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Pathophysiology Final > Psoriasis > Flashcards

Psoriasis Flashcards

1
Q

true or false: psoriasis is an autoimmune disease

A

true -> involves activated T cells:
-some auto-Ag triggers the autoimmune system which activates inflammatory T-cells-> these produce mediators of inflammation
-these mediators then enhance/promote proliferation of keratinocytes-> white/scaly bumps (aka the keratinocytes are not allowed to develop properly (premature maturation))
(not known if the enticing Ag is self-derived or not)

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2
Q

true or false: psoriasis has an unpredictable course of disease

A

true

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3
Q

true or false: psoriasis is chronic

A

it is both chronic and relapsing condition

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4
Q

psoriasis

A
  • inflammatory and hyperplastic (increase in cell #/ proliferation) disease of skin
  • characterized by erythema (redness) and elevated scaly plaques
  • non-infectious
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5
Q

epidemiology of psoriasis

A

-global prevalence range between 0.1-8.5%

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6
Q

Age of Onset

A

mean age= 23-37
current theory: 2 distinct peaks with possible genetic associations
-early onset and late onset
-age and 2 peaks are both very important however there is usually some sort of event that starts it all off

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7
Q

early onset of psoriasis

A

16-22

  • more severe and extensive
  • more likely to have affected first-degree family member
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8
Q

late onset of psoriasis

A

57-60

  • milder form
  • affected first-degree family members nearly absent
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9
Q

Etiology/ Risk factors

A
  • most prevalent autoimmune (?) condition -> most likely an autoimmune disease
  • very rarely affects N or S America aboriginals and Japanese (genetics)
  • affects M=W
  • environmental contributors
  • can occur at any age, but 2 onset peaks: 20-30 y/o and 50-60 y/o
  • external predisposing factors
  • infections
  • other associated triggers
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10
Q

explain the reasoning between he possibility of genetics playing a role in psoriasis

A
  • again, very rarely affects N/S American aboriginals and Japanese
  • at least 7 loci related to psoriasis
  • family history ranges from 35-91% of cases
  • 80% concordance in monozygotic twins
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11
Q

What different factors leads to the inappropriate immune response

A

genetic predisposition +/- predisposing factor + precipitating trigger -> psoriasis development

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12
Q

locus

A

-specific location of a gene/ DNA sequence on a chromosome

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13
Q

what are some of the external predisposing factors

A

-obesity-> increases risk of inverse psoriasis
-alcohol consumption
-smoking-> increases risk of developing the disease and increases severity of the disease
-stress
-viral/bacterial infections (ex HIV)- can predispose to disease onset or trigger relapse
predisposing= increased risk of developing disease

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14
Q

What are some infections that can lead to psoriasis

A
  • streptococcal pharyngitis (strep throat) -> CAN CAUSE FLARE OF PSORIASIS OR TRIGGER ONSET
  • Candida albicans (thrush)
  • Human immunodeficiency virus (HIV) -> INCREASES SEVERITY OF PSORIASIS
  • Staphylococcal skin infections (boils) -> CAN CAUSE FLARE OF PSORIASIS
  • Viral upper respiratory infections-> CAN CAUSE FLARE OF PSORIASIS
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15
Q

What are some other associated triggers of psoriasis

A
  • certain drugs (lithium, NSAIDS, beta-blockers, antimalarials, interferons)
  • cold, dry weather (bad for all skin conditions, including psoriasis
  • skin trauma (cuts, bruises, burns, bumps, vaccinations, tattoos) aka “Koebner phenomenon”

-cycle of smoking/ stress/ and resultant headaches leads lots of smokers to take more NSAIDS and then this increases their risk of psoriasis even more

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16
Q

describe how certain dugs can lead to psoriasis

A

NSAIDS- most important to know it can trigger psoriasis

  • interferons- given to people with auto-immune disease which can lead to psoriasis-> important to realize that these autoimmune diseases are often related and can be seen together/ signal the start of another
  • this is the same with lithium (depression); beta-blockers (heart disease), etc
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17
Q

“Koebner Phenomenon”

A
  • occurs in almost half of those who already have psoriasis
  • occurs within 7 to 14 days of injury to the dermis layer
  • therefore it is important to treat these areas asap (very well and aggressively) especially if they are in the risk factor ages/ have other risk factors
  • wounds lead to the proliferation of keratinocytes
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18
Q

Linear injury (leading to psoriasis) can be caused by:

A
  • physical injury (insect bites, cuts, scrapes, tattoos)
  • chemical burns (chemical irritants)
  • excessive rubbing (chafing, shaving)
  • sunburns
  • allergic reactions (adhesives, contact dermatitis)
  • AKA ALL PHYSICAL TRAUMA TO SKIN
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19
Q

Physiological Roles of Skin

A
  • barrier to the elements and pathogens
  • barrier to prevent moisture loss
  • thermo-regulator protecting the body from excessive heat loss or overheating
  • protects from UV radiation
  • wound repair and regeneration (if there is a wound, we want it to quickly repair)
  • synthesizes Vitamin D (fat soluble- critical for absorption of Ca)
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20
Q

Three layers of the skin

A

1) epidermis
2) dermic
3) hypo-dermis

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21
Q

epidermis

A
  • physical barrier/ protects the skin from environment

- ranges in thickness from 0.4 to 1.55mm (depending on location on the body)

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22
Q

dermis

A

-layer of connective tissue containing blood vessels (middle)

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23
Q

hypo-dermis

A

-provides structural integrity to the skin (inner)

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24
Q

What layer do the keratinocytes move up into during psoriasis?

A

epidermis

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25
Q

What is the outer most strata within the epidermis

A

-there are multiple state within the epidermis, but the outer most is the STRATUM CORNEUM

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26
Q

how often does the epidermis renew itself

A
  • 4 to 6 weeks

- this is therefore the follow-up period (if treatment is working, it should be clearing up by this time)

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27
Q

Cells types within the epidermis

A
  • keratinocytes (80-85%)
  • melanocytes (5%)
  • langerhans cells (2-5%)
  • merkel cells (6-10%)
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28
Q

keratinocytes

A
  • produce keratin
  • move from the basal cell layer to surface (also called basal cells)
  • differentiate on transit from basal cell to stratum corneum (outer skin layer)—> corneocytes
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29
Q

melanocytes

A

pigment production

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30
Q

langerhans cells

A

detects, attacks, neutralizes, and eliminates foreign bodies

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31
Q

merkel cells

A

involved in the function of touch

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32
Q

keratin

A
  • produced by keratinocytes
  • key structural material making up the outer layer (integrity) of the human skin (stratum corneum)
  • it is also the key structural component of hair and nails
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33
Q

corneocytes

A

-are keratinocytes that have completed differentiation process and lose their nuclei and cytoplasmic organelles

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34
Q

what is the stratum corneum normally comprised of?

A

dead keratinocytes (corneocytes) that have migrated from lower stratum basale

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35
Q

Are the cellular events of psoriasis fully understood?

A

-no -> there are many different theories (there are some events that are consistent amongst all the theories-> that is what we will cover)

36
Q

Current hypothesis that psoriasis is a T-cell mediated autoimmune disease

A
  • unknown skin Ags stimulate immune response
  • leads to impaired differentiation and hyper-proliferation of keratinocytes
  • langerhans are the initial army
37
Q

T-cells/ T-lymphocytes

A

-WBCs (t-lymphocytes) protect the body from “invaders” called Ags
-normally found in small numbers in the skin
-activation of T-cells (Th1 and Th17 subtypes) via antigen presenting cells (APCs) results in the release of inflammatory mediators such as cytokines and chemokines that drive the IS induced response
-they mature in the thymus
Cell-mediated immunity
(cytotoxic T-cells= CD8)

38
Q

antigens

A

-molecule capable of inducing an immune response on the part of the host organism, though sometimes antigens can be part of the host itself

39
Q

T-cell infiltration

A
  • following a stimulus (Ag presentation) T cells (Th1 and Th17) and dendritic cells become activated
  • activation leads to release of cytokines, chemokines, and other mediators of inflammation
  • epidermis infiltrated by activated (++) T-cells
40
Q

What do the activated T-cells do to the keratinocytes

A

-the induce keratinocyte proliferation thereby reducing differentiation which promotes build up as skin plaques

41
Q

What cells are classified as dendritic antigen presenting cells

A
  • langerhans cells

- t-cells

42
Q

what happens once dendritic antigen presenting cells are activated?

A

-they release cytokines, cheekiness, and growth factors that trigger keratinocyte proliferation, altered differentiation, and angiogenic tissue response

43
Q

Abnormal keratinocyte proliferation

A
  • activated t-cells induce RAPID proliferation of keratinocytes (hyper-proliferation)
  • this results in faster maturation than normal (3-5 days vs >30days)= abnormal cell differentiation (i.e. cells don’t function properly
  • both result in sales and flakes (plaques) seen in psoriasis
  • plaques contain 30x more keratinocytes than healthy skin
44
Q

differentiation

A

how generic embryonic cells become specialized cells

45
Q

proliferation

A

rapid multiplication of parts or the increase in the number of something

46
Q

Psoriasis plaque formation as seen under a microscope

A

upper: disrupted stratum corneum
below: elongated “rete ridges”-strikingly and evenly elongated, and the overlying cornfield layer contains cells with retained nuclei (parakeratosis), a pattern that reflects the increased epidermal turnover

47
Q

Major Pathogenic Changes

A

1) abnormal keratinocyte proliferation and differentiation= epidermal thickening
2) abnormal angiogenesis (formation of new blood vessels) & increased capillary permeability= bright erythema
3) accumulation of keratinocytes and neutrophils in stratum corneum= silvery sporadic scales
4) elongated “rete ridges”

48
Q

what is the most common area of psoriasis?

A

at the joints

49
Q

parakeratosis

A
  • process of differentiation whereby keratinocytes retain their nuclei (normal in mucous membranes, abnormal in skin cell differentiation)
  • leads to silvery scaly skin plaques
50
Q

What are characteristic psoriatic changes

A

-thickened stratum corneum, elongated rete, and angiogenesis

51
Q

acanthosis

A
  • elongated rete ridges

- diffuse epidermal hyperplasia (thickening of the skin)

52
Q

Should a scented lotion be recommended to someone who has psoriasis?

A

no- it will sting

53
Q

symptoms of psoriasis

A 
(from most frequently to least frequently experienced):
-scaling
-itching
-skin redness
-tightness
-bleeding -> since the skin gets so tight, when you bend/move it will break and tear open and bleed
-burning sensation
-fatigue
(-other)
54
Q

types of psoriasis

A
  • chronic plaque (psoriasis vulgaris)
  • guttate
  • flexural
  • erythrodermic
  • pulstular
  • -local forms:
  • palmoplantar
  • scalp
  • nail
55
Q

guttate psoriasis

A

=”drop” psoriasis; “eruptive” psoriasis
-presents small lesions (red, tear drop shaped) on limbs and trunk or face
-most common in children and young adults
-can occur suddenly and may be caused by infections or stress
-less scale than plaque psoriasis
(for more look on slide 31)

56
Q

flexural psoriasis

A
  • “inverse” psoriasis
  • smooth, shiny, inflammed patches; thin, minimally scaly, raw, tender, itchy, well defined plaques
  • occurs on flexor (inner) surfaces (armpits, groin, under breasts, skin folds of butt)
  • can be mistaken for candida infections
57
Q

erythrodermic psoriasis

A
  • least common
  • may occur b/c of drug rxns, trauma, emotional stress or illness
  • red, inflammatory patches with sparse scaling with some peeling of skin, itching, and some pain
  • covers 75-90% of skin surface
  • can be confused with Steven Johnson’s syndrome (dug/infectious rxn)
  • can cause epidermis to separate from dermis
  • may evolve slowly from chronic plaque psoriasis or appear as eruptive phenomenon
  • may become febrile, hypo/hyperthermic, and dehydrated
  • complications: infections, malabsorption and anemia
  • often in association with Zumbusch pustular psoriasis
58
Q

pustular psoriasis

A
  • “vonZumbusch” psoriasis
  • primarily seen in adults
  • white pustules surrounded by red skin (blisters on non-infectious pus); clearly raised
  • NO EVIDENCE THAT INFECTION PLAYS A ROLE*
  • intense itching and burning
  • localized to hands and feet
  • uncommon
59
Q

Chronic plaque (psoriasis vulgaris)

A

vulgaris=common-> most common form (80-90%)

  • red/pink, scaly plaques at least 0.5cm in diameter
  • raised, well defined flat topped plaques with sharp borders (symmetrical)
  • typically covered with silvery white scales that constantly shed
  • arms, legs, elbows, knees, genitalia, lower back and buttocks
  • occurs on the extensor surfaces (opposite the joint areas- outer part of arm or front of leg)
60
Q

true or false: a person can only have 1 type of psoriasis throughout their lifetime

A

false

-generally a person will only have 1 type, but with certain triggers the patient may develop other types

61
Q

palmo-plantar psoriasis

A
  • can be hyperkeratotic or pustular
  • limited to palms of hands and soles of feet
  • can be difficult to treat
  • possibly aggravated by trauma
62
Q

scalp psoriasis

A
  • difficult to differentiate between dandruff and seborrhea
  • can occur alone or with other psoriasis types (occurs in about 50% of patients)
  • mild form appears as dry, fine scales whereas more severe forms appear as thick, crusted plaques
  • occurs along hairline of the scalp (forehead, back of neck and around ears)
63
Q

Nail psoriasis

A
  • may be present in patients with any type of psoriasis
  • can take several forms:
  • pitting
  • subungual hyperkeratosis
  • onycholysis
  • oil-drop sign
64
Q

pitting

A
  • discrete, well-circumscribed depressions on nail surface (1mm in diameter)
  • may involve only a few fingernails or majority
  • may also involve toenails, although to a lesser degree
65
Q

Subungual hyperkeratosis

A

-silvery white crustingunderu free edge of nail with some thickening of nail plate

66
Q

Onycholysis

A
  • nail separates from nail bed at free edge
  • produces white to yellow discoloration of distal nail plate
  • this discolouration may range from 1-2mm at the distal free edge to involvement of entire nail
67
Q

oil-drop sign

A
  • pink/red colour change on nail surface
  • well-demarcated, usually circular colour change
  • separate and distinct from onycholysis
68
Q

Co-morbid conditions associated with psoriasis

A

-inflammatory bowel disease (chrohn’s, ulcerative colitis)

-type 2 diabetes (increased riskk by 62%)
CDV disease (increased risk)-> stroke, atherosclerosis, heart attacks
-obesity
  • depression (significant)-> affects qol
  • some conditions may be caused by the treatment (currently looking at cancers)
69
Q

is psoriasis contagious

A

NO

-but it can affect a persons qol b/c many people thinks it does (also affects appearance)

70
Q

psoriatic arthritis

A
  • may appear 7-10 years after psoriasis appears on the skin
  • affects patients most often with nail and scalp psoriasis between ages 30-50
  • can affect up to 30% of indivs with psoriasis
  • joint deformity, red, warm, and inflamed joint
  • located at distal joints of fingers, wrists, ankles, knees, back and neck
  • often presents as RA- must rule out with RF factor and history
  • psoriatic arthritis is important to keep in mind if the pt is repeatedly getting psoriasis in the same area/bone/joint
71
Q

general goals of treatment

A
  • tailor management to individual and address both medical and psychological aspects
  • improve qol
  • achieve long-term remission and disease control
  • minimize drug toxicity
  • evaluate and monitor efficacy and suitability of individual treatments
  • remain flexible and respond to changing needs
  • its important to discuss feasible treatment goals and make sure patient understands chronicity and relapsing nature of disease
72
Q

if a patient is in remission does this mean they are disease free and can stop their therapy?

A

NO

73
Q

measures of treatment success

A

1) clearance- disease is controlled with no signs or symptoms
2) control- response to therapy that satisfies both the patient and the physician
* CONTROL IS USUALLY MOST REALISTIC GAL IN MOD-SEVERE PSORIASIS
3) remission- disease is controlled for an extended time period either partially or completely without treatment other than routine skin care

74
Q

measures of treatment failure

A

1) exacerbation- worsening of disease
2) flare- exacerbation while on therapy and the condition is different than the original disease (size of area covered, more severe, etc)
3) rebound- exacerbation of the condition due to treatment discontinuation (usually within 3 months of stopping treatment)

75
Q

general treatment measures to reduce risks

A

reduce/eliminate potential trigger factors (stress, smoking, alcohol, trauma, drugs (NSAIDS overuse), infections)

76
Q

general topical measures (for all plaque psoriasis

A

-should be consistently used +/- other topical/ systemic treatments
-emollients/moisturizers
keratolytics
helps reduce plaque burden
strengthen stratum corneum and epidermal barrier to limit kobeners phenomenon
*should be used during remissions to maintain symptom-free time

77
Q

emollients/ moisturizers

A
  • protective film to lessen dehyrdration
  • prefer creams or ointments to lotions (increased viscosity, lipid richness and “staying power”
  • hydration of stratum corneum= enhanced penetration of corticosteroid products
  • includes petrolatum, ointment/creams, bath oils, etc
78
Q

keratolytics

A
  • soften plaques by promoting cellular desquamation
  • also helps to promote corticosteroid penetration
  • stops proliferation of keratinocytes
  • ie urea, salicylic acid, lactic acid
79
Q

treatment options

A
  • topical agents (corticosteroids, vitamin D3 analoges) -> MOST commonly used
  • systemic therapy (traditional, biologics)-> moderate to severe conditions
  • phototherapy
  • dramatically slows growth of keratinocytes- deceases rapid proliferation*
  • most treatment includes combos*
80
Q

corticosteroids as treatment

A
  • topical agent; first line of treatment
  • anti-inflammatory
  • reduces production of cytokines, reduces scaling and itching
81
Q

vitamin D3 analogues as treatment

A
  • inhibits proliferation of keratinocytes and reduces inflammation
  • recommend vit D supplements (same as with MS)
82
Q

traditional systemic therapy

A

1) methotrexate- decreases rate of proliferation of keratinocytes
2) cyclosporine- inhibits activation of t-cells

83
Q

biologics systemic therapy

A

target blocking the immunological causes involved in t-cell activation

84
Q

phototherapy as treatment

A

-UVB light
-decreases cells involved in psoriasis pathogenesis
(psoralin is added to phototherapy to increase skin responsiveness)

85
Q

treatment planning

A
  • determine previous therapies (success/failure)
  • treatment should be in stepwise manner
  • therapies are often combined to attain desired outcomes
  • consider patient feasibility (i.e. phototherapy 3-5x/ week)
  • remember psychological aspect of illness- depression
86
Q

what is the step-wise manner of which psoriasis should be treated

A

1) water- hydrate skin
2) emollients (soften skin)
3) reduce risk factors
4) apply steroid ointment (that can now penetrate
5) if this doesn’t work (aka psoriasis is really aggressive) use oral interventions

Pathophysiology Final (10 decks)

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