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CSB520 > FINAL EXAM REVISIONS - LEARNING OBJECTIVE > Flashcards

FINAL EXAM REVISIONS - LEARNING OBJECTIVE Flashcards

1
Q

What does Haematoxylin stain? What Colour?

A

Stains the Nucleus (Nuclei and Lymph node) dark blue or Purple

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2
Q

What does Eosin stain? What Colour?

A

Stains the Cytoplasm (Proteins - Muscle or cytoplasm with little nucleus) pink

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3
Q

Define Cellular Differentiation

A
  • Features in cell that show it has a function and structure

- It is a specialised Cell

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4
Q

What is a specialised Cell?

A

A Nucleus that contains microvilli attached

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5
Q

What is an undifferentiated cell?

A
  • A cell that does not have a function

- It is an Unspecialised cell

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6
Q

What is an unspecialised cell

A
  • It is a Stem Cell

- Just a Nucleus

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7
Q

What is a Gastrula made up of?

A

Ectoderm, Germ Cells, Mesoderm, Endoderm

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8
Q

Does a change in Environment cause a change in a cell?

A

Yes, in each cell there is DNA and specific strands can be turned on and turned off based on the surrounding environment
Environment is a determinant in what a cell can become.

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9
Q

Cell considered Epithelial?

A 
Skin Cells
GIT cells
Reproductive Cells
Urinary Tract Cells
Lining of Exocrine ducts
Liver Cells
Kidney Cells
Respiratory cells
Pancreas Cells
Glandular Epithelial Cells
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10
Q

Types of Epithelial Cells? There’s 7…

A 
Simple Squamous
Stratified Squamous
Simple Cuboidal
Simple Columnar
Pseudo Stratified
Transitional 
Stratified Cuboidal/Columnar
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11
Q

Feature of a Simple Squamous Epithelium:

A
  • Single Layer
  • Cytoplasm usually appears thinner than Nuclei
  • Allows gases, ions and small molecules to pass through
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12
Q

What are the 3 types of cells:

A

Labile
Stable
Permanent

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13
Q

What are Labile Cells

A

Continuously Dividing
Epithelial
Haemopoietic Stem Cells

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14
Q

What are Stable Cells

A

Divide only when required - growing tissue back
Epithelial
Smooth Muscle Cells, Fibroblasts and endothelial Cells

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15
Q

What are Permanent Cells?

A

Non-Dividing Cells
Cardiac Cells
Skeletal Myocytes
CNS Neurons

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16
Q

What is proliferation? Explain the process

A

The rapid division of a cell

DNA is unwined and replicated during the cell cycle if stimulated - G0 is cell cycle arrest - stable cells

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17
Q

Stages of the Cell Cycle

A

During the cell cycle, cells become labile

Stages: G1, S, G2, Mitosis, Cytokinesis

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18
Q

What do tissues need?

A 
Nerve Innovation
Blood and Lymphatic Supply and removal:
- Gases, Hormones and Growth Factors
Defence against invasions:
- Skin/Epidermis (fat)
- GIT
- Urogenital 
- Respiratory
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19
Q

What do Cells Need?

A 
Functional Plasma Membrane (Skin)
Ability to make RNA and Proteins
Ability to Copy and repair DNA
Functional cytoskeletal proteins
Energy (ATP)
Antioxidant Defences
Ability to remove waste including proteins
Ability to repair or destroy redundant and damaged organelles
The correct temperature, pH, etc.
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20
Q

How do cells communicate?

A

Through distant cells using chemicals released into the blood such as hormones
Through Neighbouring cells and connecting tissue (Acting in a paracrine matter)
- Epithelial Cells like to be attached to their neighbours and membranes beneath them

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21
Q

What is a Paracrine process?

A

Communication with neighbouring cells directly

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22
Q

What is an Autocrine process?

A

The cell communicates with itself

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23
Q

What is an Endocrine process?

A

The cells communicates over distance through blood

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24
Q

Mitochondria

A 
Surrounded by a double membrane
Generate ATP
Full of Oxidative Enzymes
Induces cell death
Possibly drives differentiation
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25
Q

What are Oxidative Enzymes?

A

A Bi-product of ATP that prevent the mitochondria from stealing electrons and damaging the lipid

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26
Q

Lysosomes? Types?

A 
Waste Disposal
Membrane-Bound Digestive Organelles
Primary Lysosomes
Secondary Lysosomes:
- Heterophagosomes
- Autophagosomes
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27
Q

How does the cell membrane work with Lysosomes

A

It fuses with a lysosome containting acid and breaks down constituents, thus removing waste

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28
Q

What is Autophagy? How does it work?

A

Self Eating - Nutrient Depletion - The cells shrinks itself by eating a part of itself
Reduction in cell Size

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29
Q

Mitochondria and Autophagy

A

If the mitochondria is damaged by free-radicals and cannot repair, it will need removal. The cell designates a section of the cytoplasm containing the dodgy mitochondria for removal.

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30
Q

Define Physiology:

A

Scientific Study of the function of living things

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31
Q

Define Pathology:

A

Scientific Study of Disease

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32
Q

Define Active:

A

Requiring Energy

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33
Q

Define Passive:

A

Does not require energy

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34
Q

Define Aerobic:

A

Done with oxygen

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35
Q

Define Anaerobic:

A

Done without Oxygen

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36
Q

Define Hypoxia:

A

Lack of Oxygen

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37
Q

Define Ischaemia:

A

Lack of Blood Supply - “Distruption”

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38
Q

Define Reperfusion:

A

Restoration of blood following a period of Ischaemia

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39
Q

Define Acute:

A

Sudden Onset

Sudden Severe

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40
Q

Define Chronic:

A

Long Duration of Severeness

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41
Q

What can cause Cell Stress/Injury:

A

Mutation: Tumour, impaired Function
Cell Death: Apoptosis, Necrosis
Adaptation: Autophagy, Hypertrophy, Hyperplasia, Metaplasia

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42
Q

How does cell stress occur? Flow Chart…

A

Normal Cell - STRESS - Adaptation - INABILITY TO ADAPT - Cell Injury - SEVERE, PROGRESSIVE - Irreversible Injury - Cell Death (Necrosis, Apoptosis)

Normal Cell - INJURIOUS STIMULUS - Cell Injury - SEVERE, PROGRESSIVE - Irreversible Injury - Cell Death (Necrosis, Apoptosis)

If a normal cell that undergoes cell injury is only mild and transient that reversibility can occur returning the cell back to normal.

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43
Q

What does Stress lead to?

A

Stress –> Cell Death = Apoptosis and Necrosis
Stress can stimulate either form of death depending upon the duration and severity of the application and the resources of the cell

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44
Q

Define Apoptosis:

A

Programmed cell death, Cell Suicide
Takes itself away from other organelles and kills itself - Active dismantling
Phagocytosis (removal) of apoptic bodies using Macrophages and Neighbouring cells
No inflammation or scarring
Decrease in cell number

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45
Q

Define Necrosis:

A

Sudden Death

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46
Q

Negatives with Necrosis

A

Doesn’t have time to move away from neighbouring cells
Neighbouring cells undergo Necrosis
Stimulation of Acute Inflammation
Loss and reduction in tissue function - Scarring, Calcification, Death

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47
Q

Define Infarction:

A

Area of Necrotic Tissue

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48
Q

Physiological jobs of Apoptosis:

A
  1. Embyronic Development
  2. Tissue homeostasis
  3. Removal of redundant cells
  4. Crucial for immune function
  5. Immune-mediated Killing
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49
Q

Pathological jobs of Apoptosis:

A
  1. Pathological Atrophy
  2. Transplant Rejection
  3. Autoimmune Diseases
  4. Some infections
  5. Anti-cancer treatment (Targets dividing cells)
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50
Q

Apoptosis VS Necrosis?

A
  • Apoptosis occurs in physiology and pathology. Necrosis is pathological
  • Apoptosis is Active. Necrosis is Passive
  • A single cell can die from Apoptosis. Neighbouring cells die from necrosis
  • Apoptosis does not stimulate Inflammation. Necrosis stimulates inflammation
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51
Q

What causes Adaptation?

A

Increased Workload or demand

Altered Environment

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52
Q

What is Tissue Atrophy

A

The absence of nourishment, development or growth at THE TISSUE LEVEL
A reduction in size and cell number of individual cells in a tissue/organ undergoing a combination of AUTOPHAGY and APOPTOSIS or just APOPTOSIS in ‘old’ cells
Not Reversible - occurs in permanent tissue

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53
Q

Mitochondria and Ageing

A

As we age, the mitochondria produces less anti-oxidant defences and more oxidative enzymes - more susceptible to injuries
As we age, the mitochondria becomes weaker and more damaged as free radicals increase as ATP decreases

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54
Q

What are Free Radicals?

A

Highly reactive elements that can kill the mitochondria and cause damage to cells

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55
Q

What happens to the mitochondria usually once it is damaged by free radicals? What about with ageing?

A

Usually, it would undergo autophagy where is isolates itself, fuses with a lysosome and degrades until it becomes a ‘recycling of metabolites’
When we age, the cells are too old to isolate and lose ability to undergo autophagy. This causes the mitochondria to release free radicals and damage the surrounding cells as well

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56
Q

What effect does ageing have on cells and organs?

A

A decreased ability to undergo Autophagy - Cells atrophy with age

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57
Q

Healthy Cell - Cellular response to stress (Low, Moderate and Sudden Severe Stress)

A

Healthy Cell –> Adapt Autophagy –> Apoptosis –> Necrosis

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58
Q

Old Cell - Cellular response to stress (Low, Moderate and Sudden Severe Stress)

A

Old Cell –> Apoptosis –> Necrosis

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59
Q

Physiological and Pathological examples of Tissue Atrophy

A

Physiological: INVOLUTION (Shrinkage of tissue when inactive)
Pathological: GRADUAL DECREASE IN CELL SIZE AND NUMBER

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60
Q

Atrophy vs Infarction

A 
Atrophy:
- Caused by Gradual Stress
- Involves Apoptosis (Decrease in cell number)
- Involves Autophagy (Decrease in cell size)
Infarction:
- Caused by Sudden Severe Stress
- Ischaemia
- Haemorrhagic
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61
Q

What is Metaplasia?

A

Reversible
The change from one normal/well-differentiated cell type to another normal well-differentiated cell type usually because of a change in environment
Increase risk in mutation = Increase in Cancer
- Example: Smoking causes the conductive region of the airways to go from pseudostratified epithelium with goblet cells to stratified squamous epithelial cells due to the change to a harsher environment due to carcinogens

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62
Q

Define Hyperplasia:

A

Increased number of cells
Stabile or Labile cells can undergo hyperplasia and cause an abnormal increased rate of cell division (failure of apoptosis in a labile tissue (Whats dying isnt being removed))

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63
Q

Define Hypertrophy:

A

Increase in cell size – Enlarged Organ

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64
Q

Connective Tissue Type:

A 
Myocytes - Muscle Cells
Fibroblasts
Collagen
Fat
Endothelium (lining of blood vessels)
Cartilage (Chondrocytes)
Bone (Osteoblasts, Osteocytes)
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65
Q

Are Skeletal Muscle fibers permanent?

A

Yes, but they are able to repair not replaced
ALSO:
- Contain possible 100s of nuclei in each cell

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66
Q

Are Cardiac Myocytes Permanent?

A

Yes, and there is no repair
ALSO:
- Individual cells with single, central nuclei

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67
Q

Are smooth Muscle permantent?

A

No, they are stable cells but can divide when necessary

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68
Q

What are Fibroblasts?

A

Stable cells secreting collagen

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69
Q

What is Collagen

A

A long stringy contractible protein - Stable cell

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70
Q

What is fat?

A

Adipocytes - large cells with a cytoplasm full of fat

Nucleus against the edge

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71
Q

Are the endothelium, cartilage and bone permanent cells?

A

No they are stable cells

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72
Q

Function of the Epithelium:

A 
Mechanical Stress
Chemical Stress
Secretion - Lubrication, Digestion, Excretion
Absorption
Transport
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73
Q

What are Glandular Epithelial Cells?

A

Secretory cells
Endocrine - Secrete into blood acting on receptor in distant site
Exocrine - Secretion into lumes or duct

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74
Q

Stratified Squamous Epithelium:

A

Basal cuboidal-like cells that matures as it migrates towards the surface
At some sites, a keratinised upper layeer reduces absorption but increases strength
Lines surfaces exposed to abrasion, friction, physical stress:
- Skin, oral cavity, pharynx, oesophagus, anal canal, outer cervix (ectocervix), Vagina
Labile cells

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75
Q

Simple Cuboidal Epithelium:

A 
Tall and wide
Lines protected surfaces:
- Exocrine glandular ducts
- Collecting tubules of the kidney
- Outer surface of ovary
Labile or Stable cells
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76
Q

Simple Columnar Epithelium:

A

Line surfaces involved in secretion and absorption
Sometimes microvilli are present to increase the surface area of the absorptive membrane or cilia to aid movement across the surface

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77
Q

Pseudo Stratified:

A

Located in upper respiratory tract and male reproductive system
Appears as stratified but it is simple single layer
Stable Cells

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78
Q

Transitional Epithelium:

A

Restricted to Urinary System - Renal, Calyxes, Ureters, Bladder and Urethra
Allow stretch and retraction that look columna when relaxed but cuboidal when stretched

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79
Q

Stratified Cuboidal:

A

Lines mammary glands, part of the cohchlea, germ cells of the seminiferous tubules and granulosa cells of the ovarian follicles

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80
Q

Straified Cuboidal/Columnar:

A

Rare

Some large ducts are lines by columnar on top of cuboidal

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81
Q

Other Tissues:

A

Aren’t considered connective or epithelial:

  • Mesothelial cells
  • Melanocytes
  • Neural Tissue
  • —–Meninges
  • —–Glial Cells
  • —–Neurones
  • Germ Cells
  • Lymphoid tissue and cells
  • Bone marrow and haemopoietic cells
  • RBC’s
  • Neutrophils
  • Macrophages
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82
Q

Define tumour:

A

Denotes Swelling

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83
Q

Define Benign Tumour

A

Friendly, causes no harm

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84
Q

Define Malignant Tumour

A

Potentially Fatal

Cancer

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85
Q

Can Benign Tumours be cancers?

A

NO

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86
Q

How do mutations occur?

A

Cells that are dividing have the greatest chance of sustaining a mutation
- Epithelial cells are capable of dividing and some continuously divide
- Epithelial cells are on the front line
Epithelial cancers increase in incidence as we age
It takes many mutations to create a cancer cell and we acquire mutations over time
More than 90% of cancers are Carcinomas
Non-lethal Genetic damage

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87
Q

What happens to cells if there is no adaption or it fails to adapt?

A

Dysplasia

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88
Q

What is Dysplasia?

A

A pre-cancerous exchange
Usually the immune system destroys these, but it can accumulate with age
The Genotype and phenotype are abnormal

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89
Q

What are Mutagens?

A

A substance that can cause genetic mutation
May act directly to cause damage or may do so through increasing oxidant production or reduction or reducing anti-oxidant defences causing an increase in free radicals

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90
Q

What causes mutagens?

A 
Exposure to carcinogens
UV
Alcohol
Smoking
Obesity
Genetics
Viruses
Some Chronic Inflammatory conditions - Not necessary but can happen
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91
Q

What are four classes of normal regulatory genes that are principle targets of genetic damage?

A

1- Growth promoting onoco-genes
2- Growth Inhibiting Tumour Suppressing genes
3- Genes that regulate Apoptosis
4- DNA repair genes

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92
Q

What is the molecular basis of cancer? “The essential alterations for malignant transformation?”

A
  • Self-sufficiency in growth signals
  • Insensitivity to growth-inhibitory signals
  • Evasion of Apoptosis
  • Defects in DNA repair
  • Limitless replicative potential
  • Sustained Angiogenesis
  • Ability to invade and metastasize
  • Predilection for glycolysis even in the presence of oxygen
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93
Q

Define Self-sufficiency in growth signals

A

Proliferation without any external stimuli

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94
Q

Define Insensitivity to growth-inhibitory signals

A

Ignore signals sent out by sells to stop growth

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95
Q

Define Evasion of Apoptosis

A

When DNA damage occurs, the cells is mutated enough that the apoptopic pathway has been turned off, and cells arent removed

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96
Q

Define Defects in DNA repair

A

DNA doesnt scan cells for mutations or mistakes when formed, mutations accumulate

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97
Q

Define Limitless replicative potential

A

Immortal, continuous division of cells with genetic errors

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98
Q

Define Sustained Angiogenesis

A

Formation of new blood vessels to support mutation
Benign - Neat Blood vessel formation
Malignant - Messy and out of order blood vessel formation

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99
Q

Define Ability to invade and metastasize

A

Mutated Cells can pass the basement membrane and enter blood vessel and migrate to a different site to invade and mutate more cells

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100
Q

Define Predilection for glycolysis even in the presence of oxygen

A

Cancer Cells choose not to us oxygen but rather use glucose

Aerobic glycolysis - Warburg Effect

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101
Q

What is a cancer cell called when it hasnt passed the basement membrane

A

Carcinoma in-situ

102
Q

How does a cell accumulate mutations?

A

Normal Cell undergoes DNA Damage - hopefully repairs, if it doesnt, apoptosis, but if that fails too then - Genetic Instability in the cell cycle, Unregulated division, inability to undergo further apoptosis, Invasive Cancer, Metastisis

103
Q

Benign VS Malignant

A

Benign:

  • NEVER metastisize
  • Encapsulated
  • Homogenous - uniformity between cells (Same appearance)
  • Well Differentiated
  • Cytoplasmic ratio is close to normal
  • Slow Growing

Malignant:

  • POTENTIALLY metastisise
  • Infiltrative growth
  • Heterogeneous - Lack uniformity (Different Appearance)
  • Well/poorly-differentiated or undifferentiated
  • Increased nuclear to cytoplasmic ratio
  • Fast Growing
104
Q

3 routes of metastasis?

A

1- Blood (haematogenous)
2- Lymphatics (vessels & Nodes)
3- Direct Seeding (through/within body cavities)

105
Q

What is the most common site of metastatic neoplasms?

A

Will try to travel through the capillary bed all the way to the secondary location
Secondaries: Lung then Liver

106
Q

What is the nomenclature of BENIGN connective tissue called?

A 
Fibroma - Fibroblasts
Leiomyoma - Smooth Muscle
Chondroma - Cartilage
Osteoma - Bone
Lipoma -Fat
Haemangioma - Endothelial lining of blood vessels
107
Q

What is a MALIGNANT tumour derived from connective tissue?

A

SARCOMA Suffix
“sarc” = Malignant from connective tissue origin
SUPER RARE - Less than 10% for these

108
Q

Nomenclature of epithelial BENIGN tumours?

A

Papilloma - Finger like projections
Adenoma - Glandular cells
Cystadenoma - Fluid-filled sac

109
Q

What is a MALIGNANT tumour derived from epithelial tissue called?

A

CARCINOMA suffix
“Carc” - Malignant and Epithelial cell of origin
More then 90% of cancer - Proliferation and Stress

110
Q

What type of tumour do other tissues form?

A

Malignant tumours

111
Q

What is a meningioma?

A

It is a benign tumour located in the brain and can kill

112
Q

What is a Mature Ovarian Teretoma?

A

It is a Benign dermoid cysts that is from a germ cell and isn’t fertilised but can give rise to a baby or parts of baby - hair, teeth, etc.
Monstrous Growth

113
Q

What is a Testicular Tumour?

A

An immature Teratoma

Seminoma

114
Q

Other types of Maligant tumours?

A 
Melanoma
Leukaemia
Lymphoma
Mesothelioma
Glioma
Testicular Tumour
Blastoma
115
Q

What is a Blastoma

A

Never a normal cell to begin with - during embryo genesis it got mutated.

116
Q

Different types of pathogenesis:

A

Normal Cell - Multiple mutations - Cancer (NOT BENIGN)

Normal Cell - Multiple mutations - Benign Tumour

Normal Cell - Multiple mutations - Benign Tumour - Further mutations - Cancer (NOT STABLE)

Normal Cell - Sustained Stress- Metaplasia - Multiple Mutations - Dysplasia - Further Mutations - Cancer

117
Q

What is Melanoma?

A

Number 1 Cancer in Australia
Can be Caught in dysplastic stage before metastasis
Dont need much to become aggressive - already motile
Involve:
- Eyes
- Mucus Membrane
- Skin

NOT JUST SKIN CANCER

118
Q

Pathogenesis of Melanoma?

A

Normal Cell - Multiple mutations - Cancer (NOT BENIGN)

119
Q

What is Mesothelioma?

A 
Very Aggressive
Very rare
Due to radiation exposure
Asbestos
On pleural lining
CARCINOGENS can cause
120
Q

Pathogenesis of Mesothelioma?

A

Normal Cell - Multiple mutations - Cancer (NOT BENIGN)

121
Q

Pathogenesis of Ovarian Teratoma and Leiomyoma?

A

Normal Cell - Multiple mutations - Benign Tumour

122
Q

Pathogenesis of Colon Cancer?

A

Normal Cell - Multiple mutations - Benign Tumour - Further mutations - Cancer (NOT STABLE)

123
Q

Pathogenesis of Lung Cancer?

A

Normal Cell - Sustained Stress- Metaplasia - Multiple Mutations - Dysplasia - Further Mutations - Cancer

Stress: Carcinogen exposure

124
Q

Pathogenesis for female reproductive cancer? How does it occur?

A

Normal Cell - Sustained Stress- Metaplasia - Multiple Mutations - Dysplasia - Further Mutations - Cancer

During Menstruation, cells in the endocervical canal are pushed out into a different environment that has a higher pH (Ectocervix) - Forced to adapt and become stratified to handle environment, can get mutations whilst adpating.

125
Q

Grading VS Staging:

A

Grading:

  • Nature of the cancer and aggressiveness
  • 1 to 4, indicating 4 the worst prognosis
  • Differentiation
  • Number of mitoses dividing cells
  • Varies depending on the cancer type

Staging:

  • TNM system - talks about characteristics of tumour
  • T1-T4 = Tumour size
  • N0-N3 = Number of lymph nodes that are cancerous
  • M0-M1 = Metastasis or not
126
Q

Can Cancer be cured?

A

Many ‘early’ caught cancers can be however, 30% of patients have metastases at diagnosis
5 year survival rate
Cure or remission (partial/total)

127
Q

Signs and Symptoms of Cancer?

A

Fat and Muscle Loss
Paraneoplastic Syndrome
Horomone, blood and mucous changes

128
Q

Treatments of Cancer?

A 
Surgery
Radiotherapy
Chemotherapy
Hormone therapy
Immunotherapy
Hyperthermia
129
Q

Treatment affects on host?

A

Healthy Cells lost - epithelial, immune
Mutation in health cells - Mesothelial, Lymphoid
Scars, Radiation Burns

130
Q

Types of micro-organisms?

A 
Parasites
Yeast & Fungi
Bacteria
Viruses
Prions
131
Q

What is an Innate Defence system?

A

A defence system in the immune system that the body is born with
It has the same response every time no matter the damage

132
Q

What is an Acquired Defence System?

A

A defence system in the immune system that the body adapts to.
It learns from past viruses and creates an army to to attack in the future - its specific to the virus
Involves Lymphocytes

133
Q

Innate vs Acquired?

A

INNATE:

  • Fast Response
  • Non Specific
  • Germline encoded
  • Celullar response: Neutrophils, Macrophages, Natural Killer Cells

ACQUIRED:

  • Slow Response
  • Able to differentiate between lots of targets
  • Learns and remembers
  • Has a “memory”
  • Cellular Response: T Cells and B cells
  • Humoral: Antibodies
134
Q

What is the function of a T Cell?

A

Activation of B cells and cytotoxic T cells

Travel to site and bind to the antigen

135
Q

What is the function of a B Cell?

A

Matures into a plasma cells and produces antibodies which are released into the blood and bind to the antigen
Signal Destruction

136
Q

What do the clinical manifestations of infections depend upon?

A

1- The host and principally the host response to the infection
2- Site of infection
3- Characteristics of the organism principally the intrinsic virulence of the organism

137
Q

Define Virulence

A

The ability of power of a microorganism to cause disease

Low? No destruction unless immune compromised

138
Q

What are Virulence Mechanisms?

A

Factors inherent to the organism, encoded at the molecular or gene level
Helps establish the infection causing the disease

139
Q

What do these Virulence mechanisms involve?

A

Overcoming Defences
Damaging host cells
Altering host cells and/or cytokine production
Adhesive/invasive factors, capsules, slime, fimbbriae, pili, enzymes
Toxins (exotoxins, endotoxins, enterotoxins)
Cause damage and impair host defence

140
Q

What are Sterile body sites?

A

Areas with NO microorganisms:

  • Brain and CSF
  • Blood
  • Bone and Marrow
  • Lower respiratory tract
  • Upper urogenital - Male and female reproductive system
  • Stomach
141
Q

What are Non-Sterile body sites?

A

Areas with microorganisms:

  • Skin
  • GIT
  • Upper Respiratory - Oral Cavity and Larynx
  • Lower urogenital - Female Reproductive System (Ectocervix and vagina should have microorganisms)
142
Q

What are Leukocytes?

A

White blood Cells

143
Q

Cellular Components of Leukocytes:

A

Granulocytes and Agranulocyes

144
Q

What are Granulocytes?

A 
Destroy large bacteria by throwing chemical substances at microorganisms. Release granules
Involve:
- Neutrophils - phagocytes
- Eosinophils
- Basophils
145
Q

What are Aganulocytes?

A

Involve:

  • Lymphcytes
  • Monocytes
146
Q

What happens to Monocytes when they mature?

A

When a monocytes is activated and calledupon to a specific site, it matures and becomes a macrophage

147
Q

Define Macrophage:

A

A immune cells that eats large cells that are dead

Has a long life span

148
Q

Define Interstitial Fluid:

A

Fluid between cells

149
Q

Define Oedema:

A

Increase in Interstitial flue causing a fluid build up in cavities and tissues

150
Q

High-protein Oedema Vs Low Protein Oedema:

A

High-protein oedema:
- Water and Plasma proteins are leaking into tissue - Exudate

Low-protein Oedema:
- No plasma change but water is being pushed out -Transudate

151
Q

Define Hyperaemia:

A

The Increase in blood flow to an area
Occurs actively
Vasodilation and increase in permeability causing oedema

152
Q

How is hyperaemia impacted during acute inflammation?

A

Chemical mediators are released and induce mudcle in vessel to relax - causing it to become engorged in blood

153
Q

Define Congestion:

A

Increase and accumulation in blood flow
Occurs passively
Usually not in arterial circuit but in venous circuit

154
Q

What happens if the left side of the heart is congested?

A

Lungs become congested

155
Q

What happens if the right side of the heart is congested?

A

Whole body in the venous system becomes congested

156
Q

Define Exudate:

A

Inflammatory extra vascular fluid with high protein - High-protein Oedema

157
Q

Define Transudate:

A

Extravascular fluid with low protein concentration - Low-protein Oedema
usually not caused by inflammation but by other things

158
Q

Define Pus:

A

Purulent inflammatory exudate that is high in neutrophils, cell debris and sometimes pyogenic organisms

159
Q

How does Transudate form:

A

Congestion increases hydrostatic pressure causing venous flow obstruction. The fluid leaks and goes into tissue to produce transudate making it harder to breathe. There is no change in colloidal osmotic pressure

160
Q

How does Exudate form:

A

An increase in hydrostatic pressure causing venous flow obstruction allows the leakage of fluid.
A decrease in colloidal pressure causing a decrease in protein synthesis makes the endothelial more permeable allowing protein leakage.

161
Q

Define inflammation:

A

No microorganism involved - just a disruption in blood supply - infarction due to necrosis
The body’s general response to injury and infection
The pattern of events is similar irrespective of the cause or its location

162
Q

Types of inflammation:

A

Acute and Chronic

163
Q

Define Acute inflammation:

A

The start of repair although it can lead to further injury

164
Q

Nomenclature of inflammation

A

Suffix - “itis”

  • DermatITIS
  • PancreatITIS
  • MeningITIS
  • EncephalITIS
  • BronchITIS
  • TonsillITIS
  • GastrITIS
  • HepatITIS
  • NephrITIS
165
Q

What are the indicators of Acute Inflammation? How are they caused?

A
  1. Heat –> Hyperaemia
  2. Redness –> Hyperaemia
  3. Swelling –> Oedema due to Hyperaemia and increase permeability
  4. Pain –> Stretch receptors and chemical mediators
  5. Loss of function –> Swelling and Pain
    “He Read Stories of Pain and Loss”
166
Q

Define Chemotaxis:

A

The movement or locomotion according to a chemical gradient - Similar to metastasis

167
Q

Define Chemokine:

A

Agent that induces chemotaxis

168
Q

Define cytokine:

A

Hormone of the immune system

169
Q

What is the vascular response to acute inflammation?

A

Release of soluble mediators from necrotic cells, infectious/foreign agents, nearby cells and plasma

  1. Dilation and Hyperaemia
  2. Extravasation of fluid and proteins (Oedema - exudate)
  3. Leukocyte…Neutrophil recruitment and activation

“Hyperaemia, Oedema, Neutrophil”

170
Q

Cellular components of acute inflammation

A

Neutrophil

Monocyte which matures into a macrophage

171
Q

What is extravasion?

A

Requires and intact vasculature

  1. Margination
  2. Rolling
  3. Adhesion
  4. Diapedesis
  5. Migration
172
Q

What is Phagocytosis?

A

Taking up of dead tissue

  1. Recognition and attachment
  2. Engulfment
  3. Killing and Degredation
173
Q

Aims of acute inflammation?

A

Dilute, Destroy and Clean up

174
Q

If a stimulus was Necrosis and infection, what is the response?

A

Release of chemical mediators producing a vascular and cellular response.
The Vascular Response consists of Hyeraemia and Oedema
The cellular response involves the leukocyte activation and recruitment of Neutrophils and monocytes/Macrophages

175
Q

Aims of Chronic Inflammation?

A

Wall-Off and Contain

176
Q

What are the General Features of Acute inflammation

A

Early onset (secs –mins)
Short duration (mins – days)
Involves fluid exudation (oedema) & neutrophil emigration
May result in resolution or organisation

177
Q

Define Resolution

A

Healing without scarring, restoration of structure and function
Possible following acute inflammation
Not possible in permanent cells
Depends on tissue type, extent of injury, presence of factors that can impair repair - infection, nutrition, etc.

178
Q

Define organisation

A

Healing by scarring/fibrosis
Inevitable following chronic inflammation
Possible following acute inflammation, depends on tissue type, extent of injury, presence of factors that can impair repair - infection, nutrition, etc.

179
Q

What are the outcomes of Acute inflammation

A
  1. Resolution (Healing no scar)
  2. Organisation (Healing with scar tissue)
  3. Chronic Inflammation - Worst Case Scenario
180
Q

What is the scar tissue made up of?

A

Prior to maturation, scar tissue is composed of granulation tissue
Granulation tissue:
- Macrophages
- Fibroblasts/Myofibroblasts
- Angiogenesis
Mature scar is made up of collagen fibre proteins

181
Q

What happens to collagen over time?

A

It contracts

182
Q

What does each component of granulation tissue provide?

A
  1. Macrophages - Remove any debris
  2. Fibroblasts - secrete collagen
  3. Angiogenesis - provides oxygen and nutrients
183
Q

What happens after maturation of scar tissue?

A

Fibroblasts and macrophages leave, the vessels die by apoptosis leaving an acellular collagen scar that will contract over time

184
Q

What does scarring do?

A

Functionless - just a filler to a gap where tissue has been lost
Distortion of surrounding tissue due to contraction

185
Q

Where is scarring good and bad?

A

Positive:
- Heart, small area on the skin

Negative:

  • Where a burn is located
  • Lungs (Alveoli)
  • Kidney (Tubule)
186
Q

The outcome of acute inflammation depends upon?

A

Cell/Tissue Type

Type of Injury

187
Q

What increase the chance of organisation?

A

Fibrinous Exudate

188
Q

What is fibrinous exudate?

A

Fluid with a high fibrin content which denotes greater permeability and the presence of pro-coagulative factors. It frequently occurs in linings and may be removed by fibrolysis and phagocytosis. Otherwise it may lead to the ingrowth of granulation tissue and scarring

189
Q

What is an Ulcer?

A

A lesion or ‘sore’ on a body surface like the skin or mucous membranes
Where necrotic tissue has been eroded and can be slough off and removed from the body

190
Q

What is an abscesses?

A

An Area of necrosis in a solid organ that is trapped in the body walls of the entire area with granulation tissue
If removed = cystic space
Not removed = Chronically inflammed

191
Q

Features of Chronic Inflammation?

A
  • Later onset (days)
  • Longer duration (weeks- years)
  • Involves lymphocytes & macrophages
  • Involves further injury & repeated attempts to repair
  • Always results in organisation
192
Q

Outcomes of Chronic Inflammation

A

Unresolved Acute Inflammation
Repeated Acute Injuries and inflammation
Special Cases where the immune system targets the body

193
Q

Components of Chronic Inflammation

A
  1. Continued injury/necrosis
  2. Repeated attempts at repair
    - Granulation tissue
    - —–1 Macrophages
    - —–2 Fibroblasts laying down collagen
    - —–3 angiogenesis
    - Proliferating Parenchymal cells
  3. Lymphocytes
    - T cells
    - B cells –> Plasma Cells –> Antibodies
194
Q

What are Lymphocytes?

A

Part of the acquired immune system
Contains:
- T cells
- B cells –> Plasma Cells –> Antibodies
Feature in chronic inflammation where the immune system is causing problems
- Autoimmune disorders
- Hypersensitivity disorders

195
Q

Complications of Chronic Inflammation?

A

Involves continued injury, inflammation and repeated attempts at repair
Healing inevitably by organisation

196
Q

What are the roles of the Immune System?

A

Defense against infections
Defence against tumours
Recognition of foreign proteins and tissues
Recognition of other foreign substances

197
Q

What are four parts of the immune system?

A
  1. Non-specific INNATE
  2. Specific response (slower) ADAPTIVE
  3. Non-specific reinforcement INNATE
  4. Memory ADAPTIVE
198
Q

Describe the Adaptive immune response:

A

Acquired Immunity

Involves:
- Antigen processing and presentation by macrophages

Leads to either:

  • Cell mediated response
  • Humoral (antibody) response
  • Immunologic memory

Characteristics of Adaptive Immunity:

  • Identification/determination of ‘self’ and ‘non-self’
  • Specificity (and diversity)
  • Memory
199
Q

What is a Type 1 (immediate) Hypersensitivity?

A

Overreaction to an antigen

Prototypic disorders:

  • Anaphylaxis
  • Allergies
  • Atopic asthma

Pathologic lesions:

  • Vascular dilation leading to oedema
  • Smooth muscle contraction
  • Mucous production
  • Tissue damage
  • Inflammation
200
Q

What is a Type 2 (Antibody-mediated) hypersensitivity?

A

Antibody that targets proteins for destruction

Prototypic Disorder:

  • Autoimmune hemolytic anemia
  • Goodpasture syndrome

Pathologic lesions:

  • Phagocytosis & cell lysis leading to Inflammation
  • Functional impairment without cell injury
201
Q

What is a Type 3 (Immune Complex-mediated) Hypersensitivity?

A

Prototypic Disorder:

  • Systemic lupus erythematosus
  • Some glomerulonephritis

Pathologic lesions:

  • Inflammation
  • Necrotizing vasculitis (fibrinoid necrosis)
202
Q

What is a Type 4 (cell-mediated) hypersensitivity?

A

Sensitised T Lymphocytes are the cause of the cellular and tissue injury
Induce lesions that are part of the immediate hypersensitivity reactions and are not considered a form of type 4 hypersensitivity.

Prototypic Disorder:

  • Multiple sclerosis
  • Type I diabetes
  • Rheumatoid arthritis
  • Tuberculosis

Pathologic lesions:

  • Cell destruction
  • Granuloma formation
203
Q

Order of blood flow in the circulatory system?

A

Right Atria - Right Ventricle - Lungs - Left Atria - Left Ventricle - Large Artery - Medium Artery - Small Artery - Capillary - Venule - Vein - Right Atria

204
Q

What is a Capillary?

A

1 cell think cell where gas exchange occurs

205
Q

In what direction do arteries travel?

A

Away from the heart

206
Q

In what direction to veins travel?

A

Towards the heart

207
Q

Which side of the heart if more powerful?

A

Left Side

208
Q

What is the major artery?

A

The Aorta

209
Q

Where does the Aorta go?

A

Comes out of the left ventricle and goes down wards through the thoracic chest and abdomen

210
Q

Where is the INNER ENDOthelial Lining?

A

Both artery and vein

211
Q

Arterial vs Venous

A

Arterial:

  • Smaller Lumen
  • Higher pressure
  • Thicker Muscle Layer

Venous:

  • Largen Lumen
  • Smaller Wall thickness and muscle layer
212
Q

What are the layers of the capillary?

A

Endothelial Lining and Connective Tissue

Produces anti-coagulative substances that encourage vessels to stay open and prevent clotting

213
Q

Structure of the Artery

A

Suppose to be able to push large amounts of blood to the entire body
Requires large contractions from the heart to be able to reach everywhere in the body
Has an elastic layer to hold large volumes of blood in between each heart contraction by expanding the artery
HIGH PRESSURE

214
Q

Stucture of the Vein

A

Supposed to be able to dilate and store blood
Requires skeletal muscle contraction to squish the vein closed thus pushing blood back to the heart against gravity
When muscles relax, the valves in the venous system stop backflow.
LOW PRESSURE

215
Q

What is the volume of blood?

A 
60% systemic veins and venules
15% in systemic arteries and arterioles
12% in Pulmonary blood vessels
8% Heart
5% Capillaries
216
Q

Vasodilation vs Vasoconstriction

A 
Smooth Muscle can be modified
Vasoconstriction:
- Contracts
- Increase in blood pressure
- Too High? Systemic Hypertension

Vasodilation:

  • Dilates and relaxes
  • Decrease in blood pressure and hypotension
217
Q

What are Intrinsic Mechanisms?

A

Autoregulation
Metabolic or myogenic controls
Distribute blood flow to individual organs and tissues as needed

218
Q

What are extrinsic mechanisms?

A

Neuronal or hormonal controls
Maintain mean arterial pressure (MAP)
Redistribute blood during exercise and thermoregulation

219
Q

What does the renal system do

A

Formation of urine - removal of wastes
Regulates plasma ions (NA, Cl, PO4, K, Ca2
Regulates pH (H, HCO3)
Endocrine function - Vitamin D, RAAS, EPO)
Regulation of blood volume
Regulation of blood pressure

220
Q

How does RAAS work?

A

Renin - Angiotensin 2 - Aldosterone System

When the Renal system senses ischemia, Renin is activated and uses ACE to get Angiotensin 2.

Angiotensin 2 can cause potent vasoconstriction and an increase in vascular resistance. It can also increase SNS - Increasing sympathetic tone and heart rate (force of contraction) - increasing vascular resistance.
Angiotensin 2 can trigger ADH increasing thirst and water uptake in DCT thus increasing blood volume

Angiotensin 2 triggers Aldosterone which is a horone released into the adrenal gland to act upon the kidney. It increase Na uptake in DCT, increasing blood volume

RAAS increases blood pressure and hypertension

221
Q

What is ACE

A

Angiotensin Converting Enzyme

222
Q

What is ADH

A

Anti-diuretic hormone

223
Q

What is EPO

A

Erythropoitetin

224
Q

How does EPO work

A

A decrease in oxygen in the blood causing hypoxia is identified by the kidney which releases EPO, increasing bone marrow rbc production

225
Q

What happens if the kidney fails?

A

No EPO is created causing Anaemia

226
Q

What is Haemopoisesis

A

Stem Cells that form cellular components of blood immune cells to inflammation cells

227
Q

How does Anaemia impact Fetus and Adult differently?

A

In a fetus, there are more haemopoesis = more red marrow. When there is anaemia, an increase in red marrow is easier due to its excess

In an adult there are less haemopoiesis in red marrow

228
Q

Define Anaemia:

A

A decreased number or quality of red blood cells

  • Excessive loss or RBC’s
  • Reduced Synthesis (decreases EPO, dietry deficiency of iron, vitamin B12 or folic acid
  • Increased Destruction
229
Q

Symptoms of Anaemia:

A 
Weak
Lethargic
Dizzy
Insomnia
Sad
Depressed
Confused
Breath shortness
Pale Gums
Eyelid Linings
Tachycardia and Arrhythmia
230
Q

What are the primary lymphoid organs?

A

Bone Marrow

Thymus

231
Q

What are secondary lymphoid organs?

A

Spleen
Lymph Node
Lymphoid tissues of the Alimentary Tract and Respiratory Tract

232
Q

What happens in lymph nodes?

A

Physical filtration of lymph fluid causing a removal of any particulate matter and bacteria
The cortex contains primary lymphoid follicles

233
Q

What are lymphoid follicles?

A

Are sites of B lymphocytes storage and proliferation
Includes naive lymphocytes and memory cells
Contain Germinal centers

234
Q

What are Germinal Centres?

A

Contain proliferating lymphocytes
- Antigenic stimulation –> Plasmablasts –> Proplasmocytes
Proplasmocytes move to periphery of node and mature into plasma cells (Secrete antibody)

235
Q

What happens in the spleen?

A

Filters circulating blood
Immunological response against blood borne antigens
Removal of damaged and old red cells
- B lymphocytes around arteriole
- T lymphocytes in marginal zone
- Antigen Presenting cells for immune attack

236
Q

What are the functions of the liver?

A

Digestion: Production of bile salts (from cholesterol) used in the digestion of fats
Metabolism: Carbohydrates, fats, proteins, vitamins, bilirubin, toxins
Storage of Vitamins
Metabolism of Bilirubin
Excretion of substances: Bilirubin, drugs, etc.

237
Q

Role of Metabolism?

A

Synthesis of Cholesterol, Urea
Synthesis of lipoproteins, proteins
Glucongeogenesis, glycogenesis
Detoxification

238
Q

What is the portal Triade.

A

Located on the corners of the liver lobule
Drains bile duct through
Blood supplying and transportation for metabolism
Venous and Artery enter at the same site

239
Q

How does blood drainage in liver work?

A

Blood supply arrives together from all other organs and systems through the portal tract, mix down leaky sinusoids and drain into the central vein

The central veins comes together and forms the hepatic veins and into the inferior vena cava

240
Q

Pathways to Systemic Odema:

A

Heart Failure - Increase Capillary hydrostatic pressure - Oedema

Heart Failure - Decrease Renal blood flow - Activation of RAAS - Retention of NA and H2O - increase in blood volume - Oedema

Renal Failure - Retention of NA and H2O - increase in blood volume - Oedema

Malnutrition, Decrease in hepatic Synthesis, Nephrotic syndrome - Decrease in plasma albumin - decrease in plasma osmotic pressure - oedema

241
Q

Consequences of Haemorrhages?

A

Determined by: Site, Amount Lost, Speed of Loss
Healthy adults can quickly lose >20% at a slower rate, without serious consequences
Hypovolemic shock
Iron Deficiency Anaemia

242
Q

What happens in a Haemorrhage?

A

Accumulation of blood causing a haematoma

243
Q

What is a haematoma?

A

“bruise”
Small Haematomas = Petechiae, pupura
Large Subcutaneous haematomas = Ecchymoses

244
Q

What are the signs of shock?

A

Low peripheral blood flow
Escessive symphathetic stimulation
Thirst, altered skin temperature, decreased Blood pressure, increased heart rate, decreased venous pressure, decreased urine output
Decreased cellular perfusion, increased lactic acid, Death

245
Q

Define Thrombus:

A

Blood clot that is attached to the wall of a vessel or the heart

246
Q

Define Embolus:

A

Undissolved mass travelling in the blood

247
Q

Define Aneurysm:

A

An ABNORMAL, LOCALISED, DILATION of an artery or ventricle

248
Q

What causes an infarction?

A

Haemorrhage or Ischaemia
1- Blcokage in arterial system - Ischaemia - necrosis
2- Blockage in venous system - congestion of poorly oxygentated blood - Haemorrhage - Necrosis

249
Q

What is the Normal haemostatic Process:

A

The maintenance of fluid blood and the formation of a haemostatic clot in response to injury
Naturally produces anti-coagulents

250
Q

What are the three components of normal haemostatic process?

A
  1. Vascular wall, endothelium
  2. Platelets
  3. Coagulation Cascade

CSB520 (1 decks)

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