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Endocrinology > Gestational DM and DM type 1 > Flashcards

Gestational DM and DM type 1 Flashcards

1
Q

What is DM associated with?

A
  • disturbances in carbs, fat and protein characterized by hyperglycemia
  • one of most prevalent diseases in US (24 mill individuals)
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2
Q

What does long term tx of DM emphasize?

A
  • control of blood glucose levels to prevent the acute complications of ketosis and hyperglycemai
  • long term complications such as retinopathy, neuropathy, nephropathy, and CVD can be minimized if blood glucose levels are effectively controlled
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3
Q

Why is DM such a big deal? Why do we care about it so much?

A
  • 12,000- 24,000 become blind each year secondary to DM
  • death rate due to diabetes has increased 45% since 1987
  • when kidney failure dx: it is found that 45% of pts have diabetes
  • at current rate 1/3 Americans born after 2000 will develop diabetes
  • there is an epidemic of Diabetes especially Type 2 stemming from obesity especially in the US
  • DM is associated with increased risk of stroke, heart attack, and eye, skin and foot complications
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4
Q

What occurs when there is declining level of glucose in the blood?

A
  • triggers pancreas to release glucagon which stimulates glycogen breakdown into glucose in the liver so blood glucose rises back to normal range - homeostasis
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5
Q

What occurs when there is a rise in blood glucose?

A
  • triggers pancreas to release insul which stimulates glucose uptake by tissue cells (muscle and adipose), and stimulates glycogen formation in the liver this causes blood glucose to fall back intot the normal range
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6
Q

what are the 4 diabetes classifications?

A
  • type 1 diabetes (IDDM)
  • latent autoimmune diabetes in adults (LADA)
  • type 2 diabetes (NIDM)
  • gestational diabetes
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7
Q

What is type 1 diabetes?

A
  • 5-10% of dx diabetes
  • autoimmune disease that destroys the pancreatic beta cells causing absolute insulin deficiency
  • bottom line: no insulin is being produced by the beta cells
  • oral agents are ineffective so insulin therapy is required
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8
Q

What is type 2 diabetes?

A
  • 90-95% dx cases of diabetes
  • due to both:
    decreased insulin release (not an autoimmune basis) and
    disease of insulin receptors (lack of insulin receptors) so that glucose can’t get into cells so glucose levels rise: insulin resistance
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9
Q

When is DM I usually dx?

A
  • in children and young adults
  • age of presentation has bimodal distribution:
    1st peak: 4-6 years
    2nd: 10-14 years
  • 45% of children present before age 10
  • previously known as juvenile diabetes
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10
Q

Presentation of DM I?

A
  • classic: new onset of chronic polydipsia, polyuria and wt loss with hyperglycemia and ketonemia (or ketonuria)
  • DKA
  • silent (asx) incidental discovery (unusual)
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11
Q

What is the most common presentation of DM I?

A
  • hyperglycemia without acidosis
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12
Q

2nd most common presentation of of DM I?

A
  • DKA (hyperglycemia and ketoacidosis)
    potentially life threatening complication
  • vomiting, dehydration, altered mental status, often 4-8 L depleted
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13
Q

What does DKA result from?

A
  • results from a shortage of insulin and corresponding increase in glucagon, liver releases more glucose from glycogen in response the body switches to burning fatty acids from adipose tissue and producing acidic ketone bodies that cause most of sxs and complications
  • high glucose levels spill into urine taking water and Na+ and K+ along with it in a process known as osmotic diuresis causing polyuria and dehydration
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14
Q

How is DKA tx?

A
  • with IV fluids, insulin, manage intercurrent illnesses, and infection
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15
Q

What is the triad of hyperglycemia?

A
  • polyuria
  • polydipsia
  • polyphagia
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16
Q

What are the other signs of diabetes (type 1 and 2)?

A
  • lack of energy
  • blurred vision
  • pruritus
  • candida infection
  • hyperglycemia
  • glucosuria
  • ketones in blood and urine
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17
Q

What is polyuria?

A
  • frequent urination
  • excessive or abnormally large production of urine
  • usually appears in conjunction with polydipsia (increased thirst)
  • can cause dehydration
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18
Q

What is polydipsia?

A
  • increased thirst
  • brought on by polyuria
  • one of intitial sxs of diabetes
  • non compliance of DM meds
  • doses of DM meds not adequate
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19
Q

What is polyphagia?

A
  • excessive hunger or increased appetite with (with wt loss)
  • mitochondria can’t get the glucose so metabolizes fat and protein: liver has to convert the fat and protein into ketones for energy
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20
Q

Reason for lack of energy presentation?

A
  • high levels of glucose in the blood, but the cells are lacking because insulin is the gatekeeper to allow entry into the cells
  • glucose can’t get into the cells to be used by the mitochondria so can’t make energy
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21
Q

Why is there blurred vision in diabetes?

A
  • aqueous humor in eye anteriorly
  • glucose enters aqueous humor and can distort light
  • improves or resolved with controlled glucose levels
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22
Q

Presentation of pruritus in diabetes?

A
  • itching: irritated by change in osmolality
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23
Q

Candida infection?

A
  • rash under breasts
  • vulvo-vaginal: repeated vulvitis
  • balanitis in men
  • diaper rash and recurrent thrush in infants
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24
Q

How do you dx diabetes?

A
  • FBS greater than 126 on 2 separate occasions
  • sxs of hyperglycemia and random blood sugar greater than 200 mg/dL
  • oral glucose tolerance test (OGTT)greater than 200
  • glycosylated hemoglobin (A1C): greater than 6.5%
  • loss of C peptide less than 0.8 ng/dL (produced in beta cells of pancreas)
  • urine dipstick testing: + glucose (glucose starts spilling into urine when serum is greater than 180), + for ketones
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25
Q

How do you differentiate b/t type 1 and 2?

A
  • antibodies: DM I is suggeseted by the presence of circulating, iselt-specific, pancreatic autoabs:
    glutamic acid decarboxylase (GAD65)
    40K fragment of tyrosine phosphatase (IA2)
    insulin and/or zinc transporter 8 (ZnT8)
    absence of pancreatic autoabs doesn’t rule out the possibility of T1DM
  • insulin and C-peptide levels:
    high fasting insulin and C peptide levels suggest T2DM
  • low levels or in normal range relative to concomitant plasma glucose concentration: T1DM
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26
Q

Type 1 clinical features?

A
  • typical onset age: less than 30
  • duration of sxs: weeks
  • body weight: normal/low
  • ketonuria: yes
  • rapid death: yes
  • autoabs: yes
  • complications at diagnosis: no
  • other autoimmune diseases: common
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27
Q

Type 2 clinical features:

A
  • typical onset age: greater than 50
  • duration of sxs: months to years
  • body weight: obese
  • ketonuria: no
  • rapid death: no
  • autoabs: no
  • complications at dx: 25%
  • Other autoimmune diseases: uncommon
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28
Q

How does Hb A1C work?

A
  • used in dx as well as management of disease
  • glucose enters RBCs and links up (glycates) with hemoglobin
  • hemoglobin gets stickier because of chronic elelvated blood glucose
  • Hb A1C provides overview of average blood glucose over 2-3 months (ex: 7% A1C - would be an estimated average glucose of 154 mg/dL
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29
Q

Levels of Hb A1C?

A
  • healthy non-diabetic: less than 5.6%
  • prediabetes: 5.7-6.4
  • diabetes: greater than 6.5
    ADA recommends measuring A1C 3-4x a year for type 1 and controlled type 2 diabetics, and 2x year for well controlled type 2 diabetics
  • ***don’t need to be fasting
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30
Q

Type 1 DM acute complications?

A
  • DKA
  • dehydration
  • hyperglycemia
  • infections (recurrent candidiasis)
31
Q

Diabetic chronic end organ damage complications (microvascular)

A
  • diabetic retinopathy (most common blindness in US)
  • diabetic nephropathy (most common cause of renal failure)
  • diabetic neuropathy (usually legs/feet but can be autonomic - erectile dysfunction)
32
Q

Diabetic chronic end organ damage complications (macrovascular)

A
  • CVD: CAD, MI
  • cerebrovascular disease: TIA and stroke
  • peripheral arterial disease
33
Q

Diabetes management - reaistic goals?

A
  • targeted glycemic goals: balancing act - lower the risk of complications of hyperglycemia vs hypoglycemia
  • setting realistic goals for each child and family
  • training the pt and family to provide apporpriate daily diabetes care
  • maintaining normal growth, development, and emotional maturation, with increasing independence and self care of diabetes as the child grows older
  • takes a multidisciplinary team
  • newly diagnosed (or relapsing) may need hospitilization to stabilize and get patient and family education
  • close follow up and develop good rapport
34
Q

Diabetes management team consists of?

A
  • primary care provider
  • endocrinologist
  • nurse educator
  • dietitian
  • mental health professional, who can provide pediatric specific education and care
  • T1DM is life changing dx for younger pts
  • comprehensive management by ped. diabetes team reduces the number of hospitilizations and emergency room visits and is cost effective
35
Q

What are the 2 management phases of diabetes?

A
  • initial phase: tx with insulin is initiated, pt and family are taught the most essential skills to safely manage diabetes
  • second ongoing phase: family is given further education and support to optimize glycemic control and long term management
36
Q

What is important in initial management of diabetes?

A
  • education on disease process
  • insulin admin
  • blood glucose testing
  • testing for ketonuria (especially impt in young children, insulin pump users, or those with hx of DKA)
  • hypoglycemia
37
Q

What is important in ongoing management of diabetes?

A
  • diabetes team continues to provide care, teaching, and support to child and family. Sessions with individual team members allow more in depth education and care directed toward goal of maintaining excellent glucose control
  • during these sessions, concepts that are required for glycemic control are taught and reinforced. These include interaction of insulin, diet, and exercise on blood glucose concentrations. A management regimen specific for each pt is designed to achieve the best possible glucose control. In addition the clinician should explain that strict glycemic control helps to prevent long term sequelae of diabetesl discussion should be repeated and reinforced as often as necessary, particularly if glycemic control is suboptimal
  • as child grows older, education and training are directed toward increased autonomy and self-management for the pt
38
Q

Who is self monitoring blood glucose for?-

A
  • for all pts with DM who use insulin
  • most pts who take other glucose lowering meds
  • they should self monitor to assess glucose control, adjustments of insulin and diet, and timely intervention to avoid serious hypoglycemic events
39
Q

What is glycemic index?

A

term that describes what happens after consuming a carbohydrate-containing food and takes into account:
1) rise in plasma glucose levels (primarily looking at the peak)
2) the area under the curve for 2 hour period after food is consumed
- std reference value is based on:
usually glucose or white bread
all other foods are measured against this std
not a uniform system, so the impt thing to do is look at numbers relatively

40
Q

How do different foods affect plasma glucose?

A
  • different types of carb-containing foods affect plasma glucose in a variable way
    ex:
    glucose drinks results in plasma glucose levels rising rapidly
    an apple results in a much slower rise in plasma glucose level because of digestive process
41
Q

Therapeutic goals for glycemic control?

A 
- adults (non-pregnant)
goal of therapy: less than 7% A1C
action suggested if greater than 8%
- older adults (healthy) less than 7.5% no comorbidities, longer life expectancy
complex intermediate health less than 8%
very complex/poor health: less than 8.5%

pediatric pts:
13-19 years 7.5%
6-12 less than 8%
toddlers and preschoolers less than 8.5% but greater than 7.5%

42
Q

A1C therapeutic goals?

A
  • target goals must be individualized based on pt’s circumstances
  • kids more complex: growth and mealtime behaviors
  • some concerns about frequent hypoglycemia causing neurocognitive defects, so must balance against long term effects of hyperglycemia
43
Q

2 types of insulin replacement therapy?

A
  • fixed insulin dosing

- insulin pump therapy

44
Q

Insulin replacement therapy: multiple daily injections

A
  • MDI regimen combines a baseline level of insulin using a long acting insulin
  • with premeal/snack bolus of rapid or short acting insulin
  • pre meal and pre snack bolus doses of a rapid or short acting insulin are based on 3 factors:
    premeal blood glucose level
    estimated amount of carbs to be consumed
    expected level of exercise after the meal
  • insulin glargine (lantus) is long acting insulin. it usually has a duration of action of 20-24 hours, but the half life is shorter in some pts, requiring division of the daily dose into 2 injections per day/
45
Q

How does an insulin pump work?

A

insulin is housed inside pump called a reservoir

  • insulin travels into your body through flexible tube that ends with tiny needle inserted just under the skin
  • the needle is held in place by and infusion set, a little adhesive patch on the skin
46
Q

What should you cover in an annual medical hx on pts with DM?

A
  • age and characteristics of diabetes (DKA, routine lab eval)
  • prior A1C records
  • eating patterns, nutritional status, and wt history, growth and development in children and adolescents
  • diabetes education hx
  • review of previous tx programs
  • current tx of diabetes, including meds, meal plan,and results of glucose monitoring and pts use of data
  • exercise hx
  • DKA frequency, severity and cause
  • hypoglycemic episodes
  • any severe hypoglycemia, frequency, severity and cause
  • hx of diabetes related complications
  • microvascular: eye, kidney, nerve
  • macrovascular: cardiac, CVD, PAD
  • other: sexual dysfxn, gastroparesis
47
Q

What should you cover on the physical exam?

A
  • ht and wt
  • bp determination
  • funduscopic exam: refer to ophtho for annual exams
  • thyroid palpation
  • skin exam
  • neuro/foot exam:
    inspect, palpation of DP and PT pulses, patellar and achilles reflexes, proprioception, vibration, and sensation
  • monofilament testing annually if pt is older than 10 and if pt has complaints
48
Q

Lab eval at annual exam?

A
  • A1C ( q 3 months)
  • fasting lipid profile
  • LFTs
  • TSH
  • celiac disease screening (tTG q 2-3 years)
  • kidney profile (CMP or chem7):
    serum creatinine and claculated GFR, urine albumin to creatinine (annually), UA
49
Q

Who should you make referrals to during annual exam?

A 
endocrinologist
ophtho
dietician
diabetes educator
family planning for women of reproductive age
mental health
50
Q

Gestational diabetes?

A

2-10% of expectant mothers develop GD making it one of the most common health problems of pregnancy

  • insulin receptors don’t function properly
  • hormonal changes make cells less responsive to insulin: placenta produces larger quantities of more hormones than any other human organ: human placental lactogen, and estrogen and progesterone
51
Q

Pathophys of GD?

A
  • placenta supports baby as it grows
  • hormones from placenta block the action of the mother’s insulin leading to insulin resistance
    estrogen, cortisol, human placental lactogen (vital hormones in pregnancy preservation)
  • 2nd and 3rd trimester: mom needs 3x as much insulin as normal. Growing placenta continues with insulin resistance, leading to hyperglycemia in mom
  • usually occurs about 20th to 24th week of pregnancy
  • can be measured by 24th to 28th week (check at 28 weeks)
52
Q

Result of baby from increased insulin?

A
  • Mom’s insulin doesn’t cross the placenta and excess glucose from mom does
  • baby produces more insulin to counter extra glucose crossing the placenta
    this leads to macrosomia “fat” baby… increased birth weight
53
Q

What are the GD risk factors?

A
  • age: women over 25 are more likely to develop gestational diabetes
  • family or personal hx: chances increase if a close family member has type 2 diabetes
    gestational diabetes occurred in previous pregnancy
  • wt: being overweight before pregnancy (normal wt gain of pregnancy doesn’t cause GD)
54
Q

What is recommended for GD screening?

A
  • The ADA recommends that all pregnant women who have not been identified with glucose intolerance earlier in pregnacny be screened with a 50 g 1 hr GCT b/t 24 and 28 weeks of pregancy
  • in 2005: study showed that researchers screened pregnant women for GD and randomly assigned those with GD to receive aggressive or routine tx:
    the outcome was healthier babies and fewer childbirth complications for women who received aggressive tx - demonstrated the need to screen all mothers
55
Q

IF no risk factors what are the screening recommendations?

A 
- if no RFs: screening starts at 24-28 weeks, unless sxs occur prior:
increased thirst
increased urination
wt loss in spite of increased appetite
fatigue
N/V
blurred vision
56
Q

If women have risk factors GD screening recommendations?

A
  • screening at first prenatal visit and then again at 24-28 weeks
57
Q

Initial test for GD?

A
  • glucose challenge test (GCT)
  • this test doesn’t have to be fasting
  • 50 g of glucose orally (glucola)
  • wait 1 hr and have blood glucose level drawn
  • a value equal to or above 140 mg/dL should be used as the threshold level
  • blood glucose above 130 requires a 2nd test for dx: only about 1/3 of women who test + on glucose screen actually have GD
58
Q

2nd test for GD?

A
  • 3 hr glucose tolerance test
  • this test is done in AM after overnight fast
  • 100 g of glucose soln orally
  • blood glucose levels drawn at fasting, 1 hr, 2 hrs and 3 hrs
  • having at least 2 instance of abnormal blood glucose levels at any hour indicates gestational diabetes
  • some practitioners just do 3 hr fasting and use those results
positive results: (2 or more of the following)
fasting - greater than 95
1 hr - greater than 180
2 hrs greater than 155
3 hrs greater than 140
59
Q

Complications for the baby: macrosomia?

A
  • extra glucose can cross the placenta and end up in the baby’s blood
  • baby’s pancreas makes extra insulin to process the extra glucose, and this can cause the baby to grow too large (macrosomia)
  • for a full-term pregnancy, this means a birth weight of 4500 grams (9 lbs and 14 oz) or more
  • very large babies may have difficulty during delivery and are more likely to sustain birth injuries or be born by C- section
60
Q

Complications for baby - shoulder dystocia?

A
  • baby’s shoulders may be too big to move through the birth canal. This results in a potentially life-threatening obstetrical emergency, known as shoulder dystocia. In most cases, maneuvers can be performed to free the baby, but injuries may occur under the best of care.
  • this is rare but very serious complication of gestational diabetes
61
Q

Complications for the baby - hypoglycemia?

A
  • low blood sugar (hypoglycemia) shortly after birth
  • this happens because the baby is accustomed to receiving large amounts of glucose from the mother, and their own insulin production is high
  • these infants should have their blood sugar levels checked regularly after delivery. Tx this problem involves feeding right a way.
  • The baby may need a glucose solution through an IV line to prevent low blood sugar
62
Q

Jaundice (hyperbilirubinemia) - complications for baby?

A
  • perhaps due to high levels of insulin production which tend to produces extra RBCs in utero
  • after birth RBC’s break down = bilirubin
  • a heavy load for the newborn liver
  • usually isn’t a cause for concern, but should be carefully monitored in case it doesn’t go away
  • early and frequent nursing helps with bilirubin excretion
63
Q

Stillbirth or death - complications for baby?

A
  • if gestational diabetes goes undetected, a baby has an increased risk of stillbirth or death as a newborn
64
Q

Further complicatons for baby down the road if mother had GD?

A
  • babies are at risk for obesity as children

- increased susceptibility to type 2 diabetes as adults

65
Q

complications for mom due to GD?

A
  • preeclampsia: significant increase in BP, edema, proteinuria during pregnancy
  • polyhydramnios: excess amniotic fluid around the baby: can do ultrasound to check fluid level
  • operative delivery: (C-section) - due to baby with macrosomia, gestational diabetes isn’t reason to schedule C -section, GD c section rate b/t 25-30%, majority still deliver vaginally
66
Q

Long term complications for mom?

A
  • type 2 diabetes: predilection for development as moms get older
  • gestational diabetes in another pregnancy
67
Q

Tx of GD? initial therapy

A
  • control of blood sugar: starting with diet (medical nutrional therapy) and exercise -
    nutritional counseling: smaller meals, frequent snacks
    exercise: daily walking or swimming
  • self monitoring blood sugars
  • check urine for ketones
  • fetal monitoring to assess fetal status: ultrasound with amniotic fluid index, non-stress tests (fetal heart monitor) - 3 accelerations of 15 beats/min over the baby’s normal HR within a 20 min. period
68
Q

Tx of GD for women who don’t achieve adequate glycemic control with nutritional therapy and exercise alone?

A
  • tx with insulin: FBG is greater or = to 95 or
    if 1 hr postprandial BG is greater than 130 or 2 hr glucose is greater than 120 on 2 or more occasions within 1 week interval
  • insulin is first line rather than oral -hyperglycemic agents during pregnancy
  • glyburide is reasonable alt. for women who fail diet therapy and refuse to take, or are unable to comply with insulin therapy
69
Q

Optimal glycemic goals for gestational diabetes?

A
  • preprandial: less than 95 mg/dL
  • 1 hr post meal: less than 140 mg/dL
  • 2 hr post meal: less than 120 mg/dL
  • for women with pre-existing type 1 or 2 who become pregnant:
    pre-meal, bedtime, overnight glucose: 60-99 mg/dl
    peak post-prandial glucose: 100-129 mg/dL
  • HbA1C: less than 6.0%
70
Q

What should be done after delivery?

A
  • women with GD rarely require insulin in postpartum period. As insulin resistance quickly resolves, so does the need for insulin
  • need to check fasting and 2 hr postprandial glucose levels before hospital discharge
  • breastfeeding improves glycemic control and should be encouraged in women who had gestational diabetes
  • women with gestational diabetes should be tested for diabetes 6-8 weeks after delivery via fasting blood glucose measurements on 2 occasions or a 2 hour oral 75 g glucose tolerance test
71
Q

What should GD patients be educated about after delivery?

A
  • pts should be counseled about diet and exercise, by losing weight and exercising, women can significantly decrease their risk of developing diabetes
  • lifestyle changes
  • eating a balanced diet
  • regular exercise
  • maintaining correct wt for ht
72
Q

Diabetes is the leading cause of what 2 things?

A
  • leading cause of blindness and kidney disease
73
Q

Who does DM I usually affect?

A
  • kids and is life threatening which requires extensive pt and family education

Endocrinology (22 decks)

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