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102- Theme 1 > Pathology > Flashcards

Pathology Flashcards

1
Q

State the 5 cardinal signs of inflammation.

A 
Rubor (redness)
Tumor (swelling)
Calor (increased heat)
Dolor (pain)
Functio leasa (loss of function)
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2
Q

State what is activated by phagocytosis.

What are the 3 mechanisms by which a phagolysosome causes destruction?

A

Release of soluble mediators

  1. Release of toxic radicals and Hydrogen-Oxygen products.
  2. Lower pH
  3. Digestive enzymes
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3
Q

Which two molecules promote local inflammation?

State how.

A

Cytokines
Chemokines

  1. attracting cells inc. neutrophils
  2. causing vasodilation, increased permeability (junctions between endothelial cells widens) and increased adhesion molecules on blood vessel endothelium.
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4
Q

What are the 4 possible outcomes of inflammation?

A
  1. Resolution- insult removed and the tissue heals completely.
  2. Fibrosis- insult removed but scar tissue remains
  3. Chronic inflammation- insult cannot be removed
  4. Abscess formation- inflammation causes tissue destruction to form a cavity containing lots of neutrophils and dead tissue(appears pink)
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5
Q

Suggest 5 advantages of inflammation.

A
  1. AMPLIFIES RESPONSE- small stimulus results in large local and systemic response
  2. Focuses immune response by flooding area with leucocytes.
  3. Allows fibrin formation
  4. Activates next stage of immunity ( T cell response/memory)
  5. Facilitates transport of drugs
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6
Q

Suggest 3 disadvantage of inflammation.

A
  1. Damage healthy tissue by digestion
  2. May by activated inappropriately
  3. Activated uncontrollably: septic shock
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7
Q

What is an ulcer?

Effects on a) skin b) gastrointestinal tract?

A

A macroscopically apparent loss of surface epithelium.

a) crust of dried fibrin, unlikely to lead to severe haemorrhage
b) haemorrhage, perforation, loss of defence as epithelium protect submucosa from acid and enzymes.

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8
Q

Describe the 4 main cells involved in chronic inflammation.

A
  1. Histiocytes (macrophages inside tissues)
  2. Lymphocytes (one nucleus and small cytoplasm. T: inflammation ; B: plasma cells)
  3. Eosinophils (look like cartoon sun with sunglasses as nuclei take up stain well. Involved in allergic and parasitic conditions.)
  4. Plasma cells
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9
Q

Describe what a polymorph/neutrophil is.

A

Involved in phagocytosis and bacterial killing

Has multiple joined nuclei

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10
Q

Which cell types accumulation is mediated by IgE produced by plasma cells?

A

Eosinophils

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11
Q

How is the number of eosinophil involved in an immune response related to symptoms?

A

They produce inflammatory mediators.

The more present, the more symptoms the patient suffers.

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12
Q

What is a polyp?

How may a microscopic slide of a polyp appear?

A

An abnormal growth protruding growth into a cavity

Pale due to excess fluid oedema

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13
Q

What is a monocyte ? Describe its appearance.

A

Single kidney-shaped nucleus and lots of cytoplasm.

Phagocyte but only inside tissues where its called a macrophage.

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14
Q

State three causes of chronic inflammation.

Describe the distinct pattern of chronic inflammation

Which cytokines are involved in this?

A
  1. persistent infection
  2. inability to heal ( e.g. in a peptic ulcer)
  3. immune mediated inflammatory disease (Chrohns)
  4. Prolonged exposure to toxic agents

Granulomatous inflammation - contains granuloma (collection of macrophages surrounded by lymphocytes- in order ones some scarring also)

IL-1- initiation
TNF- maintenance
IL-2- increase in size

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15
Q

What are the 5 R’s involved in bodily response to injury?

A 
Recognition of injurious agent
Recruitment of leukocytes
Removal of injurious agent
Regulation
Resolution
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16
Q

Describe the pathophysiology of acute inflammation.

A
  1. Vasodilation- this causes stasis of blood and increased hydrostatic pressure. Causes Rubor (redness) and calor (high temperature)
  2. Increased vascular permeability- Its mediated by histamine and NO. Theres damage to the endothelium by leukocytes and osmotic pressure in tissue increase and more fluid leaves vessels than moves in. Causes tumor (swelling)
  3. Exudation- (1) involves margination & rolling, (2) adhesion and (3) emigration caused by CD31
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17
Q

Whats the difference between an exudate and a transudate?

A

Transudate - exiting fluid contains few proteins and cells

Exudate- exiting fluid contains lots of proteins and cells

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18
Q

Describe the events involved in margination and rolling.

A
  1. White blood cells peripheral to RBC in capillary
  2. Transient connections between WBC’s and endothelium

Upregulated by TNF and IL1

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19
Q

State three ways in which growth can occur

A
  1. Multiplication by mitosis
  2. Auxetic - increase in cell size either by cell elongation or organelle number
  3. Accretionary - increase in extracellular tissue
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20
Q

Define labile cells, stable cells and permanent cells.

A

Labile cells- Continuously proliferate, short lifespan and rapid turnover time e.g. blood cells and epithelial cells

Stable cells (facilitative dividers)- Good regenerative ability but would normally have low cell turnover.( e.g. quiescent tissues - hepatocytes)

Permanent cells- little/no regenerate ability (cardiac muscle, neurons)

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21
Q

If a cell cannot adapt then it will likely die. Define the 4 reversible changes involved in adaptation.

What is cell injury. Example?

A
  1. Metaplasia- conversion of one mature(differentiated) cell type to another
  2. Hyperplasia- cell number increases
  3. Atrophy- cell size decrease
  4. Hypertrophy- cell size increases

Cells become so severely stressed that they can no longer adapt. In renal tubule, hypoxia causes cells to become disordered and then eventually necrotic.

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22
Q

Consider metaplasia. Give a physiological and pathological example.

A

Physiological:
Simple columnar epithelium changes to stratified squamous epithelium due to acidity of vagina.

Pathological:
Oesophagus- squamous to columnar due to gastric acid
Pseudostratified ciliated columnar epithelium changes to squamous due to smoking
Columnar endocervical mucosa to squamous once infected by HPV.

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23
Q

Consider hyperplasia. Give a physiological and pathological example.

A

Physiological:
Hormonal- increases functional capacity e.g. in breast feeding
Compensatory- when tissue is lost( partial liver resection_

Pathological:
Excess hormonal stimulation -
Endometrial (causes increased oestrogen)
Prostatic (causes increased androgens)

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24
Q

Consider atrophy. Give a physiological and pathological example.

A

Physiological:
Post menopausal atrophy of the uterus due to lack of oestrogen stimulation

Pathological:
Denervation of muscle
Malnutrition
Disuse of muscle/bone
Pressure atrophy owing to adjacent mass effect (tumour)
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25
Q

Consider hypertrophy. Give a physiological and pathological example.

A

Physiological:
Uterine lining (muscle increases during pregnancy)
Weight training

Pathological:
Cardiac hypertrophy (causes ventricular wall to increase from 1.5cm to 4cm, higher nutrition demand, coronary heart vessels don't increase in size -> MI)

Bladder hypertrophy (caused by prostatic enlargement)

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26
Q

Describe the two forms of cell death.

A

Apoptosis- programmed cell death. Membrane remains intact, nuclei fragment.

Necrosis- death due to accidental damage. Involves groups of cells. Cellular debris stimulates inflammatory cell response. Membrane becomes impaired and contents leak out.

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27
Q

Describe the mechanism by which necrosis occurs.

A 
ATP depletion
Mitochondrial damage
Influx of calcium ions
Accumulatio of oxygen radicals
Increased membrane permeability
DNA and protein damage
28
Q

Describe the three types of necrosis.

A

Coagulative -shape and architecture preserved
Liquefactive- liquefied, viscous, soft lesion usually in brain as a result on bacterial infection
Caseous- cottage cheese like (mycobacterial)

29
Q

Briefly describe the mechanism of apoptosis and give a physiological and pathological example.

A

Activation of caspase 3 leads to degradation of DNA and protein.

Pathological:
In embryogenesis( between fingers)
High turnover tissues
Elimination of autoimmune lymphocytes
Death of inflammatory cells after response

Physiological:
DNA damage
Infection
Duct obstruction

30
Q

What is autophagy?

A

A survival mechanism by which the cell breaks down its contents to maintain metabolic processes in states of nutrition deprivation.

It can be employed to combat neoplasia.

31
Q

Describe the three methods by which the body can recover from injury.

A
  1. Resolution & Scavenging - the tissue damage is limited and there is fast enough removal of debris
  2. Regeneration- extracellular matrix is intact, mild superficial injury.
  3. Repair- extracellular matrix is impaired. Severe injury. Occurs in permanent tissues such as brain and heart muscle.
32
Q

Which cells are most important in resolution and scavenging? Describe their role.

A

Macrophages
Monocytes travel to sinusoids in liver, bone marrow and spleen.
They act as filter tissue to remove abnormal cells and clear off stimuli.
Produce growth factors for the proliferation of cells in healing response

33
Q

Describe the 5 activities involved in resolution and scavenging.

A
  1. Chemotaxis (attraction of macrophages to site)
  2. Hypertrophy ( histiocytes get larger and aggregate)
  3. Pseudopodia (active movement)
  4. Pinocytosis (degradation of small molecules and ingest fluid from surroundings)
  5. Phagocytosis (ingestion of large molecules)
34
Q

Describe the importance of stem cells in regeneration.

A

They have prolonged self renewal capacity and asymmetric replication.

For example liver tissue, regeneration occurs via stem cells if stromal reticulum scaffolding remains intact

Epithelial cells increase stem cell division and decrease time it takes for cell cycle to occur.

35
Q

How is regeneration controlled?

A
  1. Interactions between macrophages and stromal reticulum scaffolding/ extracellular matrix
  2. Growth and transcriptional factors which set of signalling pathways.
36
Q

Describe repair in terms of tissue response to injury.

State the processes which lead to scar formation.

A

A response by fibroblasts that leads to the formation of fibrotic scar tissue.

Normal tissue
Tissue injury
Inflammatory response
Granulatiom tissue formation
Scar tissue
37
Q

Explain the events involved in scar formation in terms

  1. Formation of Angiogenesis
  2. Formation of granulation tissue
  3. Scar formation
  4. Scar modelling
A
  1. Vasodilation, BM degradation, migration of end cells and endothelium precursor cells from bone marrow, proliferation of end cells, maturation of end cells into tubes and finally development of blood vessel walls.
    VASCULAR ENDOTHEIUM GROWTH FACTOR
  2. Angiogenesis and proliferation of fibroblasts, new vessels are leaky which leads to oedema. Granulation tissue contains new blood vessels, fibroblasts and neutrophils.
  3. Growth factors from macrophages caused migration and proliferation of fibroblasts into gran tissue. This produces extracellular matrix proteins.
    FIBROBLAST GROWTH FACTOR & TRANSFORMING GROWTH FACTOR ALPHA
  4. interactions of collagen deposition and degradation by MMPs. Contraction of scar tissue. Type 3 collagen to type 1. Tissue only 80% strength of original tissue.
38
Q

Describe healing by a)primary intention b)secondary intention c) tertiary intention.

A

a) No loss of tissue (lacerations, bone fractures)
b) Significant loss of tissue (abscess, infection laceration that has led to necrosis of some tissue)
c) Initially left open to allow drainage and the would heals from bottom up

39
Q

Consider the local impediments to reparation of tissue.

A 
Infection
Haemotoma
Denervation
Site
Necrotic tissue
Poor blood supple
Mechanical stress
40
Q

Consider the systemic impediments to reparation of tissue.

A 
Age
Diabetes
Malignancy
Malnutrition
Anaemia
Obesity
Trauma
Vitamin C deficiency
Infection/sepsis
Drugs
41
Q

Consider the possible complications of would healing.

Give examples in the case of

a) deficient scar formation
b) excessive scar formation

A

a) dehiscence (wound rupture along a surgical line)
ulceration
b) keloid, abnormal adhesions

42
Q

Describe the microscopic appearance of granulate tissue that is being replaced by collagen

How does scar tissue differ to adjacent dermis?

How does the overlying epidermis differ from the adjacent epidermis?

A

Edge of wound = granulate tissue and acute inflammation
Centre= collagen

Less collagen, more cellular due to presence of fibroblasts

Thicker, longer protrusions (hyperplasia).

43
Q

What are the 8 things you want to know about a disease?

A 
Epidemiology- prevalence, incidence, distribution
Aetiology- cause
Pathogenesis- mechanism "how"
Pathological & clinical features
Complications
Sequalae- consequences
Prognosis
Treatment
44
Q

Describe the 8 steps involved in preparing a histological artefact.

A
  1. Receipt
  2. Data Entry
  3. Fixation
  4. Specimen dissection (in numerous planes)
  5. Processing (removing tissue fluid and replacing it with paraffin and bees wax)
  6. Embedding in wax block
  7. Microtome cutting (block cut into micron thickness)
  8. Staining in order to see specimen - Haematoxylin(purple nucleus) & Eosin (Red cytoplasm)
45
Q

What is immunohistochemistry ?

Name a protein granular cell tumours are positive for.
Which other cell type is positive for this?

A

Detection of proteins on cells

s100
Langerhan cells

46
Q

Which germ layer do epithelium originate from?

What are glands/ducts?

A

Can originate from all three germ layers (ectoderm, mesoderm, endoderm)

Specialised ingrowths of epithelium.

47
Q

Describe three types of epithelium.

A

Squamous epithelium- look like flattened circles

Columnar epithelium- nuclei at basal side

Stratified epithelium- looks cuboidal

48
Q

What are the two types of glandular epithelium? Give examples.

A

Duct- produce and secrete substances onto an epithelial surface by way of a duct. E.g. sweat, saliva, lacrimal

Ductless- endocrine glands that secrete substance directly into vascular system to distant tissues. E.g. thyroid, islets of Langerhans, adrenal glands.

49
Q

Describe 5 features of the structure of epithelium.

A
  1. Adhere to each other
  2. Tight junctions to seal borders
  3. Desmosomes for strength
  4. Gap junctions- allow transfer of molecules
  5. Cytokeratin intermediate filaments within cytoplasm to provide internal structure.
50
Q

Describe the layers of a neurovascular bundle vessel.

A

Tunica Intima- endothelium on connective tissue
Elastic intima
Tunica Media- circumferential smooth muscle
Elastic externa
Tunica Adventitia- collagen and vascular supply to wall. Outer connective tissue

51
Q

State the 10 properties/functions of skin.

A
  1. immune function
  2. secretory function
  3. vitamin d metabolism
  4. sensory function
  5. protection from infection (barrier)
  6. sexual/social significance
  7. control of body temperature
  8. waterproofing
  9. protection from injury
  10. maintenance of integrity
52
Q

Describe the three structures that make up skin.

A

Epidermis- collagen type 4, connected to BM. Stratified squamous epithelium.
Dermis- connective tissue of mesenchymal origin
Subcutaneous fat

53
Q

What are the steps of terminal differentiation of keratinous epithelium?

A 
Stratum cornum (Horny cell layer)- cornified
Stratum lucidium - only in thick skin, separates SC and SG
Stratum granulosum (Granular cell layer)
Stratum spinosium (Spinous cell layer)- contains desmosomes 
Stratum basalis (Basal cell layer)
54
Q

Describe three other cells that occur in the epidermis.

A
  1. Melanocytes- originate from neural crest and stuck to BM. 1 melanocyte provides melanin to 36 keratinocytes. Keratinocytes phagocytosise melanin from melanocyte dendrites.
  2. Langerhan cells- originate from bone marrow, dendritic and antigen presenting cells.
  3. Merkel cells- originate from neural crest. Mediate tactile sensations(pressure in skin), associated with sensory neurone endings.
55
Q

How do sebaceous glands in the face cause acne?

What do they look like at low magnification?

A

They secrete lipid rich liquids. Controlled by sex hormones.

Bunch of grapes.

56
Q

What happens in eczema?

A

Irritated skin causes increase in thicknesss of keratinous layer, cornified layer and spinous layer (acanthiosis).

57
Q

What are the two types of sweat glands? Explain.

What type of epithelium line these glands?

A 
Eccrine
All over the body
Inner secretory epithelium
Outer myoepithelium 
Responsible for temperature control

Apocrine
Axillary, nipple and groin
Responsible for body odour (bacterial fermentation)
Large irregular shaped lumen

SIMPLE CUBOIDAL

58
Q

Describe the three commonest skin cancers.

A
  1. Basal cell carcinoma- infiltrates locally, mutiple and reoccurring
  2. Squamous cell carcinoma - described as being well to poorly differentiated based on keratin level. spreads to lymph nodes, lungs, liver and brain commonly
  3. Malignant melanoma- spreads to lymph nodes, lungs, liver and brain commonly. Pagetoid patterns
59
Q

State three diseases involving melanocytes.

A
  1. Melanoma
  2. Albinism - defect in tyrosinase which controls of melanin production.
  3. Congenital naevus - birth mark, hyper pigmentation
60
Q

Name 5 surfaces covered in non-keratinised squamous epithelium

Where is the body has a thick layer of keratinised epithelium?

A
  1. Mouth
  2. Oesophagus
  3. Anal canal
  4. Cervix
  5. Vagina

Hands and foot bottom

61
Q

State 4 characteristics/functions of the keratinised layer.

A
  1. Protects against infection
  2. prevents dehydration
  3. consists of dead cells
  4. increased thickness when irritated
62
Q

Where do coronary arteries originate?

Describe the branching of coronary artery

A

Aortic root

Right coronary artery
Left circumflex coronary artery
Left anterior descending coronary artery

63
Q

What happens in atherosclerosis?

A

Intima gets thicker duet liquid deposit of plaque(oxidised fatty acids) causing narrowing artery.

Overtime the plaque becomes calcified.

All atheroma have a thin fibrous cap that can rupture resulting in a prothrombotic cascade of events resulting in a thrombus.

64
Q

Whats the difference between a thrombus and embolus?

A

A blood clot forming within a vessel = thrombus

A blood clot loving within a vessel = embolus

65
Q

What are consequences of vascular occlusion?

A

Thrombus stops blood flow resulting in ischaemia(lack of blood flow)

This leads to:
Hypoxia (lack of oxygen)
Accumulation of toxic metabolites
Reversible cell injury
Irreversible cell injury
Cell death

102- Theme 1 (10 decks)

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