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Principles Collated Flashcards > Pathology > Flashcards

Pathology Flashcards

1
Q

Definition of risk factor?

A

Social or individual factor which increases the risk of development of a disease

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2
Q

Aetiology definition?

A

Causative element in disease

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3
Q

Pathogenesis definition?

A

Sequence of events from healthy state to clinical disease

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4
Q

Sequelae definition?

A

Range of possible outcomes of disease process

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5
Q

Outcome definition?

A

Patient health or illness at a defined time

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6
Q

Necrosis requires energy. True or False?

A

FALSE

Requires no energy

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7
Q

What is necrosis? And what does it elicit?

A

Death of tissues
Pathological
-Elicits adjacent tissue response

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8
Q

Different patterns of necrosis?

A
  • Coagulative
  • Colliquative
  • Caseous
  • Gangrenous
  • Fibrinoid
  • Fat necrosis
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9
Q

Coagulative necrosis?

A

Proteins coagulate
Preservation of cell outline
-Eg MI

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10
Q

Colliquitive necrosis?

A

Necrotic material becomes softened and liquefied (PUS)
No cell structure remains
-Eg brain

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11
Q

Caseous necrosis?

A

Cheese-like

-Eg TB

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12
Q

Gangrenous necrosis?

A

Cell death by necrosis then infection on top of it

Anaerobic bacteria may grow

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13
Q

Fibrinoid necrosis?

A

Fibre deposition

-Eg damage to blood vessel in malignant hypertension

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14
Q

Fat necrosis example?

A

Eg- Acute pancreatitis

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15
Q

What process requires energy?

A

Apoptosis

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16
Q

What is apoptosis?

A

Programmed cell death
Defence against inherited injury
-Eithe physiological (normal growth) or pathological (injury, infection, chemo)

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17
Q

What is P53 and what can it lead to?

A
  • Protein

- If lost it can lead to development of cancer, which is more likely resistant to treatment

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18
Q

Where does P53 function?

A

Cell cycle at G1 (like a spell checker)

-If mistakes are found cycle is paused and repair is attempted

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19
Q

What can occur at G1 checkpoint?

A

Apoptosis

If DNA is damaged

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20
Q

G2 checkpoint?

A

Mitosis will not occur if DNA is damaged or not replicated

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21
Q

M checkpoint?

A

Mitosis stops if chromosomes are not properly aligned

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22
Q

What happens if DNA can’t be repaired?

A

Then P53 stimulates and indices apoptosis

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23
Q

What part of the cell is involved in cell aging?

A

Telomere

Shortening

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24
Q

How do chromosomes prevent degradation and fusion?

A

They are capped

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25
Q

What does cancer reactivate?

A

Telomerase gets reactivated in cancer and can become immoral

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26
Q

What causes loss of membrane integrity?

A

Failure of ion pumps
Disruption of membrane
Alteration of lipids
Cross-linking of membrane proteins

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27
Q

What are free radicals formed by?

A
  • Drugs
  • O2 toxicity
  • Reperfusion injury
  • Inflammation
  • Intracellular killing of bacteria
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28
Q

What is a metabolic disorder?

A

Biochemical abnormality which may itself be deleterious, but which also causes target organ damage, usually by accumulation of injurious agent

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29
Q

How would you inherit a metabolic disorder?

A

Autosomal recessive

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30
Q

Inherited metabolic disorder causes…?

A

Loss of function

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31
Q

What is phenylketonuria?

A

Due to accumulation of phenylalanine
Caused by deficiency in enzyme (phenylalanine hydroxylase) which converts phenylalanine to tryosine
Guthrie test - foot prick (PKU)

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32
Q

Vascular phase of inflammation?

A

Dilation and increased permeability of blood vessels

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33
Q

Exudative and cellular phase of inflammation?

A

Fluid and cells escape from permeable venules

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34
Q

What is a diagnostic feature for inflammation?

A

Neutrophil accumulation in extracellular space

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35
Q

Beneficial effects of inflammation?

A
  • Toxin dilution
  • Entry of ABs
  • Fibrin formation
  • Drug transport
  • Oxygen and nutrient delivery
  • Immune response stimulation
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36
Q

Harmful effects of inflammation?

A
  • Digestion of normal tissues
  • Swelling
  • Inappropriate inflammatory response (Type 1 sensitivity)
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37
Q

What is chronic inflammation?

A

Subsequent and often prolonged tissue reactions

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38
Q

Characteristics of inflammation?

A
  • Redness
  • Heat
  • Swelling
  • Pain
  • Loss of function
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39
Q

Why does redness occur in inflammation?

A

Due to dilation of small blood vessels

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40
Q

Why does heat occur in inflammation?

A

Increased blood flow through region

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41
Q

Why does swelling occur in inflammation?

A

Accumulation of fluid in extravascular space

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42
Q

Why does pain occur in inflammation?

A

Distortion of tissues

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43
Q

Why does loss of function occur in inflammation?

A

Inhibited by pain or swelling

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44
Q

What is in fluid exudate?

A

Proteins including immunoglobins

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45
Q

When does fibrinogen turn to fibrin?

A

On contact with ECM (Extra-cellular matric fibrin), acutely inflammed organ surfaces commonly covered in fibrin

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46
Q

What is margination?

A

Loss of intravascular fluid and increased plasma viscosity allows neutrophils into plasma (only occurs in venules)

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47
Q

What do neutrophils stimulate?

A

Inflammation

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48
Q

Adhesion of neutrophils increased by?

A

Complement C5a
Leukotriene B2
TNF

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49
Q

Endothelial expression of adhesion molecules increased by?

A

IL1
Endotoxins
TNF

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50
Q

What is chemotaxis?

A

Locomotion orientated along a chemical gradient

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51
Q

Examples of chemical mediators?

A 
Histamine 
Seratonin 
Chemokines 
Leukotrienes
Prostaglandins
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52
Q

What does histamine do?

A

-Vascular dilation

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53
Q

What are histamines released by?

A

Mast cells, eosinophils, basophils, platelets

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54
Q

Release of histamine is stimulated by?

A

C3a, C5a and lysosomal proteins (released by neutrophils)

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55
Q

What does seratonin cause?

A

Increased vascular permeability

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56
Q

What is another term for seratonin receptors?

A

5HT

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57
Q

Where are 5HT present in high concentration?

A

Platelets

58
Q

What do chemokines do?

A

Attract various leukocytes to site of inflammation

59
Q

What type of hypersensitivity are leukotrienes involved in?

A

Type 1

60
Q

What do prostaglandins do?

A

Increase vascular permeability

Stimulate platelet agregation

61
Q

What is necessary for recognition of microorganisms?

A

They must be coated with opsonin

62
Q

Examples of things acting as opsonins that could coat microorganisms?

A

Fc fragment of IgG
C3b
Collectins

63
Q

What is suppuration? What cells does it include?

A

Formation of pus

Neutrophils, bacteria, cellular debris

64
Q

Resolution?

A

Complete restoration of tissues to normal after episode of acute inflammation

65
Q

Cells involved in chronic inflammation?

A

Plasma cells
Lymphocytes
Macrophages

66
Q

Macroscopic appearance of inflammation eg chronic ulcer?

A

Breach in mucosa
Base lined by granulation tissue
Fibrous tissue extends through muscle layers

67
Q

Appearance of chronic abscess cavity?

A

Thickening of wall by fibrous tissue

68
Q

When would something appear granulomatous?

A

Crohn’s

TB

69
Q

On contact with____, __ Lymphocytes become _______ cells?

A

Antigen
B
Plasma

70
Q

What cell produces cytokines?

A

T lymphocyte

71
Q

Characteristics of reversible damage?

A
  • Reduced aerobic respiration/increased anaerobic
  • Membrane pumps fail
  • Cell swelling
  • Accumulation of lipids
72
Q

Characteristics of irreversible damage?

A
  • Severe damage to cell membranes and mitochondria
  • Leakage of enzymes
  • Nuclear changes- ATP changes, cell membrane damage
73
Q

Progression of injury/damage?

A

Attempted repair
|
Complete= regeneration/restitution
Incomplete= repair/scarring

74
Q

Labile cells. What are they? location?

A

Cells that multiply constantly throughout their short lives

-GI tract, Bone marrow

75
Q

Stable cells. What are they? Location?

A

Cells that multiply only when needed

-Hepatocytes, endothelium

76
Q

Permanent cells. What are they? Location?

A

Cells that are unable to replicate in post-natal life
-Skeletal muscle, neurones
REGENERATION of these is not possible

77
Q

Stem cells. What are they?

A

Pluripotent cells

Can differentiate into most cell types

78
Q

What becomes a fibrous scar?

A

Granulation tissues after it has undergone organisation

79
Q

What is a granuloma and when is it normally present?

A
  • Collection of macrophages (in response to foreign bodies eg bone, asbestos, TB, parasites, syphillis, malignancy)
  • FOUND in chronic inflammation
80
Q

What is differentiation?

A

Acquisition of specialized features

81
Q

Hyperplasia?

A

Increase in cell number

82
Q

What does amlodipine cause?

A

Gingival hypertrophy (overgrowth of gum tissue around teeth)

83
Q

Hypertrophy?

A

Increase in cell size

84
Q

Atrophy?

A

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

85
Q

Hypoplasia?

A

Reduced size of an organ that never fully developed to normal size

86
Q

Metaplasia?

A

One type of cell becomes another form of cell in response to stress

87
Q

Example of metaplasia?

A

Barrett’s eosophagus

88
Q

Meaning of neoplasia?

A

New growth

89
Q

Neoplasia?

A

Abnormal mass of tissue, growth which exceeds and is uncoordinated with that of normal tissues

90
Q

Describe heritage of neoplastic cells?

A

Monoclonal

-Derived from one single common ancestor

91
Q

Benign neoplasia?

A
  • No necrosis
  • N:C nucleus to cytoplasm ration normal
  • Minimal change in size/shape (pleomorphism)
  • Diploid
  • Adenoma
  • Papilloma
92
Q

Types of benign neoplasia?

A

Adenoma

Papilloma

93
Q

Malignant neoplasia?

A 
Necrosis common 
Metastatic potential 
Pleomorphic 
N:C ratio increased 
Aneuploid
Carcinoma, carcinoma in situ, sarcoma
94
Q

Carcinoma is?

A

Cancer of epithelial cell

95
Q

Carcinoma in situ is?

A

Not invading other tissues, confined to site of origin

96
Q

Sarcoma is?

A

Cancer of mesenchymal cell

97
Q

What is meaning of dysplasia?

A

Disordered growth

98
Q

What is dysplasia?

A

Pre-malignant process

Abnormal cell changes

99
Q

Angiogenesis?

A

Formation of new abnormal blood vessels

Successfully growing tumors will develop ability to create own blood supply

100
Q

Metastasis?

A

Formation of tumour implants that are discontinuous with the primary lesion

101
Q

Roues of mets?

  • Carcinoma?
  • Sarcoma?
A 
Lymphatic= carcinoma 
Sarcoma= haematogenous
102
Q

Stepwise progression of cancer?

A

Initiation- 1st mutation
Promotion- more mutations
Persistence - Malignant?

103
Q

What is involved in initiation?

A

Oncogenes
Tumour suppresors
DNA repair
Evasion of apoptosis

104
Q

What is involved in promotion?

A

Further accumulation of mutations

105
Q

What is involved in persistence?

A

Unregulated abnormal growth, can become malignant

106
Q

What do classical oncogenes do?

A

Stimulate cell proliferation (turn up genes that promote growth)
Inhibition
Dominant

107
Q

Examples of oncogenes affected by mutations?

A

RAS - colon, lung, bladder, melanoma, pancreatic
BRAF -
Myc -Lymphoma. neuroblastoma, small cell carcinoma of lung
P13K - Haematological malignancies

108
Q

What do tumour suppressors do?

A

Turn of genes that slow growth

  • Inhibit cell proliferation
  • Stimulate cell death
  • Recessive
109
Q

Examples of tumour suppressors affected by mutations?

A

P53 protein

110
Q

What is P53? What is is activated by?

A

Transcription factor

Activated by cell stress

111
Q

Dna repair genes affected by mutations?

A

BRCA 1 and BRCA2

112
Q

What malignant cells look like?

A

Usually rough and nasty

113
Q

What benign cells look like?

A

Usually smooth and round

114
Q

Epithelium cancer?

A

Carcinomas

115
Q

Glandular cancers?

A

Adenoma vs adenocarcinoma

116
Q

Squamous cancers?

A

Papilloma vs squamous cell carcinoma

117
Q

Sarcoma is malignant. True or false?

A

TRUE

118
Q

Paraneoplastic syndromes?

A

Clinical syndromes involving non-metastatic systemic effects that accompany malignant disease. They are rare disorders

119
Q

Example of an acquired metabolic disorder?

A

Diabetes

120
Q

Which diabetes is insulin dependant?

A

Type 1

121
Q

What is type 2 diabetes?

A

Non-insulin dependent

122
Q

Biochemical complications of diabetes?

A

Ketoacidosis
Non-enzymatic glycosylation
Hypoglycaemia
Lactic acidosis

123
Q

Other issues associated with diabetes?

A

Macroangiopathy
Diabetic nephropathy
Diabetic retinopathy
Cataracts

124
Q

Peripheral obesity?

A

Around around arms and thighs

125
Q

Pathogenesis of atheroma?

A
  • Fatty streak
  • Fibrofatty plaque
  • Proliferative atheroma
  • Complicated atheroma
126
Q

Aetiology of atheroma?

A

Endothelial injury

  • Response to injury
  • Macrophages + platelets
  • Lipid accumulation
  • Smooth muscle proliferation
127
Q

Complications of atheroma?

A 
Thrombosis 
Aneurysm 
Dissection 
Embolism
Ischaemia
128
Q

How hypertension and the heart works?

A
  • Left ventricular hypertrophy
  • Increased LV load
  • Poor perfusion
  • Interstitial fibrosis
  • Micro-infarcts
  • Diastolic dysfunction
129
Q

Thrombus definition?

A

Solid mass of blood constituents, formed within blood vessels

130
Q

3 parts of Virchow’s triad?

A

Vessel wall
Blood flow
Blood constituents

131
Q

Vessel wall in Virchow’s triad?

A

Loss of endothelial tissues

Inflammation

132
Q

Blood flow in Virchow’s triad?

A

Stasis

Turbulence

133
Q

Blood constituents in Virchow’s triad?

A

Platelets
Coagulation proteins
Viscosity

134
Q

What are platelets?

A

Anucleated cell fragments

135
Q

What constitutes of platelets?

A

Adherance properties
Procoagulant contents
Growth factors

136
Q

Embolism?

A

Mass of material in vascular system moving form its site of origin to lodge in the vessels in a distant site

137
Q

DVT possible causes?

A 
Post-op
Bed bound 
Travel 
Involves= 
Unilateral leg swelling 
Oedema 
Pain
138
Q

What is a PTE and it’s symptoms/risk factors?

A

Pulmonary thromboembolism

  • Sudden onset
  • Haemoptysis
  • Breathlessness
  • CV collapse and shock
  • Cardiac arrest
139
Q

What is the pathology of an MI?

A

Zonal necrosis due to sudden occlusion of blood supply

-Due to lack of nutrients and oxygen

140
Q

How long does it take neurons in brain to die without oxygen?

A

3 mins

Principles Collated Flashcards (13 decks)

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