Exam 1 Advanced Pathophysiology Mccance And Huether

Front 1

What are the eight specialized functions of cells

Back 1

movement, conductivity, metabolic absorbtion, secretion, excretion, respiration, reproduction, and communication

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Nucleus

Back 2

aids in cell division and controls of genetic information, contains DNA.

Front 3

Ribosomes

Back 3

RNA protein complexes, float freely in cytoplasm, provide sites for cellular protein synthesis

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Endoplasmic Reticulum

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Specializes in synthesis and transport of the protein and lipid components of most of the cells organelles; also protein folding and sensing cell stress

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Golgi Complex

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A network of smooth membranes and vesicles located near the nucleus; processes and packages proteins into secretory vesicles

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Lysosomes

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Digest and remove waste, digest debris from dead cells

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Mitochondria

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Cellular respiration and pathway for energy production (ATP)

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Cytoskeleton

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"bones and muscles of the cell, maintains shape and allows movement.

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Prevents water soluble molecules from entering cells across the plasma membrane

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Phospholipid bilayer

Front 10

Hydrophobic

Back 10

uncharged; water fearing

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Hydrophillic

Back 11

charged; water loving

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Plasma membrane

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Impermeable to most water-soluble molecules, but allows lipid-soluble molecules (o2/Co2) and uncharged particles such as H2o, Co2, and urea to diffuse it readily

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Prokaryotes

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contain no organelles; cyanobacteria, bacteria, and rickettsia

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Eukaryotes

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"good nucleus," ;layer with intracellular anatomy; animals

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Passive transport

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no-energy transport of uncharged molecules through any semi-permeable barrier; ex. H2o and Co2 diffusing readily across plasma membrane

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Diffusion

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Movement of a solute molecule from an area of greater solute concentration to an area of lesser solute concentration

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Filtration

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Movement of H2o and solute through a membrane b/c of a greater pushing pressure on one side of the membrane

Front 18

Osmosis

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Movement of H2o down a concentration gradient, across a semi-permible membrane from a regions of higher concentration to lower concentration

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Active Transport

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The protein transporter moves molecules against, or up, the concentration gradient. Requires the expenditure of ATP and bigger molecules suchs a protein, ions, large cells, and complex sugars

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Endocytosis

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A section of the plasma membrane enfolds substances from outside the cell, invaginates (folds inward), and separates from the plasma membrane, forming a vesicle that moves into the cell.

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Pinocytosis

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Cell drinking; involves the ingestion of fluids and solute molecules through formation of small vesicles

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Phagocytosis

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Cell eating; involves the ingestion of large particles, such as bacteria, through formation of large molecules

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Exocytosis

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Secretion of macromolecules; helps replace portions of the plasma membrane; also releases molecules synthesized by the cells into the ECF

Front 24

Endocrine Signaling

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A form of cellular communication; remote signaling by secreted molecules (hormones) in the blood to remote cells

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Paracrine Signaling

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A form of cellular communication; secretion of local chemical mediators that are quickly taken up and immobilized. Contact signaling by plasma membrane molecules.

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Synaptic Signaling

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A form of cellular communication; secretion of neurotransmitters at specialized junctions call the chemical synapse. Contact signaling via specialized junctions.

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Glycolysis

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The second phase of cellular energy production, following digestion. A glucose molecule is split and two ATP molecules are formed through oxidation

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Oxidative Phosphorylation

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Occurs in the mitochondria; process by which energy is transferred into ATP

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Mitosis

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The reproduction of somatic cells; nuclear division followed by cytokinesis (cytoplasmic division); asexual

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The result of mitosis

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2 genectically identical daughter cells from 1 parent

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Meiosis

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Cellular reproduction of a germ cell; involves 2 fissions of the nucleus; sexual

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The result of meiosis

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four gametes (sex cells)

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Hypoxia

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Lack of sufficient oxygen

Front 34

Most common cause of cellular injury

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hypoxia

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Ischemia

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reduced blood supply

Front 36

The most common cause of hypoxia

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Ischemia

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Process of cell death caused by ischemia

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1. Insufficient o2 and glucose create a situation where the cell cannot produce adequate energy

2. There is an influx of Na and Cl into the cell

3. H2o is drawn in and the cell swells

4. There is an influx of Ca

5. The mitochondria are destroyed and the cell is then unable to produce energy

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Effects of cell death

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1. Irreversible and inevitable

2. Cell swells and bursts

3. Free radicals are released

4. The inflammatory process is activated

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Free radicals

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Electrically uncharged atom or group of atoms having unpaired electrons, looks to steal other electrons, causing domino effect

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Chemical injury

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Begins with a biochemical interaction between a toxic substance and the cells plasma membrane, ultimately damaged, leading to increased permeability

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Hypothermic injury

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Intial vasoconstriction with paralysis of vasomotor control leading to vasodilation

Front 42

Results of hypothermic injury

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1. Increased membrane permeability

2. Cellular swelling

3. Increased blood viscosity

4. Ischemic injury

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Hyperthermic injury

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Burn; tissue is destroyed; injury depends on extent of injury and how many layers are involved

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Partial thickness injuries

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Capillary dilation and increased loss of protein-rich fluid (redness,swelling, and blistering)

Front 45

Full thickness injuries

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Extensive loss of fluid and plasma proteins. Cellular regeneration is not possible, so grafting is needed to protect and heal.

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Coagulative Necrosis

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Caused from hypoxia caused by severe ischemia. Protein denaturation causes protein albumin to change from a gelatinous, transient state, to a firm, opaque state

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Liquefactive Necrosis

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Results from ischemic injury to the neurons and glial cells in the brain.

Front 48

Liquefactive Necrosis

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Self digestion leads to liquid which is encapsulated in cyst and abcesses

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Caseous Necrosis

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TB

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Caseous Necrosis

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A combination of coagulative and liquefactive necrosis. The dead cells degenerate but the debris is not digested completely.

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Fat Necrosis

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Cellular death that mainly occurs in pancreas, breasts, and other abdominal structures

Front 52

Coagulative Necrosis

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Cellular death that mainly occurs in the heart, kidneys, and adrenal glands

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Fat Necrosis

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Caused by lipase. Lipases breaks down triglycerides, releasing free fatty acids, which then combine with Ca, Mg, and Na., creating opaque and chalk white soaps.

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Gangreous Necrosis

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Death of tissue resulting from severe hypoxic injury

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Dry gangrene

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Result of coagulative necrosis;dry, brown or black

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Wet gangrene

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Develops when neutrophils invade the site, causing liquefactive necrosis; site is cold, swollen, and black with foul odor.

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Gas gangrene

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Due to infection by clostridium; can lead to death if enzymes lyse the membrane of RBC's destroying their oxygen carrying capacity.

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Apoptosis

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Cellular dropping off; cellular self destruction

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Atrophy

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Reduction in cell size; may be caused by disuse, decreased hormone stimulation, or reduction in blood supply

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Hypertrophy

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Increase in cell size due to increase workload; ex. muscle

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Hyperplasia

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Increase in cell number due to an increase in cell division; ex. monthly hyperplasia of endometrium, callus

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Dysplasia

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Abnormal changes in size, shape, and organization of mature cells.

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Metaplasia

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Reversible replacement of one mature cell by another, often less differentiated cell type

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Neoplasia

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Abnormal growth of tissues, a tumor forms.

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Compensatory Hyperplasia

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An adaptive mechanism that enables certain organs to regenerate.

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Contains 2/3 of body's H2o

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ICF

Front 67

Conatins 1/3 of body's H2o

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ECF

Front 68

The sodium potassium pump maintains balance of _____ inside cells and _____ outside of cells by active transport.

Back 68

K;Na

Front 69

Hydrostatic pressure

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Arterial side of capillaries; pressure in capillaries is greater than pressure in the interstitial space

Front 70

Edema

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Accumulation of fluid in the interstitial space

Front 71

An increase in hydostatic pressure can be caused by:

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Venous obstruction or salt and water retention; ex. CHF, kidney failure, thrombophlebitis, tight clothes, prolonged sitting

Front 72

A decrease in plasma proteins yields

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A decrease in osmotic pressure, fluid release in the interstitial space; ex. malnutrition, burn injury, liver disease

Front 73

Primary factors in regulation of thirst

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A secretion of ADH and perception of thirst

Front 74

What intiates the thrist mechanism

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osmoreceptors in the hypothalamus

Front 75

Most common causes of a hypertonic cellular alterations

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1. Hypernatremia

2. reduction in ECF H2o (hypovolemia)

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Causes of hypernatremia

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1. Increased Aldosterone (Cushing's syndrome)

2. Excessive water loss r/t diarrhea, polyuria, and profuse sweating

3. Intracellular dehydrationoccurs

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Treatment for hypernatremia

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Isotonic IV fluid (D5 in H2o)

Front 78

Hypernatrima s/s

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1. Urine specific gravity <1.030

2. Hematocrit and plasma proteins will be elevated

3. Na <146

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Most common causes of hypotonic cellular alterations

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1. Hyponatremia

2. Water excess

Front 80

Causes of hyponatremia

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Pure sodium deficits; ex. diarrhea, vomitting, gi suction, diuretics, SIDH, failure of distal tubules to reabsorb Na, and burns

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Treatment for hyponatremia

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Fluid restriction and possible hypertonic solution of saline

Front 82

S/S of hyponatremia

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1. Behavioral and neurological changes, wt gain, edema, ascites, pulmonary edema, and JVD.

2. Urine specific gravity >1.010

3. Na >135

Front 83

Hyperchloremia

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1. Seen with hypernatremia and plasma HCo3 deficits

2. No s/s, treat underlying cause

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Hypochloremia

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1. Occurs with hyponatremia or an elevated HCo3

2. Seen with cystic fibroids, use of diuretics, and vomitting

3. Treat underlying cause

Front 85

Causes of hypokalemia

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Increased aldosterone, diuretics, diarrhea, vomitting, NG suction, Addison's disease, and alkalosis.

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Causes of hyperkalemia

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Oral or IV KCL, nutritional substitues, salt substitues, decreased aldosterone

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S/S of hypokalemia

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Renal function impaired, neuromuscular excitability is decreased causing skeletal muscle weaknes= smooth muscle atony and dsyryhtmias.

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S/S of hyperkalemia

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Muscle weakness, cramps, numbess, parethesis, N/D, abdominal distention, confusion, and arrythmias

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Treatment for hypokalemia

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IV potassium at 20 mEq/L

Front 90

Treatment for hyperkalemis

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IV calcium, insulin, D50, albuterol, dialysis

Front 91

Predominant ICF ion, major influence on the regulation of ICF osmolarity, fluid balance, and ICF electrical neutrality

Back 91

Potassium

Front 92

90% of ECF cations, combined with Cl, HCo3, and Na regulates EC osmotic forces and therefore regulates H2o balance.

Back 92

Sodium

Front 93

S/S of hypocalcemia

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Caused by an increase in neuromuscular excitability, paresthesis of the mouth and digits, capoedal syndrome, larygyospasm, hypereflexion, seizures, dysrhthmias, when severe convulsions, tetany, and death

Front 94

Twitch of the nose or lip when temple is tapped

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Chvostek sign

Front 95

Contraction of hands and fingers after radial artery is occluded for 5 min.

Back 95

Trousseau Sign

Front 96

Causes of hypercalcemia

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Hyperparathyroidism, bone mets with calcium reabsorption, sarcoidosis, and excess Vitamin D

Front 97

S/S of hypercalcemia

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Cause by a decrease of neuromuscular excitability, fatigu, weak, lethargy, anorexia, block, bradycardia, confusion

Front 98

Treatment for hypocalcemia

Back 98

Give IV calcium gluconate, PO CA, and decrease Ph intake

Front 99

Treatment for hypercalcemia

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Treat underlying cause, large amounts of NS, corticosteroids, and cytotoxic drug mithramycin

Front 100

Plasma membrane stability and permability are directly r/t ______ ions.

Back 100

Calcium

Ex. transmission of nerve impulses and contarction of muscles

Front 101

Decrease ph, normal or decreasing PO2, decrease HCO3; seen with Diabetic ketoacidosis, renal failure, starvation, hypoxia with lactic acid buildup, physical exertion w/o adequate caloric intake

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Metabolic acidosis

Front 102

Incresed ph, normal or increasing PO2, increase HCO3; seen with vomitting, NG suction

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Metabolic alkalosis

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Decreased ph, increase CO2, and normal or increasing HCo3; seen with emphysema, narcosis, and respiratory arrest

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Respiratory acidosis

Front 104

Increased ph, decreased Co2, normal or decreasing HCo3; seen with hyerventilation, salicylate toxicity, pain, panic, or neurogenic disorders

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Respiratory alkalosis

Front 105

The difference between primary measured cations (Na+ and K+) and primary measured anions (Cl- and HCo3-)

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Anion Gap (The magnitude of difference helps identify causes of metabolic acidosis)

Front 106

Posess contact inhibtion, controlled growth with a limited life span, uniform size and shape, normal chromosomes, perform apoptosis

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Normal cell

Front 107

Lack contact inhibtion, uncontrolled growth, immortal, anaplasia, loss of organization, abnormal chromosomes, no apoptosis

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Cancer cell

Front 108

Describe the 6 hallmarks of cancer

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1. Self sufficiency in growth signals, do not need external signals to multiply

2. Insensitivity to anti-growth signals

3. Avoid apoptosis

4. Limitless replicative potential

5. Sustained angiogenesis

6. Tissue invasion and metasis

Front 109

Angiogenesis

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Process by which BV are formed

Front 110

Most common cancers associated with children

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Leukemia and Brain

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Risks associated with childhood cancer

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prenatal exposure, exposure in utero, breast milk contents before conception

Front 112

Basic units of inheritance, composed of sequences of DNA

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Genes

Front 113

Double helix polymer, a long molecule composed of 4 nucleotides, during replication the molecule splits and each half forms a mirror of itself, yielding two new molecules

Back 113

DNA