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Biomedicine I > 10. Integumentary and Lymphatic Pathologies > Flashcards

10. Integumentary and Lymphatic Pathologies Flashcards

1
Q

Papule

A

A small, firm, elevated lesion
•Circumscribed, solid elevation of skin with no visible fluid.
•Can be either brown, purple, pink or red in colour.
•Can see “maculopapular rash” like in measles.

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2
Q

Pustule

A

Small, elevated, erythematous lesion containing pus
•Purulent material usually consists of necrotic inflammatory cells.
•These can be white or red.

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3
Q

Macule

A

Small, flat, circumscribed lesion of a different colour to normal skin
•A change in surface colour, without elevation or depression (non-palpable).

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4
Q

Nodule

A
  • Morphologically similar to a papule, but is bigger & deeper e.g. Rheumatoid Arthritis.
  • May be filled withinflamed tissue or fluid.
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5
Q

Crust

A
  • Collection of dried bodyfluid (blood plasma & exudate) & dead skin cells (ascab).
  • Exudate: any fluid that filters from the blood.
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6
Q

Lichenification

A

Thick, dry, rough plaques of thickened skin
•Visible thickeningof epidermis, with accentuated skin markings/pronounced lines.
•“Bark like” appearance.
•The hallmark of chronic eczema/dermatitis or excessive scratching.

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7
Q

Erosion

A

Shallow, moist cavity in the epidermis
•Wearing away with loss of superficial epidermis (from chemicals, friction or pressure).
•‘Ulcer’ in diabetes.

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8
Q

Keloid

A

Raised, irregular mass of collagen due to scar tissue formation
•Abnormal scar tissue that grows beyond the skin boundary.
•Strong genetic links. Vaccination site, scratching, burns.

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9
Q

Comedone (Acne)

A

Blackheads, whiteheads or red bumps due to excess sebum, keratin and debris forming a plug in the sebaceous duct of a hair follicle.
•Hormones such as testosterone can cause more and thicker oil secretions that block pores.
•Open comedo: Blackhead (acne vulgaris) -if oil is open to air it will oxidise> turns dark
•Closed comedo: Whitehead
If skin has grown over oily material it remains white.

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10
Q

Eczema/Dermatitis

A
  • The terms “eczema” and “dermatitis” are interchangeable.

* A very common chronic, pruritic, inflammatory skin condition.

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11
Q

Eczemea/Dermatitis

A
  • Flaky, dry, oedematous.

* Erythematous, pruritic (itchy), crusty, weepy lesions mostly on flexor surfaces of joints.

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12
Q

Eczema/Dermatitis: Complications

A

• Secondary bacterial infections.

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13
Q

Contact Dermatitis

A
  • An acute inflammation of the skin caused by direct contact with an agent.
  • Divided into Irritant (80%) and Allergen (20%) contact dermatitis:
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14
Q

Irritant contact dermatitis (ICD)

A
  • Non-specific inflammatory reaction to a substance contacting skin.
  • Abrasive chemicals can corrode the epidermis causing cutaneous ulceration.
  • Hands are vulnerable due to frequent occupational exposure to soap (that can abrade the lipids in skin).
  • A type called phototoxic dermatitis in which topical (e.g. perfumes) or ingested irritants are activated by exposure to UV rays.
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15
Q

Allergen Contact Dermatitis (ACD)

A
  • A Type IV delayed hypersensitivity reaction.
  • Sensitisation occurs on first exposure.
  • Pruritic, erythematous rash develops at the site on subsequent exposures.
  • Can occur with various chemicals, rubber, plants, metals.
  • Multiple allergens cause ACD and cross-sensitisation among agents is common.
  • A variant called photoallergic contact dermatitis in which a substance becomes allergenic only after it undergoes structural change triggered by UV light. e.g. sunscreens.
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16
Q

Contact Dermatitis: Signs and Symptoms

A
  • Location of symptoms can give a clue to the irritant/allergen.
  • Pruritic rash, often burning, stinging, eroded, blistered skin.
  • Irritant contact dermatitis = ulceration, burning, prickling, soreness and quicker onset of symptoms.
  • Allergen contact dermatitis= pruritis is significant, but slower onset of symptoms.
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17
Q

Contact Dermatitis: Treatment

A

Remove allergen. Steroids & anti-histamines

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18
Q

Atopic Dermatitis/Eczema

A
  • An immune-mediated inflammation of the skin due to the interaction between genetic & environmental factors.
  • Pruritus is the primary symptom.
  • Usually occurs in infancy/childhood.
  • Primarily affects children in urban areas or developed countries, and prevalence has increased over the last 30 years
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19
Q

Atopic Dermatitis/Eczema: Allergens

A
  • Foods (milk, eggs, soy, wheat, peanuts, fish).

* Airborne (dust mites, moulds, pollen).

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20
Q

Atopic Dermatitis/Eczema: Causes

A
  • Family history of atopic disorders in 2/3 of cases: asthma or allergic rhinitis.
  • Genetic weaknesses in epidermal barrier function.
  • Some patients have a mutation in the filaggrin gene: a structural protein in the stratum corneum.
  • Loss of filaggrin may result in impaired skin’s barrier function leading to entry of foreign environmentalsubstances that may trigger immune responses.
  • The skin may be deficient in ‘ceramides’ (fatty acids) increasing transepidermalwater loss.
  • IgE involved in 70 to 80% of cases “true allergy”.
  • Predominance of pathogenic staphylococcus aureus in the skin flora of 90% of patients.
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21
Q

Atopic Dermatitis/Eczema: Signs and Symptoms

A
  • Red scaly lesions on flexor surfacesand cheeks. Very itchy.
  • Broken skin on scratching ->lichenification.
  • Infection on skin (very inflamed and with pus).
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22
Q

Atopic Dermatitis/Eczema: Treatment

A

Corticosteroids, soap substitutes.

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23
Q

Urticaria (Hives)

A
  • An itchy (pruritic), red (erythematous), blotchy and raised rash resulting from swelling of the superficial skin.
  • Can develop in the pharyngeal mucosa causing swelling in the throat and obstruction of the airways.
  • Occurs due to therelease of histamine from mast cells (causing vasodilation and capillary leakage).
  • Causes: medications, food allergies, stings, stress.
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24
Q

Urticaria (Hives): Treatment

A

Anti-histamines

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25
Q

Psoriasis

A
  • Psoriasis is a chronic, autoimmune, inflammatory skin disease.
  • In psoriasis, the stratum basale is dividing too quickly making abnormal keratin, thus the stratum corneum renewal is as little as 7 days rather than 40 days.
  • There is reduced shedding and an accumulation of the stratum corneum, causing silvery scales and flakes on the skin surface.
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26
Q

Psoriasis: Causes

A
  • Autoimmune -T-Lymphocyte mediated hyperproliferation of keratinocytes.
  • Environmental, genetic and immunologic factors.
  • Genetic defect in mitotic control.
  • Susceptibility may be due to genetic defects in detoxification enzymes.
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27
Q

Psoriasis: Triggers

A

Infection, chemicals, alcohol, stress, anti-malarials, beta-blockers.

28
Q

Psoriasis: Signs and Symptoms

A
  • Red scaly plaques covered with overlapping silvery shiny scales that may bleed.
  • Characteristically involves extensor surfaces (wrists, elbows, knees) and scalp.
  • Possibly tiny dents in finger/toenails.
  • Arthritis(14% ->autoimmune).
29
Q

Psoriasis: Treatment

A

Corticosteroids, UV light therapy, methotrexate (immunosuppressant!)

30
Q

Acne Vulgaris

A
  • Blockage of sebaceous/hair follicle duct.
  • It is more common in males and the onset is typically at puberty.
  • In acne, oil that normally drains to the skin surface, gets blocked by excess skin cells inside the follicle. This provides an ideal location for bacteria to grow.
  • Acne tends to affect the face & to a lesser extent, the back.
31
Q

Acne Vulgaris: Causes

A
  • There is a high prevalence of acne in western populations. Some non-westernised populations have a complete absence of acne, which strongly points to environmental factors including diet.
  • Foods that are high in glucose & elevate insulin levels promote oil production & excess skin cell production in follicles. They also cause the testes (& ovaries) to produce testosterone. Dairy will do the same! This is a typical western diet.
  • Linked to excess testosterone (hence puberty).
  • Premenstrual hormonal imbalances.
  • Oily creams & some drugs (anabolic).
32
Q

Acne Vulgaris: Types

A
  • Closed comedomes(white heads): when the trapped sebum and bacteria stay below the skin surface.
  • Open comedomes(black heads): Oxidised lipids causes dark colour.
  • ‘Inflammatory acne’ can occur which begins as closed comedomes. Distension of the follicle occurs causing inflammation (red papules).
  • Cystscan occur when follicles rupture resulting in a pustule/nodule.
  • Large, deep pustules can break down adjacent tissue & cause scarring.
33
Q

Acne: Treatment

A
  • Roaccutane–often effective but many side effects including teratogenicity. Antibiotics.
  • Facial cleansers, contraceptive pill.
34
Q

Acne Rosacea

A
  • Chronic Inflammation of the skin associated with vascular changes, which results in flushing.
  • Often accompanied by seborrhoea(excessive discharge of sebum) but is notan inflammation of the follicles.
  • Suspected that other organs are affected too, such as the stomach & intestines.
  • More common in women.
35
Q

Acne Rosacea: Signs and Symptoms

A

• Facial flushing -redness across nose & cheeks, seborrhoea (oily skin) with papules, pustules.

36
Q

Acne Rosacea: Causes

A
  • Exaggerated vasodilatory response to hyperthermia.
  • High incidence of gastric ‘Helicobacter pylori’ found in rosacea patients (88%). Flushing reaction may be caused by gastrin (gastrin = H pylorigrowth).
  • Other causes include environmental (oil, chlorine, UV), cosmetics (e.g. paraffin), medications. stress.
37
Q

Acne Rosacea: Treatment

A

Mild local treatment with NSAIDs and antibiotics.

38
Q

Warts and Verruca

A

Benign proliferation of the skin and mucosa caused by infection with the Human Papilloma Virus (2 and 4).

39
Q

Warts and Verruca: Signs and Symptoms

A

Papularlesions with a coarse roughened surface. Usually with a red margin.

40
Q

Warts and Verruca: Treatment

A

Laser or freezing(suppression, not a cure!).

41
Q

Skin Tags

A
  • Small growths attached to skin by stalk.
  • Often neck, axilla, groin, eye lid, anus. Generally occurs in areas where skin rubs.
  • Skin coloured or darker and can bleed when knocked. They often drop off.
  • Associated with hyperinsulinaemia (common in type 2 diabetes).
42
Q

Vitiligo

A
  • The skin loses its pigmentation due to the loss of Melanocytes.
  • Onset at any age, 50% under 25 years.
  • Not contagious.
  • Noticeable in races with darker skin
43
Q

Vitiligo: Causes

A
  • May be a genetic susceptibility.
  • Autoimmune link: Increased number of ‘Langerhan cells’ ->hypothesised these cells may inhibit the proliferation of melanocytes.
44
Q

Burns

A

Injury to the skin or tissues caused by heat, cold (frostbite), electricity, radiation, chemicals (strong acid/bases).

45
Q

Burns: Signs and Symptoms

A
  • Damage of the skin withnecrosispain.

* Electrical burns injuries may extend beyond tissue damage (cardiac arrhythmia/fibrillation) etc.

46
Q

Burns: Treatment

A

Skin grafting for deep burns, fluid & electrolyte replacement, pain management.

47
Q

Burn Classification

A
  • 1st degree: affects the epidermis.
  • 2nd degree: all of epidermis and some dermis.
  • 3rd degree: extends into subcutaneous tissue.
  • 4th degree: extends into muscles and tendons.
48
Q

Burn Complications

A
  • Dehydration–due to loss of water and plasma through damaged skin surface.
  • Hypothermia –due to impaired thermoregulation and heat loss.
  • Hypovolaemic shock.
  • Infection.
  • Renal failure –if the kidneys cannot filter waste from broken down red blood cells and damaged tissue.
  • Contractures–scar tissue contracts distorting skin and impairing movement.
49
Q

Lymphangitis

A
  • Inflammation of the lymph vessel.

* Bacterial infection -usually Streptococcus.

50
Q

Lymphangitis

A
  • Swelling, painful red lines below skin surface along the lymph vessel course.
  • Fever, malaise, muscle ache, low appetite.
51
Q

Lymphangitis: Complications

A

• Infection may spread to the blood -> septicaemia (hence a medical emergency)

52
Q

Lymphodema

A
  • Localised lymphatic fluid retention associated with a compromised lymphatic system so reduced lymphatic return.
  • Obstruction of lymph vessels causes an increase in protein accumulation in the interstitial fluid.
  • increase of protein = water retention, swelling of soft tissue [stage 1 –pitting oedema].
  • increase of protein = inflammation and activation of fibroblasts [stage 2 –fibrosis of vessels].
53
Q

Lymphodema: Causes

A
  • Primary: Congenital,poorly developed lymphatics e.g. vessels.
  • Secondary: Damage to the lymphatic system caused by radiotherapy or lymph node removal. Infections e.g. cellulitis.
54
Q

Lymphodema: Signs and Symptoms

A
  • Severe fatigue of affected area.
  • Heavy, painful, swollen limb/area (‘pitting oedema’).
  • Discolouration of the skin overlying the lymphoedema.
  • Recurring skin infections in the effected limb which may lead to thickening & hardening of the overlying skin.
55
Q

Lymphodema: Complications

A

• Recurrent infection, cellulitis, lymphangitis, septicaemia.

56
Q

Lymphodema: Treatment

A

• Lymphatic drainage, treat the cause, skin brushing, herbs, diet, compression bandages, exercise.

57
Q

Lymphadenitis

A
  • Lymphadenitis describes inflammation of lymph nodes.

* Usually a bacterial infection.

58
Q

Lymphadenitis: Signs and Symptoms

A
  • Often following upper respiratory infection (i.e. Sore throat).
  • Enlarged lymph nodes that are often painful on palpation.
59
Q

Lymphadenitis: Complication

A

• Lymphangitis.

60
Q

Lymphadenitis: Treatment

A

Antibiotics

61
Q

Splenomegaly

A

• Enlargement of the spleen due to increased workload; associated with many diseases.

62
Q

Spenomegaly: Causes

A
  • Viral or bacterial infectionse.g. infectious mononucleosis (glandular fever), malaria.
  • Liver diseasessuch as cirrhosis leading to portal vein hypertension.
  • Haemolytic anaemiase.g. Thalassemia, Sickle cell anaemia.
  • Blood/lymphatic malignancies:Leukaemia & Hodgkin’s lymphoma.
63
Q

Splenomegaly: Signs and Symptoms

A
  • Abdominal pain.
  • Early satiety (due to splenic encroachment).
  • Symptoms of haemolytic anaemia due to accompanying cytopenia.
  • Palpable left upper quadrant abdominal mass.
64
Q

Splenomegaly: Complications

A
  • Anaemia, increased bleeding, frequent infections.

* Ruptured spleen.

65
Q

Optimising Lymphatic Health

A
  • Exercise is essential –lymphatic vessels rely on exercise to ‘pump’ lymph through the body.
  • High anti-inflammatory and anti-oxidant diet: green leafy vegetables, berries, omega-3 foods, nuts & seeds, turmeric, ginger.
  • Reducing oxidative stress: 7-9 hours of good quality sleep, reducing stress, healthy diet.
  • Remove common allergens from the diet to reduce the stress on the digestive and immune systems (e.g. dairy, gluten, nightshades).
  • Dry brushing and refer for lymphatic drainage.

Biomedicine I (18 decks)

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