Cellular Regulation Flashcards

1
Q

What is cellular regulation

A

Cells function within cells to maintain homeostasis including response to extra cellular signals and the way each cell produces intracellular response

Cells contain natural functions that help them respond to stress to keep them in the intact state

Want to look at ways cells respond to normal stressors

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2
Q

Proliferation

A

Normal cells reproduce new cells through cell division

Hyperplasia: increased number of cells in response to stress, increased metabolic demands, or increased hormones

Neoplasia: abnormal and progressive multiplication of cells; multiplying without a purpose and can lead to cancer

Neoplasm: new and abnormal tissue growth; uncontrolled and progressive

Neoplasia is a little controlled; neoplasm is uncontrolled

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3
Q

Differentiation

A

Acquisition of a specific cell function; new cells acquire structural, microscopic, and functional characteristics of cells they replace

Differentiation refers to how close the cells are to the parent cells they came from; the less differentiated, the more problems because they are less like the parent cells and more neoplastic

Metaplasia: change in normal differentiation- normal for type of cell but wrong location; protective response to adverse conditions; under normal control of DNA

Dysplasia: loss of DNA control over differentiation in response to adverse conditions

Anaplasia: regression to immature or undifferentiated state; no DNA control; looking at cancer that is out of control

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4
Q

Benign

A

Continues inappropriate cell growth

Retains parent morphology

Small nuclear to cytoplasmic ratio

Specific differentiated function continues; well differentiated: close to parent cell

Tight adherence to each other

No migration- does not spread to anywhere else in the body

Orderly cell growth even though cell growth is out of control

Normal chromosomes

Loss of apoptosis (orderly cell death where old cells die and we create new ones): there is no cell death resulting in the tumor

Less division than a malignant tumor

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5
Q

Malignant

A

Rapid proliferation; rapid cell division requires a lot of energy and need to increase caloric intake; may become cachectic or malnourished and thin because of energy the tumor is taking

Anaplasia- decreased cell death; no signal for apoptosis

Large nuclear to cytoplasmic ratio

Poor differentiation; no homeostatic control because DNA is different from parent cell

Lose adherence and migration

No contact inhibition

Abnormal chromosomes

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6
Q

Step 1: initiation

A

Irreversible mutation of gene but still able to carry out original function; there is an oncogene (e.g., BRCA1), there is some irreversible agent (e.g., exposed to something like benzene) that changes the cell, or some carcinogen

Something changes on initiation that changes the genetic or purpose of the cell; simply the process of changing the cell and what it does

Oncogene over expression

Irreversible event

Carcinogens change cells genes

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7
Q

Step 2: promotion

A

Enhancement of growth of initiated cell

Hormones like insulin or estrogen are big promoting agents that stimulate the growth of the cell that has mutated. Some of the cells have a threshold- there is a certain amount of promotion that needs to occur to stimulate the process

Threshold dose is required to stimulate

In obesity, there is insulin resistance which can create inflammation and other problems like hyperglycemia or anaerobic oxidation. Fat cells produce estrogen; increased estrogen leads to hyperplasia which can all lead to uterine cancers

Looking at cytokines production as an initiator; estrogen and insulin as a promoter; all which leads to progression

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8
Q

Step 3: promotion

A

The cell changes lead to an undifferentiated cell state

Increased growth rate

Increased invasive ability

Metastasis

Angiogenesis

Start with a normal cell with a mutation, end up with some hyperplasia, have some dysplasia (some change in the cell for a purpose), an in situ cancer (something that is in place and hasn’t invaded anything yet), the the invasive malignant cells

With progression, we have promoting that leads to an undifferentiated cell that starts growing faster that increases our invasive ability and have metastasis

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9
Q

Metastasis spread

A

Lymphatic system: WBCs will attack and clear the lymphatic system. With a cancer cell, it will enter the system where it will die, spread through the lymphatic system and remain dormant, or start growing a mass. Mass can break off into thoracic duct into the vasculature. Sentinel node is the first node after original tumor

Hematogenous system: invaded capillaries and venules; GI & pancreas feed into portal vein where thee liver mets; vena cava where the lung mets ; breakdown ECM (extra cellular membranes) with enzymes and goes into the venous system

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10
Q

Cancer risk: age

A

Long-term exposure to promotional agents

Decreased immune response especially with advanced ages of 70s and 80s

Hormonal changes with estrogen

Free radical production as we age and have more oxidative stress

76% of cancer occurs in people over the age of 55; children account for about 1% of all cancers

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11
Q

Cancer risk: hereditary

A

Inherited predisposition- about 5-10% of cancers are genetically linked; BRCA1 causes breast, prostate, ovarian cancers

Familial clustering- familial polyposis where there are polyps in the colon; may remove the colon when they are little because risk for dying of colon cancer is very high; more cancers in the family and looking at their genes to determine why they have so many cancers in their family

Other autosomal dominant things: retinal blastoma which is a tumor of the retina, BRCA1, familial polyposis, etc.

Chromosomes: people with a known chromosomal disorder have a much higher risk of leukemias (e.g., Down syndrome have 25% higher risk; Klinefelters syndrome have a high risk for breast cancer because males with XXY chromosomes grow breast tissue; Turners syndrome is a woman with one X chromosome and higher risk of leukemia)

Genetic testing does not detect cancer but shows if there is an increased risk

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12
Q

Cancer risk: obesity

A

Insulin resistance and increased insulin production

Increased androgen and estrogens which are proliferated in fat cells

Chronic inflammation state which puts cells in contact with cytokines which are cancerous promoting agents

Cytokines respond to these things that promote growth

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13
Q

Cancer risk: chemical

A

Form highly reactive species- looking at free radical production which are some of those promoting agents that put us at risk for cancer such as smoking, benzoprene (foods that are fried and reused fat like McDonald’s), polycystic aeromatic hydrocarbons (animal fat in charcoal in smoked meats), ethanol (metabolism interferes with DNA synthesis and repair), asbestos, benzene (bladder cancer r/t benzene in paper)

Bunds to DNA and RNA cause cell mutation

Change cell proteins and enzymes

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14
Q

Cancer risks: radiation

A

Ionizing

Ultraviolet- causes additional damage added to the initiation stage

Radon- most common; test houses for this

Medical: x-rays are 11% of our radiation risks, nuclear medicine testing like CAT or PET scans are 4%- don’t order undue tests

Increased brain tumors in kids who’ve had a head CT; want to reduce: for concussions, monitoring is better than a CT

Radiation mutates the genes by chromosome breakage; it’s the initiation stage that increases the risk

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15
Q

Cancer risks: viral

A

Viral insertion of genetic material into DNA can activate oncogene and damage suppressor genes

HPV- can cause cervical, penile, and oral cancer

EBV

HBV- can cause liver cancer

HHV-8- human herpes virus can cause throat and mouth cancer

Helicobacter pylori- bacteria that causes ulcers can put you at risk for gastric cancer

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16
Q

Cancer risk: other

A

Immune function: protect from foreign and non-self cells where T cells destroy abnormal cells so we can’t proliferate it and cause cancer

Decreased immune function= high risk for cancer; organ transplant on immunosuppressants are high risk for lymphomas

Gender: male- higher risk for prostrate and bladder (esp. in men who smoke)
Female- higher risk for breast and thyroid

Socioeconomic status- poor access to healthcare screening and counseling; poorer diet and more stress (increases cytokine hormones)

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17
Q

Assessment: history

A

Discovery of lump, mass, or lesion

Unexplained bleeding, bruising, cough, or fatigue

Change in appearance: skin and moles (ABCDE), loss of appetite, weight loss, mental status changes, bowel changes, swallow changes, pallor, unexplained bruising, persistent fevers, unexplained vomiting (may be a brain tumor from vomiting centers being pushed on by tumor), bone pain, headaches, changes in gait or personality, fatigue, new diagnosis of SIADH could be indicative of a brain tumor, new diagnosis of Cushings, hypercalcemia, new blood clot

Signs of altered body function

Family history

Risk history

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18
Q

ABCDE for skin cancer

A

A-asymmetry

B-border that is uneven, crusty, or notched

C- color that is various esp. white and or blue tends to be bad

D-diameter that is larger than a pencil eraser tends to be a melanoma

E- evolving or changing in size, shape, or color or begins to bleed or scab is often bad

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19
Q

7 warning signs of cancer

A

CAUTION

  1. Change in bowel or bladder habits
  2. A sore that does not heal
  3. Unusual bleeding or discharge
  4. Thickening or lump in breast or elsewhere
  5. Indigestion (persistent) or difficulty with swallowing
  6. Obvious change in wart or mole
  7. Nagging cough or hoarseness of voice
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20
Q

Assessment: diagnostic

A

Radiographic/X-ray- show size and location

Visualization: colonoscopy, esophoduodenaloscopy, MRI, CT, mammograms, ultrasounds

Labs: tumor markers (antigen on surface of tumor cells), CBC which shows bone marrow function

Cytologic- taking a sample of cells like a Pap smear where you look at cancer cells that exfoliate and change secretions

Tissue biopsy to look at tissue under microscope

Immunohistochemistry is looking at type of tumor markers

Microarray technology detects and quantifies the expression of large numbers of oncogenes

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21
Q

Grading a tumor

A

Dependent on the degree of differentiation

G1- well differentiated

G4- not differentiated where cells are far away from parent; difficult to determine origin of cell because so far away

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22
Q

Staging tumor size

A

Tx- not measured

T0- no evidence of tumor; may have peripheral evidence but no tumor seen

Tis- malignant cells only in superficial layer; not invaded anywhere

T1-T4 is based on size and invasion

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23
Q

Staging- regional lymph node

A

Nx- not assessed

N0- no metastasis; sentinel node is clear

N1-N3 is based on size, location, and number of lymph nodes involved

Look at sentinel node- the first lymph node past the tumor

24
Q

Staging- metastasis

A

Mx- presence not assessed

M0- none

M1-M4- distant

Looking at nearby tissue, if it’s spread into the vascular system, and where it might have gone into after the vascular system

25
Q

Terminology

A

Oma: benign tumor for parenchymal tissue (organ tissue) type

Carcinoma: malignant epithelial origin

Adenocarcinoma- gland-like structures (thyroid, parathyroid, adrenal)

Sarcoma- mesemchymal tissue (looking at non organs)

Blastoma- embryonic tissue

26
Q

Primary prevention- prevents!

A

Regular physical activity- decreasing obesity and inflammation rates

Balanced diet

Avoid known or potential carcinogens- smoking, protective gear, sunscreen

Modify associated factors

Remove at risk tissues

Chemoprevention- vitamins, minerals, antioxidants, etc.

Vaccination- HPV

27
Q

Secondary prevention- screen!

A

Mammography should begin at age 40 unless familial history, then want to start earlier or BRCA1 testing

PSA- prostate specific antigens with family history of prostate cancer; is it inflamed or cancer

PAP for cervical cancer

Colonoscopy starting at age 50 or sooner with family history

28
Q

Childhood cancers

A

Hematopoietic, nervous, soft tissue, bone, and kidney

Embryonic origin and some are mesenchymal

Lymphoblastic leukemia- look to see if they have other disorders in their genes that will focus treatment

Puberty- bone cancer (osteosarcoma is high in the teenage population), lymphoma, gonadal (boys may get testicular cancer as teenagers; girls can get ovarian cancer as teenagers but not commonly) (look at stages of growth)

29
Q

Cancer impact on function: GI

A

Cachexia- extreme body waiting and malnutrition

Increased catabolism as tumor is using a lot of energy

Treat- smaller frequent meals; nutritional supplements; enteral feeding; parenteral nutrition

Decreased appetite from N/V, mucosal changes, feeling of fullness

30
Q

Cancer impact on function, neuro, motor, and sensory

A

Invasion of bone: risk for fractures, pain, spinal cord compression, hypercalcemia

Invasion of brain: impact dependent on location; can have cognitive, sensory, personality disorders, hormonal changes

Nerve compression: pain, motor and sensation issues

31
Q

Cancer impact on function: pain

A

Tumor compression

Metastasis

Treatment

Pain is often what causes the person to be evaluated; want to relieve so they have good QOL and make sure they are comfortable but can function

32
Q

Cancer consequences- psychological

A

Fear, stress, anxiety

Familial dynamics

Financial

Self-image and identity

33
Q

Cancer treatment: surgical

A

Prophylactic- removes potential source of cancer

Diagnostic- excisional biopsy, remove all or part of the tumor

Staging- size, metastasis, etc.

Debulking- entire tumor cannot be removed r/t damage to vital organ but large amounts are removed so radiation can work better

Cure- remove all cancerous tissue; usually for skin cancers or benign tumors that are encapsulated

Palliative- not curing, may be end stage, can remove parts for improved QOL

Reconstructive/ rehabilitative- increasing function or appearance

Side effects: loss of organ function- change in appearance from loss of body part

Care-post-surgical: psychological and acceptance

34
Q

Cancer treatment: radiation therapy external

A

Gamma ray, radionuclides, or ionizing beams: effects in path or field of radiation- not always full body except leukemia; exposure- what is delivered into the tissue; radiation dose- fractionation (to decrease damage to good tissue), what is absorbed into the tissue

External beam: patient not radioactive because particles dissipate quickly

Gamma knife targets one area from different angles to decrease damage to good tissue; seen often with brain tumors

35
Q

Cancer treatment: radiation side effects

A

Acute: alopecia (possibly permanent if damage to hair follicle), cerebral edema, N/V, somnolence (very sleepy), mucositis, xerostomia (dry mouth), esophagitis, pharyngitis, anorexia, diarrhea, cystitis, vaginitis, fatigue, taste changes, bone marrow suppression

Late: cognitive, pituitary/hypothalamus (SIADH, temp regulation issues), dental caries, hypothyroid, xerostomia, cardiomyopathy, lung fibrosis (hard lung tissue, decreased respiratory function), lymphedema, bowel injury

36
Q

Radiation therapy: patient skin care

A

Wash daily with water or mild soap

Do not scrub

Do not remove ink markings

Pat dry

Use only prescribed lotions

Avoid sun exposure

Oils on skin need to be washed off with radiation therapy because oils on the skin will make it burn more

37
Q

Radiation: brachytherapy

A

Small radioactive rods placed near the tumor in the body

Internal contact with tumor; implanted- patient is radioactive, degrade or need removal; ingested- body fluids radioactive

Patient care: private room and bath, caution sign and lead shield, wear dosimeter badge (detects amount of radiation exposure) and lead apron (don’t turn back, increases exposure), do not try to conceive, limit visitor time to 30 minutes a day

No exposure to pregnant women or children if radioactive

38
Q

Cancer treatment: chemotherapy

A

Chemicals to prevent multiplication

Effect during cell division

Selection: tumor cell cycle, growth factors and size

Effect ALL body cells

Nadir- time of greatest effect on bone marrow- time of lowest WBCs, RBCs to see when they are at greatest risk for infection, anemia’s, etc.

Timed mixture

High-dose causes bone marrow depression: growth factors;m to increase WBC production; HST/BMT (hematopoietic stem cell/bone marrow transplant) may be required

39
Q

Cancer treatment: chemotherapy continued

A

IV admin requires chemo-certification; but anyone can monitor the patient once it’s up and running

PPE with chemo or patient bodily fluids: double glove or chemo glove, gown for 48 hours after administering; eye protection of risk for splashing

Vesicants- drugs damage tissue on contact: extravasation prevention; call provider for antidote if suspected

Oral- handle with gloves: do NOT split, crush, break, or chew

40
Q

Cancer treatment: chemo side effects

A

Mucositis (erosion of mouth tissue)- use soft bristled tooth brush; salt and soda swish and spit; avoid spicy, acidic, hard foods

Alopecia- whole body hair loss; avoid direct sunlight; body image

Cognitive alterations (“chemo brain”)- decreased concentration, memory loss

Peripheral neuropathy- decreased sensation; poor gait and balance, orthostatic hypotension, pain; patient education on shoes, inspecting feet, fall risk

41
Q

Cancer treatment: chemo bone marrow suppression- neutropenia

A

Cause for dose limiting and mortality; risk of infection and sepsis

ANC <500: severe infection risk
ANC= [(seg% + band%) x WBC] /100

Patient report fever >100, cough, cloudy urine, wound

Decrease purulence and pus because decreased WBCs, decreased fever response because decreased WBCs

Nursing interventions: hand washing; antibiotics with fever- blood and wound culture before; WBC daily; colony stimulating factors

42
Q

Cancer treatment: chemo bone marrow suppression

A

Anemia & consequences: blood transfusions; erythropoiesis stimulating agents (darbepoetin and epoetin alpha- both increase clot risk)

Thrombocytopenia-
Bleeding precautions: platelet transfusions; eltrombopag or romiplastin- risk of fluid retention

43
Q

Cancer treatment: chemotherapy N/V

A

Anticipatory (before going in), acute (first 24 hours, persists 1-2 days), delayed (after 24 hours of stopping chemo)

Breakthrough, emetogenic

Serotonin antagonist- block in brain and intestine (ondansetron; give before chemo starts)

Corticosteroids (dexamethasone) to decrease brain swelling

Neurokinin receptor antagonist (aprepitant) to block warfarin and oral contraceptives effectiveness

Prokinetic- increase gastric emptying (metoclopramide)

Benzodiazepines (lorazepam, Ativan)

44
Q

Cancer treatment: humoral

A

Target or block receptor and feedback loops

Direct anti tumor activity

Interleukins regulate inflammation: macrophage and NK cells to target the tumor; side effects: capillary leak syndrome (neuro- confusion, fatigue, agitation, hallucinations, depression)

Interferons slow cell division: block oncogene expression; cancer cells to normal function

45
Q

Cancer treatment: target

A

Antibody and small molecule inhibitors

Prevent growth signaling: block angiogenesis; block oncogene expression (can block cells from dividing); stimulate immune destruction

Tyrosine kinase inhibitors: side effects include N/V, fluid retention, bone marrow suppression

Herceptin will block HER-2 cancer cells

46
Q

Cancer treatment: hormonal manipulation

A
Androgen and antiestrogen: 
Hair and acne
Amenorrhea- stop periods 
Fluid retention 
Hypercalcemia 

Estrogen/ progestins:
Osteoporosis
Gynecomastia
Loss of facial hair

47
Q

Cancer treatment: HSCT/ BMT

A

Allogeneic (someone else; typically used for leukemia) and autologous (my own)

Donor identification- HLA matching

High dose chemo destroys BM (bone marrow)

GVHD- graft versus host disease: skin, gut, liver

48
Q

Oncology emergencies

A

Sepsis: neutropenia, temp >100

DIC- caused by sepsis and chemotherapy

SIADH- pituitary and small cell lung cancers

Hypercalcemia- cancers secrete PTH and bone metastasis: bone pain and renal calculi

49
Q

Oncologist emergencies: spinal cord compression

A

Tumor invaded spine

Vertebrae collapse, spinal cord damage

Sx: back pain, weakness, decreased sensation, urinary retention, constipation, decreased DTRs, vibratory sense, paralysis if not treated quickly

Treat: high dose steroids, XRT (radiation and debulking), surgery

50
Q

Oncologist emergencies: superior vena cava syndrome

A

Compression blocking venous return

Sx: pain, periorbital edema, neck and chest tightness, airway compression, worse when flat, signs of decreased venous return

Death if not treated

Treat: XRT and chemo to shrink tumors

51
Q

Oncologic emergencies: tumor lysis syndrome

A

Chemo destroys large number of cells

Hyperkalemia risk

Hyperuricemia- acute renal failure

Hyperphosphatemia

Liver occlusion

Treat: hydration; alkaline body fluids- NaHCO3, check urine pH; allopurinol for Uric acid piece

52
Q

Cancer signs in children

A

General- mass, purpura, pallor, weight loss, fatigue

Overt- white eye reflection , vomiting in morning, recurrent/persistent fever

Covert- bone pain, headache, persistent lymphadenopathy, change in gait, balance, personality

53
Q

Leukemia

A

ALL/ANLL

Overproduction of immature WBCs

Competition for metabolic elements

Dx: CBC- blasts and decreased RBC/platelet count; bone marrow flow cytometry; LP for CNS involvement

54
Q

Leukemia therapy: ALL

A
  1. Induction chemo
  2. CNS prophy
  3. Intensification
  4. Maintenance
55
Q

Leukemia therapy: ANLL

A
  1. Chemo 2-4 courses with CNS prophy

2. BMT or consolidation

56
Q

Leukemia nursing management

A
Emotional support
Pain
Infection
Hemorrhage 
Anemia
Chemotherapy 
N/V
Anorexia
Mucosal ulceration
Neuropathy
Hemorrhagic cystitis 
Alopecia
Mood changes