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
What are Oxidative Enzymes?
A Bi-product of ATP that prevent the mitochondria from stealing electrons and damaging the lipid
26
Lysosomes? Types?
``` Waste Disposal Membrane-Bound Digestive Organelles Primary Lysosomes Secondary Lysosomes: - Heterophagosomes - Autophagosomes ```
27
How does the cell membrane work with Lysosomes
It fuses with a lysosome containting acid and breaks down constituents, thus removing waste
28
What is Autophagy? How does it work?
Self Eating - Nutrient Depletion - The cells shrinks itself by eating a part of itself Reduction in cell Size
29
Mitochondria and Autophagy
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.
30
Define Physiology:
Scientific Study of the function of living things
31
Define Pathology:
Scientific Study of Disease
32
Define Active:
Requiring Energy
33
Define Passive:
Does not require energy
34
Define Aerobic:
Done with oxygen
35
Define Anaerobic:
Done without Oxygen
36
Define Hypoxia:
Lack of Oxygen
37
Define Ischaemia:
Lack of Blood Supply - "Distruption"
38
Define Reperfusion:
Restoration of blood following a period of Ischaemia
39
Define Acute:
Sudden Onset | Sudden Severe
40
Define Chronic:
Long Duration of Severeness
41
What can cause Cell Stress/Injury:
Mutation: Tumour, impaired Function Cell Death: Apoptosis, Necrosis Adaptation: Autophagy, Hypertrophy, Hyperplasia, Metaplasia
42
How does cell stress occur? Flow Chart...
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.
43
What does Stress lead to?
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
44
Define Apoptosis:
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
45
Define Necrosis:
Sudden Death
46
Negatives with Necrosis
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
47
Define Infarction:
Area of Necrotic Tissue
48
Physiological jobs of Apoptosis:
1. Embyronic Development 2. Tissue homeostasis 3. Removal of redundant cells 4. Crucial for immune function 5. Immune-mediated Killing
49
Pathological jobs of Apoptosis:
1. Pathological Atrophy 2. Transplant Rejection 3. Autoimmune Diseases 4. Some infections 5. Anti-cancer treatment (Targets dividing cells)
50
Apoptosis VS Necrosis?
- 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
51
What causes Adaptation?
Increased Workload or demand | Altered Environment
52
What is Tissue Atrophy
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
53
Mitochondria and Ageing
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
54
What are Free Radicals?
Highly reactive elements that can kill the mitochondria and cause damage to cells
55
What happens to the mitochondria usually once it is damaged by free radicals? What about with ageing?
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
56
What effect does ageing have on cells and organs?
A decreased ability to undergo Autophagy - Cells atrophy with age
57
Healthy Cell - Cellular response to stress (Low, Moderate and Sudden Severe Stress)
Healthy Cell --> Adapt Autophagy --> Apoptosis --> Necrosis
58
Old Cell - Cellular response to stress (Low, Moderate and Sudden Severe Stress)
Old Cell --> Apoptosis --> Necrosis
59
Physiological and Pathological examples of Tissue Atrophy
Physiological: INVOLUTION (Shrinkage of tissue when inactive) Pathological: GRADUAL DECREASE IN CELL SIZE AND NUMBER
60
Atrophy vs Infarction
``` 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 ```
61
What is Metaplasia?
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
62
Define Hyperplasia:
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))
63
Define Hypertrophy:
Increase in cell size -- Enlarged Organ
64
Connective Tissue Type:
``` Myocytes - Muscle Cells Fibroblasts Collagen Fat Endothelium (lining of blood vessels) Cartilage (Chondrocytes) Bone (Osteoblasts, Osteocytes) ```
65
Are Skeletal Muscle fibers permanent?
Yes, but they are able to repair not replaced ALSO: - Contain possible 100s of nuclei in each cell
66
Are Cardiac Myocytes Permanent?
Yes, and there is no repair ALSO: - Individual cells with single, central nuclei
67
Are smooth Muscle permantent?
No, they are stable cells but can divide when necessary
68
What are Fibroblasts?
Stable cells secreting collagen
69
What is Collagen
A long stringy contractible protein - Stable cell
70
What is fat?
Adipocytes - large cells with a cytoplasm full of fat | Nucleus against the edge
71
Are the endothelium, cartilage and bone permanent cells?
No they are stable cells
72
Function of the Epithelium:
``` Mechanical Stress Chemical Stress Secretion - Lubrication, Digestion, Excretion Absorption Transport ```
73
What are Glandular Epithelial Cells?
Secretory cells Endocrine - Secrete into blood acting on receptor in distant site Exocrine - Secretion into lumes or duct
74
Stratified Squamous Epithelium:
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
75
Simple Cuboidal Epithelium:
``` Tall and wide Lines protected surfaces: - Exocrine glandular ducts - Collecting tubules of the kidney - Outer surface of ovary Labile or Stable cells ```
76
Simple Columnar Epithelium:
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
77
Pseudo Stratified:
Located in upper respiratory tract and male reproductive system Appears as stratified but it is simple single layer Stable Cells
78
Transitional Epithelium:
Restricted to Urinary System - Renal, Calyxes, Ureters, Bladder and Urethra Allow stretch and retraction that look columna when relaxed but cuboidal when stretched
79
Stratified Cuboidal:
Lines mammary glands, part of the cohchlea, germ cells of the seminiferous tubules and granulosa cells of the ovarian follicles
80
Straified Cuboidal/Columnar:
Rare | Some large ducts are lines by columnar on top of cuboidal
81
Other Tissues:
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
82
Define tumour:
Denotes Swelling
83
Define Benign Tumour
Friendly, causes no harm
84
Define Malignant Tumour
Potentially Fatal | Cancer
85
Can Benign Tumours be cancers?
NO
86
How do mutations occur?
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
87
What happens to cells if there is no adaption or it fails to adapt?
Dysplasia
88
What is Dysplasia?
A pre-cancerous exchange Usually the immune system destroys these, but it can accumulate with age The Genotype and phenotype are abnormal
89
What are Mutagens?
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
90
What causes mutagens?
``` Exposure to carcinogens UV Alcohol Smoking Obesity Genetics Viruses Some Chronic Inflammatory conditions - Not necessary but can happen ```
91
What are four classes of normal regulatory genes that are principle targets of genetic damage?
1- Growth promoting onoco-genes 2- Growth Inhibiting Tumour Suppressing genes 3- Genes that regulate Apoptosis 4- DNA repair genes
92
What is the molecular basis of cancer? "The essential alterations for malignant transformation?"
- 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
93
Define Self-sufficiency in growth signals
Proliferation without any external stimuli
94
Define Insensitivity to growth-inhibitory signals
Ignore signals sent out by sells to stop growth
95
Define Evasion of Apoptosis
When DNA damage occurs, the cells is mutated enough that the apoptopic pathway has been turned off, and cells arent removed
96
Define Defects in DNA repair
DNA doesnt scan cells for mutations or mistakes when formed, mutations accumulate
97
Define Limitless replicative potential
Immortal, continuous division of cells with genetic errors
98
Define Sustained Angiogenesis
Formation of new blood vessels to support mutation Benign - Neat Blood vessel formation Malignant - Messy and out of order blood vessel formation
99
Define Ability to invade and metastasize
Mutated Cells can pass the basement membrane and enter blood vessel and migrate to a different site to invade and mutate more cells
100
Define Predilection for glycolysis even in the presence of oxygen
Cancer Cells choose not to us oxygen but rather use glucose | Aerobic glycolysis - Warburg Effect
101
What is a cancer cell called when it hasnt passed the basement membrane
Carcinoma in-situ
102
How does a cell accumulate mutations?
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
Benign VS Malignant
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
3 routes of metastasis?
1- Blood (haematogenous) 2- Lymphatics (vessels & Nodes) 3- Direct Seeding (through/within body cavities)
105
What is the most common site of metastatic neoplasms?
Will try to travel through the capillary bed all the way to the secondary location Secondaries: Lung then Liver
106
What is the nomenclature of BENIGN connective tissue called?
``` Fibroma - Fibroblasts Leiomyoma - Smooth Muscle Chondroma - Cartilage Osteoma - Bone Lipoma -Fat Haemangioma - Endothelial lining of blood vessels ```
107
What is a MALIGNANT tumour derived from connective tissue?
SARCOMA Suffix "sarc" = Malignant from connective tissue origin SUPER RARE - Less than 10% for these
108
Nomenclature of epithelial BENIGN tumours?
Papilloma - Finger like projections Adenoma - Glandular cells Cystadenoma - Fluid-filled sac
109
What is a MALIGNANT tumour derived from epithelial tissue called?
CARCINOMA suffix "Carc" - Malignant and Epithelial cell of origin More then 90% of cancer - Proliferation and Stress
110
What type of tumour do other tissues form?
Malignant tumours
111
What is a meningioma?
It is a benign tumour located in the brain and can kill
112
What is a Mature Ovarian Teretoma?
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
What is a Testicular Tumour?
An immature Teratoma | Seminoma
114
Other types of Maligant tumours?
``` Melanoma Leukaemia Lymphoma Mesothelioma Glioma Testicular Tumour Blastoma ```
115
What is a Blastoma
Never a normal cell to begin with - during embryo genesis it got mutated.
116
Different types of pathogenesis:
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
What is Melanoma?
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
Pathogenesis of Melanoma?
Normal Cell - Multiple mutations - Cancer (NOT BENIGN)
119
What is Mesothelioma?
``` Very Aggressive Very rare Due to radiation exposure Asbestos On pleural lining CARCINOGENS can cause ```
120
Pathogenesis of Mesothelioma?
Normal Cell - Multiple mutations - Cancer (NOT BENIGN)
121
Pathogenesis of Ovarian Teratoma and Leiomyoma?
Normal Cell - Multiple mutations - Benign Tumour
122
Pathogenesis of Colon Cancer?
Normal Cell - Multiple mutations - Benign Tumour - Further mutations - Cancer (NOT STABLE)
123
Pathogenesis of Lung Cancer?
Normal Cell - Sustained Stress- Metaplasia - Multiple Mutations - Dysplasia - Further Mutations - Cancer Stress: Carcinogen exposure
124
Pathogenesis for female reproductive cancer? How does it occur?
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
Grading VS Staging:
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
Can Cancer be cured?
Many 'early' caught cancers can be however, 30% of patients have metastases at diagnosis 5 year survival rate Cure or remission (partial/total)
127
Signs and Symptoms of Cancer?
Fat and Muscle Loss Paraneoplastic Syndrome Horomone, blood and mucous changes
128
Treatments of Cancer?
``` Surgery Radiotherapy Chemotherapy Hormone therapy Immunotherapy Hyperthermia ```
129
Treatment affects on host?
Healthy Cells lost - epithelial, immune Mutation in health cells - Mesothelial, Lymphoid Scars, Radiation Burns
130
Types of micro-organisms?
``` Parasites Yeast & Fungi Bacteria Viruses Prions ```
131
What is an Innate Defence system?
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
What is an Acquired Defence System?
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
Innate vs Acquired?
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
What is the function of a T Cell?
Activation of B cells and cytotoxic T cells | Travel to site and bind to the antigen
135
What is the function of a B Cell?
Matures into a plasma cells and produces antibodies which are released into the blood and bind to the antigen Signal Destruction
136
What do the clinical manifestations of infections depend upon?
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
Define Virulence
The ability of power of a microorganism to cause disease Low? No destruction unless immune compromised
138
What are Virulence Mechanisms?
Factors inherent to the organism, encoded at the molecular or gene level Helps establish the infection causing the disease
139
What do these Virulence mechanisms involve?
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
What are Sterile body sites?
Areas with NO microorganisms: - Brain and CSF - Blood - Bone and Marrow - Lower respiratory tract - Upper urogenital - Male and female reproductive system - Stomach
141
What are Non-Sterile body sites?
Areas with microorganisms: - Skin - GIT - Upper Respiratory - Oral Cavity and Larynx - Lower urogenital - Female Reproductive System (Ectocervix and vagina should have microorganisms)
142
What are Leukocytes?
White blood Cells
143
Cellular Components of Leukocytes:
Granulocytes and Agranulocyes
144
What are Granulocytes?
``` Destroy large bacteria by throwing chemical substances at microorganisms. Release granules Involve: - Neutrophils - phagocytes - Eosinophils - Basophils ```
145
What are Aganulocytes?
Involve: - Lymphcytes - Monocytes
146
What happens to Monocytes when they mature?
When a monocytes is activated and calledupon to a specific site, it matures and becomes a macrophage
147
Define Macrophage:
A immune cells that eats large cells that are dead | Has a long life span
148
Define Interstitial Fluid:
Fluid between cells
149
Define Oedema:
Increase in Interstitial flue causing a fluid build up in cavities and tissues
150
High-protein Oedema Vs Low Protein Oedema:
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
Define Hyperaemia:
The Increase in blood flow to an area Occurs actively Vasodilation and increase in permeability causing oedema
152
How is hyperaemia impacted during acute inflammation?
Chemical mediators are released and induce mudcle in vessel to relax - causing it to become engorged in blood
153
Define Congestion:
Increase and accumulation in blood flow Occurs passively Usually not in arterial circuit but in venous circuit
154
What happens if the left side of the heart is congested?
Lungs become congested
155
What happens if the right side of the heart is congested?
Whole body in the venous system becomes congested
156
Define Exudate:
Inflammatory extra vascular fluid with high protein - High-protein Oedema
157
Define Transudate:
Extravascular fluid with low protein concentration - Low-protein Oedema usually not caused by inflammation but by other things
158
Define Pus:
Purulent inflammatory exudate that is high in neutrophils, cell debris and sometimes pyogenic organisms
159
How does Transudate form:
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
How does Exudate form:
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
Define inflammation:
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
Types of inflammation:
Acute and Chronic
163
Define Acute inflammation:
The start of repair although it can lead to further injury
164
Nomenclature of inflammation
Suffix - "itis" - DermatITIS - PancreatITIS - MeningITIS - EncephalITIS - BronchITIS - TonsillITIS - GastrITIS - HepatITIS - NephrITIS
165
What are the indicators of Acute Inflammation? How are they caused?
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
Define Chemotaxis:
The movement or locomotion according to a chemical gradient - Similar to metastasis
167
Define Chemokine:
Agent that induces chemotaxis
168
Define cytokine:
Hormone of the immune system
169
What is the vascular response to acute inflammation?
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
Cellular components of acute inflammation
Neutrophil | Monocyte which matures into a macrophage
171
What is extravasion?
Requires and intact vasculature 1. Margination 2. Rolling 3. Adhesion 4. Diapedesis 5. Migration
172
What is Phagocytosis?
Taking up of dead tissue 1. Recognition and attachment 2. Engulfment 3. Killing and Degredation
173
Aims of acute inflammation?
Dilute, Destroy and Clean up
174
If a stimulus was Necrosis and infection, what is the response?
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
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Aims of Chronic Inflammation?
Wall-Off and Contain
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What are the General Features of Acute inflammation
Early onset (secs –mins) Short duration (mins – days) Involves fluid exudation (oedema) & neutrophil emigration May result in resolution or organisation
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Define Resolution
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.
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Define organisation
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.
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What are the outcomes of Acute inflammation
1. Resolution (Healing no scar) 2. Organisation (Healing with scar tissue) 3. Chronic Inflammation - Worst Case Scenario
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What is the scar tissue made up of?
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
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What happens to collagen over time?
It contracts
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What does each component of granulation tissue provide?
1. Macrophages - Remove any debris 2. Fibroblasts - secrete collagen 3. Angiogenesis - provides oxygen and nutrients
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What happens after maturation of scar tissue?
Fibroblasts and macrophages leave, the vessels die by apoptosis leaving an acellular collagen scar that will contract over time
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What does scarring do?
Functionless - just a filler to a gap where tissue has been lost Distortion of surrounding tissue due to contraction
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Where is scarring good and bad?
Positive: - Heart, small area on the skin Negative: - Where a burn is located - Lungs (Alveoli) - Kidney (Tubule)
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The outcome of acute inflammation depends upon?
Cell/Tissue Type | Type of Injury
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What increase the chance of organisation?
Fibrinous Exudate
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What is fibrinous exudate?
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
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What is an Ulcer?
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
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What is an abscesses?
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
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Features of Chronic Inflammation?
- Later onset (days) - Longer duration (weeks- years) - Involves lymphocytes & macrophages - Involves further injury & repeated attempts to repair - Always results in organisation
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Outcomes of Chronic Inflammation
Unresolved Acute Inflammation Repeated Acute Injuries and inflammation Special Cases where the immune system targets the body
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Components of Chronic Inflammation
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
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What are Lymphocytes?
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
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Complications of Chronic Inflammation?
Involves continued injury, inflammation and repeated attempts at repair Healing inevitably by organisation
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What are the roles of the Immune System?
Defense against infections Defence against tumours Recognition of foreign proteins and tissues Recognition of other foreign substances
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What are four parts of the immune system?
1. Non-specific INNATE 2. Specific response (slower) ADAPTIVE 3. Non-specific reinforcement INNATE 4. Memory ADAPTIVE
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Describe the Adaptive immune response:
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
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What is a Type 1 (immediate) Hypersensitivity?
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
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What is a Type 2 (Antibody-mediated) hypersensitivity?
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
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What is a Type 3 (Immune Complex-mediated) Hypersensitivity?
Prototypic Disorder: - Systemic lupus erythematosus - Some glomerulonephritis Pathologic lesions: - Inflammation - Necrotizing vasculitis (fibrinoid necrosis)
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What is a Type 4 (cell-mediated) hypersensitivity?
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
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Order of blood flow in the circulatory system?
Right Atria - Right Ventricle - Lungs - Left Atria - Left Ventricle - Large Artery - Medium Artery - Small Artery - Capillary - Venule - Vein - Right Atria
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What is a Capillary?
1 cell think cell where gas exchange occurs
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In what direction do arteries travel?
Away from the heart
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In what direction to veins travel?
Towards the heart
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Which side of the heart if more powerful?
Left Side
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What is the major artery?
The Aorta
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Where does the Aorta go?
Comes out of the left ventricle and goes down wards through the thoracic chest and abdomen
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Where is the INNER ENDOthelial Lining?
Both artery and vein
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Arterial vs Venous
Arterial: - Smaller Lumen - Higher pressure - Thicker Muscle Layer Venous: - Largen Lumen - Smaller Wall thickness and muscle layer
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What are the layers of the capillary?
Endothelial Lining and Connective Tissue | Produces anti-coagulative substances that encourage vessels to stay open and prevent clotting
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Structure of the Artery
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
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Stucture of the Vein
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
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What is the volume of blood?
``` 60% systemic veins and venules 15% in systemic arteries and arterioles 12% in Pulmonary blood vessels 8% Heart 5% Capillaries ```
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Vasodilation vs Vasoconstriction
``` 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
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What are Intrinsic Mechanisms?
Autoregulation Metabolic or myogenic controls Distribute blood flow to individual organs and tissues as needed
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What are extrinsic mechanisms?
Neuronal or hormonal controls Maintain mean arterial pressure (MAP) Redistribute blood during exercise and thermoregulation
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What does the renal system do
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
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How does RAAS work?
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
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What is ACE
Angiotensin Converting Enzyme
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What is ADH
Anti-diuretic hormone
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What is EPO
Erythropoitetin
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How does EPO work
A decrease in oxygen in the blood causing hypoxia is identified by the kidney which releases EPO, increasing bone marrow rbc production
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What happens if the kidney fails?
No EPO is created causing Anaemia
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What is Haemopoisesis
Stem Cells that form cellular components of blood immune cells to inflammation cells
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How does Anaemia impact Fetus and Adult differently?
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
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Define Anaemia:
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
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Symptoms of Anaemia:
``` Weak Lethargic Dizzy Insomnia Sad Depressed Confused Breath shortness Pale Gums Eyelid Linings Tachycardia and Arrhythmia ```
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What are the primary lymphoid organs?
Bone Marrow | Thymus
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What are secondary lymphoid organs?
Spleen Lymph Node Lymphoid tissues of the Alimentary Tract and Respiratory Tract
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What happens in lymph nodes?
Physical filtration of lymph fluid causing a removal of any particulate matter and bacteria The cortex contains primary lymphoid follicles
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What are lymphoid follicles?
Are sites of B lymphocytes storage and proliferation Includes naive lymphocytes and memory cells Contain Germinal centers
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What are Germinal Centres?
Contain proliferating lymphocytes - Antigenic stimulation --> Plasmablasts --> Proplasmocytes Proplasmocytes move to periphery of node and mature into plasma cells (Secrete antibody)
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What happens in the spleen?
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
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What are the functions of the liver?
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.
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Role of Metabolism?
Synthesis of Cholesterol, Urea Synthesis of lipoproteins, proteins Glucongeogenesis, glycogenesis Detoxification
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What is the portal Triade.
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
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How does blood drainage in liver work?
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
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Pathways to Systemic Odema:
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
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Consequences of Haemorrhages?
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
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What happens in a Haemorrhage?
Accumulation of blood causing a haematoma
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What is a haematoma?
"bruise" Small Haematomas = Petechiae, pupura Large Subcutaneous haematomas = Ecchymoses
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What are the signs of shock?
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
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Define Thrombus:
Blood clot that is attached to the wall of a vessel or the heart
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Define Embolus:
Undissolved mass travelling in the blood
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Define Aneurysm:
An ABNORMAL, LOCALISED, DILATION of an artery or ventricle
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What causes an infarction?
Haemorrhage or Ischaemia 1- Blcokage in arterial system - Ischaemia - necrosis 2- Blockage in venous system - congestion of poorly oxygentated blood - Haemorrhage - Necrosis
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What is the Normal haemostatic Process:
The maintenance of fluid blood and the formation of a haemostatic clot in response to injury Naturally produces anti-coagulents
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What are the three components of normal haemostatic process?
1. Vascular wall, endothelium 2. Platelets 3. Coagulation Cascade