CSB520 Mid Sem Exam LOI

Epithelial Cells Examples

- glandular (salivary and sweat glands)

- simple squamous = gas/ion exchange (alveoli)

- stratified squamous = external barrier (mouth, anus, skin)

- simple cuboidal = protection (kidney tubules)

- simple columnar = mucus (small intestine)

- pseudostratified = conducting (upper respiratory tract)

- transitional = stretch/retract (urinary)

stratified cuboidal/columnar (mammary glands)

Connective Cells Examples

- myocytes = muscle (skeletal, cardiac, smooth)

- chondrocytes (cartilage)

- endothelium (lining of blood vessels)

- osteoblasts/osteoclasts (bone)

- adipocytes (fat)

- fibroblasts (synthesises collagen)

Other Cells Examples

- mesothelial cells = lines cavities and organs

- melanocytes = melanin forming in skin

- germ cells = embryonic

- lymphocytes

- haemopoietic cells = blood cell precursor

- neutrophils = white blood cells, acute inflammation

- macrophages = detects and destroys pathogens

- Red blood cells = oxygen and nutrient transport

Labile Cells

continuously dividing = epithelial (skin, GIT, reproductive, urinary, lining of exocrine ducts), haemopoietic stem cells

Stable Cells

divide when prompted = epithelial (liver, kidney, lungs, pancreas), smooth muscle cells, fibroblasts, endothelial cells

Permanent Cells

non dividing = cardiac/skeletal myocytes, neurons

Hypertrophy

increase in cell size (reversible)

Hyperplasia

increase in cell number (reversible)

Autophagy

decrease in cell size (reversible)

Metaplasia

change from one normal, well-differentiated cell type to another (reversible)

Apoptosis

programmed cell death (not reversible)

Apoptosis vs Necrosis

Apoptosis = programmed cell death

- active (requires energy)

- pathological and physiological

- does not stimulate inflammation

can occur in single cells

Necrosis = sudden cell death

- passive (no energy)

- pathological

- stimulates inflammation

- kills neighbouring cells

Infarct, how does it occur?

Infarct = area of necrosis

- occurs when cells dies of necrosis, swells to the point of breakage, consequently killing neighbouring cells

When does atrophy vs infarction occur?

Atrophy

- mild, moderate stimulus

- duration (chronic, gradual)

- partial ischaemia

- cells with adaptive capacity

Infarction

- severe stimulus

- duration (acute, sudden)

- complete ischaemia

- cells without adaptive capacity

Effect of ageing on cells and organs

- cells are less likely to divide

- cells are less likely to undergo autophagy = less likely to withstand stress = increase chance of apoptosis and undergo necrosis at lower stress points

- organ shrinkage and loss of functional tissues (organ failure)

Hyperplasia

increase in cell number

Neoplasia

new, abnormal tissue growth

Tumour

swelling caused by abnormal tissue growth

Malignancy

presence of cancerous cells that have the ability to spread

Dysplasia

abnormal, pre-cancerous change, not an adaptation

Angiogenesis

formation of new blood vessels (wound healing, oxygen supply to organs, tumour growth)

Heterogenous

diverse cell population

Homogenous

uniform cell population

Invasive

malignancy spread beyond initial layer of tissue

Encapsulated

confined to an area surrounded by a thin, protective layer of fibrous tissue

Differentiated

mature, specialised cells

Undifferentiated

immature (stem) cells

Metastasis

cancer cells travel from primary site to distant site

Naming of epithelial tumours

Carcinoma (malignant)

- cystadenoarcinoma (secretory glandular growing in cystic pattern)

- papillocarcinoma (epithelial with fingerlike projections)

- adenocarcinoma (normal secretory glandular)

Naming of connective tumours

Sarcoma (malignant)

- leiomyosarcoma (smooth muscle)

- adiposarcoma (adipocytes)

- haemangiosarcoma (endothelial cells)

- osteosarcoma (osteoblasts/osteoclasts)

- chondrosarcoma (chondrocytes)

Naming of 'other' tumours

- leukaemia (haematopoietic cells)

- lymphoma (lymphocytes)

- melanoma (melanocytes)

- mesothelioma (mesothelial cells)

- teratoma (germ cells) = testicular (malignant), ovarian (benign)

Benign vs Malignant

Benign (non cancerous)

- don't metastasise

- encapsulated

- homogeneous

- well differentiated

- generally slowing growing

Malignant (cancerous)

- can metastasise

- infiltrative growing patterns

- heterogeneous

- can undergo due to fast growth causing outgrowth of blood supply

3 main routes of metastasis

1. blood flow - spreads through arteries and veins

2. lymph flow - move through lymph vessels

3. direct seeding - cancer cells detach from primary tumour and float to nearby locations

Common sites for metastasis

- liver (largest visceral organ = large amount of arterial blood, filters blood from GIT)

- lungs (all venous blood returns to them)

- brain/bones (lots of arterial blood)

Pathogenesis of adenocarcinoma and squamous cell carcinoma (most common primary lung cancers)

Adenocarcinoma (smoking)

- metaplasia

- dysplasia

- carcinoma in situ

- invasive carcinoma

Squamous cell carcinoma (mutation)

- hyperplasia

- dysplasia

- carcinoma in situ

- invasive carcinoma

Why are carcinomas most common in adults?

- epithelial cells (labile/stable) = proliferation = mutation

- epithelial cells (first line of defence) = exposure to carcinogens

Hyperaemia

increased blood flow to an area

Oedema

increased fluid in interstitial tissue

Exudate

high protein oedema

Transudate

low protein oedema

Effusion

oedema in a body cavity

Resolution

healing from inflammation without scarring

Organisation

healing from inflammation with scarring, results in loss of functional tissue

Ulcer

area of necrosis on body surface

Abscess

acute inflammation pus

Granulation tissue

immature scar tissue

Leukocyte (WBC)

immune cells produced in bone marrow, defends against infections, pathogens and foreign materials

Phagocyte

specialised leukocyte, engulf/digest pathogens

3 features of acute inflammation

1. hyperaemia

2. oedema (exudate)

3. neutrophils

3 possible outcomes of acute inflammation

1. resolution

2. organisation

3. chronic inflammation

Consequences of healing through organisation

- loss of functional tissue

- collagen scarring (reduces mobility)

3 main components of granulation tissue and their roles

1. macrophages - remove debris

2. fibroblasts - secrete collagen

3. angiogenesis - supply nutrient and oxygen

3 main causes of chronic inflammation

1. unresolved acute (nail in arm doesn't get removed)

2. repeated acute (arm gets repeatedly stabbed)

3. special cases (straight to chronic due to autoimmune disease)

3 features of chronic inflammation

1. ongoing injury

2. repeated attempts of repair

3. presence of lymphocytes

Negative consequences of chronic inflammation

1. inevitably involves more tissue destruction

2. requires healing through organisation = reduced functional tissue

3. increased risk of carcinoma formation

Sterile vs Non-sterile

- Sterile (should not have microorganisms)

- Non sterile (microorganisms present)

Innate vs Adaptive systems

Innate

- first line, fast

- non specific defence, acute inflammation all over

Adaptive

- slow, differentiates

- memory, responds faster to same infection

- tailored to specific targets

Autoimmune disease

sees something normal in the body and decides to attack it

Hypersensitivity

overreaction of the adaptive system to a stimulus/antigen

Immunocompromised

weakened immune system/impaired innate defences

- at risk = people with autoimmune diseases, elderly, chemotherapy patients

Congestion

passive build up of blood, happens in low pressure circuits (veins, pulmonary)

Ischaemia

lack of blood supply

Haemorrhage

damage to blood vessel, internal bleeding

Thrombus

blood clot attached to vein, artery wall or ventricle of heart

Embolus

anything undissolved travelling in blood

Aneurysm

localised abnormal ballooning out or dilation of part of a vessel/ventricle wall

Atheroma

sclerotic plaque which represents an area of chronic inflammation within the wall of an artery

Atherosclerosis

process of atheroma formation

Haematoma

bruise or accumulation of blood constituents in tissue, organ or body cavity

Pulmonary Hypertension

abnormally high pressure in pulmonary arteries

Systemic Hypertension

consistently high blood pressure against the walls of systemic arteries

Stasis

slow, stoppage or pooling of body fluid

Hypercoagulability

increased ability of the blood to coagulate

Superficial vs Deep vein thrombi

Superficial

- doesn't embolize

- prominent signs/symptoms

Deep

- embolizes

- asymptomatic

Risk factors and embolus of DVT

risks = stasis and hypercoagulability

embolism = travels to right side of heart --> lungs --> pulmonary embolus

Risk factors for the development of atherosclerosis

- increasing age

- male

- Aboriginal and Torres Strait Islander descent

- smoking

- diabetes

- systemic hypertension

Kidneys role in systemic hypertension

RAAS system

renin -> angiotensinogen -> angiotensin I -> angiotensin II -> aldosterone

- angiotensin: increased vascular resistance = increased blood pressure

- aldosterone: increased sodium absorption = increased water absorption = increased blood volume = increased blood pressure

Vascular pathologies that atherosclerosis predisposes

1. aneurysm

2. thrombus

3. embolus

Consequences of atherosclerosis in abdominal aorta

- thrombus: partial blockage, decreased blood flow

- ruptured aneurysm: death via hypovolemic shock

- embolus: endangers lower limbs when travelling downwards

Consequences of atherosclerosis in coronary arteries

ischaemia heart disease

Consequences of atherosclerosis in carotid and cerebral arteries

cerebral vascular disease

Constituents of blood

Plasma (55%)

- water (91%)

- proteins (7%)

- ions, nutrients, etc (2%)

Formed elements (45%)

- platelets

- leukocytes (neutrophils, lymphocytes, monocytes)

- erythrocytes

Organs relevant for blood synthesis/maintenance

1. bone marrow - produces RBC/WBC in response to erythropoietin

2. kidney - produces erythropoietin, aldosterone (increases blood volume), angiotensin II (increases blood pressure)

3. liver: synthesises plasma proteins (less protein = less colloidal pressure = more transudate), releases glycogen to correct low blood pressure

4. spleen - filters old/damaged RBC

Systemic arterial circuit

1. flow: left ventricle -> body -> arterioles -> capillaries

2. pressure: high

Pulmonary circuit

1. flow: right ventricle -> lungs -> left atrium

2. pressure: low

Systemic venous circuit

1. flow: capillaries -> veins -> right atrium

2. pressure: very low

Angina vs. Myocardial Infarction

Myocardial infarction (MI)

- loss of blood supply that has been prolonged, causing necrosis

- caused by occlusion of coronary artery

- only medically treated

Angina

- pain associated with ischaemia but blood is restored before any necrosis

- caused by overwork of the heart

- treated through rest

Inflammation and repair of an MI

1. acute inflammation: hyperaemia, increased vascular permeability, neutrophil infiltration to damage, exudate

2. organisation: macrophages eat necrotic tissue -> fibroblasts secrete collage -> angiogenesis sprout -> macrophages/fibroblasts leave -> angiogenesis regresses

Complications of an MI

- scar tissues is weak = increased risk of aneurysm

- functional tissue replaced with collagen = increased risk of thrombi formation due to cells not making anticoagulants

- structurally different = increased risk of arrhythmias and heart failure

Left-sided heart failure

1. forward effect - decreased blood pumped from left ventricle to systemic circuit, RAAS system

2. backward effect - pulmonary congestion = increased hydrostatic pressure = pulmonary oedema, pleural effusion

3. causes - ischaemic heart disease, systemic hypertension

4. symptoms - dyspnea (difficultly breathing when lying down)

Right-sided heart failure

1. forward effect - decreased blood pumped from right ventricle to lungs, RAAS system

2. backward effect - systemic venous congestion = increased hydrostatic pressure = peripheral oedema

3. causes - LSHF, pulmonary hypertension

4. symptoms - swelling of lower limbs, abdominal effusion, distended jugular veins

Endocarditis

1. cause: bacteria and special cases

2. consequences:

- valve stenosis (not opening correctly)

- valve incompetence (not closing correctly) = regurgitation --> left/right/global heart failure

- infectious emboli shed --> infarction/infection in organs

- not treated --> chronic inflammation --> scarring --> valve function lose

Pericarditis

1. cause: infection, autoimmune disease, secondary cancer, uraemia, spread of inflammatory response caused by MI

2. consequences:

- acute: impaired ventricular diastole (decreased cardiac output, chest pain, progress to heart failure)

- chronic: restrictive pericarditis/fusing pericardium to myocardium ( decreased cardiac output, restricts filling and contraction)

Ageing on the cardiovascular system

- fewer functional myocardial cells = increased workload for remaining cells

- hypertrophy overtime

- more collagen = stiffening

- increased chance of atherosclerosis = increased chance of systemic hypertension

- predisposes to calcification of valves = aortic mitral valve disease