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ACVD Exam > Adnexal Units (including diseases) > Flashcards

Adnexal Units (including diseases) Flashcards

Structure and function of the hair follicle, sebaceous gland, and sweat glands with important associated diseases.

1
Q

What are the functions of hair?

A
  • Thermoregulation (dependent on length, thickness, density, medulation, piloerection, and gloss)
  • Physical protection (UV, chemical, physical, microbial)
  • Social interactions (scent, piloerection, color)
  • Camouflage
  • Stem cells for wound healing
  • Dispersing sweat/sebum
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2
Q

Most hair follicles develop before birth, which do not?

A
  • All hair in marsupials
  • Secondary follicles in dogs
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3
Q

Which tissues in the hair follicle are ectodermally derived?

A
  • All epithelial components
  • Sebaceous glands
  • Apocrine glands
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4
Q

Which tissues in the hair follicle are mesodermally derived?

A
  • Hair papilla
  • Connective tissue sheath
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5
Q

Which tissues in the hair follicle are neural crest derived?

A

Melanocytes

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6
Q

Describe where hair first appears on the embryo.

A

Vibrisse on the chin, eyebrow, and upper lip for first then hair begins to form all over the head and then moves down

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7
Q

What are lanugo hairs?

A
  • First hairs formed in utero
  • Non-medulated
  • Typically shed in humans before birth
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8
Q

What genes are likely responsible for non-random placement of hair?

A
  • Homeobox genes
  • Mice with Engrailed knockout get hair on paw pads
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9
Q

How many stages are there in hair follicle development?

A

8
(7 in anagen, 8 in catagen)

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10
Q

What happens to the genes and signaling molecules that are involved in the development of the hair follicle when the individual becomes an adult?

A

Most of the become involved in hair cycling.

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11
Q

What happens first in the development of the hair follicle (stage 1 aka hair placode stage)?

A
  • An epithelial placode/hair placode/hair germ begins to form in the epidermis (goes on to form the entire epithelial portion) due to the influence of Wnt/β-catenin, EDA/EDAR, BMP, noggin, and follistatin
  • Then the mesenchymal/dermal condensate forms underneath (goes on to form the dermal papilla) under the influence of Wnt, PDGF, and Shh
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12
Q

What happens second in the development of the hair follicle (stage 2 aka hair peg stage)

A

Epithelial placode proliferates, invades the dermis, and surrounds the dermal condensate largely mediated by Shh

(later stages will go on to differentiate into inner and outer root sheath and form bulges)

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13
Q

The outer root sheath of the hair peg goes on to form 3 bulges. What does the deepest bulge form?

A

The arrector pili attachment

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14
Q

The outer root sheath of the hair peg goes on to form 3 bulges. What does the middle bulge form?

A

Sebaceous gland

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15
Q

The outer root sheath of the hair peg goes on to form 3 bulges. What does the most superficial bulge form?

A

Sweat gland

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16
Q

What does the fibroblast growth factor 5 (FGF-5) gene do during hair follicle development?

A
  • Responsible for hair length
  • Is a catagen inducer in the mature follicle (so abnormalities lead to longer hair)
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17
Q

What does the keratin-71 gene do during hair follicle development?

A

Is responsible for hair curl

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18
Q

What does the R-spondin 2 gene dictate about hair?

A

Hair size and texture (and distribution)

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19
Q

What does the Wnt/β-catenin pathway do during hair development?

A

-“master switch”
- required for hair follicle induction and initial placode development
- originates from epidermal cells
- determines differentiation into hair follicle keratinocytes
- plays an important role in regulating expression of hair shaft keratin genes as nearly all of them have Lef-1 binding sites in their promoter region
- β-catenin is the downstream mediator of Wnt signaling
- once activated β-catenin translocates to the nucleus and interacts with the LEF/TCF family of genes (Lef-1) which then impact downstream genes including homeobox genes
- these are normally inactive (except for inducing anagen) in the adult epidermis but constant activation results in pilomatricomas and trichofolliculomas

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20
Q

What does EDA/EDAR do during hair development?

A
  • Part of another major pathway that stimulates early follicle development/promotes follicle development
  • Is essential for the development of multiple ectodermal tissues (hair, teeth, glands) so mutations in this result in ectodermal dysplasias
  • Is a downstream mediator of Wnt signaling
  • Mice overexpressing this have fused follicles due to lack of proper spacing
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21
Q

What does BMP (bone morphogenetic protein) do during hair development?

A
  • Works in contrast to EDA/EDAR by inhibiting hair follicle/placode formation
  • Is essential for correct distribution of follicles and differentiation of inner root sheath/hair shaft
  • Induces catagen in the mature follicle
  • Its antagonist is Noggin
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22
Q

What does noggin do during hair development?

A
  • Antagonizes BMP
  • Promotes placode fate by increasing Lef-1 expression and works to induce anagen in the mature follicle
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23
Q

What does TGF-α/EGF do during hair development?

A

Induce catagen in the mature follicle

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24
Q

What does the Notch pathway do during hair development?

A
  • Comes from the hair bulb and outer root sheath
  • Not that important for embryonic development
  • Important for post-natal development leading to differentiation into hair and the the development of the shat and inner root sheath
  • Also appears to control the phenotype of keratinocytes as they leave the bulb matrix
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25
Q

What does the Shh (sonic hedgehog) pathway do during hair development?

A
  • Secreted in the follicular placode
  • Plays a major role in epithelial-mesenchymal signaling
  • Is essential for dermal placode maturation
  • Is responsible for the elongation of the hair germ
  • Aids in inducing anagen in the mature follicle
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26
Q

What does the Patched-1 (Ptc1) pathway do during hair development?

A
  • Is the receptor for Shh
  • Expressed in the germ cells and dermal papillae
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27
Q

What hairs are medullated vs not?

A
  • Most in companion animals and terminal hairs in humans (on scalp, eyebrows, lashes, and elsewhere after puberty)
  • Non-medullated hairs form the wool of sheep, fiber of angora goats, most Sphynx hairs, and vellus hairs on the face/arms/body of people
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28
Q

How do primary and secondary hairs differ?

A
  • Primary hairs aka outer/guard hairs are larger in diameter; bulbs deeper in the dermis; have arrector pili, sebaceous glands, and sweat glands
  • Secondary hairs aka undercoat/down hairs are more superficial and only have sebaceous glands
  • Both are medullated
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29
Q

What is the difference between simple and compound hairs?

A
  • Simple hair follicles only contain 1 hair, compound contain multiple
  • Compound hairs develop post-natally (12-28 weeks in dogs)
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30
Q

How do cat and dog hair follicles differ?

A

Cats have a higher density of hairs with more compound hairs than dogs
- Dogs: compound with 1 large primary and 2 smaller secondaries from 1 pore
- Cats: single primary follicle with 2-5 compound hair follicles around them that contain 3 primary hairs and 6 to 12 secondary hairs

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31
Q

What is acromelanism?

A

In siamese, Himalayan, Balinse, and Birman cats there is a temperature dependent enzyme that convers melanin precursors to melanin so higher temps hair is light and lower temp hair is dark

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32
Q

Describe sheep hair follicles?

A
  • Wool follicles in clusters with 3 primary follicles and 6x more secondary follicles than primary
  • Higher in wool breeds
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33
Q

Where is the mutation in curly coat/sphynx/Devon rexes?

A

Keratin 71

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34
Q

What are keratin 71 mutations associated with?

A

Wavy/curly/wooly phenotype in dogs, cats, and humans

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35
Q

What are keratin 25 mutations associated with?

A

Wavy/curly/wooly phenotype in horses, humans, and mice

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36
Q

What are keratin 27 mutations associated with?

A

Wavy/curly/wooly phenotype in cattle and mice

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37
Q

How do hair follicle keratins organize differently than other keratin intermediate filaments?

A
  • In the hair follicle, keratins organize such that they are stretched out longitudinally (“macrofibrils”) then twist
  • Are crosslinked with keratin associated proteins (KAPs) in addition to disulfide bonds to make it stronger
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38
Q

Which keratin promotes anagen in the hair follicle and how?

A

K17, attenuates TNF-a-induced apoptosis in matrix keratinocytes

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39
Q

What stimuli are involved in directing hair follicle stem cells into sebaceous cells?

A

BLIMP1

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40
Q

What molecules are involved in maintenance of stem cell quiescence in the hair follicle?

A
  • NFATc1
  • Bmp6
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41
Q

What is the primary mediator of hair follicle elongation and dermal papilla development?

A

Shh

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42
Q

What is the hair bulb?

A

Thickening of the proximal end of the hair follicle
Contains rapidly proliferating, undifferentiated matrix cells, melanocytes, and ORS cells

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43
Q

What is the follicular bulge?

A

Insertion site of the arrector pili muscle
Contains hair follicle stem cells
Not specifically present in dogs

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44
Q

What are club hairs?

A

Fully keratinized hair present during telogen and catagen

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45
Q

What is the dermal papilla?

A

Mesodermal signaling center of the hair follicle
Contains fibroblasts
Continuous with dermal connective tissue
Aaro-Perkins corpuscle below; hair matrix above

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46
Q

What is the hair shaft?

A

The hair, composed of terminally differentiated hair follicle keratinocytes
Central medulla, outer cortex, melanin granules, and hair cuticle

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47
Q

Where in the hair shaft are melanin granules most important for coloration?

A

Cortex

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48
Q

What is the inferior segment of the follicle?

A

Most distal portion AKA suprabulbar region
Extends from the bulge/ arrector pili attachment to the bulb
Cycling portion of the hair follicle (ie- not always present)

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49
Q

What is the infundibulum of the follicle?

A

Proximal portion of the follicle
Extends from the sebaceous duct to the epidermal surface

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50
Q

What is the inner root sheath?

A

Rigid tube composed of terminally differentiated hair follicle keratinocytes
Surrounded by ORS
Layers (from inside- out):
- IRS cuticle
- Huxley
- Henle
- companion

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51
Q

What is the isthmus of the follicle?

A

Middle part
Extends from the bulge/ arrector pili attachment to the sebaceous duct

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52
Q

What is the outer root sheath?

A

Outermost layer of follicle
Proximally, merges with the basal layer of the epidermis
Distally merges with the hair bulb

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53
Q

What is Adamson’s fringe?

A

Where hair becomes fully keratinized (upper margin of keratogenous zone)
- where tricholemmal keratinization ends
- dermatophyte invasion of the shaft stops here
Differentiates between regenerative vs non-regenerative portion of follicle

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54
Q

What is the dermal papilla composed of?

A

fibroblasts, collagen bundles, mucopolysaccharide rich stroma, nerve fibers,
single capillary loop

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55
Q

When is the hair bulb maximal in volume?

A

Anagen

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56
Q

What are the permanent portions of the hair follicular structure?

A

infundibulum and isthmus

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57
Q

How many hairs/follicle do chinchillas have?

A

Up to 60

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58
Q

Where are medullated hairs found on companion animals?

A

Most hairs in companion animals are medullated
Medullated hairs can be primary (outer or guard hairs) or secondary (undercoat, down hairs)

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59
Q

What do primary follicles have that secondary follicles lack?

A

Epitrichial sweat gland
+/- arrector pili
(both have sebaceous glands)

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60
Q

What animals have non-medullated hair as adults?

A

Sphynx cats
Wool of sheep
Fiber of angora goats
Human vellus hairs

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61
Q

What are the two tactile hair types in animals?

A

Sinus hairs
Tylotrich hairs

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62
Q

What is the fibrous connective tissue sheath aka hyalin membrane of the hair follicle primarily composed of?

A

Collagen III

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63
Q

Where is the outer root sheath the thickest?

A

Near the epidermis
Just a single layer of flattened cells near the bulb

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64
Q

What do the cells of the outer root sheath in the inferior segment just above the bulb look like?

A

large and contain glycogen so that their cytoplasm is clear and vacuolated

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65
Q

What do the cells of the outer root sheath do in the isthmus?

A

undergo trichilemmal keratinization (without keratohyalin granules)
- occurs where inner root sheath begins to slough
–> so is happening where where ORS is not apposed to the IRS

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66
Q

What is trichilemmal keratinization?

A

abrupt conversion of the non-keratinized ORS cells into anuclear keratin

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67
Q

Where are keratohyalin granules present in the outer root sheath?

A

Infundibulum
(keratinization is happening just like in the epidermis)

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68
Q

Where are follicular keratinocyte and melanocyte stem cells found in humans and mice?

A

ORS at the follicular bulge region

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69
Q

Where are follicular keratinocyte and melanocyte stem cells found in dogs?

A

stem cells are concentrated near the region of the arrector pili attachment
but are also widely distributed in isthmus

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70
Q

What surrounds the ORS?

A

The glassy membrane - continuous with the basement membrane
* mineralizes in toy poodles and Bedlington terriers
* can be senile change

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71
Q

Where is the inner root sheath present in the hair follicle?

A

bulb to the isthmus

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72
Q

When in the hair cycle is the inner root sheath absent?

A

telogen

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73
Q

Where does the inner root sheath keratinize and disintegrates?

A

same level where trichilemmal keratinization begins in the ORS
- at the isthmus

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74
Q

What is the inner most layer of the inner root sheath?

A

Cuticle
Forms “shingled roof pattern”
interacts with the hair shaft cuticle to anchor the hair shaft to the follicle

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75
Q

Why does the inner root sheath mold/shape the hair?

A

IRS keratinizes/ hardens in advance of the hair shaft

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76
Q

What is the outer most layer of the inner root sheath?

A

companion layer
slippage plane between the stationary ORS and the upward moving IRS
is tightly bound to the Henle layer

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77
Q

Is the Henle or Huxley layer closer to the outside of the hair follicle?

A

Henle

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78
Q

Which is the first layer of the inner root sheath to keratinize

A

Henle
*Huxley will keratinize above the Henle layer

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79
Q

What is a granules are a unique feature of the cells of the Henle and Huxley layers of the inner root sheath?

A

trichohyalin granules (pink on histopathology)
morphological hallmark of the IRS (and the hair medulla)
IRS equivalent of keratohyalin granules

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80
Q

What is the Line of Auber?

A

A line across the widest part of papilla
Most of the mitotic activity is below this line

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81
Q

What is the hair shaft epicuticle?

A

Amorphous external layer derived from cuticular cells as an exocellular secretion or from outer portion of cuticular cell membranes

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82
Q

What it the hair shaft cuticle?

A

Covers hair, interacts with the IRS cuticle shingles

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83
Q

What is the hair shaft cortex?

A

bulk of the hair shaft
between the cuticle and the medulla
composed of cornified, spindle shaped cells
provides the mechanical strength
melanin here determines hair shaft color

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84
Q

What is the inner most portion of the hair shaft?

A

medulla
composed of cuboidal cells with trichohyalin granules at the base and air/glycogen vacuoles distally
pigment may be here but doesn’t have much influence on color

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85
Q

What are two mechanisms proposed in the greying of hair?

A

depletion of the melanocytic stem cell reservoir with repeated cycling
damage to the pigmentary unit via ROS
- melanin is a ROS scavenger for the highly active matrix keratinocytes

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86
Q

What is the wild-type/classic hair color in dogs?

A

agouti
produces a light tip, a heavily pigmented body and a yellow or red base

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87
Q

What is the wild-type/ classic hair pattern in cats?

A

tabby/ agouti
produces a black tip, yellow banding in the body and a blue base

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88
Q

In what type of pattern does hair cycling in animals typically occur?

A

mosaic pattern

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89
Q

How does hair cycling in rabbits and rodents (except Guinea pigs) occur?

A

synchronized, orderly waves that starts ventrally between the front legs and progresses dorsally and caudally

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90
Q

What stage of the hair cycle dominate in most animals?

A

telogen

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91
Q

What is induction of anagen dependent on?

A

Wnt, noggin and Shh signaling (as well as KGF)

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92
Q

What happens during early anagen?

A

Onset of growth
Dermal papilla moves into the subcutaneous tissue
- via a remaining fibrous streamer
Dermal papilla becomes enclosed by hair matrix cells
Melanin production in the bulb
Hair matrix cells begin to differentiate into hair shaft and IRS
- Dependent on Wnt signaling and BMP

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93
Q

What happens during late anagen?

A

Dermal papilla is fully enclose and deep into the subcutaneous tissue
Hair shaft is fully developed and surrounded by IRS
Hair reaches the surface and club hair is lost (exogen)

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94
Q

What is IGF-1 in the context of the hair cycle?

A

A potent anagen stimulator

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95
Q

What is induction of catagen dependent on?

A

BMP s
TGF-α
FGF-5
vitamin D receptor activity

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96
Q

What happens during early catagen?

A

Melanogenesis stops
The bulb narrows and mitotic activity stops
- apoptotic keratinocytes may be visible
Dermal papilla changes shape and moves upward
Trailing connective tissue sheath becomes visible

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97
Q

What happens during late catagen?

A

Shortened hair follicle
Club hair is formed
Trailing connective tissue sheath eventually shrinks and disappears

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98
Q

What happens during telogen?

A

Hair follicle and the dermal are in more superficial dermis
Club hair firmly anchored in trichilemmal keratin
There is no IRS or trailing connective tissue sheath

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99
Q

What is exogen?

A

Shedding
Timing varies
o Early exogen – hairs actively retained
o Late exogen – hairs ready to shed
There may be a link between desquamation and shedding

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100
Q

What is kenogen?

A

Empty follicle after exogen
o Denotes prolonged telogen state ; not always pathologic
ORS with no hair or luminal cornified debris

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101
Q

Is temperature or light the most important part of the affect of season on hair growth?

A

Photoperiod
Hypothalamus, hypophysis and pineal gland are stimulated by light to produce hormones which influence hair cycling
Hair growth increases in the summer, decreases in winter, shed fall/spring

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102
Q

What is seasonal alopecia in ferrets?

A

a very dramatic spring molt

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103
Q

How does melatonin influence the hair cycle?

A

Increases the production of prolactin –> inhibits hair shaft elongation
- induces catagen in most species
- except it induces anagen in cashmere goats
Downregulates apoptosis and estrogen receptor expression in hair follicles
It is a free radical scavenger and DNA repair inducer (protective in anagen?)
Influences sex hormone concentrations which can then affect hair cycling

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104
Q

How does daylight affect melatonin?

A

Decreased production with long daylight periods

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105
Q

How does daylight affect catagen?

A

long daylight = less melatonin = less prolactin to induce catagen

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106
Q

How do thyroid hormones influence the hair cycle?

A

Thyroxine (T4) stimulates anagen and stem cell differentiation

T3 and T4 increase melanogenesis in follicles
T3 and T4 down regulate apoptosis, prevent catagen

Hypothyroid = less T3/T4 = increased number of follicles in telogen

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107
Q

How do glucocorticoids/ cortisol influence the hair cycle?

A

Role in hair cycling is not fully understood but suppress anagen
- Dexamethasone can induce catagen in mice
Reduced synthesis and increased degradation of hyaluronans and proteoglycans needed for follicular function

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108
Q

How does progesterone influence the hair cycle?

A

Poorly defined effects on hair cycling
Binds to glucocorticoid receptor in dog and cross-reacts with the testosterone receptor

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109
Q

How do estrogens influence the hair cycle?

A

Shorten anagen, promote catagen, lengthen telogen in dogs
▪ Opposite effect in people: stimulates scalp hair growth
- Possibly via anti-androgenic effects or differing receptor expression
Stimulates BMP expression
Decreases size of sebaceous glands and epidermal thickness

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110
Q

How do androgens influence the hair cycle?

A

Humans: androgens stimulate hair growth everywhere
- except the scalp where they inhibit hair growth
▪ Scalp hairs become miniaturized with a shortened anagen
Testosterone seems to have minimal effects on canine hair follicle growth

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111
Q

How does spaying/ neutering can affect coat quality?

A

Occurs in ~20% of animals
Woolly coat: increased undercoat, increased curl, dulling of color
The pathomechanism is unknown

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112
Q

Where are Langerhans cells found in the hair follicle?

A

ORS of the upper portion
- This population can serve as a reserve to repopulate the epidermis

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113
Q

What is the immune status of the lower portion of the hair follicle in a healthy state?

A

Relative immune privilege
Primarily for the ORS stem cell population and anagen bulb

114
Q

How does the lower portion of the hair follicle sustain an immune privileged state?

A

Absence of MHC class I expression
- melanocytes work to downregulate this
Bulge has increased expression of the “no danger” signal, CD200
MHC class II expression is reduced greatly in the bulb and some in the bulge
Extracellular matrix has high concentration of glycosaminoglycans
- thought to impede T-cell trafficking

115
Q

What immunosuppressive molecules does the hair follicle produce?

A

TGF-β2 and α-MSH
- impair antigen presenting cell function
- prevent NK/ CD8+ cell attacks
IL-10 and MIF (macrophage migration inhibition factor)

116
Q

What does sebum consist of?

A
  • Lipid
  • Keratohyline granules
  • Keratin
  • Associated cellular debris
  • Inorganic salts
  • Anti-microbial proteins
  • Antiviral gycoprotein interferon
  • Albumin
  • Transferrin
  • Complement
  • Glucocorticoid
  • Immunoglobulins
117
Q

What are the functions of sebum?

A
  • Lubricating
  • Antimicrobial
  • Limit water loss/are water-repelling
118
Q

What form of secretion do sebaceous glands have?

A

Holocrine

119
Q

In what species are sebaceous glands sparse and inconspicuous?

A

Pigs

120
Q

In what species are sebaceous glands numerous and prominent?

A

Cattle, horses, cats, and dogs

121
Q

What forms “lather” in horses?

A

Sebaceous secretions and protein-rich (latherin) sweat

122
Q

Where are sebaceous glands primarily located in sheep?

A

Infraorbital, inguinal, and interdigital

123
Q

Where are sebaceous glands primarily located in goats?

A

Base-of-horn glands

124
Q

What do dog and cat sebaceous glands produce more of than human sebaceous glands?

A
  • Sterol esters
  • Free cholesterol
  • Cholesterol esters
  • Wax diesters
125
Q

What do dog and cat sebaceous glands produce less of than human sebaceous glands?

A
  • Triglycerides
  • Monoglycerides
  • FFAs
  • Monoester waxes
  • Squalene
126
Q

What are the free fatty acids present in sebum and what is their primary role?

A
  • Linoleic
  • Myristic
  • Oleic
  • Palmitic acids

(are antimicrobial)

127
Q

Which bacteria are present in the hair infundibulum that produce FFAs?

A
  • Lipase producing bacteria
  • Propionibacterium and Staph
128
Q

Eccrine aka atrichial sweat glands produce secretions in what manner?

A

Merocrine

129
Q

Where do eccrine aka atrichial sweat glands empty to?

A
  • Directly onto the skin surface
  • Openings of ducts are not usually associated with hair follicles
  • Ducts penetrate cornified epithelium and have a corkscrew appearance
130
Q

Which sweat gland type is prominent in humans?

A

Eccrine

131
Q

Where are eccrine aka atrichial glands in animals?

A
  • Foot pads of carnivores
  • Frogs of horses
  • Noses of pigs and cattle
132
Q

What do apocrine aka epitrichial glands look like and where do they open to?

A
  • Distal end may be coiled into a spherical structure or may have a spiral appearance
  • Open into the hair follicle
133
Q

What are the secretions of apocrine aka epitrichial glands like and what do they contain?

A
  • Viscous and cloudy
  • Contain IgA
  • May have pheromones
  • Electrolytes (Na, K, Cl) that can be antimicrobial
134
Q

How do you test for anhydrosis in horses?

A

Inject them with epinephrine

135
Q

What is the genetic mutation leading to anhydrosis in horses?

A

Aquaporin 5

136
Q

What tonicity is equine sweat?

A

Isotonic to hypertonic due to Na, K, and Cl

137
Q

Primary follicles are located ___ in the dermis than secondary follicles and are ___ diameter.

A

1) deeper
2) larger

138
Q

What is a simple hair follicle?

A

When only a single hair is present

139
Q

What is a complex hair follicle?

A

When two or more hairs exit a pore

140
Q

Describe the organization of dog hair follicles.

A

Dogs have compound follicles with a primary hair and smaller secondary hairs that occur in clusters of 3

141
Q

Describe the organization of feline hair follicles.

A

Cats have a single simple follicle surrounded by 2-5 compound follicles with a primary hair and 6-12 secondary hairs

142
Q

Describe the organization of equine and bovine hair follicles.

A

They only have primary hair follicles

143
Q

Describe the organization of porcine hair follicles.

A

They have clusters of 3-4 primary follicles

144
Q

Describe the organization of ovine hair follicles.

A

Clusters of 3 primary follicles interspersed among secondary follicles which can be 6 or more (the number of secondary follicles is greater in wool sheep than other breeds)

145
Q

Where are sinus hairs located?

A

Around the lips, cheek, chin, and eyes (and around the carpi in cats)

146
Q

What are sinus hairs?

A
  • Hairs that grow from specialized follicles and have sensory/tactile function
  • Have a blood-filled sinus
147
Q

Why are sinus hairs so sensitive?

A

There are numerous free nerve endings within the inner dermal sheath which extend to the outer sheath

148
Q

When does the first hair cycle occur and what happens on subsequent cycles?

A

The first hair cycle occurs in the fetus and through subsequent cycles the hair increases in diameter and coarseness (puppy hair –> adult hair)

149
Q

What hair cycle stage predominates in dogs with long hair?

A

Anagen

150
Q

What stage of the hair cycle does doxorubicin affect?

A

Anagen

151
Q

What appendages do sinus hairs have?

A
  • Skeletal muscle
  • Poorly developed sebaceous glands
  • No sweat glands
152
Q

How is the acidic pH of the skin maintained?

A
  • Lactic acid and ammonia in sweat
  • Amino acids from sebum
153
Q

What are the most common pustular and nodular diseases without adnexal destruction?

A

Superficial bacterial folliculitis (common in dog and rare in cats)
Dermatophytosis
Pemphigus foliaceus
Sterile eosinophilic pustulosis
- rare, idiopathic canine disease
- sterile eosinophilic pustules and peripheral eosinophilia

154
Q

What are some pustular and nodular diseases with adnexal destruction?

A

Bacterial furunculosis (including interdigital and post-grooming)
GSD pyoderma
Acral lick dermatitis
Actinic furunculosis
Acne (once there is furunculosis)
Dermatophytic kerion
Demodicosis
Pelodera dermatitis
Eosinophilic furunculosis of the face

155
Q

What are some mural diseases of the hair follicle?

A

Inflammation directed to follicular wall, inflammation involving only infundibulum, isthmus or hair bulb
- Alopecia areata
- Mural folliculitis due to demodicosis and dermatophytosis
- Pseudopelade
- Eosinophilic mucinotic mural folliculitis in dogs
- Degenerative mucinotic mural folliculitis in cats
- Granulomatous mural folliculitis in dogs
- Follicular mucinosis

156
Q

What is telogen effluvium?

A

Rare, widespread alopecia in response to severe metabolic stress
▪ illness, parturition, surgery, anesthesia, etc
▪ Drugs: doxorubicin
Anagen is terminated and all hairs enter telogen –> shed at same time
▪ Usually 1-3 months after the inciting incident
▪ Face is usually spared
▪ Resolves spontaneously
Histopathology: kenogen but no atrophy or lots of early anagen hairs
Non-scarring

157
Q

What is anagen effluvium/ defluxion?

A

Very uncommon
Non-scarring
Anagen phase is interrupted and hair is damaged –> falls out in anagen
▪ Trichogram: hair shaft is damaged, tapered fractures of anagen hairs
Caused by toxins, chemotherapy, other insults
Hair loss occurs within days of the insult

158
Q

What is congenital hypotrichosis/alopecia?

A

May be born without normal hair (reduced number of follicles in utero)
May have hair loss within 4 wk to 6 mo of life (hair fails to regenerate/ cycle following the 2nd or 3rd catagen)
- Some forms are X-linked (EDA/EDAR mutations in ppl, dogs, cattle
- Some forms are autosomal dominant (Mexican hairless/Chinese crested)
- Some form are autosomal recessive (Sphynx)
- May be associated with other ectodermal defects

159
Q

What is aplasia of hair follicle with dental dysplasia?

A

An ectodermal defect
Congenital defect in more than one ectoderm-derived tissue
Humans: mutations in X-linked Eda gene 1
In dogs: X-linked mutation in Eda so occurs primarily in males
- multifocal alopecia of frontotemporal, sacral, abd, proximal limbs
- no arrector pili muscles, sebaceous glands or apocrine glands
- dental alternations of deciduous and permanent teeth

160
Q

What causes congenital hypotrichosis in Mexican hairless, Peruvian hairless, and Chinese crested dogs?

A

Frameshift mutation within the FOXI3
- a form of ectodermal dysplasia
- may also have abnormal teeth
Heterozygous dogs are hairless
Homozygous mutants die during embryogenesis
Variably dysplastic follicles, mostly anagen, have sebaceous/sweat glands

161
Q

What is the most common form of ectodermal dysplasia in most animals?

A

anhidrotic/hypohidrotic ectodermal dysplasia (XLED or XLHED) caused by mutations in the X-linked EDA gene

162
Q

What is congenital hypotrichosis in horses?

A

A form of hair follicle dysplasia
Otherwise normal blue roan Percheron born with a partial alopecia
- progressed to being a complete, body-wide alopecia by 1 year of age Histologic changes consisted of follicular hypoplasia and hyperkeratosis
- Catagen and telogen hair follicles predominated
- Excess melanin within the lumina of follicles and sebaceous glands
Anecdotal reports of a hereditary hypotrichosis in Arabians
- Hair loss is symmetric, on the face, primarily around the eyes

163
Q

What is congenital progressive alopecia in cattle?

A

Hair follicle dysplasia in polled Hereford cattle
- born with wiry hair and alopecia on nose and ears
- alopecia progresses with excessive scaling
- hepatic fibrosis, subtle neuro abnormalities

164
Q

What is lethal hypotrichosis in cattle?

A

Hair follicle dysplasia in Holsteins
- autosomal recessive
- generalized alopecia
- calves die within hours of birth

165
Q

What is viable hypotrichosis in cattle?

A

A hair follicle dysplasia reported in Guernsey, Jersey, Holstein, Hereford
- autosomal recessive with generalized alopecia
- dysplastic HF do not form hair shafts

166
Q

What is black hair follicle dysplasia?

A

Reported in dogs and cattle
Collies, JRTs, Münsterländer dogs, salukis, and a New Zealand huntaway dog
Autosomal recessive
Looks a lot like color dilution alopecia, just affects black hairs
▪ Disorder of melanosome transfer or migration
▪ Other color hair will be normal
Coat changes usually by 4 weeks of age (up to 1 yr)

167
Q

What causes hypotrichosis in sphynx cats?

A

Mutation in the KRT71 gene
Autosomal recessive
Abnormal shaft production without a decrease in follicle quantity
- follicles are small, curved and kinked
- infundibular hyperkeratosis and dilatation
- shafts that protrude from follicular ostia do not reach normal length

168
Q

What is color dilution alopecia?

A

Reported in dogs and cats
▪ Individuals with blue, fawn or grey/ silver coats
▪ Gradual onset, usually by 3 years of age
▪ Weimaraners have their own mild, rare form
Form macromelanosomes due to irregular melanin transfer –> hair fragility
Likely multifactorial, D-locus encodes other follicular changes
Dorsal truck largely affected
Prone to secondary infections

169
Q

What is follicular lipidosis?

A

A form of color-linked follicular dysplasia
Variable degreed of hair loss affecting mahogany points in rottweilers
Present within the first year of life
Lipid accumulation in matrix keratinocytes of anagen bulb
- Ballooning of matrix cells, nuclear pyknosis, absence bulb inflammation
- Primary > secondary hairs

170
Q

What are the common clinical features of follicular dysplasias (not ectodermal dysplasias) in water dogs and which breeds are predisposed?

A

Loss of coat following damage to hairs
- esp neck where collar lies
- periocular, flank/saddle region
Poor coat quality, color change, poor regrowth after clip
- Primary (guard hairs) affected
- Onset in puppyhood
- Progressive alopecia (may be cyclical but eventually permanent)

Portuguese/Spanish water dogs, Irish water spaniels, curly coated retrievers, Chesapeake Bay Retrievers
* all are technically described separately but share key features

171
Q

What is the follicular dysplasia seen in Siberian huskies and malamutes?

A

Onset at 3-4 months of age
Loss of primary but retention of secondary hairs
Coat color change to reddish brown.

172
Q

What is the follicular dysplasia seen in Doberman pinchers?

A

Affects red or black dogs
Onset between 1 and 4 years of age
Flank and saddle region involved initially
- With time, the hair along the dorsum is lost but retained elsewhere

173
Q

What are the histopathologic findings associated with non-ectodermal hair follicle dysplasias in dogs?

A

Normal epidermis and dermis
Infundibular dilatation and keratin plugging (hyperkeratosis)
Hair follicle w/ irregular outer contours +/- vacuolar change
Scattered clumps of melanin
Small anagen or telogen (but decreased number in anagen)
Variably distorted/atrophic (absent, fragmented, or thin) hair shafts

174
Q

What is suspected to play a role in the pathogenesis of follicular dysplasias in Irish water spaniels?

A

Abnormalities of the steroidogenic pathways
Dietary factors and sexual hormones
- Dietary changes improved coat and skin quality

Thought to be an autosomal dominant trait

175
Q

What is recurrent flank alopecia?

A

Repeated well-demarcated serpiginous alopecia w/ hyperpigmentation
- Usually affects bilateral flank > dorsal midline, thorax
Hair loss common in late autumn to early spring and resolves by late spring
- Thought to be due to photoperiod and melatonin
- Melatonin is commonly a treatment
Likely strong intrinsic components as well
Strong breed predilection so may have genetic component

176
Q

What breeds are predisposed to typical recurrent flank alopecia?

A

Boxers
Rhodesian ridgebacks
Airedale terriers
- May cross over dorsum in an “H” saddle pattern
French Bulldogs
English bulldogs
Schnauzers

177
Q

What is the histopathology of recurrent flank alopecia?

A

Mildly acanthotic epidermis
Often hypermelanotic epidermis (including SC and sebaceous glands)
Infundibula are dilated, elongated, and plugged with orthokeratosis
Lower compound HF are short, atrophic, distorted
- “witches’ feet”

178
Q
A

Recurrent flank alopecia

179
Q

What is atypical recurrent flank alopecia?

A

More common in hunting dogs (ex: German shorthair pointer)
Facial only has been reported in Dogues de Bordeaux and Cane Corso
No hyperpigmentation
Tends to be more generalized, severe, and permanent than the typical form
Histopathology is similar to “typical”

180
Q

What is alopecia X?

A

Affects plush coated breeds
- True alopecia X in Pomeranians
- Alopecia X-like in all other breeds
Usually affects between 1 and 5 years of age
Affects males > females, thought to have a hormonal component
- variable results on a large hormone panel study
- 17-hydroxyprogesterone (17-OHP) is increased
Bilaterally symmetrical hair loss and hyperpigmentation
- spares the head and distal limbs

181
Q

What are the categories of causes for an increased the percentage of hairs in kenogen?

A

1) Signals that induce a new anagen phase at the end of the telogen phase are missing/reduced
2) Exogen has occurred prematurely, follicle not ready for new anagen
3) Signals which are maintaining the anagen phase (anagen promotion) are missing

182
Q

Which hormones or stress related molecules are inducers of premature telogen?

A

Glucocorticoids
Estrogens

183
Q

Which hormones or stress related molecules prolong anagen?

A

TSH
T3/4

184
Q

Which hormones or stress related molecules are inducers of premature catagen?

A

Glucocorticoids
Estrogens
Substance P
Nerve growth factor

185
Q

Which hormones or stress related molecules are inducers of anagen?

A

TSH
T3/4

186
Q

Which hormones or stress related molecules are inhibitors of anagen?

A

Glucocorticoids
Estrogens
Testosterone
Substance P
Nerve growth factor

187
Q

This dog was born looking like this. What genetic mutation do you suspect?

A

A form of ectodermal dysplasia (probably FOX13)
White arrows: dysplastic epidermal portion of follicle
Black arrows: mesenchymal cells aggregates

188
Q

What causes the hairless phenotype of American hairless rat terriers?

A

Mutation in SGK3
Autosomal recessive
Puppies are born with a sparse, fuzzy coat over their entire body
- gradually lose it from nose back
- spare sinus hairs
- may have dental abnormalities

189
Q

A Spanish water dog presents with regionalized hair loss on the dorsum, the rump, and parts of the lateral thorax. What is occuring?

A

Follicular dysplasia in Spanish and Portuguese water dogs
note
- B: shaft and IRS formation is impaired in the suprabulbar region
- C: fragmented hair shaft
- D: Vacuolar changes in the IRS and the matrix cells

190
Q
A

Color dilution alopecia

191
Q

What non-cutaneous abnormalities have been found for Pomeranians with alopecia X?

A

7-hydroxyprogesterone (17-OHP) is increased
–> thought to be due to abnormal activity of the 21-hydroxylase enzyme
baseline cortisol concentrations correlated with progesterone concentrations
potential abnormal cutaneous steroidogenesis characterized by the dysregulation of genes
- however, relevant gene variants were not identified
suggested that there are an increased number of mitochondrial gene mutations

192
Q

What are the histopathologic findings of alopecia X?

A

reduced number of anagen follicles
relatively high number of telogen/kenogen/atrophic follicles
looks similar to endocrinopathies (esp hyperestrogenism)

193
Q

What is trichorrhexis nodosa?

A

nodes are formed along the hair shaft
hair is abnormally fragile following trivial injury
can be acquired or congenital
described in golden retrievers and horses

194
Q

What is congenital trichoptilosis?

A

a hair shaft abnormality that causes hair to split and fracture due to a defect in the hair shaft’s structure or damage to the cuticle layer
reported in related male golden retrievers

195
Q

What is medullary trichomalacia?

A

name proposed for a hair shaft abnormality that was recognized in 6 German shepherd dogs
loss of architecture, swelling, and apparent softening of the medulla, followed by longitudinal (lengthwise) splitting and breakage of the hair shaft

196
Q

What conditions have been reported in dogs that result in structural defects/breakage of the hair?

A

Trichorrhexis nodosa
Trichoptilosis
Medullary trichomalacia
Color dilution/black hair follicle dysplasia
Bald thigh syndrome

197
Q
A

Bald thigh syndrome
note that hair shafts are fractured and trichilemmal keratin is assembled underneath the hair shaft

198
Q

What is canine pattern alopecia (pattern baldness)?

A

Mostly affects breed w/ smooth hair coats
- ex. Dachshund, Boston terrier, Chihuahua
- may have genetic basis
Develops within the 1st year of life
Develop a bilaterally symmetric thin coat on the pinnae/nearby skin, caudal thighs, perineal skin, ventral neck/chest/abdomen
Alopecia thought to be associated with miniaturization of the hair follicles
- may have increased telogen
- similar to humans with female or male pattern baldness
- due to a shorted anagen phase?

199
Q

How does pituitary dwarfism affect hair coat?

A

affected dogs lack primary hairs and have prominent secondary hairs
- resulting in a puppy coat
over time, bilateral symmetrical alopecia progresses and the skin becomes hyperpigmented

200
Q

What is pili torti?

A

Secondary hairs are flattened and rotated

201
Q

What is the hair shaft disorder of Abyssinian cats?

A

Only affects whiskers and primary hairs
Onion-shaped swelling at the tip of the hair
* Fracture more easily, coat appears rough and lusterless

202
Q

What is spiculosis?

A

Reported in male Kerry blue terriers
▪ Hard, brittle follicular spicules

203
Q

What are the histopathologic features typical of hyperestrogenism?

A

decreased anagen follicles
mainly telogen and kenogen follicles
*like alopecia X
*may also have follicular atrophy

204
Q

What are the typical clinical features of hair loss associated with an endocrinopathy?

A

Nonpruritic , bilateral symmetrical hypotrichosis /alopecia
Rest of coat is dull, dry, fails to regrow after clipping
*often have other signs of the endocrinopathy
*“Zebra striped pattern” with hypothyroid in Rhodesians

205
Q

What are the histopathologic features typical of hyperadrenocorticism?

A

abundant kenogen follicles
severe follicular, dermal, and epidermal atrophy
- atrophy of sebaceous glands to
comedones
+/- calcinosis cutis

206
Q

What are the histopathologic features typical of hypothyroidism?

A

primary hairs in anagen or telogen, normal size
secondary hairs in kenogen or atrophic
epidermal hyperplasia (if concurrent infections are present)
rare dermal mucinosis

207
Q

What is post-clipping alopecia?

A

characterized by a lack of hair regrowth after clipping
underlying cause is unclear
occur more often in dogs with a long telogen HC phase
-eg. Siberian huskies and other breeds with a thick undercoat
- maybe it just takes a long time to reach anagen again
may also have to do with vascular perfusion changes

208
Q

What is traction alopecia?

A

chronic partial ischemia not associated with an underlying vascular pathology
- prolonged traction causes shearing/compression of small vessels
often on top of head in long-haired dogs
once developed, alopecia is long term and generally permanent
histopathology shows atrophy of adnexal units and dermal fibrosis

209
Q

What are flame follicles?

A

exaggerated regressing follicles with large spikes of fused keratin protruding thru ORS to vitreous layer –> result in abnormal catagen phase with overabundant tricholemmal keratin

210
Q

What is alopecia associated with ischemic dermatopathy?

A

caused by impaired vascular perfusion
- underlying vasculitis or vasculopathy
~50% of cases associated with vaccines
focal or multifocal alopecia typically at vaccine site or extremities
- may have erosions/ulcers/crusts, scale, erythema, hyperpigmentation

211
Q

What is histopathology finding associated with ischemic dermatopathy?

A

Histopathology:
- primary and secondary HFs are severely atrophic and may be absent
–> aka “fading” follicles
- Perifollicular collagen is prominent and homogenized
- +/- lymphoplasmacytic cell poor interface dermatitis
- inflammation of the vessel walls is seen rarely in dogs
–> may have loss of vascular distinction or endothelial cells

212
Q

Other than alopecia, what can high doses of doxorubicin for a long time cause?

A

ulcerative erythroderma

213
Q

What is post traumatic alopecia?

A

Reported in cats
shearing trauma to elastic skin results in separation from blood supply
looks a lot like ischemic dermatopathy

214
Q

What is proliferative, lymphocytic, infundibular mural folliculitits with apoptosis and parakeratotic casts?

A

Reported in Labrador retrievers (5 ever)
- Rare, 6 years old
- VERY THICK adherent hyperkeratotic plaques

215
Q

What neoplasia are frequently associated with widespread hair loss?

A

Pancreatic neoplasia/biliary carcinoma: Paraneoplastic alopecia (cats)
Thymoma: feline thymoma exfoliative dermatitis
Cutaneous lymphoma
Occasionally neoplasias treated with doxorubicin

216
Q

What is pseudopelade?

A

rare immune mediated skin disease in dog and cat
novel lymphocytic isthmus mural folliculitis
manifests clinically as a visually noninflammatory alopecia
causes permanent hair loss

217
Q

What is degenerative mucinotic mural folliculitis?

A

rare, presumptively immunological skin disease of cats
generalized alopecia
striking thickening of facial skin
varying degrees of lethargy
causes mural folliculitis of the isthmus with mixed infiltrate

218
Q

What is granulomatous mural folliculitis?

A

rare, presumed immunological syndrome
highly variable alopecia
may be an adverse drug reaction in dogs
associated with methimazole in cats
virus associated in goat (catarrhal fever)

219
Q

What is follicular mucinosis?

A

very rare, presumed immunologically mediated, alopecic skin disease of dog and cat

220
Q

What is alopecia areata?

A

uncommon autoimmune skin disease
Seen in humans, primates, dogs, cats, cattle, poultry, mice, and rats
causes non-scarring well demarcated alopecia +/- leukotrichia
- commonly on face/head but can affect whole body (universalis)
- may also have nail changes
- horses it is usually wide-spread but may be neck, mane, and tail
- can be pruritic if have secondary infection

221
Q

What are the typical histopathologic findings associated with alopecia areata?

A

Lymphocytic bulbitis which may progress to isthmus
- “swarm of bees”

222
Q

What causes alopecia areata and what is the treatment?

A

caused by a loss of immune tolerance
- IgG against lower hair follicle
- mostly CD3+ T cells (+/- CD8+)
- may have a genetic component
- may be triggered

Treatment is immunosuppression - maybe calcineurin inhibitor?
- mixed response
- can occur in people in the face of cyclosporine treatment

223
Q

What breed of horse is predisposed to alopecia areata?

A

Appaloosas and palominos (color not breed) are predisposed
- can have dystrophic hooves (based on one case)
*there is a genetic predisposition in humans

224
Q
A

Alopecia areata
(good differential would be cutaneous epitheliotropic lymphoma since it can preferentially affect hair follicles)

225
Q

What animals are sebaceous glands not present in?

A

Whale and porpoises

226
Q

Where on the body of mammals are sebaceous glands not present?

A

Paw pad and nasal planum

227
Q

Describe the tail gland in carnivores?

A

oval region on cats and dogs
around the 5th -7th coccygeal vertebrae
stiff, coarse hairs from simple follicles
has many large sebaceous glands

228
Q

Where are reserve cells for sebaceous glands found?

A

surrounding basement membrane

229
Q

Where do sebaceous ducts open onto?

A

infundibulum of the hair follicle

230
Q

What receptors on the sebocytes causes lipid accumulation from circulation?

A

LDL receptor
FATP4

231
Q

What hormones influence sebocytes?

A

androgens - hypertrophy and hyperplasia
estrogens and glucocorticoids - induce involution
retinoids - reduce sebum production

232
Q

What do members of the Equidae family have that is unique to their sebum?

A

Lactones

233
Q

Which carnivore species has an increased amount of sebum production?

A

Ferrets

234
Q

What is sebaceous adenitis?

A

Uncommon skin disease in the dog and rare in cats, rabbits, horses, and humans
Inflammatory condition resulting in T-cell-mediated, immunologic
destruction of the sebaceous glands
Unknown pathogenesis but may have a genetic component
- autosomal recessive in Akitas and poodles
- might be an abnormality in lipid metabolism or storage or keratinization defect
- may be associated with other diseases like hypothyroidism or Leishmaniasis

235
Q

What breeds of dogs are predisposed to sebaceous adenitis?

A

Akitas
Poodles
Havanese
Lhasa apso
Chow chow
Springer spaniel

236
Q

What are the clinical signs of sebaceous adenitis?

A

Young to middle age onset
Varying degrees of alopecia, hyperkeratosis, and seborrhea, with follicular casts
Long-coated breeds will present in the early stages with hair color and texture change
Short-coated breeds will present with annular areas of scale and alopecia
Lesions commonly start on head, cervical region and around pinnae
Can extend into the ear canal so otitis externa can occur
Secondary bacterial infections are common

237
Q

What are the histopathologic signs associated with sebaceous adenitis?

A

mild to moderate acanthosis
moderate to severe hyperkeratosis with follicular plugging
granulomatous to pyogranulomatous reactions at level of sebaceous gland
- histiocytes, neutrophils, lymphocytes and plasma cells
in chronic stages there will be a loss of sebaceous glands
perifollicular fibrosis can be present

238
Q

Where do epitrichial sweat gland ducts open onto?

A

Although they are located deep to sebaceous glands, their ducts empty into the infundibulum above the level of the sebaceous gland

239
Q

Where are epitrichial glands found in largest number and size in most species?

A

near mucocutaneous junctions, in the interdigital spaces and over the dorsal neck and rump

240
Q

Where are epitrichial sweat glands concentrated in horses?

A

mucocutaneous junctions, in the submandibular region, near the mane and coronet

241
Q

What happens to the volume of epitrichial sweat glands in thoroughbreds in the summer?

A

increases

242
Q

Where are epitrichial sweat glands found in rodents and ferrets?

A

there are no epitrichial sweat glands in rodents or ferrets

243
Q

What is the treatment of sebaceous adenitis?

A

revolves around removing scale and follicular casts from the skin and coat and improving the quality of the coat and hair regrowth
Will likely be lifelong
Topical treatments: include shampoos, humectants, and oil soaks
Oral treatments: include omega fatty acids, systemic retinoids, cyclosporine, vitamin A, tetracycline, and niacinamide
- typically not responsive to glucocorticoids
- cyclosporine has been shown to reverse histopathologic changes

244
Q

What is the structure of sebaceous glands?

A

may be simple or branched and are composed of 2-8 lobules

245
Q

What is the structure of epitrichial sweat glands?

A

coiled and saccular to tubular
secretory cells are a singular row of flat to columnar epithelial cells
duct is composed of a double layer of cuboidal cells
surrounded by a single layer of fusiform myoepithelial cells in most species

246
Q

What is aquaporin 5?

A

a water channel in horse epitrichial glands which facilitates rapid movement of fluid during thermoregulatory sweating

247
Q

What is unique about the structure of the epitrichial gland in the horse?

A

the myoepithelial cells form a loose basket-weave around the gland and the gland has a rich blood supply

248
Q

How are epitrichial glands innervated?

A

They are not directly innervated but are under the control of adrenergic agonists including epinephrine and norepinephrine

249
Q

How are epitrichial sweat glands controlled in horses?

A

autonomic adrenergic nervous control is the main mechanism
humoral control by adrenergic agonists secreted from the adrenal medulla during exercise is also important
also appears to be some autocrine control

250
Q

What causes epitrichial sweating in horses?

A

fever, exercise, heat, pain, hypoglycemia, hyperadrenocorticsm, and catecholamine release from excitement, stress or a pheochromocytoma

251
Q

What happens to the epitrichial glands of horses that are continuously exposed to adrenergic agents?

A

They become refractory

252
Q

Which immunoglobulin does epitrichial sweat contain?

A

IgA

253
Q

What is anhidrosis?

A

inability to sweat
may have a sudden onset or may be more gradual
can result in life threatening hyperthermia in horses
more common in hot, humid climates
- move them somewhere cooler and drier
ponies, thoroughbreds/warmbloods, and stock-type horses predisposed

254
Q

Why does anhidrosis occur in horses?

A
  • high levels of epinephrine –> desensitization, downregulation of cell receptors and aquaporin-5 –> degeneration of secretory cells
  • macrolides (esp erythromycin) can play a role for foals with R. equi
255
Q

What are the clinical signs of anhidrosis in horses?

A

Patchy to inadequate sweat response, reduced ability to cool down after exercise with persistent hyperthermia and tachypnea
- Acutely, they may collapse and die
If chronic, horses can have a dry coat with scale and partial alopecia of the face/neck

256
Q

How do you diagnose anhidrosis in horses?

A

History
Response to intradermal testing with epinephrine, terbutaline, or other β-2 agonists
- increasing doses 1:1,000,000 to 1:1,000
- normally, sweating occurs over the test site within minutes at all dilutions
- in anhidrotic animals, sweating only occurs at the highest concentrations of epinephrine and only after 5+ hours

257
Q

What is the structure of atrichial sweat glands?

A

small and tightly coiled and reside in the deep dermis and subcutaneous
tissues
secretory cells are cuboidal to columnar and are found in a single layer, lined by a
singly layer of fusiform myoepithelial cells
duct opens directly on the surface of skin

258
Q

What is the innervation of atrichial sweat glands?

A

They have a rich nerve supply and sweating increases due to agitation and excitement

259
Q

What are the common causes of acquired noncicatrichial alopecia due to altered hair follicle function in horses?

A

Telogen effluvium
Anagen effluvium
Seasonal alopecia
Hypothyroidism (is very rare)
Color dilution alopecia
Follicular dysplasia
Protein, copper, or iodine deficiency
Chemical toxicosis: selenosis*, arsenic, mercury, mimosine

260
Q

What are the common causes of acquired noncicatrichial alopecia due to defects in hair shafts in horses?

A

Trichorrhexis nodosa
Piedra

261
Q

What are the common causes of acquired noncicatrichial alopecia due to inflammation of the hair follicle in horses?

A

Bacterial pyoderma
Dermatophytosis
Alopecia areata
Linear alopecia

262
Q

What is noncicatrichial alopecia?

A

hair regrowth occurs if causative factors are eliminated or corrected

263
Q

What is cicatrichial alopecia?

A

permanent destruction of hair follicles; hair regrowth does not occur

264
Q

What are the causes of cicatrichial alopecia in horses?

A

Physical, chemical or thermal injury
Severe furunculosis
Neoplasia
Cutaneous onchocerciasis

265
Q

What is seasonal alopecia in horses?

A

Seen in several scenarios
1) Icelandic horses in Austria: develops in November, resolves in May/June
- feeding a better diet prevented the problem
2) Horses from the northern hemisphere: facial alopecia in spring-fall
3) Excessive spring shedding: resolves in 1-3 mo
- esp in curly coated horses on mane and tail

*maybe try melatonin?

266
Q

What are the common follicular dysplasia syndromes?

A

Mane and tail dystrophy
- esp Appaloosas but consider alopecia areata if an adult onset
Black and white hair follicle dystrophy
Persistent alopecia of the tail in curly coated horses
Color dilution alopecia

267
Q

What are the cutaneous manifestation of selenium toxicosis in horses?

A

hoof abnormalities
progressive loss of the long hairs of the mane, tail, and fetlocks

268
Q

What is proliferative, lymphocytic, infundibular mural folliculitis and dermatitis with prominent follicular apoptosis and parakeratotic casts?

A

rare condition
Labrador retrievers from North America
immune-mediated reaction
- genetic/hormonal predisposing factors
Clinical lesions included multifocal, coalescing, verrucous, crusted papules and plaques with erythematous borders and comedones or follicular casts

269
Q

What are the histopathologic findings associated with proliferative, lymphocytic, infundibular mural folliculitis and dermatitis with prominent follicular apoptosis and parakeratotic casts?

A

Ortho- and more prominent parakeratotic hyperkeratosis involving follicular infundibular epithelium, with cast formation and a papillary epidermal surface
Lymphocytic exocytosis affected all strata of follicular infundibular epithelium and epidermis
Variable numbers of acidophilic shrunken keratinocytes, often bordered by lymphocytes (satellitosis), occupied the more superficial strata of the follicular infundibular epithelium and epidermis

270
Q

What does immunohistochemistry show with proliferative, lymphocytic, infundibular mural folliculitis and dermatitis with prominent follicular apoptosis and parakeratotic casts?

A

intraepithelial CD3+ T lymphocytes and cleaved caspase-3-positive apoptotic keratinocytes

271
Q

What is the treatment of proliferative, lymphocytic, infundibular mural folliculitis and dermatitis with prominent follicular apoptosis and parakeratotic casts?

A

Immunosuppression, primarily cyclosporine

272
Q

Middle-aged female Labrador

A

proliferative, lymphocytic, infundibular mural folliculitis and dermatitis with prominent follicular apoptosis and parakeratotic casts

(a) Acanthosis and parakeratosis with hair follicle infundibula distended with parakeratotic keratin, providing a papillary appearance to the epidermis (dog 1). Haematoxylin and eosin. (b) Lymphocytes and acidophilic, shrunken keratinocytes, often closely apposed (boxes), within epithelium (dog 1). Haematoxylin and eosin. (c) Eosinophilic fluid within the parakeratotic stratum corneum at the edge of a follicular ostium and vacuoles (arrows) within the parakeratotic stratum corneum (dog 3). Haematoxylin and eosin. (d) Deep within some sections at or near the entrance of sebaceous ducts to the infundibular lumen, there is a thin cornified layer with retained nuclei and with a few apoptotic cells (dog 3). Haematoxylin and eosin.

273
Q

Which section of the hair follicle is absent in telogen?

A

The inferior portion

274
Q

What are the histopathologic hallmarks of the infundibulum in anagen and telogen?

A

stratified squamous epithelium
keratohyalin granules

275
Q

What are the histopathologic hallmarks of the upper portion of the isthmus in anagen and telogen?

A

stratified squamous epithelium
no granules

276
Q

What are the histopathologic hallmarks of the upper portion of the isthmus in anagen?

A

cornified IRS

277
Q

What are the histopathologic hallmarks of the upper portion of the isthmus in telogen?

A

trichilemmal keratin anchoring club hair
no IRS

278
Q

What are the histopathologic hallmarks of the lower portion of the isthmus?

A

glycogenated cells in ORS in anagen
cornified IRS

279
Q

What are the histopathologic hallmarks of the suprabulbar portion of the inferior portion?

A

stratified squamous epithelium
trichohyalin granules
gyclogenated cells in ORS
non-cornified IRS

280
Q

What are the histopathologic hallmarks of the bulbar portion of the inferior portion?

A

matrical cells
trichohyalin granules
dermal papilla

281
Q

The lack of which structure plays a role in why birds are so prone to hyperthermia?

A

no sweat glands in avian skin

282
Q

What glands to avians have?

A

uropygial (or preen) glands
pericloacal glands (which secrete mucus)
glands of the ear canal.

ACVD Exam (25 decks)

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