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Skin Infection Flashcards

1
Q

Explain the natural defenses of the skin and their role in preventing bacterial infections.

A

The skin’s natural defenses include:

Temperature >37°C inhibits bacterial growth.

Dryness prevents microbial colonization.

Keratin and desquamation remove pathogens.

Sebum (low pH, high lipid content) creates an antibacterial barrier.

Sweat (low pH, high salt content) inhibits microbial growth.

Skin-associated lymphoid tissue provides immune responses.

Resident microflora competes with pathogens.

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2
Q

Discuss the composition and functions of resident microflora on the skin.

A

Resident microflora includes bacteria (e.g., Staphylococci, Micrococci), fungi (e.g., Candida albicans), and mites. It protects against pathogenic microbes by competing for nutrients and secreting antimicrobial substances.

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3
Q

Differentiate between resident and transient bacteria on the skin.

A

Resident bacteria live harmlessly on the skin, mainly in the upper epidermis and hair follicles. Transient bacteria, like Staphylococcus aureus, are temporary and often introduced from external sources.

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4
Q

Outline the common bacterial species found in normal skin flora.

A

Staphylococci, Micrococci, Diphtheroids (Corynebacterium, Brevibacterium), and fungi (Malassezia) are common. Staphylococcus epidermidis predominates on the surface.

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5
Q

What are the characteristics and significance of Staphylococcus epidermidis in skin health?

A

epidermidis is a resident bacterium that inhibits pathogenic bacteria by competing for space and nutrients. It is typically non-pathogenic but may cause opportunistic infections.

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6
Q
  1. Define impetigo and describe its types and causes.
A

is an acute, contagious bacterial skin infection caused by Staphylococcus aureus (bullous type) or Group A β-hemolytic streptococci (non-bullous type). It presents as vesicles or bullae that rupture to form yellowish crusts.

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7
Q
  1. Explain the pathogenesis and clinical presentation of bullous impetigo.
A

Bullous impetigo, caused by S. aureus, primarily affects newborns and presents as larger bullae with clear fluid that turns turbid. The lesions rupture, leaving varnish-like crusts, and typically target the face, palms, and soles.

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8
Q

Discuss the complications associated with impetigo.

A

Complications include lymphangitis, lymphadenitis, Staphylococcal Scalded Skin Syndrome (SSSS), and post-streptococcal acute glomerulonephritis.

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9
Q
  1. Compare the treatment options for mild and severe cases of impetigo.
A

Mild cases: Wet compresses with antiseptics (e.g., potassium permanganate) and topical antibiotics.

Severe cases: Systemic antibiotics (e.g., flucloxacillin, erythromycin) are added, especially if nephritogenic streptococci are suspected.

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10
Q
  1. What is ecthyma, and how does it differ from impetigo?
A

Ecthyma is a deeper skin infection caused by Streptococcus pyogenes and Staphylococcus aureus. Unlike impetigo, ecthyma penetrates into the dermis, forming ulcers under crusts and often leads to scarring.

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11
Q
  1. Explain the clinical features and treatment of ecthyma gangrenosum
A

Clinical Features: Ecthyma gangrenosum presents as necrotic ulcers with a violaceous border caused by Pseudomonas aeruginosa. It is common in immunocompromised individuals and progresses rapidly without treatment.

Treatment: Requires prompt systemic antibiotics and treatment of the underlying immune deficiency.

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12
Q
  1. Discuss the differences between superficial and deep folliculitis.
A

Superficial Folliculitis: Infection at the ostium of hair follicles, usually by Staphylococcus aureus. It is self-limiting and resolves within a week.

Deep Folliculitis: Affects deeper parts of hair follicles, forming painful nodules that may rupture and scar (furuncles). Recurrent cases may need long-term antibiotics.

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13
Q
  1. What are the common causes of pseudofolliculitis barbae?
A

ingrown hairs, common in individuals with curly hair. Secondary bacterial infections may occur, typically after shaving.

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14
Q

Describe the management strategies for chronic furunculosis.

A

Strategies include improving hygiene, treating Staphylococcus aureus carriage sites with topical antibiotics, long courses of oral flucloxacillin, and addressing underlying conditions such as diabetes.

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15
Q
  1. Define carbuncles and discuss their clinical presentation
A

Definition: A carbuncle is a collection of interconnected boils.

Clinical Presentation: It appears as painful, swollen areas with multiple pus-draining openings, commonly on thick skin (nape of neck, back). Symptoms include fever and malaise.

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16
Q
  1. What are the complications of carbuncles, and how are they managed?
A

Complications: Bloodstream invasion, abscess formation, and severe pain.

Management: Includes incision and drainage, culture swabs, systemic antibiotics, and treating underlying conditions.

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17
Q
  1. Explain erysipelas, its causes, and treatment.
A

Erysipelas: An acute bacterial skin infection involving the dermis and upper subcutaneous tissue, caused by Streptococcus pyogenes.

Treatment: Intravenous penicillin for 7–10 days, rest, and supportive care.

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18
Q
  1. Differentiate erysipelas from cellulitis.
A

Erysipelas: Involves the upper dermis with well-defined, raised edges, usually on the face.

Cellulitis: Affects deeper subcutaneous tissues, with poorly defined margins, often on lower limbs.

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19
Q
  1. Describe the clinical presentation of necrotizing fasciitis and its management.
A

Presentation: Painful dusky cellulitis progressing to widespread tissue necrosis. Often associated with diabetes or surgery.

Management: Surgical debridement, intravenous antibiotics, and supportive care.

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20
Q
  1. What is erythrasma, and how is it diagnosed?
A

Erythrasma: A bacterial skin infection caused by Corynebacterium minutissimum, presenting as scaly reddish-brown patches in body folds.

Diagnosis: Coral red fluorescence under Wood’s lamp. Treated with topical or systemic erythromycin.

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21
Q

Describe the clinical features and management of staphylococcal scalded skin syndrome (SSSS).

A

Features: Caused by exfoliative toxins of S. aureus. It presents with fever, irritability, and widespread skin desquamation, particularly in infants and children.

Management: Systemic antibiotics and supportive care.

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22
Q
  1. What are the diagnostic and treatment approaches for streptococcal cellulitis?
A

Diagnosis: Clinical features of red, swollen, warm skin, systemic symptoms, and bacterial cultures.

Treatment: Systemic antibiotics like penicillin or cephalosporins.

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23
Q
  1. Explain the significance of Milian’s ear sign in erysipelas.
A

It indicates involvement of the ear pinna in erysipelas, which lacks subcutaneous tissue, distinguishing it from cellulitis.

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24
Q
  1. What are the risk factors for necrotizing fasciitis?
A

Diabetes, immunosuppression, surgical wounds, trauma, and polymicrobial infections, including streptococci and anaerobes.

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25
25. How is cutaneous tuberculosis diagnosed and treated?
Diagnosis: Biopsy, microscopy, culture, PCR, and Mantoux test. Treatment: A full multidrug antituberculosis regimen (e.g., isoniazid, rifampicin, pyrazinamide, and ethambutol).
26
D 26. Define lupus vulgaris and its clinical features.
Definition: A persistent form of cutaneous tuberculosis. Features: Reddish-brown papules forming plaques with an “apple-jelly” consistency, mainly on the head and neck.
27
27. What are the complications of scrofuloderma?
Fistulae, scarring, secondary infections, and potential spread to underlying lymph nodes or joints.
28
28. Describe the clinical presentation and risk factors of erythema induratum.
Presentation: Deep ulcerating nodules on the backs of the legs. Risk Factors: Poor circulation, often in women.
29
29. What are the types of viral warts and their associated human papillomavirus (HPV) strains?
Common warts (HPV-1, 2, 4), plane warts (HPV-3), and genital warts (HPV-6, 11, 16, 18).
30
30. Compare the clinical presentation of common warts and plantar warts.
Common Warts: Smooth papules with a hyperkeratotic surface, mainly on hands. Plantar Warts: Rough, slightly protruding lesions surrounded by a horny collar, often painful.
31
31. Explain the pathophysiology and treatment of mosaic warts.
Pathophysiology: Clusters of tightly packed warts caused by HPV on soles or palms. Treatment: Salicylic acid, cryotherapy, or surgical removal.
32
S 32. What distinguishes plane warts from other types?
Smooth, flat-topped papules commonly on the face, hands, and legs, often painless.
33
33. Discuss the management of periungual warts.
Use salicylic acid, cryotherapy, or careful curettage. Avoid damaging the nail matrix to prevent deformities.
34
34. Describe the course and complications of untreated anogenital warts.
Course: May grow into large, uncomfortable lesions. Complications: Secondary infection, discomfort, and increased risk of cervical cancer (with HPV-16, 18).
35
35. What are the treatments for stubborn or painful warts?
Options include local curettage, intralesional bleomycin, or laser therapy by specialists.
36
C 36. Describe the transmission and latency of herpes simplex virus (HSV).
Transmitted by direct contact. After the primary infection, it remains latent in nerve ganglia and can reactivate.
37
37. What are the differences between primary and recurrent herpes labialis?
Primary: Widespread painful vesicles, fever, and systemic symptoms. Recurrent: Localized lesions with fewer symptoms, triggered by stress or illness.
38
38. Explain the complications of herpes simplex virus infections.
Encephalitis, disseminated infections, eczema herpeticum, and recurrent corneal ulcers leading to scarring.
39
39. What is the treatment for herpes genitalis?
Oral antivirals like acyclovir for acute and recurrent infections, along with symptomatic relief.
40
40. Describe the stages and complications of chickenpox.
Stages: Macules to vesicles to pustules to crusts. Complications: Secondary bacterial infection, pneumonia, meningitis, and scarring.
41
41. What is herpes zoster, and how does it differ from chickenpox?
Herpes Zoster: Reactivation of dormant VZV, presenting as painful vesicles in a dermatomal distribution. Chickenpox: Primary VZV infection with widespread vesicular rash.
42
2. Discuss the management of postherpetic neuralgia.
Treated with gabapentin, pregabalin, amitriptyline, or topical capsaicin cream.
43
43. What are the risk factors and complications of disseminated herpes zoster?
Risk Factors: Immunosuppression. Complications: Visceral involvement, secondary infections, and severe neuralgia.
44
44. Describe the presentation and treatment of molluscum contagiosum.
Presentation: Pearly, umbilicated papules, often self-limiting. Treatment: Curettage, cryotherapy, or chemical agents like cantharidin.
45
. Explain the management of HFMD.
Symptomatic treatment: Pain relief, hydration, and keeping blisters clean.
46
45. What are the common clinical features of hand, foot, and mouth disease (HFMD)?
Fever, oral ulcers, and vesicular rash on hands, feet, and mouth, caused by Coxsackievirus A16.
47
47. What is the role of cryotherapy in wart treatment, and what are its limitations?
Effective for removing warts with liquid nitrogen but can be painful and may require multiple sessions.
48
48. Describe the pathogenesis of necrotizing fasciitis.
A polymicrobial infection leading to rapid tissue necrosis, often starting as cellulitis.
49
49. What are the key features of Ramsay Hunt syndrome?
Caused by herpes zoster involving the geniculate ganglion, leading to facial paralysis and auditory symptoms.
50
50. Discuss the .prevention strategies for bacterial skin infections.
Good hygiene, proper wound care, avoiding skin trauma, and treating predisposing conditions like diabetes.
51
51. Explain the relationship between eczema herpeticum and atopic dermatitis.
Eczema herpeticum occurs when HSV infects areas of atopic dermatitis, leading to widespread vesicles, fever, and possible systemic involvement.
52
52. What are the signs of herpes zoster ophthalmicus, and how is it treated?
Signs: Vesicular rash in the ophthalmic nerve distribution, corneal ulcers, and scarring. Treatment: Systemic antivirals like acyclovir and topical eye drops.
53
53. Discuss the risk factors for reactivation of latent herpes viruses.
Stress, immunosuppression, UV exposure, illness, and physical trauma can trigger reactivation.
54
54. What are the primary methods to prevent herpes simplex virus transmission?
Avoid direct contact with lesions, use barrier protection, and consider suppressive antiviral therapy for recurrent cases.
55
55. Describe the clinical differences between viral and bacterial cellulitis.
Viral cellulitis is rare, often associated with HSV or VZV, while bacterial cellulitis involves S. pyogenes or S. aureus and presents with more systemic symptoms.
56
56. What is the significance of Wood’s lamp in diagnosing skin infections?
It highlights conditions like erythrasma (coral red fluorescence) and fungal infections (green fluorescence).
57
57. Explain the treatment options for verrucae vulgaris (common warts).
Options include salicylic acid, cryotherapy, electrosurgery, or immune modulators like imiquimod.
58
58. What are the complications of improperly treated cellulitis?
Abscess formation, septicemia, nephritis, and chronic lymphedema.
59
59. Discuss the differences in presentation between erythema nodosum and erythema induratum.
Erythema nodosum: Tender red nodules, typically on shins, associated with systemic conditions. Erythema induratum: Ulcerating purplish nodules, often linked to tuberculosis.
60
60. What is the rationale for using systemic antibiotics in bacterial skin infections?
They target the underlying bacterial cause, prevent complications like abscesses, and reduce the spread of infection.
61
Explain the role of biofilms in chronic skin infections.
Biofilms protect bacteria from antibiotics and immune responses, making infections like chronic wounds harder to treat.
62
62. What are the clinical features of scabies, and how does bacterial infection complicate it?
Scabies causes intense itching and burrows; secondary bacterial infections like impetigo can worsen the condition.
63
63. Describe the differential diagnosis for pustular skin lesions.
Includes folliculitis, acne, impetigo, pustular psoriasis, and candidiasis.
64
64. What are the key features of necrotic ulcers in ecthyma gangrenosum?
Rapid onset of painful ulcers with necrotic centers, surrounded by erythema, often due to Pseudomonas aeruginosa.
65
65. How do fungal infections complicate bacterial skin conditions?
They disrupt the skin barrier, allowing bacteria to invade and complicate treatment with mixed infections.
66
66. What is the importance of bacterial culture in skin infections?
Identifies causative organisms, guides targeted antibiotic therapy, and detects resistance patterns.
67
67. Describe the differences between acute and chronic bacterial infections of the skin.
Acute infections like impetigo are sudden and short-lived, while chronic infections like furunculosis persist or recur over time.
68
68. How does immunosuppression affect skin infection risk?
It increases susceptibility to opportunistic infections like ecthyma gangrenosum and severe herpes zoster.
69
69. Discuss the clinical presentation of post-streptococcal glomerulonephritis in skin infections.
Hematuria, proteinuria, edema, and hypertension following streptococcal skin infections like impetigo.
70
70. What are the benefits of using combination therapies for skin infections?
They target multiple pathogens, reduce resistance, and treat underlying and secondary infections.
71
71. Explain the role of corticosteroids in managing inflammatory skin infections.
Reduce inflammation in conditions like pseudofolliculitis barbae but may worsen infections if used improperly.
72
72. Describe the pathophysiology of herpes simplex encephalitis.
HSV invades the central nervous system, causing inflammation and necrosis, particularly in the temporal lobes.
73
73. What are the preventive measures for chickenpox in susceptible populations?
Vaccination, isolation of infected individuals, and prophylactic antivirals in high-risk cases.
74
74. Discuss the importance of maintaining skin integrity to prevent infections.
Intact skin acts as a barrier; injuries or eczema can facilitate microbial entry.
75
75. What are the unique features of bullous impetigo compared to non-bullous impetigo?
Bullous impetigo has larger, fluid-filled blisters caused by S. aureus, while non-bullous presents with honey-colored crusts.
76
76. How is a diagnosis of necrotizing fasciitis confirmed?
Clinical signs, imaging (MRI), and deep tissue biopsy.
77
77. What are the treatment principles for cutaneous tuberculosis?
Multidrug therapy targeting Mycobacterium tuberculosis and addressing drug resistance.
78
78. Describe the clinical presentation of disseminated molluscum contagiosum.
Widespread pearly papules, common in immunosuppressed patients.
79
79. What factors influence the resolution of viral warts?
Host immune response, type of HPV, and treatment methods.
80
80. Discuss the role of vaccines in preventing HPV-associated conditions.
Prevents cervical cancer and genital warts by targeting high-risk HPV strains like 16 and 18.
81
81. Explain the differences between bacterial and viral vesicular skin lesions.
Bacterial vesicles often crust, while viral vesicles (e.g., HSV, VZV) are grouped and associated with systemic symptoms.
82
82. What are the primary diagnostic features of hand, foot, and mouth disease (HFMD)?
Fever, vesicles on palms, soles, and mouth ulcers, typically in children under five.
83
83. Describe the management of anogenital warts during pregnancy.
Avoid podophyllin; use cryotherapy or safe topical treatments like imiquimod under supervision.
84
84. What is the clinical significance of “apple-jelly nodules” in lupus vulgaris?
They indicate cutaneous tuberculosis and require histological confirmation.
85
85. Discuss the complications of untreated erysipelas.
Toxemia, septicemia, gangrene, and lymphedema.
86
86. How do you differentiate between fungal and bacterial intertrigo?
Fungal intertrigo shows satellite lesions and positive Wood's lamp findings, while bacterial forms lack these features.
87
87. Explain the rationale for prophylactic antibiotic use in recurrent bacterial skin infections.
Prevents flare-ups in at-risk individuals, like those with diabetes or immune compromise.
88
88. Describe the diagnostic process for erythrasma.
Clinical examination, Wood’s lamp (coral red fluorescence), and culture if necessary. مرجان احمر
89
89. What are the hallmark features of herpes zoster in the elderly?
Painful, unilateral dermatomal rash with a higher risk of postherpetic neuralgia.
90
90. How does vaccination reduce the burden of varicella-zoster virus?
Decreases primary infection (chickenpox) and reactivation (shingles).
91
91. What are the indications for systemic antivirals in chickenpox?
Severe cases, immunocompromised patients, or adults with a higher risk of complications.
92
92. Describe the differences in treatment approaches for localized versus systemic bacterial skin infections.
Localized: Topical antibiotics and wound care. Systemic: Oral or IV antibiotics and supportive care.
93
93. How does diabetes contribute to recurrent skin infections?
Poor glycemic control impairs immune responses and wound healing.
94
94. What is the importance of MRSA screening in recurrent furunculosis?
Identifies resistant strains and guides appropriate antibiotic therapy.
95
95. Discuss the use of cryotherapy for molluscum contagiosum.
Rapidly destroys lesions but may cause discomfort and require multiple sessions.
96
Rapidly destroys lesions but may cause discomfort and require multiple sessions.
Severe pain, rapid progression, dusky skin, and systemic toxicity.
97
97. How does the human microbiome influence skin health?
Maintains skin barrier function and competes with pathogens.
98
98. What are the complications of post-streptococcal skin infections?
Acute glomerulonephritis and rheumatic fever.
99
99. Describe the management of infected burn wounds.
Debridement, topical antimicrobials, systemic antibiotics, and skin grafts as needed.
100
100. What is the role of education in preventing skin infections?
- Promotes hygiene, early recognition of infections, and adherence to treatment.

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