Pathological Procedures Flashcards

1
Q

Define neoplasia?

A

A form of abnormal growth that is independent of normal growth regulating factors. It is always pathological

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2
Q

Outline clinical symptoms associated with a diagnosis of neoplasia?

A

Feel a mass
See enlargement of an area
Fatigue
Fever/ chils
Night sweats
Loss of appetite
Loss of weight
Pain
Headaches
Nausea
Vomiting

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3
Q

Macroscopic and microscopic appearances of uterine fibroid?

A

Macro - well-defined, Pale nodule, +/- bossalated, infarction, Haemorrhage. Can be serosa, subserosal or intramural

Micro - well-defined, spindle cells with cigar shaped nuclei, +/- atypia

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4
Q

There are 2 mechanisms for cell death what are they?

A

Apoptosis
Necrosis

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5
Q

How do apoptosis and Necrosis differ?

A

Apoptosis - programmed, no inflammatory response, no extra damage to tissues, controlled, pyknosis, karyohexis and karyolysis, active

Necrosis - incidental, responds to stimuli, inflammatory response, damage to surrounding tissues, uncontrolled, swelling and discolouration, passive

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6
Q

Define metaplasia?

A

The reversible change of one form of mature epithelium into another mature epithelium in response to an external stimuli

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7
Q

Give 2 examples of metaplasia with appropriate clinical settings

A

Cervix - hormone changes, in adolescence cause cervix to enlarge and transformation zone to move into the vagina where the pH is more acidic. Delicate columnar epithelium of the canal changes into squamous epithelium of the vagina.

Oesophagus - continual acid reflux damages the cuboidal epithelium of the Oesophagus to change into mucus secreting stomach or duodenal epithelium for protection

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8
Q

Describe the histological features of acute inflammation, including cell types and potential outcomes?

A

Neutrophil infiltrate, oedema in surrounding tissues, fibrin deposits to wall off stimulus.
Abscess formation, progression to chronic inflammation, recovery and removal of inflammatory components and debris

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9
Q

Describe the histological features of chronic inflammation, including cell types and potential outcomes?

A

Lymphocytes, histiocytes infiltrate, increase fibrin deposits, collagen laid down, cells that can regenerate do so or scar formation begins

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10
Q

Define hamatoma

A

Pool of mostly clotted blood in an organ, tissue, or body cavity

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11
Q

Define neoplasm

A

New growth of tissue that is not normal

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12
Q

Define carcinoma

A

Tumour that begins in epithelial cells

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13
Q

Define sarcoma

A

Tumour that begins in bone or soft tissue

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14
Q

Describe with examples the main routes of malignant tumour spread?

A

Adjuvent spread - to adjacent tissues, uterine to colon
Lymphatic - to nearest lymph node then through the lyphatics to be deposited at a new organ MM to lymph nodes
Transcoelimic - across body cavities ovarian to liver
Blood - through he vessel wall to a new organ colon to liver as it is filtered

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15
Q

Give 3 examples of tumour markers and their tumours of origin?

A

PSA - hyperplasia or malignancy of the prostate
CA 125 - ovarian cancer
CEA - increased risk of colon cancer

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16
Q

What are the advantages and disadvantages of using tumour markers clinically?

A

Aid diagnosis
Non-invasive tests
Direct the patient pathway

Not specific for tumours

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17
Q

What is the microscopic appearance of granuloma to us inflammation?

A

Multineucleate giant cells
Epitheloid histiocytes
Lymphocytes
Necrosis

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18
Q

Name 4 conditions where granuloma to us inflammation can occur?

A

Foreign body reaction
Infective diseases - tuberculosis
Sarcoidosis
Crohn’s disease

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19
Q

Describe the 3 pathological processes involved in the development of a thrombus, with examples?

A

Hypercoaguability - something that triggers coagulation of the body at an inappropriate time or increases the level above normal - surgery, trauma, malignancy, pregnancy, infection, IBD, Autoimmune conditions

Circulatory status - natural or acquired areas that allow blood flow to remain static - immobility, venous obstruction, varicose veins, fibrillation, dysfunction, congenital abnornalities

Vascular damage - damage to the vessel wall - cellulitis, atherosclerosis, venopuncture, fractures, long travel, disruption or break in the endothelial wall.

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20
Q

What is an embolism?

A

An obstruction of a blood vessel by an embolus

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21
Q

What is the pathological effect of an embolism

A

The tissues distal to the embolism are deprived of blood and oxygen. If severe or prolonged this will lead to tissue death

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22
Q

Name 6 types of emboli?

A

Thrombus,
Foreign body,
Air,
Metastatic tumour
Atherosclerosis /fat
Infection

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23
Q

Describe with examples, autosomal dominant disorder

A

A disorder or disease that is spread via genetic information and only requires one copy of the gene

Polycystic kidney disease
Huntington’s disease

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24
Q

Describe with examples, X-linked recessive disorder

A

Disease or disorder that is spread by the X chromosome and requires both X chromosomes to carry the gene in females and only the X chromosome in males. It’s more likely to affect males than females.

Red-green colourblindness
Haemophilia A

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25
Q

Define apoptosis

A

The process of programmed cell death

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26
Q

What are the morphological features seen in cells undergoing apoptosis?

A

Karyohexis
Karyolysis
Pyknosis
Blebbing of cytoplam

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27
Q

Give an example of a normal process in which apoptosis occurs

A

Webbing between fingers and toes during embryonic development

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28
Q

What is acute inflammation?

A

A rapid response to acute tissue injury or infection. It delivers neutrophil and immune cells to the damaged area

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29
Q

What are the classic signs of acute inflammation?

A

Heat
Pain
Redness
Swelling

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30
Q

What is the acute inflammatory process?

A

Damage - vasodilation - increased permeability - oedema - neutrofil activation and migration - phagocytosis - complement cascade activation - immunoglobulins - Fibrinogen leaved - fibrin formed - sealing stimulant and helping with scar formation

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31
Q

What is the aim of acute inflammation?

A

To isolate and contain the site of injury or infection,
Destroy toxins and microbes
Prepare the site for repair

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32
Q

What is the Macroscopic appearance of acute inflammation?

A

Red
Swollen
Exudate
+/- Necrosis

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33
Q

What is the microscopic appearance of acute inflammation?

A

Neutrophil line the vessels
Fiberous tissue has clear spaces (oedema)
Congestion

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34
Q

What are the complications that arise from acute inflammation?

A

Pus formation - abscess formation - increase in liminal pressure - immune response further damaging wall = rupture and associated comolications

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35
Q

What types of acute inflammation are there?

A

Suppurative
Fiberous
Serous

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36
Q

What is suppurative inflammation?

A

Purulent

Exudate rich in neutrophil
Often due to bacterial infections
If closed off = abscess

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37
Q

What is fibrinous inflammation?

A

Exudate rich in plasma proteins
Common to cavity membranes (Pleural, pericardium)
Can lead to adhesions between organs

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38
Q

What is serous inflammation?

A

Fluid in the response has little protein and cells (transudate)
Eg skin in response to burn

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39
Q

What is serous inflammation?

A

Fluid in the response has little protein and cells (transudate)
Eg skin in response to burn

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40
Q

What is the outcome of acute inflammation?

A

Resolution - normal architecture and function eg after Sun burn
Healing - scar formation when tissue cannot regenerate. Structural integrity with impairment of function eg modified bone after a fracture
Abscess formation - progresses to chronic inflammation eg appendicitis, lobular pneumonia

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41
Q

What happens when control of inflammatory processes fails?

A

Autoimmune disorders

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42
Q

How long does an acute inflammatory response last before it becomes chronic?

A

After 3 days

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43
Q

What types of tissue repair are there?

A

Regeneration
Replacement

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44
Q

What happens to a tissue if it regenerates?

A

Original cells type and function returned

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45
Q

In prepare what happens to the tissue if it undergoes replacement?

A

New cell/tissue type usually with some or total loss of function

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46
Q

When it comes to repair what types of tissues are there?

A

Labile
Stable
Permanent

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47
Q

What are labile tissues?

A

Tissues that constantly divide and regenerate during repair processes

Skin, mucosa and haemopoietic tissues

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48
Q

What are stable tissues?

A

Tissues that divide until fully mature then stop. Can regenerate after injury

Connective tissue, liver and pancreas

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49
Q

What are permanent tissues, in regards to repair?

A

Tissues with limited ability to replicate
Usually replaced after injury

Neurons, skeletal and cardiac muscle

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50
Q

Repair can be delayed due to what factors?

A

Stimuli remaining
Foreign body remaining
Poor nutrition
Poor circulation
Pre-exsisting diabetes
Medication (steroids)

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51
Q

What is primary intention?

A

A rapid process with a low rate of infection and only a small amount of scarring

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52
Q

What type of wound undergoes primary intention?

A

The edges of the wound are close together and fit easily together

Surgery

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53
Q

What happens during first intension?

A

Wound fills with blood
Clot forms containing fibrin
Fibrin binds the wound together
Clot dries
Infection prevented
Vasodialtion
Increase permeability
Vessel permeability increases
Oedema in surrounding tissues
Migration and activation of neutrophils
Phagocytosis of damaged tissue
Fibrin contains any infectious agents
Neutrophil die forming pus and exudate
Fibroblasts from surrounding tissue migrate to clot
Fibroblasts produce collagen and extracellular matrix components
I labile tissues capillaries revasculise the area
Fibrin clot breaks down and removed
Delicate connective tissue (granulation tissue) is laid down forming a scar

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54
Q

What is granulation tissue?

A

Delicate connective tissue that forms in wounds during repair

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55
Q

What is the function of granulation tissue?

A

The form a scar when a tissue is unable to regenerate after injury

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56
Q

What is the Macroscopic appearance of a scar?

A

Start off as a shiney red patch but become more white as the capillaries are compressed and the granulation tissue increases

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57
Q

What is secondary intention?

A

Repair process when the edges of a wound are far apart or do not fit easily together

4th degree burns
Skin tears

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58
Q

What process occurs in secondary intention?

A

Blood fills wound
Clots but fibrin is not enough to seal the wound
This slows down the repair process and the wound is still open to infection
Vasodilation
Increase permeability
Vessel permeability increases
Oedema in surrounding tissues
Migration and activation of neutrophils
Phagocytosis of damaged tissue
Fibrin contains any infectious agents
Neutrophil die forming pus and exudate
Fibroblasts from surrounding tissue migrate to clot
Fibroblasts produce collagen and extracellular matrix components
I labile tissues capillaries revasculise the area
Fibrin clot breaks down and removed
Delicate connective tissue (granulation tissue) is laid down forming a scar

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59
Q

What process occurs in secondary intention?

A

Blood fills wound
Clots but fibrin is not enough to seal the wound
This slows down the repair process and the wound is still open to infection
Vasodilation
Increase permeability
Vessel permeability increases
Oedema in surrounding tissues
Migration and activation of neutrophils
Phagocytosis of damaged tissue
Fibrin contains any infectious agents
Neutrophil die forming pus and exudate
Fibroblasts from surrounding tissue migrate to clot
Fibroblasts produce collagen and extracellular matrix components
I labile tissues capillaries revasculise the area
Fibrin clot breaks down and removed
Delicate connective tissue (granulation tissue) is laid down forming a scar
As it is harder to form a scar the wound contracts, pulling the sides together causing debilitating scars (puckering)

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60
Q

What are the differences between primary and secondary intension?

A

Secondary intention has…
Increased inflammatory response
More debris for phagocytes to remove
More risk of infection
More granulation tissue

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61
Q

What is angiogenesis?

A

Formation of new capillaries

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62
Q

What happens during granulation tissue formation?

A

Angiogenesis
Space between capillaries is filled by lymphocytes, macrophages, proliferation Fibroblasts and loose oedematous extracellular matrix
Thin walled vessels leak increasing inflammatory infiktration
Overtime vessels regress and collagen is laid down
Inflammatory cells die or return to circulation
Fibroblasts become activated, increase in size, form collagen
Collagen becomes organised forming and early scar
Fibroblasts regress
Overtime cellularity if the scar decreases

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63
Q

Give an example of specialist repair and why?

A

Bone after a fracture
Scar tissue would not be able to weight bear

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64
Q

How do bones undergo repair?

A

Following injury embryonic development is reactivated

Fracture
Bleeding
Haematoma forms
Acute inflammatory process occurs
Granulation tissue is formed (soft tissue callus)
Callus holds bone together
Stem cells from carribium layer of peristeum are activated
Cells divide forming chrondocytes and osteoblasts
Chondrocytes form cartilage nous matrix
Osteoblasts form osteoid
Granulation tissue gives way
Osteoblasts surround osteoid
Osteoid becomes mineralised to form a boney callus
Initial bone is haphazard (woven)
Over months oxsteoclasts remodel it and Osteoblasts build to form lamellar bone with trabecukated architecture

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65
Q

What causes cells to adapt?

A

An ever changing environmemt

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66
Q

Give an example of physiological adaptation to cells?

A

Thyroid gland in pregnancy
Increase TSH acts on thyroid epithelium
This is within normal range

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67
Q

Give examples of environmental (pathological) adaptations?

A

Toxins
Poisons
Infectious organisms

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68
Q

What are the possible outcomes for environmental (pathological) adaptations?

A

Malfunction
Cell death

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69
Q

What happens to cells when a stimuli is removed?

A

They revert to the normal form or undergo adaptive change

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70
Q

Give examples of adaptive change?

A

Hyperplasia
Atrophy

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71
Q

What happens if an adaptive change is sucessful?

A

The cell survives

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72
Q

What happens if an adaptive change is unsucessful?

A

The cell dies
Usually takes several morphological changes for this to occur

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73
Q

What can influence if a cell survives an adaptive change?

A

Magnitude of stimuli
Type of stimuli
Duration of stimulus
Vunerability of cell (Neurons are more vulnerable to hypoxia than Fibroblasts)
Immunosupression
Immunodeficiency
Poor nutrition

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74
Q

How can adaptive changes be seem Macroscopically?

A

Cloudy
Swelling
Hydropic degeneration
Fatty change

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75
Q

Are adaptive changes reversible?

A

Yes, generally, once stimulus is removed

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76
Q

What is autophagy?

A

Removal of damaged organelles
Synthesis of new proteins

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77
Q

What is steatosis and where can it occur?

A

Fatty change
Subleathal metabolic dearragement

Usually in high energy demanding cells
Liver due to chronic alcohol abuse
Myocardium or skeletal muscle due to lack of use

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78
Q

What is Necrosis?

A

A form of cell injury that results in the premature death by autolysis

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79
Q

What causes Necrosis to occur?

A

Stimuli that remain unchecked
Irreversible cell damage

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80
Q

What are the types of Necrosis?

A

Colliquative
Coagulative
Caseous
Fibrinoid

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81
Q

What is colliquative necrosis?

A

Dead tissue is semi-liquid
Eg ischeamia

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82
Q

What is Coagulative necrosis?

A

Dead tissue is firm
Eg abscess

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83
Q

What is Caseous necrosis?

A

Soft, cream cheese consistency
Eg tuberculosis

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84
Q

What is fibrinoid Necrosis?

A

Occurs in the walls of blood vessels?

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85
Q

What is the microscopic appearance of Necrosis?

A

Pale staining
Cytoplasmic vaculation
No definition to the cytoplasm
Nuclear condensation

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86
Q

What happens in a cell if it undergoes reversible cell damage?

A

Mitochondria fail to produce ATP
Ion pumps in membranes fail
Loss of ion fluid homestasis
Free radicles accumulate

If this fails to correct then the damage becomes irreversible

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87
Q

What happens in a cell if it undergoes lethal injury?

A

Damage to organelles
Lysosomes release autodigestion enzynes
Autolysis
Cell membranes loose specialist structures (microvilli)
Cell function is lost

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88
Q

What is apoptosis?

A

Programmed cell death. A highly organised process to alter the cell and cause cell death. Affects individual cells only

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89
Q

Give an example of pathological apoptosis?

A

Cancer

Failure of apoptosis is a key factor in cancer formation

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90
Q

Give an example of embryonic apoptosis

A

Webbing between toes and fingers

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91
Q

Give an example of regressive apoptosis?

A

Menstrual cycle and endometrium

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92
Q

List examples of causes of apoptosis?

A

Radiation
Certain viruses (HPV)
membrane damage
Mitochondrial damage
DNA damage
Immune mediated attack

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93
Q

What is process of apoptosis?

A

Cells loose specialist structures
Loose attachment to other cells
Cells become rounded
Pyknosis
Karohexis
Karolysis
Blebbing of cytoplasm
Apoptotic bopsies form expressing membrane surface factors encourage phagocytosis

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94
Q

What is the aim of apoptosis?

A

Part of embryonic development
Part of everyday cell turnover
Eliminate damaged and disease cells

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95
Q

What triggers apoptosis?

A

Intrinsic and extrinsic pathways

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96
Q

What is the microscopic appearance of apoptosis?

A

Nuclear enlargment
Pyknosis - chromatic condensation
Karohexis
Karolysis
Naked cytoplasm
Vacuoles in cytoplasm

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97
Q

What is the microscopic appearance of apoptosis?

A

Nuclear enlargment
Pyknosis - chromatic condensation
Karohexis
Karolysis
Naked cytoplasm
Vacuoles in cytoplasm

98
Q

What is an abscess?

A

A localised collection of pus following excessive tissue damage, often by pyrogenic bacteria

99
Q

What happens during abscess formation?

A

Bacteria elicit an inflammatory response
Exudate is formed composed of neutrophils
Neutrophils die, releasing lysosomal enzymes
Autolysis
Pus made up of dead and dying neutrophils, fluid from acute inflammatory response and fibrin
Pyrogenic bacteria often survive the response
More pus production
Enlargement of lesion
Acute abscess formation
Acute abscess formation
Acute abscess formation
Eventually the abscess is walled off
Becomes surrounded by granulation and Fiberous tissue
Chronic abscess formation

100
Q

What limits the abscess size?

A

The repair that forms the margins of the abscess

101
Q

What is chronic inflammation?

A

A continuation of acute inflammation. A response to prolonged exposure to a stimuli. Can lead to morbidity and mortality.

102
Q

Microscopic appearance of chronic appearance?

A

Generally lymphocytes, macrophages and plasma cells

103
Q

What types of chronic inflammation are there?

A

Specific
Non-specific

104
Q

What is non-specific chronic inflammation?

A

A continuation of acute inflammation

Acute, granulation, repair and chronic inflammation can all co-exsist

105
Q

Give an example on non-specific chronic inflammation?

A

Peptic ulcer stomach

Local chronic ulceration
Patients become infected by H. Pylori
Ulcer expands to full thickness of mucosa
H. Pylori interferes with control of acid secretion
Imbalance between damaging factors (acid and Peptic enzymes) and protective factors (mucus and alkaline secretion)
More ulceration
Circle begins again

106
Q

How does chronic inflammation demonstrate a dynamic balance?

A

If repair is favoured fiberous repair occurs then mucosa regenerates ro cover
If damage is favoured the wall thins and the risk of rupture increases

107
Q

What are the types of specific (Primary) chronic inflammation?

A

Granulomatous
Non-granulomatous

108
Q

What is the key feature of non-granulomatous chronic inflammation?

A

Activated macriphages

More efficient at phagocytosis
Secrete factors that control inflammatory cells and induce fibrosis

109
Q

What causes damage to normal tissues during an inflammatory response?

A

Phagocytosis of cells in a non-discrimatory manner

110
Q

What is granulomatous inflammation?

A

A type of chronic inflammatory response

111
Q

What is the classic appearance of granulomatous chronic inflammatory?

A

Activated epithelial macrophages and multineucleate giant cells, surrounded by lymphocytes, macrophages, Fibroblasts and varying degrees of fibrosis. Collectively called a granuloma

112
Q

In granulomatous chronic inflammation what are the multineucleate giant cells derived from?

A

Macrophages

113
Q

Give an example of immune causes of granulomatous chronic inflammation?

A

Crohn’s
Sarcoidosis

114
Q

Give an example of non-immune causes of granulomatous chronic inflammation?

A

Suture following surgery
Thorn in skin

115
Q

What is a granuloma?

A

A cluster of macrophages, multineucleate giant cells surrounded by lymphocytes, Fibroblasts and fibrosis.

Different from granulation tissue seen in acute inflammation

116
Q

An example of granulomatous chronic inflammation?

A

Tuberculosis

117
Q

Give 3 ways a virus can cause diseases, with examples?

A

Infect cells and cause death.
HIV cell death of T-lymphocytes

Cause excessive proliferation of infected cells. HPV - cervical carcinoma

Integrate themselves into the nucleus producing a latent infection. HSV - coldsores

118
Q

What immune response do most bacteria elicit?

A

Acute

119
Q

Give an example of a bacterial infection?

A

C. diff
Produces toxins that destroy the surface of the colon which in turn allows for uncontrolled growth of C. diff

120
Q

Give an example of fungal infection?

A

Candida
In the Oesophagus

121
Q

Give an example of a protazoan infection?

A

Trichomonas vaginalis
In the female genital tract

122
Q

What is hyperplasia?

A

Increased production and maturation of normal cells, in a tissue without an increase in size of the cells

123
Q

What causes hyperplasia?

A

An external stimuli such as hormones or environment

124
Q

How does metaplasia appear?

A

Cells are normal to the tissue, may give rise to modules or just overall growth of the tissue.

125
Q

What happens to hyperplasia if the stimuli is removed.

A

Hyperplasia stops +/- regression

126
Q

How does hyperplasia compare to neoplasia?

A

Neoplasia is uncontrolled growth, hyperplasia is controlled

127
Q

What are the risks of hyperplasia?

A

Atypia
Neoplastic change

128
Q

Why do some cases of hyperplasia form nodules?

A

Non-uniform hyperplasia within the organ/tissue

129
Q

Give 2 examples of hyperplasia?

A

Endometrial glands in the menstrual cycle
Modular hyperplasia I thyroid, prostate or adrenal glands

130
Q

What is hypertrophy?

A

Increase in the size of a tissue or organ brought about by enlargement of the cell, but not the number of cells

131
Q

What happens hypertrophic cells once the stimulus is removed?

A

Hypertrophy stops +/- regression

132
Q

Give 2 examples of hypertrophy?

A

Skeletal muscle following exercise
Smooth muscle following chronic obstruction by tumours

133
Q

What is hypotrophy?

A

Tissue or organ shrinks in size due to shrinking cells, not cell mumbers

134
Q

What is a common cause of hypotrophy?

A

Deficiency during development causing underdeveloped cell types

135
Q

Give an example of hypotrophy?

A

Muscle hypotrophy

136
Q

What is agenesis?

A

Complete failure of an organ to develope during embryonic development

137
Q

What is atrophy?

A

The wasting away of a normally developed organ or tissue due to degeneration of cells. Resultant reduction in function too

138
Q

What are the classic signs of atrophy?

A

Cells are usually replaced with adipose tissue or fiberous tissue

139
Q

What is the microscopic appearance of atrophy?

A

Shrinkage of cells
Reduction of organelles
Loss via apoptosis

140
Q

Give 2 examples of atrophy?

A

Muscle atrophy - lack of exercise
Ischaemic atrophy - lack of blood flow to the kidney

141
Q

What is metaplasia?

A

The reversible change of one form of mature epithelium into another form of mature epithelium in response to a stimuli

142
Q

What happens in metaplasia is the stimulus is removed?

A

It should reverse as it is an adaptive change

143
Q

What types of metaplasia are there?

A

Pathological
Physiological

144
Q

Give an example of pathological metaplasia?

A

Barrett’s oesophagus
Normal stratified squamous to gastric or small bowel cuboidal-columnar epithelium

145
Q

Give a example of physiological metaplasia?

A

Squamous metaplasia of the cervix
Endocervical columnar epithelium into staitified squamous

146
Q

What is atypia?

A

Abnormality or Deviation from the normal state

147
Q

What is the process of atypia?

A

Cells divide rapidly
Don’t mature fully before dividing again
Leads to a population of atypical cells

148
Q

What causes atypia?

A

Response to a persitently damaging stimuli.

149
Q

What happens when the stimulus causing atypia is removed?

A

The cells reach full maturation

150
Q

What is the microscopic appearance of atypia?

A

High n/c ratio
Large nuclei
Dark chromatin
+/- prominent nucleoli
Lack of specialist structures

151
Q

What is dysplasia?

A

Abnormal development of cells within a tissue

152
Q

What is the cause of dysplasia?

A

Persistent atypia that is not the result of regeneration

153
Q

Where is dysplasia often found?

A

Metaplastic tissue

154
Q

What is a potential outcome of untreated dysplasia?

A

It has the potential to become precanceeous
And the further potential for neoplasia

155
Q

What happens in neoplastic tissues once the stimulus is removed?

A

They continue

156
Q

What is the microscopic appearance of neoplasia?

A

Cells of various stars of differentiation
Commonly fail to reach full maturation

157
Q

What types of neoplasia are there?

A

Benign
Malignant
Anaplastic

158
Q

What are the characteristics of benign neoplasia and an example?

A

Generally slow growing
Remain localised
May be encapsulated
Resemble original tissue
Few mitoses
Normal or slight increase to n/c ratio
Cells are uniform

Breast fibroadenoma

159
Q

What are the characteristics of malignant neoplasm and an example?

A

Rapid growing
Spread widely
May metasasize
Not encapsulated
May fail to mature fully
Pleomorphic
Can be well or poorly differentiated

Cervical carcinoma

160
Q

What are the characteristics of anaplastic neoplasm?

A

No evidence of differentiation
Need more morphology to diagnose

161
Q

Which type of malignant neoplasm is more likely to be more invasive or aggressive? Well differentiated or poorly differentiated

A

Poorly differentiated

162
Q

What is carcinoma in situ?

A

A carcinoma is a cancer that forms in epithelial tissues.
In situ means that the cancer has remained in the tissue of origin and not spread

163
Q

What will happen to carcinoma in situ if left untreated ?

A

It will metastasise

164
Q

What is the microscopic appearance of carcinoma in situ?

A

Cell crowding
Pleomorphism
increased and abnormal mitosis
no invasion through basement membrane
changes to N/C ratio
abnormal nuclei
loss of stratification

165
Q

What is metastases?

A

The distal spread of a neoplasm away from its primary site

166
Q

What is the clinical presentation of metastases?

A

Weight loss
loss of appetite
fever
general malaise (body weakness)
+/- loss of function of specific organs or increased functions (eg parathyroid hormone produced by lung carcinoma)

167
Q

What types of modes of spread are there?

A

Local
lymphatic
vascular
transcolemic

168
Q

What is local spread of cancer and give an example?

A

The spread of cancer to surrounding tissues by a direct route

breast carcinoma to overlying skin cervical carcinoma to bladder or rectum

169
Q

What is lymphatic spread of cancer and give an example?

A

Spread of cancer via the lymphatics that drain the site of the primary tumor, it can be a long the lumen or as an emboli

Breast carcinoma to lymph nodes of the axilla
tongue carcinoma to lymph nodes of the neck

170
Q

What is vascular spread of cancer and give an example?

A

Spread via the veins that drain the sight of the primary tumor, it can invade thin walls of the vessels and then spread as an emboli

Rectal cancer spreads via the portal vein to the liver

171
Q

What is transcolemic spread of cancer and an example?

A

Spread past colemic (body) cavities emboli from primary tumor break off and float to a new site where they embed

Carcinoma of the ovary to peritoneal surfaces

172
Q

What is atherosclerosis ?

A

A disease of the arteries in which fatty plaques develop on the inner walls eventually obstruction of blood flow will occur

173
Q

What are the risk factors of atherosclerosis?

A

Age
Sex (men and menopausal women) genetic
ethnicity (African and Asian) hypertension
hyperlipidemia
smoking
physical inactivity
obesity
diabetes
stress
anxiety
depression

174
Q

What is atheroma?

A

Porridge or sludge within the arteries, affects the karge and medium arteries

175
Q

What is the process of atherosclerosis?

A

At vessel branches and other sites of turbulent flow and stress leads to expression of cell adhesion factors by the endothelium which leads to accumulation of and migration of macrophages and lymphocytes.
Epithelial dysfunction leads to increased permiability to lipoproteins, monocytes and lymphocytes leading to an inflammatory response in the intimate.
Smooth muscle migrates from the media and atherosclerosis formation begins as a fatty streak
As the fatty streaking increases a fibrous cap forms between the vessel and the lumen forming a mature plaque
Over time cap remodels and frequently undergoes calcification if the cap ruptures a thrombi is released

176
Q

What would full occlusion of a vessel due to atherosclerosis lead to?

A

Ischeamia or Infarction

177
Q

What is thrombosis?

A

A condition from where blood changes from liquid to a solid state within a cardiovascular system, during life, and produces a mass (thrombus)

178
Q

What is the difference between thrombosis and coagulation?

A

Thrombosis occurs in blood flow it is a dynamic process
Coagulation occurs in static blood.

179
Q

What are the courses of thrombosis?

A

Virchow ‘s triad

Damage to endothelium - physical or dysfunction to normal process eg hypertension, turbulent blood flow or bacterial endotoxins
Disordered blood flow - turbulent flow leads to eddy currents with focal stasis of blood flow eg immobility, obesity, varicose veins,
Abnormal homeostatic properties of blood - hypercoagulability eg inherited = IBD or acquired = surgery, trauma, pregnancy, dehydration

180
Q

What is Virchow’s triad?

A

Damage to endothelium - physical or dysfunction to normal process eg hypertension, turbulent blood flow or bacterial endotoxins
Disordered blood flow - turbulent flow leads to eddy currents with focal stasis of blood flow eg immobility, obesity, varicose veins,
Abnormal homeostatic properties of blood - hypercoagulability eg inherited = IBD or acquired = surgery, trauma, pregnancy, dehydration

181
Q

What is the microscopic appearance of a thrombi?

A

White to pink to red
granular
firm
may have layers of organization on the cut surface

182
Q

What is the microscopic appearance of a thrombi?

A

Platelets
Insoluble fibrin
Erythrocytes
Leukiocytes

183
Q

What is the thrombosis process?

A

Endothelial injury platelets adhere to exposed subepithelial collagen
Platelet activation ADP and thromboxane AZ are released triggering further plateless aggregation Platelets degranulate and coagulation cascade is activated
Soluble fibrogen becomes insoluble fibrin
Red cells become trapped
Thrombus increases in size

184
Q

What are the complications of thrombosis?

A

Occurs in large arteries and veins Affects the peripheral vessels with smaller diameter
They become occluded by the thrombi

185
Q

What is an aneurysm?

A

Loss of muscle and elastin from vessel wall leads to weakening of the wall allowing local dilation (aneurysm) rupturr is fatal

186
Q

What is an embolism?

A

The condition in which an emboli becomes lodged in an artery and obstructs the blood flow

187
Q

What are the types of emboli?

A

Venous thromboemboli
Arterial thromboemboli
Atheromatus debris
Tumor cells b
Bacterial vegetations
Fat or bone marrow
Air

188
Q

What is an example of Venus thromboemboli?

A

Deep vein thrombosis

189
Q

When does arterial thromboemboli?

A

Following myocardial infarction

190
Q

When would a fat or bone marrow emboli occur?

A

Following a fracture

191
Q

Give an example of an air emboli?

A

Nitrogen

Due to rapid changes in air pressure when deep sea diving

192
Q

How can thrombi resolved?

A

Fibrinolysis can resolve a thrombi - medications such as warfarin

193
Q

What happens if an emboli is left untreated?

A

Arteries and veins become blocked ischemia will follow in distal regions or organs and later infarction

194
Q

What is infarction?

A

The death of part or the whole of an organ that occurs when an artery carrying its blood supply is obstructed by an embolus

195
Q

What is venous infarction?

A

When an embolus blocks or prevent strainage and blood flow is impaired

196
Q

How can venous infection appear in the kidney, spleen or brain?

A

A wedge shaped infarction

197
Q

What is the process of infarction?

A

Infarction excites an inflammatory response
Replacement of an necrotic tissue with granulation tissue which undergoes fibrous repair and scarring

198
Q

What causes arterial infarction?

A

Complete or partial blockage of an artery by an emboli generally from a pre-existing atheroma

199
Q

What causes venous infarction?

A

Generally due to mechanical compression of vessels

Torsion of the testes
Hernia strangulation

200
Q

What is the process of venous infarction?

A

Blockage stops blood from leaving the tissue leading to ischemia due to stasis and eventually infarction

201
Q

What is oedema?

A

Excessive accumulation of fluid in the body tissues can be local as seen in injury or inflammation or more generally as seen in heart or kidney failure

202
Q

How is homeostasis of fluid in and out of the bloodstream maintained?

A

Hydrostatic pressure vs plasma colloid and osmotic pressure

Increase capillary pressure means lower colloid osmotic pressure

203
Q

What is capillary pressure?

A

The pressure of a fluid within the capillary

204
Q

What is of colloid osmotic pressure?

A

Pressure in the capillary due to the concentration of proteins

205
Q

Give two examples of oedema?

A

Deep vein thrombosis - impaired venous return leads to increased hydrostatic pressure and oedema around the calf
Liver cirrhosis - decreased albumin leads to decreased colloid osmotic pressure leading to ascites

206
Q

What is coagulation?

A

The process by which a colloidal liquid changing to a jelly like mass

207
Q

What is the process of coagulation?

A

It can be initiated by the contact of blood with a foreign surface (intrinsic system) or with a damage to the tissue (extrinsic system)
Both systems use coagulation factors which lead to the production of thrombin
Thrombin converts fibrinogen into fibrin and a clot is formed

208
Q

What is ionizing radiation?

A

It is used to treat cancer and during imaging
It is a mutantogenic carcinogenic and tetrogenic (abnormalities in fetus)

209
Q

What are the biological effects of ionizing radiation?

A

Effects depend on the method of delivery

The effect is cumulative - if spread out some repair can occur between doses
The field size - high power in a small area is best for the body
Cell proliferation - rapidly dividing cells are more susceptible
Hypoxia
Vascular damage

210
Q

What is the effect of radiation on a tissue?

A

Radiation kill cells
Inflammatory response
Fibrosis

211
Q

What is innate immunity?

A

It is always present
Non-specific
Includes epithelial barriers, circulating plasma proteins, phagocytic leukaocytes and natural killer cells

212
Q

What can problems with immunity lead to?

A

Congenital immunodeficiencies
Acquired immunodeficiencies
Normal response harms healthy tissue
Allergies caused by excessive or uncontrolled immune response

When self-tolerance fails it leads to autoimmune disease

213
Q

What are autoimmune disorders?

A

Disorders caused by inflammation and the destruction of tissues by the bodies own immune response

214
Q

Give three examples of autoimmune disorders and where they are found?

A

Rheumatoid arthritis - joints
Hashimotos disease - thyroid
Crohn’s disease - colon

215
Q

What is a tumour marker

A

Substance produced by a tumour that can be used to aid detection, monitor its size and the effects of treatment

216
Q

Give three examples of tumour markers?

A

CA125 - ovarian cancer
PAP - prostate cancer
Calcitonin - medullary carcinoma of the thyroid

217
Q

What is an allele?

A

Different forms of a gene, codes for variation in a genetically inherited trait

218
Q

What is a gene?

A

Part of the DNA that codes for proteins, carries hereditary information

219
Q

What is a dominant gene?

A

A gene that shows a specific trait even if it is only passed on from one parent

220
Q

Was what is a recessive gene?

A

A gene that only shows its trait when passed on from both parents

221
Q

What does homozygous mean?

A

Two of the same form of a gene

222
Q

What does heterozygous mean?

A

Two different forms of the same Gene

223
Q

What is a genotype?

A

Genetic makeup of an individual

224
Q

What is a phenotype?

A

Outwardly expressing traits of a characteristic

225
Q

What is a phenotype?

A

Outwardly expressing traits of a characteristic

226
Q

In genetics what is penetrance?

A

Probability of a genetic trait being expressed

227
Q

What are the different types of genetic disorders?

A

Chromosomal disorders
Single gene disorders
X-linked disorders
Polygenic disease

228
Q

What is a chromosomal disorder and give an example?

A

Addition or deletion of an entire/partial chromosome
Down syndrome

229
Q

What is a single Gene disorder and give an example?

A

A single gene mutant that has a large effect on the patient

Sickle cell anemia
Haemophilia

230
Q

What is a characteristic of x-linked disorders and an example?

A

Almost all are recessive
Haemophilia A and B

231
Q

What is a degenerate condition?

A

Diseases of the central nervous system mainly the grey matter

232
Q

Give two examples of disorders that affect the cerebral cortex?

A

Alzheimer’s disease
Vascular dementia

233
Q

Give two examples after disorders that affect the basal ganglia?

A

Parkinson’s Disease
Huntington’s disease

234
Q

What is a fistulate?

A

An abnormal communication between two hollow organs connecting to mucosa lined surfaces or between a hollow organ and the exterior surface

235
Q

How are fistulate caused?

A

By infection put malignancy can also lead to formation

236
Q

What are the four types of fistulate?

A

Enterovesical
Enterocolic
Enteroenteric
Enterocutaneous

237
Q

What is an enterovesical fistula?

A

Between bladder and small bowel

238
Q

What is an enterocolic fistula?

A

Between small bowel and colon

239
Q

What is an enteroenteric fistula?

A

Between adjacent loops of the small bowel
Common after surgery

240
Q

What is an enterocutaneous fistula?

A

Between small or large bowel and skin