Histology Flashcards

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1
Q

Where is inflammatory infiltrate seen in acute dermatitis?

A

In the upper dermis

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2
Q

Describe inflammatory infiltrate in acute dermatitis

A

Groups of purple cells which will be lymphocytes, seen in the upper dermis

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3
Q

Where is the main abnormality in acute dermatitis and what is seen?

A

Main abnormality is in the epidermis where bubble-like structures will be seen. These represent fluid collections and would clinically be seen as tiny blisters

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4
Q

Spongiosis

A

Fluid accumulation between the keratinocytes in the epidermis

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5
Q

True or false: spongiosis is the typical histological pattern seen in acute dermatitis

A

True

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6
Q

Epidermis in psoriasis

A

Thickened epidermis and lots of keratin in the keratin layer which is loosely packed, with the accumulation of inflammatory cells, particularly neutrophils

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7
Q

Where are nuclei normally broken down?

A

Granular layer

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8
Q

Parakeratosis

A

Retention of nuclei

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9
Q

In which condition is parakeratosis present and why?

A

Psoriasis due to rapid and abnormal differentiation of keratinocytes

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10
Q

Describe rete pegs in psoriasis

A

They are thicker and longer and often joined together

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11
Q

Histology of bullous pemphigoid

A

Epidermis splits up off the dermis at the dermo-epithelial junction so the whole of the epidermis forms the roof of the blister. If split is higher up then the roof is thinner and blister bursts more easily
Inflammatory cells within the blister – mostly eosinophils

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12
Q

Toxic dermal necrolysis is drug induced - true or false?

A

True

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13
Q

What type of cell dies in toxic dermal necrolysis?

A

Keratinocyte

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14
Q

Mortality rate with toxic dermal necrolysis?

A

25-40%

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15
Q

What does toxic dermal necrolysis result in?

A

Epidermal detachment from dermo-epidermal junction

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16
Q

What can skin failure lead to?

A

Loss of thermoregulation, increased risk of infection, failure of homeostatic function

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17
Q

Things required for healthy skin

A

Intact physical barrier
Functioning immune system
Functional vasculature
Functioning venous return and lymphatic system
Means of temperature regulation
Normal sensory nerve function to warn us about injury
Adequate nutrition

18
Q

Means of temperature regulation in healthy skin

A

Capillary dilation/constriction, functioning sweat glands

19
Q

What is a wound?

A

Any break in the skin

20
Q

What does the method of wound healing depend on?

A

Size and type of wound

21
Q

How do most surgical wounds heal?

A

Primary intention

22
Q

Primary intention healing

A

Edges approximated by stitches leading to rapid healing

23
Q

How can primary intention healing be compromised?

A

Haematoma, infection, poor suture technique, dehiscence

24
Q

What type of wounds is secondary intention healing used for?

A

Larger wounds that are too tight to stitch or where direct closure would cause significant distortion of surrounding tissues

25
Q

3 stages of secondary intention healing

A
1 = inflammation
2 = proliferation
3 = tissue remodelling
26
Q

What happens in inflammation stage of secondary intention healing?

A

Platelets form an initial clot and release inflammatory mediators.
Leucocytes debride the wound bed by phagocytosing bacteria and scavenging cellular debris
Inflammation gradually decreases and keratinocyte proliferation and new tissue formation becomes predominant

27
Q

What happens in proliferation stage of secondary intention healing?

A

Cells proliferate to re-epithelialise the wound surface
Granulation tissue formation is stimulated
Fibroblasts lay down matrix and contract the wound (fibroplasia)
Endothelial cells develop new blood vessels (angiogenesis)

28
Q

What happens in tissue remodelling stage of secondary intention healing?

A

New tissue is converted into mature scar tissue over a period of months
Fibroblasts lay down collagen to improve the tensile strength of the scar and restore the dermal matrix

29
Q

Superficial burns are erythematous/non-erythermatous, wet/dry and non-painful/painful

A

Superficial burns are erythematous, wet and painful

30
Q

What colour are deep burns?

A

White or black and charred

31
Q

Are deep burns wet or dry?

A

Dry

32
Q

Are deep burns painful?

A

No, they are numb

33
Q

Where do the burns extend in:

  • First degree?
  • Second degree/partial thickness?
  • Third degree/full thickness?
A

First degree = epidermis only
Second degree/partial thickness = epidermis and dermis
Third degree/full thickness = beyond dermis

34
Q

What are chronic wounds?

A

Wounds present >6 weeks

35
Q

What do chronic wounds often exhibit?

A

Surface slough

36
Q

What is surface slough?

A

A mixture of dead cells, polymorphs and bacteria. It is a yellow/green colour

37
Q

Effect of slough on healing of wounds

A

Inhibitory effect on healing ability of wound

38
Q

How can slough be removed?

A

Chemically, with physical debridement or larval therapy

39
Q

Where do chronic wounds tend to heal from?

A

The edges - increased risk of infection

40
Q

Factors that contribute to delayed healing of wounds

A
Infection
Poor arterial supply
Impaired venous return
Repeated trauma/friction
Poor nutritional state
Underlying systemic disease
41
Q

Factors leading to breakdown of skin: erosion and ulceration (relating to pressure sores)

A

Prolonged pressure over a bony area
Lack of blood flow
Friction from bedding/clothing
Irritation from sweat/blood/urine/faeces

42
Q

Stages of development of pressure sores

A
  • Skin is unbroken but shows a pink or reddened area. May look like a mild sunburn. Skin may be tender, itchy or painful
  • Skin is red, swollen and painful. Blisters (broken or intact) may be present. Upper layers of skin begin to die
  • Sore has broken through the skin and wound extends down to deeper layers of the skin tissue. Crater-like ulcers are present. Wound is prone to infection
  • Sore extends past the skin and into fat, muscle and bone tissue. Blackened, dead tissue called eschar may be seen in deep opened wounds