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Nataly [62]
3 years ago
12

Can anyone help ASAP pls!

Medicine
2 answers:
Kobotan [32]3 years ago
7 0

Answer:

1: respect

2: communication

3: trust

4: community

5:edibility

6: your voice matters

7: engagement

8: safety culture

9: resilience

10: diversity

Hope this helps ;)

dybincka [34]3 years ago
7 0
Glad you got help ♡
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A client with long-standing rheumatoid arthritis has frequent reports of joint pain. The plan of care should be based on the und
FromTheMoon [43]

The plan of care should be based on the understanding that chronic pain is most effectively relieved when analgesics are administered at regularly scheduled intervals.

<h3>What is Rheumatoid arthritis?</h3>

Rheumatoid arthritis may be defined as an autoimmune and inflammatory disease that is responsible for attacking the healthy cells of the immune system of your body by mistakes.

During the treatment of Rheumatoid arthritis, various drugs, as well as analgesics, are effectively delivered to the patient's body to relieve that chronic pain in joints.

Such analgesics are required to be delivered or provided at regularly scheduled intervals specifically. This activity assists the patients with a lack of chronic pain and partial movements of joints.

Therefore, it is well described above.

To learn more about Rheumatoid arthritis, refer to the link:

brainly.com/question/16920119

#SPJ1

3 0
2 years ago
Write the medical name for the disease and separate it into suffix, root, and prefix.
rusak2 [61]

Answer:

“Neurodegeneration” is a commonly used word whose meaning is believed to be universally understood. Yet finding a precise definition for neurodegeneration is much more arduous than one might imagine. Often, neurodegeneration is only casually mentioned and scarcely discussed in major medical textbooks and is even incompletely defined in the most comprehensive dictionaries. Etymologically, the word is composed of the prefix “neuro-,” which designates nerve cells (i.e., neurons), and “degeneration,” which refers to, in the case of tissues or organs, a process of losing structure or function. Thus, in the strict sense of the word, neurodegeneration corresponds to any pathological condition primarily affecting neurons. In practice, neurodegenerative diseases represent a large group of neurological disorders with heterogeneous clinical and pathological expressions affecting specific subsets of neurons in specific functional anatomic systems; they arise for unknown reasons and progress in a relentless manner. Conversely, neoplasm, edema, hemorrhage, and trauma of the nervous system, which are not primary neuronal diseases, are not considered to be neurodegenerative disorders. Diseases of the nervous system that implicate not neurons per se but rather their attributes, such as the myelin sheath as seen in multiple sclerosis, are not neurodegenerative disorders either, nor are pathologies in which neuron Perspective series.

As we have mentioned, HD has received at great deal of attention in the field of neuroscience, as it is a prototypic model of a genetic neurodegenerative disease. While it is well established that a triplet-repeat CAG expansion mutation in the huntingtin gene on chromosome 4 is responsible for HD, Anne B. Young (39) will bring us on the chaotic trail of research that aims to define the normal functioning of this newly identified protein, as well as to elucidate the intimate mechanism by which the mutant huntingtin kills neurons. Although much remains to be done, this article provides us with an update on the most salient advances made in the past decade in the field of HD, suggests pathological scenarios as to how mutant huntingtin may lead to HD, and, most importantly, discusses the many steps in the process of functional decline and cell death that might be targeted by new neuroprotective therapies (39).

While HD is by nature a genetic condition, PD is only in rare instances an inherited disease. Despite this scarcity, many experts in the field of neurodegeneration share the belief that these rare genetic forms of PD represent unique tools to unravel the molecular mechanisms of neurodegeneration in the sporadic form of PD, which accounts for more than 90% of all cases. Accordingly, Ted Dawson and Valina Dawson review, in their Perspective, the different genetic forms of PD identified to date (40). They then summarize the current knowledge on the normal biology of two proteins, a-synuclein and parkin, whose mutations have been linked to familial PD (40). The authors also discuss how these different proteins may interact with each other and how, in response to the known PD-causing mutations, they may trigger the neurodegenerative processes (40).

The recognition that many neurodegenerative diseases are associated with some sort of intra- or extracellular proteinaceous aggregates has sparked major interest in the idea that these amorphous deposits may play a pathogenic role in the demise of specific subsets of neurons in various brain diseases. Along this line, what could be a better example of “proteinopathic” neurodegenerative disease than AD, which features NFTs and senile plaques? In this context, Todd Golde (41) reviews the presumed role of amyloid β protein (Aβ) in the initiation of AD and outlines the molecular scenario by which Aβ may activate the deleterious cascade of events ultimately responsible for dementia and cell death in AD. In light of this information the author discusses the different therapeutic approaches that may be envisioned for AD (41). He also summarizes the state of our knowledge about risk factors and biomarkers for AD that can be used to detect individuals at risk for developing the disease, and to follow its progression once it has developed (41).

Explanation:

7 0
3 years ago
What does aldosterone do.
Anna [14]

Answer:

Usually, aldosterone balances sodium and potassium in your blood.

4 0
2 years ago
Tell the five most common signals of a heart attack. Explain the steps (procedures) in cardiopulmonary resuscitation (CPR).
lana66690 [7]

i got you, boy scout, im first class.

Chest pain – like an elephant sitting on chest, often radiates to left

arm, shoulder, back.

Shortness of breath

Weakness

Unusual sweating

Nausea and/or vomiting

numbness in left arm

steps:

1. Check for unresponsiveness

2. Call 911

3. Position victim

4. Open Airway – position/tilt head

5. Look, Listen and Feel for a good 5 seconds. If no breathing is heard,

felt, or seen in chest movement,

6. Give 2 breaths – check to see that the air is going into the lungs by

watching for the chest to rise as you administer each breath.

If no air is going in you must clear airway –

i. Reposition the head and try your two breaths again.

ii. Finger sweep

iii. Heimlich Maneuver

7. Once airway is open, check for carotid pulse for 5-10 seconds.

8. If NO pulse is present, begin first cycle of 15 chest compressions

to 2 breaths. The heel of the hand is used in the center of the

breastbone to give compressions. Place one hand over the other and

press STRAIGHT down.

9. Recheck pulse for a full 10 seconds after 4th cycle for return of

pulse or breathing. Continue CPR at the rate of 15/2 until help

arrives, the person is revived, or you are physically exhausted and

unable to continue.

4 0
3 years ago
Read 2 more answers
Discuss how social media may perpetuate attacks on lesbian, gays, bisexual, transgender, queers, intersex (LGBTQL) and sexual /a
solmaris [256]

Answer:

It is a fact that people of different sexuality do get attacked on the internet for "coming out" but just take a while to realize who your hurting, just because there different doesn't mean you have to go and bully them how would you feel if it happened to you? Hopefully this world will change to where we get to live in a world where we get to love who WE want without getting judged or attacked from it

3 0
3 years ago
Read 2 more answers
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