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AY Principles > Pathology > Flashcards

Pathology Flashcards

1
Q

What are the patterns of necrosis?

A 
Coagulative 
Colliquative 
Caseous
Gangrenous 
Fibrinoid 
Fat necrosis
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2
Q

2 types of metabolic disorder

A

Inherited

Acquired

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3
Q

What is phenylketonuria?

A

Accumulation of phenylalanine

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4
Q

Clinical features of phenylketonuria

A

Brain toxicity
Mental retardation
Fair skin, blue eyes
Guthrie test

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5
Q

2 types of inflammation.

A

Acute inflammation

Chronic inflammation

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6
Q

Physical characteristics of inflammation

A 
Rubor (redness)
Calor (heat)
Tumor (swelling) 
Dolor (pain)
Loss of function
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7
Q

2 phases of acute inflammation

A

Vascular phase (dilatation and increase permeability of blood vessels)

Exudative and cellular phase (fluid & cells escape from permeable venules)

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8
Q

What is exudate?

A

A fluid rich protein which oozes out of blood vessels due to inflammation

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9
Q

What is fibrinogen?

A

A soluble Ortega present in blood plasma from which fibrin is produced through the action of the enzyme thrombin

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10
Q

Examples of chemical mediators which increase vascular permeability?

A

Histamine

Bradykinin

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11
Q

Diagnostic feature of acute inflammation

A

Neutrophil accumulation in the extracellular space

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12
Q

Functions of neutrophils

A 
Kill organisms
Degrade necrotic tissue 
Ingest offending agents 
Produce chemical mediators 
Produce toxic oxygen radicals 
Produce tissue damaging enzymes
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13
Q

How do neutrophils find the site of inflammatory stimulus?

A

Chemotaxis

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14
Q

What does histamine do?

A

Vascular dilatation

Transient increase in vascular permeability

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15
Q

What is histamine release from?

A

Released by mast cells, eosinophils, basophils and platelets
(Stimulated by complement)

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16
Q

What is serotonin?

A

Amine present in platelets

Increases vascular permeability

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17
Q

What are chemokines?

A

Proteins

Attract leukocytos to site of inflammation

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18
Q

What are leukotrienes?

A

In neutrophils
Have vasoactive properties
Involved in type 1 hypersensitivity

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19
Q

What are prostaglandins?

A

Fatty acids
Increase vascular permeability
stimulate platelet aggregation

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20
Q

4 cascade systems in plasma

A

Complement system
The kinins
The coagulation factors
Fibrinolytic system

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21
Q

What are opsonins?

A

Bund to specific receptors on leukocytos and greatly enhance phagocytosis
(Tomato ketchup)

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22
Q

What is suppuration?

A

Formation of pus (neutrophils, bacteria, cellular debris)

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23
Q

What causes suppuration?

A

Almost always infection

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24
Q

What is an abscess?

A

A collection of pus surrounded by a membrane of sprouting capillaries, neutrophils and occasional fibroblasts

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25
Q

What are the beneficial effects of acute inflammation?

A

Dilution of toxins (can be carried away by lymphatics)
Entry of antibodies (increased vascular permeability)
Fibrin formation (impedes movement of microorganisms)
Transport of drugs (e.g. antibiotics)
Delivery of nutrient and oxygen (aided by blood flow)
Stimulation of immune response

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26
Q

Harmful effects of acute inflammation

A

Digestion of normal tissues
Swelling
Inappropriate inflammatory response (e.g. type 1 hypersensitivity)

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27
Q

Which factors lead to complete resolution of acute inflammation?

A

Minimal cell death & tissue damage
Organs regenerative capacity (e.g. liver)
Rapid destruction of causal agent
Rapid removal of fluid debris by good local vascular drainage

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28
Q

Why would acute inflammation progress to chronic inflammation?

A

Indigestible substances (result in chronic suppuration)
Deep seated suppuration inflammation
Recurrent episodes of acute inflammation

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29
Q

Predominant cells in chronic inflammation

A

Lymphocytes
Plasma cells
Macrophages

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30
Q

Examples of primary chronic inflammation

A

Resistant infective agents (e.g. TB, leprosy)
Foreign body reactions (e.g. Gout)
Specific diseases of unknown aetiology ( e.g. IBD)
Primary granulomatous diseases (e.g. sarcoidosis)

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31
Q

Macroscopic appearances of chronic inflammation

A 
Chronic ulcers
Chronic abscess cavity 
Thickening of wall by fibrous tissue 
Granulomatous inflammation 
FIBROSIS
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32
Q

Cell responses in acute inflammation

A

B lymphocytes -> plasma cells
T lymphocytes produced cytokines
Cytokines (recruit macrophages, produce inflammatory mediators, recruit other lymphocytes,maestros target cells, produce interferon)

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33
Q

What is a granuloma?

A

Aggregate of epithelial histiocytes

Histiocytes = macrophage present in connective tissue (secretory function)

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34
Q

Causes of granulomatous inflammation

A 
Specific infections 
Foreign bodies (endogenous, exogenous) 
Specific chemicals 
Drugs 
Unknown
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35
Q

Properties of mycobacteria

A

Slow growing in culture
Acid/alcohol fast on microscopic staining
Resistant to many antimicrobials (e.g. Penicillin)
Induce granulomatous reactions in tissue
Intracellular pathogens able to survive and replicate within neutrophils and macrophages

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36
Q

What is hyperplasia?m

A

Increase in cell number

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37
Q

Where does hyperplasia occur?

A

Hormonally sensitive organs

  • endometrium
  • breath
  • thyroid
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38
Q

Example of hyperplasia

A

Enlargement of gingival tissuesn
Hyper plastic responses within spit helium & underlying connective tissue
Various causes including certain drugs

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39
Q

What is hypertrophy?

A

Increase in cell size

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40
Q

What tissue does hypertrophy affect?

A

Muscle

  • skeletal
  • cardiac
41
Q

What is atrophy?

A

Reduction in cell size and number in an organ that was of normal size

42
Q

Causes of atrophy

A

Ageing
Lack of use
- mechanical
- functional

43
Q

What is hypoplasia?

A

Reduced sized of an organ that was never fully developed

A developmental defect

44
Q

What is metaplasia?

A

An acquired form of altered differentiation.
One fully formed cell type to another fully formed cell type
Can be part of an adaptive response to stress

45
Q

Example of metaplasia?

A

Barrett’s oesophagus

Squamous epithelial cells -> columnar epithelial cells

46
Q

Is metaplasia a neoplasticism disorder?

A

No.
Environmental changes lead to metaplasia and may if persistent lead to further changes that can manifest as dysplasia and progress to malignancy

47
Q

What is the Hayflick limit?

A

Number of times a cell can divide

48
Q

What is senescene?

A

Process of aging

49
Q

What are the 3 processes involved in regulation of cell number?

A

Proliferation
Senescene
Cell death

50
Q

What are labile cells?

A

Continuously dividing cells

e.g. surface epithelia, haematopoetic cells

51
Q

What are stable cells?

A

Cells with low level of replicative activity
May divide rapidly if stimulated
e.g. hepatocytes, fibroblasts, endothelium

52
Q

What are permanent cells

A

Non-dividing cells
Not able to renter cell cycle
e.g. neurones, skeletal & cardiac muscle

53
Q

In what types of diseases is there increased apoptosis?

A

AIDS
Neurodegenerative disorders
Reperfusion injury

54
Q

In what diseases is there decreased apoptosis?

A

Neoplasia

Autoimmune disease

55
Q

What is neoplasia?

A

Abnormal growth

56
Q

How is neoplasia classified?

A

Behavioural
- benign
- malignant
Histogenetic

57
Q

Description of benign neoplasms

A 
Resemble Norma, tissue 
No invasion 
Encapsulated 
No necrosis 
Minimal pleomorphism 
Diploid 
DO NOT METASTASISE
58
Q

Features of malignant neoplasms

A 
Invasive growth pattern 
Not encapsulated 
Necrosis common 
Pleomorphic 
Abnormal mitosis figures  
Aneuploid
MAY METASTASIISE
59
Q

Are neoplastic cells monoclonal?

A

Yes

60
Q

What is dysplasia?

A

A premalignant process

e.g. In Squamous or glandular epithelia

61
Q

What is desmoplasia?

A

The proliferation of fibroblast to produce fibrous stroma in response to malignant tumour

62
Q

What is angiogenesis?

A

Formation of new blood vessels

Control is lost in tumours - forms abnormal vessels

63
Q

Do tumour require less or more oxygen than normal cells?

A

Less

64
Q

What is metastasis?

A

Spread of a mi,grant tumour from its original site of origin

65
Q

Common sites of metastasis

A 
Regional lymph nodes 
Liver 
Lung 
Bone 
Brain 
Adrenal gland 
Skin
66
Q

Routes of metastasis?

A

Lymphatic (carcinoma)
Haematogenous (sarcoma)
Across body cavities
Direct implantation

67
Q

Role of immune system in cancer

A

May target tumour cells
Can regress some cancers (melanoma)
Immunodeficiencies - increased risk

68
Q

Main stages of cancer development?

A 
Self sufficient growth signals 
Escape from senescene 
Evasion of apoptosis 
Limitless replicative potential
Angiogenesis
Invasion & metastasis
69
Q

What is a carcinogen?

A

A substance that can lead to the development of cancer

70
Q

Can genetic predisposition have a role in cancer?

A

Yes

71
Q

What viruses can predispose to cancer?

A

SV40
HBV
HPV

72
Q

Example of RNA tumour virus

A

RSV (Rous Sarcoma Virus)

73
Q

Examples of classical oncogenes

A 
PDGF
EGFR
ras
Src
myc
74
Q

4 ways of activating Proto-oncogenes

A

Amplification
Translocation
Point mutation
Insertional mutagenesis

75
Q

Examples of tumour suppressor genes

A

p53
pRB
ALC
BRCA-1

76
Q

What are classical oncogenes?

A

Stimulate cell proliferation
Inhibit cell death
Are dominant

77
Q

What are tumour suppressors?

A

Inhibit cell proliferation
Stimulate cell death
Are recessive

78
Q

Vague symptoms that present with cancers

A

Fatigue
Weight loss
Anorexia
Fever

79
Q

Clinical presentation of cancer if it’s an ulceration with bleeding

A

Chronic blood loss - anaemia (eg colorectal cancer)

Acute blood loss - haematemesis, haemoptysis

80
Q

Clinical presentation of cancer if it’s caused a narrowing of lumen

A 
Dysphagia 
Abdominal pain 
Renal failures
Jaundice
Infection behind an obstructing lesion (e.g. pneumonia, cholangitis)
81
Q

Clinical presentation of cancer which has caused pressure or damage to adjacent structures

A 
Pain, nerve palsied (e.g. mediastinal tumours) 
Bone destruction (e.g. local invasion or primary bone tumours)
A endocrine glands (e.g. Pituitary adenomas) 
Raised intracranial pressure (CNS tumours)
82
Q

Clinical presentation of cancer if it has elicited an effusion

A 
Breathlessness (pleural effusion)
Abdominal distension (peritoneal effusion)
83
Q

Presentation if cancer has metastasised to bone

A

Pain and patholigical feature

84
Q

Presentation if cancer has metastasised to brain

A

Raised intracranial pressure, epilepsy, CVA (stroke)

85
Q

Presentation if cancer has metastasised to liver

A

Jaundice

86
Q

Presentation if cancer has metastasised to adrenal glands

A

Addisons disease

87
Q

What is paraneoplastic syndrome?

A

Symptoms/syndromes in cancer patients not directly associated with local or distant spread of tumours

88
Q

What underlying cancer presents with venous thrombosis?

A

Pancreatic carcinoma

89
Q

What is a tumour grade?

A

A histological assessment of how well differentiated tumour cells are
Well differentiated tumours tend to have a better prognosis

90
Q

What is the dukes stage grade of colorectal cancer?

A

A - confined to wall, no lymph node metastasis
B - penetrates wall, no lymph node metastasis
C - lymph node metastasis
D - metastatic disease

91
Q

TNM classification of cancer

A

T STAGE (size of tumour)

  • Tx - primary tumour cannot be assessed
  • T0 - no evidence of primary tumour
  • Tis - carcinoma in situ
  • T1-4 - size and or extent of tumour

N STAGE (lymph node involvement)

  • Nx - nodes cannot be assessed
  • N0 - no node involvement
  • N-3 - regional node metastasis

M STAGE (metastasis)

  • M0 - no distant spread
  • M1 - distant metastasis
92
Q

Treatment of HER2 breast cancer

A

Trastuzumab (herceptin) which is a monoclonal antibody

93
Q

Characteristics of IDDM

A 
Onset young 
Weight normal 
Reduced insulin levels 
Anti-islet antibodies 
Ketoacidosis 
HLA linked
94
Q

Characteristics of NIDDM

A 
Onset > 30
Overweight 
Normal or decreased insulin 
No islet antibodies 
No ketoacidosis 
No HLA linkage
95
Q

Complications of diabetes

A 
Ketoacidosis 
Lactic acidosis 
Macroangiopathy 
Diabetic neuropathy
Diabetic retinopathy - cataracts
96
Q

What is Virchows triad?

A

Hypercoagulability
Haemodynamic changes
Endothelial injury

97
Q

What are platelets?

A

Anucleated cell fragments
Adherence properties
Procoagulant contents
Growth factors

98
Q

What is an embolism?

A

A mass of magi weak in the vascular system moving from its site of origin to lodge in the vessels in a distant site

99
Q

What is infarction?

A

Zonal necrosis due to sudden occlusion of blood supply

AY Principles (11 decks)

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