Pathophysiology Unit 2

Front 1

Characteristics of benign tumors

Back 1

Differentiated; relatively normal mitosis; similar to normal cells; relatively slow growth; expanding mass; frequently encapsulated; spread remains localized; systemic effects are rare; life-threatening only in certain locations (brain)

Front 2

Characteristics of malignant tumors

Back 2

varied size and shape with large nucleii; many undifferentiated; some necrosis; mitosis increased and atypical; rapid growth; cells not adhesive, infiltrate tissue; no capsule; invades nearby tissues or metastasizes to distant sites through blood and lymph vessels; systemic effects often present; life threatening via tissue destruction and tumor spread

Front 3

Tumor nomenclature

Back 3

benign: + oma
malignant (epithelial): + carcinoma
malignant (connective): + sarcoma

some prefixes: lipo (fatty), adeno (glandular), fibro (fibrous), osteo (bone)

Front 4

Elements of carcinogenesis

Back 4

Risk factors (extrinsic and intrinsic), oncogenesis (genetic mechanism)

Front 5

Summary of oncogenesis

Back 5

Requires activation of many independently mutated genes; genes involved are those controlling DNA repair (fail); oncogenes (growth factors for cell growth and proliferation) (activated); tumor suppressing genes (inhibit cell proliferation in a tumor) (inactivated); genes controlling apoptosis (altered)

Front 6

Stages of oncogenesis

Back 6

1. Initiation- enough exposure to carcinogen to cause permanent damage to genome
2. Promotion- various chemicals/growth factors activate oncogenes and stimulate mutated cells to divide; may be reversible if promoting substance removed
3. Progression: Mutated cells acquire malignant phenotypic changes such as increased genome instability, invasiveness, metastasis.

Front 7

Characteristics of newly mutated tumor cells

Back 7

Anaplasia (altered or lack of differentiation); cells are altered in shape and size; highly anaplastic cancer cells resemble themselves more than the tissue of origin. Early mutation causes the tumor to be less differentiated and more malignant; late mutation does the opposite. cytological/histological grading of tumors- I least anaplastic, IV most anaplastic

Front 8

Changes in characteristics and function of anaplastic cells

Back 8

Do not undergo normal proliferation and differentiation; do not function properly; do not die in normal time frame; loss of contact inhibition; loss of cohesiveness and adhesiveness; impaired cell-cell communication; increase in degradative enzymes (ex- collegenase) that help in infiltration, invasion, metastasis; secretion of growth factors to stimulate angiogenesis; altered cell structure; altered tissue antigens

Front 9

Cancer warning signs

Back 9

Unusual bleeding or discharge anywhere in body; change in bowel or bladder habits; change in wart or mole; sore that won't heal; unexplained weight loss; anemia; fatigue; persistent cough or hoarseness; solid lump, often painless, anywhere in body.

Front 10

Local effects of tumor growth

Back 10

Bleeding; obstruction of ducts or tubes; ischemia from blood vessel constriction; necrosis from ischemia; infection (of necrotic tissue); inflammation from infection; pain from pressure on sensory nerves or stretching of visceral capsule (especially in late stages)

Front 11

Systemic effects of tumor growth

Back 11

Weight loss; cachexia (tissue wasting) from anorexia, tumor cell nutrient-trapping, altered metabolism, cachetic factors produced by macrophages to fight tumor; anemia from anorexia, chronic bleeding, bone marrow depression; fatigue and poor tissue regeneration from anemia; infections from decreased host resistance; bleeding from blood vessel erosion, tissue erosion, poor clotting from bone marrow depression, slow regeneration of digestive tract mucosa; paraneoplastic syndromes (tumor cells release factors that produce neurologic, endocrine, and hematopoietic syndromes and complicated diagnosis and treatment.

Front 12

Mechanisms of cancer spread

Back 12

Invasion- local spread into adjacent tissue
Seeding- local spread through body fluids or along membranes
Metastasis- distant spread through blood/lymph to develop secondary tumors; typically follow venous flow draining tumor and only small percentage of tumor cells are successful.

Front 13

Tumor staging

Back 13

Describes clinical spread of the disease. T1-T4=tumor size; N0-N3= lymph node involvement; M1-M3=metastasis

Front 14

Basic cancer treatment measures

Back 14

1. surgery for solid tumors and regional lymph nodes
2. chemo and radiation (adjuvant) for hemotologic cancers and surgery follow-up; prophylactic (protective- just in case some cancer cells remained or for cancers known to metastasize early in dev); most effective on cells undergoing DNA synthesis or mitosis; kills all cells (normal and cancer); cause bone marrow depression, epithelial damage, sterility, etc.
*radiation- kills cells and stops mitosis; blood vessel damage causes tumor cell ischemia
*chemo-interferes with protein synthesis and DNA replication or tumor cells

Front 15

Curative vs. Palliative cancers

Back 15

1. Curative- likelihood increased when tumor is small and localized; cure=5 yrs without recurrence; remission=period with no clinical signs
2. Palliative- goal is to maintain quality of life.

Front 16

Secondary treatments

Back 16

1. hormones- alter tumor's enrironment; glucocorticoids- decrease mitosis, increase erythrocyte count, increase appetite, decrease swelling; estrogens- block prostate cancer; tomoxifen (estrogen inhibitor) for breast cancer.
2. angiogenesis inhibiting drugs- block mitosis of epithelial (blood vessel walls) cells
3. analgesics- relieve pain
4. biotheraphy- immunotheraphy and biologic response modifiers (interferons, ABs, TB vaccine) to enhance immune response

Front 17

Immune surveilance hypothesis

Back 17

Immunologic mechanisms provide a means to detect, classify, prognoses, and treat cancer. Research to produce targeted therapy.

Front 18

hematogenic spread

Back 18

Tumor cells break free from primary tumor, invade surrounding extracellular matrix, enter blood vessel, protect themselves from immune system by aggregating and adhering to blood components (platelets) to form tumor emboli; stop and adhere to wall at favorable location; invade surrounding tissue and begin to replicate- dependant on presence of blood vessels and specific growth factors

Front 19

metastatic spread to lymph nodes

Back 19

May die from lack of nutrients, grow into new mass, or remain dormant; surviving cells can break free and enter venous system.

Front 20

Control of fluid balance

Back 20

1. thirst mechanism in hypothalamus
2. ADH- controls amt of fluid leaving body in urine by promoting reabsorption of water into blood from kidney tubules
3. aldosterone- controls reabsorption of Na+ and water into flood from kidney tubules.

Front 21

Hydrostatic and osmotic pressures in fluid balance

Back 21

Water moves between vascular compartment or blood and the interstitial compartment through the semi-permeable capillary membranes. Proteins and electrolytes contribute to osmotic pressure. At arteriolar end of capillary- blood hydrostatic pressure greater than interstitial hp and blood osmotic pressure, so blood moves out. At venous end- easier. HP= push, OP= pull

Front 22

Increase in serum osmolality or decrease in blood volume stimulate. .

Back 22

Thirst and edema

Front 23

Characteristics and effects of edema

Back 23

Localized or generalized; "pitting edema" where fluid accumulation exceeds tissue absorptive capacity; swelling may limit joint movement or compress blood vessels; increases distance for 02, nutrients, and waste to travel (increasing ischemia and tissue damage_

Front 24

Mechanisms of edema

Back 24

1. Increased capillary hydrostatic pressure prevents fluid return from interstitial compartment to venous ends of capillaries, or forces excessive amounts of fluid out of capillaries into tissues.
* May be from hypervolemia associated with kidney failure, pregnancy, congestive heart failure
2. Loss of plasma proteins (esp. albumin) decreases plasma osmotic pressure, increasing fluid leaving the capillaries and decreasing amt entering venous ends. *can be from too much Na+ in interstitial space (heart failure, high bp, kidney disease, too much aldosterone), kidney disease (protein loss through urine)
3. lymphatic obstruction (excessive fluid and protein not returned to circulation) (tumor, infection, lymph node removal)
4. increased capillary permeability (usually localized edema) (from inflammatory response, infection, hypervolemia) (causes increased movement of fluid and protein into interstitial space, the protein causes the fluid to accumulate)

Front 25

Dehydration

Back 25

*insufficient amt of body fluid volume.
*more serious for elderly and infants (lack fluid reserves, can't conserve fluid as well)
*often accompanied by electrolyte loss, sometimes protein loss.

Front 26

Kinds of dehydration

Back 26

1. Isotonic- proportunate loss water and electrolytes
*Na+ levels remain normal, osmosis from ICF to ECF to maintain tissue perfusion
2. Hypotonic- loss of more electrolytes than water
*Na+ levels increase, osmosis from ICF to ECF to maintain tissue perfusion.
3. Hypertonic- loss of more water than electrolytes or excessive water intake (water intoxication)
*Na+ levels decrease, osmosis from ECF to ICF. .

Front 27

Third spacing

Back 27

Fluid shift from vascular space into area where it cannot perform its normal physiologic functions as part of the circulating fluid.
*cause hypovolemia and edema
*locations are pericardial cavity, peritoneal cavity, pleaural cavity, joints, skin (burns)

Front 28

Na+ functions

Back 28

*makes up 90% of solute in extracellular fluid. impt to maintain extracellular fluid volume through effect on osmotic pressure. Also impt for nerve impulses and muscle contraction.

Front 29

Hyponatremia

Back 29

Low sodium [] in cells. Through excessive loss (sweating, vomiting, diarrhea), excessive water gains, renal failure, hormonal imbalances (excess ADH, reduced aldosterone); decreased osmotic pressure cause fluid shift into cells.

Front 30

Hypernatremia

Back 30

High [sodium] in cells. Through excessive ingestion, excessive water loss, lost of thirst mechanism, insufficient ADH; increased osmotic pressure cause fluid shift out of cells.

Front 31

Potassium functions in body

Back 31

Assists in regulation of intracellular fluid volume, role in many metabolic processes, impt in nerve conduction, muscle contraction (determines membrane potential)

Front 32

Potassium regulation in body

Back 32

Major intracellular cation; serum levels very low, intracellular levels high. Excreted in urine (aldosterone). Acidosis shifts K+ out of cells into extracellular fluids, alkalosis shifts K+ into cells.

Front 33

Acidosis/Alkalosis

Back 33

High [H+] in blood, H+ diffuse out into interstitial fluid then into cells, displacing K+ in cells to maintain electrical neutrality. K+ then diffuse into blood, leading to hyperkalemia. Alkalosis does the opposite.

Front 34

Hypokalemia

Back 34

Low serum [K+]. Caused by diarrhea, certain diuretics, excess aldosterone or glucocorticoids (Cushings syndrome), low dietary intake, insulin treatment. Causes heart arrhythmia, cardiac arrest.

Front 35

Hyperkalemia

Back 35

High [K+]. Caused by renal failure, "potassium-sparing" diuretics, aldosterone deficit, severe tissue damage (escapes into ICF), prolonged or severe acidosis. Causes heart arrhythmia, cardiac arrest.

Front 36

Functions of Calcium in body

Back 36

Structural strength (bones/teeth), maintain stability of nerve membranes by controlling permeability and excitability needed for nerve conduction, required for muscle contractions and many metabolic processes, esp. those involved in blood clotting.

Front 37

Hypocalcemia- causes

Back 37

Hypoparathyroidism (which decreases intestinal absorption of Ca++), decreased calcium intake, Malabsorption syndrome (decreased intestinal absorption of vit D or Ca++), vit D deficit, elevated serum phosphate levels (causing increased urinary excretion of Ca++), alkalosis (increased binding of Ca++ to protein)

Front 38

Hypocalcemia- effects

Back 38

Skeletal muscle spasms b/c of increased permeability and excitability of nerve membranes (Chvostek's sign- lip/face, Trousseau's sign- carpopedal (fingers) spasm induced by ischemia from blood pressure cuff). Heart arrhythmias and hypotension.

Front 39

Hypercalcemia- causes

Back 39

Uncontrolled release of Ca++ from bones due to neoplasms, hyperparathyroidism, increased intake of vit D or calcium, milk-alkali syndrome (from high milk and antacid intake)

Front 40

Hypercalcemia- effects

Back 40

Depression of neuromuscular activity, disruption of ADH function (causing polyuria), decreased blood volume, depressed renal function, accumulation of nitrogen wastes, cardiac arrest

Front 41

Magnesium- functions

Back 41

Metabolic reactions, protein and DNA synthesis

Front 42

Hypomagnesemia- causes

Back 42

Malabsorption, malnutition, diuretics, diabetic ketoacidosis, hyperparathyroidiism, hyperaldosteronism

Front 43

Hypomagnesemia- effects

Back 43

Neuromuscular hyperirritability (tremors/chorea), personality changes, tachycardia, arrhythmias, hypertension

Front 44

Hypermagnesemia- causes/effects

Back 44

Usually caused by renal failure. Depresses neuromuscular function causing lethargy, impaired reflexes, cardiac arrhythmias.

Front 45

Phosphate- functions

Back 45

Bone/tooth mineralization, metabolic processes, esp. involving ATP, buffer for a/b balance, removing H+ from body through kidneys, forming cell membranes, interacting with Ca++.

Front 46

Hypophosphatemia-causes

Back 46

Malabsorption, diarrhea, excessive Al or Mg based antacids, hyperparathyroidism, alkalosis

Front 47

Hypophosphatemia- effects

Back 47

Impaired neurologic function, impaired blood cell function

Front 48

Hyperphosphatemia-causes/effects

Back 48

Causes- renal failure (most often), tissue damage, chemotherapy.
Effects- impaired neurolo

Front 49

Chloride- functions

Back 49

Bicarbonate ions bind with metabolic acids, Cl- diffuses out of rbc into serum to maintain same [-ion] in blood. If blood [Cl-] decreases, bicarbonate ions diffuse out of rbc into serum. So low serum chloride leads to high serum bicarbonate (alkalosis)

Front 50

Hypochloremia- causes/effects

Back 50

Causes- alkalosis from vomiting (HCl loss), excessive sweating (Cl- loss)
Effects-Hyponatremia, dehydration

Front 51

Hyperchloremia- causes/effects

Back 51

Causes-excessive salt intake
Effects- Hypernatremia, fluid excess