Tissue growth disorders and dysplasia

Question 1

What are cellular adaptations? + 4 types

Answer 1

Reversible changes in size, number, phenotype, metabolic activity or function in response to changes within their environment

4 types:
Hyperplasia
Hypertrophy
Atrophy
Metaplasia

Question 2

What is hyperplasia? + a requirement
What can happen alongside it?

vs hypertrophy? - what is it, what its due to, how is it different to hyperplasia

Answer 2

Hyperplasia:
Increase in no. cells within affected organ - Only happens if cell can divide - so cant happen in muscle which has ltd proliferation capacity
Can happen alongside hypertrophy, in response to the same stimulus

Hypertrophy:
Increase in size of cells which increases size of the affected organ
Due to increase in intracellular structural components
Unlike hyperplasia, happens also in cells unable to divide

Question 3

hormonal vs compensatory hyperplasia? egs for each

Answer 3

Hormonal hyperplasia = when u need to increase functional capacity of a hormone secreting organ
- eg increase in breast glandular epithelium in puberty/pregnancy

however, Compensatory hyperplasia = need to increase tissue mass after damage or resection
- eg Liver cell regeneration after donation of one lobe + bone marrow hyperplasia

Question 4

4 examples of pathological hyperplasia?

Answer 4

Endometrial hyperplasia – imbalance between oestrogen & progesterone, therefore endometrium continues to proliferate = abnormal vaginal bleeding ! :(

Prostatic hyperplasia - due to excess androgens

Hyperplasia can cause Cancer causing mutations

HPV can lead to hyperplasia

Question 5

4 mechanisms of thyroid hyperplasia?

Answer 5

4 mechanisms:

Lack of substrate – aka iodine deficiency leads to thyroid hyperplasia
Lack of enzymes in thyroid pathway production -> dyshormogenetic thyroid hyperplasia
Autoimmune: Grave’s disease – autoantibodies that stimulate or block TSH receptor
Sporadic thyroid hyperplasia - usually in females in puberty

Question 6

Describe physiological hypertrophy, how a histological sample of it would look + 2 causes
vs
why does pathological hypertrophy occur + example

Answer 6

You would see less nuclei and more cytoplasm

Due to increased functional demand - eg skeletal muscle fibres in those who gym, + hormonal stimulation of uterus sm fibres during pregnancy

Path. hypertrophy:
Due to increased demands on tissue or organ - Eg Cardiac myocytes in response to chronic haemodynamic overload

Question 7

Atrophy is the reduction in size of a structure/organ due to a decrease in cell size and number
When is physiological atrophy seen + 2 egs of physiological atrophy?

Answer 7

Seen in embryological structures during normal development, eg thyroglossal duct

Thymus after puberty, Uterus after delivery

Question 8

6 examples of pathological atrophy

Decreased workload vs Loss of innervation vs Diminished blood supply vs Inadequate nutrition vs Loss of endocrine stimulation vs Pressure

Answer 8

Decreased workload eg bed rest = skeletal muscle atrophy

Loss of innervation eg skeletal muscle atrophy following spinal cord injury

Diminished blood supply - eg brain atrophy due to atherosclerosis

Inadequate nutrition - Cachexia in chronic inflammation & cancer

Loss of endocrine stimulation - eg endometrial atrophy due to lack of oestrogen after menopause

Pressure - A benign tumour

Question 9

What is metaplasia? + 3 types

Answer 9

Replacement of one differentiated cell type by another in order to withstand an adverse environment

Squamous
Intestinal/columnar
Connective tissue

Question 10

Describe Squamous metaplasia & 3 examples vs Intestinal metaplasia & 1 example

Answer 10

Cells go from columnar to squamous - More prone to infection as you lose protective cilia Eg:
Resp tract - chronic irritation due to cig smoke -> squamous cell carcinoma.
In excretory ducts due to stones
In endocervix as it everts

Intestinal: Squamous to columnar eg: in Barrett’s oesophagus

Question 11

connective tissue metaplasia + eg

Answer 11

Formation of cartilage, bone or adipose tissue in places that don’t usually contain them
E.g. Myositis ossificans

Question 12

agenesis vs aplasia vs atresia?

Answer 12

Agenesis: complete absence of an organ : eg Agenesis of corpus callosum -> neurodevelopmental delays

Aplasia: failure of development of the primordium -> absence of an organ
:E.g Radial aplasia= failure in radial bone development, causing limb issues. Aplasia can occur as part of broader conditions like VACTERL

Atresia: blockage or absence of an opening, Usually a hollow organ : eg Intestinal atresia= blockage of the intestine–> bowel obstruction

Question 13

hypoplasia vs dysplasia? + example for each

Answer 13

Hypoplasia: incomplete development of an organ due to a decreased number of cells E.g. Pulmonary hypoplasia due to oligohydramnios

Dysplasia: in context of development – disorganisation of cells E.g. Multicystic renal dysplasia due to urinary reflux

Question 14

heterotopia vs hamartoma?

Answer 14

Heterotopia:
Well developed nest of normal tissue at the wrong site
E.g. Gastric or pancreatic tissue in a Meckel’s diverticulum -> erosion of cell surface -> bleeding

Hamartoma:
Mass of mature but disorganised tissue at an appropriate site
E.g. Fibrous hamartoma of infancy

Question 15

3 acquired predispositions to cancer?

Answer 15

HPV 16 + 18 –> cervical cancer
H. pylori –> gastric cancer
Reproductive history: the pill, early menopause

Question 16

Premalignant lesions vs premalignant conditions?

Answer 16

pre malignant lesions:
high grade dysplasia, +
benign neoplasms at risk of malignant transformations

Premalignant conditions:
chronic ulcerative colitis -> colorectal cancer
Hepatic cirrhosis -> hepatocellular carcinoma

Question 17

Describe dysplasia as a predesposition for cancer

cytological features of malignancy?

Answer 17

nuclei become darker as they have more chromatin

Question 18

Describe cervical screening? (premalignant condition)

Answer 18

Cervical screening in women aged 25 to 64
First test for presence of HPV – if negative = nothing further done
If positive, examine cells for dysplasia (dyskaryosis)

If low-grade dysplasia: no treatment but repeat smear in 12 months as most resolve
If high-grade: treat w. LLETZ ( large loop excision of the transformation zone)

Question 19

Describe how + why we screen individuals w Barrets Oesophagus

Answer 19

Barrett’s oesophagus can -> invasive oesophageal adenocarcinoma
Must do regular endoscopies w biopsies every 2cm
Usually every 2-5 years (time interval depends on length of oesophagus involved)

Question 20

Describe how + why we screen individuals w Familial adenomatous polyposis syndrome

Answer 20

To screen for Familial adenomatous polyposis syndrome, you must do:
Annual colonoscopies w histology of polyps from 10-15 years until definitive surgery
Upper endoscopies to screen for gastric & duodenal polyps from time of onset of colonic polyposis or 20 years
Thyroid ultrasounds due to inc. risk of thyroid cancer
Provided for first degree relatives for a period defined by findings