Type 1 DM Flashcards

1
Q

what should the color be for a urine dipstick if there is NO glucose in the urine?

A

blue

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2
Q

what should the color be for a urine dipstick if there is glucose in the urine?

A

dark brown

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3
Q

if fasting, what should blood sugar be?

A

70-100

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4
Q

if not fasting, what should blood sugar stay under?

A

126

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5
Q

is T1DM still considered juvenile DM?

A

NO!

-you can diagnose people up to the age of 30 with T1DM

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6
Q

age distribution for T1DM diagnosis

A

bimodal distribution for dx of T1DM:

  • 4-6 y/o
  • 10-14 y/o
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7
Q

what risk factors are playing together to make someone develop T1DM? (HINT: 3)

A

genetics, environmental trigger, immune system dysregulation

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8
Q

if you have a genetic risk for T1DM, does that mean you WILL get T1DM?

A

no, something has to trigger it (e.g., environmental trigger)

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9
Q

what genetic risk has the highest risk of getting T1DM?

A

monozygotic twin (30% risk)

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10
Q

environmental risk factors for T1DM?

A
  • viral infection (enterovirus)
  • immunizations
  • early intro of cow’s milk to kids diet (shouldn’t do until 12 months)
  • high SES
  • obesity (more T2DM)
  • vit D deficiency
  • perinatal (maternal age, preeclampsia, neonatal jaundice)
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11
Q

what are the classic symptoms of T1DM?

A

polyuria, polydipsia, weight loss, fatigue

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12
Q

glucagon fxn?

A

stimulates glycogenolysis & gluconeogenesis

-activated when blood sugar is low -> raises blood sugar

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13
Q

when do T1 diabetics show s/sx?

A

T1 diabetics will NOT show any signs or symptoms until 80% of beta-cells are destroyed
(reason why it is hard to know true onset of disease)

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14
Q

what type of reaction is T1DM?

A

immune mediated (T cell)

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15
Q

why do T1DM have polyuria?

A

increased urinary glucose excretion -> osmotic diuresis

  • blood sugar >180, kidneys spill out glucose into urine & water follows
  • water is going to where there is higher osmolarity (osmotic diuresis)
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16
Q

what does polyuria result in?

A

hypovolemia (dehydration)

-losing water -> hypovolemia -> feel thirsty -> polydipsia

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17
Q

what do T1DM have polydipsia?

A

have increased serum osmolality and hypovolemia

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18
Q

why do T1DM have weight loss?

A

have hypovolemia and increased catabolism

-catabolism = tissue breakdown -> weight loss

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19
Q

why do T1DM have fatigue?

A

if you don’t have the sugar in your cells to make energy, you will feel fatigued

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20
Q

what should you acquire in the medical hx besides the classic sx’s for T1DM?

A

blurry vision & frequent infections

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21
Q

why do T1DM get blurry vision?

A

when have hyperglycemia, the lens of the eye begins to swell and it distorts their vision
(correctable when treat their blood sugar)
-could also be result of long-term complication

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22
Q

why do T1DM get frequent infections?

A

immune system is dysregulated, blood sugar is higher, which bacteria love

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23
Q

what types of infections should you ask a T1DM about?

A

lung, ear, skin infections

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24
Q

what are the vitals like for T1DM?

A

BP - hypotension b/c of the hypovolemia

Tachycardia - blood volume goes down so pulse goes up

Weight loss/BMI

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25
Q

what should you check for with pts skin that is T1DM?

A

hydration status - check skin turgor/mucous membranes (mouth, lips)

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26
Q

T1DM and respiratory rate

A
  • high

- might smell ketones (fats that are breaking down - fruity or acetone smell)

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27
Q

T1DM and abdomen

A
  • abdominal pain can show up but has nothing to do with pathology in the body (has to do with metabolic decompensation)
  • metabolic acidosis -> abdominal pain (secondary to acidosis)
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28
Q

what do you gather on physical exam for T1DM?

A

vitals, general appearance, hydration status, resp rate, cardio, abdomen

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29
Q

T1DM differential dx

A
  • T2DM
  • Endocrine abnormalities (Cushing, growth-hormones excess, glucagon secreting tumors)
  • urinary tract infection
  • septic shock
  • medication (growth-hormone supplements, prednisone, thiazide diuretics, statins)
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30
Q

what medications can be on diff dx for T1DM?

A
  • growth-hormone supplements
  • PREDNISONE
  • thiazide diuretics (hydrocholorthiazide)
  • statins
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31
Q

what is diagnostic of T1DM?

A

A1c ≥ 6.5%

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32
Q

what are criteria to T1DM/T2DM?

A

Once of the following:

  • random blood glucose > 200mg/dL w/sx’s
  • fasting blood glucose of ≥ 126mg/dL
  • ≥200mg/dL on glucose tolerance test (for pregnancy)
  • A1c ≥ 6.5%
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33
Q

when is glucose toxic to your blood vessels?

A

Glucose is toxic to your blood vessels if it is outside of the 70-100 range

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34
Q

where must T1 diabetics go when newly diagnosed?

A

ED

  • Need to know if patient is in DKA or not (can’t just look at them and know)
  • must be done b/w their blood could be acidotic
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35
Q

what is the leading cause of morbidity and mortality in children with T1DM?

A

DKA

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36
Q

what is DKA?

A

ketones are being broken down and blood is beginning to turn acidotic

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37
Q

can you check sometimes urine to know if they are acidotic?

A

no

-but you can check for ketones in urine, but don’t know she’s acidotic from that

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38
Q

how do you diagnose DKA?

A
  • hyperglycemia (bs >200)
  • metabolic acidosis (ph<7.3 or bicarb<15)
  • ketosis (ketones in the urine means you have A LOT in the blood), can be ketosis even if ketones only in the blood
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39
Q

symptoms of DKA

A
  • vomiting, tachypnea
  • abdominal pain (from metabolic acidosis)
  • SOB
  • mental status changes (change in LOC)

*can look just like influenza/GI illness

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40
Q

does DKA need to be fixed quickly?

A

YES!

-can lead to cerebral edema

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41
Q

DKA assessment

A

vitals, weight, neuro

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42
Q

what’s the vitals like for DKA?

A

BP -> low
Peripheral pulses -> weak (diminished)
Pulse -> high

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43
Q

why do you need the weight of the patient in DKA?

A

need to calculate how to rehydrate them so need their weight

-will be 5-10% water deficit

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44
Q

why do you need to test neuro in DKA?

A

d/t risk of cerebral edema

-do full neuro assessment

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45
Q

Labs needed to be drawn for pt in DKA?

A
  • Blood glucose (<200, not in DKA)
  • ketones
  • electrolytes (Na & K)
  • consider lactate
  • BUN & Creatinine
  • venous pH
  • CBC
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46
Q

why do you need to measure pts lactate in DKA?

A

lactate released from tissue catabolism

47
Q

why do you need to measure pts BUN & Creatinine in DKA?

A

Looking for kidney failure

-dehydration put kidneys at risk (want to make sure not causing organ damage to kidneys)

48
Q

why do you need to measure pts venous pH in DKA?

A

acidosis

49
Q

why do you need to measure pts CBC in DKA?

A

for infection

-can precipitate DKA, make them go into hyperglycemic state

50
Q

what do you need to manage when pt in DKA?

A

dehydration, hyperglycemia, sodium, potassium

51
Q

how do you fix dehydration in DKA?

A
  • gradual rehydration with isotonic fluid
  • 10mL/kg over 1 hour (max 1000ml)
  • need to calculate pts weight
52
Q

how do you fix hyperglycemia in DKA?

A
  • Insulin infusion 0.1units/kg/hr

- once bs is <300 change fluids to contain glucose (5% dextrose nl saline)

53
Q

what do you need to do with sodium in DKA?

A
  • Na needs to be monitored the whole time

- as H2O moves into the cell, serum Na will rise

54
Q

will Na stay high in DKA after giving fluid?

A

no, once you give pt fluids the Na level will god down

-fix the dehydration and monitor the Na and you will see the Na go back to normal

55
Q

what’s the K level like in DKA & physiology?

A
  • typically a total body deficit, but levels vary

- physio: insulin drives K into cells (also glucose)

56
Q

what if pt has hyperkalemia, what do you do with insulin?

A

high K; ok to give insulin b/c K will go down to normal

57
Q

what if pt has normokalemia, what do you do with insulin?

A

normal K; if give insulin will cause hypokalemia, so must also give K with the insulin

58
Q

what if pt has hypokalemia, what do you do with insulin?

A

low K; give them K FIRST!!!, then follow it with insulin b/c you don’t want to the K to go so low they go into cardiac arrest

59
Q

what electrolytes is it important to monitor for pt in DKA?

A

sodium and potassium

60
Q

what other bloodworm should you do once T1DM diagnosis has been made?

A

T1DM antibodies, thyroid antibodies, & Celiac (anti-endomysial antibodies)

61
Q

what are the T1DM antibodies? (HINT: 3) & what are they causing?

A

anti-pancreatic antibodies:

(1) insulin
(2) GAD
(3) IA2

-they are causing the destruction

62
Q

does a person need to have all 3 T1DM antibodies?

A

no, can just have 1 or 2 or all 3

63
Q

what is the fxn of the insulin antibody?

A

antibody against physiologic insulin, so insulin stops working

64
Q

what is the fxn of the GAD antibody?

A

Glutamate decarboxylase

-enzyme that is produced by the beta cells and is attacking the beta cell itself

65
Q

what is the fxn of the IA2 antibody?

A

insulinoma autoantibody

-enzyme produced in the beta cell

66
Q

what can T1DM pts end up with in terms of thyroid?

A

hypothyroidism

  • TSH not helpful initially due to loss of metabolic control
  • when TSH is high, means hypothyroidism, but will be high b/c of metabolic derangement (don’t actually have hypothyroidism)
67
Q

what antibodies will be for celiac?

A

anti-endomysial antibodies & tissue transglutaminase antibodies

  • high risk pts will end up with this
  • ask about diarrhea when eating carbs
  • NOT affected by metabolic derangement
68
Q

when is glucagon used?

A

to raise glucose levels in emergency state of hypoglycemia (when pt is unconscious or can’t swallow)
-stick them with glucagon

69
Q

what can you give a pt that is in an emergency state of hypoglycemia besides glucagon?

A

a quick acting sugar

-don’t give chocolate if they can swallow b/c it’s SLOW ACTING

70
Q

is glucagon in a liquid form?

A

no!

-it’s a powder and liquid and must be mixed at time of need

71
Q

when should T1 diabetics check their blood sugar?

A

multiple times a day (every single time they are going to eat)
-need to know what their blood sugar is before taking insulin (if bs is too low and take insulin, then bs will go really low)

72
Q

lifestyle modifications for diabetes

A

nutrition counseling
-CARB counting & glycemic index

exercise

73
Q

what happens to glucose channels when exercising?

A

when exercise, open glucose channels that allow glucose into cell -> reduces glucose levels -> hypoglycemic

74
Q

when do you check ketones and why?

A

check ketones b/c worry about DKA

check when:

  • BS >300 - if BS >250-300 then check
  • sickness - increases risk of going into DKA
75
Q

what blood sugar is considered hypoglycemic?

A

<70

76
Q

sx’s of hypoglycemia

A
  • shaky
  • teeth chattering
  • dizzy
  • tired
77
Q

what are the most common reasons people who are T1 diabetics get hypoglycemic?

A
  • took prandial insulin and forgot to eat
  • over bloused -> too much insulin
  • exercise
78
Q

sx’s of hyperglycemia

A
  • irritable
  • tired
  • thirsty
  • going to bathroom frequently
  • HA
  • blurred vision
  • zoned out
79
Q

what are the physiologic causes of hyperglycemia? (HINT: 2)

A

Dawn phenomenon and Somogyi effect

80
Q

what is the Dawn phenomenon?

A
  • surge of hormones daily around 4-5am
  • result -> high bs in the morning
  • txt -> adjust overnight basal (increase it)
81
Q

what is the Somogyi effect?

A
  • if pt is low in the early morning hours -> hormones are released and overshoot the correction
  • 1-2am same hormones start to surge in response to hypoglycemia -> hyperglycemia in the morning
82
Q

how to fix the dawn phenomenon and somogyi effect?

A

have pt check their bs in the middle of the night
-if it’s normal, it’s the dawn phenomenon (adjust basal rate), if it’s low it’s the somogyi effect (pull back basal insulin)

83
Q

how many carbs should a person have at a meal and per day?

A

45-60 grams of carbs at a meal & 180g of carbs/day

84
Q

who is the ratio of insulin to carbs determined by?

A

the medical provider

85
Q

how many units of insulin for every ___ grams of carbs?

A

1 unit for every 15-20 grams of carbs, then you check bs and adjust if need to

(if on short-acting insulin and blood sugar is normal after 2 hours, you know it’s working)

86
Q

examples of 15 grams of carbs

A

4oz of fresh fruit

1 slice of bread

1/3 cup of pasta

8oz of milk

87
Q

what is a low glycemic index? examples?

A

0-54

whole wheat pasta/bread

88
Q

do you want a diabetic to have carbs that have a high or low glycemic index?

A

want them to have carbs that have a low glycemic index (0-54)

89
Q

why are carbs with low glycemic index good?

A
  • feel less hungry
  • provide you with more energy
  • lead to weight loss
  • provide a reduced risk of diabetes
90
Q

how often should diabetics get eyes checked?

A

every year

91
Q

why is it important for diabetes to care for their feet?

A

Prone to callus build up causing them to not walk properly -> increases risk of ulcer on feet -> infection problems

92
Q

what bloodwork should diabetic get?

A

renal bloodworm to make sure not kidney failure

93
Q

lipids and diabetics

A

DM’s at increased risk for CVD

94
Q

psych and diabetics

A

monitor b/c it’s hard to deal with everything to do to manage diabetes (chronic disease)

95
Q

complications of diabetes

A

diabetic neuropathy, peripheral neuropathy, nephropathy, skin complications

96
Q

non-proliferative diabetic reintopathy

A

initial manifestation of diabetic eye disease

  • dilation of small vessels
  • vascular closure -> ischemia -> increase permeability
97
Q

signs of non-proliferative diabetic reintopathy

A

microaneyursm, hemorrhages, “cotton wool” spots, lipid exudates

ASYMPTOMATIC!!!
(may see blurred vision if edema)

98
Q

proliferative diabetic retinopathy

A
  • abnormal vascular proliferation (neovascularization)
  • late stage
  • worse visual prognosis
  • tighter glucose control needed

(don’t want pt in proliferative stage, rather non-proliferative stage)

99
Q

should a diabetic ever go blind?

A

No diabetic should every go blind because we have laser surgery to treat them before it happens

100
Q

why does diabetic neuropathy occur?

A

Neuropathy occurs not only because the patient has diabetics for a long time, but because of the variability of glucose throughout the day (same for retinopathy)

-glucose is toxic to your cells & nerves don’t like it

101
Q

primary symmetrical sensory polyneuropathy

A
  • distal lower extremities
  • early impairment can begin in the pre diabetes state
  • starts in longest axons first
  • sensory loss ascends
102
Q

what is the pattern of the primary symmetrical sensory polyneuropathy?

A

“stocking-glove”

-begins in the hands and feet -> then calf’s, then fingers

103
Q

exam for primary symmetrical sensory polyneuropathy?

A

vibratory sensation loss; altered proprioception; impaired pain, light touch, and temperature; decreased reflexes

104
Q

if patient has neuropathy what can they not feel? how is it tested for?

A

vibration (it’s decreased)

-tested by putting tuning fork on pts ankle and see if they can feel the vibration

105
Q

proprioception and neuropathy?

A

proprioception is where your joint is in space
-Take one big toe and patient closes eyes and you move their toe up and down
Patient with neuropathy won’t be able to tell where their toe is in space

106
Q

light and sharp touch and neuropathy?

A

see if can tell difference – lose being able to over time

107
Q

reflexes and DM

A

reflexes diminish slowly overtime with DM

108
Q

nephropathy pathophysiology

A

Mesangial expansion, glomerular basement membrane thickening, podocyte injury, glomerular sclerosis

  • Kidneys getting damaged because of glucose getting excreted
  • Kidneys start to spill proteins (look for albumin)
109
Q

nephropathy s/s

A

Albuminuria

Sometimes hematuria

110
Q

T1DM and nephropathy

A

Up to 30% will have increased albuminuria after 15-year duration of T1D
-Less than half of these will progress to nephropathy

111
Q

Macrosomia

A

giant baby - occurs if glucose not controlled

112
Q

why does macrosomia occur/?

A

-increased glucose from the mother crosses the placenta
-insulin does NOT cause the placenta
-fetus makes more insulin which acts like growth factor and increases size of baby
(risk for delivering huge baby)

113
Q

if tightly control mothers blood sugar, what can you prevent?

A

macrosomia