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Disease and Defense > Unit III > Flashcards

Unit III Flashcards

1
Q

What are the functions of skin?

A 
decoration/beauty
barrier
vitamin D synthesis
water homeostasis
thermoregulation
insulation/calorie reservoir
touch/sensation
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2
Q

What type of melanin produces black to brown pigment?

A

Eumelanin

*Eutopia!

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3
Q

What type of melanin produces yellow to red-brown pigment?

A

phenomelanin

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4
Q

Where do light skin melanocytes cluster?

A

top of nucleus

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5
Q

Where can you find dark skin melanocytes in the cell?

A

**larger and evenly distributed throughout the cytoplasm

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6
Q

Where do hair follicles originate?

A

In the subcutaneous fat

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7
Q

Name the four layers of the skin starting from the most superficila layer

A

stratum corneum
stratum granulosum
stratum spinosum
stratum basalis

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8
Q

What is the stratum granulosum comprised of?

A

Has Keratohyalin granules and inside granules you have profilaggrin which is a precursor to filaggrin

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9
Q

Where can you find profilaggrin?

A

In keratohyalin granules

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10
Q

What is the function of filaggrin?

A

Filaggrin cross-links keratin tonofilaments and is important in the barrier function of the skin. Filaggrin is mutated in dry skin conditions including ichthyosis and atopic dermatitis.

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11
Q

What is the function of the stratum spinosum?

A

Has a “prickly” or spiny appearance due to desmosome attachments between cells

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12
Q

What are tonofilaments?

A

protein structures (keratin filaments) that insert into the dense plaques of desmosomes on the cytoplasmic side of the plasma membrane

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13
Q

What is the function of a desmosome?

A

attaches keratinocytes to each other

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14
Q

What is the function of a hemidesmosome?

A

attach basal cells firmly to the basal lamina of the dermal

epidermal junction

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15
Q

Difference between desmosome vs hemidesmosome?

A

desmosome is attachment between cells

hemidesmosomes are attachments to the basal lamina of the dermal epidermal junction (deeper in the cell)

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16
Q

What type of cells are found in the stratum basalis?

A

keratinocytes - either a single layer cuboidal or columnar

stem cells of the epidermis found here

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17
Q

What is the stratum lucidum?

A
  • a thin, light staining band seen only in thick skin
  • cells of this layer no longer have nuclei or organelles
  • between the stratum corneum and granulosum
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18
Q

Where in the dermis is the capillary network that is blood supply for epidermis?

A

the papillary layer

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19
Q

What part of the dermis is the pathway for defense cells?

A

the papillary layer

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20
Q

What are Meissner’s corpuscles and where are they found?

A

sensory cells found in the papillary layer of the dermis

Senses **fine touch and tactile discrimination

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21
Q

What part of the dermis contains extensive collagen and elastic fibers that provide strength and flexibility?

A

The reticular layer

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22
Q

Where in the dermis do epidermal derivatives such as glands and hairs and plays a major role in their development and functioning?

A

The reticular layer

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23
Q

What part of the dermis has a pathway for major blood vessels arranged specifically to facilitate thermoregulation?

A

the reticular layer

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24
Q

What part of the dermis has a site of nerve tracts and major sensory receptors?

A

the reticular layer

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25
Q

Where are Pacinian corpuscles found and what do they do?

A

In the reticular layer. They sense vibration, pressure and touch

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26
Q

Where are langerhan’s cells found and what do they do?

A

found in the epidermis and they are essentially the immunologic barrier

“antigen presenting cells of the skin”

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27
Q

what defect causes albinism?

A

a defect in the tyrosine gene needed for the synthesis of melanin

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28
Q

What is vitiligo?

A

an autoimmune disease in which antibodies attack melanocytes and you have depigmentation

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29
Q

What are the adnexal structures?

A 
Apocrine glands
• Eccrine glands
• Hair
• Nails
• Sebaceous glands
-sweat glands
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30
Q

what organs are needed to activate vitamin D3 and 2?

A

The liver and kidneys

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31
Q

What is the mechanism of getting vitamin D from sun?

A

UV + 7 dehydrocholesterol = vitamin D

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32
Q

What is bullous pemphigoid?

A

subepidermal blisters due to an autoimmune response against BP 230 and BP 180 (Type XVII collagen) at HEMIDESMOSOMES

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33
Q

What is Epidermolysis bullosa (EB) ?

A

a group of inherited bullous disorders characterized by blister formation in response to mechanical trauma.

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34
Q

What is Junctional EB?

A

blistering due to genetic defects in Laminin 5

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35
Q

What is dystrophic EB?

A

blistering due to genetic defects in collagen XII

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36
Q

What type of epidermolysis bullosa (EB) leads to mitten hands, flexion contractures, and increased risk in squamous cell carcinomas?

A

recessive dystrophic EB

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37
Q

What is the thickest layer of the epidermis?

A

stratum spinosum

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38
Q

What filaments do desmosomes contain?

A

Contain intracellular keratin filaments (5 and 14)

also contains transmembrane proteins, desmogleins and desmocollins

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39
Q

What is Pemphigus Vulgaris?

A

intraepidermal blistering due to antibodies against desmoglein 1 and 3

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40
Q

What is epidermolysis bullosa simplex?

A

onset of blisters shortly after birth due to defects in keratin filaments 5 and 14 (found in desmosomes)

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41
Q

What does the breakdown of filaggrins form?

A

Forms Natural moisturizing factor (NMF) which binds H2O to keep skin moist

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42
Q

What disorder is caused by defective skin barrier function due loss-of-function filaggrin mutations?

A

Icthyosis Vulgaris and atopic dermatitis

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43
Q

What is the function of merkel cells and where are they found?

A

tactile sensation within the epidermis

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44
Q

What is the epidermal rete?

A

Downward projections of the epidermis that interdigitate with upward projections of the dermal papillae.

Provides strength of adherence, and also increases the surface area between the epidermis and dermis

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45
Q

What is the dermis predominantly comprised of?

A

collagen fibers, elastic fibers and ground

substance.

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46
Q

What is the significance of collagen I?

A

Makes up 85% wt of the dermis and is also the major component in bone

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47
Q

What type of collagen comprises a large part of the fetal dermis but is not a major portion of the adult dermis?

A

collegen III

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48
Q

Where is collagen IV found?

A

found in high concentration in the “basement membrane zone” which is present in the dermoepidermal junction. Also more prominent around blood vessels (think Ehlers-Danlos syndrome)

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49
Q

What is collagen VII used for?

A

found in the anchoring fibrils which are used by the

body to attach the epidermis to the dermis.

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50
Q

What type of collagen is synthesized intracellularly within fibroblasts?

A

procollagen

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51
Q

procollagen consists of how many chains?

A

3 alpha helical chains

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52
Q

under an electron microscope what is the pattern characteristic of procollagen?

A

a characteristic pattern of striations with 68 nm intervals

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53
Q

procollagen chains primary consist of what proteins?

A

Glycine - Proline - Hydroxyproline

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54
Q

What is stasis dermatitis?

A

Chronic venous insufficiency of the lower extremities associated with lower extremity edema.

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55
Q

What are some complications associated with stasis dermatitis?

A

Dryness
Itching
Allergic contact dermatitis due to use of topical preparations (i.e. topical antibiotics)
Allergic contact dermatitis (ACD) is found in 58-86% of patients with leg ulcers
Irritant Dermatitis due to wound exudates

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56
Q

How would you treat stasis dermatitis?

A 
Compression
Elevation
Exercise calf muscles
Vascular surgery
Topical steroids
Avoid allergens
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57
Q

What is the morphology of dermatitis?

A

Erythematous papules and thin plaques with scale

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58
Q

Where does inflammation take place in dermatits?

A

Epidermis and dermis

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59
Q

What is the morphology of cellulitis?

A

Warm, tender, erythematous, patches or plaques

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60
Q

Where does inflammation take place in cellulitis?

A

dermis and subcutaneous tissue

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61
Q

What is atopic dermatitis?

A

Common skin disease which may begin at any age, however a majority begin before age 5

Often associated with xerosis (dry skin) and a history of atopy (asthma, allergic rhinitis)

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62
Q

What is the diagnostic criteria for atopic dermatitis?

A

Must have: Itchy skin + Plus three or more of the following:

  • History of involvement of skin creases
  • Personal history of asthma or hay fever
  • History of dry skin within the last year
  • Visible flexural eczema
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63
Q

What is the pathogenesis for atopic dermatitis?

A
  • Barrier disrupted skin
  • Filaggrin mutation
  • Staphlyococcus aureus acts as a superantigen
  • Elevated IgE
  • Eosinophilia
  • TH2 type cytokine (IL-4, IL-5, IL-10) immune response produced
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64
Q

What’s another word for dermatits?

A

eczema

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65
Q

What is irritant contact dermatitis?

A

Non-immunologically mediated reaction resulting from a direct cytotoxic effect

-Either from a single or repeated exposure to the irritant

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66
Q

What is the most common contact dermatitis?

A

irritant contact dermatitis

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67
Q

What are examples of weak irritants?

A

o Soap and water
o Skin products (even “baby” and “hypoallergenic”)
o Perfumes
o Wool
o Raw Foods (meat, fruits, or vegetables held while preparing foods)
o Body Secretions (feces, urine, saliva, sweat)
o Friction

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68
Q

What is intertrigo?

A

an inflammatory condition of skin folds

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69
Q

What are the clinical presentations of adult dermatits?

A
  • involves eyelid and hand dermatitis
  • associated with dry skin defect in falaggrin aka ichthyosis vulgaris
  • Keratosis vulgaris – lil bumps on back of arm skin and have this more than general population
  • Hyperlinearirty of palms – prominent lines
  • Ichthyosis vulgaris – defect in falaggrin
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70
Q

What type of dermatitis typically burns more than itches?

A

irritant contact dermatitis

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71
Q

What is allergic contact dermatitis?

A

skin condition that requires contact exposure of an allergen, immune response and development of “memory” T cells

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72
Q

The biochemical elicitation of ACD is caused by what molecules?

A

inflammatory cytokines including TNFα and IL-1.

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73
Q

What is the gold standard testing for ACD?

A

patch test

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74
Q

What is the most frequent allergen?

A

nickel exposure 19.5%

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75
Q

What are risk factors for nickel sensitivity?

A

Young
Female
Ears pierced

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76
Q

What is co-sensitization and give an example

A

allergy to two allergens which are not structurally related, but are frequently used concomitantly

Bacitracin and Neomycin

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77
Q

What is a drug eruption?

A

eczematous eruptions/ drug rashes

  • Most common type of drug reaction in skin
  • Usually cell-mediated type IV hypersensitivity
  • Eruption is usually generalized
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78
Q

What is the time course of a drug eruption

A

usually 7-14 days after starting a new drug (unless the drug is an old medication)

with treatment can resolve in 1-2 weeks

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79
Q

What enhances the risk of a drug eruption?

A

viral infection

Almost 100% of pts with infectious mononucleosis will get an exanthematous eruption if given ampicillin

-HIV pts are more susceptible to drug eruptions

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80
Q

what is urticaria?

A

-Hives, wheals

Each individual lesion lasts

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81
Q

What is acute urticaria?

A

represents an immediate type I hypersensitivity reaction

mediated by IgE antibodies

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82
Q

What layer of skin is affected by urticaria?

A

No epidermal changes just inflammation in DERMIS so no scale or blisters

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83
Q

Physical features of urticarias

A
  • Dermographism - exaggerated whealing (welting)
  • Delayed Pressure Urticaria
  • Vibratory Angioedema
  • Exercise-induced urticaria
  • Cold Urticaria
  • Solar Urticaria
  • Aquagenic Urticaria
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84
Q

What is the clinical presentation of Seborrheic Dermatitis

A
  • Sharply demarcated patches (thin plaques) with pink or slightly orange-yellow erythema
  • Characterized by flaky, “greasy” scales
  • Occurs in infancy and post-puberty when sebaceous glands are active
  • Occurs in areas rich in sebaceous glands (scalp, face, ears, chest and intertriginous areas).
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85
Q

What diseases have more severe seborrheic dermatitis?

A

HIV patients

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86
Q

What disease is commonly seen with seborrheic dermatitis?

A

Parkinson’s disease

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87
Q

What is “cradle cap”

A

infant seborrheic dermatitis
Begins 1 week after birth and may persist for several months
-Often starts on the scalp and can become confluent with a thick scale covering most of the scalp
-Often seen in the inguinal folds or axillae

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88
Q

What is the pathogenesis of seborrheic dermatitis?

A

Sensitivity to yeast which can over grow in areas of oil glands and you get a rash that looks like dandruff

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89
Q

What cell type do cherry angiomas affect?

A

endothelial cells

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90
Q

What are cherry angiomas?

A

bright, red, smooth-topped papules that are primarily distributed in the truncal region

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91
Q

What is the best treatment option for small cherry angiomas?

A

Superficial electrodesiccation

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92
Q

What is infantile hemangioma?

A

Benign endothelial cell neoplasm

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93
Q

What is the most common benign tumor of childhood?

A

Infantile Hemangioma aka strawberry hemangioma or capillary hemangioma

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94
Q

What is the pattern of involution for a child with infantile hemangioma?

A

involute slowly at 10% per year
50% resolved by age 5
90% resolved by age 9

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95
Q

What is the first line of treatment for infantile hemangioma (if needed at all) during the growth phase?

A

Beta blockers

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96
Q

What is the histology of infantile hemangioma?

A

dermal proliferation of capillary-sized endothelial cell-lined vessels.

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97
Q

What do infantile hemangiomas cells stain with?

A

placenta associated vascular markers including GLUT-1

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98
Q

What is a port wine stain?

A

vascular malformation in the endothelum that leads to pink patches.

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99
Q

What is one main difference between port wine stain and hemangiomas?

A

Port wine stains do not resolve spontaneously and eventually change from a pink patch to thicker purple plaque with nodularity.

does NOT stain with GLUT-1

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100
Q

What is Sturge Weber Syndrome?

A

systemic abnormality associated with port wine stain aka “facial stain”
10-15% of capillary malformation in a V1 distribution associated with ocular and neurologic abnormalities.

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101
Q

How is port wine stain treated?

A

with vascular lasers called “pulse dye laser”

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102
Q

What is nevus sebaceus?

A

A hamartoma the presents as papillomatous, yellow-orange linear plaque on the face or scalp

lesions associated with alopecia

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103
Q

When does nevus sebaceous often occur?

A

During puberty with all the active sebaceous glands and epidermal hyperplasia busy at work

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104
Q

What are some of the complications associated with nevus sebaceous?

A

epithelial neoplasms in 10-30% *small cancer risk

epidemal nevus syndrom (neurologic abnormalities)

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105
Q

What are treatment options for nevus sebaceous?

A

Either observation or surgical excision. Make sure to do excision EARLY!

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106
Q

What is sebaceous hyperplasia?

A

common benign tumor of oil gland more frequent after middle age

distribution face > trunk > extremities

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107
Q

What treatment for sebaceous hyperplasia?

A

no treatment needed
electrodessication w/w/o curettage
trichloroacetic acid
liquid nitrogen cryotherapy

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108
Q

What treatment would you recommend with your patient who has recurrent sebaceous hyperplasia?

A

liquid nitrogen cryotherapy

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109
Q

What are Acrochordons?

A

skin tags that form in areas of rubbing like neck, axilla, and infra-mammary area

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110
Q

What is the most common form of treatment of acrochordons?

A

freezing “cryosurgery” with liquid nitrogen

-cut off

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111
Q

What cell type does acrochordon affect?

A

fibroepithelial layer of the skin

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112
Q

What is dermatofibroma?

A

Fibrous histiocytoma of the skin that appear as brown, firm papules, and range 3-10 mm in size.

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113
Q

Where are dermatofibromas most commonly found?

A

Legs

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114
Q

What is a positive dimple (Fitzpatrick) sign indicative of?

A

Dermatofibroma

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115
Q

What are treatment options for dermatofibroma?

A 
no treatment needed
surgical excision (can make make more noticeable)
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116
Q

What is a lipoma?

A

benign tumor of adipose tissue

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117
Q

What age group are lipomas most common in?

A

ages 40-60 but can still be seen in children

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118
Q

What type of collagen is a keloid mostly made up of?

A 
collagen III (early/fetal)
collage I (late/most abundant)
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119
Q

What is the difference between hypertrophic scars and keloids?

A

Hypertrophic scars do not growh beyond the boundaries of the original wound

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120
Q

What are treatment options for keloid scars?

A

topical steroids
intralesional steroids
surgical excision -best for ear keloids
surgery +/- radiation

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121
Q

What are seborrheic keratosis?

A

benign tumors of the hair follicles

primarily head, neck, and trunk

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122
Q

What is the appearance of seborrheic keratosis?

A

oval, slightly raised, light brown to black papules or plaques

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123
Q

When is the typical onset of seborrheic keratosis?

A

fourth or fifth decade with gradual increase in nuber

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124
Q

What is dermatosis pupulosa nigra?

A

Subtype of suborrheic keratosis that occur on the face of fitzpatrick skin type V or VI

*morgan freeman

125
Q

What would you call small hyperkeratotic paupules found in the ankels, feet, forearms, and dorsal hands that resemble seborrheic keratoses?

A

Stucc keratosis

126
Q

What is sign of leser-trelat?

A

rapid increase in size or number of seborrheic keratoses associated with adenocarcinoma of the stomach in 60% of cases

127
Q

Where are intradermal nevus commonly found?

A

head and neck

128
Q

Where are junctional nevus’ found?

A

commonly on plantar and palmar surfaces

129
Q

What is the primary lesion for junctional nevus?

A

macule - typically smooth, tan to brown

130
Q

What is the primary lesion of intradermal nevus’?

A

papule or nodule
dome shapes
skin colore to tan to light brown

131
Q

Where are compound nevus common found?

A

trunk and proximal extremities

132
Q

What are appropriate treatment options for nevocellular nevi?

A

shave biopsy
punch biopsy
excision

133
Q

What is a blue nevus?

A

dermal proliferation of mealanocytes that get trapped in the dermis and present with a blue color

134
Q

What are treatment options for blue nevus?

A

punch biopsy

excision

135
Q

What is a main difference between congenital nevi and acquired nevi?

A

congenital can range anywhere from 1 mm to huge size

presence of dark hairs as well

136
Q

What are the risks associated with congenital nevis?

A

risk 1% per year in large congenital nevi (>20 cm diameter)
malignant melanoma 50% appear in first 3 years
60% appear in first decade

137
Q

What is a dysplastic nevi?

A

a subgroup of nevi which have an irregular outline, variable pigmentation, indistinct borders, can be larger than 6 mm in diameter

138
Q

What is the clinical significance of dysplastic nevi

A

can lead to melanoma

139
Q

What is the criteria for familial atypical moles and melanoma (FAMM)?

A
  • The occurrence of malignant melanoma in 1 or more first- or second-degree relatives
  • The presence of numerous (often >50) melanocytic nevi, some of which are clinically atypical
  • Many of the associated nevi showing certain histologic features
140
Q

What genes are linked to hereditary melanoma?

A

CDK2NA
CDK4
CMM1

141
Q

What is cafe au lait macules?

A

subtle increase in number of melanocytes with increased melanin production

142
Q

What are multiple cafe au lait macules associated with?

A

neurofibromatosis

143
Q

What is neurofibromas?

A

soft flesh colored papules characterized by the “button hole sign”
focal proliferation of neural tissue within the DERMIS

144
Q

What type of inheritance is neurofibromatosis Type 1?

A

Autosomal dominant

145
Q

What defect causes neurofibromatosis?

A

defect in the neurofibromin gene, a tumor suppressor, on chromosome 17 for NF 1

146
Q

What signs are associated with cafe-au-lait macules indicative of NF?

A 
prepubertal child has 6 or more > 5 mm 
Crows sign (axillary freckling)
147
Q

What are factors that increase risk infantile hemangioma?

A

female
low birth weight
chorionic villus
multiple gestational

148
Q

What is the most common superficial bacterial infection of children?

A

Impetigo - streptococcus pyogenes

149
Q

What two bacterias cause impetigo?

A

streptococcus pyogenes and staphylcoccus aureus

150
Q

What is the bacteria that causes non-bullous impetigo?

A

streptococcus pyogenes

151
Q

What bacteria is associated with non-bullous and bullous impetigo?

A

Staphylococcus aureus

152
Q

Where does streptococcal/ impetigo contagiosa present?

A

commonly affects the face followed by the extremities

153
Q

What are the clinical presentations of impetigo contagiosa?

A

early primary lesion - erythematous macule with superficial blister
developed - “honey colored” yellow crust
mild lymphadenopathy

154
Q

What is the clinical presentation of bullous impetigo

A

can affect any area of the body
superficial flaccid blister that may demonstrate pus
older lesion - collapsed blister

155
Q

Staphylococcal Non-Bullous Impetigo typically affects what part of the body?

A

The face - nasal pharynx

156
Q

What type of impetigo is due to a gram positive cocci

A

streptococcus pyogenes **see chains

157
Q

How is impetigo diagnosed?

A 
clinical presentation
culture and sensitivity of crust or fluid from intact bullae
gram stain of curst or fluid from intact bullae
skin biopsy (rarely done)
158
Q

What are predisposing factors to impetigo?

A

high humidity

poor hygiene

159
Q

What are treatment options for impetigo?

A

soaking and gentle removal of crusts

topical antibiotics - mupirocin 2% ointment

160
Q

What are systemic antibiotics for impetigo?

A

cephalexin
dicloxacillin
azithromycin
clarithromycin

161
Q

Is cellulitis or impetigo more superficial?

A

Impetigo is more superficial and cellulitis is deeper in the subcutaneous layer

162
Q

What group of people have a higher risk of cellulitis?

A

very young, elderly patients, immunocompromised patients, intravenous drug users, patients with chronic ulcers

163
Q

What is erysipelas? what causes it?

A

a clinical variant of cellulitis most commonly associated with beta hemolytic streptococci - Streptococcus pyogenes

164
Q

What is cellulitis cased by?

A

Beta-hemolytic streptococci (streptococcus pyogenes), staphylococcus aureus, haemophilus influenza

165
Q

What is the clinical presentation of erysipelas?

A

sharply demarcated area of erythema “cliff drop border” commonly on the face
regional lymphadenopathy
rarely epidermis has bullae, pustules, or hemorrhagic necrosis
incubation period 2-5 days

166
Q

What is the clinical presentation of cellulitis?

A 
commonly located on the extremities
primary lesion - non palpable or subtly palpable area of painful erythema warm to the touch
lymphatic streaking
regional lymphadenopathy 
can progress to septicemia 
incubation period 2-5 days
167
Q

How would you diagnose cellulitis?

A

clinical presentation
CBC - look for leukocytosis
culture and gram stain LEADING EDGE
blood culture - usually negative

168
Q

How to treat cellulitis

A 
antibiotics - cephalexin
dicloxacillin
clarithromycin
azithromycin
fluroquinolone antibiotics
169
Q

What is a dermatophyte?

A

fungus that feeds on keratin (skin, hair, nails)

170
Q

What is the most common dermatophyte?

A

trichophyton

171
Q

trichophyton rubrum?

A

most common cutaneous pathogen

172
Q

trichophyton mentagrophytes?

A

common cause of tinea pedis

173
Q

trichophyton tonsurans?

A

common cause of tinea capitis

174
Q

microsporum canis?

A

common cause of fluorescent tinea capitis

175
Q

epidermophyton floccosum?

A

common cause of tinea cruris

176
Q

What is a frank pathogens?

A

can cause disease in a normal healthy host

177
Q

What is an opportunistic pathogen?

A

usually only causes disease in an immunocompromised host. Ex: HIV

178
Q

How would you measure virulence?

A

In terms of the number of organisms it takes to cause disease.

**dose response curve

179
Q

What are strategies the strategies viruses use for survival?

A
  1. House their DNA and RNA in small proteinaceous particles (capsid)
  2. Genome contains all the information to initiate and complete an infectious cycle
  3. Establish a relationship in a population of hosts that ranges from benign to lethal
180
Q

What is the classical system for classifying viruses?

A

Nature of the genetic material in the virion (DNA or RNA)
Symmetry of the capsid (helical or icosahedral)
Naked or enveloped
Dimensions of the virion and the capsid

181
Q

What is the baltimore system for classifying viruses?

A

classifies based on how the virus produces mRNA

DNA–> RNA –> Protein

182
Q

What is the + RNA strand?

A

ribosome ready strand that can be translated into protein

183
Q

What is the - DNA strand?

A

The DNA from which mRNA is copied

184
Q

What is the + DNA strand?

A

The DNA equivalent polarity to the mRNA

185
Q

What is unique about enveloped viruses?

A

They do not necessarily have to kill the cell in their course of replications

186
Q

What are some of the uses of viral glycoproteins found in the envelope?

A

they allow entry and host range determination
assembly and egress
evasion from the vertebrate immune system

187
Q

What is unique about the eclipse period for viruses?

A

period during which the input virus becomes uncoated. As a result, no infectious virus can detected during this time

0-12 hours

188
Q

What is the latent period?

A

The time it takes from initiation of infection to the release of new infectious virus particles from the cell about 16 hours for the adenovirus type 5

189
Q

What events take place during the latent period?

A

attachment of virus to cell
entry of virus into cell and uncoating of the viral genome
viral gene expression
viral genome replication
assembly of new viruses and egress of new virus particles from the cell

190
Q

Which enzyme do DNA viruses use to make mRNA?

A

use the host’s RNA polymerase II

191
Q

What do RNA viruses use to make mRNA?

A

They use their own RNA-dependent RNA polymerase to make mRNA and for RNA replication

192
Q

(-) stranded RNA viruses package what with them?

A

RdRp to make a +sense mRNA

193
Q

ho do + stranded RNA viruses with DNA intermediate work?

A

they package reverse transcriptase with them to make a double stranded DNA then us host encoded RNA polymerase II from transcription

194
Q

How are naked capsids release from infected cells?

A

lysis

195
Q

How are enveloped viruses released from infected cells?

A

budding from plasma membrane or the golgi apparatus or ER

196
Q

How would you study larger animal, plant cells and bacteria?

A

using light microscopy

197
Q

How would you study the pox virus or medium sized viruses?

A

you can use electron microscopy or x-ray

198
Q

How would you study a tiny ass virus?

A

x-ray or NMR

199
Q

What type of inclusion bodies are seen with cells infected by virus?

A

virions and proteins in the nucleus
protein and RNA in cytoplasm (Negri bodies)
virus protein complexes and nascent virus in cytoplasm
chromatin clumps in nucleus

200
Q

What are negri bodies?

A

protein and RNA in cytoplasm

201
Q

What is syncytia?

A

cell fusion that is a cytopathic effect of viral infections

202
Q

What are some of the morphologic cytopathic effects associated with a viral infectino?

A 
nuclear shrinking (pyknosis)
membrane proliferation
nuclear membrane proliferation
cytoplasmic vacuolization
cell fusion (syncytia)
chromosomal magination & breakage
rounding and detachment of tissue culture cells
203
Q

What does humoral immunity refer to?

A

anti-body mediated response usually protects against reinfection

204
Q

What are Type I IFNs?

A

includes alpha and beta IFN

secreted by most infected cells within hours of infection

205
Q

What are Type II IFN?

A

include interferon gamma
produced by T cell and NK cells
more restricted

206
Q

What is APOBEC3G?

A

A human protein that interferes with the replication of HIV by incorporating itself into virus particles and damaging the genetic material of the virus.

207
Q

What is Vif?

A

The HIV protein that blocks APOBEC activity can function in two ways:

(1) by binding to APOBEC3G and preventing incorporation into virus particles; and
(2) by targeting APOBEC3G for destruction and elmination.

208
Q

Type I IFNs use what pathway?

A

ISREs (interferon stimulated response elements)

209
Q

Type II IFNs use what pathway?

A

GAS (gamma activated site)

makes sense because includes interferon gamma

210
Q

IFNs signal through what pathway?

A

Jak/Stat

211
Q

What is the anti-viral state?

A

characteristic of a cell that has bound and responded to IFN at specific receptors and induces transcription of genes. The responding cell need not be infected with virus. IFN alters transcription of more than 100 cellular genes (up and down regulates). Optimal state to block viral replication.

212
Q

What is the role of PKR?

A

mediator of the IFN-induced anti-viral state

protein kinase that phosphorylates and thereby inactivates cellular translation initiation factor, resulting in decreased protein synthesis

Translation arrest

213
Q

What is the role of OAS?

A

mediator of the IFN-induced anti-viral state

2’-5’oligoadenylate synthesis activates a cellular ribonuclease that degrades mRNA

mRNA degradation

214
Q

What is the role of NK cells?

A

activated in response to interferons or macrophage-derived cytokines and serves to contain virus infections while the adaptive immune response generates antigen specific cytotoxic T cells that can clear the infection

215
Q

What are the cytokines of the innate defense?

A

IFNs, IL-1, TNFa, IL-6, IL-12, IL-18

216
Q

What are the chemokines of the innate defense?

A

IL-8, IP10, MIP1a

217
Q

What is one main difference between adaptive immunity and innate?

A

adaptive is able to target viruses with greater precision while using many of the same effector mechanisms

218
Q

What type of antibody is produced during primary virus infections?

A

IgM isotyoe

219
Q

Which antibody can facilitate complement lysis of enveloped viruses.

A

IgM and IgG

220
Q

Name a neutralizing Ab

A

IgA: inhibits virion/host attachement, neutralizes toxins/enzymes.

221
Q

Name the importance of cell mediate responses for viral infections

A

Critical for recognizing and eliminating viral INFECTED cells

222
Q

What are the two categories of adaptive defense?

A

humoral response

cell mediated

223
Q

What are the major cell types involved in the innate response?

A

Mononuclear cells
dendritic cells
NK cells

224
Q

What are the major cell types involved in the adaptive response?

A

B and T cells

225
Q

Define tropism

A

A given virus is likely to infect certain tissues and not others.

226
Q

How are enveloped viruses often trasmitted?

A

often by close contact since they are sensitive to many environmental stresses

227
Q

How are non-enveloped viruses often trasmitted?

A

they are hardier and more durable

transmitted via virus-associated objects and use repiratory or fecal/oral routes

228
Q

What is the incubation period for acute local virus infection?

A

1-3 days

229
Q

What is the incubation period for acute systemic virus infection?

A

10-21 days

230
Q

What is the duration of immunity for acute local virus infection?

A

often short (viruses rapidly mutate)

231
Q

What is the duration of immunity for acute systemic virus infection?

A

usually life long

232
Q

What is the antibody responsible for resistance to reinfection for acute local viral infections?

A

secretory IgA

233
Q

What is the antibody responsible for resistance to reinfection for acute local systemic infections?

A

serum IgG and secretory IgA

234
Q

Explain a persistent viral infections

A

refers to virus infections that continue top produce NEW virus over long period of time (Hepatitis B, rubella in neonates)

235
Q

Explain a latent viral infection

A

virus genome is relatively silent (little gene transcription, little-no disease in health host). They retain ability to re-initiate transcription and replication to produce new virus (called reactivation or recrudescence). Examples: herpes simplex virus (in dorsal root ganglia), Epstein Barr virus (B lymphocytes) and human papillomaviruses (basal epithelia). Will not see “positive” test in blood.

236
Q

What is an example of an acute local viral infection?

A

colds, diarrhea

237
Q

What is an example of an acute systemic viral infection?

A

measles and small pox

238
Q

What is an example of a chronic viral infection

A

Rubella in neonate

239
Q

What is an example of a latent viral infection

A

VZV

240
Q

What is an example of a slow/progressive viral infection?

A

aids and cancer

241
Q

What is Ehlers-Danlos syndrome?

A

A group of related disorders of COLLAGEN synthesis

242
Q

What are 4 major clinical features of Ehlers-Danlos syndrome?

A

skin hyperextensibility
joint hypermobility
tissue fragility
poor wound healing

243
Q

Elastic fibers provide the skin with..

A

resiliencey

244
Q

collagen fibers provide the skin with..

A

tensile strength

245
Q

What type of stain can be used for elastic fibers?

A

silver

**Argyrophilic

246
Q

What is solar elastosis?

A

acquired disorder of elastic due to significant sunlight exposure elastic fibers degenerate and collage bundles aggregate and clump together

247
Q

What is pseudoxanthoma elasticum?

A

mutation in the gene encoding part of the multi-drug resistant complex that results in the elastic fibers becoming enlarged, tangled, and calcified.

248
Q

Is cellulitis or dermatitis typically bilateral?

A

dermatitis

249
Q

What does atopic dermatitis look like in an infant?

A

dry red scaly areas confined to the cheeks

flushed red cheeks when exposed to cold

250
Q

What condition is associated with flexural skin?

A

atopic dermatitis:

Antecubital fossa
Popliteal fossa 
Neck
Wrists
Ankles
251
Q

Where is atopic dermatitis typically seen in adults?

A

eyelids and hands

252
Q

What are common irritants for irritant contact dermatitis?

A 
soap and water
strong acids and drugs
skin products 
wool
perfumes
raw food
body secretions
253
Q

What drugs commonly cause exanthematous eruptions?

A 
o Aminopenicillins
o Sulfonamides
o Cephalosporins
o Anticonvulsants
o Allopurinol
254
Q

What is the common clinical location of seborrheic dermatitis?

A

facial involvement
Occurs in areas rich in sebaceous glands (scalp, face, ears, chest).
Characterized by flaky, “greasy” scales

255
Q

What type of yeast is associated with seborrheic dermatitis?

A

Malassezia furfur.

256
Q

Increased seb derm is associated with what conditions?

A

Neurologic conditions, including Parkinson’s disease, head injury, and stroke
Human immunodeficiency virus (HIV)

257
Q

What percent of psoriasis have a family history?

A

36%

258
Q

What percent of the population does psoriasis affect?

A

2%

259
Q

What condition may be associated with increased risk of cardiovascular disease?

A

psoriasis

260
Q

What is a trigger for guttate psoriasis?

A

strep throat

261
Q

What percent of chronic urticaria is idiopathic/autoimmune?

A

72%

262
Q

What are the three building blocks of the dermis?

A

collagen
elastic fibers
ground substance

263
Q

What is procollagen cleaved enzymatically into?

A

tropocollagen

264
Q

What is an acquired disorder of elastic tissue?

A

solar elastosis

265
Q

What is a congenital disorder of elastic tissue?

A

pseudoxanthoma elasticum

266
Q

What disorder is caused by a mutation in the MDR gene that results in calcified, brittle elastic fibers?

A

pseudoxanthoma elasticum

267
Q

What are the components of ground substance?

A

principally of two: glycosaminoglycans - hyaluronic acid and dermatan sulphate

268
Q

What is the function of ground substance?

A

come absorb 10,000X their weight in water
under pressure can expel bound water and take it up again
facilitates nourishment of epidermis
allows water diffusion

269
Q

What molecule destroys ground substance?

A

hyaluronidase

270
Q

What molecule produces ground substance for renewal?

A

fibroblasts

271
Q

How would you restore ground substance in a saggy old faced lady?

A

give her pure hyaluronic acid

272
Q

What glues the components of ground substance (hyaluronic acid and dermatan sulphate) together?

A

fibronectins

273
Q

What is the name of the cosmetic filler agent for wrinkles?

A

Restylane

274
Q

What is Auspitz sign?

A

When thickened scales of psoriasis are removed, pinpoint bleeding occurs at that spot. **due to trauma to the capillaries in the upper part of papillary dermis

275
Q

What is verruca?

A

warts

benign, virally induced neoplasms that require an increased blood supply

276
Q

What is central thrombosed capillary loops a sign of?

A

varruca (warts)

277
Q

What is leukocytoclastic vasculitis ?

A

an insult leads to the formation of immune complexes in the walls of vessels

**palpable purpura is seen

278
Q

What type of immunopathology causes leukocytoclastic vasculitis?

A

Type III - Gell & Coombs reaction patter

immune complex mediated

279
Q

What does blanching or blanchable mean?

A

when pressure is applied lesion loses all its redness

280
Q

Is leukocytoclastic vasculitis blanchable? Why or why not?

A

no because RBCs are extravasated into the dermis

281
Q

What causes congenital insensitivity to pain?

A

mutation in the neurotrophic tyrosine receptor kinase 1 (NTRK1)

282
Q

What is type A fiber?

A

heavily myelinated, conducts rapidly
alpha (largest) - proprioception and large motor unit
beta- carries touch
gamma - spindle organs in the muscle stretch receptors
delta (smallest) fast localizing initial component of pain

283
Q

What is type C fiber?

A

unmyelinated, slow conducting

-temperature and itching sensation

284
Q

What are vellus hairs?

A

fine, thin, and apigmented

285
Q

What are three parts of the hair follicle?

A

infundibulum
isthmus
matrical region (root)

286
Q

What is the embryologic origin of the follicular unit?

A

primitive ectodermal germ

287
Q

What are the three cycles of hair growth?

A

anagen - 85% 3 years
telogen - 10-15% 3 months
catagen - 1-5% 3 wks or less

288
Q

What is the mechanism of androgenic hair loss?

A

conversion of testosterone to dihydrotestosterone

289
Q

What treatment is used for androgenic hair loss?

A

Finasterid - selective inhibitor of 5 alpha reductase

works only in MEN

290
Q

What is the relationship between sympathetic nervous system and acetylcholine secretion for the eccrine sweat gland?

A

sweating is mediated by sympathetic system but TRIGGERED by acetylcholine secrition

291
Q

What are drugs that increase acetylcholine levels?

A

neostigmine
physostigmine
organophophate- based pesticides

**results in sweating

292
Q

What are the effects of atropin poisoning?

A

has anticholinergic activity
you dont sweat
warm and flushed

293
Q

What is miliaria?

A

blocked sweat ducts

294
Q

What is chromohidrosis?

A

colored sweat from the apocrine gland

genital area

295
Q

What is anhidrotic ectodermal dysplasia?

A

mutation in EDA gene
aberrant ecrrine development - no sweating
poor temperature regulation
sparse hair, abnormal teeth.

296
Q

How would you treat hyperhidrosis?

A

botulinum toxin blocks secretion by preventing acetylcholine release

297
Q

What comorbidities are associated with psorriasis?

A

Arthritis
-Crohn’s disease
-Persistent low grade inflammation favors the development of insulin resistance, obesity and metabolic syndrome
-Metabolic syndrome patients have accelerated atherosclerosis due to
inflammation
-Cardiovascular Disease
o Patients in their 40s with severe psoriasis were more than 2x RR for
heart attack than people without skin disease
o Mild psoriasis raised the risk of heart attack by 20% for people in their
40s

298
Q

What is the difference between type A and type B influenza?

A

Type B only infects humans

Type A can affect humans and other animals

299
Q

Is type A or B influenza susceptible for antigenic shift?

A

Type A because it can affect multiple animals

300
Q

What type of influenza can you treat with matrix protein inhibitors?

A

Type A

includes: amantidine and rimantidine

301
Q

What type of influenza can you treat with Neuraminidase Inhibitors?

A

Type A and B:

a. Oseltamivir (Tamiflu)
b. Zanamivir (Relenza)
c. Peramivir (Rapivab) – only IV approved

302
Q

What population was most severely affected by the pandemic H1N1 swine flu out break?

A

you children and adults

303
Q

What is H5N1?

A

Highly pathogenic avian influenza A (H5N1) virus

mainly in birds andcan be deadly, particularly to domestic poultry. Since then, H5N1 has been responsible for outbreaks in domesticated poultry throughout SE Asia

binds to the 2, 3 linkage on hemaglutinin but has the potential to bind to our human 2,6 hemaglutinin which would be HORRIFIC!

304
Q

How Do You Determine When a Pandemic is Occurring?

A
  1. Emergence of a new influenza subtype
  2. The virus must infect humans and cause serious illness
  3. Virus must have sustained human-to-human transmission and spread easily (without interruption) among humans.
305
Q

What is respiratory syncytial virus? RSV

A

viral lower respiratory tract infection in all ages, but particularly in young children.

most common cause of bronchiolitis

306
Q

What is the influenza structure?

A

RNA virus with a segmented genome.
eight different pieces of single stranded RNA
. Surrounding the core is a lipid envelope, with a lining of matrix protein on the
inner side of the envelope.

307
Q

What is the respiratory syncytial virus structure?

A

• Single stranded, non-segmented RNA virus

308
Q

What can you do to prevent respiratory syncytial viral infection in children?

A

No vaccination at this time but you can use prophylaxis for high risk groups: palivizumab and motavizumab

Disease and Defense (4 decks)

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