Cancer Flashcards

1
Q

General overview of cancer

A

Genes inside each cell tell it when to grow, work, divide and die. Normally, our cells follow these instructions and we stay healthy. But sometimes the instructions get mixed up, causing our cells to grow and divide out of control or not die when they should.
As more and more of these abnormal cells grow and divide, they can form a lump in the body called a tumor

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2
Q

Hyperplasia

A

means that abnormal cells are dividing and increasing in number faster than normal. The cells look normal under the microscope but there are more cells than normal. Some types of hyperplasia are precancerous but most aren’t

i.e. BPH

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3
Q

Atypia

A

means that cells are slightly abnormal (atypical).

Sometimes atypia may be caused by healing and inflammation but some types of atypia are precancerous.

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4
Q

Metaplasia

A

means that there has been a change to the types of cells that are normally found in this area of the body. The cells look normal but they aren’t the type of cells that are normally found in that tissue or area. Most types of metaplasia aren’t precancerous but some are.

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5
Q

Dysplasia

A

means that cells are abnormal, there are more cells than normal, the cells are growing faster than normal and they aren’t arranged like normal cells. Dysplasia is a precancerous condition.

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6
Q

Carcinoma in situ

A

is the most severe type of precancerous change. The cells are very abnormal but have not grown into nearby tissue. Carcinoma in situ is usually treated because it has a high risk of developing into cancer.

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7
Q

Precancerous changes can be mild to severe. There are different ways of describing precancerous changes based on how mild or severe the changes are.

A

Hyperplasia
Atypia
Metaplasia
Dysplasia
Carcinoma in situ

People with precancerous conditions are usually checked regularly, so they can be treated quickly if cell changes become more severe or turn into cancer.

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8
Q

Describe normal cellular differetiation

A

Orderly process progressing from a state of immaturity to a state of maturity

Stable and will not change

Exact mechanism of normal cellular differentiation not completely understood

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9
Q

Most human tissues contain _____-stem cells.

A

predetermined, undifferentiated

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10
Q

All cells are controlled by a_______________ that determines proliferation.

A

intracellular mechanism

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11
Q

Cancer cells grown in culture are characterized by loss of

A

contact inhibition.

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12
Q

Stem cell theory of defect in cellular proliferation

A

Loss of intracellular control of proliferation results from mutation of stem cells.
DNA is substituted or permanently rearranged.

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13
Q

Two types of genes that can be affected by mutation are

A

Proto-oncogenes
Regulate normal cellular processes such as promoting growth
Tumour suppressor genes
Suppress growth

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14
Q

Proto-oncogenes

A

Genetic locks that keep cells functioning normally

Mutations that alter their expression can activate them to function as oncogenes (tumour inducing genes).

Which can interfere with normal cell growth causing the cell to become malignant.

Like a gas pedal, helping cell grow and dvide

oncogenes are like gas pedals that are stuck down - out of control

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15
Q

Tumour suppressor genes

A

Function to regulate cell growth

Suppress growth of tumours

Are rendered inactive by mutations

Result in loss of suppression of tumour growth

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16
Q

BRCA1 and BRCA2 genes

A

if mutated, increase risk of ovarian cancer and breast cancer

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17
Q

What happens to cells once they mutate

A

Cells can die from damage or by initiating programmed cellular suicide (apoptosis).

Can recognize damage and repair itself

Can survive and pass on damage to two or more daughter cells

Surviving mutated cells have potential to become malignant.

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18
Q

When do normal cells divide

A

When new cells are required

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19
Q

Malignant or cancer cells and adhereance

A

Less adherant and more mobile than normal cells

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20
Q

Normal cells adhere to

A

Other normal cells

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21
Q

Angiogenesis

A

Cancer cells have the ability to secrete a substance that stimulates blood vessel growth to support the rapidly growing mass. This is called angiogenisis

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22
Q

Do normal cells or cancer cells die more easily

A

Cancer cells do not die as easy

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23
Q

Development of cancer, origin of cancer may be

A

Radiation
Viral/bacterial
lifestyle
environemnt

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24
Q

How do cells go from normal to neoplastic

A

Mutation of cell’s genetic structure
From inherited mutation
From exposure to a chemical, radiation, or viral agent
Many carcinogens are detoxified and harmlessly excreted. If not they enter the cells nucleus and alter its DNA.
Mutated cell has the potential to develop into neoplastic cells.

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25
Q

Carcinogens

A

Radiation
Chemical
Viral

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26
Q

Cells damaged by carcinogens may

A

Self repair
Die
Replicate into daughter cells with same genetic alteration

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27
Q

Chemical carcinogens

A

Chemolytics

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28
Q

Radiation

A

Ionizing radiation can cause cancer in almost any human tissue.
Dose of radiation needed to cause cancer is unknown.
Ultraviolet radiation is associated with melanoma and squamous and basal cell carcinoma.

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29
Q

Hepatitis B and C viruses, associated with

A

hepatocellular carcinoma

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30
Q

Human papillomavirus, associated with which cancers

A

squamous cell carcinomas such as cervical, anal, and head and neck cancers

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31
Q

The withdrawal or reduction of promoting factors like ________,_______,_________, &_________ _______ can reduce the risk of cancer development

A

obesity, smoking, drinking, dietary fat, colon cancer,

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32
Q

Latent period for cancer cells

A

1-40 years

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32
Q

Critical mass

A

0.5 cm

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33
Q

1 cm cancer cell has how many cells in it

A

1 billion

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34
Q

what is a criticao mass

A

For disease to be clinically evident, tumour must reach a critical mass that can be detected.
`

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35
Q

Progression of cancer characterized by

A

increased growth rate
invasivness
Metastasis

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36
Q

Most frequent site of meastasis

A

Brain
Lung
Liver
Bone
Adrenal

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37
Q

Tumor angiogenisis

A

_________ is formation of blood vessels within tumour.

Certain segments of a primary tumour can detach and invade surrounding tissues.

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38
Q

Immunological surveillance

A

Response to tumour-associated antigens

Lymphocytes continually check cell surface antigens and detect and destroy abnormal cells.

Involves cytotoxic T cells, natural killer cells, macrophages, and B lymphocytes

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39
Q

Cytotoxic T cells

A

Kill tumour cells directly

Produce cytokines
- Natural killer cells and activated macrophages can lyse tumour cells.
- B cells produce antibodies directed to tumour surface antigens.

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40
Q

Other ways that cancer cells avoid immune response

A

Tumor burden too small to trigger a response or too great and overwhelms the immune response.

Cancer cells produce shields around cells that decrease recognition by the immune system.

Tumor invasion in bone cancer can decrease lymphocytes. Why is that concern?

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40
Q

Immunological escape-Mechanism by which cancer cells evade immune system

A

Suppression of factors that stimulate T cells
Weak surface antigens allow cancer cells to “sneak through” surveillance.
The development of tolerance of the immune system to some tumour antigens
Blocking antibodies that bind tumour associated antigens, preventing recognition

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41
Q

Benign

A

Have cells that stay in one place
Tend to have a regular and smooth shpae and have a covering called capsule
Don’t usually come bac kafter they are removed

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42
Q

Malignant tumors

A

Can grow into nearby tissue and spread to other parts of the body
Can stil come back after removal bc cancer cells might have alread yspread

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43
Q

Early detection is improtant becauce

A

Cancer is usually smaller and easier rto treat
Less chance cancer has spread

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44
Q

Primary cancer prevention

A

Drink in moderation
smoking cessation
Exercise and diet

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45
Q

CAUTION

A

Change in bowel or bladder habits
A sore that doesn’t heal
Unusual bleeding and discharge
Thickening or lump in breast or elsewhere
Indigestion or difficulty in swallowing (Thyroid)
Obvious change in wart or mole
Nagging cough or hoarseness

Also cancer cachexia
- most cancer pts die from malnutrition

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46
Q

FOBT or FIT test

A

For those whoodn’t have increased risk of colorectal cancer Q2 years after 50 years

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47
Q

Digital rectal exam

A

Exam for prostate cancer in men

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48
Q

Women screening

A

PAP smear and pelvic examinations: Q1 year until three consecutive negative exams then Q3 years until 69 years
Mammogram: Q2-3 years from 50-74 years of age;

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49
Q

Cancer is nrearly always diagnosed by

A

Expert pathologist

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50
Q

Prognostic factors

A

Favorable prognostic factors can have a positive effect on the outcome. Unfavorable prognostic factors can have a negative effect on the outcome.

Type of cancer
Subtype of cancer based on the type of cells or tissue (histology)
Size of the tumor
Stage: how far and where the cancer has spread
Grade: how fast the cancer cells are growing

51
Q

More prognostic factors

A

Age (younger)
Comorbidities
Functional status
Wt loss
Coping ability

52
Q

Stage of cancer includes

A

the size of the tumor,
which parts of the organ have cancer,
whether the cancer has spread (metastasized)
0: Cancer in situ
I: Tumour limited to tissue of origin; localized tumour growth
II: Limited local spread
III: Extensive local and regional spread
IV: Metastasis

53
Q

Grading used for

A

Describes how the cancer cells look compared to normal, healthy cells

Used to help predict how the cancer will grow and to plan treatment

Grading depends on

how different the cancer cells look from normal cells (differentiation) and other features of the tumor such as the size and shape of the cells and how the cells are arranged
how fast the cells are growing and dividing
whether there are areas of cell death in the tumor (called necrosis)

54
Q

High grade vs low grade cancer

A

Some cancers have their own grading systems, but most solid tumor cancers are given a grade between 1, 2, 3 or 4. (Solid tumor cancers, like breast or prostate cancer, form lumps.) A lower number means the cancer is a lower grade. Different parts of a tumor can have cancer cells with different grades. But the tumor is usually graded as the highest grade seen anywhere within the tumor.

55
Q

Know the TNM table

A

Tumor
Nodes
Metastasis

56
Q

Tumor classicivation TNM

A

T0 – no evidence of primary tumor
Tis – evidence of carcinoma in situ
T1, T2, T3, etc. Progressive increase in tumor size and involvement.
Tx – unable to assess tumor

57
Q

Node classication TNM

A

N0 – No regional lymph node metastasis
N1, N2, N3 – Increasing involvement of regional nodes.
Nx –Regional lymph nodes cannot be assessed clinicall

58
Q

Metasistis CLassification

A

M0 – no evidence of distant metastasis
M1, M2, M3 – Metastatic involvement
Mx- Presence of metastasis cannot be assessed.

59
Q

Most concerning s/s at cancer diagnosis

A

Cancer cacthexia

Wt loss (muscle)

60
Q

Why do palliative cancer pts recieve treatment

A

To keep them comfortable

61
Q

Surgery

A

diagnostic, preventative, eliminative, reconstructive, or palliative

62
Q

Radiation

A

local destruction of cancer cells; adjuvant (supplements surgery) and palliative.

63
Q

Biotherapy

A

Biotherapy-uses the body’s immune system to kill cancer cells.

64
Q

3 reasons why surgery is used for cancer

A

Remove tumor (Cure)
Control spread, slow process
Paliation (Causing pain)

65
Q

The removal of the primary cancerous tumor is

A

the most common operation to try and cure or control cancer.

66
Q

Risks of primary cancerous tumor

A

Some tumor cells can shed off and seed for regrowth

67
Q

Chemo definition

A

type of treatment that includes a medication or combination of medications to treat cancer. The goal ofchemois to stop or slow the growth of cancer cells. Chemo medications attack rapidly growing cancer cells, but they can also affect healthy cells that grow rapidly.

68
Q

How is chemo dilivered what route

A

IV, PO, IM, Intracavitary (peritoneal), Intrathecal (into sub-arachnoid space), intra-arterial (into artery supplying the tumor), intravessicle (directly into the bladder) or SubQ

69
Q

How long is chemo therapyu

A

Months to years

70
Q

Big concern with chemo

A

Affects bone marrow

Disrupts production of blood cells

71
Q

Why would someone be prescribed chemo

A

If cancer is in the lymph or bloodstream

If they suspect cancer has spread

72
Q

Why do combo of chemo work better

A

Attack cnacer cells at different time in cell cycle

73
Q

Focus more on THIS lecture

74
Q

Chemo delivery often occurs via

A

porta cath

Central IV line that is threaded into one of the large central veins in the chest, which empties into the heart. The vein which is used most often is the superior vena cava. This vein is preferred because it is very close to the skin and easy to find with ultrasound

75
Q

Use for porta cath

A

Blood draws
IV hydration
Chemotherapy

76
Q

How does radiation work

A

Works by making small breaks in the DNA inside cells. These breaks keep cancer cells from growing and dividing and cause them to die.

More localized than chemo

Most times in early stages to shrink tumor prior to operation

77
Q

General side effects of radiation

A

Skin problems and fatigue
Other side effects reflect the location of the XRT

78
Q

3 types of radiation

A

External
Internal
Systemic

79
Q

Internal radiation

A

Internal radiation is also called brachytherapy. A radioactive source is put inside the body into or near the tumor.

Less side effects

80
Q

Systemic radiation

A

Radioactive drugs given by mouth or put into a vein are used to treat certain types of cancer. These drugs then travel throughout the body.

81
Q

Biological therapy how does it work

A

Restore or help host immune system responses, and interfere for the cancer’s ability to metastasize or differentiate.

82
Q

Growth Factors

A

stimulate production, maturation, and release of cells from the bone marrow, increasing functional ability of blood cells. Ex. GCSF (Neupogen and Neulasta). Bone pain is common.

If chemo causes low WBCs, this can be given to increase cell count so they can continue chemo

83
Q

One of the most important responsibilities of the nurse is that of differentiating between

A

Is the effect from the drug or from the dx process

84
Q

Chemotherapeutic agents cannot selectively distinguish between normal and cancerous cells

therefore the adverse effects of chemo are caused by the destruction of normal cells especially those that proliferate rapidly like cells from the ________ ________, _____ ______ and _____________systems.

A

GI Tract, skin and hair

85
Q

When you think of the function of the bone marrow what should we monitor?

A

RBCs, Hgb, WBCs, and platlets

WBCs affected quickest and most ( a week)

Platlets 2-3 weeks

RBCs 2-3 months before affected

86
Q

Interventions for low WBC count

A

Reverse precautions

87
Q

Response to low RBC

A

Blood tranfusion, folic acid, iron

88
Q

GI system efects

A

N/V
Aorexia
Diarrhea
Toxic effects on the liver

Stomatitis (sores in mouth and upper resp tract)

Cool foods are good, Antiemetic drugs

89
Q

Integ effects of chemo

A

Alopecia
Skin rashes
Neurogenic sensations
photosensitivity
Hyperpigmentation
Extravasation

90
Q

Infection related to cancer

A

Common Sites: Lungs, GU system, Mouth, Rectum, Peritoneal cavity, blood

Caused by ulceration, compression of vital organs

Neutropenia due to disease process or tx

91
Q

Febrile Neutropenia in cancer pts

A

Increase temp, HR, RR

Infection can be rapidly fatal in cancer patients so it must be treated ASAP.

A patient with a temp higher than 38 C should go to emergency or the cancer clinic ASAP

92
Q

Tx for neutropenia

A

Preventing infection is best

Reverse protection

Hold chemo, no pets, gardening, etc.

Pharm
Granulocyte Colony-Stimulating Factors (G-CSF)
Antibiotics

93
Q

Malnutrition

A

Measure albumin, give them any food they want

Ensure, protein etc.

94
Q

Oncologival emergencies

A

Superior Vena Cava Syndrome
Due to: Obstruction of vena cava by a tumor (commonly by Lung Ca, Hodgkins and Non-Hodgkins Lymphoma)

  1. Malignant Spinal Cord Compression (MSCC)
  2. Intestinal Obstruction:

Requires urgent radiation therapy

95
Q

Superior vena cava syndrome manifestations

A

Facial Edema
Periorbital edema
Distended neck and chest veins
Headache
Seizures

96
Q
  1. Malignant Spinal Cord Compression (MSCC)
A

Due to: Tumour compressing the spinal cord (primary or metastatic tumours)

97
Q

Manifestations of Malignant Spinal Cord Compression

A

Tingling, loss of sensation, bowel and bladder function impaired/lost, paralysis pain etc.

98
Q

Treatment for Malignant Spinal Cord Compression

A

Steriods to decrease inflammation
Urgent radiation therapy

99
Q
  1. Intestinal Obstruction:
A

Complete or partial obstruction d/t swelling of the intestine or solid tumour invasion.

100
Q

Manifestations of Complete or partial obstruction d/t swelling of the intestine or solid tumour invasion.

A

Profuse, projectile vomiting with foul smelling vomit (like feces)

Ovarian cancer is a high risk

101
Q

Symptoms of Complete or partial obstruction d/t swelling of the intestine or solid tumour invasion.

A

N/V, abdom distention and pain

102
Q

Intervention for bowel blockage

A

Surgery removal
NG tube

103
Q
  1. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
A

abnormal or sustained production of ADH (occurs most often in Small Cell Lung Ca)

104
Q

Symtoms of inapproriate ADH

A

Fluid retention
Serum hypo-osmolality
Dilutional hyponatremia
Early: muscle cramps, weakness
Late: vomiting/ abd cramping/ seizures/ coma
Decreased urine output

105
Q

Treating SIADH

A

Fluid restriction
Treat the cause

106
Q

Oncological Hypercalcemia

A

Most common condition metabolic oncolgoical emergency

-Has a poor prognosis,80% of patients with hypercalcemia will die within a year and there is a median survival of 3 to 4 months.

-Cancer-related hypercalcemia is the leading cause of hypercalcemia in hospitalized patients.

107
Q

What causes hyperCa in cancer pts

A

Increased breakdown of bone tissue (osteoclastic activity) due to malignancy (multiple myeloma) or bony metastases (from lung, breast, etc). Or release of parathyroid like substance from certain cancers.

108
Q

Clijnical manifestations of hyperCa

A

Confusion
Apathy/ Depression/ Fatigue
Muscle weakness
ECG changes
Anorexia/ Nausea/ vomiting
Polyuria/ nocturia

severe muscle weakness, decreased deep tendon reflexes, kidney stones, irregular heartbeat even heart attack.

109
Q

Calcium measurement

A

It’s the ionized calcium that you are concerned about because ionized calcium is the physiologically active form of calcium; calcium bound to albumin is inactive. Standard lab tests usually measure the total calcium.

110
Q

Ionized vs Total Calcium

A

Ionized CAN be calculated from total

111
Q

HyperCa tx

A

Mobility
Hydration***
Calcitonin
Loop diuretic
Bisphotphonates
Glucocorticoids

112
Q

. Tumor Lysis Syndrome (TLS):

A

Follows the destruction of a large number of neoplastic / cancer cells due to chemo or radiation allowing for vast numbers of intracellular electrolytes to enter the blood stream. Often causes changes in potassium, phosphorous and uric acid levels.

113
Q

Tumor Lyusis synd most comon in which pts?

A

Most commonly seen in patients with highly aggressive hematologic cancers (ie high-grade lymphomas and acute leukemias

Usually occurs when effective chemotherapy has begun, but can occur after radiation and/ or spontaneously

114
Q

Hyperkalemia can cause serious and occasionally fatal — ___________

A

Dysrrythmias

115
Q

Tumor Lysis syndrom labs

A

HyperKalemia
Hyperphosphatemia
Hypocalcemia
Hyperuricemia

116
Q

Tx for TLS

A

Lots of Fluids**
Alipuronal - reducing buildup of uric acid in the blood

117
Q

What is allopurinol? Why do you think it would be used in Tumor Lysis syndrome?

A

TO preserve the kidneys

118
Q

Hyper viscosity Syndrom

A

Hyper viscosity syndrome is a condition that occurs when your blood becomes so thick that your body’s overall blood flow decreases.

It can be caused by blood cellschanging shape or by an increase in serum proteins, red blood cells, white blood cells, or platelets.

119
Q

Classic hyperviscosity

A

includes mucosal bleeding, visual abnormalities, and neurological abnormalities

119
Q

LOOK on slides for HVS

120
Q

Standard of care for managing hyperviscosity

A

therapeutic apheresis

121
Q

Cardiac Tamponade

A

Fluid accumulation in the pericardial sac, constriction of the pericardium by a tumour, or percarditis secondary to radiation.

122
Q

S/S of Cardiac tamponade

A

Heavy feeling over the chest
Tachycardia
SOB
Cough
Distant heart sounds
Dyspahgia and many more…..

123
Q

Treament for cardiac tamponade

A

Treatment- Reduce the fluid around the heart and mange symptoms

124
Q

Managing physical symptoms

A

Treating fatigue with steriods
Constipation - must be on bowl protocol

Dyspnea - treated with chest tube draining
- pace activites
- Narcotics reduce. experience of breathlessness
- Fans

N/V
Assessing and treating cause

Dehydration
- Oral hygeine
- Giving fluid

Anorexia/Cachexia
Meds to help make you eat

125
Q

Vomiting or pain treated first

A

Nausea/vomiting