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Semester 2 Missed Lectures > Pathological Processes > Flashcards

Pathological Processes Flashcards

1
Q

What is pathology?

A

The study of disease and cellular dysfunction.

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2
Q

What is disease?

A

A pathological condition that is characterised by identifiable signs or symptoms.

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3
Q

What is autolysis?

A

Self-digestion of tissues.

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4
Q

What do fixatives do and what is the rate of formalin penetration?

A

They inactivate tissue enzymes and denature proteins to prevent bacterial growth and putrefaction. It also hardens tissues.

It penetrates at 1mm/hour, when submerged in 10x volume of fixative.

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5
Q

How do you remove the water from a tissue?

A

Dehydration using alcohol, followed by the replacement of alcohol with xylene (also removes the lipid).

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6
Q

What do cytokeratins show a marker of?

A

Epithelial differentiation, and can give information about the primary site of a carcinoma.

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7
Q

What does molecular pathology look for?

A

Mutations in DNA, RNA or proteins.

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8
Q

What do DNA mutations and mRNA levels show?

A

DNA mutations = mutations in genes.
mRNA levels = expression of genes, which can be used to predict how a tumour may behave.

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9
Q

What are the clinical details given in a histology report?

A

Age/ gender.
Past medical history.
Signs and symptoms.
Risk factors.
Endoscopic findings.
Clinical teams’ diagnoses.

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10
Q

What is said in the macroscopic, microscopic and conclusion sections of a histology report?

A

Macroscopic = details of sample received and its size.

Microscopic = description of the tissue under the microscope and differential diagnoses.

Conclusion = what the diagnosis is.

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11
Q

What is the hearts response to injury?

A

There is an initial insult, causing the myocytes to work harder.
Adaptation occurs, causing cardiac myocyte hypertrophy.
Continued insult and adaptation occurs, leading to ventricular hypertrophy.
The continuing insult increases the requirement for the heart for oxygen, leading to the second insult of hypoxia.
The insufficient oxygen supply leads to ischaemia and myocardial infarction, an irreversible cell injury and death.

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12
Q

What does the degree of injury depend on?

A

The tissue type.
The type of injury.
The severity of the injury.
The length of the injury.

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13
Q

What are some non-environmental cause of cell injury?

A

Genetic/ ageing - inborn errors in metabolism, enzyme deficiencies and dysfunctional proteins.

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14
Q

What are some toxins that can cause cell injury?

A

Alcohol.
Drugs.
Asbestos.
Poisons.
Pollutants.
Insecticides.
Herbicides.

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15
Q

What are the two types of immune mediated injury?

A

Hypersensitivity reaction - excessive immune reactions, such as anaphylaxis.

Auto-immune reactions - immune system attacks itself, causing tissue damage.

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16
Q

Outline some physical agents that can cause tissue injury.

A

Trauma.
Extreme temperatures.
Electric currents.
Radiotherapy.

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17
Q

What nutritional/ dietary abnormalities can cause cell injury?

A

Obesity.
Anorexia.
Deficiencies or excesses, particularly in fat or salt, B12, folate and vitamin D.

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18
Q

What can excess intracellular calcium activate?

A

ATPases - reducing ATP levels.
Phospholipases - breaks down the cell membrane.
Proteases - breaks down organelles.
Endonucleases - breaks down DNA.

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19
Q

What transport proteins control free radical formation?

A

Transferrin binds iron to prevent the Fenton reaction from occurring.
Ceruloplasmin binds copper to prevent free copper from being available.

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20
Q

What do heat shock proteins do and how do cells adapt for this?

A

They help re-fold damaged proteins or label them for degradation.

Cells decrease protein synthesis and increase heat shock protein synthesis.

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21
Q

What is pathological apoptosis caused by?

A

Viral infection and cells with damaged DNA.

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22
Q

What is fat necrosis seen in?

A

Acute pancreatitis and direct trauma to fatty areas.

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23
Q

What 3 molecules are released by injured cells and what can their effect on the body be? When would they be seen?

A

Potassium - is cardiotoxic and can cause heart attacks. Seen in major burns.

Enzymes - can cause a breakdown of molecules. Seen in liver disease, MI and pancreatitis.

Myoglobin - decrease in renal function and tea-coloured urine. Seen in extreme athletes and when an elderly person falls and lays on a muscle for a prolonged period of time.

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24
Q

What do the complications of infarction depend on?

A

Any alternative blood supply.
The speed of ischaemia.
The type of tissue involved.
The oxygen content of the blood.

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25
Outline the process of how excess alcohol can cause death.
Excess ethanol increases the NADH/NAD+ ratio, increasing fatty acid synthesis and accumulating the fat in the liver. The continued consumption of alcohol causes inflammation of the liver, damaging the hepatocytes. There is then abnormal cellular accumulations, such a toxic bilirubin, leading to necrosis, fibrosis and cirrhosis. They then have liver failure and the liver cannot carry out its normal functions, leading to death.
26
What are the differences between exudate and transudate?
Exudate is caused by an increase vascular permeability, whereas transudate is not. Exudate is protein rich but transudate is not. Exudate occurs in inflammation, but transudate occurs in heart/hepatic/renal failure.
27
How can leucocytes increase vascular permeability?
Enzymes and ROS are released by activated inflammatory cells and can degrade the endothelial cells, increasing vascular permeability.
28
What proteins delivered in the exudate can help with inflammation?
Fibrin is delivered which acts as a mesh to limit the spread of toxins. Immunoglobulins are delivered for opsonisation.
29
What is the structure of a neutrophil?
It has a purple staining, trilobed nucleus.
30
How do neutrophils roll and adhere to endothelial cells?
They roll through selectins that are expressed on endothelial cells. They adhere through the binding of integrins (expressed on neutrophils) to the selectins, changing the adhesion from a low to high affinity state.
31
How does the neutrophil change for chemotaxis?
Re-arrangement of neutrophil cytoskeleton, stimulated by chemoattractants, such as bacterial peptides, IL-1, TNF and C5a.
32
What is hereditary angio-oedema? What can it cause?
Autosomal dominant deficiency in C1-esterase inhibitor Patients have itchy cutaneous oedema of the skin. They often have intestinal oedema, causing pain and can die of sudden death due to larangyeal oedema.
33
What is alpha-1 antitrypsin deficiency, and what do patients develop?
Autosomal recessive resulting in low levels of alpha-1 antitrypsin. It is a protease inhibitor, meaning proteins are broken down by proteases released from neutrophils. Patients develop emphysema due to the destruction of parenchymal tissue, and liver disease due to incorrect protein folding. Results in liver damage and cirrhosis.
34
What are the characteristics of chronic inflammation?
It has a slow onset. There is a variable duration. It has a variable appearance. It limits damage and initiates repair. It can cause debilitating symptoms.
35
Why do macrophages in the lung appear dark red/ brown?
They have phagocytosed carbon.
36
What gives macrophages their foamy appearance?
Phagolysosomes - the addition of lysosomes to material that has been phagocytosed.
37
What are the functions of macrophages?
To phagocytose pathogens, necrosis and debris. Antigen presenting to T-cells. Cytokine release to accumulate immune cells at the site of damage.
38
Describe the appearance of plasma cells.
They are oval in shape with a large nucleus to one side that contains clumps of chromatin that lines the edge. There is peri-nuclear clearing - a site of lighter appearance as a ‘shadow’ due to the presence of Golgi.
39
Where are Langhans, Touton and foreign body giant cells seen?
Langhans = tuberculosis. Touton = fat necrosis. Foreign body = foreign bodies present.
40
What are the proportion of cells seen in rheumatoid arthritis, chronic gastritis and Whipple’s disease? What is the significance of this?
Rheumatoid arthritis = mainly plasma cells. Chronic gastritis = mainly lymphocytes. Whipple’s disease = mainly macrophages. The proportion of cell types can help influence a diagnosis.
41
What is granulomatous inflammation?
Chronic inflammation and the presence of granulomata.
42
What are the two different types of granuloma and what distinguishes them?
Foreign body = destruction of foreign material containing few lymphocytes. Immune mediated = destruction and removal of pathogens with many lymphocytes. It can be idiopathic and can undergo central necrosis.
43
Why are mycobacterium difficult to destroy?
They have thick cell walls and mycolic acids which are resistant to macrophages.
44
What is special about mycobacterium granulomata, and what is the appearance?
It has central caseous necrosis which is bright pink in structure with the epitheliod histiocytes and lymphocytes around the outside.
45
What is a biopsy and a resection?
Biopsy - the removal of a small amount of tissue for diagnosis. Resection - the removal of tissue/ organ to relieve symptoms.
46
How and why do giant cells form?
When macrophages are unable to phagocyte something, they release cytokines which stimulate the fusion of macrophages.
47
What is regeneration?
The re-growth of cells with minimal evidence of injury.
48
What are the differences between unipotent, multi potent and totipotent stem cells?
Unipotent stem cells differentiate to become one type of cell. Multipotent stem cells can differentiate to become several different types of cells. Totipotent stem cells can differentiate to become any type of cell.
49
What is fibrous repair?
The replacement of functioning tissue with a scar.
50
What are the 4 stages of scar formation?
Haemostasis - the prevention of blood loss. Inflammation - the accumulation of immune cells, leading to the digestion of a blood clot. It is acute and then chronic. Proliferation - angiogenesis occurs with proliferation of fibroblasts, myofibrosblasts and formation of extracellular matrix, forming granulation tissue. Remodelling - laying down of collagen and contracting as the cell population is reduced.
51
What is the role of endothelial cells in fibrous repair?
To proliferate and form capillaries to deliver nutrients and other cells to the site of injury.
52
What is the structure and function of fibroblasts?
They have a spindle-shaped nucleus with cytoplasmic extensions. They secrete collagen and elastin.
53
Where is type 4 collagen found?
Basement membranes, lens of the eye, glomerular filtration.
54
What is contact inhibition?
Where cells proliferate until they come into contact with other cells, where cadherins bind to prevent further proliferation.
55
What is the regenerative capacity like in adipocytes, melanocytes and the CNS?
Adipocytes cannot regenerate. Melanocytes tend to repair the too little or too much. The CNS cannot regenerate, meaning severed axons do not grow back.
56
What is an ulcer?
A break in the skin, in the lining of an organ or on the surface of a tissue.
57
What are 4 different types of ulcers?
Venous. Arterial. Diabetic. Pressure.
58
What is haemostasis?
The consequence of a tightly regulated process, maintaining fluid status in vessels.
59
What are the 3 components of haemostasis? What is the goal of haemostasis?
1) Vascular wall. 2) Platelets. 3) Coagulation cascade. The goal of haemostasis is to make a clot, control clotting and break the clot down.
60
What is involved in platelet aggregation?
The cross-linking of platelets to form a platelet plug.
61
What factors are involved in the formation of a platelet plug?
62
If both PT and APTT are elongated, what does this suggest?
There is a defect in the common pathway of the clotting cascade.
63
What are the functions of (activated) protein C and protein S?
Protein C is to inactivate activated factors 8 and 5. Protein S acts as a co-factor for protein C.
64
What does antithrombin do and what is it activated by?
It inactivates thrombin, and is activated by heparin.
65
What are some causes of thrombocytopenia?
66
What is the difference between immune thrombocytopenic purpura and thrombotic thrombocytopenic purpura?
Immune = only low platelets with no other cause. Thrombotic = platelets and red blood cells are broken down.
67
What are the signs and symptoms in haemolytic-uraemia syndrome? Who does it occur most in?
Signs = low RBCs, acute kidney injury and low platelets. Symptoms = bloody diarrhoea, fever, vomiting and weakness. It occurs most in children with E. Coli.
68
Who are abnormal factor V Leiden and antiphospholipid syndrome seen most commonly in?
Factor V Leiden abnormality seen in Caucasians, and antiphospholipid syndrome seen in other ethnicities.
69
How do direct oral anticoagulant drugs work? Give an example.
Inhibit thrombin or factor Xa. Apixaban/ edoxaban.
70
What is a clot?
A mass of blood outside the cardiovascular system
71
What is the difference between an arterial and venous thrombus in appearance and components?
Arterial is pale, granular and shows lines of Zahn. It contains fewer cells. Venous is soft, gelatinous and is a deeper red in colour. It has a higher cell count.
72
What is arteriosclerosis?
The thickening of the walls of arteries and arterioles associated with loss of elasticity, most commonly due to hypertension or diabetes mellitus.
73
What does endothelial dysfunction lead to cells doing, increasing the risk of atherosclerosis?
Monocytes moving into the intima and differentiating into macrophages. Platelet adhesion - PDGR released. Smooth muscle cell migration and proliferation. LDL and cholesterol crossing into the intima.
74
What are the microscopic appearance changes of unstable plaques from stable plaques?
Disruption of the internal elastic lamina and fibrous cap. Damage extending into the media. New blood vessels growth into the plaque from the adventitia. Thrombus formation.
75
What can atherosclerosis in the peripheral arteries cause?
Acute limb ischaemia. Intermittent claudication. Critical limb ischaemia. Gangrene.
76
What are some defects with lipid metabolism that increases ones risk of atherosclerosis?
Apolipoprotein defects - ApoE defects, ApoA1 defects or deficiencies. Enzyme defects - lipoprotein lipase defect. Receptor defects - LDL receptor defects.
77
What are 3 infectious organisms that cause increase the risk of atherosclerosis?
Chlamydia pneumoniae. Helicobacter pylori. Cytomegalovirus.
78
What needs to occur first to allow lipid to enter the wall of the artery?
Chronic endothelial damage.
79
What does the size of a cell population in adults depend on the rate of?
Cell proliferation. Cell differentiation. Cell death by apoptosis.
80
Why is atrophy an adaptive mechanism?
Because the decrease in size or number of the cells decreases the demand of oxygen and nutrients on that tissue, allowing other areas of the body to get sufficient oxygen and nutrients.
81
At what point is atrophy no longer reversible?
When the parenchymal tissue is replaced by connective tissue.
82
What is involution? Give a physiological example.
The normal programmed shrinkage of an organ. It is seen with the thymus.
83
What can benign prostatic hyperplasia cause the bladder to do?
Undergo hypertrophy due to the increase in urinary retention.
84
What is carcinomatosis?
Extensive metastatic disease.
85
What is differentiation?
The process of becoming different by growth or development.
86
What is the primary and secondary site of a malignant neoplasm?
The primary site is the site of origin of the malignant neoplasm. The secondary site is the site that the malignant neoplasm spreads to, that is discontinuous of the primary site.
87
What does anaplastic mean?
There is no resemblance to any tissue.
88
What is the difference in thickness between mild, moderate and severe dysplasia?
Mild = lower 1/3rd. Moderate = lower 2/3rds. Severe = full thickness.
89
What 3 events are required for invasion of a malignant neoplasm require, and what is this process called?
Altered adhesion, stromal proteolysis and motility. It is called epithelial to mesenchymal transition.
90
How does the adherence of a malignant neoplasm change?
There is reduced E-Catherine expression, meaning that it is not longer in contact with other cells. Reduced integrin expression, meaning that it is no longer bound to the basement membrane.
91
What is involved in stromal proteolysis?
Altered expression of proteases - metalloprotinases. Degradation of the basement membrane, allowing for invasion. Utility of nearby non-neoplastic cells.
92
What nearby non-neoplastic cells does the neoplasm use and what do they provide?
Stroma, fibroblasts, endothelial cells and inflammatory cells. They utilise the growth factors and proteases.
93
What is required for motility of the neoplasm?
Changes in the actin cytoskeleton.
94
Why are the symptoms experienced by paraneoplastic syndromes important?
They can be the first sign of a neoplasm. They can cause clinical problems and be fatal. They can cause the wrong treatment to be given.
95
What is Trousseau’s sign of malignancy?
Thrombus formation due to hyper-coagulable blood.
96
What is the function of the TP53 gene?
It induces apoptosis in mutated cells.
97
How can obesity cause cancer?
Adipose tissue can increase inflammation, make growth hormones and growth factors. This causes the cells to divide more often, which can act as an initiator or promoter.
98
What are first and second classes of carcinogens?
First class = initiators. Second class = promoters.
99
What is the AMES test used for?
It is to see whether a chemical can cause DNA mutations.
100
What do proto-oncogenes encode, generally?
Oncoproteins.
101
What is Li-Fraumeni syndrome, and what does it increase the risk of?
102
What virus does having sex earlier increase the risk of developing?
HPV - human papilloma virus.
103
What types of cancer does smoking increase the risk of?
104
What increases the risk of malignant mesothelioma the most?
UV radiation.
105
What is the adenoma-carcinoma sequence?
The progression of a neoplasm through adenoma to carcinoma, through deactivating APC tumour suppression genes and activating KRAS proto-oncogenes.
106
What do seminoma neoplasms look like under a microscope?
Fibrous septae with lymphocytes inside.
107
Mutations in BRCA1 and 2 genes can predispose to breast cancer. What other cancers can mutations in these predispose to?
Ovarian, prostate, pancreatic and melanomas.
108
What is Gleason’s pattern scale used for and what is the criteria it is based on?
It is used for prostate grading. It is based off of the presence and shape of glands.
109
What commonly causes osteosclerotic lesions in the spine?
Metastatic prostate cancer.

Semester 2 Missed Lectures (5 decks)

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