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MP321 > week 5 > Flashcards

week 5 Flashcards

1
Q

functions of the skin

A
  1. A physical barrier to noxious agetns and the entry of pathogens. Not a barrier to everything though, for example lipophilic chemicals such as nicotine patches can pass through. Waterproof covering.
  2. Immunological barrier to the ingress of pathogenic organisms
  3. Assists in the retention of heat and regulation of body temperature
  4. Retains moisture and osmotic balance within the body
  5. Sensory organ for touch
  6. Excretion (sweat)
  7. Vitamin d production
  8. protection from sunlight
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2
Q

eccrine sweat glands

A

secrete directly onto skin surface. thermoregulation, salt excretion, antibactierals

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3
Q

apocrine sweat glands

A

bud fatty secretions off into enclosed areas like hair follicles. especially found in axilla and pubic areas

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4
Q

pilosebaceous unit

A

can change lipid content to modulated sweat evaporation to control thermoregulation, if there is obstruction of sebum secretion it may become infection, causing acne and other skin conditions.

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5
Q

what is the epidermis composed of ?

A

anucleuc dead cells (cornified)

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6
Q

order of skin outside to inside

A

dead anuclear ‘squamous’ layer -> granular layer with keratin in vacuoles -> spindle layer with early differentiation -> germinal layer

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7
Q

germinal layer

A

; stem cells replicate and constantly divide and renew. They then migrate upwards based on a potential difference of a very small charge. Also, melanocytes which produce pigment.

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8
Q

spindle layer cells

A

form tight junctions, anchored with adhesion proteins, cells glued into a sheet-like structure. Differentiate and rise up further. This layer contains large Langerhans cells specific to the skin.

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9
Q

granular layer

A

; further migration and differentiation into the granular layer where cells have vesicles containing keratin fibre. Gets its name from its granular appearance under a microscope. The keratin strengthens them making them tough.

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10
Q

squamous layer

A

essentially dead as anuclear. Tough because of keratin tightly joined. Tough waterproof barrier to the outside world and pathogens. Dead skin cells constantly shed off making dust.

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11
Q

glabrous

A

non hairy skin

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12
Q

meissner corpuscle

A

responds to light pressure

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13
Q

Pacinian corpuscle

A

responds to deeper pressure

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14
Q

merkel cells

A

respond to sustained light pressure

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15
Q

4 stages of wound healing

A

haemostasias, inflammation, proliferation, remodelling

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16
Q

process of haemostasias in wound healing

A

Fibrin is released by platelets. It is cross linked to make a plug to stop bleeding, helps prevent infections taking hold. Langerhan cells patrol the local area. Neutrophils are recruited and the release of histamine causes vasoconstriction.

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17
Q

process of inflammation in wound healing

A

Chemotactic factors are released into the bloodstream. Monocytes move in by diapedesis. More neutrophils are attracted. Mast cell activation. A cycle of inflammation. Combats opportunistic infections.

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18
Q

process of proliferation in wound healing

A

Helps to form a scab on top of the wound. Scab detaches as skin grows underneath. Endothelial cell proliferation promotes angiogenesis. Fibroblast proliferation fills the underlying connective tissue and the skin.

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19
Q

process of remodeling in wound healing

A

Skin repairs itself at the surface. Wound edges come together to form a contiguous barrier. Healing continues underneath. Myofibroblasts make pseudopods and migrate forward dragging cells behind them. Gradually this enables the ends to come together. Can take months to fully heal.

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20
Q

indirect factors affecting wound healing

A

Age, nutrition, diabetes, autoimmune diseases, obesity, genetic disease and immobility

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21
Q

direct factors affecting wound healing

A

Body site, infection, vascular supply, oxygenation, mechanical stress

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22
Q

biochemistry of tanning

A

UV light exposure induces double-stranded breaks in DNA in keratinocytes. This causes activation of p53 protein. Transcription of proopiomelanocortin (POMC) occurs. POMC is cleaved into 2 species. Β-endorphin acts as a local analgesic. Α-Melanocyte stimulating hormone (MSH) causes melanocytes to produce a pigment. Melanosomes transfer pigment to keratinocytes.

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23
Q

acne cause and treatment

A

a result of oily skin and the colonisation of block pilosebaceous units. Topical benzoyl peroxide is a treatment option, as well as tetracycline but should only be considered if symptoms are severe.

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24
Q

impetigo cause and treatment

A

a bacterial infection in the skin usually caused by S. aureus or S. pyogenes. It is very contagious. Non-bullous type pinhead pustules on red skin that erupt to give a yellow-brown crust after skin injury. Topical treatment with bacitracin or mupirocin.

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25
Q

ecthyma cause and treatment

A

progresses from untreated impetigo causing a deeper infection. Treat with warm compresses and antibiotics e.g., dicloxacillin.

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26
Q

folliculitis cause and treatment

A

infection of hair follicles by S. aureus portraying as red pustules that eventually rupture. Topical clindamycin and erythromycin on affected areas if necessary and anti-bacterial soap. Larger abscesses may need to be drained

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27
Q

necrotizing fasciitis cause and treatment

A

infection of subcutaneous tissue which can occur after surgery or trauma. Can be caused by S. pyogenes but often involves a mixture of bacteria. Fatal without proper treatment, surgical intervention is required along with parenteral antibiotics such as gentamycin and clindamycin.

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28
Q

what is the most common infectious fungus

A

Trichopyton

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29
Q

5 forms of tinea

A
  1. Pedis (athletes foot)
  2. Cruris (jock itch)
  3. Capitis (cradle cap)
  4. Corporis (ringworm)
  5. Unguium (infection of nails)
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30
Q

treatment of tinea

A

terbinafine, clotrimazole or econazole

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31
Q

Tinea versicolor cause and treatment

A

caused by the widespread yeast malassezia furfur, more common in hot climates. Results in lightened pigmentation of the skin in upper body and limbs. Treatment is selenium sulphide shampoo or topical antifungal agents.

32
Q

Candidiasis cause and treatment

A

caused by yeast candida albicans which is part of the normal microbiota. Can be associated with poor oral hygiene and dentures. Treat with topical antifungals, plus possibility of systemic antifungals such as ketoconazole, fluconazole.

33
Q

viral infections of the skin

A

herpes simplex type 1, coldsores, herpes varicella zoster, warts

34
Q

herpes simplex type 1 and coldsore cause and treatment

A

virus resides in dorsal ganglia until reactivated. Acyclovir is the preferred treatment.

35
Q

herpes varicella zoster cause and treatment

A

during chicken pox the virus travels to sensory ganglia where it remains for life. Usually resolves with rest and analgesics but acyclovir can be used, especially if virus is disseminated.

36
Q

warts cause

A

benign skin tumours caused by infection with the human papilloma virus (HPV) have dark necrotized blood vessels at the heart of the wart. Many strains of HPV, but most are benign.

37
Q

parasitic infections of the skin

A

scabies and headlice

38
Q

how is tuberculosis spread

A

when a person inhales droplets from a cough or sneeze by an infected person.

39
Q

main causes of antimicrobial resistance

A
  • Poor compliance
  • Inadequate treatment and diagnosis
  • Poor healthcare infrastructure
  • Lack of education
  • Global location causes severe logistical issues
40
Q

why is tuberculosis hard and difficult to treat?

A

the disease is able to cause many complex symptoms. M. tuberculosis has a very complex cell wall. After treatment, a small percentage of bacteria many remain in a dormant state in macrophage. These can become reactivated many years later.

41
Q

how many phases of tuberculosis treatment?

A

2

42
Q

what 4 drugs are given in the initial phase of TB treatment?

A

Rifater, Isoniazid, Rifampicin and Pyranzanimide

43
Q

how long is the initial TB treatment phase carried out

A

Duration of 2 months but can be extended until sensitivity testing is completed. Its purpose is to reduce the bacterial population as rapidly as possible, preventing resistance. Helps to reduce the chance of reactivation (PZA).

44
Q

why is PZA only active during the initial phase

A

PZA is only active during initial phase due to host immune response lowering the pH in macrophages

45
Q

what drugs used in continuation phase?

A

combination of RIF (Rifampicin) and INH (Isoniazid), Rifinah or Rimactazid

46
Q

bacteriostatic

A

inhibit growing bacteria

47
Q

bactericidal

A

kill bacteria outright

48
Q

discuss PZA’s bactericidal and bacteriostatic properties

A

PZA is bactericidal against TB at low pH but bacteriostatic against growing bacteria.

49
Q

bactericidal drugs are __ effective at reducing bacterial populations

A

more

50
Q

first line drugs in treating TB

A

superior efficacy with acceptable toxicity. These include; Isoniazid, Rifampicin, Pyrazinamide, Ethambutol, Streptomycin.

51
Q

second line drugs in treating TB

A

have less efficacy and/or worse side effects. These include; p-Amino Salicyclic acid, Fluoroquinolones, capreomycin, kanamycin, amikacin, ethonamide, prothionamide, cycloserine.

52
Q

how does rifampicin work?

A

prevents protein synthesis binding to DNA-dependent RNA polymerase b-subunit. It has broad spectrum bactericidal activity, helps sterilize “persistors” and active mycobacteria

53
Q

how does Isoniaid work?

A

isonicotinic acid hydrazide. This drug targets the ketoenoyl-reductase enzyme InhA in cell wall mycolic acid biosynthesis. It is a prodrug – activated to a binding complex with InhA

54
Q

how does pyrazinamide work?

A

a bactericidal against “persisting” slow growing mycobacteria. Mode of action is unclear, but it is a prodrug requiring activation to the acid form pyrizinoic acid (POA). Requires low pH macrophage environment (intracellular.)

55
Q

tissue schizonticides

A

inhibit the growth of pre-erythrocytic stages of the parasite in liver. sometimes called casual prophylactices.

56
Q

hypnozoitocides

A

are only used to eradicate the dormant liver stage of vivax infections – primaquine. Disrupts the REDOX process in the pentose-phosphate pathway.

57
Q

Blood schizonticides

A

act rapidly and only on the erythrocytic stage of the infection. Some used prophylactically but mainly for treating established malarial infections. Prevent hemozoin formation leading to cell death by binding to heme in the parasite.

58
Q

chlamydia trachomatis gram negative or gram positive

A

negative

59
Q

does chlamydia have a peptidoglycan layer in the cell wall?

A

no

60
Q

discuss the two forms of chlamydia

A

1) elementary body (infective form) - infect columnar epithelial cells
2) reticulate body (non-infectious form)

61
Q

diagnosis of chlamydia

A

urethral/cervical swab/rectal swab, midstream urine put through a sucrose phosphate (2SP) transport medium then cell lines treated with cycloheximide or nuclei acid amplification test.

62
Q

treatment of chlamydia

A

used to be 1g azithromycin but changed to 100mg for seven days of doxycycline. Alternative options include erythromycin 500mg for 10-14 fays. 200mg BD for 7 days of ofloxacin can be used in pregnancy.

63
Q

is Neisseria gonorrhoeae gram negative or positive?

A

negative

64
Q

male and female symptoms of gonorrhea

A

male; mucopurulent urethritis and dysuria
female; vaginal discharge, dysuria, dyspareunia and mild lower abdominal pain.

65
Q

stages of neisseria infection

A

1) Deposited on mucous membranes during sexual activity
2) Attachment of bacteria using fimbriae to microvillus on non-ciliated columnar epithelial cells.
3) Bacteria gain cellular entry by parasite-directed endocytosis.
4) Bacteria transported to basement membrane and released by exocytosis where they multiply in the subepithelial tissue. This results in various inflammatory cells being recruited and various factors released
5) Cellular damage and inflammatory exudate accumulates in lumen

66
Q

treatment of n.gonorrhea

A

uncomplicated infections 1g ceftriaxone IM as a single dose if susceptibility unknown. 500mg ciprofloxacin as a single dose if susceptibility known. Azithromycin 2g as a single dose. Gentamicin 240mg intramuscularly as a single dose plus azithromycin 2g orally.

67
Q

anogentital warts

A

causes by human papilloma viruses. spread skin to skin contact or indirect contract presenting on genetals, anus and groin region. If less than 4cm2 skin surface involved, then home treatment with topical podophyllotoxin. Four treatment cycles consist of BD application for 3 days followed by 4 days rest. Imiquimod for refractory cases. Alternatives include cryotherapy or electrocautery

68
Q

anogential herpes

A

caused by HSV1 or 2. Transmission by skin-to-skin contact or indirect. 80% may experience no symptoms or very mild symptoms. Incubation period 4-14 days. Diagnosis by sampling blister – PCR. Treatment with 400mg acyclovir TDS for 5 days HSV-1 50% of at least one recurrence. HSV-2 80% chance of at least one recurrence

69
Q

methods used for sterilization

A

heat (steam and dry heat)
radiation (g-rays, high energy electrons)
gaseous (formaldehyde)
filtration (subsequent aseptic processing)

70
Q

parenteral products should be ___

A

be pyrogen free, practically-free from particles, physiological compatible in terms of pH, tonicity

71
Q

how do moist heat and dry heat work to sterilize

A

moist - denatures cell wall and cytoplasmic constituetns and/or hydrolysis
dry heat - denatures by oxidation

72
Q

how is heat transferred in dry heat sterlisation

A

conduction, convection and radiation

73
Q

what radiation is used in radiation sterilization

A

gamma-rays and high energy electron beams

74
Q

what is ethylene oxide commonly mixed with to reduce risk of explosion?

A

an inert gas such as carbon dioxide or dicholorodifluoromethane

75
Q

what are filters made of?

A

polymers such as cellulose esters, PTFE, Nylon and polysulfone

76
Q

finding time to steady state

A

5 x t1/2

MP321 (5 decks)

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