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2002MSC Pathophysiology > ETE > Flashcards

ETE Flashcards

1
Q

Neoplasia

A

new growth

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2
Q

Tumour

A

Tumour - swelling / inflammation

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3
Q

Benign

A

– microscopically innocent, localised, non-spread, removable

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4
Q

Malignancy

A

Malignancy – invade adjacent structures, metastasize to distal organs, cure = found early

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5
Q

Anaplasia

A

Anaplasia - lack of differentiation

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6
Q

What is the cause of neoplasia and tumours?

A
  • Non-lethal genetic mutation leading to tumour cells and excessive and unregulated proliferation
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7
Q

Benign and malignant neoplasm characteristics?

A

Benign and malignant neoplasm characteristics?
- Clonal neoplastic cells = parenchyma
- Reactive stroma which growth/evolution is dependant on
- Naming based on parenchymal cells affected

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8
Q
A

How do you name benign neoplasms?
- “-oma” to cell of origin
- Fibrous tissue = fibroma
- Cartilage = chondroma

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9
Q

In Benign neoplasms what are adenomas?

A

In Benign neoplasms what are adenomas?
- Epithelial benign tumour

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10
Q

How do you name malignant neoplasms?

A

How do you name malignant neoplasms?
- If of mesenchymal – add “sarcoma”
o Fibrosarcoma
- If of epithelial origin (any 3 germ layers) – add “carcinoma”
o Epidermis (ectodermal origin)
o Renal tubular cells (mesodermal origin)
o Cells lining intestine (endodermal)

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11
Q

If neoplasm is epithelial original & from stratified squamous epithelium or glandular pattern what’s it called?

A

If neoplasm is epithelial original & from stratified squamous epithelium or glandular pattern what’s it called?
- Squamous cell carcinoma
- Adenocarcinoma

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12
Q
A

If a neoplasm of epithelial origin is tissue origin as well…?
- Bronchogenic squamous cell carcinoma
- Renal cell carcinoma

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13
Q
A

What’s the difference between carcinoma vs. Sarcoma?
- Carcinoma = skin or tissue cells lining internal organs (kidney, liver)
- Sarcoma = grows in body’s connective tissue (fat, blood vessels, nerves, bones, cartilage)

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14
Q

Name 3 characteristics of benign and malignant tumours & germ layers?

A

Name 3 characteristics of benign and malignant tumours & germ layers?
- contain cells from single germ layer
- more than one germ layer = endo, meso, ectoderm = teratoma
o well differentiated = benign teratoma
o poorly differentiated = malignant teratoma

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15
Q

Benign & Malignant Neoplasms – Differentiation / Anaplasia

A

Benign & Malignant Neoplasms – Differentiation / Anaplasia
Benign
- WELL differentiated
- E.g. lipoma – parenchymal cells almost identical to adipocytes
Malignant tumours
- Differentiated or completely Undifferentiated parenchymal cells
- E.g. thyroid adenocarcinoma = normal appearing follicles
- Squamous cell carcinoma = normal squamous epithelial cells

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16
Q

Differentiation/ anaplasia of malignant neoplasms? What does anaplasia do?

A

Differentiation/ anaplasia of malignant neoplasms? What does anaplasia do?
- POORLY differentiated = ANAPLASTIC
- Anaplasia =
o Pleomorphism – varied size, shape
o Abnormal nuclear morphology – abundant chromatin
o Mitoses – cell division (M phase) - proliferative

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17
Q

What does differentiation and anaplasia cause to the body?

A

What does differentiation and anaplasia cause to the body?
Loss of polarity
- Cells grow together
Abnormal nuclear morphology
- Tumour giant cells
Metaplasia
- Replacement of one cell type with another (e.g. oesophageal reflux)

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18
Q

Do well differentiated tumours retain cellular function? And how do we detect glandular hyperplasia?

A

Do well differentiated tumours retain cellular function? And how do we detect glandular hyperplasia?
- YES – poorly differentiated don’t
- E.g. glandular adenomas = increased hormone production
- Cellular products can be measured in blood to detect glandular hyperplasia
o Squamous cell carcinomas elaborate keratin
o Hepatocellular carcinomas secrete bile contents

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19
Q

How long until you can clinically detect a tumour?

A

How long until you can clinically detect a tumour?
- Palpation or x-ray
- 1 gm = 1,000,000,000 cells
- Cell replications = 1, 2, 4, 8, 16, 32, 64, 128, 256
- Assume cell cycle of 3 days = 30 divisions x 3 days each = 90 days
- 10 more divisions = 1 kg
o MAX compatible with LIFE
o 10 divisions x 3 days = 30 days
o Life expectancy 4 months from first mutation

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20
Q
A

If a tumour has been detected at >1gm what does this mean?
- Its completed ¾ of its lifespan
- Often too late – mutations allowing it to metastasis

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21
Q

When should we aim to detect cancer cells?

A

When should we aim to detect cancer cells?
- Earlier stages at <10mg = 24-25 divisions

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22
Q
A

What 3 factors determine tumour growth?
- Doubling time
- Fraction of cells dividing
- Rate of cell death

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23
Q

Define ‘Rates of growth’ + growth fraction (high & low) + senescent?

A

Define ‘Rates of growth’ + growth fraction (high & low) + senescent?
- Tumour cell doubling time is equal or greater than normal cells
- More benign (differentiated) neoplasms = lower growth rate and fraction

  • Growth faction
    o Proportion of cells undergoing division in tumour / number of cells in tumour
    o No. of parenchymal cells dividing¬¬¬__ x 100
    o No. of cells parenchymal in tumour
    o HIGH GROWTH FRACTION = leukemia/ lymphoma, lung cancers
    o LOW GROWTH FRACTION = colon, breast cancers (10%)
  • Senescent
    o Cells that stop dividing, die and exit cell cycle
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24
Q

Define tumour kinetics

A

Define tumour kinetics
- Fast growing tumours = increased cell turnover = increased growth and apoptosis

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25
Q

Why are malignant tumours an exception to growth rate?

A

Why are malignant tumours an exception to growth rate?
- As they progressively slow their growth with maturation
- Affected by hormones/blood supply
- Tumours that spontaneously resolve are extremely rare = untreated = fatal

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26
Q

How does local invasion affect cancer growth?

A

How does local invasion affect cancer growth?
Progressive
- Infiltration within parent organ
- Destruction surrounding tissue
- Poor demarcation
- Rows of cell penetrating margin
- No boundaries = breaks skin
- Resection = lots of healthy tissue removed
- Invasiveness defines benign/malignant tumours

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27
Q

What is metastasis?

A

What is metastasis?
Tumours removed from primary tumour – to secondary organ
Metastatic = malignant
- Cells permeated into vessels, lymphatics, body cavities
- Two malignant cancers rarely metastasise
- 30% patients solid tumours possess mets = poor prognosis

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28
Q

What are the 3 pathways of spread?
1.

A

What are the 3 pathways of spread?
1. Direct seeding of body cavities/surfaces
2. Lymphatic spread
3. Haematogenous spread

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29
Q
A

Describe direct seeding of body cavities/surfaces?
- When malignant neoplasm breaks into open field
- Within peritoneal cavity
- Ovarian cancer – all peritoneal surfaces covered
- Metastasis to liver, vertebrae, colon

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30
Q

Describe lymphatic pathways of spread?

A

Describe lymphatic pathways of spread?
- Most common spreading – carcinomas
- Invade lymphatic vessels, to nodes to follow lymphatic drainage – blood
- E.g. breast cancer – along internal mammary arteries – infra/supraclavicular nodes
- lymph nodes can stop further spread
- symptoms: tumour lump, gland swelling

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31
Q

Describe haematogenous pathway of spread?

A

Describe haematogenous pathway of spread?
- Sarcomas
- Tumour cells come to rest in first capillary bed
- Tumour cells in renal vein move to the lungs -> in the rental artery move to kidney -> in the small intestine move to liver
- Some vascular sites infrequently involved - muscle, spleen due to a phenomenon termed homing

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32
Q

Summary for distinguishing benign/malignant neoplasms

A

Benign - e.g. leiomyoma
- slow growing
- non-inavasive
- well differientiated

Malignant (leiomyosarcoma)
- large
- rapid growth
- necrosis
- metastatic
- poorly differentiated

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33
Q

Where are neoplasms most common in men and women

A

Where are neoplasms most common in men and women
Men: prostate, lung, colorectal
Women: breast, lung, colo-rectal

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34
Q

What are the percentages of death rates in cancer?

A

What are the percentages of death rates in cancer?
- Last 15-20 yrs decreased 18.4% in male top cancers
- Last 10-15 yrs decreased 10.4% in women top cancers

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35
Q
A

What percentage is environmental and genetic factors influencing sporadic cancer?
- 65% environmental
- 26-42% genetic

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36
Q

How many deaths % does obesity and smoking cause?

A

How many deaths % does obesity and smoking cause?
Obesity 14-20%
Smoking – 90% lung

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37
Q

What age are most cancer in and why ?

A

What age are most cancer in and why ?
More than > 55 years
Due to somatic DNA mutation
Decline in immune function

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38
Q

How do cancers genetically develop?

A

How do cancers genetically develop?
- Autosomal dominant inherited cancer syndromes
- Defective DNA repair syndromes
- Familial cancers

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39
Q
A

How do non-hereditary factors cause cancer?
- Develop at sites of chronic inflammation
- Asbestosis, GI inflammation, H. pylori (causes compensatory proliferation, production of ROS)
- Precancerous conditions
o Chronic gastritis, UC

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40
Q

What are key features/pre-recs of cancer development?

A

What are key features/pre-recs of cancer development?
- Non-lethal damage
o DNA mutation via environment or inherited
- Tumours formed by expansion of single damaged cell

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41
Q

What four classes of mutations predisposed to cancer?

A

What four classes of mutations predisposed to cancer?
1. Growth promoting oncogenes
2. Growth inhibiting tumour suppressor genes
3. Genes regulating apoptosis
4. Genes involved in DNA repair

42
Q

What mechanisms of cancer development are there?

A

What mechanisms of cancer development are there?
Carcinogenesis  multistep process
- Tumour cells possess multiple genetic mutations
- Excessive growth, metastasis
- Cells become more malignant
Transformation
Progression
Proliferation of genetically unstable cells 
Tumor cell variants heterogeneity

43
Q

What are the 7 key attributes in tumour malignant transformation?

A

What are the 7 key attributes in tumour malignant transformation?
1. Self-sufficiency in growth signals – oncogene activation
2. Insensitivity to growth inhibition – TGFb, CDKs
3. Evasion of apoptosis – p53 inactivation
4. Limitless replicative potential
5. Sustained angiogenesis
6. Ability to invade/metastasise
7. Defects in DNA repair

44
Q

What are oncogenes?

A

What are oncogenes?
Genes controlling autonomous growth
Created by mutations in proto-oncogenes

45
Q

Describe what RAS oncogenes are?

A

Describe what RAS oncogenes are?
- G protein that binds to guanosine phosphate (GTP)
- Activation of GFRs dissociates GDP from RAS
- When GTP binds to RAS, activation downstream MAPK pathway, floods nucleus with mitogenic stimuli

46
Q

What are the most important cyclins?

A

What are the most important cyclins?
D, E, A, B
Cyclins bind to CDKs, phosphorylate proteins and drive cell cycle
Cyclin D binds CDK4 drives G1

47
Q

Describe cyclins, CDKs and inhibitors role in the cell cycle:

A

Describe cyclins, CDKs and inhibitors role in the cell cycle:
D-CDK4/6, E-CDK2 regulate the G1-S transition by phosphorylation of the RB protein. A-CDK2/1 are active in the S phase. B-CDK1 is essential for the G2-M transition. Two families of CDKIs can block activity of CDKs and progression through cycle – p16, 15, 18, 19 act on C-CDK4/6. P21, 27, 57 can inhibit ALL CDKs.

48
Q

What are the 3 insensitivities to growth inhibition?

A

What are the 3 insensitivities to growth inhibition?
1. Quiescence - Activation temporary cell cycle arrest
2. Senescence – induction permanent cell cycle arrest
3. Apoptosis – triggering cell cycle arrest

49
Q

How does the invasion of apoptosis occur?

A

How does the invasion of apoptosis occur?
- Mutations in genes promote apoptosis = increased cell growth = neoplasia
- Apoptosis = programmed cell death to prevent damaged cell reproducing
- Extrinsic apoptosis
o Fas receptors

50
Q

Invasion of cell apoptosis summary:

A

Invasion of cell apoptosis summary:
Cancer cells evade apoptosis
- Mutation = ↓ Fas
- Gain of function = increased BCL-2 protein
o 85% B cell lymphomas
o Increased BCL-2/BCL-XL. ↓ apoptosis
- ↓p53 activity, ↓BAX, BAK

51
Q

How do cells grow more than >2mm?

A

How do cells grow more than >2mm?
ANGIOGENSIS – vascularisation
Increased angiogenesis = increased vasculogenesis

52
Q

Appearance/ morphology freckle

A

Appearance/ morphology freckle
Appearance
* 1-3mm (small)
* Tan-red
* Light brown macules
o Seen AFTER SUN exposure
Morphology
* Increased pigmentation of basal keratinocytes
* Slightly enlarged (increased synthesis melanin)

53
Q

Appearance/ morphology Lentigo

A

Appearance/ morphology Lentigo
* Common
* Benign localised hyperplasia of melanocytes
* Mucous membrane + skin
* 5-10mm
* Tan brown
* DO NOT darken from UV
* Linear melanocyte hyperplasia above basement membrane

54
Q

Appearance/ morphology Melanocyte Nevus (mole)

A

Appearance/ morphology Melanocyte Nevus (mole)
* < 6mm (small)
* Flat to elevated, round boarders
* Many types
* Acquired nevi common
* Junction + compound
* Pregnancy (more common as hormonal response)
Morphology
* Junctional
* Aggregates/nest of cells along epi/der boarder
* Nuclei rounded
* Compound
* Nests into dermis
* Epidermal nest can dissipate
* More raised than junctional
* Junctional -> compound = maturation
* Deepening of roots, loss of pigment, low tyrosinase, high cholinesterase activity
* Deep maturation - deep neural like cells - melanoma (no maturation) from benign
* Possible transformation of nevi -> melanoma

55
Q

What is the skin composed of?

A

What is the skin composed of?
- Squamous epithelial cells
o Protective keratin protein and cytokines
- Melanocytes
o Epidermis  melanin, protection UV
- Dendritic cells
o Epidermis  Langerhans cells  immune function, migrate to lymph nodes
o Dermis  Dendrocytes

56
Q

What three steps are in the cutaneous immune system?
A.

A

What three steps are in the cutaneous immune system?
A. Non activated
B. Innate
C. Adaptive

57
Q

Define the 3 steps, non activated, innate and adaptive of the cutaneous immune system:

A

Define the 3 steps, non activated, innate and adaptive of the cutaneous immune system:
A. Non activated
a. Absence of inflammation  stationary + transitory immune cells survey ready for response
b. Langerhans cells, dermal dendritic cells, granulocytes and monocytes
B. Innate
a. Response to epithelial injury/ antigen presentation = recruits nonspecific effector cells  neutrophils and eosinophils
b. Inflammation, activated Langerhans cell, cytokines and chemokines  attacked by activated dendric cell + fibroblast and migrate to local lymph node
C. Adaptive
a. When antigen presented recognised by T cells  antigen-specific skin-homing T cells recruited, T cell receptor response
b. Activated langerhans cell, dermal fibroblasts, dendric cells with TCR + CLA T cells recruited to right antigen

58
Q

5 Steps of maturation of non-dysplastic nevi

A

5 Steps of maturation of non-dysplastic nevi
* A - Normal skin - scattered dendritic melanocytes within epi basal cell layer
* B - Junctional nevus
* C - Compound nevus
* D - Dermal nevus
* E - dermal nevus with neurotization (extreme maturation)

59
Q

Describe Dysplastic nevi: precursors, morphology, pathogenesis (5 steps)

A

Describe Dysplastic nevi: precursors, morphology, pathogenesis (5 steps)
Precursors:
- Precursor to melanoma
- Flat, raised, dark pebbly surface
Morphology
- Enlarged and can fuse together
- Nevus cells replace basal membrane
- Enlarged irregular nucleus
- Release of melanin  dermis
Pathogenesis
* Development nevi -> melanoma stepwise process
o Mutations, epigenetic changes
 CDKN2A, CDK4 (Dysplastic nevus syndrome) + NRAS + BRAF

A. Lentiginous melanocytic hyperplasia
B. Lentiginous junctional nevus
C. Lentiginous compound nevus with abnormal architecture and cytologic features (dysplastic nevus)
D. Early melanoma/ in radial growth phase
E. Advanced melanoma (vertical growth phase) with malignant spread into the dermis and vessels

60
Q

Define aetiology, pathophysiology, morphology + clinical presentation of MELANOMA

A

Define aetiology, pathophysiology, morphology + clinical presentation of MELANOMA
Clinical features
- Asymptomatic
o Itching pain
o Changes in colour/shape
o ABCDE - Asymmetry, irregular Boarder, uneven Colour, Diameter, Evolving
Morphology
- Radial growth – NO metastasis
- Shift to vertical growth
o Deep dermal infiltration
o Needs excision – melanocytes
Pathogenesis
- Inherited factors + sun exposure
o Upper back for men and legs for women
o 10-15% family
o Mutations in RB tumour suppressor protein

61
Q

Define aetiology, pathophysiology, morphology + clinical presentation of SQUAMOUS CELL CARCINOMA (SSC)

A

keratosis of basal cells in epithelium, ↑ stratum corneum
* Second most common tumour -sun
* More men than women
* Detected small and excised
* Epidermal SSC are – scaly red lesions, advanced lesions may ulcerate
MICRO Morphology
* Atyptical enlarged hyperchromatic nuclei
* All levels of dermis: areas of keratinisation, necrosis and stratum corneum
INVASIVE morphology
* Lesions nodular and ulcerated
* “tongues” of atypical squamous epithelial have gone into basement membrane into dermis
Pathogenesis
* DNA damage UV radiation – sun
* Immunosuppression
* Tobacco
* P53 mutation in acitic keratosis

62
Q

Define aetiology, pathophysiology, morphology + clinical presentation of BASAL CELL CARCINOMA

A

dilated blood vessels, basal cell proliferation, usually in epithelium
* Most common invasive cancer
* Slow growing, rarely metastisise
* On sun exposed skin
Morphology
* Pearly papules (purple like blobs)
* Invades bone, facial sinuses
* Tumour cells resemble normal basal cells
o Multifocal growths
o Nodular lesions
 Stroma retracts away from carcinoma
Pathogenesis
* One allele mutated, second allele acquired by UV exposure
* 40-60% have p53 mutations
o 60% of these UV radiation hallmark

63
Q

What’s the basic structure of blood vessels?

A

What’s the basic structure of blood vessels?
- Endothelial, smooth muscle cells, ECM (elastin, collagen, glycosaminoglycans)

64
Q

What are the 3 concentric layers in blood vessels?

A

What are the 3 concentric layers in blood vessels?
- Intima  endothelial cells and connective tissue
- Media  internal elastic lamina, smooth muscle cells, external elastic lamina)
- Adventitia  connective tissue, nerve fibres, vasa vasorum

65
Q
A

What is the structure and function of arterial categories?
- Large + elastic
- 2mm – 100 um
- Configuration  based on metabolic needs
- Changes in ECM and media – aging

66
Q

What are the three main processes of vessel development, growth and remodelling

A

What are the three main processes of vessel development, growth and remodelling
1. Vasculogenesis
a. Formation of blood vessels in utero  VEGF growth factors essential  quiescence induced by pericytes
2. Angiogenesis
a. Formation of new vessels in adulthood
3. Arteriogenesis
a. Remodelling/ adaptation of arteries

67
Q

What is the response of vascular components due to injury?

A

What is the response of vascular components due to injury?

  • Endothelial cells
    o Maintain non-adherent neutral surface  prevents haemostasis
    o Possess different transcriptional activities along vascular tree
     Endothelial cells and pericytes remain impermeable
    o Can become activated  induce gene expression
     Cytokines, lipids, viruses
     Normal when rectified
  • Endothelial dysfunction
    o Altered phenotype
    o Impaired vasoreactivity
    o Adhesive to inflammatory cells  increased thrombosis, atherosclerosis
  • Vascular smooth muscle cells
    o Vascular repair
    o Proliferate, synthesise ECM collagen, elastin + cytokines
    o Respond to physiological stimuli regulate vascular tone  PDGF, endothelin-1, INF-y, IL-1
68
Q

What does intimal thickening cause?

A
  • Loss/dysfunction endothelium = VSMC growth = ECM = thickening
  • Damage = hyperplasia of VSMC and recruitment of adjacent ECs
    o To cover wound
    o Thickening is normal
    o Neointimal VSMCs can divide
    o Healing permanently increases thickness = prolonged damage = arteriosclerosis + occlusion
    1. Recruitment of smooth muscle cells/precursor cells to the intima
    2. Smooth muscle cell mitosis
    3. Elaboration of extracellular matrix
69
Q

What is hypertensive vascular disease definition and diagnosis?

A

Where BP must be maintained
Hypertension = >139 S or >89 D mmHG
* Increased atherosclerosis
* 25% hypertensive
Diagnosis
* Often delayed = silent killer
* Atherosclerosis, renal disease, cardiac hypertrophy
* ½ die of IHD
* 1/3 stroke

70
Q

Define hypertensive vascular disease in terms of increased/↓ BP

A

↓ BP
= ↓ dilation = increased nitric oxide, prostacyclin
= ↓ cardiac output = ↓ HR, contractility and blood volume
* CO influenced by NA+ and H2O, ↓pH, hypoxaemia
* Total peripheral resistance influenced by tone and compliance

Increased BP
= increased cardiac output, HR, contraction and volume
= Increased constriction = increased angiotensin II, thromboxane

71
Q

How are the kidneys and hypertension related?

A
  • Renin-angiotensin-aldosterone system !!!!
    o Regulates vasoconstriction and Na+ homeostasis
     Renin secretes from juxtaglomerular cells
     Then renin + angiotensinogen I to II by ACE in lungs
     Angiotensin II stimulates vasoconstriction and aldosterone release = increased Na+ reabsorption = Increased blood volume and pressure
     Kidney releases prostaglandins and NO
     Myocardium releases natriuretic factors = ↓ Na+ reabsorption
72
Q

How are tubular cells involved in kidney filtration and hypertensive vascular disease?

A
  • Tubular cells must reabsorb 99.5% sodium from kidneys
    o 98% via ion channels
    o 2% by renin-angiotensin system
    o ↓ Na+ excretion implicated as a final common pathway of essential hypertension
    o If pressure increases  increases GFR  increased Na+ excretion = hypertension slowly develops
73
Q

Define arteriosclerosis + atherosclerosis

A

Define arteriosclerosis + atherosclerosis
Arteriosclerosis  “hardening of the arteries” – wall thickening/elasticity loss – Mockeberg medical sclerosis (calcified sclerosis of muscular arteries)

Atherosclerosis  “gruel and hardening” – IHD/stroke

74
Q

What is the epidemiology of atherosclerosis

A

What is the epidemiology of atherosclerosis
* High in western countries
* Age, gender, genetics
* Premenopausal women lower risk – protected by estrogen
* Post menopausal women higher risk
* Modifiable risk factors – hyperlipidemia, hypertension, smoking, diabetes
* Other risk factors – inflammation, metabolic syndrome, lazy

75
Q

In atherosclerosis what 2 modifiable risk factors play a big role?

A
  • Hyperlipidemia and hypercholesterolemia
    o Stimulate atherosclerosis development LDL
    o LDL delivers cholesterol to tissues
    o HDL transprots lipids from tissue to liver
    o Diet big role
     Omega 3 = ↓ LDL
     Exercise + alcohol = increased HDL
     Obesity + smoking = ↓ HDL
76
Q

What biochemistry levels should you be at in cholesterol?

A

Total, HDL, LDL
* Normal / high risk tryglycerides = less 1.1 / more 2.1 mM
* Normal / high risk cholesterol = more 6.2 mM total

77
Q

What 3 causes cause atherosclerosis

A

Hypertension
* Systolic and diastolic pressure high = increased risk by 60%
Smoking
* One pack per day doubles risk
DM
* Induces endothelial damage
* Diabetic = double risk

78
Q

What is the pathogenesis of atherosclerosis? 2 ways

A

2 main
1. Intimal hyperplasia
2. Vascular thrombus formation
a. Response to injury
b. Response to retention
c. Oxidative modification hypothesis

79
Q

Drawing of pathogenesis of atherosclerosis

A
  1. Chronic endothelial injury
    a. Hypertension
    b. Smoking
    c. Toxin
    d. Virus
  2. Response to injury – endothelial dysfunction
    a. Increased permeability, monocyte adhesion + emigration
  3. Smooth muscle recruitment to intima
    a. Macrophage activation
  4. Macrophages and smooth muscle cell engulf lipid
  5. Smooth muscle proliferation, collagen, and other ECM deposition, extracellular lipid
80
Q

What is the cell progression of atherosclerosis

A

Preclinical phase
= Normal artery  fatty streak  fibrofatty plaque  advanced vulnerable plaque
Clinical phase
= wall weakening – aneurysm + rupture  plaque rupture – occlusion by thrombosis  progressive plaque overgrowth – critical stenosis

81
Q

What consequences are there from atherosclerosis?

A
  • Stenosis = Blockage to blood flow, initial complication, exertional angina (70% occlusion)
    o Can cause cardiac/gut/muscle/brain ischaemia  pain/necrosis
  • Plaque eruption/ thrombosis = partial / complete flow restriction, acute ischaemia
82
Q

What is an aneurysm ?

A

What is an aneurysm ?
* Localised abnormal dilation of blood

83
Q

What is a dissection?

A

What is a dissection?
* Blood enters arterial wall, dissects vascular intima and adventitia and leads into the media

84
Q

Pathogenesis of vascular aneurysm

A

Pathogenesis of vascular aneurysm
* Vascular damage overwhelms ECM connective tissue

85
Q

Name 2 diseases/ conditions of aneurysm and dissection?

A

Name 2 diseases/ conditions of aneurysm and dissection?
* Marfan syndrome
o Poor quality ECM
o Defective fibrillin
o Poor TGF-B activity
* Vitamin C deficiency

86
Q

What is abdominal aortic aneurysm (AAA)
*

A

What is abdominal aortic aneurysm (AAA)
* Caused by Atherosclerosis, hypoxia, necrosis,
o Thrombosis
o Males >50 yr old
Morphology
* 25 cm long, 15cm wide
* Intima shows atherosclerosis
Clinical consequences
* Peritoneal haemorrhage
* Occlusion distal artery
* Lower limb embolism
* Abdominal mass
* Morality rate pre-rupture surgery 5%. POST = 50%

87
Q

Give aneurysm treatments

A

Give aneurysm treatments
- Surgical clipping = prevents blood into aneurysm and rupture
- Endovascular coiling/stent = impedes blood flow into aneurysm and rupture

88
Q

Describe aortic dissection

A

Describe aortic dissection
When blood separates intima/media/adventitial layers
* Common in 40-60 yrs old men

89
Q

Describe pathogenesis of aortic dissection

A

Describe pathogenesis of aortic dissection
* Hypetension – ischemic injury
* Marfan syndrome – affects ECM deposition and weakens arterial wall

90
Q

How much blood does the blood pump?

A

How much blood does the blood pump?
* 6,000 L/day
* 40 million x a year
* Most common death world wide 1/3 deaths less than 75 yr old

91
Q

Describe structure / function of heart?

A

Describe structure / function of heart?
* 250-350g
* Wall = RV 0.3-0.5cm & LV = 1.3 cm-1.5cm
* SA node fasted beat 60-100 bpm
* Conduction system – muscle – electrically excitable – Ca2+ release – actin/myosin – SA node – AV node – bundle of his – right/left bundle branches – purkinje network

92
Q

Name 3 main causes of heart valve dysfunction?

A

Name 3 main causes of heart valve dysfunction?
1. Nodular calcification
2. Direct collagen damage
3. Fibrotic thickening

93
Q

What 6 factors cause cardiac dysfunction?

A

What 6 factors cause cardiac dysfunction?
1. Pump failure
2. Blood flow obstruction
3. Regurgitant flow
4. Shunted flow
5. Cardiac conduction
6. Rupture of heart vessel

94
Q

IHD # of death/year and causes ?
 

A

IHD # of death/year and causes ?
 
7 million!!!!
* Caused by myocardial ischemia
o Lack of oxygen and nutrients
o 90% IHD = atherosclerotic blockage
* IHD is a late manifestation of CAD

95
Q

What is IHD empidemiology
*

A

What is IHD empidemiology
* 500 K American die/year
* 50% less than 20-30 yrs ago
* ↓ smoking, medication, surgery helps
* Mortality rates increasing atm = fatty foods

96
Q

What is IHD empidemiology
*

A

What is IHD empidemiology
* 500 K American die/year
* 50% less than 20-30 yrs ago
* ↓ smoking, medication, surgery helps
* Mortality rates increasing atm = fatty foods

97
Q

IHD pathogenesis

A

IHD pathogenesis
1. Normal
a. Atherosclerosis
2. Fixed coronary obstruction
a. Plaque disruption OR
b. Severe fixed coronary obstruction = IHD
3. Thrombosis causes
a. Mural thrombosis with obstruction
b. Occlusive thrombosis

98
Q

Difference between stable angina and unstable angina

A

Difference between stable angina and unstable angina
Stable angina → where arteries are stenosed
Unstable angina → plaque rupture + partial thrombosis + vasospasm

99
Q

List times of myocardial responses

A

List times of myocardial responses
Onset of ATP depletion = seconds
Loss of contractibility = less 2 mins
ATP reduced to 50% = 10 min
ATP reduced to 10% = 40 min
Irreversible injury = 20 min-40 min
Microvascular injury = more 1 hr

100
Q

Consequences of MI

A

Consequences of MI
Heart rupture
1. Of necrotic/inflamed free wall (3-7 days)
2. Ventricular septum (L/R shunt)
3. Papillary muscle (regurgitation)

Pericarditis Myocardial inflammation extends into pericardium (2-3 days)

Right ventricular infarction Results in venous congestion, systemic hypotension

2002MSC Pathophysiology (8 decks)

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