Class notes
Human Pathology notes
- Course
- Institution
Detailed notes on the course with pictures included
[Show more]
Seller
Follow
ninajunakovi
Content preview
THEME 1: NEOPLASIADERMATOPATHOLOGY
NEOPLASIA
− neoplasm = genetically driven growth of cells → benign, pre-malignant, malignant
− tumour:
o always a formation of mass
o can be genetically driven → neoplasm
o can be due to other causes e.g., inflammation
− neoplasm → isn’t always a mass e.g., leukaemia
− benign neoplasm:
o slow and local growth
o no metastases
o no atypia/anaplasia (stop looking like precursors)
o moles, wards (bradavice)
o isn’t always premalignant
− malignant neoplasm:
o often rapid growth/proliferation (mitosis in tissues)
o infiltration in other tissues → metastasizing
o atypical cells → dysplasia = abnormal
development of cells within tissues or organs
− multiple genetic aberrations in different genes → usually
at least 6 genes need to be hit:
1. autonomous cell proliferation → growth
2. new vessels formation → growth
3. loss of cell apoptosis → growth, survival
4. loss of differentiation → loss of function
5. loss of cell contact inhibition → invasion
6. growth in and out of the vessels → metastasis
→ different mutations need to occur for each step
→ every new hit leads towards malignancy
→ also keeps happening within tumours, however, it doesn’t spread
− cancer genes:
o (proto)oncogenes = code for proteins promoting for cell growth, gain of function mutation
(activation or gain of expression)
o tumour suppressor genes = code for proteins inhibiting cell proliferation or inducing cell
apoptosis, loss of function mutation (loss of gene or loss of expression) → needs to mutate
in both alleles
o DNA repair genes = code for proteins controlling and repairing the genome, loss of function
mutation (also 2x) → accumulation of DNA errors
o viral genes = incorporated into human genes and cause cancer
,− genetic alterations:
o mutations:
▪ small
▪ substitution = activation of oncogenes → hotspot mutation = a continuous
activation of the gene & inhibition of tumour suppressor → stop codon
▪ insertion/deletion = + frame shift → inhibition of tumour suppressor & - frameshift
→ gain or loss of function
o copy number variations:
▪ large
▪ sections of the genome are repetead in a
chromosome
▪ gain of oncogenes
▪ loss of tumour suppressor genes
o chromosomal translocations:
▪ expression/activation of oncogenes
▪ part of a chromosome is fused to another
chromosome → fusion of 2 genes
− somatic mutation:
o acquired
o only in certain cells of the body
o dependent on a carcinogen
− germline mutations:
o often in the family history
o congenital (urođeno)
o present in all cells of the body
o can give the susceptibility for cancer
CLINICAL PATHOLOGY
− clinical pathologist = a medical specialist who diagnoses disease by investigating tissues (and cells)
of patients
− pathological investigation of skin tumours:
1. assessment of the differentiation line → from which tissue/cells the tumour derived
2. establishing whether the tumour is benign or malignant
1 + 2 = diagnosis
3. determine the tumour stage → measuring invasion depth or looking at which tissues it invaded
→ dyeing the margins before cutting
4. establishing whether the margins are free of tumour
→ determines clinical management: tumour size, necessity of (re)excision and its margins, necessity of
adjuvant radiotherapy, node excision, and adjuvant systemic therapy
,− example:
− pathological examination of skin excision:
o skin excision with marked margins
o cut with bread loaf technique
o representative material goes under
the microscope → the thinner slices
− diagnosis:
o routine histology = sufficient in most
cases, H&E (haematoxylin and eosin)
staining, H/purple – nucleus & E/pink
– cytoplasm
o immunohistochemistry = usage of an antibody directed against an antigen only expressed
on tumour cells, the binding is visualized by the 2nd antibody with an enzyme which then
converts a chromogen into an insoluble stain on the section, used for determining the
tumour/cell origin and for the malignant character of the tumour
o molecular pathology → used to make diagnosis and for determining treatment options
SKIN TUMOURS
− the largest organ, aging, lifelong exposure to UV light, tanning bed → increase of skin cancer
− every cancer cause has its own mutational signature
− other causes: viral infection (HPV), hereditary
− different skin structures: epidermis, dermis, hair follicles, oil and sweat glands, nerves, fatty tissue,
lymph vessels, melanin cells, immune cells → all can give rise to different tumours
− basal cell carcinoma/BCC:
o most frequent skin cancer → becoming an epidemic
o derived from hair follicles
o clinical behaviour: locally aggressive, can be mutilating, however, hardly ever metastizes
o location: always present in the skin, frequent around the eyes and the nose, not found on
mucosa, palms, and soles → similar to hair follicles
, o histology: large dark nuclei with very
little cytoplasm
o etiology (the cause of a disease or an
abnormal condition): UV-specific
mutation, age > 40, only Caucasians,
areas with cumulative sun-
exposition (face and hands)
− squamous cell carcinoma/SCC:
o common and rising
o derived from keratinocytes (major
cell type of the epidermis)
o mostly in areas with cumulative
sun-exposition
o mutilating, but only 2% of them
can metastize
o histology: always show
keratinization (forming of keratin,
dying skin cells)
o etiology: UVB → tumours develop
on the sun-exposed sites, UV-
specific mutation & HPV → larger
cells with better margins and
irregular nuclei, hypertrophic
epidermis, no invasive growth,
especially in immune compromised patients
o 2 types of dysplasia: actinic keratosis (UVB) & Morbus Bowen (HPV)
MELANOCYTIC TUMOURS
− melanocyte:
o pigment producing cell
o in the basal layer of the epidermis
between keratinocytes
o 1 melanocyte communicates with
30-40 keratinocytes via dendrites
o melanin granules protect
keratinocytes against UV
o darker skin → more melanin
produced, same number of
melanocytes
BENIGN MELANOCYTIC TUMOURS → NEVUS (MADEŽ)
− develop mostly in the first 2 years of life
− most people have 20-30 nevi
− neoplasms → genetically driven → 60% BRAF gene & 20% NRAS gene mutations
The benefits of buying summaries with Stuvia:
Guaranteed quality through customer reviews
Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.
Quick and easy check-out
You can quickly pay through credit card or Stuvia-credit for the summaries. There is no membership needed.
Focus on what matters
Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!
Frequently asked questions
What do I get when I buy this document?
You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.
Satisfaction guarantee: how does it work?
Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.
Who am I buying these notes from?
Stuvia is a marketplace, so you are not buying this document from us, but from seller ninajunakovi. Stuvia facilitates payment to the seller.
Will I be stuck with a subscription?
No, you only buy these notes for $7.31. You're not tied to anything after your purchase.
Can Stuvia be trusted?
4.6 stars on Google & Trustpilot (+1000 reviews)
80435 documents were sold in the last 30 days
Founded in 2010, the go-to place to buy study notes for 14 years now