Pathology Flashcards

1
Q

Common complications of diabetes?

A

Angina, MI, Peripheral vascular disease

Kidney failure

Skin infections

Cataracts

Neuropathy

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2
Q

What is non-enzymatic glycosylation?

A

Glucose combining with AAs and proteins without the need for enzymes

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3
Q

Examples of how glycated proteins can cause pathology?

A

Glycated collagen and ECM traps LDL

Glycated cell-surface receptors affects their function e.g. activation of inflammatory cells

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4
Q

What does polyol pathway disruption cause, and what is it?

A

It is when hyperglycaemia causes influx of glucose to the inside of the cell, metabolised to sorbitol and fructose

These increase osmotic pressure cause cellular swelling and accumulation of pro-inflammatory cytokines

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5
Q

What does activation of protein kinase C in diabetes lead to?

A

Production of VEGF

Production of pro-inflammatory cytokines

Increase in endothelin-1 and decrease in NO

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6
Q

Three main molecular pathways for pathology in diabetes?

A

Glycated proteins

Polyol pathway disruption

Activation of protein kinase C

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7
Q

Two types of angiopathy in diabetes?

A

Microangiopathy - Leaky, and thicker basement membranes, in capillaries, arterioles and venules

Macroangiopathy - Atheroma

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8
Q

Three reasons atheroma production is accelerated in diabetic patients?

A

Glycation of ECM in arterial walls traps LDL

Infalmmation causes damage to endothelium due to increased cytokines and vasoconstriction

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9
Q

What organ is particularly affected by diabetic microangiopathy?

A

The kidney, thickening of the glomerulus

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10
Q

Three eye conditions that are more likely to occur in diabetics?

A

Cataract - due to sorbitol production

Glaucoma - growth of abnormal vessels

Diabetic retinopathy - microangiopathy causes haemorrhages in retinal vessels

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11
Q

What is the multistep hypothesis of carcinogenesis?

A

That carcinoma cells are clones of one single cell that accumulates a series of genetic alterations causing it to become cancerous

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12
Q

What is dysplasia?

A

The stage where cells show neoplastic characteristics but are contained within the basement membrane and are not yet invasive

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13
Q

Histological features of dysplasia/neoplasia?

A

Hyperchromatic - darker nuclei than usual

Irregular and varying in size and shape

Nuclear/cytoplasmic ratio is increased

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14
Q

Stages of the adenoma-carcinoma sequence in the colon?

A

1: The aberrant crypt focus - loss of tumour suppressant APC
2: Low-grade dysplasia - Mutated KRAS (proto-oncogene) causes increased proliferation

Adenomas: benign polyps form

3: High-garde dysplasia - the polyp generates more gene abnormalities and undergoes more abnormal growth, still benign
4: Cancer

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15
Q

4 most common pathological gynaecological diagnoses?

A

Endometriosis

Fibroids

Endometrial cancer

Cervical cancer

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16
Q

What is endometriosis?

A

The presence of endometrial glands or stroma in abnormal locations outside the uterus

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17
Q

What does endometriosis cause?

A

Infertility

dysmenorrhoea

dyspareunia (pain after intercourse)

Pelvic pain

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18
Q

Treatment options for endometriosis?

A

Progestagens

GnRH analogues

Laser ablation

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19
Q

What is a fibroid?

A

Leiomyoma (benign smooth muscle tumour)

Most commonly found in myometrium

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20
Q

Symptoms in fibroids?

A

Abnormal bleeding

Compression of the bladder

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21
Q

Fibroid risks?

A

Increased risk of:

  • Miscarriage
  • Fetal malpresentation
  • Uterine malcontractions
  • Postpartum haemorrhage
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22
Q

Fibroid (leiomyomata) treatments?

A

Surgery

Hormonal manipulation

Arterial embolisation

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23
Q

The two pathogenetic groups leading to endometrial cancer?

A

1: Background prolonged oestrogen stimulation related to obesity and anovulatory cycles
2: Poorly differentiated, older age

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24
Q

Most common histological type of endometrial cancer?

A

60% - endometrial adenocarcinoma

Good prognosis

25
Q

Where are samples taken from in cervical screening?

A

Transformation zone

26
Q

How is HPV associated with cervical cancer?

A

Infection present in 99.7% of invasive cancers

27
Q

What is a medullary carcinoma?

A

A carcinoma of calcitonin secreting cells

28
Q

Process of amyloid formation/deposition?

A

Abnormal proteolysis of a protein causes it to take on a beta-pleated sheet structure, it is insoluble in this form and is deposited.

29
Q

What are carcinoids?

A

Endocrine tumour with neurosecretory granules in their cytoplasm

30
Q

Main defining features of small-cell carcinoma?

A

Very aggressive, normally in lung

31
Q

Three main ways a pituitary tumour can present?

A

Compress and destroy surrounding tissue causing pituitary insufficiency

Secrete active hormone

Compression effects of adjacent structures e.g. compression of optic chiasm causing bitemporal hemianopsia

32
Q

What effect does dopamine have on prolactin secretion?

A

Suppresses it

33
Q

Symptoms of excess prolactin?

A

Amenorrhoea breast lactation

34
Q

What are islet cell neoplasms?

A

Benign or malignant neoplasms of the pancreas secrete active hormones

35
Q

Two types of germ cell tumours?

A

Seminoma (>30) and non-seminomatous

36
Q

Markers of germ cell tumours?

A

Non-seminomatous:

  • alpha-fetoprotein
  • βHCG

Seminomatous:
- PLAP

37
Q

Germ cell tumour prognosis?

A

Chemoradiosensitive, cure is likely

38
Q

What are leydig cell tumours’ features?

A

Often secrete androgens

Can occur at any age

Can secrete oestrogen (causing gynaecomastia)

39
Q

Key marker for prostate tumour?

A

PSA - prostate specific antigen

40
Q

Management of prostate cancer

A

Surgery

Radiotherapy

Hormonal manipulation:

  • Orchidectomy
  • gonadorelin analogues (to suppress LH)
  • anti-androgens
41
Q

Three main criteria for prognostic factors for neoplasia, and examples within them?

A

Tumour itself: size/histological type

Host: Age of host/presence of other conditions/Compliance with therapy

Environment: Availability of treatment, expertise of caregiver

42
Q

Meanings of T and N and M in TNM tumour classification?

A

T - local spread of tumour

N - Involvement of regional lymph nodes

M - Distant metastases

43
Q

What are co-morbidities?

A

Other diseases that a patient may have

44
Q

4 classifications of diabetic retinopathy?

A

Pre-proliferative

Proliferative
- New vessels growing

Maculopathy
- Macular oedema

Advanced diabetic eye disease

  • Neovascular glaucoma
  • Traction detachments of new blood vessels become fibrosed and pull on the retina
45
Q

3 Main causes of retinopathy?

A

Leakage

Occlusion

New blood vessel growth

46
Q

Key features of diabetic retinopathy seen down an opthalmoscope?

A

Haemorrhages

Hard exudate

Cotton wool spots - cloudy swelling of retina, sign of vascular insufficiency to nerve fibre resulting in hold up of axoplasmic flow

Vessel changes:

  • Venous beading - dilated veins with beaded, uneven edges, venous loops
47
Q

Steps in treating a diabetic foot infection?

A

Resuscitation

Antibiotics

Surgery

Optimise arterial flow

Control swelling

Off-load

48
Q

Initial causes of a diabetic foot infection?

A

Skin defect e.g. minor trauma, tinea pedis

Sensory neuropathy

49
Q

What to check in a diabetic foot examination?

A

Look for: swelling/colour/hair growth

Feel for: Dorsalis pedis pulse/posterior tibial pulse/temperature gradient

Capillary refill

Check for: areas of redness/wasting/fixed deformities

50
Q

Theories explaining the pathology of ageing?

A

Loss of homeostasis causing cell injury/death

Genetic theories: Gene regulation dysfunction and somatic mutations

Cellular theories: Free-radicals/oxidative stress

51
Q

What is the epitope of the antigen?

A

the specific region of the antigen that reacts with variable region of the antibody

52
Q

What are hybridoma cells?

A

B-lymphocytes that are secreting a specific antibody that have been fused with malignant tumour cells so that enough antibody can be produced indefinitely

53
Q

What does monoclonal mean?

A

Derived from a single cell

54
Q

How does the test strip of a pregnancy test produce it’s colour change in a positive reaction?

What lab technique is this an example of?

A

At the bottom there is an antibody against hCG, bound to the bottom
hCG binds to this antigen
There is another antibody against hCG with an enzyme attached which then reacts with a dye molecule that then turns pink

ELISA

55
Q

Difference in immunohistochemistry and ELISA?

A

In immunohistochemistry the molecule we are testing for is on the slide and the followed by a primar and secondary antibody and dye, there is no ‘sandwich’ effect

56
Q

What part of the cell is the oestrogen receptor located in?

A

The nucleus

57
Q

What is carcinoma in situ (CIN)?

A

Carcinoma that is not malignant but has neoplastic changes, can reverse itself or go on to become malignant

58
Q

Two most common types of cervical carcinoma?

A

Squamous cell carcinoma and adenocarcinoma