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Stephanie Talbot

Module 7.1: Discuss The Pre-operative Assessment

Hx:
1. age >65 increases risk 2. drug, alcohol, tobacco use, 3. current medications 4. use alternative therapies 5. past surgeries & how tolerated 6. ALLERGIES

Module 7.1: Discuss The Pre-operative Assessment


Physiological

assessment: Neurologic- LOC, motor & sensory fxn, risk falls Cardiovascular & respiratory Renal & hepatic fxn Musculoskeletal fxnarthritis-may affect position

Fluid/e-lyte balance- no K+ imbalances Contageous dxneed to clear up before surgery Medication hx- do need heart, respiratory, seizure meds

Module 7.1: Discuss The Preoperative Assessment Psychosocial assessment: 1. Level of anxiety 2. Ability to cope 3. Family or support persons

Module 7.1: Discuss The Preoperative Assessment


diagnostics:

Urinalysis- bun, creatinine, fasting glucose, protein, pathogens, sp.gr, e-lyte balance CBC-RBC, WBC Platelet, Hct, Hgb

Pt, PTT INR AST, ASL (liver fxn) Type and crossmatch X-ray, EKG ABGs

Module 7.1: What are the NSG Interventions during the pre-operative period? Hx & physical Baseline Vs, skin prep Preoperative teaching Confirmation informed consent NPO and bowel preparation, administration regular meds, drains, tubes Removal personal items Offer bed pan Administer pre-op drugs, raise side rails i.d pt, surgical site and procedure one last time

Module 7.1 : What are the Preoperative Medications?


Anticholinergic
Inhibits PNS response
1. 2. 3.

Atropine- decrease saliva, gastric juice production and sweat Scopolamine- inhibits emesis and motion sickness Robunol- decreases gastric juices

Sedatives, anxiolytics, hypnotics Benzodiazepines Used as introduction to

S.E: dry mouth, orthostatic hypotension, urinary retention, constipation, thick, dry pulmonary secretions, blurred vision, tachycardia

anesthesia: decreases anxiety, induces sleep, relaxes muscles Lorazapam (ativan) Diazepam (valium) Flurazepam (dalmane) Midzolam (versed) S.E: confusion and amnesia

Module 7.1 : What are the Preoperative Medications and their S.E?
Antiemetics
Inhibit nausea and

Antihistamines

vomiting Trimethobenzamide (tigan) Ondansetron (zofran) Aprepitant (emend) Metaclopramide (reglan) S.E: headache, dizziness, diarrhea, fatigue

Used to enhance effects anesthesia


Hydroxazine (atarax,

vistaril)

Informed consent
Discuss criteria informed consent The physicians What is the nurses role in informed consent? To witness that the

responsibility to give informed consent and explain all risks involved, outcomes etc. Involves: Adequate information Understanding and comprehension Voluntary signing

signature was given voluntarily

Intraoperative period
Who is responsible for positioning

Allergies?

The nurse and the rest of the surgical team

Always assess for allergies

Nurse pads boney prominences and secures limbs when needed

Common:
Latex Betadine- contained

in shell fish

Intraoperative period
Discuss spinal anesthesia.
Is local anesthesia injected into the

subarachnoid space into the CSF


An epidural

is injected into the epidural space

Useful for cardiac and respiratory patients Watch for spinal headache and hypotension

If have complications give EPINEPHRINE


If have systemic rx. Watch for CNS stimulation

followed by CNS depression

Postoperative period
Complications
Complications

Anaphylactic rxs Malignant

DVT, Respiratory problems Emergency delirium-

hyperthermia Shock, Hypo/hypertension Dysrhythmias Fluid/e-lyte imbalances: overload, Hypokalemia

hypoxia check Delayed emergence Confusion , N/V Hypo/hyperthermia Decreased UOP Wound problems: infection, dehiscence, evisceration

Postoperative period
Lab tests, results &
WBC=4000-10000/mm
Neutrophils-55-70% Macrophage-28% Monocyte-3-4% Eosinophil-1-2% Basophil-1%

interpretation:
HCT=35=34%, HgB=12-18g/dL,
platelet=200,000-200,000, RBC=45million PT, PTT, INR- increase suggest bleeding BUN=20-30mg/dL, creatinine=.6-1.0mg/dL Increase suggest kidney problem

Fasting glucose=70-110mg/dL ABG: acidosis/alkalosis E-lytes: Na+ and K+ Liver fxn tests (AST, ASL)-

increase suggest liver problem

Postoperative Period: Discuss the nsg interventions of the PACU.


Monitor respiratory

auscultate BS, maintain airway Monitor cardiovascular status-assess skin temp, pulses, heart rate, BP Musculoskeletal- ask pt move limbs Neurologic- assess LOC, call pts name

Temperature

hypothermia/hyperther mia
Normal temp <100.4 in 1st 24hrs

Fluid/e-lyte- monitor

I/O, weights Pain-most pain after 1226 hrs

Assess q2

Renal status- assess I/O,

expect 800-1500 in 1st 24hrs

What are the phases of shock


Initial: Decrease C.O leads to decrease tissue perfusion & O2 needs of cells anaerobic metabolism lactic acid production.

S/S slight increase BP

Compensatory: SNS activated and releases epinephrine and norepinephrine causing vasoconstriction of periphery..shunts blood to heart and brain

s/s: slightly normal BP, tachypnea, cool dry pale skin, thirst

What are the phases of shock


Progressive: Body cant maintain compensations, hypoxia sets in vital organs, anoxia sets in in nonvital organs continued production lactic acid

s/s: decreased: LOC, BP, increased: HR, RR, hypothermia, cool, clammy pale skin

refractory: Exacerbation anaerobic metabolism vasodilation and leaky capillaries, proteins leak into tissues, blood pools, respiratory/cardiac arrest DEATH

Section 4.1: NG tubes


Discuss NG tube to suction

w/ nsg interventions
3 types sxn: Intermittent- used single lumen tubes- 80-100mmHg High-100-120mmHg not used Continuous-used double lumen tubes-60-120mmHg

Verify placement Connect sxn wall occlude

Introduce self and I.D pt,

explain procedure Hand hygiene

to det. If working properly, listen for sxn Connect to NG tube-watch for gastric contents Assess appearance gastric contents Document Check connections q30min for 2hrs to assure proper fxning

Section 4.1: NG Tubes


Demonstrate the correct administration of tube feeding.
i.d pt Verify placement and patency tube: Air bolus & auscultate Aspirate, pH X-ray

Aspirate stomach contents, if >100 or double hold Instil 30-60 cc H2O Administer feeding Instil 30-6- cc H2O

Section 4.2:
Discuss the Types of wound healing 1. Primary intention- wound approximated ex. Surgery 2. Secondary intentionwound allowed to stay open & fill in with granulation tissue ex. P-ulcer 3. Tertiary intention- wound stays open 3-5dys decrease edema and infection, then closed via primary intention ex. Dirty wounds What are the various drains?
Jackson Pratt & Hemovac-

closed systems to maintain sxn, empty drainage, open port and put pressure on device, then recap port to establish sxn Penrose drain- open gravity system Purpose drains= to promote healing of the underlying structures

Section 4.3: IVs


Local complications
1.

Systemic complications
1.

2.

3.

4.
5.

Infiltration/extravation- edema above the site, cool skin, leaky fluid, mottled skin D/C, cold compress Thrombosis- clot in vein red, swollen painful site D/C , cold compress Phlebitis-inflamed vein red, pain at site 1. D/C, warm compress Thrombophlebitis- D/C, cold then warm compress Infection- red, pain, drainage, pus 1. D/C, express drainage.

2. 3. 4.
5. 6.

Embolism: air, pulmonary, catheter (place left side &trendelenburg for air, tourniquet catheter) Hematoma- put pressure on site Systemic infection Speedshock-stop infusion, notify DO, VS Circulatory overload- elevate HOB, keep warm, assess edema, decrease rate, notify DO Allergic rx.

Section8.1: Inflammation
Define inflammation
The response of the tissues to damage

s/s: Red Swollen Pain site Loss function heat

Section8.1: Inflammation: Stages of inflammation


Vascular &cellular response

Exudate production
Exudate consists dead cell,

Histamine release in

response to injury vasoconstriction followed by vasodilation & influx blood into injured area Fluid, proteins, leukocytes into site, as blood slows leukocytes emigrate into tissues and engulf pathogens. This causes bone marrow produce and release more WBC

WBC, pathogen etc Thromboplastin, fibrinogen and platelets form network to wall off area

Section8.1: Inflammation: Stages of inflammation


Reparative (Regeneration)
Presence WBC stimulate healthy cells to divide Minor wound replaced cells through re-

epathilization Major wounds for scar-granulation tissue

Section8.1: Inflammation
Discuss the medications of inflammation (SE)
1. 2.

Discuss local heat/cold application.


Heat causes vasodilation &

3.
4. 5. 6. 7.

Decongestants- Sudafed Antihistamines-block histamine effects Sympathomimeticepinephrine CorticosteroidsAntipuritic- topical lotions ex. Calamine lotion Mast cell stabilizercromalyn blocks leukotrines immunotherapy

increases blood flow to the area Cold causes vasoconstriction DO NOT GIVE HEAT WHEN:
1st 24hr after trauma,

Haemorrhaging, Malignant tumour, Skin conditions cause redness, blisters DO NOT GIVE COLD WHEN: Open wound, poor circulation, allergy/hypersensitivity to cold

Section 5.3: Thyroid Gland: Differentiate between Hyper/Hypothyroidism


Hypothyroidism: Decreased thyroid hormones T3, T4, TH Cause: Lithium, destruction thyroid, atrophy thyroid, lack iodine NSG: Monitor BP, HR, shock due to deceased C.O, administer synthroid, assess chest pain and dyspnea s/s: every-thing slows

down

Decreased: metabolism,

UOP, HR (bradycardia) Constipation, dysrhythmias, chest pain activity & cold intolerance Dyspnea Dry, scaly skin MYXEDEMA COMA

Section 5.3: Thyroid Gland: Differentiate between Hyper/Hypothyroidism


Hyperthyroidism: Increased thyroid hormone: T3, T4, TH Causes: Autoimmune disorder Excessive release thyroid NSG: Monitor VS, decrease environment stimuli, keep cool Administer anti-thyroid meds: PTU, methinazole (tapazole), SSKI, Lugals soln, radiation therapy to decrease size, bblockers tx tachycardia (propanolol-inderal; atenololtenormin). Assess stridor Watch agranulocytosis

s/s:everything speeds up

Warm, moist skin Expthalamous Goiter Tachycardia Increased: RR, HR, BP, metabolism Weight loss Heat intolerance Muscle weakness and wasting Increased tissue sensitivity THYROID STORM

Section 5.3: Pituitary Gland


Discuss Cushings: Characterized by increased cortisol Causes: Pituitary tumours Prolonged use corticosteroids NSG: Assess/monitor fluid overload Prevent skin breakdown
Administer Mitotane to decrease

s/s:
Weight gain, acne,

ACTH Restrict fluid & Na+ ingestion Monitor I/O, weight, & sp. Gr Radiation therapy, surgery, bblockers Assess psychosocial needs

Hirsutism, hypervolemia Increased: HR, BP Straie Activity intolerance Hypergylcemia Poor wound healing

Section 5.3: Thyroid Gland: Discuss Thyroidectomy

Want to shrink thyroid prior to removal so administer

radiation (make sure increase fluid intake to help excrete it), SSKIs and thyroid drugs until it is within normal size and fxning.

Section 5.3: Thyroid Gland


What are the parathyroid
NSG:
Monitor I/O, VS Administer furosemide to increase

glands and their fxn?

Parathyroid glands release

PTH-essential Ca2+ /P3+ balance

Acts on bone, kidney and intestines

Causes: excessive ingestion Ca2+ & VitD, increased PTH production, kidney dx s/s: increase: bone fractures, HR, constipation, lethargy, dyspnea, n/v, anorexia, psychosis, arthritis

excretion Administer calcitonin to decrease bone Ca2+ release Administer mithromycin to bind Ca2+ for excretion Labs: Bun, CBC, creatinine, Ca2+ etc Remove parathyroid gland

Section 6.1: Pain


Discuss Pain & endogenous opiods
Pain is an unpleasant sensory

PRN medications
Give these as needed

experience (nocioception)
Transduction-pain stimulus-

release chemical mediators Transmission-impulse travels to brain to tell of pain Modulation-release of endogenous opioids, serotonin and norepinephrine to inhibit (dampen) painful impulses Perception-you sense the pain

Section 6.1: Pain


What is tolerance?
The max amt of pain person

Discuss PCA
Patient controlled analgesia-

willing to tolerate without seeking pain relief

permits patients to administer doses of analgesia Predetermined dose administered Safety mechanisms prevent overdose

Section 6.1 Pain


Discuss use of analgesics in the elderly. Use around-the-clock dosing Be aware of adverse affects NSAIDS ( bleeding, nephrotoxicity)and acetaminophen (hepatotoxicity) Start low and go slow for increasing dose Avoid meperidine, codeine, and propoxyphene Use non-drug pain relief measures

Section 8.2: Hypersensitivity


Describe self-tolerance.
The ability to recognize
Describe immunocompetence. The ability of the immune

self-cells from non-self cells

system to identify and fight foreign substances.

Section 8.2: Hypersensitivity


Differentiate between hypersensitivity rx &

autoimmune disease.
A hypersensitivity reaction is an overreaction in

response to an invader or injury An autoimmune disease is a disorder in which the body attacks its own cells, failing to recognize self-cells from non-self cells

Section 8.2: Hypersensitivity


Name the organs of immunity. Thymus gland Bone marrow Tonsils Lymph nodes spleen

Section 8.2: Hypersensitivity


Name the cells of the immune response. Neutrophils- destroys microorganisms & foreign proteins Monocytes (phagocyte)- engulfs and delivers pathogen to lymphocyte Lymphocyte:

B-lymphocyte- fxns in antibody-mediated reactions T-lymphocyte- fxns in cell mediated reactions 1. Cytotoxic T- kills cells containing foreign proteins 2. Memory T3. Helper T-CD4+- recognition of self cells 4. Suppressor T-CD8+-inhibits hypersensitivity rxs

Section 8.2: Hypersensitivity


Name the cells of the immune response cont... Natural Killer cells-seeks and kills viruses and cancer Dendritic cells- destroy antigens at site of contact ex. Skin and mucous membranes Cytokines- chemical messenger between macrophage, b-cell and t-cell. Instructs to:

Change proliferation, activation, secretion and differentiation

Section 8.2: Hypersensitivity


Differentiate between humoral and cell mediated immunity
What does humoral and cell mediated immunity protect against?

Humoral immunity. It is termed

Humoral immunity protects

antibody-mediated immunity (through the B-cell system). Characterized by the production of antibodies in response to a foreign substance Cell-mediated immunity is initiated through the T-cell system. Responsible for immunity within the cell through the recognition of antigens within the cell.

against: Bacterial viral infections Respiratory gastrointestinal pathogens Cell-mediated immunity protects against: Transplant rejection Tumours Contact hypersensitivity Fungal infections

Section 8.2: Hypersensitivity


What are some examples of humoral and cell

mediated immunity?
Humoral- bacterial infections, anaphylactic shock,

transfusion reactions Cell mediated-First Read The Contract

Fungal infections, rejection of transplants, tumours, and contact hypersensitivity

Section 8.2: Hypersensitivity: Discuss the 5 types of hypersensitivity rxs


Type 1: Atopic Allergy Over-reaction in response to an antigen or injury IgE and histamine release Ex. Allergic rhinitis (hay fever), anaphylactic rxs, and allergic asthma Type 2: Cytotoxic Involves IgG & the engulfing of self cell containing a foreign protein (gets phagocytised and lysed). Ex. Autoimmune hemolytic anemia, thrombocytopenia, myasthenia gravis Tx: plasmaphoresis & D/C the offending antigen

Section 8.2: Hypersensitivity: Discuss the 5 types of hypersensitivity rxs


Type 3: Antibody-complex. Occurs due to excess antigens in the system Involves IgG & IgM Antibody-antigen complex is formed, which is deposited in the vessels and tissues leads to inflammation and damage of the tissues

Type4: Immune complex


sensitized T-cells attach

Ex. Rheumatoid arthritis, lupus

to an antigen forming an immune complex which releases lymphokines stimulates antigen to destroy the pathogen Ex. Poison ivy, graft rejection, positive TB test, sarcoidosis

Tx: antihistamines,

prednisone

Section 8.2: Hypersensitivity


What type of hypersensitivity rx involves IgE?

What are the s/s type 1 rxs?


Nasal congestion, runny nose Itchy, watery eyes & skin Wheals and flares Hives (uticaria), erythema Angeodema (swollen lips,

Hypersensitivity 1 type

reactions which are atopic allergic reactions Also involve the release of histamine See an increase in eosinophil count

tongues, & eyes) Mucus production Bronchospasm, stridor Dysrhythmias, rapid weak pulse hypotension

Section 8.2: Hypersensitivity


How do you treat type 1 rxs?
1. 2.
What classification of hypersensitivity involves IgG or IgM? Give ex.

3. 4. 5.
6. 7.

Antihistamines- inhibit effects histamines Decongestants- phenylephrine, pseudophedrine Sympathomimetic- epinephrine Corticosteroids- allergic rhinitis Antipuritic- topical lotions ex. Calamine lotion, camphor, methanol, phenol Mast-cell stabilizer- inhibit release histamines and leukotrinescromalyn (nasalcrom) Immunotherapy- adm. Small amts of allergen in progressive strengths to build immunity.

Hypersensitivity type 2-

cytoxic Ex. Autoimmune hemolytic anemia, ABO rxs

Section 8.2: Hypersensitivity


What type of reaction involved in transplant rejection?

Which type of hypersensitivity rx involves IgG & IgM ?

Hypersensitivity type 4:

Hypersensitivity type 3: in

immune-complex sensitized T-cells

response to excessive antigens in system antigen-antibody complex which deposits in blood vessels, tissues and joints.

Section 8.2: Hypersensitivity


List the s/s of type IV hypersensitivity rxs.
Immune complex of sensitized T cells Cell mediated response that occurs within 24-48hrs T-cell release mediators which trigger macrophage to

destroy the antigen tissue damage (no histamine in this rx) Puritis, vesicles, localized burning, scaling

Section 8.2: Hypersensitivity


What type of immunity fights anaphylactic shock, transfusions, and bacterial infections?

Humoral immunity fights

anaphylactic shock, transfusion reactions and bacterial infections

What is the purpose of cellmediated immunity? Provides immunity (protection) within the cell Fights: First Read The Contract: Fungal infections Rejection of transplants Tumours Contact hypersensitivity

Section 8.2: Hypersensitivity


What changes occur in the immune systems of the elderly

which increase their susceptibility to infection? Elderly have decreased immune fxn which increases their risk of infection Have decreased thymus gland which: Decreases amount of differentiation T-cells More pre-curser cells Delayed hypersensitivity response

Section 8.2: Hypersensitivity


What foods should you avoid if you have a latex allergy?
Differentiate between autoimmunity and immunodeficiency.

Bananas Avocados Plant foods

Autoimmunity is an immune response against self. Antibodys or lymphocytes attack healthy cellscant recognize ex. Lupus, rheumatoid arthritis.
Tx=plasmaphoresis

Complications=hypotension and citrate toxicity Immunodeficiency is the decreased ability of the immune system to protect self due to decreased WBC, improper development or illness ex. Cancer and its treatment

Section 8.2: Hypersensitivity


Describe plasmaphoresis and what are its two major

complications? The removal of plasma containing components that cause dx ex. Antigen-antibody complexes Complications: Hypotension Citrate toxicity

Section 8.2: Hypersensitivity


Differentiate between active and passive immunity.
Active immunity results from exposure to an

antigen or disease Passive immunity results from the induction of antibodys to protect against disease

Section 8.2: Hypersensitivity: Define anaphylaxis (state


causes, s/s, tx)
overreaction in response to Anaphylaxis is an extreme

an antigen

Causes: antibiotics

(penicillin, vanco, tetracycline), insect bite, contrast media, local anesthetic, opiods, food allergies, heat/cold, exercise, insulin, adrenocorticotropic hormone, vasopressin, whole blood and cryoprecipitate, shell fish, pollen

s/s: feelings apprehension, agioedema, bronchoconstriction, wheezes, stridor, weak rapid pulse, dysrhythmias, shock Tx: assess respiratory fxn, put airway and O2, d/c drug causing problem, admin epinephrine, antihistamines, Theophylline, Albuterol, elevate HOB 45 degrees

Section 8.2: Hypersensitivity


Differentiate between antigen-complex and delayed hypersensitivity rxs (include ex).
Antigen complex is a type 3 hypersensitivity rx

involving foreign proteins. Complex is deposited in blood vessels, tissues and joints Delayed hypersensitive rx are type 4 reactions involving sensitized T-cells...due to excessive antigens in the system

Section 8.2: Hypersensitivity


Describe immunosuppressive therapy and when is it used?
Immunosuppressive therapy is the suppression

of CD4 cells (immunity and inflammation) Used to prevent organ rejection in transplants Occurs with the use of corticosteroids, radiation Complications: Increases risk of infection and cancer

Section 8.2: Hypersensitivity


What type of immunity is important for the prevention of cancer and its metathesis after exposure to carcinogens?
Cell mediated immunity because in cell

mediated immunity there is recognition between the cells that belong to you and those that do not as well as the recognition between normal and abnormal cells

Section 8.2 HIV


What is immunodeficiency? Immunodeficiency is a decrease in immune fxn due to decreased WBC or improper fxning WBC
State the difference between primary and secondary immune deficiency

Primary immune

deficiency is congenitalborn with it Secondary immune deficiency occurs due to medical treatment or disease

Section 8.2 HIV


What causes of HIV
Exposure to the HIV virus

What cell does HIV attack?


CD4+ t-cell

via blood and body fluids

Section 8.2 HIV


What is the normal T-cell (CD4+) level and the complication of having decreased T-cells?
Normal CD4+=800-1200/uL

See immune problems @ 200-499/uL


See extreme immune problems <200/uL

Having a decrease in T-cells leaves you susceptible to opportunistic infections and disease like cancer

Section 8.2 HIV


What is the difference between HIV and AIDS? HIV is the presence of virus AIDS is the presence of the virus and opportunistic infections
Explain the s/s HIV (clinical manifestations)
Acute infection: Flu-like symptoms Chronic: Early: asymptomatic Intermediate: CD4+-200-499 Oral hairy leukopenia Karposi sarcoma Herpes Shingles Oral candidias Night sweats, diarrhea Headache Late: CD4<200 Opportunistic infections and cancer, wasting syndrome, aids dementia

Section 8.2 HIV


Describe the pathophysiology of HIV. Virus enters body (retrovirus) Finds CD4 cell and enters it Forces CD4 to replicate its DNA, incorporating it into human cell Causes destruction and damage to CD4

Section 8.2 HIV


What type of HIV person is most infectious? The person who has a high viral load one who has just contracted the dx but not yet diagnosed
What do you do if you get a needle stick? PEP recommended:

Basic: 2 drugs

Zidovudine &

lamivudine/emtricitabin
Expanded: 3 drugs

Section 8.2 HIV


I.D the most common opportunistic infections in HIV patient.

Pneumocystis jiroveci

pneumonia Pneumocystis carinii pneumonia Karposi sarcoma Oral candidias Oral hairy leukopenia Varicella zoster Herpes TB

What is the lymphocyte count of the pt with AIDS? <200uL

Section 8.2 HIV


What drugs cause immunosuppression?
Cytotoxic drugs Corticosteroids

Cyclosporine- prevents transplant rejection


Radiation therapy

Section 8.2 HIV


What tests are used to identify HIV positive people?

How is HIV transmitted?


Sexual contact (risky sex,

Western blot test ELISA-enzyme linked

immunosorbent assay Viral load tests- measure amt virus in the blood

multiple partners, anal, vaginal, oral) Blood transfusions Sharing needles Perinatal transmission to newborns Work risk (exposure blood and body fluids)

Section 8.2 HIV


How do you treat individuals infected with HIV?
Multidrug cocktail: AZT, retroivir Routine testing viral load

Good nutrition
Rest Decreased stress

Avoid infections

Section 8.3: Cancer


What is cancer?
Cancer is the malignant growth of cells It is uncontrolled growth

Cancer cells have no fxn

What is a benign cell? Normal cells growing in the wrong place or at the wrong time.

.
Section 8.3: Cancer: List the characteristics of a normal cell
Limited divisibility Smaller nuclear to

cytoplasm ratio Apoptosis- preprogrammed cell death Differentiated functioneach cell has a specific function for the body Tight adhesion- cells held tightly together by proteins

Morphology: each cell has specific appearance, shape and size Regulated and controlled growth- cells only divide when they have to and when they do it is controlled and regulated Diploid chromosomeshumans have 23 pairs Non-migratory- doesnt wander Contact inhibition- cells stop dividing once surrounded on all sides by cells

Section 8.3: Cancer: List the characteristics of a benign cell

Continuous or inappropriate growthnot needed for normal fxn Small nuclear to cytoplasm ratio Specific morphologylook like the parent cells

Specific differentiation

in fxn- performs fxns of parent cell ex. Endometriosiswhen grows abnormal place still acts like endometrial tissue Tight adherence and doesnt wander Has orderly growth and not invasive

Section 8.3: Cancer: List the characteristics of a cancer cell.


Rapid and continuous Chromosomes-

cell division Anaplasia- no longer look like the parent cell Loos adhesion- they dont produce fibronecton Migration- wander every-where because of the loose adhesion

ANEUPLOIDY- have broken, lost, damaged too long/short chromosomes Specific fxn lost Does not adhere to contact inhibition

Section 8.3: Cancer


Differentiate between carcinogenesis and oncogenesis.

Define Malignant transformation

These terms mean the same thing cancer

The transformation of a normal cell into a

development.

cancer cell

Section 8.3: Cancer: Describe the steps of Malignant Transformation


Initiation
Activation of oncogenes

promotion
Any substance which

(they are turned on excessively--overexpressed) by a carcinogen (cancer causing agent chemical, physical or viral) After initiation cell must be able to divide to be cancer

supports or enhances the growth of the cell ex. Hormones like estrogen and insulin

Section 8.3: Cancer: Describe the steps of Malignant Transformation


Progression
As the cell gets larger it needs

Metastasis
Occurs when a tumour

its own blood supply because the cells in the center become hypoxic TAF(tumour angiogenesis factor) stimulates blood vessel growth Once have blood vessels cells cont grow and divide often change from parent cell allowing it to become more malignant

breaks off from the primary tumour and establishes its own colony

Section 8.3: Cancer


Discuss the classification of cancer:

Tissue of origin: 1. Originates glandular tissue=carcinoma 2. Originates connective tissue=sarcoma 3. Originates embryonic tissue=blastoma 2. Biologic behaviour 3. Anatomic site 4. Degree of differentiation1.

Section 8.3: Cancer: Histologic classification


How is cancer graded?
Is graded based on appearance and

differentiation Aids is diagnosis, prognosis and treatment of disease

Section 8.3: Cancer


What is grading?
The classification of cancer

What is ploidy?
The classification of cancer

by cellular characteristics
What is staging? The classifying of cancer based on its clinical manifestations

based on the number of chromosomes and appearance

Section 8.3: Cancer: List the grades of cancer.


Grade1: tumour cells well differentiated and closely

resemble the cells from which they arose Grade2: tumour cells moderately differentiated and have some characteristics of the parent cell Grade3: tumour cells poorly differentiated but tissue of origin can still be established Grade 4: tumour cells poorly differentiated and can no longer determine tissue of origin

Section 8.3: Cancer: List the stages of cancer. TNM Classification


TNM= tumour, node and metastasis PRIMARY TUMOUR (T)- T0-cant be assessed, no evidence, T1-4-increasing size primary tumour REGIONAL LYMPH NODES (N)-N0-cant be assessedN1-3-increasing involvement regional lymph nodes DISTANT METASTASIS (M)-M0-no evidenceM1distant metastasis.

Section 8.3: Cancer:


What factors influence cancer development? 1. Exposure to carcinogens 2. Immune function 3. Genetic predisposition Name the main mechanism of carcinogenesis. 1. Oncogene activation

Suppressor genes prevent oncogenes from being overly expressed, but when suppressor genes get damaged oncogenes are over expressed causing cells to become cancerous

Section 8.3: Cancer: Risk Factors


Oncogene activation
Environmental factors ex. Physical, chemical or viral

Immune function
Advancing age Genetic predisposition

Section 8.3: Cancer


Discuss the warning signs of cancer (CAUTION) C=change in bowel habits A= a non-healing sore U= unusual discharge/bleeding T=thickening/lump I=indigestion/difficulty swallowing O= obvious change in a mole or wart N=nagging cough/hoarseness

Section 8.3: Cancer


Discuss cancer prevention and detection Discuss cancer prevention and detection

Primary prevention: Avoidance known cancer causing agents- ex. Smoking, use of sun block Modifying associated factorsex. Healthy diet, limit alcohol, safer sex Removal at risk tissuesremoval moles, polyps, etc Chemoprevention- use of drugs, chemicals etc ex. Celecoxib and aspirin reduces risk colon cancer vaccination

Secondary prevention: Screening tests:

Yearly mammogram & breast exam women>40 Yearly PAP women >18 Colonoscopy women & men>50 Yearly fecal occult all adults Yearly prostate exam men>50

Section 8.3: Cancer Treatment: What are some treatment modalities for cancer?
Surgery
1.

2.

3. 4.

biopsy -the removal of some/all of the suspected tissue for examination and testing Debunking-(cancer control/cytoreductive)-removal of parts of a malignant tumour decreasing cancer numbers increasing chances of other treatment working Curative- removal all cancer tissue Reconstructive/rehabilitation-increase fxn, appearance or both

Section 8.3: Cancer Treatment: What are some treatment modalities for cancer?

Radiation therapy
the purpose of radiation therapy is to destroy cancer

cells with minimal damage to normal cells. Use least amt radiation to destroy most amt cells

What are the two ways radiation therapy can be

delivered?
Teletherapy- radiation is external to the patient

(distant), patient isnt radioactive. To be effective must irradiate same place daily---so need tattoo it. Brachytherapy-radiation is within the patient as to have direct contact with the tumour, patient is radioactive.

Section 8.3: Cancer Treatment: What are some treatment modalities for cancer?
s/e: Dry skin, erythema ,changes in taste, anorexia, n/v Fatigue Weight loss, xerostomia: dry mouth; mucositis- irritation, inflammation or ulceration mucosa Bone marrow suppression (WBC, RBC, platelets) NSG: Provide periods rest during activities Monitor weight Small frequent meals High protein, high calorie diet Frequent oral care Administer antibiotic, topical /systemic analgesics, antiemetic

Section 8.3: Cancer Treatment: What are some treatment modalities for cancer?
What are the complications of bone marrow suppression?
What tx can be given to help decrease the risk of infection?

Decreased: WBC,

Biological Response

erythrocytes, platelets increases risk infection, hypoxia and fatigue Tendency to bleed Common cause death during tx

Modifiers- stimulate bone marrow production of immune system cells

Section 8.3: Cancer Treatment: What are some treatment modalities for cancer?
Chemotherapy: How does chemotherapy cure & increase survival times?
By damaging DNA & interfering with cell division Kills metastic cells-systemic tx

Section 8.3: Cancer Treatment: What are some treatment modalities for cancer?
How is chemotherapy delivered?
IV-major complication

Intraarterial-via artery

is extravation-leaks leads tissue damage recommend central vascular device (groshogg, PICC, infusion ports using Huber needle, infusion pumps)

supplies the tumour Intrathecal-injecting chemo into subarachnoid space Intravisical-into the bladder

Section 8.3: Cancer Treatment: What are some treatment modalities for cancer?
S.E:
1. 2. 3. 4. 5. 6.

n/v

7.

Hemorrhagic cystitis Heart damage Anemia Neutropenia (decreased neutrophils) Thrombocytopenia Alopecia Mucositis

Section 5.2: Fluid/e-lyte balance


Describe Hypernatremia (included causes & s/s)
Na+>145mE/L, s/s: Dry, sticky mucous membranes, swollen, red dry tongue, weakness NSG: Monitor I/O, assess restlessness, disorientation, labs, ,encourage fluid, limit Na+ intake

Causes
Excessive intake Renal failure Corticosteroids Cushings syndrome Diabetes insipidus Heat stroke

Section 5.2: Fluid/e-lyte balance


Describe hyponatremia (included causes & s/s)
Na+<135mEq/L s/s: Lethargy, muscle twitching, abdominal cramps, anorexia, n/v, seizure NSG: Assess manifestations, monitor I/O, Na+ levels, dietencourage high sodium foods, limit water if needed

Causes:
Excessive diaphoresis Diuretics Wound drainage Renal dx NPO Low intake

Section 5.2: Fluid/e-lyte balance


Describe Hypokalemia (include causes &s/s)
K+<3.5: NEVER ADMIN K+

Causes
v/d Heavy perspiration Use K+ wasting drugs Poor intake Hyperaldosteronism For those on digoxin monitor

IV PUSH!!!!! s/s:
Muscle weakness, leg

cramps, fatigue, lethargy, anorexia, n/v, cardiac dysrhythmias, weak pulses

NSG: Monitor HR, administer K+, monitor pain, eat K+ rich foods, safety

for toxicity cause Hypokalemia increases toxicity risk

Section 5.2: Fluid/e-lyte balance


Describe Hyperkalemia (include causes &s/s) Causes
Renal failure Hypoaldosteronism K+ conserving diuretics
K+>5 s/s: Diarrhea, irritability, confusion, cardiac dysrhythmias/ARREST, muscle weakness, decreased HR, irregular pulse NSG: Monitor cardiac status, ECG, admin diuretics ex. Glucose and insulin (pushes K+ back into cells quickly via IV), admin. KAYEXALATE

Section 5.2: Acidosis


Define Metabolic acidosis
Characterized by decreased

Define Respiratory acidosis


Characterized by decreased

pH and decreased bicarbonate levels


Ex. Diabetic ketoacidosis,

pH with an increased CO2


Ex. Hypoventilation, COPD,

shock

starvation

Kidneys compensate by

Lungs kick in and start

blowing off CO2 to compensate, so CO2 levels fall in response (blow off the acid)

retaining bicarbonate, thus bicarb levels rise

Section 2.1: Emergency preparedness


Describe the stages of a disaster. 1. Non-disaster stage(interdisaster)- pre-plan when vulnerable to disaster. 2. Pre-disaster stage- know of pending disaster, warnings, evacuation 3. Impact stage- disaster occurred, assess damage, death, loss of property, injury 4. Emergency stage- help arrives, recovery 5. Reconstruction stage- restoration, rebuild, mitigation