Exam 1 Flashcards
tumor staging
Staging: clinical spread of cancer -> treatment and prognosis
- TNM: T - tumor size (1-4), N - lymph node involvement (0-3), M - metastasis (0-1)
tumor grading
examination of differentiation
Scale of 1-4 (4 is poorly differentiated) - tumor grade ¾ doesn’t respond well to treatment
What is the purpose of a pap smear,what does the clinician look for when examining the collected specimen
To catch cancer early, the clinician looks for dysplasia, anaplasia, and neoplasia
Look for differentiation of cells
Amiocentesis
at 16 weeks of gestation, a clinician inserts needle through abdominal cavity into amniotic sac and collects fluid. Puts the fluid in petri dich and replicates the cells. Thye stop the replication and look at the chromosomes. When babies are in amniotic fluid they shed skill cells.
Chorionic villi (extensions on the placenta)
with sampling, you go transabdominally or transvaginally and collect chorionic villi. Then you put them in a petri dish and have them grow, and then you do a carrier type and look at the chromosomes. Can be done at ten weeks.
cardiac dysrythmias
caused by hyper and hypo kalemia
Cell free DNA testing
some fetal cells enter maternal circulation, so do a blood test on mom and separate mom cells from fetal cells. Grow cells and do a carrier type. Can be done at 10 weeks. Non invasive procedure - but upon finding genetic abnormality, you are advised to perform one of the other two tests.
Resolution
cells were not damaged beyond recovery, they can recover and return to normal function (does not require mitosis)
Regeneration
replacement of lost or necrotic tissue with tissue that is structurally and functionally identical, healthy neighboring cells undergo mitosis and proliferate to replace the cells lost in the tissue
Scar formation
dead cells are replaced by a different cell type than the original. First granulation tissue forms (highly vascularized connective tissue) and then it matures into fibrous tissue. Area loses its function.
complication of scar formation
Conrtactures and obstructions - scar is smaller than wound but can limit function
Adhesions (can hold loops of intestines together)
Hypertrophic scar tissue (orignal wound size but raised) excessive deposition of connective tissue
Keloid: excessive scar formation / deposition and growth of connective tissue outside of margins
Dry gangrene
lack of arterial blood supply but venous flow carries fluid out of tissue. Dry, shrinks, skin wrinkles, dark brown / black. Spreads slowly and symotoms are not as marked as wet gangrene. Clear line of demarcation between gangrenous area and healthy tissue. Confined to extremities - external. (diabetes)
Wet gangrene
lack of venous flow lets fluid accumulate in tissue. Area is cold, swollen, pulseless, moist, black. Bulbs form on surface, liquefation occurs, foul odor from bacteria. No line of demarcation between normal and dead tissue. Spread of damage tissue is rapid, affects internal organs and extremities.
Gas gangrene
clostridum infection. Bacterial infection that produces gas in tissue. Deadly. Bubbles kill muscle cells. Massive spreading edema, hemolysis of RBCs, hemolytic anemia, hemoglobinemia and renal failure
Connective tissue repair
1) hemostasis, angiogenesis, and ingrowth of granulation tissue
2) emigration of fibroblasts and deposition of the extracellular matrix
3) maturation and reorganization or the fibrous tissue (remodeling) usually starting during first 24 hr of injury
Cutaneous healing stages
inflammatory phase, proliferative phase, remodeling phase
inflammatory phase
starts right after injury and preps the wound for healing
Hemostasis
Vascular phase - vasoconstriction followed by vasodilation
Cellular phase - migration of phagocytic cells that digest and remove invading organisms and cellular debris - cleaning up the site
proliferative phase
build up of new tissue to fill the wound space
Formation of granulation tissue
Wounds that heal by secondary intention have more necrotic debris and exudate that must be removed and requires a larger amount of granulation tissue
Epithelialization (no loss of function)
migration , proliferation, and differentiation of epithelia cells at the wound edges
remodeling phase
increases the strength of the wound
Liquefaction necrosis
brain tissue dies or bacterial infection (leaves a hole)
Coagulative necrosis
hypoxic injury leading to infarctions → myocardial infarction (tissue architecture/cell outlines are preserved despite dead cells) (leaves discolored area of regular shaped organ)
Caseous necrosis
dead cell persis indefintely as soft, cheese like debris -> found in TB patient’s lungs
promote wound healing
Youth, good nutrition, adequate hemoglobin, effective circulation, clean undisturbed wound, no complications or chronic conditions
delay wound healing
advanced age (reduced mitosis), poor nutrition, anemia, circulatory problems, irritation, bleeding, infection.
Downs
3 chromosomes for 21
Edwards
3 chromosomes for 18
Klinefelters
extra x chromosome in male XXY
Turners syndrome
single x chromosome XO
stage 1 TNM
T1 – 2 cm or less, No – no lymph node involvement, Mo - no metastasis
stage 2 tnm
between 2 - 5 cm, N1 – lymph node involvement (1-3 under arm), Mo - no metastasis
stage 3 tnm
t3 larger then 5 cm, N1 to N2 – lymph node involvement (3-9 under arm), Mo - no metastasis
stage 4 tnm
T4 – tumor any size but fixed to chest wall, N3 – greater than 10 lymph nodes are involved or has spread to clavicular node involvement (spread), M1 – metastasis to distant organ
Atrophy
cells get smaller (esp when not used)
Hypertrophy
cells get larger - think working out: not more cells, just bigger
Hyperplasia
muscle gets bigger because there are more cells in the tissue
Metaplasia
cell under stressful condition changes to a cell type that can deal with the stress (acid reflux)
Dysplasia
precancerous state, cells being to vary in shape in size, develop large nuclei, increased rate of mitosis.
Anaplasia
associated with malignancy or cancer. Cells are undifferentiated, have variable nuclei, cell structure, and mitotic figures.
Neoplasm
tumor or new growth, benign or malignant.
local and systemic signs/symptoms of inflammation
swelling , redness, pain, heat/warmth, loss of function
vascular stage of acute inflammation
vasodilation and capillaries become more permeable
vasodilation
Increasing blood flow to the injured area
Mediators include histamine and nitric oxide
Redness and warmth results
increased capillary permeability
Allowing exudate to escpate into the tissues
Mediators include histamine, bradykinin, and leukotrienes
Swelling, pain, and impaired function result
Cellular stage of acute inflammation
White blood cells enter the injured tissue:
Chemotaxis
Destroying infective organisms
Removing damaged cells
Releasing more inflammatory mediators to control further inflammation and healing
Diapedesis - WBCs move from blood vessels to harmed tissue
Increase body temp (fever)
Vasoconstriction
Shivering
Increased BMR
Curl up body
Decreased rate of replication of invading organism, sequesters iron
Decrease body temp
Vasodilation
Sweating
Lethargy
Extend body
granulation tissue
Highly vascularized connective tissue
Benign
well differentiated. Cells look and act like the cells in the normal tissue. Non cancerous - cells that make up tumor contain well differentiated cells.
Malignant
less differentiated. Cells look less like cells in the normal tissue
Cancerous, undifferentiated cells. Do not look or act like normal cells in the tissue.
Cells often do not mature (differentiate) to do the job the tissue is supposed to do.
hereditary cancer
Retinoblastoma (rb)
Brca 1 and brca 2
paraneoplastic syndromes
hormones or factors secreted by tumor cells, symptoms are caused by substacnes that the tumor releases.
(ADH ACTH PTH related protein
Promote or inhibit blood clot formation )
Tumor markers
enzymes, antigens, hormones used for screening, for diagnosis, establishing prognosis, monitoring treatment and for detecting relapse
AFP
oncofetal antigens - liver cancer
CEA
carcinoembryonic antigen - colorectal cancer
hCG
human chorionic gonadotropin - gestationsion tumors or testicular cancer
PSA
prostate specific antigen - prostate cancer
CA 125
ovarian cancer
complications of chemotherapy
Affects both neoplastic cells and rapidly proliferating normal cells
Bone marrow depression: limiting factor with chemotherpay. Blood cell count must be taken before each treatment. Bone marrow is depressed, wbc level is low, pt is now susceptible to infection
nausea/vomitting: due to stimulation of the emetic center of the brain or damage to the mucosal lining of the digestive tract
Anorexia
Hair loss
Breakdown of skin and mucosa linings
mutagenic /carcinogenic (cause other mutations)
Teratogenic (cause birth defects)
Azoospermia or oligospermia (decreased sperm count, change in menstrual cycle, destory ovaries)
Changes in menstrual cycle → amenorrhea
Cellular resistance - adapt to chemo
SIADH
Excess production of ADH
causes Hyponatremia and its s/s
hypoaldosteronism
Hyponatremia, hyperkalemia
Hyperaldosteronism
Hypokalemia
dystrophic calcification
calcium on dead and dying tissue, visible to nake eye
Normal calcium levels
Microscopic deposits of calcium colts into injured tissue
Often visible to naked eye
Gritty sand like grains to firm hard rock like material
Calcium phosphate
Components of the calcium deposits come from dead or dying cells
Ie advanced atherosclerosis, damaged heart valves, TB lesions
Metastatic calcification: high calcium levels, deposited in any soft tissue (not dead tissue)
Occurs in normal tissue and is caused by increased serum calcium levels (lung, kidney, blood vessles) → abnormality in calcium metabolism
Hyperparathyroidism, hyperparathyroidism in renal failure, bone destruction
Ie immobilized patients, paget disease, cancer with metastatic bone lesions
potassium sparing
aldactone/spironolactone
Causes hyperkalemia
potassium wasting
Lasix and hydrochlorothiazide
hypokalemia
Intermittent fever
fever returns to normal at least once every 24 hours
Remittent fever
fever does not go down and varies a few degrees in either direction
Sustained fever
the temperature remains above normal with minimal variations
Recurrent or relapsed fever
there is one or more episodes of fever. Each as long as several days with one or more days of normal temperature in between episodes
Initiation stage of carcinogenesis
initial mutation occurs
Promotion stage of carcinogenesis
mutatued cells are stimulated to divide in an unregulated manner
progression stage of carcingogenesis
cells acquire malignant appearances. Tumor cells compete with one another and develop more mutations, which make them more aggressive → appearance of tumor/you have a tumor
causes of edema
Increased capillary pressure (transudative)
Decrease osmotic/oncotic pressure (transudative)
Lymphatic obstruction (transudative)
Increased capillary permeability (exudative)
electrolyte imbalance in a patient with diabetes insipidus
Comes from lack of ADH
Hypernatremia
leukopenia
Bone marrow breakdown from chemo prevents the production of WBCs (neutrophils), leading the patients to be at risk for infection
A patient is given an IV infusion of albumin, a plasma protein, what will happen to the levels of bound, ionized and total calcium in this patient and what are some signs and symptoms
More albumin means more calcium binding - more bound ca and less ionized ca. More total ca.
41)What happened to the physiological active form of calcium during acidosis
more ionized calcium (more h+ binding to oxygen, leaving less room for calcium to bind)
Alkalosis
less ionized calcium - more bound calcium because the calcium can bind to the oxygen
Proto-oncogenes
code for normal cell division proteins
Growth factors, growth factor receptors, transcription factors, cell cycle proteins, apoptosis inhibitors
Oncogene
proto oncogenes mutate to these
Increased activated or they are activated
Tumor suppressor gene
inhibit cell division
Mutations inhibit or decrease
electrolyte imbalances you would expect to see in a patient suffering from kidney failure
Sodium decreases
Potassium increases
Calcium decreases
Phosphate increases
Magnesium increases
H+ increases
* blood volume increases (but this is not an electrolyte)
How can you tell if patient is retaining fluid
By weighing them same time of day and in same apparel - a few pounds gained within a day is most likely not due to eating.
What happens to potassium in acidosis and alkalosis
Acidosis: k leaks out of cells and enters the blood (hyperkalemia) increases
Alkalosis: k levels in the blood decrease (hypokalemia)
different types of exudate
Serous: mostly water
Fibrinous: thick and sticky with a lot of fibrin and cell content
Purulent: thick, yellow-gree → designating an infection (pus) - white heads
bloody /hemorrhagic → if blood vessels are damaged (if you popped a blister and it bled)
Membranous, pseudomembranous: necrotic cells with fibropurulent exudate (mucous membranes)
naming benign tumors
tissue name + oma
Lipoma, osteoma, chondroma
Benign tumor of liver: hepatoma
Benign tumor of fat: lipoma
naming malignant tumors
Epithelial tissue: tissue name + carcinoma
malignant tumor of liver - hepatocarcinoma
Glandular tissue: tissue name + adenocarcinoma
meschymal/connective tissue: tissue name + sarcoma
Malignant tumor of fat - liposarcoma
Transudative edema
Increased hydrostatic pressure / low oncotic pressur: high in fluid, low in protein (heart failure, nephrotic syndrome, cirrhosis
Exudative edema
inflammation - high in fluid and protein
aldosterone
tells kidneys to secrete potassium and hold onto sodium
