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Pathophysiology > UNIT 5 > Flashcards

UNIT 5 Flashcards

1
Q

Describe Normal Cells

A
  • Cells in the body are organized into commented known as tissues: orderly arrangement and differentiated to carry out the cells functions (ex: endothelial tissue and glandular tissue)
  • Cells interact and communicate with each other in different ways: neurotransmitters, hormones, channels (gap junctions)
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2
Q

Describe Cell Division

A

Cells reproduce by mitosis

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3
Q

Explain Mitosis in Regards to Cell Division

A

-Mitosis is a highly regulated event in the lift of the cell:
genetically controlled through DNA and inhibitors and stimulators operate in balance
-Mitotic rate varies greatly from cell to cell: non dividing, always dividing and dormant

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4
Q

Mutations

A
  • Mutations are changes in DNA sequence that are passed onto daughter cells during mitosis: mutants have variable effects on cell (altered cell function, altered cell structure and incompatible with cell viability
  • Mutations affect protein sequence with any cellular protein susceptible: cellular enzymes and cell components involved in regulation of mitosis
  • Mutations are caused by a variety of factors such as, chemical exposure, viral infection, electromagnetic radiation
  • In addition, rapid rates of cell division may increase likelihood of infidelity in DNA replication process: ex constant proliferative (regenerative) stress in some chronic infections
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5
Q

Naming Tumours

A
  • Tumours may have common n ames (ex: colon cancer and lung cancer)
  • Tumours may also be named eponymously (ex: hodgkin’s disease)
  • Tumours names are standardized using a system: root word reflects cell of origin (ex: osteo –> bone or lip –> fat
  • Simple suffix ‘oma’ on root word usually denotes benign tumour (ex: lipoma)
  • Suffix word denoting malignant tumour is derived from tissue of origin: epithelial tissue = carcinoma (ex: adenocarcinoma) and connect tissue = sarcoma (ex: osteosarcoma)
  • Exception to the ‘rules’ (lymphoma and melanoma)
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6
Q

Describe Pathophysiology of Malignancy

A
  • Changes in cells and tissues: loss of normal tissue organization, loss of growth inhibition, loss of contact inhibition, loss of cell-cell communication and loss of tissue function
  • Changes in cell surface: expression of new surface structure (surface antigens)
  • Changes in local environment: tissue damage may be assisted by the enzyme secretion (ex: collegenase) or interior tumour necrosis or angiogenesis
  • Tumour speed into adjacent tissue: assisted by enzyme secretion (ex: collegians)

See notes for an example

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7
Q

Malignancy- Local Effects (Pain)

A
  • May be caused by pressure of mass on sensory nerves or expansion of organ capsule (ex: kidney)
  • May be secondary to cancel sequelae: inflammation, infection, schema, haemorrhage or infection may follow necrosis and ulceration (often seen in impaired host resistance in cancer patient)
  • Pain is not usually present in early cancers
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8
Q

Malignancy- Local Effects (Obstruction)

A
  • Caused by compression of passage/ duct (3 types)

- May restrict flow of: blood (results in ischemia), lymph (results in edema), air (results in respiratory impairment)

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9
Q

Malignancy- Systemic Effects (Weight Loss)

A
  • Proliferating cancer diverts nutrients from normal tissues
  • Altered metabolism
  • Anorexia, fatigue, pain and stress
  • Cachexia is a severe wasting of tissues often seen together with anorexia (some immune system products (cytokines) are ‘cachectic factors’
  • Loss of appetite, altered metabolism contribute to fatigue and weakness
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10
Q

Malignancy- Systemic Effects (Infection)

A
  • Decline host resistance
  • Chemotherapy suppresses immunity
  • Loss of mobility and muscle strength
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11
Q

Malignancy- Systemic Effects (Hemorrhage)

A
  • Ulceration in tissues
  • Erosion of BV’s by tumours
  • Thrombocytopenia (low platelets (ex: in blood cell cancers)
  • Malnutrition (may prevent looting factor production
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12
Q

Malignancy- Systemic Effects (Anemia)

A
  • Anorexia and malnutrition
  • Haemorrhage
  • Bone marrow depression (ex: blood cell cancers and chemotherapy)
  • Anemia exacerbates fatigue, weakness and poor tissue regeneration
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13
Q

Malignancy- Systemic Effects (paraneoplastic syndromes)

A

-Tumours may secrete bioactive substances that affect function of tissue: ex: some lung cancers secrete adrenocorticotropic hormone (ACTH) –>
Elevated adrenal glucocortioid secretion –>
Mimics Cushing’s disease
-Paraneoplastic syndromes may confound patient diagnosis and care

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14
Q

Diagnostic Tests- Blood Tests

A

-May see evidence of blood cell cancers by microscopic examination (ex: differential WBC count)

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15
Q

Diagnostic Tests- Medical Imaging

A
  • X-rays
  • Ultrasound
  • Magnetic resonance imaging (MRI)
  • Computed tomography (CT)
  • Position emisson tomography (PET)
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16
Q

Diagnostic Tests- Chromosomal Analysis

A
  • Provides info about status of nuclear integrity

- Ex: philadelphia

17
Q

Diagnostic Tests- Cytological Analysis

A
  • Provides definitive diagnosis of cancer

- Performed on tissue biopsy (surgical removal)

18
Q

Diagnostic Tests- Test for Tumour Makers

A
  • Caner cells express novel proteins (tumour specific proteins)
  • Sometimes, these proteins may be secreted into the coruscation and be detachable through serologic tests
19
Q

Diagnostic Tests- Usefulness of Serology caries from Cancer to Cancer

A
  • Screening
  • Confirming diagnosis
  • Staging
  • Monitoring course of disease
  • Detecting recurrence
20
Q

Describe Diagnostic Serological Tests (3)

A
  • Carcinombryonic antigen (CEA): usefulness in colorectal cancer, but not useful in screening. Maybe: levels may correlate to poor prognosis or monitoring response to CRx of metastasees
  • Human Chronic Gonadotropin (hCG) used in testicular cancer and in pregnancy
  • Alpha-fetoprotein (AFP): used to test liver cancer and down syndrome in prenatal screening
21
Q

Describe Cancer Spreading

A
  • Metastasis = cancer spread to distant sites
  • Malignancies spread by different methods: local invasion (spread, but not metastasis), lymphatic (metastasis) and bloodstream (metastasis)
  • Original tumour is called primary tumour
  • Tumours arising as a result of metastasis are secondary tumours. Secondary tumours are identical to the primary tumour, regardless of their new location
22
Q

The 3 Mechanisms for Cancer Spread

A
  • Invasion (local and regional)
  • Metastasis
  • Seeding (implantation)
23
Q

Describe Characterizing Malignant Tumours

A

Location of tumour: malignant tumour may remain initially localized and non-invasive beyond basement membrane: referred to as carcinoma ‘in situ’ (epithelial cancer ‘in place’)

24
Q

Describe the Etiology of Cancer

A
  • Carcinogenesis: what are the causes of cancer?
  • Risk Factors and prevention (self study)
  • Host defense: what defences are in place?, failure to defences?, how does the host fight back?
25
Q

Describe Carcinogenesis

Etiology of Cancer

A
  • At the most basic level, cells become malignant (‘transform’) because of DNA changes: changes usually occurs over a long period of time
  • Carcinogenesis (generation of cancer): process of malignant transformation
  • Cancer may result from: combination of several factors and repeated exposure to single risk factor
  • Some malignancies have well documented risk factors such as HPV (cervical cancer), Epstein-Barr Virus Infection (burkitt’s lymphoma), UV exposure (melanoma) and atomic radiation (leukemia)
  • However, cancer causes are complex because they are difficult to establish precise etiology (ex: not every cigarette smoker develops lung cancer)
26
Q

Describe the Stages of Carcinogenesis - One

A

Exposure to ‘initiators’ or ‘procarginogens’:

  • causes first irreversible mutations in DNA
  • May be a spontaneous mutation or exposure to environmental factor
  • Does not cause an active tumour
  • most things can damage DNA ex: tomatoes damage DNA
    ex: breast cancer -> exposure to DNA -> mutation from high amount of estrogen)
27
Q

Describe the Stages of Carcinogenesis - Two

A

Exposure to ‘promoters’:

  • Ex: hormone chemicals
  • More DNA mutations
  • Loss of differentiation (dysplasia or anaplasia may be seen)
  • Increased mitotic rate
  • Onset of tumour
28
Q

Describe the Stages of Carcinogenesis - Three

A

Continued exposure:

  • more mutations
  • malignant tumour developement
29
Q

Describe Host Defences - DNA Repair Systems

Etiology of Cancer

A

DNA repair systems: active to reverse mutation frequency

  • Xeroderma pigmentosa is a genetic deficiency in DNA repair system that reverses
  • Greatly increased frequency of skin cancer
30
Q

Describe Host Defences - Cancer Suppressor Genes

Etiology of Cancer

A

Cancer Suppressor Genes: (tumour suppressor genes aka prevents tumours (slows growth)): they slow down cell division, repair DNA mistakes, Direct Apoptosis

  • Act like a brake pedal on a car, keeping cell from dividing to quickly
  • If tumour suppressor gene mutates, cells can lose growth regulation
  • Ex: BRCA1 or BRCA2 (breast cancer genes)
31
Q

Describe Host Defences - Immune Responses

Etiology of Cancer

A

Immune Responses play important roles:

  • Neoplastic cells may express new cell surface marker that may be recognized as foreign by immune system
  • Immune surveillance looks for presence of ‘non-self’ (prevents progression of very small tumours)
  • T cells try to kill tumours after they’ve established (basis of experimental therapies)
32
Q

Describe Immune Responses

A

Immune system failure elevates risk of cancer:

-Immunodeficiencies (ex: aids) may result in appearance of unusual cancers (ex: kaposi’s sarcoma)

33
Q

Cancer Therapy: depends on? its goal?

A

Depends on:

  • Type of cancer
  • Location
  • Sensitivity to the therapeutic agent

Goal:

  • Cure (eliminate all cancer cells from the body)
  • Palliative (reduce symptoms to prolong life and make individual more comfortable)
34
Q

Cancer Therapy Continued - Radiation Therapy

A
  • X-rays, gamma rays (radium, cobalt) or high energy electrons or protons
  • Induces mutations or other changes in DNA.. so cells will die: most effective against rapidly dividing cells (like tumours), prevents tumour cell mitosis (prevents growing) and damages BV’s (causes ischemia in tumour)
  • Some Cancers are resistant to radiation damage
  • Radiation may be administered pre-operatively (ex: to debulk) or several weeks (healing time) post-operatively
35
Q

Cancer Therapy Continued - Radiation Therapy: 2 Types

A

External:

  • Use outside source and direct radiation beam onto area of interest
  • No internalization of radioactivity

Internal:

  • Implant radioactive ‘seeds’ into tumour (brachytherapy): ex: cervical, prostate and oral cancers
  • Inject radioactive chemical into blood stream: ex: inject radioactive iodine to threat thyroid cancer
36
Q

Cancer Therapy Continued - Radiation Therapy: Adverse Effects of Radiation

A

Damage to healthy tissues with rapid cell division rates:

  • mucosal tissues (GI, gums): bleeding, vomiting and diarrhea
  • Hematopoetic cells (bone marrow depression): leukopenia (low WBC increase risk of infection) and risk of infection; bleeding tendency
  • Epithelial tissues (skin, hair follicles): sunburn- like inflammation and/or hair loss

Teratogenesis: may be seen in treatment of ovarian or testicular cancer (lead to birth defects damaging age and sperm

37
Q

Cancer Therapy Continued - Cytotoxic Chemotherapy

A
  • In some tumours (ex: ‘sensitive’), chemotherapeutic agents may be used by themselves or in a combination with other treatment approaches
  • Usually, combination cytotoxic therapy is employed: several drugs acting on different parts of the cell cycle
  • Usually administer high doses of chemicals, allowing time in between treatments to allow normal tissues to recover: especially recovery of host cells (ex: neutrophils
    • chemo can kill people with cancer, because it can introduce more problems
38
Q

Cancer Therapy Continued - Cytotoxic Chemotherapy: Adverse Effects of Cytotoxic Chemotherapy

A

Damage to normal cells (as in radiation damage):
-Bone marrow depression: risk of hemorrhage, risk of infection (including opportunistic infections) and may limit frequency of therapy until leukocytes count rises

GI Mucosal Damage: Vomiting (also by stimulation of CNS vomiting centre)

Damage to Oral Mucosa: malnutrition (makes eating uncomfortable)

39
Q

Cancer Therapy Continued - Cytotoxic Chemotherapy: Other Types of Chemotherapy

A

Steroid Hormones or Antagonists:

  • Ex: tamoxifen (estrogen antagonist/breast cancer drug) blocks growth promoting effects of estrogen on certain breast cancers
  • Ex: estrogen may slow growth of prostate cancer

Glucocorticoids (ex: prednisone, dexamethasone):

  • Decreases mitosis
  • Decrease inflammation associated with cancer
  • Improve sense of well being
  • Used in Treatment of chemotherapy-assoicated nausea

Biological Response Modifiers (immunomodulators):

  • promote immune responses
  • not yet considered for first line therapy
  • very expensive about $500 a day

Antibodies:

  • made naturally in acquired, humeral immune responses
  • Can also be mass produced in laboratories
  • Therapeutic antibodies are specific for proteins that may be overexposed in certain cancers

Angiogenesis Inhibitors:

  • prevents formation of new blood vessels
  • try to starve the tumour cells of nutrients and oxygen

Pathophysiology (9 decks)

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