NURS 6501 – Advanced Pathophysiology Week 1 Quiz

NURS 6501 – Advanced Pathophysiology Week 1 Quiz

  1. A 12-year-old male is diagnosed with Klinefelter syndrome. His karyotype would reveal which of the following?
    1. XXY

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  1. The nurse is teaching staff about the most common cause of Down syndrome. What is the nurse describing?
    1. Maternal nondisjunction
  1. A nurse is discussing the movement of fluid across the arterial end of capillary membranes into the interstitial fluid surrounding the capillary. Which process of fluid movement is the nurse describing?
    1. Hydrostatic pressure
  1. What principle should the nurse remember when trying to distinguish aging from disease?
    1. It is difficult to tell the difference because both processes are believed to result from cell injury.
  1. What causes the rapid change in the resting membrane potential that initiates an action potential?
    1. Sodium gates open, and sodium rushes into the cell, changing the membrane potential from negative to positive.
  1. During childhood, the thymus decreases in size, and this is referred to as _____ atrophy.
    1. Physiologic NURS 6501 – Advanced Pathophysiology Week 1 Quiz
  1. Sodium and water accumulation in an injured cell are a direct result of:
    1. Decreased ATP production
  1. A 50-year-old male was recently diagnosed with Huntington disease. Transmission of this disease is associated with:
    1. Delayed age of onset
  1. What is the diagnosis of a 13-year-old female who has a karyotype that reveals an absent homologous X chromosome with only a single X chromosome? Her features include a short stature, widely spaced nipples, reduced carrying angle at the elbow, and sparse body hair.
    1. Turner Syndrome
  1. What is the role of cytokines in cell production?
    1. Provide growth factor for tissue growth and development
  1. A eukaryotic cell is undergoing DNA replication. In which region of the cell would most of the genetic information be contained?
    1. Nucleolus
  1. A patient has severe mental retardation caused by a deletion of part of chromosome 5. What genetic disorder will the nurse see documented in the chart?
    1. Cri du chat syndrome NURS 6501 – Advanced Pathophysiology Week 1 Quiz
  1. The student is reviewing functions of the cell. The student would be correct in identifying the primary function of the nerve cell as:
    1. Communication
  1. How are potassium and sodium transported across plasma membranes?
    1. By adenosine triphosphate enzyme (ATPase)
  1. After a geneticist talks to the patient about being a chromosomal mosaic, the patient as the nurse what that means. How should the nurse respond?  You may ____ genetic disease(s).
    1. Have a mild form of the
  1. A runner has depleted all the oxygen available for muscle energy. Which of the following will facilitate his continued muscle performance? NURS 6501 – Advanced Pathophysiology Week 1 Quiz
    1. Anaerobic glycolysis
  1. A patient who has diarrhea receives a hypertonic saline solution intravenously to replace the sodium and chloride lost in the stool. What effect will this fluid replacement have on cells?
    1. Cells will shrink
  1. A patient has a heart attack that leads to progressive cell injury that causes cell death with severe cell swelling and breakdown of organelles. What term would the nurse use to define this process?
    1. Necrosis
  1. A nurse reading the chart and sees the term oncotic pressure. The nurse recalls that oncotic pressure (colloid osmotic pressure) is determined by:
    1. Plasma proteins
  1. An aide asks the nurse why people who have neurofibromatosis will show varying degrees of the disease. Which genetic principle should the nurse explain to the aide?
    1. Expressivity
  1. A cell is isolated, and electrophysiology studies reveal that the resting membrane potential is -70 millivolts. The predominant intracellular ion is Na+, and the predominant extracellular ion is K+.  With voltage change, which of the following would result in an action potential?
    1. Na+ rushing into the cell
  1. A 13-year-old girl has a karyotype that reveals an absent homologous X chromosome with only a single X chromosome present. What medical diagnosis will the nurse observe in the chart?
    1. Turner syndrome
  1. A 15-year-old female is diagnosed with Prader-Willi syndrome. This condition is an example of:
    1. Gene imprinting
  1. A 55-year-old male with a 30-year history of smoking is examined for respiratory disturbance. Examination of his airway (bronchial) reveals that stratified squamous epithelial cells have replaced the normal columnar ciliated cells.  This type of cellular adaptation is called:
    1. Metaplasia
  1. A group of prison inmates developed tuberculosis following exposure to an infected inmate. On examination, tissues were soft and granular (like clumped cheese).  Which of the following is the most likely cause?
    1. Caseous necrosis NURS 6501 – Advanced Pathophysiology Week 1 Quiz

4 thoughts on “NURS 6501 – Advanced Pathophysiology Week 1 Quiz”

  1. The key characteristic of cachexia is a weight loss of greater than 5% within the previous 12 months or
    a BMI (body mass index) of lower than twenty kg/m2.
    Nonetheless, in the case of CKD, because
    of a bent for elevated physique weight in affected sufferers,
    detecting low BMI would not be a great choice resulting in a late analysis,
    despite the very fact that it is a legitimate and sensitive
    method to regulate cachexia [13, 17]. In protein–protein docking, the
    energy of interaction between two proteins is measured by method of international power
    with a high (negative) world vitality value considered because the interplay
    efficiency of a protein with its receptor [18,30].
    In this examine, MSTN interacted with ACVRIIB with a
    worldwide vitality of −61.sixty three, while MSTN–MIF1 and MSTN–MIF2 interacted with world energies of −59.sixty nine and −53.91, respectively.
    These differences between global energies point out that MIF1 and MIF2 weakened MSTN–ACVRIIB binding.

    Its effects are influenced by complicated mechanisms together with transcriptional and epigenetic regulation and modulation by extracellular binding proteins.

    Due to its actions in selling muscle atrophy and cachexia,
    myostatin has been investigated as a promising therapeutic goal to counteract
    muscle mass loss in experimental models and patients affected
    by totally different muscle-wasting situations.

    Furthermore, growing evidence signifies that myostatin, past to regulate skeletal muscle development, may have a role in many physiologic
    and pathologic processes, similar to obesity, insulin resistance,
    cardiovascular and persistent kidney illness.
    Focusing On this system might operate as an area for creating medicine in cachexia remedy and antagonism of melanocortin receptors can present a therapeutic technique for inflammation-mediated cachexia in CKD.
    It has been reported that central blockade of MC4-R may
    cut back uremic cachexia in experimental animals [11, 21].
    The administration of agouti-related peptide (AgRP)- an MC4-R
    antagonist- in mice with CKD, led to the augmentation of meals consumption, regulation of
    basal metabolic fee, as well as the enhancement of complete body weight and lean body mass.
    Hence, AgRP administration improves uremic cachexia without nutritional effects by involving muscle mass modulation through myostatin and IGF-I steadiness [9].
    Muscle mass will increase by IGF-I whereas myostatin inhibits muscle mass development [146].
    Cheung and coworkers assessed the protective effect of
    pegylated leptin receptor antagonist (PLA) in cachectic mice with CKD.
    Their results indicated that PLA therapy (7 mg/kg per day) could
    enhance appetite, weight acquire, lean mass in addition to muscle perform, together with decreasing vitality
    expenditure, and recovering hepatic ranges of TNF-α and IL-6 mRNA.

    It’s a negative regulator of muscle progress and may regulate the number and measurement of muscle fibers.
    Discuss to your physician before taking any supplements or making
    main changes to your day-to-day routine. Remember that one of
    the simplest ways to maintain muscle mass safely is to engage in regular train,
    eat a nutrient-dense and nutritious diet that accommodates enough protein, and get enough rest and recovery.
    However, persisting concerns have been raised relating to the long-term
    results of myostatin inhibition (like muscle imbalance and respiratory illness risk) based
    mostly on its impression on livestock and experimental animals.

    Some researchers suppose that there are no straightforward and fast solutions to these considerations, which need to be fastidiously addressed in future medical trials [24, 25].

    Some widespread names for ecdysterone embody ecdisten, ecdysone, isoinokosterone, 20-hdroxyecdysone and β-ecdysterone.
    Regardless Of these potential advantages, no analysis has supported these claims in human fashions.

    One Other class of MSTN inhibitors is fusion proteins, typically in the form of soluble activin receptors,
    which act as ligand traps by binding MSTN and stopping its additional interactions.
    Acceleron, now owned by Merck, first brought ligand traps to
    medical trials with ramatercept in 2008. Ramatercept
    is a fusion protein consisting of human IgG linked to
    the extracellular domain of ActRIIB, appearing as a soluble form of ActRIIB,
    which binds MSTN and different TGF-β members.
    In a part 1 trial involving girls, complete muscle volume (TMV)
    was improved by roughly 5.1% following a
    single injection of 3 mg/kg [62].
    You see, most roids or anabolics build muscle by making the
    muscle cells you’ve larger . Funding for this study was
    supplied by a NASA Cooperative Settlement NCC8-242 to BioServe House Applied
    Sciences and in type contributions of myostatin inhibitor from Amgen Inc.

    Thank you to the Leinwand Laboratory within the Department of Molecular,
    Cellular and Developmental Biology on the
    College of Colorado at Boulder for assist with strategies improvement and access to laboratory sources.
    Due To This Fact, sustaining muscle throughout weight reduction is critical to maintaining a healthy weight over time.
    Therefore, when performing a therapeutic realignment of the
    backbone and distal joints, tight muscles and weak muscles dramatically impact
    the result of therapeutic interventional support.

    ACE-031 is a soluble type of ACVRIIB, and varied studies on an Amyotrophic Lateral Sclerosis mouse mannequin have shown a single dose of ACE-031 will increase muscle mass
    and strength. This fusion protein of ACVRIIB and IgG1-Fc acts by binding to MSTN, and thus, disrupts its inhibitory effect (Campbell et al., 2017).
    Experiments on ACE-031 had been subsequently suspended because of potential safety issues
    of epistaxis and telangiectasia. Ghrelin is largely produced in gastric
    oxyntic mucosa (DeBoer, 2011), and ghrelin treatment reduces proinflammatory cytokine release in cachexia patients (Kishimoto et al., 2012).
    Moreover, increases in anabolic activity by ghrelin enhance GH release and scale back the consequences of irritation, which provides promise for the therapy of cachexia (Yanagi et al., 2018).

    Nevertheless, it may be very important observe that the use
    of myostatin inhibitors in enhancing athletic efficiency is taken into account unethical and will have antagonistic health results.
    Myostatin (or progress differentiation factor-8,
    GDF-8) is a unfavorable regulator of muscle progress and a member of the remodeling growth
    factor-β household [7]. Numerous molecular mechanisms regulating
    protein synthesis and degradation are influenced by
    myostatin [8]. Myostatin also negatively regulates
    the activation and self-renewal of satellite tv for pc cells (SC) by inhibiting the progress of SC into the S phase of the cell cycle [9].
    In addition, myostatin reduces IGF-Akt pathway exercise resulting in decreased protein synthesis
    initiation and increased translocation of Forkhead field protein O1 (Foxo1) into the
    nucleus. Earlier research reported an increased myostatin mRNA expression in skeletal muscle after 5 days of single-leg immobilization [10] and a rise in myostatin mRNA and protein expression after 3 days of unilateral decrease limb
    suspension in wholesome young men [11]. Whereas Jones et al.
    [12] confirmed no change in myostatin mRNA expression after 2-wk of single-leg immobilization, although
    there was an increased tendency of myostatin mRNA.
    Scientific research investigating using pharmaceutical myostatin inhibitors for stimulating muscle growth have yielded underwhelming outcomes [13].

    Several latest research analyses conclude
    that animal models of myostatin blockade merely have
    not translated to human fashions [14, 15]. Epicatechin (EC) is a prominent catechin present in cocoa beans — and to a lesser diploma in tea
    leaves — together with epigallocatechin gallate (EGCG), epigallocatechin (EGC), and epicatechin gallate (ECG) [3].
    Epicatechin and associated catechins have characteristically excessive antioxidant exercise, making them attractive therapeutic candidates
    for oxidative stress-induced health conditions (e.g. cardiovascular disease,
    muscle atrophy, and continual inflammation) [4].

    The dietary supplements have been provided pre-mixed
    right into a chocolate pudding to match the flavour and texture to
    take care of blinding. Epicatechin is a pure plant compound from
    a powerful group of phytochemicals generally known as flavanols.
    Consuming foods rich in epicatechin in addition to
    including a high quality epicatechin supplement could
    help you boost circulation, enhance your coronary heart health, promote muscle
    development, and even shield you against age-related muscle wasting
    and other health issues. As a pure anabolic compound, laxogenin stacks properly with epicatechin to
    boost muscle progress. Two serum separation vacutainer tubes and one EDTA vacutainer
    tube was obtained from every topic. The serum vacutainers were
    separated by way of centrifugation a 6,000 rpm for 20 minutes.
    One serum separation tube and the EDTA tube have been sent to Quest Diagnostics (Dallas, TX)
    for assay of a regular clinical chemistry profile and complete blood cell counts to make sure safety of supplementation in the course of the protocol.

    Following differentiation, myotubes were
    either untreated (vehicle control), or treated with UA concentrations between 0.002 and a hundred µM for a period of 24 h.
    No statistically vital loss of cell viability was noticed with 24 h remedy with UA concentrations ≤ 50 µM,
    whereas at a focus of a hundred µM, there was a ~ 40% significant decline
    in cell viability (Fig. 1A). This research offers evidence of
    UA’s metabolic benefits in major human myotubes, notably enhancing basal- and insulin-stimulated glucose uptake and supressing
    MSTN expression. These findings suggest UA could be an effective nutraceutical for mitigating insulin resistance and warrants further investigation.
    It also phosphorylates and inhibits Forkhead field O1 (FoxO1), which is a
    transcription issue that represses GLUT4 gene transcription [131].
    MSTN inhibition upregulates the PI3K/Akt pathway, resulting in an increase expression of GLUT4
    [132, 133]. Additionally, MSTN inhibits the activation of adenosine monophosphate-activated protein kinase (AMPK), a crucial regulator of mitochondrial biogenesis
    and power metabolism, which additionally promotes GLUT4 translocation in response to insulin-independent power stress [129, 134].
    Furthermore, MSTN knockout has been reported to upregulate
    adiponectin, a regulator of adipocyte energy metabolism that improves insulin sensitivity and stimulates AMPK [134–136].

    In our examine, transgenic mice overexpressing MSTN propeptide exhibited a major increase in serum adiponectin levels when fed a high-fat
    food plan, whereas sustaining normal levels of blood insulin, resistin, and leptin [121].
    The mouse hindlimb suspension (HS) mannequin mimicked lots of the
    modifications that happen with spaceflight-induced muscle
    atrophy and lack of function3,43,forty nine,50.

    As discussed above, in the course of the activations of various signaling processes, and
    thus, the activations of atrophic genes, MSTN interacts with a
    lot of totally different proteins, which supplies clues for the design of peptide
    inhibitors of MSTN. MSCs divide symmetrically to extend their
    number, or asymmetrically to supply cohorts of committed satellite cells and consequently progenitors after they’ve been activated.
    Myogenic progenitors multiply and eventually differentiate by fusing with different myogenic progenitors or injured fibers to be able to restore fiber integrity and function (Dumont et al., 2015; Dueweke et al.,
    2017). SM consists of muscle fiber with
    a unique construction, which mainly consists
    of actin and myosin filaments that permit muscles to contract and relax.
    Each muscle fiber represents a muscle cell, which
    has a elementary cellular unit generally known as the sarcomere.
    Fascicules are shaped by bundles of myofibers, and muscle tissue is fashioned by bundles of
    fascicles, with each layer being contained by the ECM and maintained by cytoskeletal networks
    (Lieber and Friden, 2000).
    Another talked-about technique of inhibiting myostatin is thru the consumption of epicatechin,
    a member of the flavonoid family of chemical substances that management pigmentation in crops [31].

    In both people and animals, myostatin is a hormone that acts as
    a kind of “brake” that tells muscle tissue to stop growing, which helps to stop them from getting too massive.
    Uneven muscle growth is a possibility if you don’t stick with a regimented training and restoration schedule.

    Unchecked muscle progress can exhaust tendons and ligaments, rising the danger of damage.
    SwissChems is a trusted name within the peptide world, and their Myostatin delivers a potent formulation designed to target myostatin inhibition directly.
    Nevertheless, Welle did mention some unwanted aspect
    effects in the mice come the end of the research.
    Myostatin is considered an inhibitor of satellite cell activation and in consequence skeletal muscle hypertrophy.
    One promising complement which has suppressed blood ranges of myostatin by 44% is a proprietary
    bioactive ingredient, Myo-T12, which is follistatin derived from
    fertile rooster egg yolk isolate. Therefore
    the aim of this study was to investigate the results of MyoT12 on skeletal muscle development and strength in recreationally skilled
    people. Over 20% of cancer deaths in human patients
    is brought on by cachexia, a symptom of cancer that causes
    the lack of muscle and fats regardless of adequate diet.

    In the muscles, more glucose means extra power that enhances performance and muscle constructing.
    It acts on granulosa cells to set off the discharge of progesterone,
    minimizing the fluctuations in the menstrual cycle.
    Research focused on follistatin 344 as a potential cancer remedy suggest that it negatively impacts certain cancers such because the prostate, esophagus, and skin (7).
    Perhaps, probably the most ground-breaking findings of mice-based studies counsel that follistatin 344 can help in some specific
    forms of cancer therapy. Some myostatin inhibitors have progressed into scientific improvement as summarized
    in Table 1. There has been progress in evaluating antimyostatin therapies in animal models of muscle losing problems.
    Some packages have progressed into clinical growth with preliminary outcomes showing positive impression on muscle quantity.

    Total RNA concentration was decided spectrophotometrically (SpectraMax 384
    Plus and SoftMax Pro Software Program, SpectraDrop Micro-Volume Microplate, Molecular Devices, San Jose, CA) by optical density (OD) at 260 nm using an OD260 equal to 40 μg/μl.
    Reverse-transcription to synthesize cDNA was carried out with 100 ng of complete RNA template utilizing the qScript Flex cDNA Kit following manufacturer’s
    specs (Quantabio, Beverly, MA). The familiarization session was primarily used to
    introduce the members to the exercise protocol and to the exercise and testing instrumentation. The members sat on every cycle ergometer to be used for testing and the
    seat was adjusted to the suitable top in order that knee flexion was ~20–25 degrees at full extension. The participant cycled against no resistance
    for a short period to verify the proper seat peak.

    He has this theory because when adults have skilled will increase
    in muscle mass because of lower myostatin ranges,
    it’s been sarcoplasmic hypertrophy. Primers for glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and myostatin had been commercially synthesized (Integrated DNA Applied Sciences, Coralville, IA).
    The forward primer sequence used for GAPDH was ACCACAGTCCATGCCATCAC, and
    the reverse primer sequence used was TCCACCACCCTGTTGCTGTA (21).
    The ahead primer sequence used for myostatin was CTACAACGGAAACAATCATTACCA,
    and the reverse primer sequence used was GTTTCAGAGATCGGATTCCAGTAT (22).

    The ranges of LA, CK, LDH, SOD, and MDA in the hippocampal
    tissue had been measured in accordance with the manufacturer’s
    protocol. The absorbance was measured at 450, 530, 532, 550, 620, 640, and 660 nm utilizing
    a spectrophotometer or microplate reader. Skeletal muscle,
    as a motor organ, has a high vitality demand, and its cellular items possess
    a massive quantity of mitochondria, all of which require correct quality
    control.
    (–)-Epicatechin has been shown, by a number of studies, to increase
    capillary and mitochondrial density, lower myostatin expression and increase follistatin expression in people (12, 24).
    The results of this research revealed an inhibitory effect of
    (–)-epicatechin supplementation on improvement of peak
    relative cardio power and mitochondrial density as decided by skeletal muscle SDH
    protein content in response to cycle coaching.
    These observations had been observed regardless of equal will increase
    in peak power obtained during the peak oxygen consumption test.
    The PLA group increased relative peak VO2 by an average of seven.4 ± 5.7 ml/kg/min whereas the EPI group solely elevated
    by a mean of two.0 ± 4.four ml/kg/min.
    The serum from the remaining separation tube was
    separated, labeled, and stored in micro centrifuge tubes at -80°C for later evaluation.
    Following completion of the study, samples were analyzed for lively testosterone, free testosterone,
    and cortisol with an enzyme immunoassay (EIA) assays
    using Goat-Anti-rabbit IgG (GARG) coated microplates. Assays had
    been performed using a Jitterbug microplate shaker
    (Boekel Scientific-Philadelphia, PA) and a Tricontinent Multiwash Advantage microplate washer (Grass Valley,
    CA).

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