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DPC > Group 8/30/19 > Flashcards

Group 8/30/19 Flashcards

1
Q

Learning issues

A

Motor/movement pathways in the brain and spinal cord (Ch 56 Guyton and Hall)
Pharmacodynamics: drug-receptor relationship (Katzung part of ch2)
Embryology of Muscular skeletal system (Sadler ch 11)
Pathology of Cell Adaptation, Injury, and Death (Rubins ch. 1)

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2
Q

what is the main function of the lateral corticospinal tract?*

A

voluntary movement of the contralateral limbs

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3
Q

what is the first order neuron of the lateral corticospinal tract?*

A

UMN (upper motor neuron): cell body in the first motor cortex descends ipsilaterally (through posterior limb of internal capsule)

  • most fibers decussate at cuadal medulla (pyramidal decussation)
  • then it descends contralaterally
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4
Q

what is the first synapse of the lateral corticospinal tract?*

A

cell body of the anterior horn (spinal cord)

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5
Q

what is the second order neuron of the lateral corticospinal tract?*

A

LMN (lower motor neuron): leaves the spinal cord

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6
Q

what is the second synapse and projection of the lateral corticospinal tract?*

A

NMJ (neuromuscular junction) to muscle fibers

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7
Q

primary motor cortex: where is it located and what is its function?

A
  • located anterior to the central sulcus
  • has control of different muscle areas of the body
  • topographically proportionate to fine motor control, greatest area for hands
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8
Q

what are some differences and similarities between primary motor cortex and premotor area?

A
  • premotor area located anterior to primary motor cortex
  • has control of different muscle areas of the body and similar topographical representation as primary motor cortex
  • nerve signals from here have much more complex patterns of movement than patterns from primary motor cortex
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9
Q

what are mirror neurons?

A

these become active when the person performs a specific motor task or when they observe the task being performed by others

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10
Q

location and function of the supplementary motor area

A
  • located in the longitudinal fissure
  • gives bilateral muscle contractions
  • provides finer motor control
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11
Q

Broca’s area location and damage effect

A
  • damage to this area will make it impossible for the person to speak whole words, although they’ll be able to speak and may small utterances
  • located anterior to the primary motor cortex
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12
Q

motor apraxia: cause and symptoms

A
  • caused by damage to the area for hand skills, which is in the premotor area immediately anterior to the primary motor cortex
  • damage here makes hand movements uncoordinated and nonpurposeful
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13
Q

motor signals are transmitted directly from the cortex to the spinal cord through the ? tract through multiple accessory pathways that involve which structures?

A
  • corticospinal tract

- basal ganglia, cerebellum, nuclei of the brainstem

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14
Q

Betz cells

A

giant pyramidal cells that are in the pyramidal/corticospinal tract. Found only in the primary motor cortex, and they transmit nerve impulses to spinal cord very fast.

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15
Q

where is the red nucleus, what signals does it receive and where do these synapse, what tracts are associated with it?

A
  • located in the mesenchephalon
  • receives many direct fibers from primary motor cortex through corticorubral tract and some from corticospinal tract
  • the fibers synapse in the magnocellular portion of the red nucleus
  • large cells from magnocellular portion give rise to rubrospinal tract which crosses to opposite side in lower brainstem
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16
Q

what part of the red nucleus is like the motor cortex, but how is it different?

A
  • magnocellular portion of red nucleus has somatographic representation of all the muscles of the body
  • less developed fineness of representation of different muscles
  • allows discrete movements but not fine movements
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17
Q

what is the extrapyramidal system?

A
  • all parts of the brain and brainstem that contribute to motor control but are not part of the direct corticospinal-pyramidal system
  • includes pathways through the basal ganglia, reticular formation of brainstem, vestibular nuclei, and red nuclei
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18
Q

what kinds of signals are transmitted by pyramidal neurons, and how are these triggered?

A
  • dynamic signals: excited at high rate for short period at the beginning of muscle contraction, cause rapid development of force
  • static signals: fire at a slower rate continuously, to maintain the force of contraction
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19
Q

what is the effect of removing the primary motor cortex, aka the area pyrmaidalis?

A
  • if premotor and supplementary motor areas are still intact, you’ll still be able to do gross postural and limb “fixation” movements
  • will have loss of voluntary control of discrete/fine movements of distal segments of limbs, especially hands and fingers
  • normally it supplies continual tonic stimulatory effect on motor neurons; so if removed, hypotonia results
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20
Q

what is the effect of lesions in the motor cortex and adjacent parts of the brain like the basal ganglia?

A

muscle spasm results in afflicted muscle areas on the opposite side of the body, since motor pathways cross to the opposite side

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21
Q

what are the structures in the brainstem?

A

medulla, pons, mesencephalon

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22
Q

what the major functions of the brainstem?

A
  • contains sensory and motor nuclei that perform functions for face and head
  • controls respiration, cardiovascular system, some gastrointestinal, equilibrium, eye movements, and other stereotyped movements of the body
  • way station for command signals from higher neural centers
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23
Q

what are the major nuclei of the brainstem?

A

pontine reticular nuclei, vestibular nuclei, and medullary reticular nuclei

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24
Q

what are the main functions of the reticular nuclei of the brainstem?

A
  • pontine reticular nuclei excite antigravity muscles

- medullary reticular nuclei relax the same muscles

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25
Q

how does the vestibular nuclei play a role in antigravity muscles?

A
  • vestibular nuclei work with the pontine reticular nuclei to excite antigravity muscles
  • it selectively controls the excitatory signals to different antigravity muscles to maintain equilibrium in response to signals from the vestibular apparatus
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26
Q

what is the vestibular apparatus, its location, and what are the two labyrinth parts?

A
  • the vestibular apparatus is a sensory organ for detecting sensations of equilibrium
  • located inside the bony labyrinth in the temporal bone
  • contains membranous tubes and chambers called the membranous labyrinth, which is the functional part
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27
Q

where are the maculae located and what are the two different types and their roles?

A
  • located inside of each utricle and succule of the membranous labyrinth of the vestibular apparatus
  • macula of utricle lies in a horizontal plane and helps determine the orientation of the head when it’s upright
  • macula of saccule lies in a vertical plane and signals head orientation when the person is lying down
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28
Q

what is the function of the kinocilium and stereocilia?

A
  • the kinocilium is a large cilium coming out of a hair cell of the equilibrium apparatus, with smaller stereocilia to one side
  • bending towards the kinocilium triggers fluid channels and receptor membrane depolarization
  • bending away the kinocilium closes ion channels and causes receptor hyperpolarization
  • has directional sensitivity and allows person to keep equilibrium of head
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29
Q

what is the role of the semicircular ducts and how do they work?

A
  • three semicircular ducts, anterior, posterior, and lateral, that represent all 3 planes in space to respond to rotation of head
  • the end of each duct has an enlarged end called an ampulla, filled with fluid endolymph
  • person’s head turns, fluid flows through duct and ampulla, bends cupula (crest outside of ampulla)
  • hair cells on cupula get bent, leads to signal in vestibular nerve
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30
Q

how do we detect linear acceleration?

A
  • the maculae, which has statoconia, is in the utricle and saccule of the membranous labyrinth and plays a role in detection of linear acceleration
  • does not sense linear velocity
  • body will thrust forward and statoconia will fall backward on hair cell cilia and cause signal
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31
Q

location and function of the flocculonodular lobes

A
  • the flocculonodular lobes are in the cerebellum

- play a role in dynamic equilibrium signals from the semicircular ducts during rapid changes in direction of motion

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32
Q

location and function of the uvula

A
  • in cerebellum

- plays a role in static equilibrium

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33
Q

path and function of the medial longitudinal fasciculus

A
  • medial longitudinal fasciculus transmits signals to the brainstem from the vestibular nuclei and cerebellum
  • causes corrective movements of the eyes every time the head rotates, so they can remain fixed on a visual object
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34
Q

hydropic swelling

A
  • a reversible increase in cell swelling from acute cell injury, like chemical/biological toxins, viral/bacterial infections, ischemia, excessive heat/cold
  • characterized by large, pale cytoplasm and normally located nucleus
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35
Q

ischemic cell injury: causes and effects*

A
  • inadequate blood supply to meet demand
  • mechanisms include decreased arterial perfusion, decreased venous drainage, and shock
  • ATP can’t be produced by aerobic metabolism, so cell uses anaerobic metabolism
  • leads to pH imbalances and injurious free radicals
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36
Q

what causes oxidative stress, what are some examples and their effects?

A
  • reactive oxygen species (ROS) can cause cell and tissue injury
  • include activated oxygen like O2- (superoxide), H2O2 (hydrogen peroxide), OH* (hydroxyl radical)
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37
Q

antioxidant defenses: what options are available and what are some examples

A
  • cells have antioxidant defenses that convert ROS to less reactive species
  • include detoxifying enzymes (eg catalse, SOD, GPX) and exogenous free radical scavengers (eg vitamins E, C, and retinoids)
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38
Q

role of p53 in oxidative injury

A
  • p53 helps to prevent and repair DNA damage. Maintains expression of antioxidant genes to promote cell survival.
  • if DNA damage is irreparable, p53 activates cell death
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39
Q

intracellular storage: what are some examples, like xanthoma, lipofuscin, melanin, anthracosis, ferritin, hemosiderin

A

-can store fat, glycogen, lysosomes, cholesterol (xanthoma are bad clusters), lipofuscin (undigestable mixture of lipids and proteins), melanin (brown-black pigment in skin), anthracosis (stored carbon in lungs or lymph nodes), iron-storage proteins (ferritin and hemosiderin)

40
Q

calcification: what is dystrophic vs metastatic calcification

A
  • dystrophic calcification causes macroscopic calcium salt deposits in injured tissues, from extracellular deposition from circulation or interstitial fluid. Interferes with blood flow.
  • metastatic calcification reflects degranged calcium metabolism and is associated with increased serum calcium concentrations (ie hypercalcemia)
41
Q

hyperplasia: what is it, what are some causes*

A
  • controlled proliferation of stem cells and differentiated cells that leads to an increase in the number of cells
  • can be caused by changes in hormonal concentration, increased physiologic requirements, chronic injury
42
Q

metaplasia: cause and effect*

A
  • reprogramming of stem cells so that one cell type is replaced to create another that can adapt to a new stress
  • usually due to exposure to an irritant, such as gastric acid (Barrett esophagus), cigarette smoke (respiratory ciliated columnar epithelium is replaced by stratified squamous epithelium)
43
Q

dysplasia: what is it, what are the signs*

A
  • disordered, precancerous epithelial cell growth
  • characterized by loss of uniformity of cell size and shape (pleomorphism), loss of tissue orientation, nuclear changes (increased nuclear cytoplasmic ratio and clumped chromatin)
44
Q

what are the reversible changes that happen to a cell after it’s injured?*

A
  • cellular and mitochondrial swelling occurs, leading to decreased ATP and decreased activity of Na/K and Ca pumps
  • ribosomal/polysomal detachment, which decreases protein synthesis
  • membrane blebbing (small knobs protrude from cell)
  • nuclear chromatin clumping
45
Q

hypertrophy: what is it?*

A

-an increase in structural proteins and organelles that increases the size of cells or an organ and increase its functional capacity

46
Q

loss of muscle mass: what is the effect, what are some causes, including sarcopenia?

A
  • a loss of just 5% of lean body mass can impair function
  • diseases that can cause weight loss include cancer, congesstive haert failure (CHF), COPD, AIDS, rheumatoid arthritis (RA), aging (loss of muscle mass in aging is sarcopenia)
47
Q

turnover as postmitotic cells

A
  • neurons and cardiac myocytes cannot undergo mitosis, but committed progenitor cells in the brain and heart can proliferate and differentiate in response to cell loss and injury
  • leads to low rate of cell loss and replacement among cells
48
Q

ubiquitin and ubiquitination: how is it carried out

A

-Ub activator enzyme (E1) activates ubiquituin (Ub), Ub conjugating enzymes (E2) and Ub ligases (E3) bind to make ubiquitinated protein, DUB enzymes help with deubiquitination, to release protein and Ub

49
Q

proteasomes and cell homeostasis: what do proteasomes do, their importance, 20S vs 26S vs DUBs

A
  • proteasomes function to destroy targeted proteins or misfolded/damaged proteins
  • mutations to normal proteasomal function are lethal
  • 20S proteasomes help to degrade oxidized proteins, 26S proteasomes degrade polyubiquitinated proteins
  • deubiquitinating enzymes (DUBs) are proteases that remove Ubs from poly-Ubs chains and their partner proteins
50
Q

UPS and disease: what is the link between UPS and disease?

A
  • mutations in Ub pathway can cause diseases, tumor development
  • UPS plays a role in gene expression, like activating NFkB
  • DUBs are critical to gene expression and can activate tumor suppressor proteins
51
Q

autophagy: what is it and what is it important for, what are macrophagy and microphagy and what enzymes and structures does the former involve?

A
  • autophagy is a catabolic process by which cytoplasmic targets are recognized and delivered to the lysosomes for digestion. Important for cellular physiology and adaptation to adversity
  • Macroautophagy is responsible for handling bulk portions of cytoplasm. Takes things up via phagophore in membrane to destroy
  • This process along with microphagy targets damaged cellular organelles, aggregated proteins and other injurious materials, engulfed by lysosomal membranes and degraded
52
Q

molecular chaperones and chaperonopathies: what is the role of chaperones, what is proteostasis, and what are chaperonopathies?

A
  • some defective proteins require interaction with molecular chaperones and enter the autophagic system via the chaperone-mediated autophagy (CMA)
  • ongoing quality control of chaperones, which make sure proteins are folded correctly and remove defective ones, is called proteostasis
53
Q

pathology of necrotic cell death: what is necrosis, what is coagulative and liquefactive necrosis?*

A
  • necrosis is enzymatic degradation and protein denaturation of cell due to exogenous injury, which leads to intracellular components leaking. It’s an inflammatory process, unlike apoptosis.
  • necrosis occurs when hostile external forces overwhelm the cells’ adaptive abilities, usually affects geographically localized groups of cells. Leads to inflammation and cell injury.
  • coagulative necrosis is the appearance of dead or dying cells, including pyknosis (smaller nucleus, chromatin clumps, basophilic), karyorrhexis (nucleus breaks up into smaller fragments), karyolysis (nucleus extrudes from the cell)
  • liquefactive necrosis is when the rate of necrotic cells dissolves faster than the rate of repair, creates an abscess in the tissue
54
Q

pathology of apoptotic cell death: what are signs that the cell is undergoing apoptosis?*

A
  • characterized by deeply eosinophilic cytoplasm and basophilic nucleus, pyknosis (nuclear shrinkage), karyorrhexis (fragmentation caused by endonuclease-mediated cleavage)
  • cell membrane typically remains intact without significant inflammation, unlike necrosis
  • DNA laddering (fragments in multiples of 180bp)
  • usually occurs in single cells or small groups of cells
  • once the self-destructive process of apoptosis propels a cell to DNA fragmentation and cytoskeletal dissolution, the apoptotic body remains, and it’s phagocytosed by tissue macrophages
55
Q

ischemic injury and reperfusion

A
  • massive influx of Ca2+ through a damaged plasma membrane is key to ischemic cell damage
  • reperfusion is the restoration of blood flow after a period of ischemia, but the process can cause damage because new oxygen can combine with free radicals to form additional ROS
  • the cell can heal from short periods of ischemia, but longer periods are associated with deterioriation and death
56
Q

apoptosis: what is it, which pathways does it include, what happens to the cell*

A

-apoptosis is ATP-dependent programmed cell death, important for development, eliminating obsolete cells, deleting mutant cells and defending against infection
-includes intrinsic and extrinsic pathways, both activate caspases (cytosolic proteases) which leads to cellular breakdown including cell shrinkage, chromatin condensation, membrane blebbing, and formation of apoptotic bodies, which are then phagocytosed
,important for development, eliminating obsolete cells, deleting mutant cells and defending against infection

57
Q

extrinsic pathway of apoptosis: what are the two pathways and what do they do?*

A

2 pathways where certain plasma membrane receptors are activated by their ligands

  1. ligand receptor interactions (FasL binding to Fas [CD95] or TNF-alpha binding to its receptor TNFR). Cytoplasmic domains of the receptors bind to death domains of docking proteins, to form a death-inducing signaling complex (DISC), and the docking proteins stimulate downstream caspases
  2. immune cell (cytotoxic T-cell release or perforin and granzyme B)
58
Q

intrinsic pathway of apoptosis: when will it happen, what are the proteins involved, proapoptotic vs antiapoptotic

A
  • initiated by intracellular stresses and mitochondria plays a central role
  • involved in tissue remodeling in embryogenesis. Occurs when a regulating factor is withdrawn from a proliferating cell population, and also happens after exposure to injurious stimuli (like radiation, toxins)
  • regulated by Bcl-2 family of proteins. BAX and BAK are proapoptotic (antisurvival), while Bcl-2 and Bcl-xL are antiapoptotic (prosurvival)
  • BAX and BAK form pores in the mitochondrial membrane, leads to release of cytochrome C from inner mitochondrial membrane into the cytoplasm, and the activation of caspases
  • Bcl-2 keeps the membrane impermeable, and prevents cytochrome C release. Bcl-2 overexpression causes a decrease in caspase activation and tumorigenesis.
59
Q

endoplasmic reticulum Ca2+ release and apoptosis

A
  • ER stores calcium, and if it releases it and it’s prolonged, that can cause apoptosis due to activation of caspases
  • calcium released may be taken up by the mitochondria, causing MPTP to open, releases Cyt c, activates downstream apoptosis pathways
60
Q

role of mitochondrial proteins in apoptosis

A
  • outside stresses such as altered mitochondrial membrane potential or ROS affect the mitochondrial matrix
  • MPTP opens, which is a barrier that goes through the inner mitochondrial membrane, disrupts the content of the mitochondrial matrix, and disrupts energy production from the mitochondria
  • permeabilization of the outer membrane causes several michondrial molecules (eg Cyt c) to exit cytosol, activate caspases and result in cell death
61
Q

necroptosis

A
  • if PCD is independent of caspases is activated, cells can undergo a fate that is like necrosis
  • FasL or TNF-alpha binds to their receptor
  • Leads to a receptor-bound complex that incorporates caspase-8, E3 Ub ligases, receptor-interacting proteins RIP1 and RIP3, leads to cell death by necroptosis
62
Q

anoikis

A
  • anoikis is a variety of apoptosis that occurs in epithelial cells
  • caused by the loss of cell adhesion or inappropriate cell adhesion
  • helps to efficiently delete cells that have been displaced from their proper residence
63
Q

granzymes and apoptosis

A
  • if cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells recognize a cell as foreign, they will activate caspase signaling
  • these lymphocytes will release perforin (punches hole in plasma membrane) and granzymes (use mitochondria to activate caspases)
64
Q

pyroptosis

A
  • pyroptosis is a cell death program that relies on caspase-1, released by an inflammasome
  • infectious agents interact with cell membrane receptors called pattern recognition receptors to stimulate inflammatory reactions
  • promotes cell swelling and death
65
Q

NETosis: what is it produced by, what do they do, what are signs in the cell?

A
  • neutrophil extracellular traps (NETs) are structures produced by polymorphonuclear granulocytes
  • they kill bacteria and pathogens to defend against infection by autophagy and NADPH activity
  • Characterized by destruction of cell’s nucear envelope and the membranes of the cytoplasmic granules, chromatin disaggregation
66
Q

entosis

A
  • cells that are not phagocytes engulf nearby living cells

- usually seen in tumors

67
Q

what germ layer does the muscular system develop from? Which part of the layer is each muscle type derived from?

A
  • mesodermal germ layer

- skeletal muscle from paraxial mesoderm, smooth and cardiac muscle from visceral (splanchnic) mesoderm

68
Q

which muscles are derived from the somites versus the somitomeres (both come from the paraxial mesoderm)?

A
  • somites give rise to the muscles of the axial skeleton, body wall, and limbs
  • somitomeres give rise to the muscles of the head
69
Q

what parts of the dermomyotome do muscle tissues develop in? What do these cells form, where do they go next?

A
  • progenitor cells for muscle tissues are derived from the ventrolateral (VLL) and dorsomedial (DML) edges (lips) of the dermomyotome
  • Cells from both regions form the myotome
  • Some cells from the VLL migrate across the lateral somitic frontier into the parietal layer of the lateral plate mesoderm
70
Q

what does the lateral somitic frontier separate, and what are the two domains called?

A
  • the lateral somitic frontier separates the two mesodermal domains in the embryo
  • two domains are the paraxial and abaxial domain
  • each myotome receives its innervation from spinal nerves derived from the same segment as the muscle cells
71
Q

primaxial domain: where is it, what cells are in it, where do they get their signals, what muscles do they form?

A
  • the primaxial domain comprises the region around the neural tube and contains only somite-derived (paraxial mesoderm) cells
  • these muscle cells do not cross the frontier, and receive many of their signals from the neural tube and notochord
  • form the muscles of back, some muscles of shoulder girdle, and intercostal muscles
72
Q

abaxial domain: where is it, what cells are in it, where do they get their signals, what muscles do they form?

A
  • abaxial domain consists of the parietal layer of the lateral plate mesoderm together with somite cells that have migrated across the lateral somitic frontier
  • muscle cells here have crossed the frontier (from the VLL edge of the myotome) and enter the lateral plate mesoderm
  • receive signals for differentiation from lateral plate mesoderm
  • form muscles of the infrahyoid, abdominal wall, and limb muscles
73
Q

innervation of axial skeletal muscles: epaxial (above the axis) muscles (back muscles) are innervated by ?, whereas hypaxial (below the axis) muscles (body wall and limb muscles) are innervated by ?

A
  • epaxial (back) muscles are innervated by dorsal primary rami
  • hypaxial (body wall and limb) muscles are innervated by ventral primary rami
74
Q

what type of precursor cell does skeletal muscle develop from, how does it progress to forming muscle?

A
  • precursor cells called myoblasts fuse and form long, multinucleated muscle fibers
  • myofibrils appear in cytoplasm, and cross striations develop by third month
75
Q

how do tendons develop, what is the transcription factor needed?

A
  • tendons for the attachment of muscles to bone are derived from sclerotome cells lying adjacent to myotomes at the anterior and posterior borders of somites
  • transcription factor SCLERAXIS regulates development of tendons
76
Q

what are some genes that regulate muscle development?

A
  • MyoD and MYF5 are muscle-specific genes
  • part of a family of transcription factors called myogenic regulatory factors (MRFs)
  • this group of genes activates pathways for muscle development
77
Q

patterns of muscle formation are controlled by connective tissue where myoblasts migrate. Where are the tissues derived from for different sections of the body?

A
  • head region connective tissues derives from neural crest cells
  • cervical and occipital regions differentiate from somitic mesoderm
  • body wall and limbs differentiate from parietal layer of lateral plate mesoderm
78
Q

where are the voluntary muscles of the head region (including tongue, eye, and pharyngeal arches) derived from?

A

paraxial mesoderm (somitomeres and somites)

79
Q

when does limb musculature start to form, what does it form from?

A
  • starts with condensation of mesenchyme near base of limb buds
  • mesenchyme came from muscle cell precursors from somites that migrate into limb bud to form muscles
  • tissue for pattern of muscle formation derived from parietal layer of lateral plate mesoderm
80
Q

where does cardiac muscle develop from, how does it develop?

A
  • cardiac muscles develop from visceral mesoderm
  • myoblasts adhere to each other with attachments that will develop into intercalated discs
  • special bundles of muscle cells with irregularly distributed myofibrils become visible as Purkinje fibers for the conducting system of the heart
81
Q

serum response factor (SRF)

A

a transcription factor responsible for smooth muscle cell differentiation

82
Q

myocardin and myocardin-related transcription factors (MRTFs)

A

these act as coactivators to enhance the activity of SRF, to initiate the genetic cascade responsible for smooth muscle development

83
Q

Which signals induce VLL vs DML cells?

A
  • signals from lateral plate mesoderm (BMPs) and overlying ectoderm (WNTs) induce VLL cells
  • signals from the neural tube and notochord (SHH and WNTs) induce DML cells
84
Q

what are most smooth muscles derived from?

A

visceral mesoderm

85
Q

where are smooth muscles of the pupil, mammary gland, and sweat glands derived from?

A

ectoderm

86
Q

potency

A

-the concencentration (EC50) or dose (ED50) of a drug required to produce 50% of that drug’s maximal effect

87
Q

efficacy

A

the extent or degree of an effect that can be achieved in the intact patient

88
Q

what is used to characterize the quantal dose-effect curve, and what does it mean?

A
  • median effective dose (ED50)

- the dose at which 50% of people exhibit the same quantal effect

89
Q

therapeutic index

A
  • relates the dose of a drug required to produce a desired effect to that which produces an undesired effect
  • usually defined as the ratio of TD50 to ED50
90
Q

therapeutic window

A

-the range between the minimum toxic dose and the minimum therapeutic dose

91
Q

idiosyncratic responses

A
  • an unusual response to a drug, infrequently observed

- may be caused by genetic differences in metabolism of the drug or immunological mechanisms

92
Q

tolerance

A

responsiveness to the drug usually decreases as a consequence of continued drug administration

93
Q

tachyphylaxis

A

the responsiveness of the drug diminishes rapidly after the administration of the drug

94
Q

what are some factors that can influence a person’s drug responsiveness?

A
  • alterations in the concentration of the drug that reaches the receptor
  • variation in the concentration of an endogenous receptor ligand
  • alterations in the number or function or receptors
  • changes in the components of response distal to the receptor; biochemical processes in responding cell and physiologic regulation by interacting organ systems
95
Q

what are some ways in which there may be both beneficial and toxic effects of drugs?

A
  • no drug causes a single, special effect; it can likely bind to multiple types of receptors, but have different affinities
  • the same receptor-effector mechanism may lead to beneficial effects but also toxic ones
  • drugs may produce both beneficial and toxic effects, depending on the tissues they act on and the separate effector pathways
  • beneficial and toxic effects can be mediated by different types of receptors

DPC (11 decks)

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