Histology Foundations Flashcards

(79 cards)

1
Q

What is the process of preparing a histological specimen?

A

Fixation (formaldehyde), embedding (with paraffin), slicing and staining (e.g. H&E)

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2
Q

What does haematoxylin stain show?

A

It is blue/purple = basophilic.
It binds to anionic or acidic components (negative charge).
Binds phosphate groups of nucleic acids (nuclei are blue)

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3
Q

What does eosin stain show?

A

It is pink/orange = eosinophilic
It binds to cationic tissue components (positive charge).
Binds to ionized amino acid groups of proteins - can be intracellular (cytoplasmic) proteins or extracellular proteins e.g. collagen
Red blood cells are very eosinophilic

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4
Q

What are amphophilic cells?

A

Stain with both acid (eosin) and basic (haemotoxylin) dyes

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5
Q

What are the four basic tissue types?

A

Connective tissue
Epithelia
Muscle
Neural tissue

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6
Q

What is connective tissue?

A

Basic type of tissue with mesodermal origin that provides structural and metabolic support for other tissues and organs throughout the body.

It is a large and continuous compartment throughout the body, located between and within organs.

Made of a few cells and large mass of extracellular matrix, (consists of fibres embedded in ground substance and also has fluid = ECF)

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7
Q

What is the dominant component of connective tissue that determines the properties of each type of connective tissue?

A

Extracellular matrix

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8
Q

What are the different types of ECM?

A

Embyronic connective tissue
Connective tissue proper - can be loose or dense (regular or irregular).
Specialised connective tissue = bone, cartilage, adipose tissue, blood, haemopoietic tissue and lymphatic tissue

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9
Q

What are the components of blood?

A

Fluid (plasma) and cells

It is a connective tissue but doesn’t have fibres or ground substance

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10
Q

What is plasma composed of?

A

It is an aqueous medium composing of water (90%), protein (8%), inorganic salts (1%), lipids (0.5%) and sugar (0.1%)
It is in equilibrium with ECF so can be transferred into cells when needed

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11
Q

What are the main proteins in plasma?

A

Proteins make up 8% of plasma. The three mean groups of proteins in plasma:

  1. Blood coagulation proteins
  2. Albumin
  3. Globulins (alpha = proteases, antiproteases and transport proteins, beta = transferrin and other transport proteins, gamma = immunoglobulins)
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12
Q

What are the cells of blood?

A

Three major functional classes:

  1. RBC (erythrocytes)
  2. WBC (leukocytes)
  3. Platelets (thrombocytes)
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13
Q

What is haematocrit?

A

Measures the percentage of blood volume that is made of RBCs = RBC volume/whole blood volume (normally 45%)

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14
Q

What is the life span of platelets?

A

8-10 days

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15
Q

What are the types of leukocytes?

A
Granulocytes (neutrophils, eosinophils and basophils)
Mononuclear leukocytes (lymphocytes and monocytes)
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16
Q

What are the histologic features of neutrophils?

A

3-5 lobed nuclei
May show a Barr body in females
1.5-2x the size of RBCs

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17
Q

What are the histologic features of eosinophils?

A

Bilobed nucleus
1.5-2x the size of RBCs
Contain large eosinophilic granules

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18
Q

What are the histologic features of basophils?

A

Bilobed nucleus

Large basophilic granules

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19
Q

What are the histologic features of lymphocytes?

A

Mononuclear
no granules
Round densely staining nucleus and little cytoplasm
Three main types = T cells, B cells and NK cells

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20
Q

What are the histologic features of monocytes?

A

Largest WBC
Oval or bean shaped nucleus
Paler nucleus and more cytoplasm than a lymphocyte

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21
Q

What is a haemopoietic stem cell?

A

Pluripotent progenitor cell for blood cells. Also progenitor for osteoclasts.
Capable of self renewal, proliferation and differentiation
Few circulate in the blood

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22
Q

What is erythropoiesis?

A

Formation of RBCs
Takes about 1 week and three main features are:
1. Cells decrease in size and extrude the nucleus
2. There is progressive loss of organelles
3. Progressive increase in cytoplasmic Hb content - become more eosinophilic

Process =
1. HSC
2. Unipotent SC
3. Proerythroblast - basophilic because still has RER
4. Normoblast - involved in Hb synthesis, decreasing RER and increasing Hb. Nucleus gets extruded.
There is a transition from basophilia to eosinophilia
5. Reticulocyte - no nucleus but some organelles. Need a special stain to see.
6. Erythrocyte (eosinophilic, no organelles)

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23
Q

What is extracellular matrix made of?

A

Fibres (elastic fibres, collagen fibres and reticular collagen) and ground substance

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24
Q

What are the functions of ECM?

A
Structural/mechanical support
Signalling pathways
Metabolic regulation
Controlling cell growth and differentiation
Binds and stores growth factors
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25
What are the types of collagen?
Type I - main structural collagen found in connective tissue proper, bone, tendons and ligaments Type II - Hyaline cartilage Type III - reticular fibres. Reticulin is prominent in highly cellular organs Type IV - Basement membranes Type VII - anchors fibrils to basement membranes (links ECM to BM)
26
What causes Marfan syndrome?
Mutation in fibrillin-1 gene resulting in abnormal elastin
27
What are the components of ground substance?
= amorphous semi-solid gel. Components: - GAGs - acidic (negatively charged - attracts water and sodium), can be linked to proteins (= proteoglycans). Predominant GAG in loose ground substance is hyaluronic acid. - Glycoproteins - glycosylated proteins = fibronectin, fibrillin and laminin.
28
What are the cells in connective tissue?
Resident cells: - fibroblasts and myofibroblasts - macrophages - mast cells - mesenchymal stem cells - adipocytes (in fat) - chondrocytes (in cartilage) - osteoblasts (in bone) Wandering cells: - lymphocytes - eosinophils - basophils - plasma cells
29
What are the functions of the basement membrane?
It is the interface between the support tissue (ECM) and the parenchymal cells. It provides structural support Control of epithelial cell growth and differentiation Selective barrier for the flow of nutrients, metabolites and other molecules
30
What produces basement membrane?
Mainly produces by the cells that are being supported (e.g. by epithelial cells)
31
What cells have a basal lamina?
Muscle cells, adipocytes and schwann cells
32
What are the components of the basement membrane?
``` GAGs e.g. heparin sulphate Collagen type IV Structural glycoproteins (laminins and fibronectin) ```
33
What are the types of epithelia?
Surface epithelia (lines surfaces and lumina) and glandular epithelia (involved in secretion - can be single cells e.g. goblet cells, invaginations forming glands in an organ/tisse and solid organs e.g. pancreas, thyroid)
34
What are the functions of epithelia?
- Protection - Barrier - selective absorption - Absorption - esp GIT - Secretion - Receptors - smell, taste
35
What are the defining features of epithelia?
Exhibit polarity, connected by cell junctions, supported by a basement membrane and avascular
36
Where is simple squamous epithelium found?
``` = single layer of squamous epithelia Line all blood vessels and the heart (endothelium) Lines body cavities (mesothelium) Alveoli lining Glomeruli ```
37
Where is simple cuboidal epithelium found?
= single layer of cuboidal cells Involved in selective diffusion e.g. in renal tubules Also thyroid follicles (follicular cells)
38
Where is simple columnar epithelium found?
= single layer of columnar cells (nuclei at the base) Non ciliated found in stomach, small intestine, large intestine, gall bladder, bile ducts, endometrium and endocervix Ciliated found in fallopian tubes and bronchioles
39
What is the respiratory system mainly lined by?
Pseudostratified ciliated columnar epithelium
40
What is simple columnar epithelium best adapted for?
secretion
41
What is simple cuboidal epithelium best adapted for?
diffusion
42
What is stratified squamous epithelium best adapted for?
withstanding abrasion
43
What is transitional epithelium?
Urothelium Stratified Lines the urinary tract Best adapted for expansion and contraction
44
Where is stratified squamous epithelium found?
Where you get wear and tear - oesophagus, anus, oral cavity and vagina. Most is non keratinising
45
Where is stratified cuboidal epithelium found?
Some ducts, not common
46
What are the types of intercellular junctions?
Tight or occluding Adherens (link actin) Desmosomes (links intermediate filaments) Gap junctions (made of connexins)
47
What order would thou see the different junctions in a junctional complex from luminal end to basal end?
1. Tight junction (most luminal) 2. Zonula adherens (just below TJ) 3. Gap junction 4. Desmosomes 5. Hemi desmosomes on basal plasma membrane (not lateral)
48
What are CAMs?
``` Cell adhesion molecules 4 main groups of CAMs: - Cadherins - Integrins - Selectins - Immunoglobulins superfamilyu (ICAM, CCAM, PECAM) ```
49
What is the lamina propria?
Supportive connective tissue under the basement membrane that contains blood vessels
50
What is the muscularis mucosae?
Thin smooth muscle layer underlying lamina propria. Separates the lamina propria from submucosa in GIT
51
What is the structure of skin?
1. Covered by epidermis (keratinising stratified squamous epithelium, continuously replicating, produces non living layer of keratin) 2. Dermis = connective tissue (consists of fibrous and fibroadipose tissue that supports the epidermis physically and metabolically) - contains blood vessels, nerves, hair follicles, sweat glands, sebaceous glands and sensory receptors 3. Hypodermis/subcutaneous tissue - mainly adipose tissue and sweat and hair follicles
52
What are intercellular bridges?
Important feature of stratified squamous epithelium | They are slender cytoplasmic strands that connect adjacent cells.
53
What are the different patterns of necrosis?
``` Coagulative Caseous Liquefactive Fat Fibrinoid ```
54
What is coagulative necrosis?
"Ghost outlines" - architecture maintained | Typical of infarction in solid organs except the brain
55
What is caseous necrosis?
Cheese like appearance No distinct cell borders Most often seen in necrotising granulomatous inflammation due to TB
56
What is liquefactive necrosis?
Characterised by digestion of dead cells resulting in transformation of the tissue into a viscous liquid mass or cavity Typical of cerebral infarction and abscesses
57
What is fat necrosis?
Not really a specific pattern of necrosis | Refers to destruction of fat, classically as a consequence of release of lipase's in the setting of acute pancreatitis
58
What is fibrinoid necrosis?
Special form of necrosis usually seen in association with immune reactions involving blood vessels Deposition of immune complexes leads to leakage of fibrin resulting in necrosis with an intense bright pink appearance on H&E
59
What is dystrophic calcification?
Deposition of calcium in tissues despite normal blood calcium levels
60
What are the four abnormal pigments?
1. Carbon - common (exogenous) 2. Lipofuschin - wear and tear pigment (accumulates with age) 3. Melanin 4. Haemosiderin - usually pathological, occurs when there is excess iron e.g. following haemorrhage
61
What are the systemic signs of inflammation?
``` Tachycardia Malaise Anorexia Fever Rigor/Chills Weight loss Anaemia if chronic ```
62
What are the main features of acute inflammation?
Neutrophils, fluid and protein exudate, vasodilation and macrophages
63
What are the main features of chronic inflammation?
Macrophages, lymphocytes, plasma cells and associated with fibrosis/scarring
64
What are the three components of acute inflammation?
1. Vascular response: increased vascular permeability - endothelial activation allows for increased delivery of cells, chemical mediators and proteins - If there is vascular injury there will be a transient arteriolar constriction and then arteriolar-> capillary-> venous dilation 2. Exudate: cells, fluid, proteins - suppurative, fibrinous or serous exudate 3. Variable necrosis
65
What are the 3 main types of exudate?
Purulent/suppurative - neutrophil rich Fibrinous - fibrin rich. Tends to occur on serial surfaces of an organ Serous - not many cells, mainly fluid
66
How is vascular permeability increased in inflammation?
Happens largely in the venues 1. Retraction of endothelial cells (leads to intercellular gaps) - most common cause - short term contraction of endothelial cells induced by histamine, bradykinin, leukotrienes - long term contraction induced by IL-1 and TNF 2. Injured endothelium - leakage begins immediately after injury and continues until thrombosis and repair has occurred 3. Leukocyte-mediated vascular injury - Leukocytes can accumulate and release toxic mediators that injure the endothelium 4. Increased transcytosis
67
How do leukocytes migrate through the endothelium?
1. TNF and IL-1 activate the endothelium 2. Endothelium expresses P-selectin and E-selectin (not normally present) 3. Leukocytes transiently bind to the selections through glycoproteins (sialyl-lewis X) and roll along the endothelium 4. The endothelium expresses ICAM-1 (low amounts normally but more in inflammation) and leukocytes bind to it via integrins (stronger binding) 5. Chemoattractants in the inflamed tissue attracts the leukocytes 6. To get into the tissue, the leukocyte binds PECAM-1 (near the gaps between endothelial cells) 7. Leukocytes move into tissue (diapedesis)
68
What is the timeline for acute inflammation?
``` Injury Biochemical changes Few hours- acute inflammation 6-7 hours can see histological features 6-24 hours neutrophils predominate 24-48 hours macrophages predominate ```
69
What is fibrinous inflammation?
Characteristic of inflammation on the linings of body cavities (meninges, pleura, pericardium etc). The exudate contains fibrin (created by cleavage of fibrinogen) which can be removed by fibrinolysis or macrophages. If the fibrin is not removed from the EC space then there is organisation and scarring.
70
What is the difference between a transudate and an exudate?
Exudate = Extravascular fluid that has a high protein content and contains cellular debris. implies increased vascular permeability (due to inflammation). Transudate = fluid with low protein content and little/no cellular material. It occurs when there is normal vascular permeability but increased hydrostatic pressure (and/or decreased colloid osmotic pressure) that causes fluid to move out of the vessel without an increase in permeability.
71
What mediators are responsible for the features of acute inflammation?
Vasodilation = NO, Prostaglandins, histamine Vascular permeability = Histamine, serotonin, bradykinin, leukotrienes. Endothelial activation = TNF, IL-1 Chemotaxis = Complement components, bacterial components, chemokines Tissue damage = Neutrophil granule contents, NO, ROS Pain = PGs, bradykinin Fever = IL-1, IL-6, TNF, PGs (PGE2)
72
What are the four main outcomes of acute inflammation?
1. Resolution - damage neutralised and tissue damage minimal. Will occur if ECM is in tact. 2. Healing by repair - damage neutralised and some tissue damage. Organisation through phagocytosis and granulation tissue formation 3. Abscess formation - Marked neutrophilic response with tissue destruction 4. Chronic inflammation - Persisting damage with tissue destruction. Organisation with continued inflammation.
73
When do you get scar tissue formation?
When there is necrosis, when the tissue can't regenerate due to cell type (permanently differentiated cells) or lack of stem cells, when there is chronic inflammation and when the structural framework/connective tissue (BM or ECM) is damaged
74
What are the main features of healing by repair?
``` Inflammation Angiogenesis Migration and proliferation of fibroblasts Scar formation Connective tissue remodelling ```
75
What is granulation tissue?
An intermediary tissue in scar healing - can be vascular or fibrous. Vascular GT occurs at least 1 week after injury and fibrous GT occurs a couple of weeks after. Hallmark of healing by repair Appears between 24 and 72 hours
76
What are the components of granulation tissue?
Inflammatory cells - macrophages, lymphocytes, eosinophils New blood vessels (mainly capillaries) - new vessels are thin and leaky. VEGF is important Fibroblast migration and proliferation (due to PGF, TGFb, FGF) Deposition of ECM
77
What is the difference between early and late granulation tissue?
Early GT is very cellular and late GT is very vascular
78
What is healing by primary intention?
Healing of a narrow wound with closely opposed edges e.g. surgical incision. Healing is fast and there is less scar tissue is edges remain closely opposed.
79
What is healing by secondary intention?
Occurs when there are larger wounds to fill in with granulation tissue. Takes longer for GT and scar tissue to form and more likely to become complicated.