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Pathological Processes > Session 1 > Flashcards

Session 1 Flashcards

1
Q

What is a disease?

A

A pathological condition of a body part, an organ or a system characterised by an identifiable group of signs or symptoms

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2
Q

What is the difference between sign and symptom?

A 
Sign = objective
Symptom = observed by patient
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3
Q

Disease can be considered to be what?

A

Consequence of failed homeostasis with consequent morphological and functional disturbances (tissue, organ or whole person level)

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4
Q

What is pathology?

A

Study of sufferinng - disease and unferstand the process of disease - explain why patients experience symptoms and guides treatment - can involve diagnosis

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5
Q

Describe the different branches of pathology?

A 
Chemical pathology
Haematology
Cellular pathology (histopathology and cytology) - Neuropathology, Forensic pathology, Paediatric pathology
Immunology
Medical microbiology - Virology
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6
Q

What is chemical pathology?

A

Clinical biochemistry

Biochemical investigations - endocrinology, diabetes, lipidology, thyroid disease, inborn errors of metabolism

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7
Q

What is haematology?

A

Diseases of blood (leukaemias), blood clotting, blood transfusion and bone marrow transplantation

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8
Q

What is cellular pathology?

A

Examine organs, tissues and cells for diagnosis and treatment and autopsies

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9
Q

What does neuropathology include examination of?

A

Brain, spinal cord, nerves and muscle

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10
Q

What is forensic pathology?

A

Medicolegal investigation of suspicious or criminal deaths

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11
Q

What is paediatric pathology?

A

Children - samples/autopsies

Foetal/Perinatal/Paediatric

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12
Q

What is immunology?

A

Diseases of the immune system - allergy, autoimmunity and immunodeficiency

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13
Q

What is virology?

A

Study of infectious diseases - antibiotics

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14
Q

What is microscopic diagnosis?

A

Definitive diagnosis
e.g. between fat necrosis and cancer
Important before major surgeries to remove lesions

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15
Q

What is the difference between histology and cytology?

A

Histology - core biopsies, cancer resection specimens, excised skin lesions, endoscopic biopsies
Cytology (disaggregated cells) - fine needle aspirates of breast, thyroid, salivary glands, lungs, effusions. cervical smears, sputum or urine

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16
Q

What are the advantages of histology?

A
  • can be therapeutic and diagnostic
  • can assess architecture and cellular atypia
  • info on completeness of excision / staging and grading
  • better for immunohistochemistry and molecular testing
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17
Q

What are the advantages of cytology?

A
  • faster and cleaner
  • non/minimally invasive and safe
  • cells in fluids
  • preliminary test before other investigations
  • higher inadequate and error rates
  • confirms/discludes cancer/dysplasia - not used for many other diagnoses
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18
Q

How can pattern recognition help you to reach a diagnosis?

A

Normal or not?
Inflammatory or neoplastic (growth)?
Benign or malignant?
Primary tumour or metastasis?

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19
Q

What do you need to consider when cancer is a possible diagnosis?

A

Influences decisions on further treatment and management

  • type of cancer
  • stage of cancer - metastasis?
  • grade of cancer - how different is it?
  • completeness of excision and if margins are involved - which ones?
  • likely efficacy of further treatments -> ER/Her2 receptors - oestrogen receptor
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20
Q

What are the different stages of obtaining a report from a pathological specimen?

A 
Fixation
Cut-up (trimming)
Embedding (processing)
Blocking
Microtomy
Staining
Mounting
Microscopy
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21
Q

What is fixation?

A

Tissue autolysis begins when blood supply is cut off
Block this by process of fixation - inactivate enzymes and denature proteins - prevents bacterial growth and hardens tissue
Can use FORMALIN

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22
Q

What is trimming or cutting up?

A

Specimen is examined and cut up

Samples are taken and placed in a cassette - placed in racks of formalin

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23
Q

What is embedding or processing?

A

Need to remove water and add paraffin wax to allow samples to be cut very thinly

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24
Q

What is blocking?

A

Tissue is put into a metal tray and paraffin wax is allowed to set

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25
Q

What is microtomy?

A

Very thin setions are made - using a microtome

Can see through the sections

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26
Q

What is staining?

A

Usually with H&E
H = nuclei are purple
E = cytoplasm and CT are pink

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27
Q

What is mounting?

A

Mounting medium applied to slide - coverslip on top - preserves tissue

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28
Q

What is microscopy?

A

Ready to be looked at by a pathologist

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29
Q

What is immunohistochemistry?

A
  • demonstrates substancees in/on cells by labelling them with specific antibodies
  • antibody joined to an enzyme that catalyses a colour change
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30
Q

What substances can be used for immunohistochemistry?

A

Any antigenic substances can be demonstrated:

  • contractile protein actin - identifies SMCs
  • cadherins - cell adhesoon molecules, deficient in some carcinomas
  • hormone receptors e.g. ER/PR
  • Her2 receptor - growth factor receptor, predicts response of cancer to Herceptin
  • microorganisms e.g. CMV, HPV, Herpes Simplex
  • cytokeratins - present in almost all epithelia - intracellular fibrous proteins - shows tissue specific distribution and can be used in combination
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31
Q

What is molecular pathology?

A

Studies how diseases are caused by alterations in normal cellular molecular biology - due to DNA, RNA or proteins being altered

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32
Q

What are the different ways altered DNA, RNA or proteins can be seen?

A

FISH - e.g. copies of Her2 gene in breast cancer
Sequencing DNA from cancer tissue - see if there is a mutation on a specific gene
mRNA expression profiling - level of activity in different genes can be detected

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33
Q

What are frozen sections?

A

Method of hardening tissue quickly - can be done quickly during an operation to establish presence and nature of a lesion

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34
Q

What are the different sections seen in a histology report?

A 
Clinical history
Macroscopic
Microscopic
Conclusion
Reported by:
35
Q

All cells have effective mechanisms to deal with wild changes in?

A

Environmental conditions

36
Q

More severe changes in environment leads to?

A

cell adaptation
cell injury
cell death

37
Q

What does the degree of injury depend on?

A
  • type
  • severity
  • type of tissue
38
Q

What are the causes of cell death?

A

Hypoxia
Toxins
Physical agents - direct trauma, extremes in temperature, changes in pressure, electric currents
Radiation
Microorganisms
Immune mechanisms
Dietary insufficiency and deficiencies, dietary excess

39
Q

What is hypoxia?

A

Hypoxia is not the same as ischaemia
Hypoxia = not enough O2
Ischaemia = reduced blood supply

40
Q

What are the causes of hypoxia?

A

Hypoxaemic hypoxia
Anaemic hypoxia
Ischaemic hypoxia
Histiocytic hypoxia

41
Q

What is hypoxaemic hypoxia?

A

Arterial content of O2 is low - reduced absorption secondary to lung disease

42
Q

What is anaemic hypoxia?

A

Decreased ability of haemoglobin to carry oxygen - anaemia/CO poisoning

43
Q

What is ischaemic hypoxia?

A

Interruption to blood supply - caused by blockage of a vessel or heart failure

44
Q

What is histiocytic hypoxia?

A

Inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes - cyanide poisoning

45
Q

How can the immune system damage the body’s own cells?

A

Hypersensitivity reactions - host tissue is injured secondary to an overly vigorous immune reaction e.g. urticaria (hives)
Autoimmune reactions - immune system fails to distinguish self from non-self e.g. Grave’s disease of the thyroid

46
Q

What are the cell components susceptible to injury?

A

Cell membranes - plasma membrane/ organellar membranes
Nucleus - DNA
Proteins - structural (enzymes)
Mitochondria - oxidative phosphorylation

47
Q

What happens at a molecular level in hypoxia?

A

reversible injury -> ischaemia -> mitochondria (less OP) -> less ATP made ->
Increase in glycolysis -> decrease in pH and glycogen -> clumping of nuclear chromatin
Decrease in Na+ pump -> more Ca2+, H20, Na+ and less K+ -> cellular swelling, loss of microvilli, blebs, ER swelling and myelin figures
Detachment of ribosomes -> less protein synthesis -> lipid deposition

48
Q

What occurs during prolonged hypoxia?

A 
Increase in Ca2+
ATPase - decreased ATP
Phospholipase - decreased phospholipids
Protease - disruption of membrane and cytoskeletal proteins
Endonuclease - nuclear chromatin damage
49
Q

Causes other than hypoxia for cell injury?

A
  • sequence of events for other insults may be different but as the cell has a limited responses to injury, outcome often similar
  • other forms of injury might attach different key structures - extreme cold damages mebranes internally
  • free radicals also damage membranes primarily
50
Q

What is a free radical?

A

Reactive O2 species - single unpaired electron in an outer orbit - unstable configuration
OH, O2-, H2O2

51
Q

How do you produce free radicals?

A
  • normal metabolic reaction
  • inflammation
  • radiation
  • contact with unbound metals within the body
  • drugs and chemicals
52
Q

How can you control free radicals?

A
  • antioxidant system: donate electrons to the free radical - vitamins ACE
  • metal carrier and storage proteins (transferrin, ceruloplasmin) sequester iron and copper
  • enzymes that neutralise free radicals
53
Q

How do free radicals injure cells?

A

Free radicals overwhelms the anti-oxidant system - oxidative imbalance
Most important target = lipids in cell membranes - causes lipid peroxidation
Oxidise proteins, carbohydrates and DNA - molecules have become bent out of shape - mutagenic and carcinogenic

54
Q

How do protect the cell from injury?

A
  • heat shock proteins - aims to mend misfolded proteins and maintains cell viability
  • unfoldases or chaperonins
55
Q

What will you see in hypoxic injured or dying cells under the microscope?

A
  • cytoplasmic changes
  • nuclear changes
  • abnormal cellular accumulations
56
Q

In reversibe cell injury what will be seen under the microscope?

A
  • swelling of cells and organelles due to sodium-potassium pump failure
  • cytoplasmic blebs
  • clumped chromatin due to reduced pH
  • ribosome detadchment due to failure of energy-dependent process of maintaining ribosomes in the correct location
57
Q

In irreversible cell injury what will be seen under the microscope?

A
  • increased cell swelling
  • nuclear changes - pyknosis, karyolysis, karryorhexis
  • swelling and rupture of lysosomes
  • membrane defects
  • appearance of myelin figures
  • lysis of endoplasmic reticulum due to membrane defects
  • amorphous densities in swollen mitochondria
58
Q

Define oncosis?

A

Cell death with swelling, spectrum of changes tha occur in injured cells prior to death

59
Q

Define necrosis?

A

In a living organism the morphological changes that occur after a cell has been dead for some time

60
Q

Define apoptosis?

A

Cell death with shrinkage, cell death induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins

61
Q

When is necrosis seen?

A

When there is damage to cell membranes and lysosomal enzymes are released into the cytoplasm and digest the cell - contents leak out of the cell and inflammation is seen - necrotic changes develop over a no of hours - necrotic tissue is removed by enzymatic degradation and phagocytosis by white cells -> can lead to dystrophic calcification

62
Q

What is coagulative necrosis?

A

Cells are dying and their proteins denature and coagulate - ischaemia of solid organs - cellular architecture is somewhat preserved - ghost outline of cells

63
Q

What is liquefactive or colliquitive necrosis?

A

Proteins undergo autolysis in which proteins undergo dissolution by the cells own enzymes - enzyme degradation is greater than denaturation - enzymatic digestion of tissues - ischaemia in loose tissues - preserve of many neutrophils

64
Q

What are the two special types of necrosis?

A

Caseous necrosis - contains amorpheus debris - not as uniform as coagulative - looks like cheese - associated with infection e.g. TB
Fat necrosis - looks like bits of wax dropped on tissue

65
Q

What is gangrene?

A

Necrosis visible to the naked eye
Exposure to air = dry gangrene - coagulative necrosis
Infection with a mixed bacterial culture = wet gangrene - liquefactive necrosis
Gas gangrene is wet gangrene where the tissue has become infected with anaerobic bacteria that produces visible and palpable bubbles of gas within the tissues

66
Q

What is infarction?

A

Necrosis caused by a reduction in arterial blood flow

67
Q

What is a red infarct?

A

RED = haemmorhagic infarct occurs where there is extensive haemmorhage into dead tissue - dual blood supple and numerous anastomoses - raised venous pressure, reperfusion and loose tissue

68
Q

What is a white infarct?

A

WHITE = anaemic infarct occurs in solid organs after occlusion of an end artery e.g. thrombosis or embolism

69
Q

What are the consequences of ischaemia?

A
  • none
  • death
    Depending on: alternative blood supply, speed of ischaemia, tissue involved and O2 content of blood
70
Q

What is ischaemia-reperfusion injury?

A

If blood flow is returned to a damaged but not yet necrotic tissue, damage sustained can be worse than if blood hadn’t been returned - increased no of neutrtophils (inflammation), free radicals, complement proteins

71
Q

Many molecules leak out of injured cells as their membranes are disrupted, for example…?

A
  • causes local inflammation
  • more general toxic effects
  • high conc in blood

Potassium
Enzymes - aid in diagnosis
Myoglobin - released from dead myocardium and striated muscle

72
Q

What is apoptosis?

A

Death of a single cell due to activation of an internally controlled suicide programme - can be a normal physiological process or can occur when a cell is damaged

73
Q

What are the characteristic appearances of apoptosis?

A
  • apoptotic cells are shrunken and appear intensely eosinophilic
  • chromatin condensation, pyknosis and karryorhexis are seen and take on a distinctive appearance
  • cytoplasmic budding
  • apoptotic bodies are removed by macrophage
  • no leakage of inflammation as there is no leakage of cell contents
74
Q

What is the characteristic of DNA breakdown?

A

Not random, internucleosomal damage of DNA

75
Q

When is apoptosis described as a physiological process?

A

Hormone controlled involution

Embryogenesis

76
Q

When is apoptosis described as a pathological process?

A

Cytotoxic T cell killing of virus infected or neoplastic cells
When cells are damaged, particularly with damaged DNA

77
Q

What are the 3 phases of apoptosis?

A

Initiation
Execution
Degradation and phagocytosis

78
Q

What are abnormal cellular accumulations?

A

If a cell cannot metabolise something it will remain in the cell
Can derive from:
- cell’s own metabolism
- extraceullular space e.g. spilled blood
- outer environnment e.g. dust

79
Q

What are the five main groups of accumulations?

A 
Water and electrolytes
Lipid - triglycerides and cholesterol
Proteins
Pigments
Carbohydrates
80
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts within tissue - can be localised (dystrophic) or generalised (metastatic)

81
Q

What is dystrophic calcification?

A
  • occurs in an area of dying tissue, in atherosclerotic plaques, in aging or damaged heart valves and in TB lymph nodes
  • no abnormality in calcium metabolism or serum calcium or potassium concentrations
  • local change or disturbance in the tissue favours the nucleation of hydroxyapatite crystals
82
Q

What is metastatic calcification?

A

Body wide disturbance - hydroxyapatite crystals are deposited in normal tissues throughout the body when there is hypercalcaemia secondary to disturbances in calcium metabolism

83
Q

What is cellular aging?

A

They accumulate damage to cellular constituents and DNA - may also accumulate abnormally folded proteins
Decline in ability to replicate - related to length of chromosomes - with each division telomeres are shortened and when the telomeres reach a critical length, the cell can no longer divide

Pathological Processes (2 decks)

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