Brainscape's Knowledge GenomeTM

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


See full index

Patho > Derm/Nero Exam > Flashcards

Derm/Nero Exam Flashcards

1
Q

What does the neural crest give rise to?

A

Posterior root ganglia, sensory (CN), autonomic ganglia, adrenal medulla (extension of neural crest cells), melanocytes, pancreatic islets

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

What is Colchicine?

A

medication used to treat gout that blocks microtubule development & may cause neural tube defects

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

What is the alar plate?

A

part of the neural tube that makes up the posterior portion (sensory, dorsal horn)

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

What is the basal plate?

A

part of neural tube that makes up anterior portion (motor, ventral horn)

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

What are glial blasts?

A

premature glial cells - astrocytes, epyndymal cells, oligodendrocytes, microglial cells

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

What day does the neural fold touch?

A

21

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

What day does the superior neuropore close?

What condition results if it fails to close?

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

What day does the inferior neuropore close?

A

30

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

What does the ectoderm develop into?

A

Sensory organs, epidermis, nervous system (CNS/PNS).

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

What does the mesoderm develop into?

A

Bone, muscle, dermis, urogenital systems, circulatory system.

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

What does the endoderm develop into?

A

GI system, liver, pancreas, respiratory system

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

What is neurulation and when does it occur?

A

the process of neural tube formation, embryonic stage (2-8 wks)

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

What develops in the fetal stage?

A

Polyneuronal development (migration of cells, 50% die, completed by 25th week), and myelination (finished by 3yrs - corticospinal tracts & cortical association fibers)

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

Causes of closure 1 problems? (spine above the sacrum)

A

Folic acid deficiency, metabolic teratogens = spina bifida

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

Closure 2 problems? (superior head)

A

Maternal hyperthermia, folic acid defic, metabolic teratogens = anencephaly

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

Closure 3 problems? (face)

A

usually resistant = mid-facial clefts

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

Closure 4 problems? (posterior head)

A

Maternal hyperthermia = cephalocele

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

Closure 5? (Sacrum)

A

valproic acid exposure = sacral closure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the benign epidermal tumors?

A

Seborrheic Keratosis, Acanthosis Nigricans, fibroepithelia polyp (skin tag), epidermal inclusion cyst, adnexal tumors: eccrine, apocrine.
*Derived from keratinizing stratified squamous epitheilum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Types of AN?

A

Benign (80%): autosomal dominant with variable penetrance, a/w obesity or endocrine abnormalities; Malignant: middle aged/older, a/w GI adenocarcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

GI adenocarcinomas effect on pigment?

A

stimulate fibroblasts to lay more keratin down causing increased pigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the pathogenesis of AN? What other disorders have the same mutation?

A

FGFR3 - achondroplasia, thanatophoric dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Morphology of fibroepithelial polyp? Associated disorders?

A

Fibrovascular cores, covered by benign squamous epithelium, can undergo ischemic necrosis d/t torsion.
*Diabetes, obesity, intestinal polyps. May be more prominent/numerous in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What makes up an epidermal cyst?

A

Keratin and lipid debris from sebaceous secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Morphology of epidermal inclusion cyst

A

wall resembles nL epidermis, center filled w/ laminated strands of keratin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Morph of pilar or trichilemmal cysts

A

Wall: resembles follicular epithelium w/o granular cell layer
Center: filled w/ homongenous mixture of keratin & lipid

27
Q

Morph of dermoid cyst

A

Wall: similar to epidermal inclusion w/ multiple appendages budding outward (w/I dermal layer)

28
Q

Morph of steatocystoma simplex

A

resembles sebaceous gland duct from which numerous compressed sebaceous lobules originate. Different from multiplex: a missense mutation in keratin

29
Q

Imipuimod

A

activates immune system by stimulating Toll-like receptors (to destroy cells)

30
Q

Hallmark of AK?

A

parakeratosis

31
Q

Bowen’s disease

A

SCC in situ, if no invasion through DEJ - sharply defined, red, scaling plaques involving all levels of epidermis

32
Q

SCC pathogenesis

A

DNA damage d/t UV = p53 mutation, dampens immune surveillance by langerhan or NK/lymphocytes in dermis, sensed by kinases normally upregulating p53 expressioin, and if mutated, the response cannot occur. A/w immunosuppression (chemo, organ transplant or steroid use). Implication of HPV 5 & 8

33
Q

BCC facts

A

Most common invasive cancer, BLUE PALISADING NESTS. immunosuppression or inherited defects in DNA repair may cause (xeroderma pigmentosum). May contain melanin

34
Q

BCC morphology

A

resemble nL basal cell layer, arise from epidermis or follicular epithelium. 2 Patterns: multifocal growths (from epidermis), or nodular lesions (grow downwards into dermis)

35
Q

Gorlin syndrome

A

nevoid BCC syndrome, dominant:PTCH gene mutation, 2nd nL allele inactivated by UV light. PTCH encodes receptor for sonic hedgehog gene. absence of PTCH causes activation of SMO leading to BCC.

  • before age 20
  • a/w: medulloblastomas, ovarian fibromas
36
Q

Ligand independent signal transuction is in which disease?

A

BCC - mutated PTCH won’t bind to SMO, and SMO will be activated leading to constant proliferation.

37
Q

Non BCCS pathogenesis

A

genetic: PTCH or p53 mutation –> xeroderma pigmentosa

38
Q

Merkels cell carcinoma?

A

Very malignant & lethal. Connected to nervous system

39
Q

Acute Dermatoses

A

Urticaria, eczema, erythema multiforme

40
Q

Chronic Dermatoses

A

Psoriasis, seborrheic dermatitis, lichen planus, lupus erthymatosus

41
Q

Difference between urticaria and angioedema?

A

Angioedema has deeper edema of dermis and subQ fat

42
Q

Pathogenesis for urticarial:

A
  • Ag induced release of vasoactive mediators from mast cells through IgE Ab
  • ASA can be instigator (AA produce only LKT)
  • Complement mediated urticarial: hereditary angioneurotic edema (def of C1 inhibitor)
43
Q

How does C1 inhibitory deficiency work?

A

C1–>C1a always activated, causing constant C3a/C5a activation which have receptors on mast cells causing degranulation

44
Q

What is seen in persistent eczema?

A

Raised, scaling plaques d/t acanthosis and hyperkeratosis

45
Q

Hallmark of eczema?

A

Epidermal spongiosis

46
Q

Types of dermal melanocytosis

A
  • Mongolian spot
  • nevus of Ota and Ito
  • melanocytes in dermis that actively synthesize melanin
  • blue color (Tyndall effect)
47
Q

Differences between Ota/Ito?

A

Ota: CN V1 & V2
Ito: posterior supraclavicular and lateral brachiocutaneous nerves

48
Q

What cells are important in dermal immunity and repair?

A
  • fibroblasts
  • perivascular mast cells
  • dendrocytes
49
Q

How is melanin synthesized?

A

Tyrosine to DOPA (by tyrosinase), DOPA to melanin

50
Q

Differences in melanin in AA and whites?

A
  • whites: degraded faster, only in basal layer
  • AA: melanosomes present throughout all layers, and are larger with more dendritic processes, can produce more melanin too.
51
Q

What are Langerhans cells?

A

Bone marrow derived, epidermal, immigrant cells.

  • regulate contact hypersensitivity, allograft rejection & GVH.
  • express MHC-1, MHC-2, Fc IgG & IgE
52
Q

Layers of the dermis

A
  • Papillary: loose CT beneath the epidermis

- Reticular: dense dermal collagen (tougher, deeper)

53
Q

Onycholysis

A

Separation of nail plate from nail bed - trauma, infxn, spontaneous

54
Q

Acanthosis

A

diffuse epidermal hyperplasia (chronic irritation)

55
Q

Papillomatosis

A

Surface elevation caused by hyperplasia & enlargement of contiguous dermal papilla

56
Q

Acantholysis

A

Loss of intercellular cohesion btwn keratinocytes (pemphigus vulgaris)

57
Q

Spongiosis

A

Intracellular edema of epidermis

58
Q

Hydropic swelling

A

Intracellular edema of keratinocytes, seen in viral infxns.

59
Q

Exocytosis

A

Infiltration of epidermis by inflammatory cells

60
Q

Vacuolization

A

formation of vacuoles w/I or adjacent to cells

61
Q

Lentiginous

A

linear pattern of melanocyte proliferation w/I epidermal basal layer

62
Q

What are basaloid cells?

A

Nests of tumor cells resembling normal basal cell layer of the epidermis

63
Q

Bowen’s disease?

A

In situ carcinomas of skin caused by HPV infection

Patho (2 decks)

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