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General Med 1 > Path - Anatomy - Exam 3 > Flashcards

Path - Anatomy - Exam 3 Flashcards

1
Q

Define agenesis

A

The complete absence of an organ or part of an organ

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2
Q

Define aplasia:

A

The almost complete lack of development of an organ, or part of an organ The clue is the presence of an anlarge (a rudiment that indicates where the organ is supposed to be).

Sometimes the word is used to indicate that there is a lack of any multiplying cells in an organ, i.e. aplastic anemia.

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3
Q

Define hypoplasia:

A

The lack of development of an organ to a full or mature size.

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4
Q

Define atrophy:

A

The acquired reduction in the size of an organ after its mature dimensions have been obtained

Applies to both a reduction in number and/or in size of component cells.

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5
Q

Define hypertrophy:

A

Reversible enlargement of an organ due to an increase in the size of component cells


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6
Q

Define Hyperplasia:

A

Reversible enlargement of an organ due to increase in the number of specialized cells

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7
Q

What are some of the causes of generalized atrophy?

A
  • inadequate nutrition
  • old age
  • disseminated malignancy
  • chronic infection
  • radiation/chemotherapy using antimetabolites
  • disuse – i.e. prolonged bed rest
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8
Q

What are some of the causes of localized atrophy?

A
  • ischemia
  • pressure
  • disuse (decreased work load)
  • hormonal
  • immunological, i.e. pernicious anemia
  • toxic and metabolic conditions
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9
Q

Discuss these quantitative growth abnormalities (atrophy, hypertrophy, hyperplasia) and their causes.

A
  • atrophy
  • hypertrophy
  • hyperplasia

Causes:
a) Atrophy: G1
Reduced RNA and protein synthesis in G1 results in failure to grow and replicate (atrophy)

b) Hypertrophy:
i) Inhibition of DNA synthesis only, results in cell enlargement without cell division
ii) Block in mitosis results in cell enlargement without division 

c) Hyperplasia: G0
Block in pathway to G0 will result in cells continuing in cell cycle to produce increased cell numbers

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10
Q

What could cause agenesis, aplasia or hypoplasia?

A

a) Hereditary – pygmies
b) environmental
c) physical, i.e. trauma, tradiation
d) chemical – thalidomide, alcohol etc
e) Microbiological, rubella, CMV, other herpes, parvo B19 etc

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11
Q

What are the four mechanisms of atrophy?

A
  1. Decreased anabolism
  2. Increased catabolism
  3. Reduced cell replication
  4. Increased apoptosis
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12
Q

Describe how hypertrophy and hyperplasia arise in relation to the normal cell cycle and give examples in physiological and pathological circumstances.

A

a) Hypertrophy:
i) Inhibition of DNA synthesis only, results in cell enlargement without cell division
ii) Block in mitosis results in cell enlargement without division 

b) Hyperplasia: G0
Block in pathway to G0 will result in cells continuing in cell cycle to produce increased cell numbers

Physiological circumstances:

  • female breast at puberty, pregnancy and lactation – hypertrophy and hyperplasia
  • Bone marrow hyperplasia – anemia
  • Lymphoid hyperplasia – infections
  • Compensatory – kidney removal

Pathological:

  • prostatic hypertrophy and hyperplasia
  • parathyroid hyperplasia
  • thyroid hyperplasia
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13
Q

Define metaplasia and describe pathways by which this process may occur

A

Reversible change from one adult cell type to another adult cell type.
NOTE: In terms of neoplasia, malignancy often preceded by metaplasia
Adaptive response
Pathways:
- Usually arises by a proliferation and transformation of immature stem cells or undifferentiated mesenchymal cells along a different pathway.
- Brought about by changed in signals
Causes:
- trauma
- chronic irritation/inflammation
- hypovitaminosis A
- Cigarette smoke

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14
Q

Give examples of metaplasia in various tissues and explain the significance of this process.

A
  • Respiratory tract – squamous metaplasia
  • smoking
  • chronic infection
  • Bladder, renal pelvis, cervix – squamous metaplasia
  • chronic irritation/infection
  • Stomach and oesophagus – goblet cell metaplasia
  • chronic inflammation
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15
Q

What is a neoplasm?

A
  • An abnormal mass/new (neo-) growth of tissue
  • Growth is not co-ordinated

  • Persists after removal of inciting stimulus (if any is identified)

  • May have secondary changes: e.g. ulceration
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16
Q

Define adenoma

A

A benign epithelial neoplasm that forms glands OR which derives from glandular tissue

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17
Q

Define papilloma

A

A benign epithelial neoplasm characterised by the formation of finger-like projections from the epithelial surface

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18
Q

Define teratoma

A

A tumour composed of ecto, endo and/or mesoderaml tissues, usually multiple, foreign to the site of origin.

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19
Q

Definae hamartoma

A

A tumour-like malformation composed of differentiated tissues normal to the site of origin. (iris, pulmonary, renal)

NOT a neoplasm

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20
Q

Define blastoma

A

A tumour composed of embryonic cells – very primitive cells

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21
Q

Define choristoma

A

A mass of histologically normal tissue in an abnormal location

NOT a neoplasm

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22
Q

Define polyp

A

Any growth or mass protruding from a mucous surface

It may not be a neoplasm

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23
Q

Define tuberculoma

A

A tumour-like mass resulting from the enlargement of a caseous tubercle.

NOT a neoplasm

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24
Q

Define mycetoma

A

A chronic disease due to infection by various fungus or actinomycetes affecting the foot, hands, legs or internal organs.

NOT a neoplasm.

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25
Q

Define anaplasia

A

A condition of cells in which they have poor cellular differentiation, losing the morphological characteristics of mature cells and their orientation with respect to each other and to endothelial cells.

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26
Q

Define pleomorphism

A

Pleomorphism is a term used in histology and cytopathology to describe variability in the size, shape and staining of cells and/or their nuclei. It is a feature characteristic of malignant neoplasms, and dysplasia.

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27
Q

Define metastasis

A

The development of secondary malignant growths at a distance from a primary site of cancer.

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28
Q

What does carcinoma refer to?

A

Malignant epithelial

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29
Q

What is cancer?

A

Malignant neoplasm

A tumour having the properties of anaplasia, invasiveness and metastasis.

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30
Q

What does sarcoma refer to?

A

Malignant mesenchymal

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31
Q

Define dysplasia

A

The enlargement of an organ or tissue by the proliferation of cells of an abnormal type, as a developmental disorder or an early stage in the development of cancer.

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32
Q

What factors are used to classify neoplasms?

A
  • Behavioural

  • Histogenetic

  • Descriptive

  • Site of origin
  • Embryological – ecto, endo or mesodermal
  • Aetiological – usually not known
  • Molecular – emerging. I.e. HER 2, BRAF ALK positive
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33
Q

What is the difference between benign and malignant?

A

Benign – remains localized

Malignant – not localized. Can be primary or secondary

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34
Q

What is the difference between hyperplasia, dysplasia and neoplasia?

A

In hyperplasia, there is an increase in the number of cells in an organ or tissue that appear normal under a microscope. In dysplasia, the cells look abnormal under a microscope but are not cancer. Hyperplasia and dysplasia may or may not become cancer.

Neoplasia is the development of a tumor, which means cell division is not being controlled.

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35
Q

What are the key macroscopic features of benign tumors (vs malignant)?

A
  • may have a capsule and be circumscribed
  • no invasion
  • uniform, less haemorrhagic
  • rarely necrotic
  • grows slower
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36
Q

What are the key microscopic features of benign tumors (vs malignant)?

A
  • well differentiated
  • low nucleus: cytoplasm ratio
  • usually not pleomorphic (variability in size and shape of cells) (but exceptions)
  • low mitotic rate
  • no invasion (exceptions)
  • no metastasis
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37
Q

What are the key macroscopic features of malignant tumors (vs benign)?

A
  • tends not to have a capsule and may not be circumscribed
  • invasion
  • necrosis common
  • haemorrhage common
  • grows faster
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38
Q

What are the key macroscopic features of malignant tumors?

A
  • variable differentiation
  • high nucleos: cytoplasm ratio
  • pleomorphism
  • hyperchromasia
  • variable mitotic rate, abnormal mitosis
  • necrosis
  • invasion
  • vascular invasion
  • reaction to invasion (desmoplasia – growth of fibrous or CT)
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39
Q

What are the four key features that differentiate benign and malignant tumors?

A
  1. Differentiation – benign is well
  2. Rate of growth – benign is slow
  3. Local invasion – none for benign
  4. Metastases – no for benign
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40
Q

What is differentiation and what are the different types of differentiation?

A

The extent to which neoplastic cells resemble comparable normal cells morphologically and functionally

a) well differentiated – tumor cells resemble mature normal cells (benign)
b) Intermediate – moderately differentiated
c) Poorly differentiated/undifferentiated – poor or no resemblance
d) Anaplasia – extreme lack of differentiation

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41
Q

What factors does tumor grade depend on?

A

High grade (poor, undifferentiated) vs low

  • differentiation
  • nuclear pleomorphism
  • mitotic rate
  • vascular proliferation
  • necrosis
  • others, i.e. proliferation index
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42
Q

What are some of the biochemical markers of cancers?

A
  • HER2 – breast, stomach
  • BRAF – melanoma, colon, rectum, thyroid
  • EGFR – lung
  • KRAS – colon, rectum, pancreas
  • ASLK positive – lung
  • Oestrogen and progesterone receptors – breast

Allows for target therapy

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43
Q

What are pre-cancerous lesions?

A

Premalignant lesions are morphologically atypical tissue which appears abnormal under microscopic examination, and in which cancer is more likely to occur than in its apparently normal counterpart.

  • Either dysplasia or benign tumor.
  • Confined to the epithelium
  • Morphological expression of disturbance of growth regulation
  • Individual cells similar to malignant cells
  • Pre-neoplastic lesion
  • Low vs high grade
  • Carcinoma in situ – very severe dysplasia
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44
Q

How pre-cancerous lesions progress to malignancy?

A
  • lesions are first localized, often asymptomatic
  • penetrate the basement membranes/capsules
  • movement through extracellular matrix
  • penetrate vascular channels (most cells don’t survive journey)
  • exit to new tissue
  • survival and growth as metastasis evoking angiogenesis
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45
Q

How can cancer spread?

A
  • local direct invasion
  • lymphatic dissemination
  • haematogenous dissemination
  • spread across cavities
  • intraepithelial spread
  • others – implantation, fine needle aspiration tract
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46
Q

What is the aetiology of neoplasms?

A
  • genetic
  • chemical
  • hormonal
  • radiation
  • microbial organisms
  • chronic diseases (i.e. ulcers)
  • immune system disorders
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47
Q

What are the genetic predispositions of cancer?

A

a) autosomal dominant inherited cancer syndromes
b) Defective DNA repair syndromes and resulting DNA instability (lynch)
c) Familial cancers (breast, colon etc)

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48
Q

What are the non hereditary predisposing factors of cancer?

A
  1. Non neoplastic:
    - chronic atrophic gastritis
    - solar keratosis of the skin
    - ulcerative colitis
    - Barrett disease
  2. Neoplastic:
    - benign neoplasms
    - dysplasia
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49
Q

What are some carcinogenic agents?

A

a) chemical
b) radiation
i) UV – squamous and basal cell carcinoma melanoma
ii) ionizing radiation
c) oncogenic viruses and other microbes
- HepB – liver cancer
- EBV – Burkitt’s lymphoma, nasopgaryngeal carcinoma
- HPV - carcinoma of cervix
- H. pylori – gastric carcinoma and lymphoma

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50
Q

Provide a scheme of cancer staging and tumour grading.


A 
TNM cancer staging (site dependant):
-	T: tumor
- size
- extent of spread
-	N: Nodal status
- number
- groups
- size etc
-	M: Metastasis
Eg. T3N1M0

Clinical staging: I, II, III, IV

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51
Q

Provide an overview of the epidemiology of cancer in WA.

A

5 leading primary tumor sites for cancer mortality:

  1. lung (M+F)
  2. colorectal (M)
    breast (F)
  3. prostate (M)
    colorectal (F)
  4. Melanoma (M)
    Pancreas (F)
  5. Unknown primary
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52
Q

What are some of the effects of all neoplasms?

A
  • local/pressure effects
  • abnormal functional activity
  • obstruction of vessels, tubes and ducts
  • bleeding, secondary infection by ulceration
  • rupture of blood vessels
  • pain
  • raised intracranial pressure

Benign tumors are rarely responsible for death directly.

Malignant can also:

  • metastasize
  • replace/destroy native tissue/organs by crowding or invasion
  • cachexia (wasting)
  • paraneoplastic syndromes
  • psychological effects
  • effects of therapy
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53
Q

What are the Bradford Hill Considerations of data?

A
  1. strength of association
  2. consistency of the observation (reproducibility)
  3. specificity to a disease
  4. temporality (cause before disease)
  5. gradient (dose-response)
  6. plausibility (biology)

  7. coherence (with natural history of disease)
  8. experimentation (with significance)
  9. analogy (similar known causes)
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54
Q

How can carcinogens in cigarette smoke cause cancer?

A
  • metabolic activation by ‘DNA adduct’

- Direct DNA damage

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55
Q

What is an example of a gene mutation found in tobacco-induced cancer?

A
  • P53 mutation*
  • LRAS
  • PTEN
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56
Q

How does smoking increase cardio vascular disease risks?

A

A. development of atherosclerotic changes

  • chronic inflammation
  • lipid abnormalities
  • endothelial dysfunction

B. induction of hypercoagulable state

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57
Q

What are common examples of occupational exposure to chemical and physical agents?

A
  • carbon monoxide
  • asbestos
  • lead
  • UV radiation
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58
Q

How does asbestos cause disease?

A
  • direct interaction with cells
  • reactive oxygen species – macrophages attempt to digest it
  • chronic inflammation
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59
Q

What are some asbestos related diseases?

A
  • Asbestosis (fibrosis)
  • Mesothelioma
  • Adenocarcinoma – massive risk increase with smoking
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60
Q

What are some of the consequences of lead poisoning?

A

a) Acute
- GIT pain (colic)
- demyelination neutopathy (weakness)

b) Chronic
- decreased IQ
- cognitive decline
- renal dysfunction
- anemia
- hypertension

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61
Q

What are some gaseous air pollutants and what can they lead to

A
  • ozone
  • sulfur dioxide
  • nitrogen dioxide

Can lead to:

  • production of free radicals
  • airway reactivity
  • lung inflammation
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62
Q

Why can carbon monoxide be a problem?

A
  • Hb has 200x greater affinity for CO than O2

- CNS ischemia

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63
Q

What are some of the consequences of UV radiation?

A
  • sunburn
  • collagen damage
  • carcinoma/melanoma
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64
Q

What is hyperthermia and what are the consequences?

A

Core 41-42 degrees

Consequences:

  • confusion
  • cardiac and respiratory dysfunction
  • vasodilation
  • oedema
  • clotting
  • acidosis
  • denaturation of cell proteins
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65
Q

What is hypothermia and what are the consequences?

A

Core 35 degrees

Consequences:

  • confusion
  • loss of shiver response
  • diuresis
  • cardiac arrhythmia
  • pulmonary oedema
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66
Q

What are some examples of physical environmental agents that cause disease?

A
  • burns
  • trauma
  • electrocution
  • ionizing radiation
  • nutritional:
    a) obesity
    b) malnourishment
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67
Q

What is cytology and what are the 3 main areas?

A

Morphological study of cells by themselves

  1. gynaecological (pap smears)
  2. non- gynaecological
  3. fine needle aspiration (FNA)
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68
Q

What is a pap smear and why is it used?

A
  • cells from transformation zone of cervix obtained via spatula or brush
  • smeared onto slide, fixed and stained using papanicolaou method
  • +/- liquid based technique
  • diagnosis of inflammatory conditions
  • candida
  • trichomonas
  • Diagnosis of viral infections
  • HSV
  • HPV
  • Malignant lesions and their precursors
  • CIN 3 (cervical intraepithelial neoplasia)
  • squamous cell carcinoma
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69
Q

For non-gynaecological cytology, what specimen types can be taken?

A

a) Fluids
- pleural
- peritoneal
- pericardial
- CSF
- urine

b) Brushings
- bronchial
- bile duct

c) Washings
- peritoneal
- bladder
- renal pelvis

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70
Q

Should non-gynaecological cytology samples be fixed or unfixed?

A

Either

If unfixed – should be refrigerated to prevent degeneration of cells
If fixed – alcohol fixative (95% ethanol)

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71
Q

Why is non-gynaecological cytology done?

A 
To diagnose:
-	inflammatory conditions
-	infections
-	malignancy
To exclude malignancy

Example – haematuria (blood in urine) – urologist performs cystoscopy and sees tumor and takes biopsy.

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72
Q

What can be assessed by FNA?

A 
Virtually any organ or mass
Either direct (superficial and palpable) or under image guidance (ultrasound or CT)

How is a FNA sample produced?

  • material obtained smeared on slides
  • fixed and air-dried
  • cell block and be made for ancillary studies
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73
Q

What is tissue pathology (histopathology) and what types are there?

A

The microscopic examination of tissue in order to study the manifestations of disease.

a) Biopsies
- skin, breast, GIT, liver, kidney, cervix, brain

b) Surgical excisions
- inflammatory/infectious/infarct
- benign neoplasm
- malignant neoplasm

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74
Q

/What is the lab process for specimens?

A
  1. Specimen received with request form:
    - patient details
    - specimen location
    - clinical info
    - requesting doctor
  2. Specimen fixed in 10% neutral buffered formalin
  3. Examined by pathologist
  4. Required tissue selected and placed in cassettes
  5. Processed overnight then embedded in paraffin wax
  6. Paraffin block sectioned
  7. Section transferred onto slide
  8. H&E stain
  9. Examination
  10. Report issued
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75
Q

What is histopathology used to diagnose?

A
  • inflammatory conditions
  • infections
  • benign neoplasms
  • malignant neoplasms
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76
Q

In histopathology, how are microbes studied?

A

Fresh tissue required for organism culture and providing antibiotic sensitivities.

  • bacteria: gram stain
  • H. pylori: Toluidine blue
  • Giardia: giemsa stain
  • Fingi: silver stain
  • Mycobacteria: Ziehl Neelsen

Also special stains for iron, mucin and elastin.

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77
Q

What are the types of malignant lesions?

A
  1. Carcinoma (epithelial tissue of skin of lining of internal organs)
    - squamous cell
    - adenocarcinoma
    - neuroendocrine
  2. Sarcoma (CT or other non-epithelial tissue)
  3. Melanoma (melanin forming cells)
  4. Lymphoma (lymph nodes)
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78
Q

What is immunohistochemistry and what is it used for?

A

TUMORS. Uses antibodies to detect different antigens in the tissue sections.

Used to:

  • differentiate between different tumor types
  • determine site of primary tumor in metastatic lesions
  • measure of proliferative activity in tumors
  • determine tumor response to treatment
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79
Q

How is a breast carcinoma diagnosed?

A

Triple test:

  1. clinical
  2. radiology
  3. histopathology
    - core biopsy
    - post surgical excision
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80
Q

For a breast carcinoma, what does histopathological assessment of the surgical excision determine?

A
  1. tumor type and grade
  2. invasive vs in situ
  3. presence/absence of lymphovascular space invasion
  4. adequacy of surgical excision
  5. lymph node status
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81
Q

What is immunohistochemical staining used to determine in breast carcinomas?

A
  • oestrogen and progesterone receptors
    hormone therapy: tamoxifen and aromatase
  • HER2 staining
    therapy: herceptin
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82
Q

Common causes of iron deficiency:

A

a) blood loss
- GI
- menstrual
- other
b) inadequate intake – vegetarian
c) Inadequate absorption
- coeliac disease
- gastritis
- calcium impairs absorption
- ascorbic acid aids absorption
d) Increased requirements
- pregnancy
- children

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83
Q

Common causes of iron overload:

A

a) Hereditary
- HFE haemochromatosis (type 1)
- non-HFE haemochromatosis (type 2-5)
b) Acquired
c) Iron loading anemias
- thalassaemia major
- sideroblastic anemia
- chronic haemolytic anemia

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84
Q
  1. Discuss the absorption, transport and storage of iron in the body.
A
  • Reduced to ferrous state – ferric reductase
  • Transport into enterocyte – divalent metal transporter 1
  • Released – ferroporin + hephaestin
  • Hepatocytes – take up
    a) free iron
    b) transferrin-bound iron – via TR1 and TR2
  • TR2 – sensor for circulating TBI – expression of hepcidin
  • Hepcidin – down regulates ferroportin-mediated release

In intestine:
- In the duodenal enterocyte (cell of the lining of the intestine), dietary iron is reduced to the ferrous state by duodenal ferric reductase.
- Then transported into the cell by divalent metal transporter 1
- It is released by way of ferroporin, facilitated by hephaestin, into circulation
In liver:
- hepatocytes take up iron from circulation either as free iron or transferrin-bound iron(TBI) (if latter, it’s taken up via transferrin receptor 1 and 2)
- TR2 may serves as a sensor of circulating TBI, thereby influencing expression of the iron regulatory hormone hepcidin
- Hepcidin is secreted into circulation, where it down regulated the ferroportin-mediated release of iron from enterocytes, macrophages and hepatocytes.

85
Q

Discuss the sequelae of iron deficiency and iron overload.

A

Deficiency:

  • often asymptomatic
  • weakness
  • headache
  • irritability
  • fatigue
  • difficult exercising
  • brittle nails
  • delayed growth in infants and children
  • neurological sequelae

Overload:

  • organ damage
  • cirrhosis
  • diabetes
  • cardiomyopathy
  • arthritis
  • testicular failure
  • bronzing of the skin
86
Q

Describe the basic measurements performed for the assessment of iron

A
  1. Ferritin – reflects iron stores. Low DOESN’T indicate iron deficiency and high doesn’t confirm overload.
  2. Iron – low doesn’t indicate deficiency, and high doesn’t indicate overload
  3. Transferrin – binds two iron molecules in circulation
  4. %Transferrin saturation = iron/transferrin x 50%
  5. Red Cell Indices:
    a) MCH – low = hypochromic
    b) MCV – low = microcytic
  6. Soluble Transferrin Receptor (sTfR) – up-regulated in deficiency
  7. HFE genotyping if suspecting overload

If anemic, these will all be low. Low RBC indices could also mean frank anemia.

If overload:

  • increased transferrin saturdation
  • +/- increased ferritin
  • HFE genotype
  • Signs of end organ damage from iron deposition, i.e. abnormal LFT.
87
Q

Describe the measurements performed in the assessment of iron deficiency as an adjunct to red cell indices transferrin saturation, ferritin and soluble transferrin receptor.

A

Soluble Transferrin Receptor (sTfR) – up-regulated in deficiency

88
Q
  1. Describe tests used for assessment and monitoring of iron overload
A
  1. Ferratin
  2. Iron
  3. Transferrin
  4. %Transferrin
  5. HFE genotyping – also identifies those at risk
  6. Signs of end organ damage
89
Q

Define a vitamin.

A

Any of a group of organic compounds which are essential for normal growth and nutrition and are required in small quantities in the diet because they cannot be synthesized by the body.

90
Q

Name the vitamins typically associated with vitamin deficiency disease, and the resulting diseases.

A

Vitamin A:

  • xeropthalmia
  • hyperkeratosis (abnormal thickening of outer layer of skin)
  • pruritis (severe itching of the skin)
  • growth retardation
  • susceptibility to infection

Vitamin D:

  • rickets in children
  • osteoporosis in adults

Vitamin E:

  • progressive sensory and motor neuropathy
  • ataxia – loss of control of bodily movements
  • retinal degeneration
  • haemolytic anemia

Vitamin K:
- bleeding

Folate:

  • megaloblastic anemia
  • pregnancy – low birth weight premature, neural tube defects

B1: (Thiamine)

  • Beriberi
  • Cardiomyopathy
  • Polyneuritis

B2: (Riboflavin)

  • angular stomatitis (inflammation of mucous membrane in mouth)
  • glossitis (inflammation of the tongue)
  • dermatitis

B3 (Niacin)
- pellagra:

B6: (pyridoxine)

  • nonspecific stomatitis
  • glossitis
  • neurological complications

B12:

  • megaloblastic anemia
  • atrophic glossitis
  • neuropathy and demyelination of the CNS

Vitamin C:
- scurvy

91
Q

Discuss the role of vitamin measurement in the diagnosis of vitamin deficiency diseases.

A

Assays. Vitamin K not available.
Supplementation may be easier, cheaper, quicker.

B12:

  • assay of B12 levels in serum
  • BUT low normal reference interval may still be deficient, therefore measure ‘active B12’.
92
Q

What could you suspect a lump is on epithelial tissue?

A
  • carcinoma
  • adenoma
  • papilloma
93
Q

Describe the skin as a barrier to infection

A

Stratum corneum = mechanical barrier

Disruption allows penetration of pathogens into deeper layers.
Bacteria may penetrate into deeper layers via lymphatic’s

Capillary plexus allows dissemination of pathogens. Also brings acute inflammatory cells and chemokines.

94
Q

Describe the microbiological causes, pathogenesis, presenting symptoms and signs, investigation and treatment of Impetigo (school sores):

A

Also cause pyoderma

Microbiological causes: Usually S. pyogenes
Also other step and staph aureus.

Presenting symptoms and signs:
-	Itchy rash with red papules, plaques on arms, hands and face
-	painless lesions
-	well child
-	heal without scaring
May be confused with herpes

Pathogenesis:
Minor skin trauma allows entry (i.e. bite, scratch)

Investigation:
- skin swap

Treatment:

  • topical antibiotics, i.e. fucidin
  • oral antibiotics, i.e. flucloxacillin
95
Q

Describe the microbiological causes, pathogenesis and investigation of Tinea:

A
  • tinea pedis – feet
  • tinea corpus – body, ring worm
  • tinea cruris – warm, moist, creases
  • tinea capitis – scalp
  • tinea (or pitriasis) versicolor – Malassezia furfur
  • tinea unguium – onchomycosis. Fungal nail infections. Nails thick, crumbly and discolored.

Microbiological causes:
Dermatophyte infection
Most common: Trichophyton rubrum

Pathogenesis:

  • fungi that invade epidermis and cause inflammation
  • invade keratinized tissues, hair follicles, nails
  • release proteinases and keratinases into skin
  • spread through stratum corneum

Signs and symptoms:

  • burning, itching, tingling in toe space
  • annular lesions

Investigation:

  • skin scrapings or nail clippings – fungus is active in the advancing margin of the lesion
  • microscopy and culture

Treatment:

  • topical clotrimazole given twice daily
  • given until 2 weeks post resolution of skin lesions
96
Q

Describe the microbiological causes, pathogenesis, presenting symptoms and signs and treatment of Paronychia:

A

Microbiological causes:

  • Usually staph aureus
  • can be oral flora, strep, gram –ve or anaerobes
  • candida albicans usually if chronic

Pathogenesis:

  • breakdown of protective barrier between nail and nail fold
  • can result from nail biting, finger sucking, manicuring, artificial nail placement

Presenting symptoms and signs:

  • soft tissue infection around fingernail
  • acutely painful, red, swollen fingernail

Treatment:

  • warm water soaks 3-4 times a day
  • oral antibiotic, i.e. Augmentin or Clindamycin
  • if it progresses to an abscess, drain promptly
  • If chronic, keep dry, warm soaks and topical antifungal

Chronic paronychia:

  • symptoms > 6 weeks
  • episodic inflammation, pain and swelling
  • usually after exposure to water: housekeepers, dishwashers, bartenders, swimmers
  • main cause: Cadida albicans
97
Q

Describe the microbiological causes, pathogenesis, presenting symptoms and signs of Dactylitis:

A

Microbiological causes:
- usually GAS infection (group A strep = pyogenes)

Pathogenesis:
- finger suckers or nail biters

Presenting symptoms and signs:

  • painful pustules on fingertips
  • sausage-shaped, painful swelling of fingers and toes
98
Q

Describe the microbiological causes, pathogenesis, presenting symptoms and signs of Bullous Impetigo:

A

Microbiological causes:
- staph aureus

Pathogenesis:

  • SA produced toxins
  • Bullous impetigo if local spread
  • Generalized spread = staph scalded skin syndrome (SSSS)

Presenting symptoms and signs:

  • fluid filled blisters
  • pop and leave sores
99
Q

Describe the microbiological causes, pathogenesis, presenting symptoms and signs of Toxic Shock Syndrome:

A

Microbiological causes:

  • staph: menstrual or non-menstrual related
  • strep – usually associated with deep GAS infection

Pathogenesis:

  • due to release of toxins
  • cause rash and organ dysfunction
  • strep TSS: 50% mortality
  • staph TSS: 5% mortality

Presenting symptoms and signs:
- rash and organ dysfunction

100
Q

Describe the microbiological causes, pathogenesis, presenting symptoms and signs, and treatment of Folliculitis:

A

Microbiological causes:

  • usually S aureus
  • hot tub folliculitis = pseudomonas aeruginosa
  • Candida, Malassezia furfur

Presenting symptoms and signs:

  • spots
  • infection of hair follicles/apocrine glands

Treatment:

  • local measures, i.e. saline compress
  • topical antibacterials and/or antifungalds

Variations:

  • Folliculitis barbae – shaving bumps
  • Hot-tub Folliculitis
101
Q

Describe the microbiological causes, pathogenesis, presenting symptoms and signs, and treatment of Furuncles:

A

Microbiological causes:
- usually S aureus

Pathogenesis:

  • from preceding folliculitis
  • areas subject to friction/perspiration and contain follicles, i.e. neck, face, axillae, buttocks
  • Predisposing factors: obesity, diabetes mellitus, steroids, leukemia

Presenting symptoms and signs:

  • a plague of boils
  • deep inflammatory nodule

Treatment:

  • application of moist heat usually sufficient
  • +/- anti-staph antibiotics (if fever/cellulitis)

Recurrent furunculosis:

  • relatively common and not associated with a defect
  • prophylaxis:
  • general skin care
  • care of clothing, bedding
  • staph decolonisation
102
Q

Describe the microbiological causes, presenting symptoms and signs, and treatment of Carbuncle:

A

Microbiological causes:
- mainly S aureus

Presenting symptoms and signs:

  • deep infection, contagious furnucles
  • cluster of boils
  • painful, discharging legions
  • unwell, i.e. fever
  • usually nape of neck, back or thighs
  • Complications:
  • cellulitis
  • bacteremia

Treatment:

  • surgical drainage AND
  • antibiotics
103
Q

Describe the microbiological causes, pathogenesis, presenting symptoms and signs, and treatment of Erysipelas:

A

Microbiological causes:
- beta haemolytic strep (usually GAS)

Pathogenesis:

  • involves cutaneous lymphatics
  • predisposing factors:
  • tinea
  • venous insufficiency
  • stasis ulcerations
  • skin disease, i.e. dermatitis
  • insect bite

Presenting symptoms and signs:

  • superficial bacterial skin infection
  • involves cutaneous lymphatics
  • fiery red, indurated, tense plaque
  • clearly demarcated borders (as opposed to cellulitis – indiscreet margins)
  • face or extremities

Treatment:
- Penicillin

104
Q

Describe the microbiological causes, pathogenesis, presenting symptoms and signs, investigation and treatment of Cellulitis:

A

Microbiological causes:
- causative pathogen rarely identified

Pathogenesis:
Predisposing factors:
-	tinea pedis
-	chronic venous or arterial ulcers
-	primary skin diseases (eczema etc)
-	minor trauma, recent surgery
-	leg oedema, i.e. RH failure, venous incompetence, lymphedema.
-	Immunodeficiency

Presenting symptoms and signs:

  • acute bacterial infections of skin and soft tissues
  • presents as a diffuse, spreading erythematous rash
  • maybe fever and chills after rash
  • abscesses, bullae/vesicles may form
  • often lymphangitis, regional lymphadenopathy or lymphadentitis

Investigation:

  • swab blister fluid
  • results may be misleading

Treatment:

  • antibiotics directed at S aureus and B-haemolytic strep
  • flucloxacillin
  • 1st gen cephalosporins
  • clindamycin
  • IV if significant fever or systemic upset, facial cellulities lymphangitis, obesity
  • HITH therapy used commonly
105
Q

Describe the role of venous insufficiency in skin and soft tissue infections

A

Venous insufficiency causes pooling of blood

106
Q

List common cellulitis masqueraders

A
  • lipodermatosclerosis – secondary to venous stasis
  • erythema nodosum
  • pyoderma gangrenosum
107
Q

What are the two types of fungus and their characteristic features?

A

a) Moulds
- characteristic structure – hypha – elongated filaments which may branch. Gives moulds velvety appearance.
- mycelium – interconnected network of hyphae

b) Yeasts
- unicellular, spherical or egg shaped bodies

c) dimorphic – may exist as mould or yeast form

108
Q

How are fungi classified?

A
  1. Site of infection
    - superficial
    - cutaneous
    - subcutaneous
    - deep
  2. Source and route of acquisition
    - exogenous
    - inhalation, through skin
    - endogenous - commensals
  3. Level of virulence
    - virulence to cause disease in normal immune systems
    - opportunistic (immunodeficiency)
109
Q

Where would you find superficial and cutaneous mycoses?

A

Epidermis

Hair shafts and nails may be involved

110
Q

What are common types of superficial and cutaneous mycoses?

A 
Superficial:
-	pityriasis versicolor
o	no living tissue invaded
o	no inflammation
o	malassezia furfur
o	asymptomatic - cosmetic
  • white piedra
  • black piedra
    o both hair shafts producing nodules
Cutaneous: - no living tissue
-	dermatophytosis (ringworm, tinea)
o	no living tissue invaded
o	inflammatory response in living epidermis
o	3 causal fungal genera:
- Trichophyton
- microsporum
- epidermophyton floccosum
  • mucocutaneous candidiasis
    o invasion of living part of epidermis of mucosa
    o inflammation
111
Q

What is the typical appearance of skin lesions caused by dermatophytes?

A
  • Annular lesion which spread centrifugally
  • May be sharply defines
  • Dry scaly skin in center
  • Slightly raised
  • Inflamed spreading margin
  • Tends to heal in centre
  • May itch and burn
112
Q

What are the characteristic features of candidiasis?

A
  • mainly exist in yeast form
  • reproduce by budding
  • in human tissue, they may be found in the form of yeasts, hyphae or pseudohyphae
  • most common pathogen: C. albicans
  • opportunistic fungus
  • Infection of skin and nails may occur when local or systemic immunity is impaired or the balance of normal bacterial flora is altered
  • Life threatening if systemic
113
Q

Where does candidiasis occur?

A

Occurs in parts of body constantly moist:
o vulva and mucous membrane of vagina
o nappy area of babies
o sweaty, intertriginous areas, i.e. beneath breasts

114
Q

What are the symptoms are candidiasis on mucous membranes?

A

Classical discharge:

  • milky white
  • thick with curd-like chunks
  • inflamed, swollen mucosa
  • painful and itchy
115
Q

What features are shared by fungi causing subcutaneous mycoses?

A
  • soil fungi
  • introduced into the skin by trauma
  • resulting infections typically chronic
  • rarely become systemic
116
Q

What are the types of subcutaneous mycoses?

A
  • mycetoma (Madura foot)
  • sporotrichosis
  • chromoblastomycosis
  • pheohyphomycosis
  • hyalohyphomycosis
  • zygomycosis
117
Q

What is a fungal mycetoma?

A

Typically see:

  1. tumefaction – tumor like swelling
  2. draining sinuses
  3. granules – small collections of mycelia in concrete matrix

Lesions grow over months to years
May be destructive to underlying fascia, bone, cartilage and muscle

Most common species = Madurella

118
Q

What is sporotichrosis?

A

Caused by:
Sporothrix schenckii

Features:

  1. a small papule on the periphery at the site of foreign body trauma
  2. gradual development of an enlarging, non-healing ulcer
  3. appearance of pus filled red swellings moving up the limb (following 
lymphatic channels)
  4. these swellings may discharge pus
  5. the infection progresses over a number of months if untreated, and 
gradually heals

Chronic, localized infections
Follows traumatic implantation, soil saprophytes

119
Q

What are the clinical forms of sporotrichosis?

A
  • lymphocutaneous
  • pulmonary
  • meningeal
  • osteoarticular
  • disseminated
  • other
120
Q

What is lymphocutaneous sporotrichosis?

A
  • Development of a papule days-weeks after cutaneous injury
  • Usually ulceration of primary lesion, frainage not grossly purulent and no odour
  • Recurrence of similar nodular lesions with overlying erythema along the lymphatics proximal to the primary lesion
  • Mild pain and no systemic symptoms
121
Q

How is lymphocutaneous sporotrichosis diagnosed?

A

Gold standard – culture

Histopath: mixed granulomatous and pyogenic process
3-5mm diameter, oval-cigar shaped with multiple buds – flower like

Aspirated material or biopsy of lesions

122
Q

What is the treatment for lymphocutaneous sporotrichosis?

A
  • itraconazole
  • continue 2-4 weeks after all lesions have resolved
  • success rate – 90-100%
  • rarely causes long term morbidity
123
Q

What is chromoblastomycosis?

A

Features:

	- small scaly nodule at the site of inoculation 
	- spreads slowly as a scaly, whitish thickened plaque 
	- over time becomes raised and warty 
	- may develop into a large “cauliflower”-like lesion
124
Q

What is Phaeohyphomycosis?

A

Clinical features determined by immunological status of host.
Typical in the normal host is cystic form.
In immunocompromised – paranasal sinuses or the brain

125
Q

What are the risk factors for tinea ?

A 
-	exposure to organism via:
o	shower floors
o	changing rooms
o	hotel, gymnasium carpets and rugs
-	enhanced by warm, moist conditions of skin
-	frequent washing with sop and inadequate rinsing
-	use of disinfectants
-	mechanical irritation
126
Q

What are the different types/sites of tinea?

A
  1. Infection of skin (stratum corneum):

    - i. tinea cruris (inguinal),

    - ii. tinea pedis (feet),

    - iii. tinea manuum (hand) - typically the palms
    - iv. tinea imbricata (rare in Australia)
  2. Infection of hair:

    - i. tinea capitis (scalp),

    - ii. tinea barbae (facial skin/hair),
  3. Infection of nails:
    - i. Tinea unguium
  4. Infection of the upper dermis:

    - i. Majocchi’s granuloma (rare; not covered here)
  5. Miscellaneous
    - i. Piedra, tinea nigra & others (rare; not covered here)
127
Q

What are the 3 common species that tinea?

A
  • Trichophyton
  • microsporum
  • epidermophyton floccosum

Most common human dermatophyte = Trichophyton rubrum

128
Q

How does tinea unguium start and what happens?

A
  • infection starts at free edge, on side of underneath (sub-ungual)
  • nails become thick, crumbly and discolored, with varying degrees of oncholysis
  • often have fungal infections at other sites
129
Q

-

What are the types of tinea unguium?

A

a) DLSO - distal and lateral nail borders (most common)
b) SWO – superficial white onychomycosis – upper surface of nail plate
c) PSO – proximal subungual onychomycosis – nail invasion directly from nail fold

130
Q

What are the details about tinea imbricata?

A

Cause: Trichophyton concentrcum

  • concentric of annular plaques
  • significant scale covering hairless skin surfaces
  • squamous plaques become thick and lamella – looks overlapping (imbricated)
  • like lace, fish scales or tiles

Aetiology:

  • begins in childhood
  • tropics with high humidity, high poverty index, rural/remote, poor hygiene and overcrowding

Treatment:

  • systemic and topical antifungal treatment
  • responses sub-optimal
131
Q

What is pityriasis? (tinea versicolor)

A

Cause:
Malassezia furfur

  • chronic, superficial
  • doesn’t penetrate into tissue
  • induced no cellular response
  • small hypo/hyper pigmented macules
  • trunks, shoulders, arms

Diagnosis:

  • Skin scrapes
  • Dixon’s agar or olive oil supplements required to grow it
132
Q

What are the key differences between cutaneous and subcutaneous mycoses?

A

Cutaneous:

  • very common
  • usually invade keratinous structures
  • common in healthy individuals
  • management is topical +/- systemic antifungals

Subsutaneous mycoses:

  • less common
  • environment fungi with inoculation injury
  • more common in immune system dysfunction
  • management is systemic antifungals +/- surgery
133
Q

List the epithelial tumors of the skin

A

List the epithelial tumors of the skin

  • Epidermal and trichilemmal cysts
  • Verrucae (warts)
  • Molluscum contagiosum
  • Solar lentigo
  • Seborrheic keratosis
  • Basal cell carcinoma
  • Actinic keratosis
  • Squamous cell carcinoma
  • Keratoacanthoma
  • (Adnexal Neoplasms)
134
Q

What are epidermal and trichilemmal cysts?

A

Usually derived from hair follicles

a) Epidermal cyst:
- 1-4cm
- punctum (small opening on top)
- rupture with keratin granuloma is common
- secondary infection may occur

b) Tricholemmal Cyst:
- usually on scalp
- no punctum
- rare proliferating variant

135
Q

What are viral warts?

A

Caused by HPV.

Clinical types:
-	verruca vulgaris
-	verruca plana
-	verruca plantaris (sole of foot)
-	condyloma acuminatum (genital)
Usually regress
You know it’s a wart if you see koilocytes = vacuolated keratinocytes. Means HPV
136
Q

What is Molluscum contagiosum?

A
  • umbilicated papules caused by poxvirus
  • spread by direct contact
  • children, young adults
  • infects follicular infundibula
  • typically resolves
137
Q

What is Solar lentigo?

A
  • pigmented macules on sun-exposed skin
  • elongation of rete ridges
  • keratinocyte hyperpigmentation
  • variable minimal melanocytic proliferation
  • most important DDx is lentigo maligna
138
Q

What is Seborrheic keratosis?

A
  • typically multiple lesions (grampa)
  • develop middle age
  • predilection for trunk, forehead
  • sharly demarcated – ‘stuck on’
  • waxy surface
  • lese-trelat sign (tate)
  • Common types of histological patterns:
    o Acanthotic (uniform cuboidal cells)
    o Papullomatous/hyperkeratotic
    o Reticular
    o May see pseudohorn cysts
139
Q

What is ‘irritated’ Seborrheic keratosis?

A
  • Red thing
  • Variable inflammatory changed
  • Reactive architectural/cytological change
  • True dysplasia rare – not pre-malignant
140
Q

What is a basal cell carcinoma?

A
  • About 70% of skin cancer

  • Predominantly in sun damaged skin

  • H+N>trunk>other sites

  • High probability of subsequent lesions

  • Rare genetic predispositions (e.g. Gorlin’s syndrome)
141
Q

What are the histological types of basal cell carcinomas?

A
  • Numerous histological types
  • Practically:

  • Superficial
  • Nodular
  • Aggressive sub-types:
  • Infiltrating
  • Micronodular

  • Sclerosing/Morpheic

  • Metatypical/Basosquamous

You might see cystic areas. (clear but granular large holes)
You might get blue cells forming a little line like a fence.

142
Q

What is Actinic keratosis?

A
  • Dysplastic proliferation of keratinocytes (grampa)
  • Marker of solar damage and risk of skin cancer
  • Low rate of progression to SCC
  • Occur on:

  • Sun exposed sites

  • Fair skin

  • Middle aged/Elderly
  • Common substrate for “keratin horn” (15% SCC)
  • Variants:

    • Hyperkeratotic
    • Pigmented

    • Actinic cheilitis (on lower lip)
    • Lichenoid
 (inflammation)
    • Atrophic

Will see orthokeratosis (Hyperkeratosis with no nuclei) but it doesn’t invade into lower tissue.

143
Q

What is an intraepidermal Squamous cell carcinoma?

A
  • Bowen’s disease
  • Erythematous plaque
  • Sun-exposed or protected skin
  • Acanthotic epiderm, i.e. pleomorphic mitotic figures
  • Adnexal colonization frequent
144
Q

What is Squamous cell carcinoma?

A
  • Sun-damaged skin
  • Tenderness, thickness on palpitation
  • Generally low risk of metastasis

High risk sites:

  • ear
  • lips
  • vilva and penis

Other risk factors:

  • clinical size>2cm
  • > 2mm thickness
  • clark level 4 or 5
  • PNI
  • Poorly differentiatied
145
Q

What is Keratoacanthoma?

A
  • rapidly growing crateriform lesion
  • usually involutes
  • clinically and histologically overlap with some types of SCC
  • generally managed as SCC
  • may see central erupting core of keratin
146
Q

/What are Adnexal tumors?

A 
Wide variety of tumours benign and malignant: 
• Follicular
• Apocrine

• Sebaceous

• Eccrine

• Mixed differentiation
147
Q

What are the major reaction patterns of inflammatory dermatosis?

A
  1. Lichenoid
    - lichen planus
  2. Psoriasiform
    - psoriasis
  3. Spongiotic
    - atopic eczema
  4. Vesiculobullous
    - bullous pemphigoid
  5. Granulomatous
    - sarcoidosis
  6. Vasculopathis
    - urticarial
    - leukocytoclastic vasculitis
148
Q

/What are the minor reaction patterns?

A
  1. epidermolytic hyperkeratosis
  2. acantholytic dyskeratosis
  3. cornoid lamellation
  4. papillomatosis
  5. acral angiofibromas
  6. eosinophilic cellulitis with flame figures
  7. transepidermal elimination
149
Q

/What are the patterns of inflammation?

A
  1. Superficial perivascular inflammation
  2. Superficial and deep dermal inflammation
  3. Folliculitis and perifolliculitis
  4. Panniculitis (inflammation of subcutis)
150
Q

What is a lichenoid reaction?

A
  • characterized by epidermal basal layer damage – it won’t be as clear as it should be and may have signs of inflammation (blue dots)
  • basal vacuolar change or cell death. Cells will be in holes. If dead – diskeratosis (pink bit of keratin left)
  • accompanying inflammatory infiltrate
    o lymphocytes
    o histiocytes
    o eosinophils
151
Q

Describe an example of a lichenoid reaction.

A

Lichen Planus.

  • also look for hyperkeratosis
  • wedged shaped hypergranulosis (thickened granular layer)
  • epidermal hyperplasia
  • band like lichenoid inflammatory infiltrate
  • basal vacuolar change with formation of colloid bodies and civatte bodies. (keratin)
  • May have subepidermal clefting
  • Direct immunofluorescence – cytoid bodies
152
Q

What is a psoriasiform reaction?

A
  • regular epidermal hyperplasia with elongation of the rete ridges
  • increased mitotic activity
  • associated inflammatory infiltrate
    o lymphocytes
    o polymorphs
    o histiocytes
153
Q

Describe an example of a psoriasiform reaction.

A

Psoriasis.

  • regular epidermal hyperplasia
  • elongated clib shaped rete ridges
  • parakeratosis (retains nuclei)
  • mild spongiosis
  • superficial dermal perivascular lymphocytic infiltrate
  • thinning of supra-papullary plated
  • *neutrophilling infiltration
154
Q

What is a spongiotic reaction?

A
  • intraepidermal and intercellular edema – fluid will push cells apart and you will see desmosomes
  • ‘eczematous reaction’
  • associated inflammatory infiltrate
155
Q

Describe an example of a spongiotic reaction.

A

Eczema.

Wet, weaping rash.

156
Q

What is a Vesiculobullous reaction?

A
  • blisters
  • the presence of vesicles or bullae at any levels within the epidermis or at the dermo-epidermal junction
    o intracorneal and subcorneal
    o intraepidermal
    o suprabasilar
    o subepidermal
    o miscellaneous
157
Q

Describe an example of a Vesiculobullous reaction.

A

Bullous pemphigoid.

  • Autoimmune disease characterized by the production of autoantibodies to the bullous pemphigoid antigen related to hemidesmosomes
  • subepidermal vesicle containing mainly eosinophils
  • lymphocytic and dense eosinophilic infiltrate
  • linear IgG and C3 localised to roof of vesicle
  • superficial dermal edema especially in pre-bullous lesions
  • clean break takes base off
  • fluorescence – line along base
158
Q

What is a granulomatous reaction?

A
  • chronic dermal inflammation with infiltration of histiocytes or epithelioid histiocytes
  • a granuloma is an aggregate of epithelioid histiocytes
    o sarcoidal
    o tuberculoid
    o necrobiotic
    o suppurative
    o foreign bodies
159
Q

Describe an example of a granulomatous reaction.

A 
Sarcoidosis. 
-	tight and naked granulomatous inflammatory infiltrate 
-	usually no necrosis
-	well circumscribed 
-	various inclusion bodies – none of which are specific for this disease
o	asteroid vodies
o	schaumann bodies
o	calcium oxalate crystals
o	hamazaki-wesenberg bodies
160
Q

What is a vasculopathic reaction?

A

Diseases of the blood vessels comprising 6 groups. I.e.:

  • urticaria
  • vasculitides (i.e. *leukocytoclastic vasculitis)
  • endothelial proliferation
  • endothelial damage
    o necrosis
    o nuclear dust
    o red cell extravasation
    o increased permeability
  • immune complex deposition
  • different to other tissue where acute/chronic inflammation is shown as neutrophilic/lymphocytic infiltration only
161
Q

Describe leukocytoclastic vasculitis.

A
  • nuclear dust, origin = leucocytes
  • also called hypersensitivity vasculitis
  • affects small vessels in the superficial dermis
  • fibrinoid necrosis – will see lots of fibrinogen
  • swollen endothelium
  • perivascular lymphocytic infiltrate, nuclear dust and red cell extravasation.
  • Clinically – palpable and purple
162
Q

What are the relevant non-neoplastic and neoplastic pigmentary disorders?

A

Non-neoplastic pigmentary disorders:

  • vitiligo
  • melisma
  • post-inflammatory pigment alteration
  • ephelis

Neoplasms:

  • (solar lentigo)
  • lentigo simplex
  • melanocytic naevi
  • melanoma
163
Q

Describe vitiligo.

A
  • acquired loss of pigmentation due to inflammatory destruction of melanocytes
  • histology: loss of melanocytes within the epidermis
164
Q

Describe melisma:

A
  • symmetrical hyperpigmented patched, usually face
  • hyperfunctioning melanocytes reacting to sun
  • hormonal association
165
Q

Describe post-inflammatory pigment alteration (PIPA).

A
  • occurs after a variety of inflammatory and traumatic processes
  • histology: melanophages in superficial dermis
166
Q

Describe ephelis.

A
  • melanocytes producing more melanin than they should, but normal numbers of melanocytes
  • wax ad wane
  • histology: normal epidermal architecture with increased keratinocyte pigmentation.
167
Q

Describe Lentigo Simplex:

A
  • small, flay darkly pigmented macule
  • fewer than ephelides, more darkly pigmented and do not wax/wane
  • a true melanocytic proliferation

Histology:
- melanocytes still single, not in nests, but there are just more of them in epidermal ridges

168
Q

What are the clinical and histological features of common benign melanocytic naevus (moles)?

A

Clinical:

  • small
  • well circumscribed
  • even coloration

Histology:

  • symmetrical
  • cells predominantly in nests
  • round to oval, even nuclei
  • maturation as the cells get deeper
  • classified as junctional, compound, intradermal
169
Q

What are the common types of benign naevi?

A

a) spitz naevus – red dome often mistaken for melanoma
b) blue naevus – dendritic melanocytes
c) large/giant congenital naevus – risk of melanoma
d) dysplastic naevus? (technically not benign)

170
Q

Describe a dysplastic naevus.

A

Clinical:

  • larger than benign naevi (>6mm)
  • irregular borders
  • variable colouration

Histological:

  • less symmetrical
  • more single cell growth
  • some larger, darker nuclei
  • fibrosis in the upper dermis
  • cytological atypia
171
Q

What is a melanoma?

A

A malignant rumor derived from melanocytes

172
Q

What are the ABCDE features of melanoma?

A

Any one of ABCDE is cause for concern

  • Asymmetrical
  • Border irregularity – poorly circumscribed
  • Colour variability
  • Diameter - >6mm as guide
  • Evolving – i.e. changing
173
Q

What are the microscopic features of melanoma?

A

• Asymmetrical

• Poorly circumscribed

• Single cells predominate over nests

• Growth in continuity from one rete ridge to another
• Extension into the upper levels of the epidermis
– Pagetoid spread

– “buckshot” scatter
• Cytological atypia

– Nuclear enlargment, hyperchromasia, irregularity
– Prominent nucleoli

174
Q

What is a melanoma in situ?

A

Growth within the epidermis – lacks metastatic potential

175
Q

What is the radial growth phase of melanoma?

A
  • growth within the epidermis (in situ) as well as microinvasion into the superficial dermis
  • microinvasion limited to single cells and small cell nests
  • lacks metastatic potential
176
Q

What is the vertical growth phase of melanoma?

A
  • invasive melanoma within the dermis
  • dermal nests larger than the epidermal nests
  • mitotic figures
  • implies capacity for metastatic spread
177
Q

What are the prognostic indicators of melanoma?

A
  • tumor thickness (Breslow thickness)
  • level of invasion (Clark level)
  • ulceration
  • mitotic rate
  • lymphovascular or perineural invasion
  • satellite lesions
178
Q

What are some of the types of melanoma?

A
  • superficial spreading melanoma – most common
  • nodular melanoma – no/minimal intraepidermal component
  • lentigo maligna melanoma - elderly, predominantly single cell growth pattern
  • acral lentiginous melanoma
  • not associated with the sun
  • acral sites – hands and feet, maybe under nail
179
Q

Describe the histology of melanoma regression,

A
  • lymphocytes
  • scarring
  • melanin-containing macrophages
180
Q

What is the ideal type of biopsy for melanoma?

A

Complete excision with 2mm margin.

Partial biopsies:

  • are less accurate (different degrees in different zones)
  • carry a higher risk of misdiagnosis – under staged
181
Q

What mutation might be tested for in regard to melanoma?

A

BRAF

  • BRAF is a serine-threonine kinase
  • Mutations found in 66% of melanomas
  • BRAF mutations lead to activation of kinase activity – MAPK pathway (mitogen activated protein kinase)
  • Also common in naevi
  • Not alone sufficient for melanoma development
  • Specific BRAF inhibiting drugs have been developed which are selective for V600E mutation – used to treat patients with metastatic melanoma
182
Q

What are mesenchymal tumors?

A

Practically, they can be though of as non-epithelial, non-melanocytic, non-lymphomatous skin tumors.

183
Q

What are some of the types of mesenchymal tumors of the skin?

A
  • tumors of fat
  • tumors of fibrous tissue
  • tumors of blood vessels and lymphatics
  • tumors of muscle
  • tumors with nerve sheath differentiation
184
Q

What are malignant mesenchymal tumors called?

A

Sarcomas

185
Q

Describe benign tumors of fat.

A

Name: lipomas

Clinically Features:

  • age 40+
  • associated with obesity
  • may be very large
  • bright yellow homogenous fat with fine fibrous capsule and trabeculae
  • greasy cut surface

Histological features:

  • composed of mature adipocytes with uniform nuclei resembling normal white fat
  • small amounts of fibrous tissue
  • occasional blood vessels
186
Q

What are the variants of lipoma?

A

These are benign tumors with similar macroscopic appearance but variable microscopic appearance.

  • spindle cell lipoma
  • chondroid lipoma
  • pleomorphic lipoma
  • angiolipoma - capillaries more prominent
187
Q

Describe a malignant fat tumor.

A

Name: liposarcoma

3 main types:

a) atypical lipotamous tumour/well differentiated liposarcoma
b) myxoid/round cell liposarcoma
c) pleomorphic liposarcoma

Deep soft tissue

188
Q

What is a dedifferentiated liposarcoma?

A

A biphasic tumor that includes an undifferentiated sarcomatous component.

189
Q

What would MDM2 genetic amplification indicate?

A

Well-differentiated tumors.

190
Q

What are some of the tumors of fibrous tissue?

A

a) Dermatofibroma
b) Defmatofibrosarcoma protuberans (DFSP)
c) Atypical Fibroxanthoma (AFX)

191
Q

Describe Dermatofibroma.

A
  • benign
  • common site: legs of women 20-50
  • recurrence not common

Histology:

  • tumor is composed of fibroblastic and histiocytic cells arranged in sheets or intersecting fascicles
  • mixed population of cells – inflammatory cells consisting of lymphocytes, plasma cells and foamy histiocytes are also seen
  • the stroma contains delicate collagen fibers in between cells
  • mitotic activity not increased
  • cytologic atypia absent
  • no sharply defined borders
  • usually show entrapment of surrounding dermal collagen
  • overlying epithelial hyperplasia and hyperpigmentation
192
Q

Describe DFSP.

A
  • well differentiated primary fibrosarcoma of the skin
  • slow growing, can be locally aggressive and recur, but rarely metastasize
  • firm, solid nodules mostly found on trunk

Histology:

  • composed of fibroblasts arranged radially in a stroriform patter (irregular pattern denoting a straw mat)
  • mitoses present
  • often show deep extendion into subcutaneous fat
  • lace-like pattern
193
Q

What are the key differences between Dermatofibroma and DFSP?

A
  • the deep margin of DF usually shows limited infiltration into subcut tissues, whereas DFSP has more extensive infiltration.
  • DSFP has more homogenous population of tumor cells, lacks inflammatory cells, foamy histiocytes and giant cells
  • Stratiform pattern more pronounced in DFSP
  • Mitotic activity increased in DFSP
  • DF = factor 13a positive
  • DFSP = CD34 positive
194
Q

Describe AFX.

A
  • generally rapidly growing nodular lesions in sun exposed areas of older patients
  • rapid growth
  • usually polypoid without ulceration.
  • 1-6cm
  • local excisions usually curative and recurrence is rare

Histology:

  • composed of atypical, pleomorphic spindle cells
  • storiform or fascicle pattern
  • abundant mitoses, but some mitotic figures atypical
  • use immunohistochemistry to exclude melanoma, spindled squamous cell carcinoma or leiomyosarcoma. AFX will be negative for S-100, melan A, desmin and cytokeratins.
  • overlying epidermis uninvolved
195
Q

What are some of the tumors of histiocytes?

A

a) Juvenile Xanthogranuloma (JXG)

b) Fibroepithelial polyp/skin tag/acrochordon

196
Q

Describe JXG.

A
  • cutaneous histiocytic lesion usually seen in infancy and childhood
  • most patients develop lesions by 6 months
  • excellent prognosis – most regress spontaneously
  • yellow or brown

Histology:

  • composed of sheets of histiocytes (eosinophilic cytoplasm) in dermis and extending to the flattened epidermis
  • hallmark = touton giant cell
  • inflammatory cells found in moderate numbers
197
Q

Describe Fibroepithelial polyp/skin tag/acrochordon.

A
  • benign
  • middle aged and older people – trunk, face and interigous areas
  • soft flesh coloured tumor attached to skin by a slender stalk

Histology:
- fibrovascular cored covered in squamous epithelium

198
Q

Name and describe a benign tumor of smooth muscle.

A

Leiomyoma = benign

Subtypes based on location:

  • nipple or scrotum
  • pilar leiomyoma
  • angioleiomyoma

Histology:

  • intersecting fascicles
  • cigar shaped nuclei
  • no atypia
  • no mitotic activity
  • no necrosis
199
Q

Name and describe a malignant tumor of smooth muscle.

A

Leiomyosarcoma = malignant

a) Dermal:
- arise from pilar muscles or genital smooth muscles
- middle aged males
- metastasis rare

b) Subcutaneous:
- arise from vascular smooth muscle
- greater tendency for metastasis

Compared to leiomyoma:

  • more cellular
  • cytological atypia
  • mitoses
  • necrosis
200
Q

Name and describe a benign tumor of blood vessels.

A

Haemangiomas

a) capillary Haemangiomas – thin walled capillaries
b) juvenile Haemangiomas
c) cavernous Haemangiomas – large, dilated vascular channels
d) lobular capillary Haemangiomas (‘pyogenic granuloma’)
– polypoid, often ulcerate and bleed
- will look like lobulated polyp, capillary sized vessels

201
Q

Name 2 malignant tumors of blood vessels.

A
  1. Angiosarcoma

2. Kaposi Sarcoma

202
Q

Describe Angiosarcoma.

A
  • head and neck in eldery
  • associated with chronic lymphedema
  • post radiation therapy
  • slow growing but highly aggressive
  • metastasize to regional lymph nodes and organ
203
Q

Describe Kaposi Sarcoma

A
  • vascular neoplasm caused by HHV8 and highly associated with AIDS
  • Four forms:
    o Classic (older men)
    o Endemic African
    o Transplant-associated
    o AIDS-associated
  • Cutaneous lesions progress from patched to plaques to nodular tumors

Histology:

  • spindle cells forming slits with extravasated RBCs
  • hemosiderin laden macrophages
  • lymphocytes
  • fibrosis
  • minimal atypia
204
Q

List 2 benign neural tumours.

A
  1. Neurofibroma (nerve sheath)
  2. Neuroma (nerve fibers and schwann cells)

Describe a neurofibroma.

  • benign nerve sheath tumour
  • mixture of schwann cells, perineural cells, fibroblasts, mast cells
  • sporadic or related to neurofibromatosis
  • 3 growth patterns
    o superficial cutaneous neurofibroma - pedunculated
    o diffuse neurofibroma – plaque like elevation of skin
    o plexiform neurofibroma – nerve roots or large nerves
205
Q

Describe a neuroma.

A
  • benign non neoplastic overgrowth of nerve fibers and schwann cells
  • usually post traumatic
  • painful
  • common subtypes:
    o amputation or traumatic neuroma
    o morton neuroma

Histology of amputation neuroma:
- irregular organization of nerve fibers immersed in scar tissue

206
Q

How are lymphomas of the skin divided? Give two examples.

A

Divided loosely into B cell and T cell proliferation.

Examples:
Mycosis fungoides = a cutaneous T cell Lymphoma
Primary Cutaneous Follicle Centre Cell Lymphoma = a cutaneous B cell lymphoma

207
Q

Describe Mycosis fungoides.

A
  • a cutaneous T cell Lymphoma
  • elderly or adults
  • skin-homing CD4+ T helper cells
  • progression: patch, plaque, nodule/tumor
  • often misdiagnosed early as eczema
  • usually remains localized to skin for many years, but may evolve into generalized lymphoma

Histology:

  • may look similar to dermatitis – increased lymphocytes
  • neoplastic lymphocytes form a band-like zone in upper dermis
  • convoluted nuclear membrane – this would be unusual for dermatitis
208
Q

Describe Primary Cutaneous Follicle Centre Cell Lymphoma.

A
  • presents with solitary or localized skin lesions on the scalp, forehead or trunk
  • erythematous plaques or nodules
  • nodular diffuse pattern
209
Q

Overview:

A

MESENCHYMAL TUMORS:

  1. Fat Tumors:

a. Lipoma = benign fat tumor
i. spindle cell lipoma
ii. chondroid lipoma
iii. pleomorphic lipoma
iv. angiolipoma

b. Liposarcoma = malignant fat tumor
i. atypical lipotamous tumour/well differentiated liposarcoma
ii. myxoid/round cell liposarcoma
iii. pleomorphic liposarcoma

  1. Fibrous Tissue Tumors:

a. Dermatofibroma
b. Defmatofibrosarcoma protuberans (DFSP)
c. Atypical Fibroxanthoma (AFX)

  1. Histiocytic Tumors:

a. Juvenile Xanthogranuloma (JXG)
b. Fibroepithelial polyp/skin tag/acrochordon (benign)

  1. Smooth Muscle Tumors:

a. Leiomyoma (benign)
b. Leiomyosarcoma (malignant)

  1. Blood Vessel Tumors:

a. Haemangiomas (benign)
i. capillary Haemangiomas
ii. juvenile Haemangiomas
iii. cavernous Haemangiomas
iv. lobular capillary Haemangiomas

b. Angiosarcoma (malignant)
c. Kaposi Sarcoma (malignant)

  1. Neural Tumours:

a. Neurofibroma (benign)
b. Neuroma (benign)

LYMPHOMAS:

  1. T cell lymphoma:
    Mycosis fungoides
  2. B cell lymphoma:
    Primary Cutaneous Follicle Centre Cell Lymphoma

General Med 1 (24 decks)

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