Exam 1 Flashcards
(124 cards)
1
Q
Describe chemical components, structure, and function of cell membrane
A
Composed of lipids, proteins, and carbohydrates. Function is to separate and maintain chemical environments.
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Q
Cellular membrane lipids
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majority are phospholipids, amphipathic
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Q
Cholesterol function in cell membrane
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affects fluidity and permeability
4
Q
Transport through lipid bilayer
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small hydrophobic molecules and gases can get through (O2, CO2, N2, benzene). Large and charged ions cannot (H+, Na+, glucose)
5
Q
Lipid rafts
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Interactions between specific lipids (cholesterol, saturated lipids, and glycosylated lipids) in plane of cell membrane drive formation of lipid rafts. They are enriched in saturated phospholipids, sphingolipids, glycolipids, cholesterol, lipated proteins, and GPI anchored proteins. They segregate specific elements in order to regulate their interactions with other cell membrane components.
6
Q
Carbohydrate molecules and cell surface
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Function to protect, cell to cell interaction (ganglioside GM1 acts as a cell surgace receptor for the bacterial toxin that causes diarrhea of cholera)
7
Q
Functions of membrane proteins
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receptors, transport-channels, enzymes, structural
8
Q
Cytoskeleton function and components
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filamentous scaffold of proteins that contribute to the internal organization of cytoplasm and stabilization of cell membrane. Consists of microtubules, actin filaments, and intermediate filaments. Actin filaments and microtubules generate forces to drivve cell shape and motility.
9
Q
What keeps cells shape
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Proteins
10
Q
Types of SIGNAL molecules
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steroids, polypeptides, proteins
11
Q
Examples of intracellular receptors
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steroid and thyroid hormones.
12
Q
List 3 classes of cell surface receptors.
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- Ion channel linked
- G protein-linked
- Enzyme-linked
13
Q
Ion channel linked cell surface receptors
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Ach receptor at neuromuscular junction, neurotransmittter receptors, serotonin, GABA, and glycine. Permeable to Na+, K+, and Ca+
14
Q
List components of G protein linked receptor signaling machinery
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3 subunits- alpha, beta, and gamma. (beta and gamma form stable complex, BYsubunit). Upon stimulation, GPCR undergoes conformational change that expose intracellular sites that activate G protein. This catalyzed dissociation of GDP bound to the Ga subunit and its replacement with GTP, leading to dissociation of Ga from BY subunit. Ga-GTP and GBy-subunit complexes are freely able to active downstream effectors. Targets of dissociated components are enzymes or ion channels in plasma membrane, and they relay signal onward.
15
Q
Give examples of chemicals that activate stimulatory and inhibitory G protein subunits.
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G1 anf Gs regulate activity of adenylate cyclase, altering cAMP levels.
Gs stimulates adenylyl cyclase, associated with adrenaline, B1, glucagon, and ACTH.
Gi inhibits adenylyl cyclase lowering level of cAMP and it is activated by receptor for somatostatin, muscarinic receptor.
16
Q
Endoplasmic reticulum
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Rough (ribosomes)- protein synthesis
Smooth- lipid synthesis
17
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Golgi apparatus
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Substances synthesized in ER get transported here for further processing and distribution
18
Q
3 types of endocytosis
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phagocytosis, pinocytosis, and receptor mediated endocytosis
19
Q
Diffusion vs Active transport
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Diffusion: movement is always down concntration gradient. Active movement against concentration gradient, requires ATP
20
Q
Differentiate Simple and facilitated diffusion
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Simple: Through membrane or channel proteins (ion channels), NOT carrier proteins. lipophilic molecules, water, small molecules (urea). Rate inreases with increasing concentration gradient.
Facilitated: SPECIFIC CARRIER PROTEIN helps transport substances across membrane down conc gradient. Saturation kinetics (rate will not necessarily increase with increase in concentration gradient). ex.) glucose, amino acids, chloride bicarbonate transport.
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Q
Factors that affect rate of diffusion
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Concentration, membrane electric potential, pressure.
22
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Osmosis
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flow of water across semi permeable membrane from solution with low solute concentration to one with high solute concentration
23
Q
Primary active transport example
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Na/K ATPase- 3 Na out, 2 K in. establishes negative voltage inside the cells. Activated by insulin and beta 2 adrenergic agonists.
24
Q
Seconday active transport example
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glucose/na, di and tripeptides, H+ and HCO3-
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Pyrimidine bases
cytosine and thymine
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Purine bases
Guanine and adenine
27
Describe basic structure of DNA
DNA- made up of nucleotides (sugar plus base GCAT plus phosphate) Bases are facing inside and interact with each other via hydrogen bonds creating rungs of helical ladder. Railing of ladder is sugar and phosphare groups connected by phosphodiester bonds.
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Chromatin
DNA wound around histone and nonhistone proteins.
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Describe structure of RNA
Bases GUAC. robose sugar. single stranded. hairpin and loops structure. Located in nucleus and cytoplasm. short lifetime.
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Transcription
process by which storage information in DNA is copied into new molecule of RNA
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List different types of RNA molecules.
Messenger RNA-carries genetic code to cytoplasm, makes proteins
Transfer RNA- carries amino acids to ribosomes to be used in assembly of protein. contains anticodon region that can read mRNA
Ribosomal RNA- form ribosomes with ribosomal proteins
Small nuclear and cytoplasmic RNA- regulatory RNAs
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Describe steps in translation/protein synthesis
Codon (3 base sequence) on mRNA codes for specific mRNA. mRNA goes to ribosome. tRNA comes and if anticodon region on tRNA matches codon on mRNA, the amino acid attached to tRNA will attach, eventually creating specific link of amino acids. This process stops when it hits the stop codon and ribosome leaves.
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Polyribosomes
Sinle mRNA can be translated by several ribosomes at the same time. cluster of ribosomes attached to single mRNA are called polyribosomes.
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Energetics of protein synthesis
ATP used to attach amino acids to tRNA molecule. 2 GTP will be used to attach amino acid to polypeptide chain and to move chain along ribosome.
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How is gene expression regulated?
During transcription, between transcription and translation, during translation, and after translation
MicroRNA- targets mRNA and destroys it to regulate gene expression
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Life cycle of cell
G1 cell grows, leaves if neuron cell. S phase regulate, DNA polymerase checks for errors, G2 prep for division, M mitosis (nutclear division) then cytokinesis (cytoplasmic division)
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Prophase
centrisoles make mitotic spindle, chromosomes become condensed.
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Prometaphase
nuclear envelope dissolves. microtubles attach to chromosomes at centromeres.
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Metaphase
chromosomes line up at center of cell forming metaphase plate
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Anaphase
chromatides of each chromosome are pulled apart toward opposite cell poles.
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Telophase
Two set of chromatides are completely separated, nuclear membrane develops around each set, cytoplasm divides.
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Define proto-oncogenes and tumor suppressor genes and discuss their role in cancer formation
Proto-oncogenes normally function to regulate cell growth, promote cell division. Dysregulaiton of expression leads to uncontrolled cell proliferation.
Tumor suppressor genes- proteins that negatively regulate gell growth by inhibiting cell division. Loss of function or **reduced** function of the tumor suppressor can lead to cancer
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Causes of genetic diseases
Abnormalities during mitosis/meiosis resulting in abnormal number of chromosomes
Chromosomal rearrangements (deletion, replacement, duplication)
Alterations in DNA sequence
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Describe two common classes of numerical chromosomal abnormalities. Give examples of aneuploidy.
Polyploidy and aneuploidy.
Polyploidy-more than one pair. Triploidy is most common. 3 copies of chromosomes. 1-3% of pregnancies. Triploids rarely sirvive to term.
Aneuploidy- one or more individual chromosomes are missing from a single set. Trisomy- 3 copies of a particular chromosome in one set in an otherwise dipoloid cell. Seex chromosome trisomy, Monosomy.
Autosomal trisomy- Trisomy 13, Trisomy 18, Trisomy 21.
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Autosomal Trisomy
Trisomy 13- (Patau syndrome)
Trisomy 18 (Edwards syndrome)
Trisomy 21 (Down syndrome)
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Sex chromosome trisomy
XXX, XXY, XYY. Relatively few problems, normal life span
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Monosomy
lack of chromosome. Autosomal monosomy is embryonic lethal.
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Sex chromosome monosomy (Turner syndrome)
Physical deformities of neck, aortic stenosis, renal abnormalities, hypothyroid, liver disease, DM.
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Locus
position of a gene on a chromosome
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Allele
variations of a gene
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Homozygous
Same alleles at a locus
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Heterozygous
Different alleles at a locus
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Genotype
Genetic constitution of an individual
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Phenotype
Observable characteristics of a cell or organism
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Dominant vs recessive
A character is dominant if it manifests in the heterozygote and recessive if it does not
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Autosomal dominant
Only one mutated copy needed to affect person. 50% of children will be affected with disease. Males and females have disease. ex) Marfan syndrome, Huntington disease, familial adenomatous polyposis
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Penetrance
percent of individuals that carry diseased allele that develop the disease. Some diseases may skip generations. ex) Huntingtons disease is 99% penetrance.
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Autosomal recessive
Two copies of gene are needed to have affcted child. 25% of children are affected. ex) sickle cell anemia, cystic fibrosis
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X linked dominant
All daughters of affected male will have disease. No sons of affected male will have disease.
Affected mom gives disease to 50% of sons and daughters
Ex) Rhett's syndrome, hypophosphatemia
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X linked recessive
Males only need one bad X to get it, so they are more often affected.
Daughters of affected male carry, 50% sons of affected mom have it.
ex) hemophilia A, color blindness, muscular dystrophy
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Mitochondrial diseases
ONLY FEMALES GIVE IT TO THEIR CHILDREN. males and females can both get sick, but only females transmiss it
62
Describe the mechanism of membrane potential formation
Membrnae potential arises when there is a difference in the electrical charge on the two sides of the membrane.
Potassium (mostly inside the cell) leaks out of cell down its concentration gradient. This creates negative charge inside the cell, drawing K back inside cell. When number of K leaving=number of K reentering cell, membrane potential achieved.
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Ion channels
- selective
- gated (open via voltage, ligand intracellular or extracellular, muchanically/stretch gated).
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voltage gated channels vs ligand gated channels
voltage gated-specific (Na, Ca, etc)
Ligand gated- less specific, neurotransmitters act as ligands. ex) Ach receptor
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Nernst Equation
Way to calculate equilibrium potential for K+ based on concentrations of potassium inside and outside the cell
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Goldman equation
calculated membrane potential takng into account 3 ions K Na and Cl and their leak channel permeabilities.
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What ion primarily establishes resting membrane potential in the neuron?
K+
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Resting potential
Difference in electrical charges across the membrane in resting excitable cells. It is the combination of equilibrium potentials for those ions to which the membrane is permeable. Goldman's equation can be used to find this. Contributers: K and Na diffusion potential and Na/K ATPase
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Depolarization
More positive charge in cell (Na and Ca in, K no longer moving out)
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Repolaraization
Becoming more negative (K out, Cl in)
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Stages of action potential
Resting stage- resting membrane potential d/t K and Na gradients and ATPase
Depolarization stage- membrane becomes very permeable to Na, lots of Na flows in
Repolarization- Na channels close, K channels open, K leaves cell.
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voltage gated K vs Na channels
Na slow to close deactivation gate, K slow to open. Both open in response to less negative membrane potential (depolarization)
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How does hypocalcemia affect cardiac action potential?
It leads to increased permeability of Na+ channels, which are activated by very slight change in membrane potential. This can lead to spontaneous discharge in peripheral nerves and tetany
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Phases of cardiac myocyte action potential
Phase 4: Resting membrane potential, voltage gated channels closed,
Phase 0: rapid Na+ influx, Na+ channels open
Phase 1: K+ channels open, K+ efflux
Phase 2: Ca+ channels open, Ca+ influx, plateau
Phase 3: Ca+ channels close, K+ channels remain open, K+ efflux and repolarization to resting membrane potential
Phase 4: resting membrane potential
75
What do QRS and T wave correspond to in regards to cardiac myocyte action potential?
QRS-Na+ channels open, Na+ influx. T wave-K+ channels open, K+ efflux.
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Automaticity
Repetitive self inducing discharges due to pacemaker neurons. occurs in heart, smooth muscle, and neurons in CNS. Causes heart beat, intestinal peristalsis, and control of breathing.
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Pacemaker activity in SA node
Phase 4- depolarization by hyperpolarization activated cyclic nucleotide gated channel (HCN) generates "funny" current. Na influx.
Phase 0: Ca+ channels open, Ca+ influx for further depolarization. slower upstroke d/t lack of Na+ channels (mostly Ca+)
Phase 1 and 2 are absent
Phse 3: K+ channels open, repolarization
Phase 4: Na influx
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Rectification
voltage gated ion channels that pass current (positive charge) more easily in one direction than the other
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Propagation of action potential
After initiation of action potential positive electrical charges are carried by Na+ ions through the membrane for short distance along the axon. This causes depolarization/initiation of action potential in new area-action potential spreads.
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What reestablishes na+ and K+ gradient?
Na+ K+ ATPase
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Saltatory conduction vs passive conduction
Saltatory- myelinated, faster
Passive-slow and energy consuming
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Refractory period
New action potential cannot be initiated because Na+ channels are inactivated
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How do local anesthetics work?
Work on activation gate of Na+ channels making it harder to open Na+ channels.
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Hyperkalemia
Mild- peaked T waves in all leads (repolarization)
Severe- prolonged ST segment, widening of QRS (sine wave EKG)
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Hypokalemia
U wave after T wave, distorted ST segment.
86
Describe muscle tendon, fasicle, and fiber
Muscle tendon holds many skeletal muscles composed of groups of muscle fibers called fasicles. Fibers contain myofibrils which contain sarcomeres.
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T tubules
Invaginations in sarcolemma that carries action potential hitting muscle fiber to all the sarcoplasmic reticulums surrounding myofibral sarcomere (contractile unit of muscle cell). Inside contains same components of extracellular fluid.
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Sarcoplasmic reticulum components
Terminal cisternae-closely associated with T tubules. Stores Ca+
Longitudinal segments- contains ATP dependent Ca+ pumps. Responsible for resequestering Ca+ into the sarcoplasmic reticulum during relaxation of muscle fiber
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Sarcomere
portion of myofibril that lies between 2 Z discs. Composed of thin and thick myofilaments with M line in the middle.
Thick filament- myosin with myosin head
Thin filament-actin, troponin, and tropomyosin
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Thick Filament
Myosin with myosin head. Myosin head-actin binding site, ATP binding site, and light chains. When myson head is bound to actin, it's called a cross bridge.
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Thin filament
Composed of actin (binds to actin site on myosin head), tropomyosin (hides actin from myosin during muscle relaxation), and troponin (troponin complex=3 protein subunits I, T, and C. I=strong affinity for actin, T=strong affinity for tropomyosin, C=strong affinity for Ca+).
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myBP
regulates positioning of myosin and actin for interaction and acts as a tether to the myosin heads, limiting their mobility. (holds thick and thin filaments together)
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Titin
anchors in Z disc, interacts with actin and myosin (holds thick and thin filament to Z disc)
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Role of calcium in muscle contraction
contraction- ca+ is released into cytoplasm, bind to TnC on troponin complex and expose myosin binding site on thin filament.
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Cross bridge cycling
when ca+ in cytoplasm, ADP and phos bind to myosin head, primes for attachment to actin. power stroke, adp released. ATP comes to detach myosin from actin, resulting in ADP and phos on head, primed for another power stroke.
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Frank Starling curve
increasing actin myosin interaction produces optimal sarcomere stretch/stroke volume.
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Sources of energy for muscle contraction
local ATP stores, then creatine phosphate, then fatty acids for moderate exercise and glucose for intense exercise.
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Fast vs slow fibers
fast-less blood supply, paler, easily fatigued
slow- smaller, extensive blood vessels, fatigue resistant.
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Summation
action potentials fuse together when they are super close, resulting action potential is stronger because there is more calcium , it hasnt been removed.
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Tetanus
response to multiple stimuli delivered at fast rate, sufficient to produce fused contraction
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Refractory period
longer in cardiac muscle tissue to prevent heart from going into tetany. Period where a second stimulus will not cause contraction in mucle.
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dystrophin complex
anchors myofibril to sarcolemma (plasma membrane) so whole thing contracts as a single unit
Muscular dystrophy- defects of dystrophin complex
Duchenne muscular dystrophy- completel loss of dystrophin complex, destruction of muscle cells, necrotic muscle cells.
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Motor unit
all muscle fibers innervated by single nerve
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neuromuscular junction
between nerve ending and muscle fiber
105
Describe events at neuromuscular junction when action potential of motor nerve arrives at presynaptic nerve terminal.
depolarization of action potential opens Ca+ ion channels. Mg+ can compete here. If enough Ca+ gets in, Ach vesicle is transported over by SNARE proteins to cell membrane of presynaptic terminal and release Ach into cleft between nerve terminal and muscle fiber. Ach binds to Ach receptor, Na+ channels open, and Na+ flows into cell. End plate potential. only reaches 30mV because Na+ channels are inactivated in response to depolarization. Acetylcholinesterase degrades Ach
106
Explain how depolarizing and non-depolarizing muscle relaxants work
Non-depolarizing: (Roc) competitive antagonist against Ach for Ach receptor. Prevent Ach from binding to Ach receptor.
Depolarizing (succs): depolarizes end plate and is more resistant to Achesterase than Ach. Na+ channels are inactivated and need a low membrane potential to reactivate. So these prevent the Na+ channels from becoming activated. Not good in pt with prolonged immobility- more sensitive spread of Ach receptors.
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Dihydropyridine receptor
action potential triggers this voltage gated receptor in T tubule to trigger Ca+ release from SR via ryanodine receptor
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SERCA (sarcoendoplasmic reticulum calcium ATPase)
located in walls of SR, energy dependent process that pumps Ca+ away from myofibrils back into sarcoplasmic tubules. Calsequestrin binds Ca+ and helps SR sequester Ca+ back to storage.
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Role of Cl- in muscle contraction
Cl- channels reside in T tubule. K+ tends to accummulate in T tubule, so Cl- helps bring membrane potential back down.
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Myotonia congenita
Defective Cl- channels, muscle stiffness and sudden forceful movement d/t build up of K in T tubules.
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Compare and contrast cardiac and skeletal muscle
Cardiac- has branched myofibrils with **adherens** junctions that enable heart to contract forcefully without ripping fibers apart. **Gap junctions** allow free exchange of solutes in cytoplasm of cell. Can create action potential on own, not by nerves like skeletal muscle. Less prominment SR, relies more on intracellular and **extracellular Ca+**. **Refractory period is very long** so tetanus is not possible. **NCX pump** via secondary active transport exchanges Na+ for Ca+ to relax.
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Cardiac ischemia and contractility
death of cells increases K+ locally, increasing resting membrane potential, Na+ channels are inactivated in this environment, leading to partial persistent systole and slow or blocked conduction
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Malignant hyperthermia
mutation in ryanodine receptor, causing massive Ca+ release into cytoplasm. Accelerated muscle metabolism with metabolic acidosis.
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List 2 major types of smooth muscle
Multiunit- Individual smooth muscle cells contract independently of one another, all cells electrically insulated from one another by collagen and glycoproteins, controlled mainly by nerve signals
Unitary-contract together as a single unit. Gap junctions (action potentials can travel from one cell to next. Controlled by non nervous stimuli
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Caveolae
Invaginations on smooth muscle in close proximity to SR.
116
Explain how chemical, mechanical, and electrical stimuli cause smooth muscle contraction
smooth muscle contractions happens d/t
- intrinsic activity of pacemaker cells
- neurally released transmitters
- circulating or locally generated hormones/signalling molecules.
- mechanical stimuli by passive stretching of smooth muscle.
- electrical stimuli (depolarization of smooth muscle opens voltage dependent ca+ channels)
ALL of these **increase intracellular calcium**
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Myogenic contraction
Smooth muscle ability to contract in absence of autonomic or hormonal stimulation. Occurs either due to pacemaker activity within the smooth muscle or due to the response of smooth muscle itself to stretch
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Bayliss Effect
increasing pressure in certain blood vessels causes vasoconstriction. Increased intraluminal pressure activates non-selective cation channels in plasma membrane of smooth muscle cells, causing membrane depolarization and muscle contraction
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Explain how smooth muscle contraction occurs.
Ca+ enters cytoplasm of cell, binds to calmodulin, Ca+-Calmodulin activate myosin light chain kinase, which phosphorylates myosin head, allowing it to interact with actin.
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How do smooth muscle maintain prolonged contraction without significant ATP exposure?
Myosin head can be dephosphorylated while it is still attached to actin, creating a **latchbridge.** Myosin head stays attached to actin, contracting smooth muscle.
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Rho kinase
in smooth muscle, Rho kinase inhibits myosin phosphorylase (which dephosphorylates myosin head) this promotes smooth muscle contraction
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How is smooth muscle relaxed
ATP dependent transporters on cell, Na/Ca antiport transport proteins, SR Ca+ ATPase.
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Management of patients with hypokalemic periodic paralysis
- caused by mutation in skeletal muscle Na+ channel
- Avoid large carbohydrate meals
- Avoid hypothermia
- glucose containing solutions that cause intracellular shift of K+ should be avoided. (Beta adrenergic agonists)
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Microcephaly
due to asymmetric mitotic spindle orientation during mitotic division
