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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
What are the beneficial effects of acute inflammation?
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
26
Harmful effects of acute inflammation
Digestion of normal tissues Swelling Inappropriate inflammatory response (e.g. type 1 hypersensitivity)
27
Which factors lead to complete resolution of acute inflammation?
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
28
Why would acute inflammation progress to chronic inflammation?
Indigestible substances (result in chronic suppuration) Deep seated suppuration inflammation Recurrent episodes of acute inflammation
29
Predominant cells in chronic inflammation
Lymphocytes Plasma cells Macrophages
30
Examples of primary chronic inflammation
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)
31
Macroscopic appearances of chronic inflammation
``` Chronic ulcers Chronic abscess cavity Thickening of wall by fibrous tissue Granulomatous inflammation FIBROSIS ```
32
Cell responses in acute inflammation
B lymphocytes -> plasma cells T lymphocytes produced cytokines Cytokines (recruit macrophages, produce inflammatory mediators, recruit other lymphocytes,maestros target cells, produce interferon)
33
What is a granuloma?
Aggregate of epithelial histiocytes Histiocytes = macrophage present in connective tissue (secretory function)
34
Causes of granulomatous inflammation
``` Specific infections Foreign bodies (endogenous, exogenous) Specific chemicals Drugs Unknown ```
35
Properties of mycobacteria
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
36
What is hyperplasia?m
Increase in cell number
37
Where does hyperplasia occur?
Hormonally sensitive organs - endometrium - breath - thyroid
38
Example of hyperplasia
Enlargement of gingival tissuesn Hyper plastic responses within spit helium & underlying connective tissue Various causes including certain drugs
39
What is hypertrophy?
Increase in cell size
40
What tissue does hypertrophy affect?
Muscle - skeletal - cardiac
41
What is atrophy?
Reduction in cell size and number in an organ that was of normal size
42
Causes of atrophy
Ageing Lack of use - mechanical - functional
43
What is hypoplasia?
Reduced sized of an organ that was never fully developed | A developmental defect
44
What is metaplasia?
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
Example of metaplasia?
Barrett's oesophagus | Squamous epithelial cells -> columnar epithelial cells
46
Is metaplasia a neoplasticism disorder?
No. Environmental changes lead to metaplasia and may if persistent lead to further changes that can manifest as dysplasia and progress to malignancy
47
What is the Hayflick limit?
Number of times a cell can divide
48
What is senescene?
Process of aging
49
What are the 3 processes involved in regulation of cell number?
Proliferation Senescene Cell death
50
What are labile cells?
Continuously dividing cells e.g. surface epithelia, haematopoetic cells
51
What are stable cells?
Cells with low level of replicative activity May divide rapidly if stimulated e.g. hepatocytes, fibroblasts, endothelium
52
What are permanent cells
Non-dividing cells Not able to renter cell cycle e.g. neurones, skeletal & cardiac muscle
53
In what types of diseases is there increased apoptosis?
AIDS Neurodegenerative disorders Reperfusion injury
54
In what diseases is there decreased apoptosis?
Neoplasia | Autoimmune disease
55
What is neoplasia?
Abnormal growth
56
How is neoplasia classified?
Behavioural - benign - malignant Histogenetic
57
Description of benign neoplasms
``` Resemble Norma, tissue No invasion Encapsulated No necrosis Minimal pleomorphism Diploid DO NOT METASTASISE ```
58
Features of malignant neoplasms
``` Invasive growth pattern Not encapsulated Necrosis common Pleomorphic Abnormal mitosis figures Aneuploid MAY METASTASIISE ```
59
Are neoplastic cells monoclonal?
Yes
60
What is dysplasia?
A premalignant process e.g. In Squamous or glandular epithelia
61
What is desmoplasia?
The proliferation of fibroblast to produce fibrous stroma in response to malignant tumour
62
What is angiogenesis?
Formation of new blood vessels | Control is lost in tumours - forms abnormal vessels
63
Do tumour require less or more oxygen than normal cells?
Less
64
What is metastasis?
Spread of a mi,grant tumour from its original site of origin
65
Common sites of metastasis
``` Regional lymph nodes Liver Lung Bone Brain Adrenal gland Skin ```
66
Routes of metastasis?
Lymphatic (carcinoma) Haematogenous (sarcoma) Across body cavities Direct implantation
67
Role of immune system in cancer
May target tumour cells Can regress some cancers (melanoma) Immunodeficiencies - increased risk
68
Main stages of cancer development?
``` Self sufficient growth signals Escape from senescene Evasion of apoptosis Limitless replicative potential Angiogenesis Invasion & metastasis ```
69
What is a carcinogen?
A substance that can lead to the development of cancer
70
Can genetic predisposition have a role in cancer?
Yes
71
What viruses can predispose to cancer?
SV40 HBV HPV
72
Example of RNA tumour virus
RSV (Rous Sarcoma Virus)
73
Examples of classical oncogenes
``` PDGF EGFR ras Src myc ```
74
4 ways of activating Proto-oncogenes
Amplification Translocation Point mutation Insertional mutagenesis
75
Examples of tumour suppressor genes
p53 pRB ALC BRCA-1
76
What are classical oncogenes?
Stimulate cell proliferation Inhibit cell death Are dominant
77
What are tumour suppressors?
Inhibit cell proliferation Stimulate cell death Are recessive
78
Vague symptoms that present with cancers
Fatigue Weight loss Anorexia Fever
79
Clinical presentation of cancer if it's an ulceration with bleeding
Chronic blood loss - anaemia (eg colorectal cancer) | Acute blood loss - haematemesis, haemoptysis
80
Clinical presentation of cancer if it's caused a narrowing of lumen
``` Dysphagia Abdominal pain Renal failures Jaundice Infection behind an obstructing lesion (e.g. pneumonia, cholangitis) ```
81
Clinical presentation of cancer which has caused pressure or damage to adjacent structures
``` 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
Clinical presentation of cancer if it has elicited an effusion
``` Breathlessness (pleural effusion) Abdominal distension (peritoneal effusion) ```
83
Presentation if cancer has metastasised to bone
Pain and patholigical feature
84
Presentation if cancer has metastasised to brain
Raised intracranial pressure, epilepsy, CVA (stroke)
85
Presentation if cancer has metastasised to liver
Jaundice
86
Presentation if cancer has metastasised to adrenal glands
Addisons disease
87
What is paraneoplastic syndrome?
Symptoms/syndromes in cancer patients not directly associated with local or distant spread of tumours
88
What underlying cancer presents with venous thrombosis?
Pancreatic carcinoma
89
What is a tumour grade?
A histological assessment of how well differentiated tumour cells are Well differentiated tumours tend to have a better prognosis
90
What is the dukes stage grade of colorectal cancer?
A - confined to wall, no lymph node metastasis B - penetrates wall, no lymph node metastasis C - lymph node metastasis D - metastatic disease
91
TNM classification of cancer
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
Treatment of HER2 breast cancer
Trastuzumab (herceptin) which is a monoclonal antibody
93
Characteristics of IDDM
``` Onset young Weight normal Reduced insulin levels Anti-islet antibodies Ketoacidosis HLA linked ```
94
Characteristics of NIDDM
``` Onset > 30 Overweight Normal or decreased insulin No islet antibodies No ketoacidosis No HLA linkage ```
95
Complications of diabetes
``` Ketoacidosis Lactic acidosis Macroangiopathy Diabetic neuropathy Diabetic retinopathy - cataracts ```
96
What is Virchows triad?
Hypercoagulability Haemodynamic changes Endothelial injury
97
What are platelets?
Anucleated cell fragments Adherence properties Procoagulant contents Growth factors
98
What is an embolism?
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
What is infarction?
Zonal necrosis due to sudden occlusion of blood supply

AY Principles (11 decks)

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