Medical Nutrition Therapy - E. Endocrine & Metabolic Disorders (p. 15-20) Flashcards

1
Q

Type 1 DM is insulin _______.

A

Insulin dependent. Depends on exogenous insulin.

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2
Q

Type 2 DM is insulin ________.

A

Resistance May need insulin.

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3
Q

*Normal Blood Glucose level:

A

*Casual: 70-100 mg/dL *2 hr post-prandial:

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4
Q

Indicative of Diabetes- *Fasting Plasma Glucose (FPG):

A

*FPG: >126 mg/dL

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5
Q

Indicative of Diabetes- *Glucose tolerance test (GTT):

A

*GTT: >200 mg/dL

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6
Q

Indicative of Diabetes- *Symptoms of DM + casual glucose >__ mg/dL

A

*Symptoms of DM + casual glucose >200 mg/dL

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7
Q

Indicative of Diabetes- *HgA1C:

A

*HgA1C: >6.5%

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8
Q

In the GTT, a patient without diabetes will present with a _______ curve.

A

*SLOPED

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9
Q

In the GTT, a diabetic patient will present with a _________ curve.

A

*ROUNDED

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10
Q

Glycosylated Hemoglobin (HGA1C) measures the % of ______ that is carrying ______. It is a measure of long-term blood glucose control over 2-3 months.

A

HGBA1C measures the % of hemoglobin that is carrying insulin.

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11
Q

Normal HGBA1C: Goal for diabetics:

A

Normal HGBA1C:

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12
Q

The goal for all diabetics is to maintain normal blood glucose. Pre-prandial: __-___ Post-prandial:

A

Pre-prandial: 70-130 Post-prandial:

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13
Q

For Type 1 DM, ________ CHO is recommended if doing fixed daily doses of ____. Integrate insulin therapy with usual eating habits. Monitor _______ and adjust ______ doses for amount of food eaten. For exercise, reduction in insulin dosage may be the best choice.

A

Consistent CHO if doing fixed doses of insulin Monitor glucose and adjust insulin doses for food eaten.

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14
Q

Risk factors for gestational diabetes include: 1. 2.

A

BMI >30 History of GDM

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15
Q

GDM usually develops (and is tested for) at 24-28 weeks gestation by a _____ _____ _____. Blood glucose will most likely return to normal following delivery, but with an increased risk for developing ____ ____ _____, which women will need to be tested for regularly.

A

Glucose tolerance test Increased risk for developing Type 2 DM.

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16
Q

GDM increases risk of ______ ______ (large for gestational age) and fetal _________ at birth.

A

GDM increases risk for fetal macrosemia (large baby) and fetal hypoglycemia at birth.

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17
Q

The ______ _____ compares the blood glucose response of a food to a standard load of glucose. Glucose = 100. Foods with ____ index produce greater satiety.

A

Glycemic index Foods with low index produce greater satiety.

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18
Q

Carbohydrate counting 1 CHO serving = __ g CHO

A

15 g

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19
Q

Rapid-Acting insulin Onset: Duration:

A

Rapid-Acting insulin Onset: 5-15 min Duration: 4 hrs

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20
Q

Short-Acting Insulin Onset: Duration:

A

Short-Acting Insulin Onset: 30-45 min Duration: 3-6 hrs

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21
Q

Intermediate-Acting Insulin Onset: Duration:

A

Intermediate-Acting Insulin Onset: 2-4 hrs Duration: 10-16 hrs

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22
Q

Long-Acting Insulin Onset: Duration:

A

Long-Acting Insulin Onset: 2-4 hrs Duration: 20-24 hrs

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23
Q

This oral glucose-lowering medication PROMOTES INSULIN SECRETION.

A

GLUCOTROL

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24
Q

This oral glucose-lowering medication ENHANCES INSULIN ACTION. Also suppresses hepatic glucose production.

A

GLUCOPAHGE (metformin)

25
Q

**The increase in early morning blood glucose due to increased hepatic production after overnight fast. Usually happens between 2 and 8 AM

A

Dawn phenomenon

26
Q

A complication of uncontrolled diabetes - hyperglycemia due to lack of insulin (insulin deficiency).

A

Ketoacidosis

27
Q

**Symptoms of DKA include: -Polyuria (leading to ______) -Increased _______ (respiratory compensation-inc respiration to inc CO2 excretion) -Fruity odor on breath (_________)

A

Symptoms of DKA include: Polyuria (leading to dehydration) -Increased pulse (respiratory compensation-inc respiration to inc CO2 excretion) -Fruity odor on breath (ketones)

28
Q

**Treatment of DKA includes:

A

Insulin therapy, rehydration (electrolyte replacement)

29
Q

Abnormally low blood glucose due to excess insulin or lack of food. (in DM) Symptoms include slow pulse, clammy skin, hunger, weak)

A

Acute Hypoglycemia

30
Q

**Treatment of HYPOGLYCEMIA begins with __ g CHO from glucose tablets, ______, ______. Wait 15 minutes, and check again. If still

A

Treatment of hypoglycemia begins with 15 g CHO from glucose tablets, fruit juice, sugar. Wait 15 minutes, and check again. If still

31
Q

The 3 LONG-TERM effects of uncontrolled diabetes include:

A

Neuropathy (peripheral and autonomic ie. gastroparesis) Retinopathy (leads to blindess) Nephropathy (leads to decreased kidney function)

32
Q

Condition caused by overstimulation of the pancreas or increased insulin sensitivity. BG falls below normal (

A

Postprandial or Reactive hypoglycemia

33
Q

**The goal in postprandial or reactive hypoglycemia is to prevent marked ____ in BG that would stimulate more ______.

A

The goal in postprandial or reactive hypoglycemia is to prevent marked RISE in BG that would stimulate more INSULIN.

34
Q

**Postprandial/Reactive hypoglycemia diet therapy: Avoid ____ sugars _____, _____ meals Consistent ___ intake

A

Postprandial/Reactive hypoglycemia diet therapy: Avoid simple sugars Small, frequent meals Consistent CHO intake

35
Q

Adrenal cortex insufficiency, or ________ disease, is characterized by a deficiency of _______ ______.

A

Addison’s disease Adrenal hormone deficiency

36
Q

Adrenal hormones include: __________ (stimulates gluconeogenesis, inhibits insulin, SO INC BG - in its absence, BG is DEC) __________ (increases reabsorption of fluid and ions by the kidney - in its absence, increased losses) __________ (influences body composition)

A

CORTISOL: (stimulates gluconeogenesis, inhibits insulin, SO INC BG - in its absence, BG is DEC) ALDOSTERONE: (increases reabsorption of fluid and ions by the kidney - in its absence, increased losses) ANDROGEN: (influences body composition)

37
Q

Symptoms of adrenal cortex insufficiency (Addison’s disease), due to absence of adrenal hormones include:

A

Hypoglycemia Sodium loss, dehydration Tissue wasting, weight loss

38
Q

The primary therapy for Addison’s disease is:

A

Hormone replacement

39
Q

Condition characterized by EXCESS secretion of thyroid hormone. T3 and T4 are ELEVATED. Increased BMR–>weight loss.

A

HYPERthyroidism

40
Q

Condition characterized by DEFICIENCY of thyroid hormone. T3 low/normal ; T4 is LOW. Decreased BMR–>weight gain.

A

HYPOthyroidism

41
Q

Enlargement of the thyroid gland due to insufficient thyroid hormone.

A

Goiter

42
Q

Type of goiter (enlargement of the thyroid gland) due to inadequate iodine intake. IODINE is essential for the production of THYROID HORMONE.

A

Endemic goiter

43
Q

Disorder of PURINE metabolism, leading to increased serum URIC ACID. Uric acid deposits in joints–>pain, swelling

A

GOUT

44
Q

Gout diet therapy: Avoid high ____ foods (organ meats, sweetbreads, anchovies, sardines, herring, mackerel, scallops, beer) However, low _____ diet may not be effective because the body produces it.

A

Purine (organ meats, sweetbreads, anchovies, sardines, herring, mackerel, scallops, beer)

45
Q

An inborn error of metabolism characterized by missing the enzyme that would have converted GALACTOSE–>GLUCOSE.

A

Galactosemia

46
Q

Galactosemia is treated solely by ____.

A

DIET. Galactose and Lactose free No organ meats, milk/milk product

47
Q

_____ cycle defects: Inborn error of metabolism characterized by the inability to synthesize urea from ammonia –> ammonia accumulation.

A

Urea cycle defects Symptoms: vomiting, anorexia, lethargy, seizures, coma

48
Q

Diet therapy for urea cycle defects: ___________ restriction BASED ON TOLERANCE. (Restriction to reduce ammonia buildup)

A

Protein restriction based on tolerance

49
Q

Inborn error of metabolism characterized by missing the enzyme PHENYLALANINE HYDROXYLASE, which converts PHENYLALANINE –> TYROSINE. Phenylalanine accumulates.

A

Phenylketonuria (PKU)

50
Q

Diet therapy for PKU: Restrict __________. Supplement _______.

A

Restrict PHENYLALANINE. Supplement TYROSINE.

51
Q

Sources of ___________: Dairy Eggs Meat, poultry, fish Nuts Beans **ASPARTAME (ie. Equal-very high in PHE)

A

Phenylalanine

52
Q

Children with PKU have a higher incidence of ________ _______ due to HIGH CHO, LOW PTN intake.

A

Dental caries

53
Q

Inborn error of metabolism where there is a deficiency of GLUCOSE-6-PHOSPHATASE in the liver, so the liver cannot convert GLYCOGEN–>GLUCOSE. Impairs glycogenolysis–>Hypoglycemia

A

Glycogen storage disease

54
Q

Diet therapy for glycogen storage disease: Provide consistent supply of _____ _____ with CORNSTARCH (exerts a lower and delayed BG peak). High ___, Low Fat

A

Diet therapy for glycogen storage disease: Provide consistent supply of EXOGENOUS GLUCOSE with regular intervals of CORNSTARCH (exerts a lower and delayed BG peak). High CHO, Low Fat

55
Q

Inherited disorder of amino acid metabolism.

A

Homocystinurias

56
Q

Homocystinuria is characterized by severe elevations in ________ and ________, and excess excretion of _________ in urine.

A

Homoecystinuria is characterized by severe elevations in METHIONINE and HOMOECYSTEINE, and excess excretion of HOMOCYSTEINE in urine.

57
Q

Homocystinuria associated with low levels of vitamin __, vitamin __ and _____. **Treatment is to provide HIGH levels of these 3 nutrients. If they don’t respond - low protein, low methionine diet

A

Homocystinuria associated with low levels of B6, B12 and FOLATE. **Treatment is to provide HIGH levels of these 3 nutrients. If they don’t respond - low protein, low methionine diet

58
Q

Inborn error of metabolism of the BCAAs (leucine, isoleucine, and valine). Poor sucking reflex, anorexia, FTT, sweet burnt maple syrup odor of sweat and urine

A

Maple Syrup Urine Disease (MSUD)

59
Q

Diet therapy for MSUD: Restrict _____ Provide adequate energy from ___ and ___ to spare ___.

A

Diet therapy for MSUD: Restrict BCAA Provide adequate energy from CHO and FAT to spare AA (PTN).