Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Med I > Rosacea & Insects > Flashcards

Rosacea & Insects Flashcards

1
Q

Driving Factors of Acne Vulgaris

A

Follicular hyperkeratinization (occurs when the cells of the follicle become cohesive and do not shed normally onto the skin’s surface)

Increased sebum production

Cutibacterium acne within the follicle

Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Microcomedo

A

Considered the precursor for the clinical lesions of acne vulgaris (First stage of acne)

Increased sebum production
Follicular hyperkeratinization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Closed Comedome - Whitehead

A

Accumulation of sebum and keratinous material converts a microcomedo into a closed comedo

Small or no opening of the follicle to the skin
Build-up of sebaceous material
Inflammation surrounding the follicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Open Comedome - Blackhead

A

The follicular orifice is opened with continued distension, forming an open comedo

Opening of pore dilates
Build-up of sebaceous material
Inflammation surrounding the follicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Inflammatory Papule (Pimple)

A

Follicular rupture and presence of bacteria contributes to the development of inflammatory lesions

Bacterial byproduct causes inflammation and infection in the surrounding skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Inflammatory Pustule

A

Immune system sends white blood cells to fight infection and creates pus in the pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Nodule or Cyst

A

Follicle wall bursts and a capsule is created via enzymes secreted by white blood cells to contain infection.

Marked inflammation is present in addition to erythema and tenderness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Contributing Factors to Acne Vulgaris

A

Androgens (sex hormones) stimulate the growth and secretory function of sebaceous glands

Mechanical trauma can rupture comedos, causing inflammatory lesions

Stress seams to have an effect on severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Topical Retinoids

A

Beneficial for both comedonal and inflammatory lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Topical Antimicrobial Therapies

A

Beneficial for inflammatory lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Oral Antibiotics

A

For severe inflammatory acne

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Benzoyl Peroxide

A

Decreases the emergence of antibiotic resistant bacteria

Often used in conjunction with other therapies (topical retinoids, antimicrobial therapies, oral antibiotics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment of Comedonal (noninflammatory) Acne

A

Topical Retinoid - Tretinoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Treatment of Mild Papulopustular and Mixed Acne

A

Benzoyl peroxide +/- topical antibiotic (erythromycin, clindamycin) and topical retinoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of Moderate Papulopustular and Mixed Acne

A

Benzoyl peroxide + topical retinoid + oral antibiotic (tetracycline class)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment of Severe Acne

A

Retinoid + oral abx (tetracycline class) + benzoyl peroxide

OR

Oral isotretinoin monotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment of Acne during Pregnancy

A

Some acne medications are teratogenic

Retinoids are super contraindicated in pregnancy

Safe regimen for pregnancy: oral erythromycin, topical clindamycin, topical azelaic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Acne Rosacea

A

Chronic skin disorder of the central face

  • Most prevalent in fair-skinned individuals
  • Female > Males
  • Usually emerges in 30s
  • Estimated 1-10% in white population
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pathogenesis of Acne Rosacea

A

Not well understood

  • Abnormalities in immunity
  • UV damage
  • Vascular dysfunction
  • Inflammatory reactions to cutaneous microorganisms
20
Q

Presentation of Acne Rosacea

A

Erythema of central face, persisting for months or more

Nose, cheeks, chin, and forehead are commonly affected

Four subtypes:

  • Erythematotelangiectatic
  • Papulopustular
  • Phymatous
  • Ocular
21
Q

Erythematotelangiectatic Rosacea

A

Chronic redness of central face

Flushing (wet or dry)

Skin sensitivity

Dry appearance

Telangiectasias

22
Q

Papulopustular Rosacea

A

Papules and pustules of central face

Inflammation can be confluent

NO comedones

23
Q

Phymatous Rosacea

A

Tissue hypertrophy causing irregular contours

Mostly nose but can involve cheeks, forehead and chin

Mostly affects men

24
Q

Ocular Rosacea

A

Often coincides with other types of rosaceas

> 50% of those with other types

Children and adults

May precede, coincide, or follow

Dry eyes, pain, itching, blurry vision, photosensitivity, blepharitis (An inflammation of the eyelid that affects the eyelashes or tear production), keratitis (Inflammation of the clear tissue on the front of the eye (cornea).), conjunctivitis, stye.

25
Q

Treatment of Erythematotelangiectatic Rosacea

A

First line: behavior changes

  • avoid trigger
  • sun protection
  • gentle skin care

Second line

  • laser and pulsed light therapy
  • topical brimonodine
26
Q

Treatment of Papulopustular Rosacea

A

Mild-Moderate
1st Line topicals: (Metronidazole, Azelaic acid)
2nd Line topicals: ivermectin and sulfacetamide-sulfur

Moderate-Severe or failed topical tx
Oral abx:
- Tetracyclines: doxycycline, minocycline, tetracycline
- Macrolides: clarithromycin, azithromycin, erythromycin

27
Q

Treatment of Phymatous Rosacea

A

Early Disease: Isotretinoin

Advanced Disease: surgical debulking and/or laser ablation

28
Q

Treatment of Ocular Rosacea

A

Refer to Ophthalmologist

Topical abx, cyclosporin (immunosuppressive drug), oral abx

29
Q

Degree of Envenomation

A

Grade 1: Local pain and paresthesias at the sting

Grade 2: Local symptoms as well as remote pain and paresthesias

Grade 3: EITHER cranial nerve OR somatic skeletal neuromuscular dysfunction

Grade 4: Both cranial nerve dysfunction AND somatic skeletal neuromuscular dysfunction

30
Q

Characteristic Signs of Envenomation

A

Local pain exacerbated by tapping near the sting site (tap sign)

Cranial nerve dysfunction
•Hypersalivation
•Abnormal eye movements 
•Blurred vision
•Slurred speach
•Tongue fasciculations

Somatic skeletal neuromuscular dysfunction
–Fasciculations
–Shaking and jerking of the extremities
–Opisthotonos (arching of the back)
–Emprosthotonos (tetanic forward flexion of the body)
–Fever up to 104°F from excess motor activity

31
Q

Severe envenomations require monitoring for…

A 
•Respiratory compromise
–Suctioning of oral secretions
–Endotracheal intubation 
•Myocardial infarction
•Hyperthermia
•Rhabdomyolysis
32
Q

Common Clinical Presentation of Bee Stings

A

Commonly result in a local reaction

Swelling, erythema lasting a few hours to 1-2 days

Treat with cold compress

33
Q

Large Local Reaction (LLR)

A

Bee Stings will cause a different response about 10% of the time

–Exaggerated erythema and swelling
–Gradually enlarges over 1-2 days
–Resolves in 5-10 days
–Cold compress, prednisone, antihistamines, NSAIDs

34
Q

Widow Bites

A

Cause a small local reaction

  • Often cause few symptoms because no venom injected
  • Blanched circular patch, surrounding red perimeter and a central punctum

•Venom causes catecholamine release
–Intermittant radiating pain
–Abdominal/chest/back pain and muscle spasm
–Local/regional diaphoresis, HA, N/V

35
Q

Common Recluse Bites

A

Often painless initially
•Progress to severe pain in 2-8 hours
•Usually a red plaque or papule with central pallor
•May see two small puncture marks within the erythema
•Vesiculation can occur
•Resolves in a week

36
Q

Rare Recluse Bites

A

severe ulcerative necrosis can occur
•Dark, depressed center develops after 1-2 days

  • Systemic symptoms
    •N/V, h/a, fever, chills
    •Rarely, renal failure, hemolytic anemia, hypotension, DIC, rhabdomyolysis can occur
37
Q

Vitiligo

A

an acquired skin depigmentation via an autoimmune process directed against melanocytes

38
Q

Epidemiology of Vitiligo

A 
–1% of worldwide population
–Affects males and females equally
–Onset peaks in 2nd/3rd decades
–Subtype (generalized vitiligo) can be associated with other autoimmune disease in 20-30% of patients
–Family history in 20-30% of patients
39
Q

Clinical Presentation of Vitiligo

A

presents as milk-white macules with homogenous depigmentation and well-defined borders

  • Slowly progressive
  • Spontaneous repigmentationin 10-20%
40
Q

Diagnosis of VItiligo

A
  • Consider screening for other autoimmune diseases

* Skin biopsy will show epidermis devoid of melanocytes

41
Q

Treatment of Vitiligo

A

Treatment focuses on prevention and repigmentation therapy

  • Treatment
  • Topical and systemic corticosteroids (first line)
  • Calcineurin inhibitors
  • Narrowband ultraviolet B phototherapy (extensive disease)
  • Skin grafts
  • Sunscreen
  • Makeup (Covermark, Dermablend)
  • Ask about psychological distress
42
Q

Hidradenitis Suppurativa (Acne Inversa)

A

Chronic inflammatory skin disorder involving the hair follicle

Results from the cycle of follicular occlusion, rupture, and the associated immune response

  • Occurs in the axillary, inguinal and anogenital regions
  • 1-4% prevalence
  • Female > male; no racial predilection
  • Avg age of onset = 23 –Rarely before puberty or after menopause

Other factors: genetics, mechanical stress, obesity, smoking, diet

43
Q

Progression of Hidradenitis Suppurativa

A

Begins with a single, deep-seated, inflammatory nodule

  • More nodules form as disease progresses
  • May form an abscess that opens to the skin
  • Purulent drainage occurs if ruptured

As the disease progresses:

  • Sinus tracts
  • Comedones
  • Scarring
44
Q

Diagnosis of Hidradenitis Suppurativa

A

Based on lesion, location, chronicity, and relapse

45
Q

Treatment of Hidradenitis Suppurativa

A 
•Local tx:
–topical clindamycin
–Intralesionalcorticosteroids
•Systemic antibiotics
–Doxycycline or minocycline
•Anti-androgenic agents 
•Surgery
–Punch debridement (nodules) or wide excision (scarring)
•Severe, refractory cases
–TNF inhibitors
–Oral retinoids

Used in conjunction with lifestyle modifications

46
Q

Complications of Hidradenitis Suppurativa

A
  • Fistulae
  • Strictures and contractures
  • Lymphatic obstruction
  • Infectious complications
  • Squamous cell cancer
  • Malaise, depression, suicide

Clin Med I (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions