MNT idk what last time Flashcards

1
Q

Insulin functions and counter-regulatory hormone

A

Insulin is hormone produced by the beta-cells of the pancreas. It is necessary for use or storage of body fuels / glucagon

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2
Q

glucagon function and counter-regulatory hormone

A

a hormone produced by the a-cells of the pancreas that causes an increase in blood glucose levels by stimulating the release of glucose from liver glycogen stores / insulin

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3
Q

somostatin function and counter u know what

A

a polypeptide hormone secreted from the stomach,small intestine,and pancreas that tends to inhibit other gastrointestinal secretions and motility/ft decreases motility of the stomach and intestine and inhibits or regulates the release of severalGI hormones.

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4
Q

lab values to diagnose dm

A
AIC ≥ 6.5% 
 FPG ≥ 126 
 2 hour PG ≥ 200 during OGTT 
 In patients with classic symptoms of hyperglycemia or 
hyperglycemic crisis, a random PG ≥ 200
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5
Q

Diagnosis for gdm

A

plasma glucose level of 140/dl/mg
gtt
fasting 95 mg/dl
6.5

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6
Q

diagnosis for igt

A

the 2-hour blood glucose is between 140 and 199 mg/dl.

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7
Q

What weeks in the pregnancy we test for GDM?

A

24-28 weeks

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8
Q

Explain why decrease CHO in the morning is needed.

A

to CHO not as well tolerated at breakfast due to

increased cortisol and growth hormones

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9
Q

What are the recommendations of grams for CHO for the morning?

A

30 g

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10
Q

Characteristics for type 1 dm

A

Primary defect is pancreatic beta-cell destruction which leads to absolute insulin
deficiency.
Beta-cell destruction rates vary person to person but typically faster in infants
and children.
Pancreas produces much more insulin than is needed, so possible destruction of
beta-cells starts occuring months or years before symptoms occur. Hyperglycemia
doesn’t occur until > 90% of insulin secretory beta-cells are destroyed.
Immune-mediated diabetes mellitus: autoimmune destruction of
beta-cells in pancreas or idiopathic
auto-immune, environmental, genetic

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11
Q

characteristics of type 2 dm

A

Insulin resistance
• Target tissues: muscle, liver, adipose cells
Pancreatic beta-cell failure
• May increase secretion of insulin at first to compensate for resistance
• Eventually it will not be able to keep up
Age ≥ 45
 Ethnicity: African American, Hispanic, Native American, Asian American, Pacific
Islander
 Family History (parents and siblings)
 HDL ≤ 35 and TG ≥ 250
 HTN
 Obesity with BMI ≥ 25
 History of IFG or IGT
 Vascular

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12
Q

insulin

A

U- 100 concentration = 100 units of insulin per ml of fluid
 Onset – when it starts working
 Peak – most action
 Duration – how long
 Injections via syringe or pen
RAPID ACTING
Examples: Insulin lispro (Humalog)
• Insulin aspart (Novolog)
• Insulin glulisine (Apidra)
• Onset: < 15 minutes
 Peak: 60 – 90 minutes
 Duration: 3 – 5 hours
 Less hypoglycemic episodes than regular
REGULAR INSULIN
 Short acting
 Onset: 30 – 60 minutes
 Peak: 2 – 3 hours
 Duration: 5 – 8 hours
 Take 30 – 60 minutes before meals
 Example: Humalog R
INTERMEDIATE-ACTING
 Neutral protamine Hagedorn (NPH) – only one that is
available
 Cloudy appearance
 Onset: ~ 2 hours
 Peak: 6 – 10 hours
 Duration: 10 – 16 hours
LONG-ACTING INSULIN
 Slow dissolution at injection site – makes it relatively constant and has
peakless delivery over 24 hours
 Acidic – so can’t mix with others
 Given at bedtime – important that it is given at consistent time daily
 Ex: Insulin glargine (Lantus)
 Insulin determir (Levemir) – absorbed from tissues quickly and then is
bound to albumin in bloodstream. Prolonged action of 17 hours
lispro - All have an onset of action within
15 minutes, a peak in activity at 60 to 90 min, and a duration of action of 3 to 5 hours. They result in fewer hypoglycemic episodes compared with regular insulin.
regular - is a short-acting insulin with an onset of action 15 to 60 minutes after injection and a duration of action ranging from 5 to 8 hours. For best results the slow onset of regular insulin requires it to be taken 30 to 60 minutes be- fore meals.
NPH - NPH is the only available intetmediate-aaing insulin (Lente insulin has been discontinued). Its appearance
is cloudy,and its onset of action is about 2 hours after injection, with a peak effect from 6 to 10 hours.
basal - analog that becauseof its slow dissolution at the injection site results in a rela- tively constant and peaklessdelivery over 24 hours

insulin - combination rapid acting or short acting pumped continuous with bolus

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13
Q

Insulin secretagogues Sulfonylureas

A

drugs administered orally to lower blood glucose levels/ katp channel of pancreatic beta cells
Sulfonylureas: promote insulin secretion by beta cells of the
pancreas
 Disadvantages: weight gain and hypoglycemia
 Examples:
• Glipizide (Glucotrol)
• Glyburide (Glynase Prestabs)
• Glimepiride (Amaryl)

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14
Q

Meglitinide

A

lower blood levels /pancreatic beta cells

secretagogues

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15
Q

Biguanide

A

enhance insulin action / liver

metaformin

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16
Q

Thiazolidinediones

A

drugs administered orally that are used to control or lower blood glucose level/ liver
TZDs or glitazones
 Decrease insulin resistance in peripheral tissues and thus enhance
ability of muscles and fat to take up gluocse
 Improve lipids and don’t cause hypoglycemia on their own
 Adverse effects: weight gain and edema
 Examples:
• Actos

17
Q

Alpha-glucosidase inhibitors

A

intestines/ blockes glucose digestion/absorbtion
Delay CHO absorption in small intestine by inhibiting enzymes that
digest CHO
 Lower post-prandial glycemia
 GI side effects include: flatulence, diarrhea, cramping, abdominal pain
 Examples:
• Acarbose (Precose)
• Miglitol (Glyset)

18
Q

Januvia

A

The mechanism of DPP-4 inhibitors is to increase incretin levels (GLP-1 and GIP),[2][3][4] which inhibit glucagon release, which in turn increases insulin secretion, decreases gastric emptying, and decreases blood glucose levels.

19
Q

Byetta, Human Amylin

A

increases insulin secretion

20
Q

benefits of exercise and grams needed for longer and 30 mins

A

Physical activity should be an integral part of the treat- ment plan for persons with diabetes. Exercise helps all per- sons with diabetes improve insulin sensitivity, reduce car- diovascular risk factors, control weight, and improve well-being
15 grams

21
Q

how are ketones formed

A

Ketones are formed when there is not enough sugar or glucose to supply the body’s fuel needs. This occurs overnight, and during dieting or fasting. During these periods, insulin levels are low, but glucagon and epinephrine levels are relatively normal. This combination of low insulin, and relatively normal glucagon and epinephrine levels causes fat to be released from the fat cells. The fats travel through the blood circulation to reach the liver where they are processed into ketone units. The ketone units then circulate back into the blood stream and are picked up by the muscle and other tissues to fuel your body’s metabolism. In a person without diabetes, ketone production is the body’s normal adaptation to starvation. Blood sugar levels never get too high, because the production is regulated by just the right balance of insulin, glucagon and other hormones.

22
Q

Sogmogyi and Dawn Phenomenon

A

dawn -Body needs less insulin from (1 – 3 AM) than at dawn (4 – 8 AM)
T1DM – make sure long-acting insulin doesn’t peak at this time.
Increased need for insulin will cause BG to be higher at dawn
Overnight excessive hepatic glucose production (common in T2DM)
Metformin often used

sogmogi - Rebound hyperglycemia”
Hypoglycemia triggers secretion of counter-regulatory hormones
Glucagon, epinephrine, growth hormone, cortisol
Hepatic glucose production stimulated
Decrease evening insulin dose or take long-acting insulin

23
Q

guidelines for sickness

A

DKA risk during acute illness: flu, colds, vomiting, diarrhea
MNT: 150 – 200 gm CHO/day to prevent DKA
45 – 50 gm CHO every 3 – 4 hours along with medication adjustments
Monitor BG at least 4 times daily
Obtain liquids
Call health care provider if sick more than 1 day

24
Q

hypoglycemia

A

BG normally: 60 – 100
Affects small number of people
Symptoms when BG < 65
Brain and nervous system are starved of glucose causing:
Sweating, shaking, weakness, hunger, headaches, irritability

25
Q

Macrovascular

A
\: large blood vessels
Metabolic syndrome
Dyslipidemia
Hypertension
BP goal: <130/80
If higher need MNT to HTN right away
26
Q

Microvascular

A

Nephropathy
First sign: microalbuminuria or incipient nephropathy
Screening after 5 years with T1DM and at Dx of T2DM and then annually
Screening also: Serum creatinine to estimate GFR
Glucose control can help slow the progression
Low PRO diets – not shown to decrease progression
ADA EBNPG – recommend < 1 gm/kg/day PRO
Retinopathy
Regular eye exams are very important
3 stages of diabetic retinopathy:
Nonproliferative diabetic retinopathy (NPDR):
Microaneurysms of capillaries to retina, new blood vessels formed
Moderate to very severe NPDR
Gradual loss of retinal microvascular occurs – retinal ischemia
Proliferative Diabetic retinopathy
New vessels are fragile, hemorrhage, cause scar tissue, eventual retinal detachment
Neuropathy
60 – 70% of people with DM have nerve damage due to chronic high levels of BG
BG control prevents progression but does not reverse
Peripheral neuropathy – nerve sensation of hands and feet
Autonomic neuropathy – various organ systems (ex: heart, GI system)

27
Q

mnt for cho, pro, fiber

A

CHO = CHO – don’t cut out one particular type
• Sucrose (50% glucose/50% fructose)
• Starch (100% glucose)
 Consistent intake of CHO = improved glycemic control
Cardioprotective recommendations: 25 – 30 grams/day
• 7 – 13 grams soluble fiber
• Not shown to actually improve blood glucose control
 Studies show 44 – 55 grams improve glycemia
Usual intake 15 – 20% of calories
 Caution: diabetic nephropathy or if high saturated fat intake
 Does not slow absorption of CHO
Limit saturated and trans fat
• Omega 3 FA (2 – 3 servings fish/week)
• Supplements: decrease TG but increase LDL

28
Q

goals of mnt

A

Goal: eat foods that keep blood gluocse levels as stable as possible
the goals for mnt for diabetes emphasize the role of lifestyle in improving glucose control, lipid and liprotein profiles, and blood pressure. Improving health through food choices and physical activity is the basis of nutrition recommendations for the treatment

29
Q

reactive hypoglycemia

A

less than 50 mg/dl
Idiopathic reactive hypoglycemia is characterized by nor- mal insulin secretion but increasedinsulin sensitivity and, to some extent, reduced response of glucagon to acute hypo- glycemia symptoms

alimentary low blood glucosemanifesting as weakness,perspiration, hunger, nausea,anxiety,and remors
I to 2 hours after a meal

30
Q

Glysosylated hemoglobin

A

Normal in person without diabetes: 4 – 6% (Avg. BG 70 – 126)
 Glucose attaches to hemoglobin overtime. The more glucose the
hemoglobin is exposed to in the bloodstream the more becomes attached.
 RBC has life span of 2 – 3 months
 Test tells how well control BG has been in past months
 Not as reliable in people with conditions that increase RBC
turnover/lifespan (ESRD, Pregnancy, CF, anemia

31
Q

urine testing

A

Urine or blood testing can be used to detect ketones. Testing for ketonuria or ketonemia should be performed regularly during periods of illness and when blood glucose levels consistendy exceed 240 mg/dl (1

32
Q

Self blood glucose monitoring (reasons for high or low blood sugars) and scheduling Type 1/Type 2

A

is usedon a day- to-day basisto managediabeteseffectivelyand safely;how- ever,laboratory measurementof glycatedhemoglobin pro- vides the best availableindex of overall diabetescontrol.
For mostpatientswith type1diabetes,SMBG isrecommended four or more times a day, before each meal and at bedtime. SMBG in patients with type 2 diabetes should be sufficient to facilitate reaching glucose goals and is often performed one to four times a day, often before breakfast and before and 2 hours after the largest meal but only 3 or 4 days per week. When adding to or modifiing therapy, type 1 and qpe 2 patients with diabetes should tesr more often than usualespecially2 hours after meal

AIC is best indicator (4 – 6% = 70 – 126); at least twice year
 Possible 8x per day: before all meals, 2 hours after meals, bedtime
and middle of night
 Typical:1 - 4 x per day: AM fasting and before and 2 hours after
largest meal of the day (only 3 -4 times per week)
 More or less testing depending on how controlled
medications/insulin/diet is

33
Q

Glycemic index

A

Glycemic index (GI): compares physiologic effects of CHO on
glucose. Compares postprandial glucose after 50 grams of sample
food compared to effects of 50 grams of glucose or 50 grams of
white bread

34
Q

Non-nutritive sweeteners

A

are ok

35
Q

MNT when dealing with alcohol intake and DM

A

Light to Moderate intake (1 women/2 men)
• Associated with decreased risk CHD possibly due to concomitant
increase in HDL and improved insulin sensitivity associated with
alcohol intake.
 Eat with alcohol to reduce risk alcohol-induced hypoglycemia

36
Q

insulin pump

A

Provides basal rapid-acting or short-acting insulin pumped
continuously in micro amounts via subcutaneous catheter 24 hours
per day
 Boluses are given before meals
 Person must be committed to checking BG at least 4 times per day,
monitor CHO intake/food logs, and be able to use technology of
pump