inflammatory process.

72
Q

What are some of the major inflammatory mediators?

A

Eicosaniods, Platlet activating factor, Histamine, Cytokines

73
Q

What are the 5 broad groups of anti-inflammatory drugs?

A
  1. Inhibit the cycle-oxygenase (COX) enzymes (NSAIDS and - coxibs)
  2. Modify disease process (disease modifying anti-rheumatic drugs for DMARDS) and including other immunosuppressants
  3. Belong to the glucorticoid Family
  4. Are anti-cytokine and other biological agents
  5. Others.. including antihististamines and gout medications.
74
Q

Explain glucocorticoids (corticosteroids).

A

Produced from cholesterol in adrenal cortex and released as needed
Power to anti-inflammatory and immunosuppressive actions
Mechanism of action is not well understood.

75
Q

What is the therapeutic use of glucocorticoids?

A

Asthma- Decreased inflammation in airways
Rheumatoid Arthiritis (RA)- Decrease immune system destruction of joints (require long term therapy)
Skin diseases - decrease inflammation causing dermatitis, psoriasis, eczema
Ocular Disease: Inflammatory eye Disease
Spinal Trauma- Reduce inflammation and irreversible destruction of nervous tissue

76
Q

What are the side effects of glucocorticoids?

A

immunosuppression, Suppression of pituitary-adrenal axis, Inhibition of growth/cell division. osteoporosis, Cushing syndrome, Secondary Diabetes.

77
Q

What are some commonly used anti-inflammatory steroids?

A

Hydrocortisone, Prednisone, Dexamethasone.

78
Q

What is Local anaesthetics?

A

Prevent of relieve pain by interrupting nerve conduction.
Mechanism is the reversible blocking of Na+ channels to stop or decrease the intuition and propagation of action potentials.

79
Q

What is LA used for? and its administration routes

A

Minor Surgery, Dental Surgery, Obstetrics.
Intradermal, Subcut, Intrathecal (into subarachnoid space ie into CSF)
Topical

80
Q

What are some other modifiers of Na+ channels?

A

Tetrodotoxin (TTX) - Found in puffer fish
Certain species of scorpions, spiders, Marine cone shells, poison arrow frogs.

81
Q

What is General Anaesthetic?

A

Rapid and pleasant induction/ recovery, a wide safety margin, low toxicity, No cardiovascular or respiratory depression.

82
Q

What are the different stages of anaesthesia?

A

Stage One (Analgesia), Stage Two ( Excitement), Stage three (Surgical Anaesthesia), Stage IV (Medullary Paralysis)

Stage two is very dangerous - try to avoid this stage.

83
Q

What are the general actions of GA? (Nervous system, Cardiovascular and respiratory systems)

A

The effects on the nervous system - Inhibit synaptic transmission by reduction of transmitter release, inhibition of action of transmitter, reduction of excitability of postsynaptic cells.

Cardiovascular and Respiratory: All anaethestics lower excitability and cardiac contractibility, some agents can increase the sympathetic discharge, some agents can cause arrhythmias (Halothane), all anaesthetics (expect N2o and ketamine) depress respiration.

84
Q

What are the different types of GA drugs that can be inhaled?

A

Isoflurane (Widely used, few adverse effects), Desflurane (Used in obsessive patients in bariatric and day surgery, may cause respiratory tract irritation - coughing, bronchospasm), Halothane (Used had declined due to accumulation of toxic metabolites), Nitrous Oxide (N20, Widely use odourless gas, low potency, rapid induction and recovery , not toxic unless used for prolonged exposures.

85
Q

Briefly explain intravenous GA

A

Rapid Acting, unconsciousness unless then 20 secs, Stage 1 to Stage 3 quickly to avoid Stage 2.
Normally used induction of anaesthesia followed by inhaled agents
Mechanism of Action verifies between GABA or Glutamate (NMDA) receptors modules.

86
Q

Drugs used of IV GA

A

Propofol, Thiopental, Ketamine

87
Q

what is the difference between inflammatory and non-inflammatory joint disease?

A

Absence of synovial membrane inflammation, lack of systemic signs and symptoms, normal synovial fluid analysis.

88
Q

What is inflammatory joint disease?

A

Commonly called arthritis, inflammatory damage or destruction in synovial membrane or articular cartilage and by systemic signs of inflammation

89
Q

What is osteoarthritis (OA)?

A

Degeneration and loss of articular cartilage, sclerosis of bone underneath cartilage and formation of bone spurs.
Also called degenerative joint disease.
Incidence increases with age, primary disease is idiopathic.

90
Q

What are some signs and symptoms of OA?

A

Mild Discomfort -> Disability, Joint Pain, Joint Stiffness, Joint Effusion

91
Q

What drugs are given for mild-moderate pain in OA?

A

NSAIDs, combination of Paracetamol/opiod.

92
Q

What drugs are given to someone with OA for local inflammation?

A

Corticosteroid

93
Q

What drugs are given for moderate - severe pain involved with OA?

A

NSAIDs (Ibuprofen; Cox 2 inhibitors (celecoxib)

94
Q

What is gout and hyperuricaemia?

A

Metabolic disorder that disrupts the body’s control of uric acid production or excretion. Occurs when the uric acid concentration increases to high enough levels to crystallise.

95
Q

What is the treatment of gout and hyeruricaemia?

A

NSAID or alternative
A Glucocorticoids

NSC2500 - Pharm & Physiology (9 decks)

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