I need a review for a exam of Advanced Pathophysiology .Attached a studyguide and Text book units

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Chapter 1

Cellular Biology

Wanda Morancy, DNP, APRN, FNP-BC

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UNIT I

Chapters 1, 2 and 3

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Significance of Cells

All body functions depend on the integrity of the cells.

Understanding cellular biology is necessary to understand disease.

An overwhelming amount of information reveals how cells are a multicellular “social” organism.

Cellular communication (“cellular crosstalk”) is at the heart of cellular biology.

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Cellular communication “cell crosstalk” is at the heart of cellular biology

Prokaryotes vs. Eukaryotes

Prokaryotes

Nucleus (single, circular chromosome)

Cyanobacteria, bacteria, and rickettsiae

Eukaryotes

Complex cellular organization

Membrane-bound organelles

Well-defined nucleus

Higher animals, plants, fungi, and protozoa

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Cells become specialized thru process of differentiation or maturation

Cellular Functions

Movement

Conductivity

Metabolic absorption

Secretion

Excretion

Respiration

Reproduction

Communication

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Structure and Function of the Cellular Components of Eukaryotic Cell

Three general components:

Plasma membrane

Cytoplasm

Intracellular organelles

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

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Nucleus is largest membrane-bound organelle and is found at the center of cell.

Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Nucleus

Structure

Nuclear envelope

Nucleolus

Deoxyribonucleic acid (DNA)

DNA replication, repair, and transcription

Histone proteins

Functions

Cell division and control of genetic information

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Nucleolus is inside of nucleus and largely composed of RNA, most of the cellular DNA and DNA binding proteins.

Primary function of nucleus is cell division and control of genetic information

Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Fills the space between the nucleus and the plasma membrane

Structure

Cytoplasmic matrix

Cytosol

Cytoplasmic organelles

Functions

Synthesis and transport

Eliminates wastes

Metabolic processes

Maintenance

Motility

Storage

Cytoplasm

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Cytoplasmic Organelles

Ribosomes

Structure: Ribonucleic acid (RNA) protein complexes; free vs. attached ribosomes

Function: Synthesize proteins

Endoplasmic reticulum

Structure: Network of tubular or saclike channels; smooth vs. rough endoplasmic reticulum

Function: Site of protein synthesis; senses cellular stress

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Ribonucleoproteins function as “trucks” carrying messages (mRNA) from nucleus to ribosomal sites of protein synthesis.

Endoplasmic reticulum is the cell’s factory that specializes in creating and transporting protein and lipid components of the cell’s organelles. It is a network.

Cell Function and Structure Video

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d) Question 1

Ribosomes are nucleoproteins that:

Are synthesized in the mitochondria and secreted into the cytosol.

Are synthesized in the cytoplasma.

Consist of a network of cisternae.

Synthesize a signal recognition sequence.

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ANSWER AND RATIONALE: 4. Synthesize a signal recognition sequence. Newly formed ribosomes synthesize a signal recognition sequence recognized by particles in the cytosol.

1. Ribosomes are synthesized in the nucleolus.

2. Ribosomes are synthesized in the nucleous.

3. The endoplasmic reticulum is composed of cisternae.

Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Cytoplasmic Organelles (cont’d)

Golgi complex

Structure

Flattened, smooth membranes

Secretory vesicles and cisternae

Proteins from the endoplasmic reticulum that are packaged in the Golgi complex

Clathrin-coated vesicles

Functions

“Refining plant” and directs traffic

Processes, secretes, and releases substances, especially protein from cells

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Cytoplasmic Organelles (cont’d)

Lysosomes

Structure

Saclike structures that originate from the Golgi

Primary vs. secondary lysosomes

Functions

Intracellular digestion system

Hydrolases: 40 digestive enzymes

Role in autodigestion and autophagy

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Cytoplasmic Organelles (cont’d)

Peroxisomes

Structure

Contain oxidative enzymes.

Are the major sites of oxygen utilization.

Functions

Detoxify compounds and fatty acids.

Break down substances into harmless products.

Synthesize specialized phospholipids for nerve cell myelination.

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Cytoplasmic Organelles (cont’d)

Mitochondria

Structure

Is surrounded by a double membrane.

Increased inner membrane surface area is provided by cristae.

Functions

Is responsible for cellular respirations and energy production.

Participates in oxidative phosphorylation.

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Cytoplasmic Organelles (cont’d)

Vaults

Are also called ribonucleoproteins.

Structure

Are shaped as octagonal barrels.

Have multiple arches.

Function

Are the cell’s “truck” that carry messenger RNA (mRNA).

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Cytoplasmic Organelles (cont’d)

Cytosol

Structure

Gelatinous, semiliquid portion of the cytoplasm

55% of the total cell volume

Functions

Intermediary metabolism involving enzymatic biochemical reactions

Ribosomal protein synthesis

Storage

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Cytoplasmic Organelles (cont’d)

Cytoskeleton

“Bones and muscles” of the cell

Maintains the cell’s shape and internal organization

Permits movement of substances within the cell and movement of external projections

Mechanotransduction

Microtubules—provides strength

Centrioles

Microfilaments: Actin

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Plasma membranes

Control the composition of the space or compartment they enclose.

Enclose the cell.

Provide the selective transport system.

Provide cell-to-cell recognition.

Provide cellular mobility and shape.

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Plasma membrane encloses the cell and by controlling the movement of substances across it, exerts a powerful influence on metabolic pathways

Very important to physiologic function because controls the composition of the space or compartment they enclose

Plasma membranes control cell polarity, the direction of cells can mean the difference between normal function and disease state such as cancer.

Plasma membrane also help with cell to cell recognition.

Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Plasma membrane composition

Bilayer of lipids and proteins not uniformly distributed

Can separate into discrete units called microdomains

Solid-gel phase; fluid-liquid crystalline phase; liquid-ordered phase

Caveolae

Lipids

Amphipathic lipids

Hydrophilic and hydrophobic

Lipid rafts

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Amphipathic lipids- water loving and water hating side.

Membranes define the cell;s boundaries. Powerful influence of metabolic pathways b/c control movment of substances from one compartment to another.

Structure of Phospholipid molecule

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A, Each phospholipid molecule consists of a phosphate functional group and two fatty acid chains attached to a glycerol molecule. B, The fatty acid chains and glycerol form nonpolar, hydrophobic “tails,” and the phosphate functional group forms the polar, hydrophilic “head” of the phospholipid molecule. When placed in water, the hydrophobic tails of the molecule face inward, away from the water, and the hydrophilic head faces outward, toward the water. (From Raven PH, Johnson GB: Understanding biology, ed 3, Dubuque, IA, 1995, Brown.)

Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Plasma membrane composition (cont’d)

Proteins

Are made from a chain of amino acids known as polypeptides.

Are the major “workhorses” of the cell.

Include integral, peripheral, and transmembrane.

Functions

Receptors

Transporters

Enzymes

Surface markers

Adhesion molecules

Catalysts

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Function of Plasma Membrane Proteins

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Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d) Question 2

The plasma membrane of a cell is:

Permeable to water soluble molecules movement into the cell.

Composed primarily of amphipathic molecules.

Dimpled because of peripheral membrane proteins.

Impermeable to lipid-soluble molecules.

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ANSWER AND RATIONALE: 2. Composed primarily of amphipathic molecules. These molecules are polar with a hydrophobic (uncharged, water hating) portion and a hydrophilic (charged, water loving) portion.

1. The plasma membrane is impermeable to the movement of water-soluble molecules into the cell.

3. The plasma membrane is dimpled because of the presence of caveolae, cave-like indentations.

4. Lipid-soluble molecules like oxygen diffuse readily through the plasma membrane.

Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Proteolytic cascade

Tightly orchestrated sequence of events that cause the breakdown of protein

Four major cascades

Caspase-mediated apoptosis (cell death)

Blood coagulation cascade

Matrix metalloproteinase cascade

Complement cascade

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Proteostasis is a state of cell balance of the processes of prtein synthesis, folding, and degradation. It is vital to cellular health

Proteases= enzymes that cause the breakdown of proteins. Proteases are involved in the physiologic regulation of essential prcesses by participating in a tightlyorchestrated sequence of events termed a proteolytic cascade. FOUR major proteolytic cascades with disease relevance are candidates for treatment modalities

Dysregulation of proteases features prominently inmany human diseases, including cancer, autoimmunity, and neurodegenerative disorders.

Structure and Function of the Cellular Components of Eukaryotic Cell (cont’d)

Cellular receptors

Protein molecules on the plasma membrane, cytoplasm, or nucleus

Proteins that bind with ligands (smaller molecules)

Must fit together

Plasma membrane receptors:

Determine with which ligands a cell will bind.

Determine how the cell will respond to the binding.

Ligand-receptor complex initiates interactions, causing adenylyl cyclase to transform adenosine triphosphate (ATP) to messenger molecules that stimulate specific responses in the cell.

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Cell receptors are protein molecules on the plasma membrane in the cytoplasm, or in the nucleus capable of recognizing and binding smaller molecules called ligands

Cell-to-Cell Adhesions

Allow cells to form tissues and organs

Extracellular matrix

Structure

Meshwork of fibrous proteins in a watery, gel-like substance of complex carbohydrates

Macromolecules

Collagen

Elastin

Fibronectin

Fibroblasts

Functions

Regulate cell growth, movement, and differentiation

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Cells are held together by 3 means: extracellular membrane, cell adhesion molecules in the cell’s plasma membrane and specialized cell junctions

Cell matrix includes 3 protein fibers” collagen, elastin, and fibronectin, they all help to regulate cell growth and differentiation

Cell-to-Cell Adhesions (cont’d)

Basement membrane (basal lamina): Thin tissue layer underlying many organs

Specialized cell junctions

Hold cells together

Allow small molecules to pass from cell to cell

Desmosomes—bands or belts

Tight junctions—barriers to diffusion

Gap junctions—clusters of communicating channels

Junctional complex

Gating

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Cells are held together by3 diff means: extracellular matrix- ECM/basement membrane, cell adhesion molecules in the cell’s plasma membrane, and specialized cell junctions

3 Main types of cell junctions: desmosomes. Tight junctions and gap junctions

Cellular Communication

Maintains homeostasis; regulates growth and division; coordinates functions

Contact-dependent signaling

Plasma membrane-bound receptors

Gap junctions

Paracrine signaling

Autocrine signaling

Hormonal signaling

Neurohormonal signaling

Neurotransmitters

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Cellular Communication (cont’d)

Examples: 3 Main Ways

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Receptors are found in the plasma membrane via specific molecules that affect the cell itself and others in direct physical contact with it

By receptor proteins inside the target cell and the signal molecule has to enter the cell to bind to them

Form protein channel (gap junctions) that directly coordinates the activities of adjacent cells

In neurohormonal signaling, hormones are released into blood by neurosecretory neurons. Then the neurons communicate directly with cells they innervate by releasing chemicals or neurotransmitters at specialized junctions called chemical synapses. The neurotransmitter (chemical) then jumps across the synapse cleft and comes in contact with the postsynaptic target cell. This is another example of cellular communication and is possible due to plasma membrane receptors.

Cellular Communication (cont’d) Question 3

Which information is correct regarding neurotransmitters?

Act on the cells that produce and secrete them.

Act on nearby cells that also take them up and destroy them.

Are produced by neurosecretory neurons and transmitted via the blood.

Diffuse across the synaptic cleft and act on postsynaptic receptors.

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ANSWER AND RATIONALE: 4. Diffuse across the synaptic cleft and act on postsynaptic receptors. Neurotransmitters are produced and released into the synaptic cleft and act on cells or receptors on the postsynaptic cell.

1. Signaling cells act on the cell that produces and secretes them by autocrine signaling.

2. In paracrine signaling, cellular mediators act on nearby cells.

3. Neurohormonal signaling is produced by blood-borne transmission of the products of neurosecretory neurons.

Signal Transduction

Signal cell to target cell by receptor proteins

Extracellular first messengers

Convey instructions to the cell’s interior

Transfer, amplify, distribute, and modulate

Channel regulation—opens and closes gate

Second messengers

Two pathways

Cyclic adenosine monophosphate (cAMP)

Calcium (Ca++)

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Signals are passed b/w cells when a particular ytype of molecule is produced by one cell – the signaling cell – and received by another – the target cell –bymeans of a receptor protein that recognizes and responds specifically to the signal molecule.

Involves signals or instructions from extracellular chemical messengers that are conveyed to the cell’s interior for execution

Second messengers are used when ligands (smaller molecules) cannot enter target cells to cause a desired intracellular response. So ligands send orders by binding with receptors on the surface membrane of cells.

Two most important second messenger pathways are cyclic adenosine monophosphate (cAMP) and calcium (Ca++)

cAMP pathway causes the surface receptor to eventually activate the enzyme adenylyl cyclase. The G protein acts as the middle man between the receptor and adenylyl cyclase. G protein include GTP guanosine triphosphate or GDP guanosine diphosphate

Signal Transduction Pathway

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Schematic of a Signal Transduction Pathway. Like a telephone receiver that converts an electrical signal into a sound signal, a cell converts an extracellular signal (A) into an intracellular signal. B and C, An extracellular signal molecule (ligand) binds to a receptor protein located on the plasma membrane, where it is transduced into an intracellular signal. This process initiates a signaling cascade that relays the signal into the cell interior, amplifying and distributing it en route. Amplification is often achieved by stimulating enzymes. Steps in the cascade can be modulated by other events in the cell. D, Different cell behaviors rely on multiple extracellular signals.

Various Cell Responses to Signals

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Cellular Metabolism

Metabolism

Chemical tasks of maintaining essential cellular functions

Provides the cell with energy

Anabolism

Energy using

Catabolism

Energy releasing

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The task of maintaining essential cellular function

Anabolism (upward) is the energy using process of metabolism

Catabolism (downward) is the energy releasing process

Metabolism gives the cell the energy it needs to produce cellular structures.

Cellular Metabolism (cont’d)

Role of adenosine Triphosphate (ATP)

Is created from the chemical energy contained in organic molecules.

When molecules of carbohydrate, lipid, and protein are catabolized, this energy is transferred to ATP.

Is used in the synthesis of organic molecules, muscle contraction, and active transport.

Functions

Storage

Transfer of energy

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ATP, Adenosine Triphosphate, functions as an energy transferring molecule. Molecules of carbohydrates, lipid and protein store energy and when catabolized transfer energy to ATP.

Cellular Metabolism (cont’d)

Food and production of cellular energy

Digestion

Glycolysis and oxidation

Occurs in the cytoplasm

Aerobic or anaerobic (substrate phosphorylation)

Six ATP molecules for each molecule of glucose

Citric acid cycle

Is called Krebs cycle or the tricarboxylic acid cycle (TCA).

Oxidative phosphorylation

Occurs in the mitochondria; is the mechanism by which energy produced from carbohydrates, fats, and proteins is transferred to ATP.

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Food is first digested from larger molecules to smaller ones of simple sugars, fatty acids and glycerol. All takes place outside of the cell – 3 phases: Digestion glycolysis and oxidation, and citric acid cyclic

Glycolysis and oxidation when smaller molecules are further broken down in the cytoplasm. Sugars are split and then converted to pyruvate that is then turned to Acetyl CoA that like ATP releases energy when hydrolyzed.

Citric acid cycle (Krebs cycle) is the 3rd phase of catabolism of proteins, lipids and polysaccharides. It is during this phase that most of the ATP is generated

Oxidative phosphorylation- Occurs in the mitochondria; is the mechanism by which energy produced from carbohydrates, fats, and proteins is transferred to ATP.

Membrane Transport: Cellular Intake and Output

Solutes—dissolved substances

Electrolytes

Cation (+)

Anions (–)

Measured in milliequivalents per liter (mEq/L) or milligrams per deciliter (mg/dl)

Nonelectrolytes

Glucose, urea, and creatinine

Do not dissociate when placed in solution

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Various types of items that can move across cell membrane via transport

Membrane Transport: Cellular Intake and Output (cont’d)

Passive transport

Occurs when water and small, electrically uncharged molecules move through pores.

Does not require energy.

Diffusion: Concentration gradient

A solute is moved from an area of greater concentration to an area of lesser concentration.

Passive mediated transport: Facilitated diffusion

A protein transporter moves solute molecules through cellular membranes without expending metabolic energy.

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Passive transport occurs when water and small, electrically uncharged molecules move through pores.

Includes diffusion, filtration, and osmosis

Difference in concentration is known as concentration gradient

Diffusion enables movement down a concentration gradient, solubles to move from high concentrated areas to lower concentrations to achieve equilibrium

Facilitated diffusion also moves molecules down the concentration gradient

Membrane Transport: Cellular Intake and Output (cont’d)

Passive transport (cont’d)

Filtration: Hydrostatic pressure

Water and solutes move through a membrane because of a greater pushing pressure (force) on one side of the membrane than on the other side.

Osmosis

Water moves “down” a concentration gradient.

Osmotic pressure: Is the amount of hydrostatic pressure required to oppose the osmotic movement of water.

Oncotic pressure or colloid osmotic pressure: Is the overall osmotic effect of colloids, such as plasma proteins.

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In the vascular system, hydrostatic pressure is the blood pressure generated in vessels by the contraction of the heart. For example blood reaching the capillary bed

Osmosis is movement of water down concentration gradient

Membrane Transport: Cellular Intake and Output (cont’d)

Tonicity

Effective osmolality of a solution

Osmolarity: Measure of the number of milliosmoles per liter of solution or the concentration of molecules per volume of solution

Osmolality: Measure of the number of milliosmoles per kilogram of water or the concentration of molecules per weight of water

Isotonic: Same osmolality or concentration of particles (285 mOsm/kg) as the intracellular fluid (ICF) or extracellular fluid (ECF)

Hypertonic: Concentration of more than 285 to 294 mOsm/kg

Hypotonic: Lower concentration; more dilute than body fluids

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Isotonic has same osmolality as the ICF ECF. For example diarrhea is a loss of isosmotic fluid from the GI tract. So isotonic solutions like D5 Water, NS 0.9% NaCL can be used to replenish fluid loss

Hypotonic solution has lower concentration and is more dilute than body fluids. Water is a hypotonic fluid

Hypertonic solution has higher concentration of particles than ICF or ECF. An example is 3% NaCL solution

It is important to know tonicity when correcting water and soluble imbalances in order to administer the proper differnet types of replacement solutions.

Passive Diffusion

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Passive Diffusion of Solute Molecules Across the Plasma Membrane. Oxygen, nitrogen, water, urea, glycerol, and carbon dioxide can diffuse readily down the concentration gradient. Macromolecules are too large to diffuse through pores in the plasma membrane. Ions may be repelled if the pores contain substances with identical charges. If the pores are lined with cations, for example, other cations will have difficulty diffusing because the positive charges will repel one another; diffusion can still occur, but it occurs more slowly.

Hydrostatic Pressure and Oncotic Pressure in Plasma

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Hydrostatic Pressure and Oncotic Pressure in Plasma. 1, Hydrostatic pressure in plasma. 2, Oncotic pressure exerted by proteins in the plasma usually tends to pull water into the circulatory system. 3, Individuals with low protein levels (e.g., starvation) are unable to maintain a normal oncotic pressure; therefore, water is not reabsorbed into the circulation and, instead, causes body edema.

Active Transport & Na/K Pump

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Membrane Transport: Cellular Intake and Output (cont’d)

Active transport (cont’d)

Transport by vesicle formation (cont’d)

Endocytosis—taking in (cont’d)

Can be clathrin-mediated: Is rapid and enables the cell to ingest large amounts of specific ligands.

Can be caveolae-mediated: Functions as uptake vesicles but are also important sites for signal transduction.

Can be clathrin-caveolin independent.

Exocytosis—expelling

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Endocytosis is a cellular internalizing process during which a section of the plasma membrane enfolds substances from outside the cell, invaginates and separates from the plasma membrane to form a vesicle that moves inside the cell.

Endocytosis mediates cellular uptake of nutrients, helps to counteract exocytosis and maintain homeostatis.

Membrane Transport: Cellular Intake and Output (cont’d) Question 4

A nurse knows that active transport requires:

Receptors capable of recognizing and binding with specific molecules

A hydrostatic pressure gradient between intracellular and extracellular regions

A molecule bound to a ligand that moves the substance down the gradient

The presence of pores in the cell membrane with no energy expenditure

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ANSWER AND RATIONALE: 1. Receptors capable of recognizing and binding with specific molecules. Active transport requires the use of specific receptors matched with molecules and the expenditure of energy.

2. A hydrostatic pressure gradient moves water by passive transport.

3. Molecules bound to a ligand may use active transport, but ligand binding is not mandatory and it moves it up the gradient, not down.

4. Passive transport occurs through pores in the cell membrane and active transport requires energy.

Movement of Electrical Impulses

Resting membrane potential: Difference in voltage across the plasma membrane

All body cells are electrically polarized.

Inside of the cell is more negatively charged than the outside.

Action potential

Depolarization- more positively charged

Threshold potential

Repolarization

Refractory period

Absolute and relative

Hypopolarization and hyperpolarization

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Two types of solutes exist in body fluids: electrolytes and nonelectrolytes. Electrolytes are electrically charges and dissociate into constituent ions when placed in solution Nonelectrolytes do not dissociate when placed in solution.

All body cells are electrically polarized.

Inside of the cell is more negatively charged than the outside.

The differene in electrical charge or voltage is known as the resting membrane potential

When an excitable (nerve or muscle) cell receives an electrochemical stimulus, cations enter the cell causing a rapid change in the resting membrane potential known as the action potential. Action potential moves along the cell’s plasma membrane and is transmitted to an adjacent cell. The action potential is how electrochemical signals convey information from cell to cell.

Depolarization in cells occurs when cells are- more positively charged and its polarity is neutralized

Repolarization process in which negative polarity of the resting membrane potential is reestablished. As sodium channels begin to close, potassium channels begin to open. Potassium permeability increases and sodium permeability decreases.

Refractory period, absolute occurs when plasma membrane cannot respond to an additional stimulus during most of the action potential

Relative refractory period takes place during latter phase of action potential where potassium permeability increases, a stronger than normal stimulus can evoke an action potential

Movement of Electrical Impulses Question 5

A nurse recalls depolarization occurs when the:

Cell is more negatively charged and its polarity is negative.

Sodium-potassium (Na+/K+) pump removes sodium from the cell.

Voltage-regulated channels open, and Na+ enters the cell.

Cell decreases by 25 to 30 millivolts and reaches threshold.

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ANSWER AND RATIONALE: 3. Voltage-regulated channels open and Na+ enters the cell. Depolarization occurs when threshold potential is reached due to a leak of Na+ into the cell. Voltage-dependent sodium channels open and allow rapid entry of Na+ into the cell.

The depolarized cell is more positively charged, and its polarity is neutralized.

2. The Na+ - K+ pump removes Na+ from the cell during repolarization.

4. Threshold potential is achieved when potential is depolarized by 15 to 20 millivolts.

Cellular Reproduction: The Cell Cycle

Necessary for life

Reproduction of gametes: Meiosis

Mitosis (nuclear) vs. cytokinesis (cytoplasmic)

Chromatin vs. chromosomes vs. chromatids

Interphase

G1 phase—gap

S phase—DNA synthesis

G2 phase—RNA and protein synthesis

M phase—mitosis occurs

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Cellular reproduction in body tissues involves mitosis (nuclear division) and cytokinesis (cytoplasmic division)

Only mature cells are capable of division. Maturation occurs during a stage of cellular life called interphase (growth phase)

The alteration between mitosis and interphase in all tissues with cellular turnover is known as the cell cycle.

The cell cycle is the reproductive process that begins after interphase in all tissues with cellular turnover. The four phases of the cell cycle are a) the S phase b) the G2 phase c) the M phase and d) the G1 phases. The M phase (mitosis involves four stages: prophase, metaphase, anaphase, and telophase.

Cellular Reproduction: The Cell Cycle (cont’d)

Mitosis is divided into four phases:

Prophase

Metaphase

Anaphase

Telophase

Two identical diploid cells or daughter cells are produced.

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Cellular Reproduction: The Cell Cycle (cont’d)

Different rates of cellular division

Completed cycle takes approximately 12 to 24 hours.

Different rates occur in the phases.

Growth factors

Are also called cytokines.

Platelet-derived growth factor stimulates connective tissue growth.

Several other types of growth factors are identified.

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Cell reproduction- completed cycle takes approximately 12 to 24 hours.

Tissue Formation

Cells to tissues to organs to tracts or systems

Founder cells

Chemotaxis

Contact guidance

Stem cells

Self renewal

Multipotency

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Tissue Types

Epithelial

Connective

Muscle

Neural

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Epithelial Tissue

Covers most internal and external body surfaces

Simple vs. stratified

Squamous

Cuboidal

Columnar

Pseudostratified

Structures: Cilia and microvilli

Functions

Protection, absorption, secretion, and excretion

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Connective Tissue

Structure

Ground substance

Fibers

Collagenous (white), elastic (yellow), and reticular

Loose and dense connective tissue

Examples

Cartilage, bone, vascular, adipose, and organs

Functions

Framework for forming organs, binding, supporting, and storing excess nutrients

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Also serves as storage sites for excess nutrients

Muscle Tissue

Structure

Composed of myocytes

Examples

Smooth

Skeletal

Cardiac

Functions

Contractile tissue, enabling both voluntary and involuntary movement

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Long, thin and contractile fibers

Neural Tissue

Structure

Neurons

Synapses

Cell body

Axons

Dendrites

Functions

Receive and transmit electrical impulses very rapidly across junctions called synapses

Neurotransmitters

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Composed of highly specialized cells called neurons that receive and and transmit electrical impulses very rapidly across junctions called synapses.

Chapter 2

Altered Cellular and Tissue Biology

Wanda Morancy, DNP, APRN, FNP-BC

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Cellular Adaptation

Is the cell’s response to escape and protect itself from injury.

Adaptive changes in cells:

Atrophy: Decrease in cell size

Hypertrophy: Increase in cell size

Hyperplasia: Increase in cell number

Metaplasia: Reversible replacement of one mature cell type by another less mature cell type

Dysplasia: Deranged cellular growth; is not a true cellular adaptation but rather an atypical hyperplasia

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Adaptation is a reversible, structural or functional response to both normal or physiologic conditions and adverse or pathologic conditions. For example the uterus adapting to pregnancy by enlarging.

In comparison, myocardial cells are forced to enlarge in response to uncontrolled BP that causes the heart to pump harder.

Cellular Adaptation (cont’d)

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Atrophy is a decrease in cellular size, probably includes the following mechanisms of decreased protein synthesis, increase protein catabolism or both

Hypertrophy is an increase in the size of cells by increases work demands or hormonal stimulation. Can be physiologic or pathologic adaptation

Hyperplasia is an increase in the number of cells caused by an increased rate of cellular division

Dysplasia or atypical hyperplasia is an abnormal change in size, shape and organization of mature tissue cells Not considered a true adaptive process. Usually occurs in cervix cells and other epithelial cells in the resp tract. Does not indicate cancer and may not progress into cancer.

Metaplasia is the reversible replacement of one mature cell type by another less mature cell type that is less differentiated. Usually occurs in the bronchial when new immature cells with no cilia replace older cells that have better protective mechanisms such as mucous production and cilia. This occurs in the presence of cigarette smoking. Once smoking stops, bronchial metaplasia can be reversed. But prolonged exposure can cause cancerous transformation of the cells to occur.

Cellular Adaptation (cont’d)

Atrophy

Physiologic

Occurs with early development, similar to the thymus

Pathologic

Results from decreases in workload, use, pressure, blood supply, nutrition, hormonal stimulation, and nervous stimulation

Disuse

Decreased protein synthesis, increased protein catabolism, or both

Ubiquitin-proteasome pathway

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Cellular Adaptation (cont’d)

Hypertrophy

Caused by increased work demand or hormones

Trigger signals: Mechanical and trophic

Physiologic

Pathologic

Hyperplasia

Caused by increased rate of cellular division

Physiologic

Compensatory: Allows organs to regenerate

Hormonal: Replaces lost tissue or supports new growth

Pathologic

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Cellular Adaptation (cont’d) Question 1

Which information is correct regarding pathologic hyperplasia?

Pathologic hyperplasia:

Produces an abnormal proliferation of abnormal cells.

Is an adaptive mechanism that enables organ regeneration.

Increases cell size.

May occur in response to growth factors.

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ANSWER AND RATIONALE: 4. May occur in response to growth factors. Pathologic hyperplasia can occur in response to hormones and growth factors.

Pathologic hyperplasia produces an abnormal proliferation of normal cells. Dysplasia refers to abnormal changes in the size, shape, and organization of mature cells.

Compensatory hyperplasia enables organ regeneration and is a normal process. Pathologic hyperplasia is not normal.

3. Pathologic hyperplasia increases cell number. Hypertrophy is an increase in the size of cells and consequently in the size of the affected organ.

Cellular Adaptation (cont’d)

Dysplasia

Refers to abnormal changes in the size, shape, and organization of mature cells.

Can be called atypical hyperplasia.

Does not indicate cancer.

Metaplasia

Is the reversible replacement of one mature cell by another less mature cell type.

Replacement of normal bronchial columnar ciliated epithelial cells by stratified squamous epithelial cells

Is a reprogramming of stem cells.

‹#›

Cellular Injury

Leads to injury of tissues and organs, determining structural patterns of disease.

Injured cells may recover (reversible injury) or die (irreversible injury).

Causes cell stress.

Is acute or chronic and reversible or irreversible.

Can involve necrosis, apoptosis, autophagy, accumulation, or pathologic calcification.

‹#›

Cellular injury is caused by a lack of oxygen( hypoxia), free radicals, caustic or toxic chemicals, infectious agents, unintentional or intentional injury, inflammatory and immune responses, genetic factors, insufficient nutrients or physical trauma from many causes. Injurious stimuli cause cell stress

Cellular Injury (cont’d)

Injury and Responses

‹#›

Free radicals can cause a) lipid peroxidation or the destruction of unsaturated fatty acids, b) alterations of proteins, and c) alterations in deoxyribonucleic acid (DNA)

Cellular Injury (cont’d)

Four biochemical themes:

Adenosine triphosphate (ATP) depletion

Oxygen and oxygen-derived free radicals

Intracellular calcium and loss of calcium steady state

Defects in membrane permeability

‹#›

Cellular Injury (cont’d)

Cellular injury can lead to cell death by:

Decreased ATP production

Failure of active transport mechanisms (sodium-potassium [Na+/K+] pump)

Cellular swelling

Detachment of ribosomes from endoplasmic reticulum

Cessation of protein synthesis

Mitochondrial swelling from calcium accumulation

Vacuolation

Leakage of digestive enzymes from lysosomes; autodigestion of intracellular structures

Lysis of the plasma membrane

Death

‹#›

Cellular Injury (cont’d)

Causes

Lack of oxygen (hypoxia)

Free radicals

Caustic or toxic chemicals

Infectious agents

Unintentional and intentional injury

Inflammatory and immune responses

Genetic factors

Insufficient nutrients

Physical trauma from many causes

‹#›

Cellular Injury (cont’d)

Hypoxic injury—lack of oxygen

Ischemia

Lack of blood flow into vessels that supply the cell with oxygen and nutrients

Anoxia

Cellular responses

Decrease in ATP, causing failure of the Na+/K+ pump and sodium-calcium exchange

Cellular swelling

Reperfusion injury

‹#›

Cellular Injury (cont’d)

Free radicals and reactive oxygen species (ROS)—oxidative stress

Electrically uncharged atom or group of atoms having an unpaired electron

Results in membrane damage

Types of damage

Lipid peroxidation

Alteration of proteins

Alteration of deoxyribonucleic acid (DNA)

Mechanisms for inactivation of free radicals

Mitochondrial oxidative stress

‹#›

Cellular Injury (cont’d) Question 2

A nurse knows that free radicals may be produced by:

Protein peroxidation

Metabolism of exogenous chemicals or drugs

Spontaneous decay of superoxide

Vitamins E and C supplements

‹#›

ANSWER AND RATIONALE: 2. Metabolism of exogenous chemicals or drugs. The metabolism of certain drugs like carbon tetrachloride results in breakdown products that include free radicals.

1. Lipid peroxidation is a response to free radicals whereby unsaturated fatty acid molecules are destroyed. Free radicals are produced when alterations of proteins cause fragmentation of polypeptide chains.

3. Superoxide may spontaneously decay into water and hydrogen peroxide, ridding the body of free radicals.

4. Vitamins E and C are antioxidants and may inactivate or terminate the actions of free radicals.

Cellular Injury (cont’d)

Chemical injury

Direct toxicity to the cell

Damage to or destruction of plasma membrane

Reactive free radicals and lipid peroxidation

Examples:

Lead

Carbon monoxide

Ethanol

Mercury

Social or street drugs

‹#›

Initial insult in chemical injury is damage or destruction of the plasma membrane

Cellular Injury (cont’d)

Lead

Exposure during neurologic development can result in learning disorders, hyperactivity, and attention problems.

Most common source is paint in older homes (children) and at work (adults).

Toxicity affects central and peripheral nervous systems.

Prevention is the key.

Treatment may include chelation therapy.

‹#›

Cellular Injury (cont’d)

Carbon monoxide (CO)

Is colorless and odorless.

Produces hypoxic injury.

Directly reduces the oxygen-carrying capacity of blood, and promotes tissue hypoxia.

CO’s affinity for hemoglobin is 200 times greater than that of oxygen; it quickly binds with the hemoglobin, preventing oxygen molecules from doing so.

‹#›

Cellular Injury (cont’d)

Ethanol (alcohol)

Results in major nutritional deficiencies, especially folate.

Is metabolized in the liver.

Has a protective effect with the cardiovascular system, up to a point.

Acute alcoholism affects the central nervous system (CNS).

Chronic alcoholism affects primarily the liver and stomach.

Alcohol-induced liver disease (fatty liver, alcoholic hepatitis, cirrhosis)

Acute gastritis

Can cause fetal alcohol syndrome.

‹#›

Cellular Injury (cont’d) Question 3

Which of the following is true about alcohol?

Alcohol (ethanol):

Is metabolized via the microsomal P450.

Is primarily metabolized and excreted by the kidneys.

Increases activation of methionine, an essential amino acid.

Can produce hypermagnesemia with chronic use.

‹#›

ANSWER AND RATIONALE: 1. Is metabolized via the microsomal p-450. This is the primary pathway for oxidation of ethanol. Most of the alcohol in blood is metabolized to acetaldehyde in the liver by three enzyme systems: alcohol dehydrogenase (ADH), the microsomal ethanol-oxidizing system (MEOS; CYP2E1), and catalase. The major pathway involves ADH, an enzyme located in the cytosol of hepatocytes. The microsomal ethanol oxidizing system (MEOS) depends on cytochrome P-450 (CYP2E1), an enzyme needed for cellular oxidation.

2. Ethanol is metabolized in the liver.

3. Methionine activation is decreased by ethanol.

4. Chronic alcohol use is associated with a number of nutritional deficiencies including hypomagnesemia. A large intake of alcohol has enormous effects on nutritional status. Major nutritional deficiencies include magnesium, vitamin B6, thiamine, and phosphorus.

Cellular Injury (cont’d)

Mercury

Two major sources are fish and dental amalgams.

Recommendation: Pregnant women, nursing mothers, and young children should avoid eating fish with a high mercury content.

Social or street drugs

Most popular and dangerous drugs include methamphetamine (“meth”), marijuana, cocaine, and heroin.

‹#›

Cellular Injury (cont’d)

Unintentional and intentional injury

Falls, motor vehicle injuries, poisonings (unintentional)

Medications are the leading cause of child poisoning.

Homicide, suicide (intentional)

Blunt force

Sharp force

Gunshot wounds

Errors in health care

Medication errors are the leading cause.

‹#›

Unintentional and intentional injuries are an important health problem in the US. Death caused by injuries is more common in men than women and higher among blacks than among whites and other racial groups. Medication miscalculations are the leading cause of errors in health care. Activation of inflammation and immunity, which occurs after cellular injury or infection involves powerful biochemical and proteins capable of damaging normal (uninjured and uninfected) cells.

Cellular Injury (cont’d)

Asphyxial injuries

Cause: Failure of cells to receive or use oxygen

Suffocation

Strangulation

Hanging

Ligature

Manual

Chemical asphyxiants

Drowning

‹#›

Cellular Injury (cont’d)

Infectious injuries

Pathogenicity or virulence of a microorganism

Disease-producing potential

Invasion and destruction

Toxin production

Production of hypersensitivity reactions

‹#›

Cellular Injury (cont’d)

Immunologic and inflammatory injuries

Phagocytic cells

Immune and inflammatory substances

Histamine

Antibodies

Lymphokines

Complement

Proteases

Cause membrane alterations

Occur after cellular injury or infection

Are capable of damaging normal (uninjured and uninfected) cells

‹#›

Cellular Injury (cont’d)

Injurious genetics and epigenetic factors

Nuclear alterations

Alterations in the plasma membrane structure, shape, receptors, or transport mechanisms

Example:

Sickle cell anemia

‹#›

Genetic disorders can injure cells by altering the nucleus and the plasma membrane’s structure, shape, receptors or transport mechanisms.

Cellular Injury (cont’d)

Injurious nutritional imbalances

Essential nutrients are required for cells to function normally.

Proteins, carbohydrates, lipids, and vitamins

Alter cellular structure and function, especially transport mechanisms, chromosomes, nucleus, and DNA.

Examples:

Deficient intake

Excessive intake

‹#›

Deprivation of essential nutrients (proteins, carbs, lipids and vitamins) can cause cellular injury by altering cellular structure and function, particularly of the transport mechanisms, chromosomes, nucleus and DNA.

Cellular Injury (cont’d)

Temperature extremes and climate change

Hypothermic injury

Slows cellular metabolic processes

Produces reactive oxygen species

Hyperthermic injury

Heat cramps; heat exhaustion; heat stroke

Malignant hyperthermia; neuroleptic malignant syndrome

Drug-induced hyperthermia

Burns

Overheating; sudden infant death syndrome

‹#›

Injurious physical agents include temperature extremes, and climate change, changes in atmospheric pressure, ionizing radiation, illumination, mechanical stresses (eg repetitive body movements) and noise.

Cellular Injury (cont’d)

Sudden increases or decreases in atmospheric pressure

Blast injury

Decompression sickness or caisson disease

“The bends,” diver disease

High-altitude illness

High-altitude pulmonary edema

High-altitude cerebral edema

Acute mountain sickness

‹#›

Cellular Injury (cont’d)

Ionizing radiation

Any form of radiation capable of removing orbital electrons from atoms

X-rays, gamma rays, alpha and beta particles

Mechanism of damage

Deterministic

Stochastic

Effects of ionizing radiation

Somatic

Genetic

Fetal

‹#›

Cellular Injury (cont’d)

Ionizing radiation (cont’d)

Bystander effects: Cells not in the directly radiated field are affected by the radiation; referred to as horizontal transmission.

Genomic instability: Generations of cells derived from an irradiated progenitor cell appear normal, but time lethal (i.e., irreversible) and nonlethal mutations appear; referred to as vertical transmission.

‹#›

Cellular Injury (cont’d)

Illumination injury

Eyestrain, obscured vision, and cataract formation

Caused by light modulation

Mechanical stresses

Physical impact, strain, and overexertion

Noise

Acoustic trauma and noise-induced hearing loss

‹#›

Manifestations of Cellular Injury

Cellular accumulations (infiltrations)

Harm cells by “crowding” organelles and by causing excessive (and sometimes harmful) metabolites

Water

Cellular swelling

Lipids and carbohydrates

Usually affects the liver (e.g., fatty liver)

Glycogen

Observed in genetic disorders: Glycogen storage diseases

Accumulation: Excessive vacuolation of the cytoplasm

‹#›

Accumulations harm cells by “crowding” the organelles and by causing excessive and sometimes harmful metabolites to be produced during their catabolism. The metabolites are released into the cytoplasm or expelled into the extracellular matrix.

Manifestations of Cellular Injury (cont’d)

Cellular swelling

‹#›

Manifestations of Cellular Injury (cont’d)

Cellular accumulations (infiltrations)

Proteins

Excess accumulates primarily in the renal convoluted tubule and in the immune B lymphocytes

Pigments

Melanin, hemoproteins, bilirubin

Calcium

Dystrophic calcification, psammoma bodies, metastatic calcification

Urate: Uric acid

Excess causes gout

‹#›

Manifestations of Cellular Injury (cont’d)

Systemic manifestations

Fatigue and malaise

Loss of well-being

Altered appetite

Fever

Leukocytosis

Increased heart rate

Pain

Other signs and symptoms

‹#›

Systematic manifestations of cellular injury include fever, leukocytosis, increased heart rate, pain, and serum elevations of enzymes in the plasma.

Cellular Death

Two types of cellular death:

Necrosis

Includes inflammatory changes

Apoptosis

No inflammatory changes

Type 1—cell death (caspases)

Type 2—autophagic cell death

‹#›

Necrosis is the sum of the changes after local cell death and includes the processes of inflammation and cellular lysis.

Cellular Death (cont’d)

Necrosis and Apoptosis

‹#›

Cellular Death: Necrosis

Necrosis

Sum of cellular changes after local cell death and the process of cellular autodigestion (autolysis)

Necrosis processes

Karyolysis

Nuclear dissolution and chromatin lysis

Pyknosis

Clumping of the nucleus

Karyorrhexis

Fragmentation of the nucleus

‹#›

Cellular Death: Types of Necrosis

Coagulative necrosis

Kidneys, heart, and adrenal glands

Protein denaturation

Abnormality in intracellular calcium

Liquefactive necrosis

Neurons and glial cells in the brain

Hydrolytic enzymes form liquid-filled cyst or forms pus

‹#›

Cellular Death: Types of Necrosis (cont’d)

Caseous necrosis

Tuberculosis pulmonary infection

Combination of coagulative and liquefactive necroses

Cheese-looking substance that is walled off

Fat necrosis

Breast, pancreas, other abdominal organs

Action of lipases

‹#›

Cellular Death: Types of Necrosis (cont’d)

Gangrenous necrosis

Clinical term

Dry vs. wet gangrene

Gas gangrene

‹#›

102

Cellular Death: Types of Necrosis (cont’d)

Dry Gangrene

‹#›

Cellular Death: Apoptosis

Apoptosis

Is programmed cellular death.

Is characterized by the “dropping off” of cellular fragments called apoptotic bodies.

Is the active process of cellular destruction.

Can occur normally or pathologically.

Dysregulated apoptosis:

Is excessive or not enough.

Can lead to cancer, autoimmune disorders, neurodegenerative diseases, and ischemic injury.

‹#›

Apoptosis which is a different type of cellular death is a process of selective cellular self-destruction called programmed cell death. Other forms of programmed cell death (type 2) include autophagic (eat oneself) cell death

104

Cellular Death: Autophagy

“Recycling center”

Eats itself

Self-destructive process

Survival mechanisms

‹#›

Aging and Altered Cellular and Tissue Biology

Aging is normal, inevitable, and universal.

Accumulation of damaged macromolecules

Human lifespan is the time from birth to death.

Maximal human lifespan is 80 to 100 years.

Life expectancy is the average number of years of life remaining at a given age.

Current generation may have a shorter life span than previous generations.

‹#›

One of the hallmarks of the aging process is the accumulation of damaged macromolecules. The emerging focus in the biology of aging includes examining the impact of epigenetic and genetic changes, inflammation , oxidative stress, metabolic and endocrine regulation, intrauterine and lifelong patterns of health, decline in cell renewal by adult stem cells and accumulates cell damage related to cancer and aging.

106

Aging and Altered Cellular and Tissue Biology (cont’d)

Degenerative extracellular changes

Collagen binding and cross linking

Increase in free radicals effects on cells

Structural alterations

Peripheral vascular disease and oxidative stress

Cellular aging

Atrophy, decreased functioning, loss of cells

4977 deletion or common deletion

‹#›

Aging and Altered Cellular and Tissue Biology (cont’d)

Tissue and systemic aging

Progressive stiffness and rigidity

Frailty

Complex clinical syndrome

Involves oxidative stress, dysregulation of inflammatory cytokines and hormones, malnutrition, physical inactivity, and muscle apoptosis

‹#›

Aging and Altered Cellular and Tissue Biology (cont’d) Question 4

A nurse remembers that aging is associated with:

Reduced cross-linking of collagen

Reduced degradation of collagen

Increased cross-linking of collagen

Increased collagen synthesis

‹#›

109

ANSWER AND RATIONALE: 3. Increased cross-linking of collagen. Aging affects the extracellular matrix with increased cross-linking, decreased synthesis, and increased degradation of collagen.

1. Aging is associated with increased cross-linking.

2. Aging is associated with increased degradation of collagen.

4. Aging is associated with reduced collagen synthesis.

Somatic Death

Is the death of the entire person.

Does not involve an inflammatory response.

Postmortem changes include:

Complete cessation of respirations and circulation

Algor mortis: Reduced temperature

Livor mortis: Purple skin discoloration

Rigor mortis: Muscle stiffening

Postmortem autolysis: Putrefactive changes associated with the release of enzymes and lytic dissolution

‹#›

Somatic death is death of the entire organism (person). Postmortem change is diffuse and does not involve the inflammatory response.

Postmortem changes include:

Complete cessation of respirations and circulation

Algor mortis: Reduced temperature

Livor mortis: Purple skin discoloration

Rigor mortis: Muscle stiffening

Postmortem autolysis: Putrefactive changes associated with the release of enzymes and lytic dissolution

110

Chapter 3

The Cellular Environment: Fluids and Electrolytes, Acids and Bases

Wanda Morancy, DNP, APRN, FNP-BC

‹#›

Distribution of Body Fluids

Total body water

Intracellular fluid (ICF): Inside the cell

Extracellular fluid (ECF): Outside the cell

Interstitial fluid

Intravascular fluid

Cerebrospinal fluid (CSF)

Lymphatic, synovial, intestinal, biliary, hepatic, pancreatic, pleural, peritoneal, pericardial, and intraocular fluids

Sweat

Urine

‹#›

Fluid fluctuations can influence excitability of cells and electrolyte balance. Can also influence pH and cellular function of enzyme cells

112

Aging and Distribution of Body Fluids

Total body water (cont’d)

Newborn: 75% to 90% of body weight

Childhood: 60% to 65% of body weight

Adults: 60% of body weight

Older adults: Percent declines with age

Men have a greater percentage of body water when compared with women

‹#›

Water Movement between the ICF and ECF

Osmolality

Osmotic forces

Sodium for the ECF

Potassium for the ICF

Aquaporins

A family of water channel proteins that provide permeability to water

‹#›

Water moves freely among body’s compartments and is transported by either osmotic or hydrostatic pressure.

114

Water Movement between the ICF and ECF (cont’d)

Osmosis: Is how water moves between the ICF and ECF compartments.

Water moves between the plasma and interstitial fluid through osmosis and hydrostatic pressure, which occur across the capillary membrane.

Net filtration: Is the movement across the capillary wall.

As described according to the Starling law or hypothesis

‹#›

-Osmosis

115

Water Movement between Plasma and Interstitial Fluid

Starling hypothesis

Net filtration is equal to the forces favoring filtration minus the forces opposing filtration

Forces favoring filtration

Capillary hydrostatic pressure (blood pressure)

Interstitial oncotic pressure (water pulling)

Forces opposing filtration or forces favoring reabsorption

Plasma oncotic pressure (water pulling)

Interstitial hydrostatic pressure

‹#›

Alterations in Water Movement: Edema

Accumulation of fluid in the interstitial spaces

Causes:

Increased capillary hydrostatic pressure (venous obstruction) Outward movement of water from capillary->interstitial space

Decreased plasma oncotic pressure (losses or diminished production of albumin) Attracts water from interstitial space->capillary

Increased capillary permeability (inflammation and immune response)

Lymph obstruction (lymphedema)

Sodium retention

‹#›

Edema is a problem of fluid distribution

117

Alterations in Water Movement: Edema (cont’d)

Causes

‹#›

Page 107, very important to understand Figure 3-2.

118

Alterations in Water Movement: Edema (cont’d)

Clinical Manifestations

Localized vs. generalized

Dependent edema

Pitting edema

“Third space”

Swelling and puffiness

Tighter-fitting clothes and shoes

Weight gain

Treatment

Elevate edematous limbs

Use compression stockings or devices

Avoid prolonged standing

Restrict salt intake

Take diuretic agents

‹#›

Alterations in Water Movement: Edema Question 1

A person with heart failure has edema in the lower legs and sacral area. The nurse suspects this condition is due to a(n):

Increase in plasma oncotic pressure

Decrease in capillary hydrostatic pressure

Decrease in lymph obstruction pressure

Increase in capillary hydrostatic pressure

‹#›

120

ANSWER AND RATIONALE: 4. Increase in capillary hydrostatic pressure. Heart failure produces salt and water retention and subsequent volume overload, which increases capillary hydrostatic pressure which leads to edema.

1. An increase in plasma oncotic pressure produces movement of fluid from the interstitial space into the vascular space which would decrease edema.

2. A reduction in capillary hydrostatic pressure decreases the force for filtration of fluid from the capillary which would decrease edema.

3. A decrease in lymph obstruction would not cause edema; an increase in lymph obstruction would lead to edema.

Overview of Electrolytes

Electrolytes are in both ECF and ICF compartments but are in different concentrations.

Some electrolytes are more concentrated in the ICF compartment, as compared with the ECF compartment.

All electrolytes move across compartments but must be in balance for optimal health.

‹#›

Overview of Electrolytes

Cation

Potassium (K+)

Anions

Phosphate

Organic ions

Intracellular

Extracellular

Cation

Sodium (Na+)

Anions

Chloride (Cl–)

Bicarbonate (HCO3–)

‹#›

Na+ and Cl– Balance

Sodium

Is the primary ECF cation.

Regulates osmotic forces.

Roles include:

Neuromuscular irritability, acid-base balance, cellular reactions, and transport of substances

Is regulated by aldosterone and natriuretic peptides.

Chloride

Is the primary ECF anion.

Provides electroneutrality.

Follows sodium.

‹#›

Sodium and water balance are intimately related. Chloride levels are generally proportional to changes in sodium level.

123

Na+ and Cl– Balance (cont’d)

Renin-angiotensin-aldosterone system

Aldosterone

Increases reabsorption of sodium by the distal tubule of the kidney

Natriuretic peptides

Decreases tubular resorption, and promotes urinary excretion of sodium

Atrial natriuretic peptide

Brain natriuretic peptide

Urodilantin (kidney)

‹#›

Na+ and Cl– Balance (cont’d)

Renin-Angiotensin-Aldosterone system

‹#›

-https://www.youtube.com/watch?v=fqOfOvwlz-g

-Kidneys secrete renin when blood volume, blood pressure and renal blood flow reduces.

-Renin stimulates formation of angiotensin I .

-ACE is released by pulmonary vessels and converts angiotensin I to angiotensin II. Angiotensin II causes vasoconstriction, elevates systemic blood pressure and stimulates secretion of aldosterone.

-Aldosterone promotes sodium and water reabsorption by proximal tubules of kidneys. Also stimulates excretion of potassium and reduces ECF concentration of potassium.

125

Water Balance

Is regulated by thirst perception and the antidiuretic hormone (ADH)

Thirst perception

Osmolality receptors (osmoreceptors)

Stimulated from hyperosmolality, dry mouth, plasma-volume depletion

Increases water intake

Baroreceptors

Stimulated from depleted plasma volume

Causes release of ADH

‹#›

-Water balance regulated by sensation of thirst and by action of the antidiuretic hormone (ADH). These are initiated by increase in plasma osmolality (occurs in water deficit or sodium excess) or decrease in circulating blood volume.

-Water is reabsorbed by renal tubules once ADH is released to restore plasma volume and blood pressure

126

Water Balance (cont’d)

ADH

Is released when there is an increase in plasma osmolality or decrease in circulating blood volume.

Is also called arginine vasopressin.

Increases water reabsorption.

‹#›

Water Balance (cont’d)

Antidiuretic hormone

‹#›

Water Balance Question 2

A person reports severe diarrhea for 2 days. The nurse understands this stimulates a(n):

Reduction in aldosterone secretion

Reduction in renin secretion

Increase in antidiuretic hormone secretion

Increase in natriuretic peptide secretion

‹#›

129

ANSWER AND RATIONALE: 3. Increase in antidiuretic hormone secretion. Hypovolemia stimulates volume sensitive receptors and baroreceptors and results in secretion of antidiuretic hormone to increase water reabsorption.

1. Volume depletion produces an increase in aldosterone secretion through the activation of the renin angiotensin aldosterone system.

2. Volume depletion produces an increase in renin secretion and initiates the renin angiotensin aldosterone system.

4. Volume depletion results in reduced secretion of natriuretic peptides. Natriutetic peptides are diuretics which would make more loss of fluid.

Alterations in Na+, Cl–, and Water Balance

Isotonic alterations

Total body water change with proportional electrolyte change

Isotonic volume depletion (hypovolemia)

Isotonic volume excess (hypervolemia)

‹#›

Isotonic refers to when solution has the same concentration of solutes as the plasma. Occurs when TBW change is accompanied by proportional changes to the amount of electrolytes and water.

130

Alterations in Na+, Cl–, and Water Balance: Hypertonic Alterations

Hypernatremia

Serum sodium >147 mEq/L

Related to sodium gain or water loss

Water movement from the ICF to the ECF

Intracellular dehydration

Manifestations: Intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia

Treatment: Isotonic salt-free fluids given slowly (D5 Water) until serum Na returns to normal

‹#›

-Occurs when osmolality of ECF is elevated above normal (> 294 mOsm)

-Hypernatremia is most common cause. Hypertonicity of ECF attracts water from ICF.

-Fluid replacement must be given slowly to prevent cerebral edema.

131

Alterations in Na+, Cl–, and Water Balance: Hypertonic Alterations (cont’d)

Hyperchloremia

Occurs with hypernatremia or a bicarbonate deficit.

Is usually secondary to pathophysiologic processes.

Is managed by treating the underlying disorders.

Give water (D5 Water) and stop fluid loss

‹#›

-Must give water and stop fluid loss.

132

Alterations in Na+, Cl–, and Water Balance: Hypertonic Alterations (cont’d)

Water deficit

Dehydration

Pure water deficits

Renal free water clearance

Manifestations

Tachycardia, weak pulse, and postural hypotension

Elevated hematocrit and serum sodium levels

Headache, dry skin, and dry mucous membranes

Treatment: Give water, and stop fluid loss

Hypotonic saline solutions or 5% dextrose in water

‹#›

Alterations in Na+, Cl–, and Water Balance: Hypotonic Alterations

Decreased osmolality

Hyponatremia or free water excess

Hyponatremia decreases the ECF osmotic pressure, and water moves into the cell

‹#›

Occurs when osmolality of ECF is less than normal (<280 mOsm) usually due to sodium deficit or free water excess

134

Alterations in Na+, Cl–, and Water Balance: Hypotonic Alterations (cont’d)

Hyponatremia

Serum sodium level <135 mEq/L

Sodium deficits cause plasma hypoosmolality and cellular swelling

Pure sodium deficits; low intake; dilutional hyponatremia; hypotonic hyponatremia; hypertonic hyponatremia

Manifestations: Lethargy, headache, confusion, apprehension, seizures, and coma

Treatment:

Depends on underlying disorder

Restrict water intake

Administer intravenous (IV) fluids

‹#›

Hypertonic saline solutions are used sparingly in cases of Hyponatremia or presence of seizures.

135

Alterations in Na+, Cl–, and Water Balance: Hypotonic Alterations (cont’d)

Hypochloremia

Is usually the result of hyponatremia or elevated bicarbonate concentration.

Some causes are:

Vomiting

Metabolic alkalosis

Cystic fibrosis

Treat the underlying cause.

Small amounts of hypertonic IV solutions (0.3% NaCl when neurologic symptoms are severe

‹#›

Alterations in Na+, Cl–, and Water Balance: Hypotonic Alterations (cont’d)

Water excess

Compulsive water drinking, causing water intoxication

Decreased urine formation

Syndrome of inappropriate ADH (SIADH)

ADH secretion causes water reabsorption

Manifestations: Cerebral edema, muscle twitching, headache, and weight gain

Treatment: Fluid restriction; may need hypertonic sodium chloride IV solution

‹#›

Potassium

Is the major intracellular cation.

Aldosterone, insulin, epinephrine, and alkalosis facilitate K+ into the cells.

Insulin deficiency, aldosterone deficiency, acidosis, and strenuous exercise facilitate K + out of the cells.

The sodium-potassium (Na + /K +) pump maintains concentration.

‹#›

-Predominant ICF ion, functions to regulate ICF osmolality, maintain the resting membrane potential and deposit glycogen in liver and skeletal muscle cells.

-Potassium balance is maintained by renal excretion of K+ absorbed from GI tract

- All help to regulate levels of ICF potassium, most important is aldosterone via renal excretion

138

Potassium (cont’d)

Is essential for the transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction.

Regulates ICF osmolality and deposits glycogen in liver and skeletal muscle cells.

Kidneys, aldosterone and insulin secretion, and changes in pH regulate K+ balance.

K+ adaptation allows the body to accommodate slowly to increased levels of K+ intake.

‹#›

Potassium adaptation- process by which body slowly adjusts to increased levels of K+.

139

Hypokalemia

Potassium level <3.5 mEq/L

Causes:

Reduced potassium intake

Increased potassium entry into cell

Increased potassium loss

Treatment:

Replace potassium orally and/or intravenously

Manifestations:

Membrane hyperpolarization causes:

Decreased neuromuscular excitability

Skeletal muscle weakness

Smooth muscle atony

Cardiac dysrhythmias

U wave on electrocardiogram (ECG)

‹#›

Hyperkalemia

Potassium level >5.5 mEq/L

Rare as a result of efficient renal excretion

Causes:

Increased intake

Shift of K+ from ICF to ECF

Decreased renal excretion

Hypoxia

Acidosis

Insulin deficiency

Cell trauma

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Hyperkalemia (cont’d)

Mild attacks

Tingling of lips and fingers, restlessness, intestinal cramping and diarrhea, T waves on the ECG

Severe attacks

Muscle weakness, loss of muscle tone, flaccid paralysis, cardiac arrest

Treatment

Calcium gluconate, insulin and/or glucose, Na+ bicarbonate, cation exchange resins, dialysis

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Administration of glucose stimulates insulin secretion. Insulin facilitates cellular entry/uptake of potassium.

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Calcium

Most calcium is located in the bone as hydroxyapatite

99% in bone

1% in plasma and body cells

Is necessary for:

Structure of bones and teeth

Blood clotting

Hormone secretion

Cell receptor function

Muscle contractions

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-Calcium is a major cation necessary ion in the structure of bones and teeth, in blood clotting, in hormone secretion and the function of cell receptors and in membrane stability.

143

Phosphate

Similar to calcium, most phosphate (85%) is also located in the bone.

Is necessary for high-energy bonds located in creatine phosphate and adenosine triphosphate (ATP) and acts as an anion buffer and needed for muscle contraction energy.

Calcium and phosphate concentrations are rigidly controlled.

Ca++ x HPO4= = K (K is a constant)

If the concentration of one increases, the concentration of the other decreases.

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Phosphate acts as a buffer in acid-base regulation and provides energy for muscle contraction

144

Calcium and Phosphate

Regulated by three hormones:

Parathyroid hormone (PTH)

Increases plasma calcium levels via kidney reabsorption.

Vitamin D

Is a fat-soluble steroid; increases calcium absorption from the gastrointestinal (GI) tract.

Calcitonin

Decreases plasma calcium levels.

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Parathyroid glands secrete PTH

145

Hypocalcemia

Calcium levels <8.5 mg/dl

Causes:

Inadequate intake or absorption

Decreases in PTH and vitamin D

Blood transfusions

Treatment:

Calcium gluconate, calcium replacement, decrease phosphate intake

Manifestations:

Increased neuromuscular excitability (partial depolarization)

Muscle spasms

Chvostek and Trousseau signs

Convulsions

Tetany

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Hypercalcemia

Calcium levels >12 mg/dl

Causes:

Hyperparathyroidism

Bone metastasis

Excess vitamin D

Immobilization

Acidosis

Manifestations:

Decreased neuromuscular excitability

Muscle weakness

Manifestations (cont’d):

Kidney stones

Constipation

Heart block

Treatment:

Oral phosphate

IV normal saline

Bisphosphonates

Calcitonin

Corticosteroids

Mithramycin

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Hypophosphatemia

Causes: Intestinal malabsorption and renal excretion, vitamin D deficiency, antacid use, alcohol abuse

Manifestations: Diminished release of oxygen, osteomalacia (soft bones), muscle weakness, bleeding disorders (platelet impairment), leukocyte alterations

Treatment: Treat underlying condition such as respiratory alkalosis and hyperparathyroidism

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Hyperphosphatemia

Causes: Exogenous or endogenous addition of phosphate to ECF, long-term use of phosphate enemas or laxatives, renal failure

High phosphate levels, related to low calcium levels

Manifestations: Same as hypocalcemia with possible calcification of soft tissue

Treatment: Treat underlying condition, aluminum hydroxide, and dialysis

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149

Magnesium

Is an intracellular cation.

Is stored most in the muscle and bones.

Interacts with calcium.

Has a plasma concentration of 1.8 to 2.4 mg/dl.

Is a co-factor in intracellular reactions, protein synthesis, nucleic acid stability, and neuromuscular excitability.

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-Major ICF cation, second to potassium, that is principally regulated by PTH

-Small intestine and kidneys balance metabolism of magnesium

150

Hypomagnesemia and Hypermagnesemia

Hypomagnesemia

From malabsorption

Associated with hypocalcemia and hypokalemia

Neuromuscular irritability

Tetany, convulsions

Increased reflexes

Treatment: Magnesium sulfate

Hypermagnesemia

From renal failure

Skeletal muscle depression

Muscle weakness

Hypotension

Respiratory depression

Bradycardia

Treatment: Avoid magnesium; dialysis

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Familiarize yourselves with the symptoms and treatment related to electrolyte loss and excess.

151

Acid-Base Balance

Increasing H+ pH scale Decreasing H+

pH—What is it?

Negative logarithm of the H+ concentration

0 7 14

Very acidic Neutral Very alkaline

Each number represents a factor of 10.

If the solution moves from a pH of 7 to a pH of 6, then the H+ ions have increased tenfold.

If H+ is high in number, pH is low (acidic).

If H+ is low in number, pH is high (alkaline).

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152

pH represents negative logarithm of hydrogen ion concentration in solution

Acid-Base Balance (cont’d)

Acids are formed as end-products of protein, carbohydrate, and fat metabolism.

To maintain the body’s normal pH (7.35-7.45) the H+ must be neutralized by the retention of bicarbonate or excreted.

Bones, lungs, and kidneys are major organs involved in the regulation of acid-base balance.

pH below 6.8 = death.

pH above 7.8 = death.

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Acid-Base Balance (cont’d)

Acid-base balance is mainly concerned with two ions:

Hydrogen (H+)

Bicarbonate (HCO3–)

Alterations of hydrogen and bicarbonate concentrations in body fluids are common in disease processes.

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-Different body fluids have different pH values

-Renal and respiratory systems, together with the body’s buffer systems are the principal regulators of acid-base balance.

154

Acid-Base Balance (cont’d)

Carbonic acid (H2CO3)

Can be eliminated as carbon dioxide (CO2) gas via the lungs

Volatile Acids in the Body

Nonvolatile Acids in the Body

Sulfuric, phosphoric, and other metabolic acids

Is eliminated by the renal tubules with the regulation of HCO3–

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Acid-Base Balance (cont’d)

Sources of H+ ions

CO2 diffuses into the bloodstream where the following reaction occurs:

Regulated by the Lung Regulated by the Kidney

CO2 + H2O  H2CO3  HCO3–+ H+

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Acid-Base Balance (cont’d)

pH control mechanisms

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Buffering Systems

Buffer: Chemical that can bind excessive H+ or OH– without a significant change in pH

Located in the ICF and ECF

Consist of a buffering pair: weak acid and its conjugate base

Most important plasma buffering systems: carbonic acid–bicarbonate system and hemoglobin

Associate and dissociate very quickly (instantaneous)

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-Buffering occurs in response to changes in acid-base balance. Buffers can absorb excess H+or OH- in order to minimize fluctuations in pH.

-Buffers are present both in ICF and ECF and function in pairs, a weak acid and a base.

-Most important plasma buffer system is bicarbonate-carbonic acid and hemoglobin

-Most important intracellular buffer systems are phosphate and protein

-Renal buffers are ammonia and phosphate

158

Carbonic Acid– Bicarbonate Buffering

Operates in the lung and the kidney.

The greater the partial pressure of carbon dioxide (pCO2), the more carbonic acid is formed.

At a pH of 7.4, the ratio of bicarbonate to carbonic acid is 20:1.

Bicarbonate and carbonic acid can increase or decrease, but the ratio must be maintained.

Lungs can decrease carbonic acid.

Kidneys can reabsorb or regenerate bicarbonate but do not act as fast as the lungs.

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Carbonic Acid– Bicarbonate Buffering (cont’d)

If bicarbonate decreases, then the pH decreases and can cause acidosis.

pH can be returned to normal if carbonic acid also decreases.

This type of pH adjustment is called compensation.

The respiratory system compensates by increasing or decreasing ventilation.

The renal system compensates by producing acidic or alkaline urine.

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Other Buffering Systems

Protein buffering

Proteins have negative charges; as a result, they can serve as buffers for H+; mainly intracellular buffer with hemoglobin

Respiratory and renal buffering

Respiratory: Acidemia causes increased ventilation; alkalosis slows respirations

Renal: Secretion of H+ in urine and reabsorption of HCO3–; dibasic phosphate and ammonia

Cellular ion exchange

Exchanges of K+ for H+ in acidosis and alkalosis

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Acid-Base Imbalances

Normal arterial blood pH

7.35 to 7.45

Obtained by arterial blood gas (ABG) sampling

Acidosis

pH is less than 7.35

Systemic increase in H+ concentration

Alkalosis

pH is greater than 7.45

Systemic decrease in H+ concentration or excess of base

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Acid-Base Imbalances (cont’d)

Four categories

Respiratory acidosis—Elevation of pCO2 as a result of ventilation depression

Respiratory alkalosis—Depression of pCO2 as a result of hyperventilation

Metabolic acidosis—Depression of HCO3– or an increase in noncarbonic acids

Metabolic alkalosis—Elevation of HCO3–, usually as a result of an excessive loss of metabolic acids

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-Respiratory acidosis occurs in presence of co2 retention via way of metabolic production of carbon dioxide related to alveolar malfunction usually due to respiratory obstruction

-Occurs when there’s decreased concentration of plasma carbon dioxide in the presence of alveolar hyperventilation

-Metabolic acidosis occurs when concentration of non-carbonic acids increase or bicarbonate is lost from extracellular fluid or cannot be regenerated by the kidneys.

-Occurs when bicarb concentration is increased, usually caused by excessive loss of metabolic acids.

163

Metabolic Acidosis

Causes

Lactic acidosis

Renal failure

Diabetic ketoacidosis

Diarrhea

Starvation

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Metabolic Acidosis (cont’d)

Noncarbonic acids increase or bicarbonate (base) is lost from ECF or cannot be regenerated by the kidney.

pH drops below 7.35

HCO3– drops: less than 24 mEq/L

Compensation: Hyperventilation and renal excretion of excess acid

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Metabolic Acidosis (cont’d)

Manifestations:

Headache

Lethargy

Kussmaul respirations

Treatment:

Bicarbonate

Lactate-containing solutions: Lactate converted into bicarbonate in the liver

Treat the underlying cause(s)

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Metabolic Acidosis (cont’d)

Anion gap

Used cautiously to distinguish different types of metabolic acidosis.

By rule, anions (–) should equal cations (+).

Not all normal anions are routinely measured.

Represents unmeasured negative ions.

Normal anion gap is 10 to 12 mEq/L.

Normal anion gap or elevated anion gap with metabolic acidosis may help determine the cause.

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-Key to remember is that it’s used to determine type of metabolic acidosis

167

Metabolic Alkalosis

Causes

Prolonged vomiting

Gastric suctioning

Excessive bicarbonate intake

Hyperaldosteronism with hypokalemia

Diuretic therapy

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Metabolic Alkalosis (cont’d)

Bicarbonate concentration is increased, usually from excessive loss of metabolic acids (Cl –)

pH is elevated above 7.45.

HCO3– is elevated above 26 mEq/L.

Compensation: Hypoventilation; kidneys conserve H+ and eliminate bicarbonate.

Manifestations: Weakness, muscle cramps, and hyperactive reflexes with signs of hypocalcemia

Treatment: Sodium chloride, potassium, chloride IV (chloride replaces HCO3-)

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Respiratory Acidosis

Causes

Depression of the respiratory center (brainstem trauma, oversedation)

Respiratory muscle paralysis

Disorders of the chest wall (kyphoscoliosis, pickwickian syndrome, flail chest)

Disorders of the lung parenchyma (pneumonitis, pulmonary edema, emphysema, asthma, bronchitis)

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Respiratory Acidosis (cont’d)

Occurs with alveolar hypoventilation

pH is below 7.35.

CO2 elevates from hypercapnia (>45mmHg)

Compensation: Is not as effective since kidneys take time but conserve bicarbonate and eliminate H+

Manifestations: Headache, restlessness, blurred vision, apprehension, lethargy, muscle twitching, tremors, convulsions, coma

Treatment: Restore adequate ventilation; may need mechanical ventilation; administer IV lactate fluids

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Respiratory Alkalosis

Causes

High altitudes

Hypermetabolic states, such as fever, anemia, and thyrotoxicosis

Early salicylate intoxication

Anxiety or panic disorder

Improper use of mechanical ventilators

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Respiratory Alkalosis (cont’d)

Occurs with hyperventilation and decreased plasma CO2 (hypocapnia)

pH above 7.45

CO2 is decreased below 38 mm Hg

Compensation: Kidneys decrease H+ excretion and bicarbonate absorption

Manifestations: Dizziness, confusion, tingling of extremities (paresthesias), convulsions, and coma with signs of hypocalcemia

Treatment: Paper bag; treat hypoxemia and hypermetabolic states; administer IV chloride fluids

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Summary

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Changes in the concentration of hydrogen in the blood cause acid-base imbalances, an increase in concentration causes acidosis and a decrease causes alkalosis.

174

Question 3

A person arrives in the emergency department after a loss of consciousness and the develop-ment of Kussmaul respirations. The individual has a history of diabetes and 2 days of vomiting and diarrhea. The nurse suspects the person has:

Respiratory alkalosis

Respiratory acidosis

Metabolic alkalosis

Metabolic acidosis

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175

ANSWER AND RATIONALE: 4. Metabolic acidosis. Diabetic ketoacidosis results in an increase in noncarbonic acids and a decrease in bicarbonate ion which produces metabolic acidosis.

1. Respiratory alkalosis is produced by alveolar hyperventilation and reduction in carbon dioxide concentration.

2. Respiratory acidosis is produced by alveolar hypoventilation and increase in carbon dioxide concentration.

3. Metabolic alkalosis is produced by an excess of bicarbonate ion.

Question 4

A person with a history of chronic lung disease arrives in the clinic with a 1-week history of a productive cough, hypoventilation, headache, and muscle twitching. The nurse suspects the person is experiencing:

Respiratory acidosis

Respiratory alkalosis

Metabolic acidosis

Metabolic alkalosis

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176

ANSWER AND RATIONALE: 1. Respiratory acidosis. Respiratory acidosis is produced by alveolar hypoventilation, which is commonly found in individuals with chronic obstructive pulmonary disease. Headache and muscle twitching are symptoms of elevated carbon dioxide levels produced by hypoventilation.

2. Respiratory alkalosis is produced by alveolar hyperventilation and reduction in carbon dioxide concentration. Symptoms of respiratory alkalosis include dizziness, confusion, paresthesia, convulsions, and coma.

3. Metabolic acidosis is produced by an increase in noncarbonic acids and/or a decrease in bicarbonate ion. Symptoms of metabolic acidosis include headache, lethargy, Kussmaul respirations, anorexia, nausea and vomiting, dysrhythmias, and coma.

4. Metabolic alkalosis is produced by an excess of bicarbonate ion. Symptoms of metabolic alkalosis include muscle weakness, muscle cramps, hyperreflexia, paresthesias, tetany, and seizures.

A 17-year-old boy is admitted to the pediatric intensive care unit after surgery. The teen requires débridement of a wound on his sacrum (triangular bone at the base of the spine). His mother attributes this to difficulty in repositioning him because of his size. He has been in a persistent vegetative state for almost 4 years after suffering a traumatic brain injury as a result of a self-inflicted gunshot to his head.

Cell Case Study

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Discussion Questions

The sacral area is covered with which type of tissue?

Muscle

Neural

Epithelial

Connective

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178

A large portion of the area is removed because of ischemia and cell death. The teen suffers from tissue:

Apoptosis

Necrosis

Catabolism

Metabolism

Discussion Questions

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179

While recuperating, the teen has generalized and dependent swelling. His wound is healing well with no noted redness or drainage.

Cell Case Study

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The pathophysiologic process of edema is related to an increase in the forces favoring fluid filtration into tissues. This is caused by:

Lymphatic obstruction

Decreased plasma oncotic pressure

Venous obstruction

Increased capillary permeability

Discussion Questions

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181

Practice Questions

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A 48-year-old woman has a malignant lymphoma. She is treated with a chemotherapeutic agent which resulted in decrease cell size, as documented on abdominal CT scans. By which of the following cellular adaptive mechanisms has her neoplasm primarily responded to therapy?

a. Atrophy

b. Hyperplasia

c. Hypertrophy

d. Displasia

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An obese 36-year-old man is seen in his primary care physician’s office after suffering from a weekend of nausea, vomiting, and diarrhea. She is slightly febrile, complains of feeling dizzy when going from a sitting to a standing position (orthostatic hypotension), and remains nauseated. He has not vomited or had any loose stools since the previous evening. According to the history provided, she did not keep any food or liquids down for more than 48 hours. Based on initial clinical observations and reported history, the clinician assumes that the woman is suffering from dehydration and hypovolemia (decrease in plasma level). As expected, laboratory results demonstrate:

a. Hypokalemia as a result of renal compensation for volume depletion

b. Metabolic acidosis as a result of decreased levels of HCO3

c. Hypernatremia as a result of renal tubular reabsorption

d. Respiratory alkalosis as a result of increased water loss from fever

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Which of the following electrolyte disturbances is typical of metabolic alkalosis?  

a. Hyperkalemia

b. Hypernatremia

c. Hypokalemia

d. Hyponatremia

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A client is admitted to the hospital and is being prepared for a craniotomy. The client is very anxious and scared of the impending surgery. After an anxiety attack, the client loses consciousness. While you order a Stat blood gas, you expect to find which of the following acid base imbalance due to hyperventilation and anxiety?

a. Respiratory alkalosis

b. Respiratory acidosis

c. Metabolic alkalosis

d. Metabolic acidosis

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Which cellular adaptation describes an increase in the number of cells in response to an increased workload?

a. atrophy

b. hypertrophy

c. hyperplasia

d. metaplasia

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