Pathophysiology Flashcards

1
Q

diffusion potential

A
  1. voltage by ions diffuse across the cell membrane
  2. ions diffuse the membrane must be permeable to that ion + concentration gradient
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2
Q

equilibrium potential

A

diffusion and electrical forces are balanced both sides membrane

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3
Q

membrane potential

A
  1. difference in voltage inside and outside cell.
  2. in nerve and muscle cells, generate nerve impulses, action potentials, muscular contractions.
  3. changes membrane potential hormone secretion
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4
Q

Electrical potential

A

ability of separated electrical charges, opposite polarity (+ and -) to do work volts (V)

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5
Q

Potential difference

A

1.difference between the separated charges - one side of the membrane to the other
2. relatively small - (mv)

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6
Q

Extra and intracellular fluids

A

1.electrolyte solutions containing - 150-160 mmol/L positively charged ions, equal concentration negatively charged ions.
2. generate and conduct membrane potentials
3. accumulation of the ions on the surface membrane - resting membrane potential (RMP

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7
Q

cell membrane

A
  1. regulate substances(particles/ions) enter and leave the cell
    2 . Movement through the cell passively (without using energy), or actively (using energy).
    3.engulf a particle - endocytosis or exocytosis
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8
Q

chemical gradient

A

difference in the number of particles on either side membrane creates

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9
Q

electrical gradient

A

difference in charged particles or ions

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10
Q

electrochemical gradient

A

(collectively) particles influence both

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11
Q

Three Processes of passive movement

A

Diffusion, Osmosis, Facilitated Diffusion

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12
Q

Diffusion

A
  1. area of higher concentration 1 side of the membrane to an area of lower concentration on the other side. - equally distributed - bth sides
  2. lipid-soluble molecules like oxygen, alcohol, carbon dioxide, fatty acids
  3. small openings (pores) in the membrane
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13
Q

The rate (speed) of diffusionl

A
  1. The number of openings cell membrane (fast/slow)
  2. Temperature - rates increase , direct proportion increased temperatures.
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14
Q

Osmosis

A

1.movement of water area of low solute (few substances dissolved in water) area of high solute (many particles in the water) - equilibrium is achieved.

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15
Q

Aquaporins

A

Channels water moves through

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16
Q

Facilitated Diffusion

A

transport protein lipid insoluble or large molecules pass lipid insoluble or large molecules pass otherwise would not be able
pass . e.g transmembrane movement glucose

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17
Q

transmembrane movement of glucose

A
  1. Glucose associates with unique transport proteins on the outer surface membrane. through the membrane
    released into the intracellular space
  2. speed number of available transport proteins
  3. Rate bind to and release substance transporting
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18
Q

small ions like sodium and potassium

A
  1. electrical charge, it is difficult to pass through the lipid layer of the cell membrane.
  2. .n many instances, cells require a rapid movement of ions either in or out of the cell in order to function.
  3. hasten their movement, their way across is via facilitated diffusion through selective ion channels
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19
Q

Ion channels

A

1.integral proteins - span the width of the cell membrane
2. Specific stimuli cause these proteins to open a channel (or gate) -ions can easily move across
3. channels are very selective - , only allowing passage ions matched

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20
Q

Active transport

A

cells use energy to move ions against an electrical or chemical gradient.

most studied active transport system

sodium-potassium (Na+/K+)-ATPase pump.

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21
Q

sodium-potassium (Na+/K+)-ATPase pump.

A

1.pump moves sodium from inside the cell to the extracellular region and returns potassium to the inside
2. Energy used for this process - splitting the high-energy phosphate bond in ATP by the enzyme ATPase.
3. If process did not occur, sodium would remain in the cell and water would follow, cell to swell.

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22
Q

two types of active transport systems

A

primary and secondary

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23
Q

primary active transport

A

ATP is used directly to transport the substance.

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24
Q

secondary active transport

A

1.energy is derived from the primary active transport of one substance - usually sodium
2. the cotransport of a second substance
3a. sodium leaves the cell by primary active transport - concentration gradient developed.
3b. storage of energy sodium is wanting to diffuse back into the cell.

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25
Q

secondary active transport

A

Two groups of secondary active transport are available.

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26
Q

Cotransport (symport)

A

sodium ions and the solute transported in the same direction.

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27
Q

Counter-transport (antiport)

A

sodium ions and the solute being transported in the opposite direction.
E.x intestine when glucose and amino acid absorption is paired with sodium transport.

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28
Q

Biomacromolecules -proteins, polysaccharides, and nucleic acids,

A
  1. extremely large size, cannot be transported across cell membranes by carrier proteins
  2. require special transport methods
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29
Q

Endocytosis

A
  1. molecule outside of the cell is enclosed - invagination - cell membrane -
  2. vesicle inside the cell
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30
Q

Endocytosis 2 Types

A

pinocytosis and phagocytosis.

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31
Q

Pinocytosis

A
  1. cell drinking
  2. engulfs small solid or fluid particles i.e proteins and electrolytes
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32
Q

Phagocytosis

A
  1. “cell eating”
  2. membrane engulfs and then kills microorganisms or other particulate matter.
  3. particle is enclosed, a phagosome is formed
  4. move into the cytoplasm
  5. joins with a lysosome to be destroyed
    Macrophages and leukocytes (particularly neutrophils). Wbc
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33
Q

Exocytosis

A
  1. secretes intracellular substances into the extracellular space. - opposite of endocytosis -
  2. important for removing cellular debris and releasing hormones made in the cell
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34
Q

Epithelial tissue

A
  1. body’s outer surface lines the inner surfaces, and forms glandular tissue.
  2. three distinct surfaces
  3. basal surface attached to an underlying basement membrane.
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35
Q

Basal Surface

A

avascular, meaning it is lacking its own blood vessels. oxygen and nutrients from the capillaries of the connective tissue on which it rests.

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36
Q

Shapes + arrangements (number of layers present)

A
  1. squamous (thin and flat), cuboidal (cube shaped), and columnar (resembling a column).
  2. simple (single layer of cells), stratified (more than one layer of cells), and pseudostratified (all cells are in contact with the basement membrane, but some do not extend to the surface).
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37
Q

Connective tissue

A
  1. extracellular matrix that supports and holds tissues together.
  2. a. connective tissue proper [ 1) loose (areolar), (2) adipose, (3) reticular, and (4) dense connective tissue.]
    b. specialized connective tissue [ 1. cartilage, 2.bone, and 3.blood cells. ]
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38
Q

Muscle tissue

A
  1. move the skeletal structures
  2. pump blood through the heart
  3. a)contract the blood vessels and visceral organs b.) accomplish this by contraction
  4. two types of fibers - produce these contractions - thin(actin) and thick (myosin) filaments.
  5. three types - skeletal, cardiac, and smooth
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39
Q

Nervous tissue

A

1.communication between peripheral tissues and the central nervous system.
2. controlling body function + sensing and moving about the environment resp. 2 internal and external stimuli.
3. two types
a) neurons (function in communication)
B) glial cells (support the neurons.)

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40
Q

cell junctions

A

1.cells are held together, by junctions, spaces between cells filled with extracellular matrix.
2.made mostly of epithelial tissue.

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41
Q

intercellular contacts

A

1.(fb) Adhesion molecules .
2. important to form the shape of the body and to create pathways for communication.

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42
Q

three basic types of intercellular junctions

A
  1. Tight junctions - epithelial tissue. fluids from entering the intercellular spaces - connecting neighboring cells
  2. Adhering junctions -prevent cell separation - strong adhesion between cells.
  3. Gap junctions - join neighboring cell membranes - channels in the cytoplasm of each cell.
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43
Q

Cellular Adaptation

A

1.cell - adapt to changes in the internal environment - stressors arise
2. stress becomes,or the cell cannot adapt effectively, cell injury and death can occur.
3. a) changing in size (atrophy and hypertrophy) b) by changing in number (hyperplasia) c) changing type or form (metaplasia and dysplasia)

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44
Q

Atrophy

A
  1. decrease in the size of an organ or tissue resulting from a decrease in the mass of pre-existing cells
  2. usually a result of disuse, nutritional or oxygen deprivation, aging, diminished endocrine stimulation, or denervation (lack of nerve stimulation in peripheral muscles caused by injury to motor nerves).
  3. can be caused by a decrease in cell number or a decrease in cell size.

https://portagelearning.instructure.com/courses/2455/files/900502/preview
Atrophy of cells in endometrium.
Left: A woman of reproductive age has a normal thick endometrium. Right: a 75-year-old woman’s endometrium shows atrophic cells and cystic glands.

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45
Q

Hypertrophy

A
  1. increase in the size of an organ or tissue due to the increase in size of the cells that comprise it.
  2. cell size - workload - increase in workload (stress) brings about an increase in cell size
  3. protein synthesis and the size and/or number of intracellular organelles are all increased.
  4. can occur under normal physiologic or pathologic conditions
  5. enlargement of the left ventricle in someone with a diagnosis of heart disease

https://portagelearning.instructure.com/courses/2455/files/900516/preview

myocardial hypertrophy

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46
Q

Hyperplasia

A
  1. increase in the size of an organ or tissue caused by an increase in the number of cells making up that organ or tissue.
  2. i.e glandular proliferation breast tissue during pregnancy.
  3. some cases, hyperplasia can occur in conjunction with hypertrophy
  4. During pregnancy; uterine enlargement is caused by both hypertrophy and hyperplasia of the smooth muscle cells in the uterus.
  5. pathologic hyperplasia can progress to dysplasia (see below) and eventually cancer.
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47
Q

Metaplasia

A
  1. replacement of one differentiated tissue
    2.usually occurs in response to chronic irritation and inflammation.
  2. transformation of cells allows for a higher likelihood of survival - less than optimal environment. i.e
    4.metaplasia is reversible - removal of the stressor ; persistent stress dysplasia
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48
Q

Barrett esophagus

A
  1. metaplasia ex. chronic gastroesophageal reflux disease (GERD) - normal squamous epithelium - lower esophagus changes to columnar-lined epithelium - better handle the stress of acid.
  2. Barrett esophagus - primary risk factor - esophageal adenocarcinoma
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49
Q

Dysplasia

A
  1. abnormal cellular growth, cells that vary in size, shape, and organization.
  2. proliferation of precancerous cells
  3. ot byproduct of longstanding pathologic hyperplasia
  4. ot byproduct of metaplasia secondary to chronic irritation and/or inflammation.
  5. reversible, in theory, alleviation of inciting stress - stress, carcinoma (irre
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50
Q

cervical intraepithelial neoplasia (CIN)

A
  1. dysplasia ex.
  2. precursor to cervical cancer
  3. cervical cancer - series of epithelial changes
  4. early detection with annual Papanicolaou (Pap) smears are key
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51
Q

Cellular Da

A

(1) Injury from physical agents
(2) Injury from biologic agents
(3) Chemical injury
(4) Radiation injury
(5) Injury from nutritional imbalances.

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52
Q

Injury from physical agents

A

1.mechanical forces
i.e (a) fractured bone
(b) extremes of temperature (burns)
(c) electrical forces

https://portagelearning.instructure.com/courses/2455/files/900483/preview

Electrical burn of the skin

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53
Q

Injury from biologic agents

A

1.viruses
2.parasites
3.bacteria

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54
Q

Chemical injuries

A

1.drug toxicities
(alcohol, Rx/OTC drugs, street drugs)
2.carbon tetrachloride
3.lead toxicity
4.mercury toxicity

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55
Q

Radiation injuries

A
  1. result of ionizing (cancer treatment)
  2. ultraviolet (sunburn)
    3.nonionizing (thermal burns) radiation
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56
Q

Injury from nutritional imbalances

A

nutrient excess or deficiency

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57
Q

Necrosis

A
  1. cell death in an organ or tissues - living person
  2. unlike apoptosis - necrosis sets off inflammatory immune response
    3.necrosis ; cell death often interferes with cell replacement and tissue regeneration
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58
Q

Coagulative necrosis

A

1.most often from a sudden cutoff of blood supply to an organ (ischemia)
2. prt - heart and kidney

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59
Q

Liquefactive necrosis

A

1.some of the cells die but their catalytic enzymes are not destroyed.
2. oft/cmy brain infarcts or abscesses

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60
Q

Caseous necrosis

A
  1. part of granulomatous inflammation
    2.tuberculosis
61
Q

Gangrenous necrosis

A
  1. significant amount of tissue undergoes necrosis
  2. dry or moist
  3. blockage of arterial blood supply and normally affects the lower extremities or the bowels.
62
Q

dry gangrene

A
  1. the affected tissue becomes dehydrated.
  2. shrinks back and becomes dark brown or black in color
  3. spread slow
63
Q

wet gangrene

A

1.affected area is cold, swollen, and pulseless
2. skin is moist, black, and distended
3. Blebs (small blisters) skin’s surface
4. liquefaction occurs
5. foul odor is caused by bacterial action
6. spread rapid

64
Q

mechanisms of cell injury

A

1.free radical formation
2.hypoxia
3.disruption of intracellular calcium homeostasis

65
Q

Free radicals

A

1.highly reactive chemical species
2.unpaired electron - outer orbit
3.unstable, enabling them to disrupt and damage cells and tissues.

66
Q

Reactive oxygen species (ROS)

A

1.oxygen-containing molecules- include free radicals and nonradicals

67
Q

Oxidative stress

A

1.generation of ROS exceeds the body’s ability to neutralize and eliminate them.
2.Oxidative damage a) cancer, b) amyotrophic lateral sclerosis (ALS), and c) age-related functional declines.

68
Q

Antioxidants (vitamins A, C, E)

A

1.molecules that inhibit the reactions of ROS.
ex. a) enzymes (catalase), b) nonmetal elements (selenium), c) metals (zinc) and d) vitamins (A, C and E).

69
Q

hypoxic cell injury

A
  1. low oxygen delivery to the tissues.
    2.Decreased oxygen impairs oxidative metabolism
  2. decreased production of ATP
    4.ATP is the primary source of energy cell
  3. the lack of ATP during hypoxia leads to cellular injury
  4. necessary metabolic processes cannot be efficiently carried out.
  5. longer tissue is without an oxygen supply, the greater the chance of per damage
    ex. Brain cells, for example - reversible damage after 4-6 minutes of oxygen deprivation
70
Q

Causes hypoxic cell injury

A
  1. anemia (reduced oxygen-carrying red blood cells),
  2. Ischemia (obstruction of arterial blood flow)
  3. carbon monoxide poisoning
  4. decreased perfusion of tissues (heart failure, shock)
  5. poor oxygenation of blood (from lung disease).
  6. longer tissue is without an oxygen supply, the greater the chance of per cellular injury.
  7. after 4-6 minutes of oxygen deprivation - Brain cells - irre damage
71
Q

Hypoxia

A
72
Q

Hypoxia

A
  1. causes failure of the ATP-dependent sodium/potassium cell membrane pump
  2. Inactivation - increase in intracellular Na+ (and consequently water) levels, resulting in cellular and organelle swelling.
  3. Leakage of intracellular enzymes through the permeable cell membrane into the extracellular fluid. key clinical indicator of cell injury and death
73
Q

Calcium

A
  1. second messenger for many cell reactions.
  2. Under normal conditions, intracellular calcium levels are lower than extracellular levels.
  3. rise in intracellular calcium- inappropriately activate several enzymes - potentially damaging effects.
74
Q

Apoptosis

A
  1. programmed cell death
  2. eliminates cells worn out, produced in excess, developed improperly, genetically damaged.
  3. responsible for several normal physiologic processes

https://us-west-1.cdn.h5p.com/orgs/1291155232022224198/organization/content/1292060794331636838/images/file-65021685da90f.jpg
Slide 1: separation of webbed fingers and toes in embryo

https://us-west-1.cdn.h5p.com/orgs/1291155232022224198/organization/content/1292060794331636838/images/file-6502176d73257.jpg
Slide 2: development of neural connections; neurons that do not establish synaptic connections and receive survival factors may be left to undergo apoptosis

https://us-west-1.cdn.h5p.com/orgs/1291155232022224198/organization/content/1292060794331636838/images/file-650217c214a9b.jpg
Slide 3: removal of cells from intestinal villi; new epithelial cells continuously form in the crypt, migrate to the villus tip as they age, and undergo apoptosis at the end of their life span

https://us-west-1.cdn.h5p.com/orgs/1291155232022224198/organization/content/1292060794331636838/images/file-65021847280f7.jpg
Slide 4: removal of aging blood cells

75
Q

cell

A

1.smallest functional unit of life
2. share similar functions are organized into tissues
3. cell and tissue characteristics - important as most disease processes initiated at the cellular level.

76
Q

eukaryotic cells

A

three primary structures - functional components
1. the nucleus
2. (2) the cytoplasm
3. the plasma membrane

77
Q

nucleus

A
  1. command center of the cell
  2. contains hereditary material in the form of DNA and RNA
  3. Deoxyribonucleic acid (DNA) is essential for the life of the cell.
  4. Genes are the uniquely inherited traits passed on from one generation to the next
  5. Three types of ribonucleic acid
    (1) messenger RNA (mRNA), (2) ribosomal RNA (rRNA), and (3) transfer RNA (tRNA)
  6. ribonucleic acids move 2 cytoplasm - synthesis of proteins
78
Q

Chromatin

A

1.complex structure - DNA-associated proteins- nuclear matrix
2. alteration in chromatin + DNA hypermethylation - progression of neoplasms

79
Q

nucleolus

A

1.inside the nucleus
2. rRNA is processed and assembled into ribosomes
3. five different chromosomes
4. part of the genetic code

80
Q

nuclear envelope

A
  1. surrounds the nucleus
  2. contains two nuclear membranes
    3.Certain materials - both directions - nuclear pores - a) fluids b)electrolytes c)RNA d)proteins, f)hormones.
81
Q

ribosomes

A
  1. site of protein synthesis
82
Q

Golgi apparatus

A
  1. stacks of thin, flattened vesicles or sacs
    2.substances produced in the ER, modify them, and package them - secretory granules - vesicles
83
Q

cytoplasm

A
  1. most cellular functions are carried ou
  2. solution - a) water b)electrolytes c)proteins, d)fats, e) glycogen molecules
  3. organelles - a)ribosomes b) the ER c) Golgi complex d) the mitochondria f) lysosomes
84
Q

endoplasmic reticulum (ER)

A
  1. extensive system - interconnected membranes - flat vesicles
  2. connect various parts - cell
  3. transportation system - substances
  4. two distinct regions - rough ER - smooth ER
85
Q

rough ER

A
  1. carry ribosomes
    2.synthesize lysosomal enzymes
    3a.Digestive enzymes - pancreas
    3b.plasma proteins - liver cells
86
Q

smooth ER

A
  1. no rib
  2. a) lipids b) lipoproteins c)steroid hormones
    3a.enzymes synthesize lipid molecules
    3b.regulate intracellular calcium
    3c. metabolize + detoxify c hormones and drugs
87
Q

Lysosomes

A
  1. digestive capacity of the cell
  2. small sacs- powerful hydrolytic enzymes -
  3. hen - break down a)cell excess, b)cellular components c) foreign substances
    4.Lysosomal enzymes - acid hydrolases - require an acidic environment - work best
  4. fully functional - vital role - normal metabolism certain substances
  5. 2 mthds break down phagocytosed
    heterophagy or autophagy

https://portagelearning.instructure.com/courses/2455/files/900383/preview

88
Q

lysosomal storage diseases

A

1.specific lysosomal enzyme is absent or inactive
2. inability to digest certain cellular substances
3.potentially toxic accumulation within the cell
4. i.e Tay-Sachs - glycogen storage disease

89
Q

glycocalyx (cell coat)

A

1.microscope- fuzzy layer - cell surface
2. complex carbohydrate chains
3a) attached to either protein
or
3b) lipid molecules
4.outside portion of the membrane
5. cell-to-cell recognition and adhesion

90
Q

lectins

A
  1. specific carbohydrate-binding proteins
    2.associated with the cell coat
  2. many important functions
    a) anti-tumor b) antifungal, c) immunomodulatory d) HIV-1 reverse transcriptase inhibitory processes
91
Q

Heterophagy

A
  1. digestion substance phagocytosed- outside of the cell
  2. cell membrane - inward- external materials into the cell - phagosome
  3. Primary lysosomes fuse phagosomes
  4. secondary lysosomes
  5. Neutrophils and macrophages (wbc)
92
Q

Proteasomes

A

1.small organelles
2. made of protein complexes
3. breakdown of proteins
4. target mis-formed proteins or polypeptide chains - no quality control of the cell.

93
Q

Autophagy

A
  1. digestion of damaged cellular organelles
  2. must remove for the cell to continue to function properly
  3. i.e cells undergoing atrophy
  4. Secondary lysosomesbreak down most a)proteins, b)carbohydrates c)lipids
  5. cannot break down remain in the cytoplasm- residual bodies-exocytosis.
94
Q

mitochondria

A

1.“power source” of the cell
2. transform organic compounds (energy in food) into cellular energy. - cellular respiration - aerobic metabolism
3.oxygen
4.Cells -store energy in compounds (ATP)
5.fuel cellular activities
6. mitochondria -cell varies between cell types
7a significantly higher number of mitochondria - muscle cells - contract frequently
7b significantly fewer mitochondria epithelial (skin) cells - lower energy demands

95
Q

cytoskeleton

A

network
microtubules microfilaments intermediate filaments
-control cell shape and movement-

96
Q

Microtubules

A

protein subunits - tubulin

97
Q

Peroxisomes

A
  1. smaller than lysosomes
  2. aid in the control of free radicals
  3. enzyme that breaks down peroxides
  4. peroxisomes not do their job highly unstable chemical compounds- damage- cytoplasmic molecules
    5.break down hydrogen peroxide to a)water b) long-chain fatty acids c)bile acids
98
Q

apoptosis

A
  1. programmed cell death
  2. Mitochondria play role -
  3. disease states
    a) if not appropriately regulated by the body -
    b) damaged or malfunctioning cells are not removed
  4. low rate of apoptosis - cancers - cells- allowed to abnormally divide.
  5. high rate - apoptosis - degenerative disease
99
Q

Microtubules

A
  1. protein subunits - tubulin
  2. disassemble in one location, reassemble in another
  3. many functions
    a) maintenance of cell form b)intracellular transport c) formation of cellular structures i.centrioles ii. basal bodies iii. cilia iv.flagella
100
Q

Centrioles

A
  1. organelle structurally identical basal bodies
    2.made of microtubules
    3.during cell division-form the mitotic spindle-separate and move the chromosomes
    4.
101
Q

Basal bodies

A
  1. organelle structurally identical centrioles
  2. form the organized microtubules
  3. in cilia and flagella

https://portagelearning.instructure.com/courses/2455/files/900377/preview

Microtubules and microfilaments of the cell

102
Q

Cilia

A

1.microtubule-filled cellular extensions 2.function in cell motility
3.Ciliated cells have many cilia
4. flagellated cells - 1 (whip-like tail)
5.cilia(unlike flagellum) -many epithelial linings -a) nasal sinuses b) bronchi in the upper respiratory system c) photoreceptors of the eye d)odorant receptors of the olfactory system e)hair cells in the inner ear
5. cilia, immotile diseases can occur
i.e immotile cilia syndrome
a)ciliated regions of the respiratory tract move potentially harmful bacteria out of the lungs b) move potentially harmful bacteria out of the lungs
c)failure=chronic lung disease called bronchiectasis

103
Q

Microfilaments

A

1.thin, threadlike structures, provide support to the cell
2.three types of microfilaments
i.Thin microfilaments -actin filaments in muscle
ii.a Intermediate filaments- diameter size between thick and thin. ii.b maintain support and shape of the cell ii.c epidermal keratinocytes of the skin , glial cells of the nervous system
iii. Thick myosin filaments - primarily muscle cells.

104
Q

Muscle contraction

A

1.cross-bridging between the thin actin and thick myosin filaments

105
Q

Microfilaments

A

1.microvilli of the intestine
2.Intermediate filaments

106
Q

neurofibrillary tangle

A

1.disruption of the microtubule protein and neurofilaments-
neurofibrillary tangle-
2. seen with Alzheimer disease

107
Q

plasma (cell) membrane

A
108
Q

Disease

A
  1. llness leading to abnormal physiological function of an organ, body structure, or an entire system
  2. born with a disease, or they can acquire it over the course of their lifetime
    3.steps - a)etiology, b)pathogenesis, c)morphologic changes
    d)clinical manifestations
    f) diagnosis
    g) clinical course
109
Q

Etiologic factors

A

1.causes of a disease
a.) physical forces (trauma, burns, radiation),
b.)chemical agents (poisons, alcohol)
c.)biologic agents (bacteria, viruses)
d.) genetic predisposition,
e.) nutritional excesses or deficiencies
2. most etiologies are idiopathic (unknown) and/or nonspecific in nature
3. agents can affect
a.) single organ/body structure (isolated burn or a broken bone )
b.) several organs, an entire system,
c.) multiple systems (sickle cell anemia or cystic fibrosis.)
4. md - multiple etiologic factors cancer, heart disease, or diabetes

110
Q

Risk factors

A
  1. predisposition to a given disease
  2. congenital - present at birth,
  3. acquired - occur after birth. -
  4. Congenital conditions - heredity, environmental factors, or a combination of both
  5. physical injury, exposure to infectious agents, dietary deficiencies or excesses
  6. most diseases are a result of an interaction of heredity and the environment
111
Q

Pathogenesis

A
  1. development of a disease process
  2. cascade of events cellular and tissue level - initial point of contact with an etiologic agent
    to ultimate manifestation disease.
112
Q

Morphology

A
  1. structure of cells or tissues
  2. Morphologic changes - gross and microscopic changes
    characteristic of a given disease
113
Q

Histology

A
  1. study of cells at the tissue level.
  2. Diagnosis of many diseases - thin - histologic sections of human tissue under a microscope
114
Q

Lesion

A
  1. Pathological or traumatic injury or organ or tissue
  2. Radiographs,ultrasonagraphy, and/or biopsy
  3. Evaluate morphological characteristics of a lesion
115
Q

Clinical Manifestations

A
  1. seen and heard through physical examination
  2. signs and symptoms -
    3.
116
Q

What is predictive value?

A

The ability of a test result or observation to predict the presence of a given disease or condition.

117
Q

Define positive predictive value.

A

The proportion of true-positive results that occurs in a given population.

118
Q

In a breast cancer screening program, what does the positive predictive value represent?

A

The group of women having ‘suspect breast nodules’ that were later found to have breast cancer.

119
Q

What is negative predictive value?

A

The true negatives in a given population.

120
Q

What role does prevalence play in predictive value?

A

It plays a bigger role than sensitivity and specificity in determining predictive value.

121
Q

How can the clinical course of a disease be categorized?

A
  1. Acute 2. Chronic 3. Subacute
122
Q

What characterizes an acute disorder?

A

Somewhat severe but self-limiting.

123
Q

Define chronic disease.

A

Long-term, usually continuous, with exacerbations of symptoms and remissions.

124
Q

What is subacute disease?

A

A disease that is not as severe or prolonged as acute or chronic.

125
Q

What is epidemiology?

A

The study of disease occurrence in human populations.

126
Q

What factors do epidemiologists examine in their studies?

A
  1. Spread of infectious diseases 2. Risk factors for multifactorial diseases 3. Patterns and characteristics of affected populations
127
Q

Why must epidemiologists consider global travel?

A

It influences the spread of diseases that were once localized.

128
Q

What is disease frequency?

A

A measurement used to predict whether a disease is on the rise or in decline.

129
Q

Define prevalence.

A

The number of people with the disease in a population in a given time.

130
Q

How is incidence defined?

A

The number of new cases in a population at risk during a specified time.

131
Q

How is morbidity defined?

A

The effect of an illness on one’s life.

132
Q

What do mortality statistics deal with?

A

The cause of death in a population.

133
Q

What is the natural history of a disease?

A

The progression of that disease when no treatment is provided.

134
Q

What factors are considered in making a prognosis?

A
  1. Anticipated survival time 2. Potential complications 3. Risk of treatment 4. Patient’s personal health and social history
135
Q

What are the three categories of disease prevention?

A
  1. Primary 2. Secondary 3. Tertiary
136
Q

What is primary prevention?

A

Attempts to eliminate risk factors to prevent disease from occurring.

137
Q

Give an example of primary prevention.

A

Vaccinating children to prevent disease.

138
Q

What is secondary prevention?

A

Aims to detect and treat disease early, usually while asymptomatic and curable.

139
Q

Provide an example of secondary prevention.

A

Going to the doctor for an annual Pap smear to detect early cervical cancer.

140
Q

Define tertiary prevention.

A

Occurs after diagnosis and aims to reduce complications and/or deterioration.

141
Q

Give an example of tertiary prevention.

A

Use of prescribed medication after a heart attack to reduce future risk.

142
Q

What is evidence-based practice?

A

The conscientious reliance on current best, scientific evidence in making decisions regarding patient care.

143
Q

What do clinical practice guidelines aim to inform practitioners about?

A

How to best deliver health care in certain circumstances.

144
Q

List the different types of epidemiologic studies.

A
  1. Cross-sectional studies 2. Case-control studies 3. Cohort studies
145
Q

What do cross-sectional studies involve?

A

Simultaneous collection of information to classify exposure and outcome status.

146
Q

What is the focus of case-control studies?

A

Comparing case subjects (known outcome) to control subjects (without outcome).

147
Q

What are cohort studies also referred to as?

A

Longitudinal studies.

148
Q

Why is monitoring disease progression important?

A

It significantly impacts patient care.

149
Q

What must clinicians and researchers understand to effectively combat disease?

A

How changes that occur with disease impact the body at organ, tissue, and cellular levels.