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Write a brief report about the metabolic syndrome.

A brief description what a metabolic syndrome is, the hormones,the nutrients, blood sugar and the body tissues and and bodysystems affected.

How does the metabolic syndrome differ between men andwomen?

Metabolic syndrome relationship to thyroid health.

The possible effect of diet soda on metabolic syndrome.

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Irving Heathcote
Irving HeathcoteLv2
28 Sep 2019
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Related questions

Robert is a 55 - year - old truck driver with Type 2 Diabetes. His blood sugars are uncontrolled as evidenced by (AEB) A1C >10 and he complains of increasing n umbness in his feet and fingers, frequent urination during the day and overnight. Robert has a history of hypertension and hyperlipidemia.

Ht 6´3” (1.90m) Wt 242 lb (11 0 kg) BMI 30, BP: 155/90 mm Hg

Medications (daily) : Lantis 80 units at HS, Metformin 100 0mg BID, simvastatin 40 mg, enalapril 10 mg,

Lipid profile

• TC: 228 mg/dL , TG: 545 mg/dL , HDL - C: 39 mg/dL , LDL - C: 136 mg/dL

SMBG shows shows:

Aggregate mean: 218 mg/dL, Standard deviation: 48 (n = 68) over last 30 days

Frequency – 2 x/day

Fasting ( 6 AM): 173 mg/dL, Standard deviation: 35 (n = 21)

Prebreakfast (9 AM): 248 mg/dL, Standard deviation: 30 (n = 6)

Prelunch: (1 PM): 193 mg/dL, Standard deviation: 47 (n = 17)

Predinner (6 PM): 195 mg/dL, Standard deviation: 33 (n = 11)

Bedtime (n = 9): 260 mg/dL, Standard deviation 34 (n = 13)

Range: 69 mg/dL to 304 mg/dL

Food and nutrition history

Due to his job, Robert is often away from home for extended periods of time and he eats at truck stop diners, where he selects hamburgers, fried eggs with bacon and deep fried foods; he eats large quantities of chips and beef jerky as snacks. He drinks diet soda and almost no water. On weekends, when Robert is at home, he enjoys drink ing beer (8 to 10 - 12 - oz cans) and making barbecues.

1. What observations do you have about Robert’s diet? ( 1)

2. Calculate Robert’s EER using two methods for determining Robert’s calorie requirements (show your work) (2)

3. What lifestyle factors could have inc reased the risk for Robert’s diabetes diagnosis? (2)

4. What criteria are used to Diagnose Metabolic Syndrome? Can you diagnose Metabolic Syndrome for Robert? Why or why not? (4)

5. List diabetic symptoms that Robert is showing (3)

6. Explain the pathophysiology of these symptoms (3)

7. What labs would be elevated if you suspect Robert is dehydrated? (2)

8. What is considered to be good control for BS (blood sugar) for someone with diabetes and what is considered poor control? (4)

9. Explain how Robert’s medications help control his diabetes (3)

10. Robert’s physician wants to initiate mealtime insulin injections. What dietary guidelines will you give to Robert regarding his food choices? (2)

11. What are some common causes of hypoglycemia and what w ill you recommend to Robert if he experiences hypoglycemia? (4)

Roger Maxwell is very health-conscious. He runs, swims, and hikes; follows a lowcarbohydrate diet; and generally feels great. He sees a physician when he needs to, in addition to annual physical exams at the large company where he is an engineer. He'd never allow himself to get so out of shape that heart disease would be a risk. Because of his strict adherence to this healthy lifestyle, Roger is surprised when a medical intern, gazing at his yearly elecfrocardiogram (ECG) at his work physical, clearly picks up on something.

"What? What are you looking at?" Roger blurts out while buttoning up his shirt.

"Oh, it's probably nothing." But she doesn't look like it's probably nothing.

"The heart murmur? My mom's been telling me about it since childhood. Not a big deal. The doctors called it something last year, something I never heard of." "Did you check it out?" asks the intern.

"Nah. It wasn't bothering me, so I forgot about it. Why? What's wrong?"

"Well, maybe you should ask the doctor to explain it again and suggest what to do."

"About what?"

"The doctor will explain it. Please don't worry, though," says the intern as she rushes off to the next patient.

Roger's electrocardiograms had in fact been showing that he has had long QT syndrome, and not a heart murmur, for many years. The doctor explains that this is a problem with the heart's rhythm, and not its valves. Roger goes home and Googles long QT syndrome right away. What he finds concerns him enough to alert his relatives.

Long QT syndrome is a lengthening in the time that it takes the ventricles (the lower two heart chambers) to recover after a contraction, called the QT interval on an electrocardiogram. This delay is called torsade de pointes, and it causes lightheadedness upon standing or even fainting, as blood pressure drops when the heart rhythm becomes abnormal. If the arrhythmia turns into the more erratic condition called ventricular fibrillation, it can be deadly. Some cases •of sudden cardiac arrest in people who apparently do not have heart disease are in fact due to long QT syndrome. This 'may have been the case with Roger's aunt, Amelia, his mother's sister, who died at age 34 of what was thought to be a heart attack, but, now Roger realizes, was more likely an arrhythmia. Still, with only one affected relative, Roger had never thought of his aunt's •early demise as a family history, especially since his mother is healthy.

Roger reads that in people with some forms of long QT syndrome, fatal arrhythmia can be triggered by intense emotions or a sudden loud sound. The first recorded case of the condition was a little girl, who collapsed dead •when her teacher suddenly yelled at her. Her older brother had died in a similar circumstance. Suddenly, Roger remembers that his daughter Sheila faints very easily. She even passed out once at a rock concert because she got so excited. He'd never panicked over it because his mother fainted easily, too. A pattern was emerging.

Long QT syndrome is caused by mutations in any of at least 10 genes that encode either proteins that form parts of ion channels (potassium, sodium, or calcium) or proteins that affect the functioning of these channels. Ion channels control the spread of nerve impulses and the resulting muscle contraction. The time for the heart's reeovery after a beat, called repolarization, extends the period when ions are trapped inside heart muscle cells because the channels are blocked, too slow to open, or too quick to close in people who are at elevated risk due to inheriting a mutation. People with long QT syndrome can experience arrhythmia if they take certain drugs that prolong the QT interval. These drugs include certain antibiotics, antidepressants, and diuretics ("water pills").

Roger reads about the different genes and drug combinations that cause long QT syndrome on Wikipedia, and then he scans www.genetests.org to find labs that test for all of them. Only then does he make an appointment with a cardiologist, and he arranges to have his blood and that of his daughter and mother sent to one of the labs. Two weeks later, he learns that they all have a dominant mutation in a gene called HERG (for "human ether-a-go-go") that causes long QT syndrome type 2 (LQT2). Even healthy family members could have inherited the mutation, because 15 percent of people with long QT syndrome do not have symptoms. The concern is their increased risk of developing symptoms in the future—perhaps suddenly.

Question 1 : Roger is upset that in the past doctors had not been more insistent that he follow up on the abnormal ECG pattern. When he mentions this to his primary care physician, she answers, "I didn't say anything because you are so healthy, and people who have cardiac arrest from long QT do so in young adulthood. You're too old to worry about it." But Roger should be worried, because

a. he looks younger than he is, so could still be at risk

b. the condition can be inherited, so others in the family could be affected.

c. he could die at any time.

d. he can no longer take antibiotics.

e. long QT syndrome can cause cholesterol to build up in his coronary arteries.

2. Individuals who should take genetic tests for long QT syndrome are

a. all the people in generation IV.

b. Eric, Joan and Peter, and then Dylan, Anika, Sean, Keri, and Anna if a parent has the mutation.

c. Juanita, Larry, Joan, Peter, and Ellie.

d. Abe, Sara, Craig, Philip, Edwin, and Yvonne.

e. Only those who are athletic.

3. The mode of inheritance of long QT syndrome in the Maxwell family is

a. X-Iinked recessive

.b. autosomal recessive.

c. autosomal dominant.

d. sex-limited.

e. X-Iinked dominant.

4. Some people who inherit the same mutation as Roger do not experience any symptoms. This means that the mutation is

a. variably expressive.

b. genetically heterogeneic.

c. polygenic.

d. incompletely penetrant.

e. dominant.

5). The fact that mutations in any of several genes can cause long QT syndrome means that the condition is

a. variably expressive.

b. genetically heterogeneic.

c. polygenic.

d. incompletely penetrant.

e.recessive.

6). The risk that Sean, Keri, or Anna has inherited the family's mutation for long QT syndrome is

a. 1

b. ¾

c. ¼

d. ¼

e. 1/8

7) Roger is relieved that he does not have- LQT7, which affects skeletal as well as cardiac muscle, causing short stature and scoliosis. He is also glad that he doesn't have LQT8, which causes many symptoms, or either of two types that also cause deafness. These other forms of the condition, with more than one symptom, exhibit

a. invariable expressivity.

b. complete penefrance.

c. genetic homogeneity.

d. pleiotropy.

e. phenocopy.

8) The reason that mutations in different genes all cause the same phenotype of extended QT interval on an ECG is that

a. the heart is an extremely complex organ.

b. the genes all encode proteins that affect ion channels essential for maintaining heartbeat.

c. the genes all encode the same protein.

d. the mutations all affect the genes in the same way.

e. the QT interval is highly variable, even within individuals at different times.

9). A phenotypic pattern in a family that could be due to inherited long QT syndrome is

a. sudden cardiac death in one or more young people and individuals who faint easily.

b. many individuals who eat a very fatty diet and are sedentary but do not develop heart disease.

c. many individuals with hypertension.

d. many individuals who suffer heart attacks after age 50.

e. a family with rnany athletes who have very low heart rates because of intense and frequent exercise.

The people of Malaysia belong to three communities: the local people called Malays, immigrants from South India called Tamils, and immigrants from China. During the early 20th century, the Malays lived mainly in coastal villages, the Tamils worked on rubber estates, and the Chinese worked in tin mines. In general, the people were very poor and they consumed a limited variety of foods.[1] Rice was the staple diet of all three communities and therefore the key source of caloric and nutrient content. Malays typically grew their own rice and dehulled it before consuming it; dehulling partially removes the aleurone layer of the rice seed. Following their South Indian food habits, the Tamils ate parboiled rice, and the Chinese ate polished white rice imported from Thailand. It was found that among the three Malaysian communities, the Chinese community was much more prone to suffer from some degree of sub-optimal thiamin intake. Out of every 1,000 Chinese inhabitants, about 120 had mild thiamin deficiency, about 80 had severe thiamin deficiency, and about 16 people had died of it. Suboptimal intake of thiamin was rare in Malays and was not reported at all in Tamils.[1] Thiamin, also called Vitamin B1, is required for all tissues, and its deficiency causes the disease Beriberi. Less severe deficiency results in non-specific symptoms such as weight loss, malaise, irritability, and confusion. Although the origin of the word Beri-beri is disputed, it is believed to be a Philippine word meaning “I can’t, I can’t” and was probably coined to refer to the lack of neuromotor coordination in people afflicted with this disease.[2] Thiamin is water-soluble and is stable in the acidic medium. It is unstable to heat, oxygen, and UV light in neutral and alkaline medium. The active form of thiamin is thiamin pyrophosphate (TPP). This active form is a cofactor for pyruvate dehydrogenase and transketolase enzymes that are involved in the metabolism of carbohydrates. These enzymes play an important role in the biosynthesis of a number of cell constituents such as neurotransmitters, pentoses, and reduced equivalents, used in oxidant stress. The human body cannot store thiamin and therefore requires a continuous supply of the vitamin. The thiamin in an individual on a thiamin-free diet typically depletes in fewer than two weeks. Thiamin absorption is affected by compounds, called thiamin antagonists or anti-thiamin factors, that alter the structure of thiamin. These compounds include alcohols, polyphenols, flavonoids, and thiaminase, a heat labile enzyme found in certain foods.[2] In affluent countries, where the diet is rich in thiamin, the most common cause of thiamin deficiency is excessive alcohol consumption. Alcohol intake affects thiamin status in two ways. First, alcoholics get a significant percentage of their daily energy intake from alcoholic beverages, which are nutrient deficient. In other words, alcoholics replace their consumption of nutrient dense foods that are part of their normal diet with the consumption of nutrient deficient alcohol. Second, alcohol inhibits the intestinal ATPase involved in the absorption of thiamin.[4] Sub-clinical thiamin insufficiency associated with excessive alcohol consumption produces an encephalopathy called Wernicke-Korsafoff syndrome. Patients with this syndrome have a higher than normal incidence of abnormal transketolase, which has a very low binding affinity to TPP. This problem can be overcome by putting patients on high-dose thiamin therapy. Some patients, however, might have a form of abnormal transketolase that does not bind at all with TPP. Such people do not respond to high-dose thiamin therapy.[4] Thiamin deficiency is observed in individuals who have low thiamin intake and a diet rich in polished rice, especially if their diet also consists of anti-thiamin factors such as tea, coffee, raw fermented fish, and betel nuts. The minimum amount of thiamin needed by the body can increase because of increased physiological or metabolic demands arising from pregnancy and lactation, heavy physical exertion, illnesses like cancer, liver diseases, hyperthyroidism, and surgery. Since TPP is required for carbohydrate metabolism, the recommended dietary allowances for thiamin are based on the assumption that its intake is related to total energy intake. The recommended dietary allowance in the United States is 0.5 mg/1000 Kcal.

Questions
1. Thiamin deficiency was observed only in the Chinese community even though all three
communities had the same staple (rice) diet. Explain.
2. On packages of enriched rice sold in supermarkets, the rice preparation directions state that the
rice should not be washed before cooking. Explain.
3. Severe metabolic acidosis caused by high levels of lactate is often associated with thiamin
deficiency. Explain.
4. Provide two plausible explanations for what might cause above normal levels of pyruvate in blood
and urine. How can one determine which of the two explanations is correct?
5. Why does thiamin utilization increase among cancer patients?
6. A negative correlation exists between the need for thiamin and the amount of fat in the diet.
Explain.

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