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
2
Q
What type of melanin produces black to brown pigment?
A
Eumelanin
*Eutopia!
3
Q
What type of melanin produces yellow to red-brown pigment?
A
phenomelanin
4
Q
Where do light skin melanocytes cluster?
A
top of nucleus
5
Q
Where can you find dark skin melanocytes in the cell?
A
**larger and evenly distributed throughout the cytoplasm
6
Q
Where do hair follicles originate?
A
In the subcutaneous fat
7
Q
Name the four layers of the skin starting from the most superficila layer
A
stratum corneum
stratum granulosum
stratum spinosum
stratum basalis
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
9
Q
Where can you find profilaggrin?
A
In keratohyalin granules
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.
11
Q
What is the function of the stratum spinosum?
A
Has a “prickly” or spiny appearance due to desmosome attachments between cells
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
13
Q
What is the function of a desmosome?
A
attaches keratinocytes to each other
14
Q
What is the function of a hemidesmosome?
A
attach basal cells firmly to the basal lamina of the dermal
epidermal junction
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)
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
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
18
Q
Where in the dermis is the capillary network that is blood supply for epidermis?
A
the papillary layer
19
Q
What part of the dermis is the pathway for defense cells?
A
the papillary layer
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
21
Q
What part of the dermis contains extensive collagen and elastic fibers that provide strength and flexibility?
A
The reticular layer
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
23
Q
What part of the dermis has a pathway for major blood vessels arranged specifically to facilitate thermoregulation?
A
the reticular layer
24
Q
What part of the dermis has a site of nerve tracts and major sensory receptors?
A
the reticular layer
25
Where are Pacinian corpuscles found and what do they do?
In the reticular layer. They sense vibration, pressure and touch
26
Where are langerhan's cells found and what do they do?
found in the epidermis and they are essentially the immunologic barrier
"antigen presenting cells of the skin"
27
what defect causes albinism?
a defect in the tyrosine gene needed for the synthesis of melanin
28
What is vitiligo?
an autoimmune disease in which antibodies attack melanocytes and you have depigmentation
29
What are the adnexal structures?
```
Apocrine glands
• Eccrine glands
• Hair
• Nails
• Sebaceous glands
-sweat glands
```
30
what organs are needed to activate vitamin D3 and 2?
The liver and kidneys
31
What is the mechanism of getting vitamin D from sun?
UV + 7 dehydrocholesterol = vitamin D
32
What is bullous pemphigoid?
subepidermal blisters due to an autoimmune response against BP 230 and BP 180 (Type XVII collagen) at HEMIDESMOSOMES
33
What is Epidermolysis bullosa (EB) ?
a group of inherited bullous disorders characterized by blister formation in response to mechanical trauma.
34
What is Junctional EB?
blistering due to genetic defects in Laminin 5
35
What is dystrophic EB?
blistering due to genetic defects in collagen XII
36
What type of epidermolysis bullosa (EB) leads to mitten hands, flexion contractures, and increased risk in squamous cell carcinomas?
recessive dystrophic EB
37
What is the thickest layer of the epidermis?
stratum spinosum
38
What filaments do desmosomes contain?
Contain intracellular keratin filaments (5 and 14)
also contains transmembrane proteins, desmogleins and desmocollins
39
What is Pemphigus Vulgaris?
intraepidermal blistering due to antibodies against desmoglein 1 and 3
40
What is epidermolysis bullosa simplex?
onset of blisters shortly after birth due to defects in keratin filaments 5 and 14 (found in desmosomes)
41
What does the breakdown of filaggrins form?
Forms Natural moisturizing factor (NMF) which binds H2O to keep skin moist
42
What disorder is caused by defective skin barrier function due loss-of-function filaggrin mutations?
Icthyosis Vulgaris and atopic dermatitis
43
What is the function of merkel cells and where are they found?
tactile sensation within the epidermis
44
What is the epidermal rete?
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
45
What is the dermis predominantly comprised of?
collagen fibers, elastic fibers and ground
| substance.
46
What is the significance of collagen I?
Makes up 85% wt of the dermis and is also the major component in bone
47
What type of collagen comprises a large part of the fetal dermis but is not a major portion of the adult dermis?
collegen III
48
Where is collagen IV found?
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)
49
What is collagen VII used for?
found in the anchoring fibrils which are used by the
| body to attach the epidermis to the dermis.
50
What type of collagen is synthesized intracellularly within fibroblasts?
procollagen
51
procollagen consists of how many chains?
3 alpha helical chains
52
under an electron microscope what is the pattern characteristic of procollagen?
a characteristic pattern of striations with 68 nm intervals
53
procollagen chains primary consist of what proteins?
Glycine - Proline - Hydroxyproline
54
What is stasis dermatitis?
Chronic venous insufficiency of the lower extremities associated with lower extremity edema.
55
What are some complications associated with stasis dermatitis?
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
56
How would you treat stasis dermatitis?
```
Compression
Elevation
Exercise calf muscles
Vascular surgery
Topical steroids
Avoid allergens
```
57
What is the morphology of dermatitis?
Erythematous papules and thin plaques with scale
58
Where does inflammation take place in dermatits?
Epidermis and dermis
59
What is the morphology of cellulitis?
Warm, tender, erythematous, patches or plaques
60
Where does inflammation take place in cellulitis?
dermis and subcutaneous tissue
61
What is atopic dermatitis?
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)
62
What is the diagnostic criteria for atopic dermatitis?
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
63
What is the pathogenesis for atopic dermatitis?
* 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
64
What's another word for dermatits?
eczema
65
What is irritant contact dermatitis?
Non-immunologically mediated reaction resulting from a direct cytotoxic effect
-Either from a single or repeated exposure to the irritant
66
What is the most common contact dermatitis?
irritant contact dermatitis
67
What are examples of weak irritants?
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
68
What is intertrigo?
an inflammatory condition of skin folds
69
What are the clinical presentations of adult dermatits?
- 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
70
What type of dermatitis typically burns more than itches?
irritant contact dermatitis
71
What is allergic contact dermatitis?
skin condition that requires contact exposure of an allergen, immune response and development of “memory” T cells
72
The biochemical elicitation of ACD is caused by what molecules?
inflammatory cytokines including TNFα and IL-1.
73
What is the gold standard testing for ACD?
patch test
74
What is the most frequent allergen?
nickel exposure 19.5%
75
What are risk factors for nickel sensitivity?
Young
Female
Ears pierced
76
What is co-sensitization and give an example
allergy to two allergens which are not structurally related, but are frequently used concomitantly
Bacitracin and Neomycin
77
What is a drug eruption?
eczematous eruptions/ drug rashes
- Most common type of drug reaction in skin
- Usually cell-mediated type IV hypersensitivity
- Eruption is usually generalized
78
What is the time course of a drug eruption
usually 7-14 days after starting a new drug (unless the drug is an old medication)
with treatment can resolve in 1-2 weeks
79
What enhances the risk of a drug eruption?
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
80
what is urticaria?
-Hives, wheals
| Each individual lesion lasts
81
What is acute urticaria?
represents an immediate type I hypersensitivity reaction
| mediated by IgE antibodies
82
What layer of skin is affected by urticaria?
No epidermal changes just inflammation in DERMIS so no scale or blisters
83
Physical features of urticarias
- Dermographism - exaggerated whealing (welting)
- Delayed Pressure Urticaria
- Vibratory Angioedema
- Exercise-induced urticaria
- Cold Urticaria
- Solar Urticaria
- Aquagenic Urticaria
84
What is the clinical presentation of Seborrheic Dermatitis
- 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).
85
What diseases have more severe seborrheic dermatitis?
HIV patients
86
What disease is commonly seen with seborrheic dermatitis?
Parkinson's disease
87
What is "cradle cap"
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
88
What is the pathogenesis of seborrheic dermatitis?
Sensitivity to yeast which can over grow in areas of oil glands and you get a rash that looks like dandruff
89
What cell type do cherry angiomas affect?
endothelial cells
90
What are cherry angiomas?
bright, red, smooth-topped papules that are primarily distributed in the truncal region
91
What is the best treatment option for small cherry angiomas?
Superficial electrodesiccation
92
What is infantile hemangioma?
Benign endothelial cell neoplasm
93
What is the most common benign tumor of childhood?
Infantile Hemangioma aka strawberry hemangioma or capillary hemangioma
94
What is the pattern of involution for a child with infantile hemangioma?
involute slowly at 10% per year
50% resolved by age 5
90% resolved by age 9
95
What is the first line of treatment for infantile hemangioma (if needed at all) during the growth phase?
Beta blockers
96
What is the histology of infantile hemangioma?
dermal proliferation of capillary-sized endothelial cell-lined vessels.
97
What do infantile hemangiomas cells stain with?
placenta associated vascular markers including GLUT-1
98
What is a port wine stain?
vascular malformation in the endothelum that leads to pink patches.
99
What is one main difference between port wine stain and hemangiomas?
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
100
What is Sturge Weber Syndrome?
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.
101
How is port wine stain treated?
with vascular lasers called "pulse dye laser"
102
What is nevus sebaceus?
A hamartoma the presents as papillomatous, yellow-orange linear plaque on the face or scalp
lesions associated with alopecia
103
When does nevus sebaceous often occur?
During puberty with all the active sebaceous glands and epidermal hyperplasia busy at work
104
What are some of the complications associated with nevus sebaceous?
epithelial neoplasms in 10-30% *small cancer risk
| epidemal nevus syndrom (neurologic abnormalities)
105
What are treatment options for nevus sebaceous?
Either observation or surgical excision. Make sure to do excision EARLY!
106
What is sebaceous hyperplasia?
common benign tumor of oil gland more frequent after middle age
distribution face > trunk > extremities
107
What treatment for sebaceous hyperplasia?
no treatment needed
electrodessication w/w/o curettage
trichloroacetic acid
liquid nitrogen cryotherapy
108
What treatment would you recommend with your patient who has recurrent sebaceous hyperplasia?
liquid nitrogen cryotherapy
109
What are Acrochordons?
skin tags that form in areas of rubbing like neck, axilla, and infra-mammary area
110
What is the most common form of treatment of acrochordons?
freezing "cryosurgery" with liquid nitrogen
-cut off
111
What cell type does acrochordon affect?
fibroepithelial layer of the skin
112
What is dermatofibroma?
Fibrous histiocytoma of the skin that appear as brown, firm papules, and range 3-10 mm in size.
113
Where are dermatofibromas most commonly found?
Legs
114
What is a positive dimple (Fitzpatrick) sign indicative of?
Dermatofibroma
115
What are treatment options for dermatofibroma?
```
no treatment needed
surgical excision (can make make more noticeable)
```
116
What is a lipoma?
benign tumor of adipose tissue
117
What age group are lipomas most common in?
ages 40-60 but can still be seen in children
118
What type of collagen is a keloid mostly made up of?
```
collagen III (early/fetal)
collage I (late/most abundant)
```
119
What is the difference between hypertrophic scars and keloids?
Hypertrophic scars do not growh beyond the boundaries of the original wound
120
What are treatment options for keloid scars?
topical steroids
intralesional steroids
surgical excision -best for ear keloids
surgery +/- radiation
121
What are seborrheic keratosis?
benign tumors of the hair follicles
primarily head, neck, and trunk
122
What is the appearance of seborrheic keratosis?
oval, slightly raised, light brown to black papules or plaques
123
When is the typical onset of seborrheic keratosis?
fourth or fifth decade with gradual increase in nuber
124
What is dermatosis pupulosa nigra?
Subtype of suborrheic keratosis that occur on the face of fitzpatrick skin type V or VI
*morgan freeman
125
What would you call small hyperkeratotic paupules found in the ankels, feet, forearms, and dorsal hands that resemble seborrheic keratoses?
Stucc keratosis
126
What is sign of leser-trelat?
rapid increase in size or number of seborrheic keratoses associated with adenocarcinoma of the stomach in 60% of cases
127
Where are intradermal nevus commonly found?
head and neck
128
Where are junctional nevus' found?
commonly on plantar and palmar surfaces
129
What is the primary lesion for junctional nevus?
macule - typically smooth, tan to brown
130
What is the primary lesion of intradermal nevus'?
papule or nodule
dome shapes
skin colore to tan to light brown
131
Where are compound nevus common found?
trunk and proximal extremities
132
What are appropriate treatment options for nevocellular nevi?
shave biopsy
punch biopsy
excision
133
What is a blue nevus?
dermal proliferation of mealanocytes that get trapped in the dermis and present with a blue color
134
What are treatment options for blue nevus?
punch biopsy
| excision
135
What is a main difference between congenital nevi and acquired nevi?
congenital can range anywhere from 1 mm to huge size
| presence of dark hairs as well
136
What are the risks associated with congenital nevis?
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
What is a dysplastic nevi?
a subgroup of nevi which have an irregular outline, variable pigmentation, indistinct borders, can be larger than 6 mm in diameter
138
What is the clinical significance of dysplastic nevi
can lead to melanoma
139
What is the criteria for familial atypical moles and melanoma (FAMM)?
- 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
What genes are linked to hereditary melanoma?
CDK2NA
CDK4
CMM1
141
What is cafe au lait macules?
subtle increase in number of melanocytes with increased melanin production
142
What are multiple cafe au lait macules associated with?
neurofibromatosis
143
What is neurofibromas?
soft flesh colored papules characterized by the "button hole sign"
focal proliferation of neural tissue within the DERMIS
144
What type of inheritance is neurofibromatosis Type 1?
Autosomal dominant
145
What defect causes neurofibromatosis?
defect in the neurofibromin gene, a tumor suppressor, on chromosome 17 for NF 1
146
What signs are associated with cafe-au-lait macules indicative of NF?
```
prepubertal child has 6 or more > 5 mm
Crows sign (axillary freckling)
```
147
What are factors that increase risk infantile hemangioma?
female
low birth weight
chorionic villus
multiple gestational
148
What is the most common superficial bacterial infection of children?
Impetigo - streptococcus pyogenes
149
What two bacterias cause impetigo?
streptococcus pyogenes and staphylcoccus aureus
150
What is the bacteria that causes non-bullous impetigo?
streptococcus pyogenes
151
What bacteria is associated with non-bullous and bullous impetigo?
Staphylococcus aureus
152
Where does streptococcal/ impetigo contagiosa present?
commonly affects the face followed by the extremities
153
What are the clinical presentations of impetigo contagiosa?
early primary lesion - erythematous macule with superficial blister
developed - "honey colored" yellow crust
mild lymphadenopathy
154
What is the clinical presentation of bullous impetigo
can affect any area of the body
superficial flaccid blister that may demonstrate pus
older lesion - collapsed blister
155
Staphylococcal Non-Bullous Impetigo typically affects what part of the body?
The face - nasal pharynx
156
What type of impetigo is due to a gram positive cocci
streptococcus pyogenes **see chains
157
How is impetigo diagnosed?
```
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
What are predisposing factors to impetigo?
high humidity
| poor hygiene
159
What are treatment options for impetigo?
soaking and gentle removal of crusts
| topical antibiotics - mupirocin 2% ointment
160
What are systemic antibiotics for impetigo?
cephalexin
dicloxacillin
azithromycin
clarithromycin
161
Is cellulitis or impetigo more superficial?
Impetigo is more superficial and cellulitis is deeper in the subcutaneous layer
162
What group of people have a higher risk of cellulitis?
very young, elderly patients, immunocompromised patients, intravenous drug users, patients with chronic ulcers
163
What is erysipelas? what causes it?
a clinical variant of cellulitis most commonly associated with beta hemolytic streptococci - Streptococcus pyogenes
164
What is cellulitis cased by?
Beta-hemolytic streptococci (streptococcus pyogenes), staphylococcus aureus, haemophilus influenza
165
What is the clinical presentation of erysipelas?
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
What is the clinical presentation of cellulitis?
```
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
How would you diagnose cellulitis?
clinical presentation
CBC - look for leukocytosis
culture and gram stain LEADING EDGE
blood culture - usually negative
168
How to treat cellulitis
```
antibiotics - cephalexin
dicloxacillin
clarithromycin
azithromycin
fluroquinolone antibiotics
```
169
What is a dermatophyte?
fungus that feeds on keratin (skin, hair, nails)
170
What is the most common dermatophyte?
trichophyton
171
trichophyton rubrum?
most common cutaneous pathogen
172
trichophyton mentagrophytes?
common cause of tinea pedis
173
trichophyton tonsurans?
common cause of tinea capitis
174
microsporum canis?
common cause of fluorescent tinea capitis
175
epidermophyton floccosum?
common cause of tinea cruris
176
What is a frank pathogens?
can cause disease in a normal healthy host
177
What is an opportunistic pathogen?
usually only causes disease in an immunocompromised host. Ex: HIV
178
How would you measure virulence?
In terms of the number of organisms it takes to cause disease.
**dose response curve
179
What are strategies the strategies viruses use for survival?
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
What is the classical system for classifying viruses?
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
What is the baltimore system for classifying viruses?
classifies based on how the virus produces mRNA
| DNA--> RNA --> Protein
182
What is the + RNA strand?
ribosome ready strand that can be translated into protein
183
What is the - DNA strand?
The DNA from which mRNA is copied
184
What is the + DNA strand?
The DNA equivalent polarity to the mRNA
185
What is unique about enveloped viruses?
They do not necessarily have to kill the cell in their course of replications
186
What are some of the uses of viral glycoproteins found in the envelope?
they allow entry and host range determination
assembly and egress
evasion from the vertebrate immune system
187
What is unique about the eclipse period for viruses?
period during which the input virus becomes uncoated. As a result, no infectious virus can detected during this time
0-12 hours
188
What is the latent period?
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
What events take place during the latent period?
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
Which enzyme do DNA viruses use to make mRNA?
use the host's RNA polymerase II
191
What do RNA viruses use to make mRNA?
They use their own RNA-dependent RNA polymerase to make mRNA and for RNA replication
192
(-) stranded RNA viruses package what with them?
RdRp to make a +sense mRNA
193
ho do + stranded RNA viruses with DNA intermediate work?
they package reverse transcriptase with them to make a double stranded DNA then us host encoded RNA polymerase II from transcription
194
How are naked capsids release from infected cells?
lysis
195
How are enveloped viruses released from infected cells?
budding from plasma membrane or the golgi apparatus or ER
196
How would you study larger animal, plant cells and bacteria?
using light microscopy
197
How would you study the pox virus or medium sized viruses?
you can use electron microscopy or x-ray
198
How would you study a tiny ass virus?
x-ray or NMR
199
What type of inclusion bodies are seen with cells infected by virus?
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
What are negri bodies?
protein and RNA in cytoplasm
201
What is syncytia?
cell fusion that is a cytopathic effect of viral infections
202
What are some of the morphologic cytopathic effects associated with a viral infectino?
```
nuclear shrinking (pyknosis)
membrane proliferation
nuclear membrane proliferation
cytoplasmic vacuolization
cell fusion (syncytia)
chromosomal magination & breakage
rounding and detachment of tissue culture cells
```
203
What does humoral immunity refer to?
anti-body mediated response usually protects against reinfection
204
What are Type I IFNs?
includes alpha and beta IFN
| secreted by most infected cells within hours of infection
205
What are Type II IFN?
include interferon gamma
produced by T cell and NK cells
more restricted
206
What is APOBEC3G?
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
What is Vif?
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
Type I IFNs use what pathway?
ISREs (interferon stimulated response elements)
209
Type II IFNs use what pathway?
GAS (gamma activated site)
makes sense because includes interferon gamma
210
IFNs signal through what pathway?
Jak/Stat
211
What is the anti-viral state?
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
What is the role of PKR?
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
What is the role of OAS?
mediator of the IFN-induced anti-viral state
2’-5’oligoadenylate synthesis activates a cellular ribonuclease that degrades mRNA
mRNA degradation
214
What is the role of NK cells?
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
What are the cytokines of the innate defense?
IFNs, IL-1, TNFa, IL-6, IL-12, IL-18
216
What are the chemokines of the innate defense?
IL-8, IP10, MIP1a
217
What is one main difference between adaptive immunity and innate?
adaptive is able to target viruses with greater precision while using many of the same effector mechanisms
218
What type of antibody is produced during primary virus infections?
IgM isotyoe
219
Which antibody can facilitate complement lysis of enveloped viruses.
IgM and IgG
220
Name a neutralizing Ab
IgA: inhibits virion/host attachement, neutralizes toxins/enzymes.
221
Name the importance of cell mediate responses for viral infections
Critical for recognizing and eliminating viral INFECTED cells
222
What are the two categories of adaptive defense?
humoral response
| cell mediated
223
What are the major cell types involved in the innate response?
Mononuclear cells
dendritic cells
NK cells
224
What are the major cell types involved in the adaptive response?
B and T cells
225
Define tropism
A given virus is likely to infect certain tissues and not others.
226
How are enveloped viruses often trasmitted?
often by close contact since they are sensitive to many environmental stresses
227
How are non-enveloped viruses often trasmitted?
they are hardier and more durable
| transmitted via virus-associated objects and use repiratory or fecal/oral routes
228
What is the incubation period for acute local virus infection?
1-3 days
229
What is the incubation period for acute systemic virus infection?
10-21 days
230
What is the duration of immunity for acute local virus infection?
often short (viruses rapidly mutate)
231
What is the duration of immunity for acute systemic virus infection?
usually life long
232
What is the antibody responsible for resistance to reinfection for acute local viral infections?
secretory IgA
233
What is the antibody responsible for resistance to reinfection for acute local systemic infections?
serum IgG and secretory IgA
234
Explain a persistent viral infections
refers to virus infections that continue top produce NEW virus over long period of time (Hepatitis B, rubella in neonates)
235
Explain a latent viral infection
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
What is an example of an acute local viral infection?
colds, diarrhea
237
What is an example of an acute systemic viral infection?
measles and small pox
238
What is an example of a chronic viral infection
Rubella in neonate
239
What is an example of a latent viral infection
VZV
240
What is an example of a slow/progressive viral infection?
aids and cancer
241
What is Ehlers-Danlos syndrome?
A group of related disorders of COLLAGEN synthesis
242
What are 4 major clinical features of Ehlers-Danlos syndrome?
skin hyperextensibility
joint hypermobility
tissue fragility
poor wound healing
243
Elastic fibers provide the skin with..
resiliencey
244
collagen fibers provide the skin with..
tensile strength
245
What type of stain can be used for elastic fibers?
silver
| **Argyrophilic
246
What is solar elastosis?
acquired disorder of elastic due to significant sunlight exposure elastic fibers degenerate and collage bundles aggregate and clump together
247
What is pseudoxanthoma elasticum?
mutation in the gene encoding part of the multi-drug resistant complex that results in the elastic fibers becoming enlarged, tangled, and calcified.
248
Is cellulitis or dermatitis typically bilateral?
dermatitis
249
What does atopic dermatitis look like in an infant?
dry red scaly areas confined to the cheeks
| flushed red cheeks when exposed to cold
250
What condition is associated with flexural skin?
atopic dermatitis:
```
Antecubital fossa
Popliteal fossa
Neck
Wrists
Ankles
```
251
Where is atopic dermatitis typically seen in adults?
eyelids and hands
252
What are common irritants for irritant contact dermatitis?
```
soap and water
strong acids and drugs
skin products
wool
perfumes
raw food
body secretions
```
253
What drugs commonly cause exanthematous eruptions?
```
o Aminopenicillins
o Sulfonamides
o Cephalosporins
o Anticonvulsants
o Allopurinol
```
254
What is the common clinical location of seborrheic dermatitis?
facial involvement
Occurs in areas rich in sebaceous glands (scalp, face, ears, chest).
Characterized by flaky, “greasy” scales
255
What type of yeast is associated with seborrheic dermatitis?
Malassezia furfur.
256
Increased seb derm is associated with what conditions?
Neurologic conditions, including Parkinson's disease, head injury, and stroke
Human immunodeficiency virus (HIV)
257
What percent of psoriasis have a family history?
36%
258
What percent of the population does psoriasis affect?
2%
259
What condition may be associated with increased risk of cardiovascular disease?
psoriasis
260
What is a trigger for guttate psoriasis?
strep throat
261
What percent of chronic urticaria is idiopathic/autoimmune?
72%
262
What are the three building blocks of the dermis?
collagen
elastic fibers
ground substance
263
What is procollagen cleaved enzymatically into?
tropocollagen
264
What is an acquired disorder of elastic tissue?
solar elastosis
265
What is a congenital disorder of elastic tissue?
pseudoxanthoma elasticum
266
What disorder is caused by a mutation in the MDR gene that results in calcified, brittle elastic fibers?
pseudoxanthoma elasticum
267
What are the components of ground substance?
principally of two: glycosaminoglycans - hyaluronic acid and dermatan sulphate
268
What is the function of ground substance?
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
What molecule destroys ground substance?
hyaluronidase
270
What molecule produces ground substance for renewal?
fibroblasts
271
How would you restore ground substance in a saggy old faced lady?
give her pure hyaluronic acid
272
What glues the components of ground substance (hyaluronic acid and dermatan sulphate) together?
fibronectins
273
What is the name of the cosmetic filler agent for wrinkles?
Restylane
274
What is Auspitz sign?
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
What is verruca?
warts
| benign, virally induced neoplasms that require an increased blood supply
276
What is central thrombosed capillary loops a sign of?
varruca (warts)
277
What is leukocytoclastic vasculitis ?
an insult leads to the formation of immune complexes in the walls of vessels
**palpable purpura is seen
278
What type of immunopathology causes leukocytoclastic vasculitis?
Type III - Gell & Coombs reaction patter
immune complex mediated
279
What does blanching or blanchable mean?
when pressure is applied lesion loses all its redness
280
Is leukocytoclastic vasculitis blanchable? Why or why not?
no because RBCs are extravasated into the dermis
281
What causes congenital insensitivity to pain?
mutation in the neurotrophic tyrosine receptor kinase 1 (NTRK1)
282
What is type A fiber?
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
What is type C fiber?
unmyelinated, slow conducting
| -temperature and itching sensation
284
What are vellus hairs?
fine, thin, and apigmented
285
What are three parts of the hair follicle?
infundibulum
isthmus
matrical region (root)
286
What is the embryologic origin of the follicular unit?
primitive ectodermal germ
287
What are the three cycles of hair growth?
anagen - 85% 3 years
telogen - 10-15% 3 months
catagen - 1-5% 3 wks or less
288
What is the mechanism of androgenic hair loss?
conversion of testosterone to dihydrotestosterone
289
What treatment is used for androgenic hair loss?
Finasterid - selective inhibitor of 5 alpha reductase
| works only in MEN
290
What is the relationship between sympathetic nervous system and acetylcholine secretion for the eccrine sweat gland?
sweating is mediated by sympathetic system but TRIGGERED by acetylcholine secrition
291
What are drugs that increase acetylcholine levels?
neostigmine
physostigmine
organophophate- based pesticides
**results in sweating
292
What are the effects of atropin poisoning?
has anticholinergic activity
you dont sweat
warm and flushed
293
What is miliaria?
blocked sweat ducts
294
What is chromohidrosis?
colored sweat from the apocrine gland
| genital area
295
What is anhidrotic ectodermal dysplasia?
mutation in EDA gene
aberrant ecrrine development - no sweating
poor temperature regulation
sparse hair, abnormal teeth.
296
How would you treat hyperhidrosis?
botulinum toxin blocks secretion by preventing acetylcholine release
297
What comorbidities are associated with psorriasis?
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
What is the difference between type A and type B influenza?
Type B only infects humans
| Type A can affect humans and other animals
299
Is type A or B influenza susceptible for antigenic shift?
Type A because it can affect multiple animals
300
What type of influenza can you treat with matrix protein inhibitors?
Type A
includes: amantidine and rimantidine
301
What type of influenza can you treat with Neuraminidase Inhibitors?
Type A and B:
a. Oseltamivir (Tamiflu)
b. Zanamivir (Relenza)
c. Peramivir (Rapivab) – only IV approved
302
What population was most severely affected by the pandemic H1N1 swine flu out break?
you children and adults
303
What is H5N1?
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
How Do You Determine When a Pandemic is Occurring?
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
What is respiratory syncytial virus? RSV
viral lower respiratory tract infection in all ages, but particularly in young children.
most common cause of bronchiolitis
306
What is the influenza structure?
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
What is the respiratory syncytial virus structure?
• Single stranded, non-segmented RNA virus
308
What can you do to prevent respiratory syncytial viral infection in children?
No vaccination at this time but you can use prophylaxis for high risk groups: palivizumab and motavizumab
